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["Code","Preferred Name","Synonyms","Definition","Semantic Type"]
["C957","10-Deacetyltaxol","10-Deacetyltaxol|benzenepropanoic acid, beta-(benzoylamino)-alpha-hydroxy-, 12b-(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,6,11-trihydroxy-4a,8,13,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca(3,4)benz(1,2-b)oxet-9-yl ester, (2aR-(2aalpha,4beta,4abeta,6beta,9alpha(alphaR*,betaS*),11alpha,12alpha,12aalpha,12balpha))-","An analog of paclitaxel with antineoplastic activity.  10-Deacetyltaxol binds to and stabilizes the resulting microtubules, thereby inhibiting microtubule disassembly which results in cell- cycle arrest at the G2/M phase and apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C28780","117-126:FGF-5 Peptide","117-126:FGF-5 Peptide|Fibroblast Growth Factor-5 (117-126) Peptide","A fragment of fibroblast growth factor-5 (FGF-5). Originally isolated from a renal cell carcinoma cell line that overexpressed FGF-5, FGF-5:117-126 peptide is recognized by tumor infiltrating cytotoxic T lymphocytes. Overexpressed by several cancer cell types, this peptide is being tested as a potential target for antineoplastic immunotherapies. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C49172","11C Topotecan","11C Topotecan|11C topotecan","A semisynthetic derivative of camptothecin, a cytotoxic, quinoline-based alkaloid extracted from the Asian tree Camptotheca acuminata radiolabeled with carbon 11 (11C) with antineoplastic and radiotracer properties. During the S phase of the cell cycle, topotecan inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death. Quantitation of 11C topotecan accumulated in tumor tissues by positron emission tomography (PET) may help predict responses to topotecan therapy.","Indicator, Reagent, or Diagnostic Aid|Pharmacologic Substance"]
["C28781","11D10 AluGel Anti-Idiotype Monoclonal Antibody","11D10 AluGel Anti-Idiotype Monoclonal Antibody|TriAb","A monoclonal anti-idiotype antibody adsorbed to aluminum hydroxide gel (AluGel) with potential antineoplastic activity.  11D10 AluGel anti-idiotype monoclonal antibody mimics the human milk fat globule (HMFG) antigen found in breast and other cancers.  Vaccination with 11D10 AluGel anti-idiotype monoclonal antibody may induce a host antibody response against tumor cells positive for the HMFG antigen. (NCI04)","Immunologic Factor"]
["C41441","12-Allyldeoxoartemisinin","12-Allyldeoxoartemisinin","A semi-synthetic analogue of Artemisinin - a sesquiterpene lactone extracted from the dry leaves of Artemisia Annua (sweet wormwood) used as anti-malaria agent. Limited data is available on Artemisinin antineoplastic activity.","Chemical Viewed Functionally"]
["C2494","13-Deoxydoxorubicin","13-Deoxydoxorubicin|GPX-100","An analogue of the anthracycline antineoplastic antibiotic doxorubicin.  13-Deoxydoxorubicin intercalates DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.  This agent was designed to be a non-cardiotoxic anthracycline antibiotic.","Antibiotic|Organic Chemical"]
["C62553","14C BMS-275183","14C BMS-275183|[14C] BMS-275183","An orally bioavailable taxane compound, a C-4 methyl carbonate analogue of paclitaxel, labeled with radioactive carbon 14, with potential antineoplastic and radioimaging activities. BMS-275183 binds to tubulin and as a result inhibits microtubule disassembly or assembly. This leads to cell cycle arrest at the G2/M phase, thereby resulting in an inhibition of cell division and ultimately cell death. BMS-275183 may be useful for treating multi-drug resistant tumors as it does not appear to be a substrate for P-glycoprotein.","Indicator, Reagent, or Diagnostic Aid|Pharmacologic Substance"]
["C29796","2,6-Diaminopurine","1H-Purine-2,6-diamine|2,6-DIAMINOPURINE|2,6-Diaminopurine|9h-purine-2,6-diamine|DAP","One of a number of organic compounds that share a similar purine structure and possess antiviral and antitumor properties. 2,6-Diaminopurine nucleosides are versatile synthetic precursors for specific N-6 modifications of antiviral and antitumor agents. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide"]
["C126754","2,6-Dimethoxyquinone","2,5-Cyclohexadiene-1,4-Dione, 2,6-Dimethoxy- (9CI)|2,5-Cyclohexadiene-1,4-Dione, 2,6-Dimethoxy-|2,6-DMBQ|2,6-Dimethoxy-1,4-Benzoquinone|2,6-Dimethoxy-p-Benzoquinone|2,6-Dimethoxy-p-Quinone|2,6-Dimethoxybenzoquinone|2,6-Dimethoxycyclohexa-2,5-Diene-1,4-Dione|2,6-Dimethoxyquinone|p-Benzoquinone, 2,6-Dimethoxy-","A methoxy-substituted benzoquinone and bioactive compound found in fermented wheat germ extracts, with potential antineoplastic and immune-enhancing activity. 2,6-Dimethoxyquinone (2,6-DMBQ) inhibits anaerobic glycolysis thereby preventing cellular metabolism and inducing apoptosis. As cancer cells use the anaerobic glycolysis pathway to metabolize glucose and cancer cells proliferate at an increased rate as compared to normal, healthy cells, this agent is specifically cytotoxic towards cancer cells. In addition, 2,6-DMBQ exerts immune-enhancing effects by increasing natural killer (NK) cell and T-cell activity against cancer cells.","Organic Chemical"]
["C116618","2-Deoxy-D-glucose","2-DG|2-Deoxy-D-glucose|Deoxyglucose","A non-metabolizable glucose analog in which the hydroxyl group at position 2 of glucose is replaced by hydrogen, with potential glycolysis inhibiting and antineoplastic activities. Although the exact mechanism of action has yet to be fully elucidated, upon administration of 2-deoxy-D-glucose (2-DG), this agent competes with glucose for uptake by proliferating cells, such as tumor cells. 2-DG inhibits the first step of glycolysis and therefore prevents cellular energy production, which may result in decreased tumor cell proliferation.","Pharmacologic Substance"]
["C1165","2-Ethylhydrazide","2-Ethylhydrazide","A podophyllic acid derivative of podophyllotoxin, a substance extracted from the mandrake root Podophyllum peltatum.  Possessing potent antineoplastic properties, 2-ethylhydrazide binds to and inhibits topoisomerase II and its function in ligating cleaved DNA molecules, resulting in the accumulation of single- or double-strand DNA breaks, the inhibition of DNA replication and transcription, and apoptotic cell death.","Organic Chemical|Pharmacologic Substance"]
["C80036","2'-F-ara-deoxyuridine","1-(2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl) Uracil|1-(2'-deoxy-2'-fluoro-beta-D-arabinofuranosyl) uracil|1-(2-DEOXY-2-FLUORO-.BETA.-D-ARABINOFURANOSYL)URACIL|2'-F-ara-deoxyuridine|FAU","A deoxyuridine prodrug with potential antineoplastic activity. Upon cellular uptake, 2'-F-ara-deoxyuridine (FAU) is phosphorylated by thymidine kinase to FAU monophosphate and subsequently methylated in the 5'-position by thymidylate synthase (TS) to its activated form, 1-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl) 5-methyluracil monophosphate (FMAUMP). FMAUMP is incorporated into DNA leading to an inhibition of DNA synthesis and so cell growth. The catalytic activity of TS is critical to activation of FAU and subsequent incorporation into DNA. FAU may be beneficial in the case of tumors with high TS activity that are resistant to TS inhibitors.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C29794","2-Fluoroadenine","1H-Purin-6-amine, 2-fluoro- (9CI)|2-Fad|2-Fluoro-1H-purin-6-amine|2-Fluoroadenine|Adenine, 2-fluoro-|BRN 0610958|Purine, 6-amino-2-fluoro-|SRI 774","A fluorinated heterocyclic 2-ring compound. 2-fluoroadenine is the base moiety for many carbocyclic and acyclic nucleoside analogues, which may be used in antineoplastic studies.","Hazardous or Poisonous Substance"]
["C82408","2G-1 TCR Retroviral Vector-Transduced Lymphocytes","2G-1 TCR Retroviral Vector-Transduced Lymphocytes|PG13-A(F/K)-F-SGSG-T2a-B(opt)(2G-1 TCR) Retroviral Vector-Transduced Lymphocytes","A preparation of autologous human T-lymphocytes isolated from renal cell cancer (RCC) patient and transduced with 2G-1 TCR, a retroviral vector encoding the alpha and beta chains of a T-cell receptor that recognizes TNF-related apoptosis inducing ligand (TRAIL) bound to death receptor 4 (DR4), with potential immunostimulating and antineoplastic activities. After transduction, expansion in culture, and introduction into the RCC patient, 2G-1 TCR retroviral vector-transduced lymphocytes may stimulate a cytotoxic T lymphocyte (CTL) response against RCC cells with TRAIL bound to DR4 on their surfaces. TRAIL, a member of the TNF superfamily, is a homotrimeric type II membrane protein that rapidly induces oligomerization of receptor intracellular death domains and apoptosis in a variety of tumor cells when bound to its receptors; DR4 (TRAIL receptor 1), a member of the TNF receptor family, is overexpressed by a variety of malignant cell types.","Cell|Pharmacologic Substance"]
["C120474","2-Hydroxyestradiol","(17beta)-Estra-1,3,5(10)-Triene-2,3,17-Triol|2-HYDROXYESTRADIOL|2-Hydroxy-17beta-Estradiol|2-Hydroxyestradiol-17beta|2-Hydroxyestradiol|2-OH-E2|2-OH-Estradiol|2-OHE2","A metabolite formed during the metabolism of 17beta-estradiol by hydroxylation of the carbon at position 2 by the CYP450 enzymes 1A1/1A2. Theoretically, 2-hydroxyestradiol (2-OHE2) is able to undergo redox cycling, which generates active radicals and induces DNA damage; however, this estradiol metabolite is very unstable in vivo and is quickly inactivated by catechol-O-methyltransferase (COMT)-mediated O-methylation and converted to 2-methoxyestradiol (2-MeE2). 2-MeE2 exerts antineoplastic activities through its estrogen receptor antagonistic effect and the induction of apoptosis in susceptible cancer cells.","Organic Chemical"]
["C63947","2-Hydroxyestrone","1,3,5(10)-Estratrien-2,3-diol-17-one|2-HYDROXYESTRONE|2-Hydroxyestrone|2-OHE(1)|2-OHE1|Catecholestrone|Estra-1,3,5(1)-Trien-17-One, 2,3-Dihydroxy-","A metabolite formed during the catabolism of estrone by the liver through the hydroxylation of the carbon at position 2 by cytochrome P450 (CYP) enzymes, including CYP1A1 and 1A2, with potential anticarcinogenic activity. The mechanism of action for the antitumor activity of 2-hydroxyestrone is not known but this metabolic product has minimal estrogenic activity compared to the parent compound and other estrone metabolites. Additionally, O-methylation of this compound produces 2-methoxyestradiol (2-MeOE2), which is a potent inhibitor of both cell proliferation and angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C85482","2-Hydroxyflutamide Depot","2-Hydroxyflutamide Controlled-Release Formulation|2-Hydroxyflutamide Depot|Liproca","A depot formulation containing a bioresorbable, controlled-release, calcium sulphate-based paste of the nonsteroidal antiandrogen 2-hydroxyflutamide (2-HOF) with potential antineoplastic activity. Upon injection into the tumor site in the prostate, 2-hydroxyflutamide depot slowly releases 2-HOF, which competitively binds to androgen receptors (ARs), blocking the binding of dihydrotestosterone (DHT). This may inhibit androgen-dependent DNA and protein synthesis, resulting in tumor cell growth arrest and decreased cellular proliferation. In addition, 2-HOF inhibits nuclear uptake of androgen in androgen-responsive tissues.","Pharmacologic Substance"]
["C105401","2-Hydroxyoleic Acid","2-Hydroxyoleic Acid|2-OHOA|2OHOA|Minerval","An orally bioavailable, synthetic analog of the fatty acid oleic acid, with potential antitumor activity. Upon administration, 2-hydroxyoleic acid (2OHOA) activates sphingomyelin synthase (SMS), thereby increasing the concentration of sphingomyelin (SM) and diacylglycerol (DAG) in the tumor cell membrane and decreasing membrane levels of phosphatidylethanolamine (PE) and phosphatidylcholine (PC). This restores the normal, healthy levels and ratios of membrane lipids. By restoring normal membrane lipid structure and composition, this agent inhibits membrane-protein associated signaling and the aberrant activity of signaling pathways in certain tumor cells, including the Ras/MAPK and PI3K/AKt pathways. This inhibits tumor cell proliferation, induces tumor cell differentiation, and eventually can cause cell death.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C965","2-Methoxyestradiol","(17beta)-2-Methoxyestra-1,3,5(10)-triene-3,17-diol|2-METHOXYESTRADIOL|2-MeE2|2-MeOE2|2-Methoxy Estradiol|2-Methoxyestradiol|2-methoxyestradiol|2ME2|Panzem","An orally bioavailable estradiol metabolite with potential antineoplastic activity.  2-Methoxyestradiol inhibits angiogenesis by reducing endothelial cell proliferation and inducing endothelial cell apoptosis.  This agent also inhibits tumor cell growth by binding to tubulin, resulting in antimitotic activity, and by inducing caspase activation, resulting in cell cycle arrest in the G2 phase, DNA fragmentation, and apoptosis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C62603","2-Methoxyestradiol Nanocrystal Colloidal Dispersion","2-Methoxyestradiol Nanocrystal Colloidal Dispersion|Panzem NCD","An orally bioavailable liquid formulation containing the small molecule 2-methoxyestradiol with potential antineoplastic activity. 2-Methoxyestradiol, a naturally occurring estradiol metabolite, exerts its antitumor effect by inhibiting endothelial cells as well as tumor cells through multiple mechanisms. This agent binds to tubulin and disrupts microtubule formation, thereby preventing mitosis and subsequent cellular proliferation. In addition, 2-methoxyestradiol induces caspase activation, resulting in cell cycle arrest in G2 phase and apoptosis in due course. This agent also down-regulates hypoxia inducible factor-one alpha (HIF-1a). The nanocrystal colloidal dispersion increases the absorption of 2-methoxyestradiol, thereby improving its bioavailability, which results in enhanced drug plasma levels.","Organic Chemical|Pharmacologic Substance"]
["C120472","2-Methoxyestrone","2-MeE1|2-MeOE1|2-Methoxyestrone|2-OMeE1|3-Hydroxy-2-Methoxyestra-1,3,5(10)-Trien-17-One","A metabolite formed during the methylation of 2-hydroxyestrone (2-OHE1) by catechol-O-methyltransferase (COMT), with potential anticarcinogenic and minimal estrogen activities. The mechanism of action for the antitumor activity of 2-methoxyestrone (2-OMeE1) is not known. A high 2-methoxyestrone (2-OMeE1)/2-OHE1 ratio indicates higher methylation efficiency and correlates with a lower cancer risk.","Organic Chemical"]
["C99130","2-O, 3-O Desulfated Heparin","2-O, 3-O Desulfated Heparin|CX 01|CX-01|CX01|O-desulfated Heparin|ODSH|PGX-100|PGX-ODSH|PGX100","A heparin derivative in which the 2-O and 3-O sulfate groups of heparin are removed and that lacks anticoagulant activity, with potential anti-inflammatory, immodulatory and antineoplastic activities. Upon administration, 2-O, 3-O desulfated heparin (ODSH) binds to both chemokine stromal cell-derived factor 1 (SDF-1 or CXCL12) and CXC chemokine receptor 4 (CXCR4). This prevents the interaction of CXCL12 with CXCR4, blocks CXCR4 activation, and may result in decreased proliferation and migration in CXCR4-overexpressing tumor cells. In addition, inhibition of CXCL12/CXCR4 interaction may induce mobilization of hematopoietic cells from the bone marrow into the blood.  In addition, ODSH prevents the interaction of the receptor for advanced glycation end-products (RAGE) with its ligands, including advanced glycation end-products (AGEs), Mac-1(CD11b/CD18), the nuclear pro-inflammatory protein high mobility group box protein-1 (HMGB-1), carboxymethyl lysine-bovine serum albumin (CML-BSA) and members of the S100 calgranulin family. In addition, this agent inhibits the enzymes heparanase, cathepsin G, and human leukocyte elastase, which are involved in inflammation and metastasis. ODSH also binds to platelet factor 4 (PF4 or CXCL4) and may prevent PF4's inhibitory effect on platelet production.  Altogether, this may inhibit tumor cell invasiveness and metastasis. ODSH also binds to platelet factor 4 (PF4 or CXCL4) and may prevent PF4's inhibitory effect on platelet production. This may increase platelet production. Unlike heparin, this agent does not induce heparin-induced thrombocytopenia (HIT). RAGE, a receptor belonging to the immunoglobulin superfamily, plays a key role in inflammation and is overexpressed in a variety of cancers. CXCR4 is a chemokine receptor belonging to the G protein-coupled receptor (GPCR) family that plays an important role in chemotaxis, chemoresistance and angiogenesis, and is upregulated in several tumor cell types. The interaction between CXCL12/CXCR4 induces retention of hematopoietic cells in the bone marrow.","Pharmacologic Substance"]
["C29475","3'-C-ethynylcytidine","1-(3-C-ethynyl-beta-D-ribo-pentofuranosyl)cytosine|3'-C-Ethynylcytidine|3'-C-ethynylcytidine|ECdy|ECyd|TAS-106","A synthetic cytidine nucleoside containing a covalently bound ethynyl group with potential antineoplastic and radiosensitizing activities. 3'-C-ethynylcytidine is metabolized in tumor cells to ethynylcytidine triphosphate (ECTP), which inhibits RNA synthesis by competitive inhibition of RNA polymerases I, II and III; subsequently, RNase L is activated, resulting in apoptosis. RNase L is a potent antiviral and antiproliferative endoribonuclease that cleaves singled stranded RNA, causes 28s rRNA fragmentation, and activates Janus Kinase (JAK), a mitochondrial-dependent apoptosis signaling molecule.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C116619","4-1BB Agonist Monoclonal Antibody PF-05082566","4-1BB Agonist Monoclonal Antibody PF-05082566|PF-05082566|PF-2566","A fully human, agonistic immunoglobulin (Ig) G2 monoclonal antibody (mAb) targeting 4-1BB (CD137, TNFRSF9), with potential immunostimulating activity. Upon administration, PF-05082566 binds to and activates 4-1BB expressed on various immune cells, such as CD8-positive and CD4-positive T cells and natural killer (NK) cells. This enhances 4-1BB-mediated signaling, induces cytokine production and promotes anti-tumor immune responses. 4-1BB, a member of the tumor necrosis factor (TNF)/nerve growth factor (NGF) family of receptors, plays an important role in the regulation of immune responses.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C123823","4H11-28z/fIL-12/EGFRt-expressing Autologous T-lymphocytes","4H11-28z/fIL-12/EFGRt+ Genetically-modified T Cells|4H11-28z/fIL-12/EFGRt+ T Cells|4H11-28z/fIL-12/EGFRt-expressing Autologous T-lymphocytes|Autologous 4H11-28z/fIL-12/EFGRt+ Genetically-modified T Cells|Autologous HLA-A2/NY-ESO-1-specific TCR Gene-transduced T-lymphocytes|Autologous MUC16ecto-targeting EGFR-secreting T Lymphocytes","A preparation of genetically modified autologous T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) targeting the human tumor-associated antigen (TAA) MUC16ecto and encoding the human pro-inflammatory cytokine interleukin-12 (IL-12), fused to the signaling domain of the zeta chain of the TCR/CD3 complex (28z), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, 4H11-28z/fIL-12/EGFRt-expressing autologous T-lymphocytes are directed to and induce selective toxicity in MUC16-expressing tumor cells. In addition, the T-cells secrete IL-12 which induces secretion of interferon-gamma, promotes the activation of natural killer cells (NKs), and induces cytotoxic T-cell responses against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T-cells and can promote elimination of those cells through a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. MUC16, a transmembrane protein and glycosylated mucin, is overexpressed on the cell surface of the majority of ovarian cancer cells but not on healthy cells. MUC16ecto is the extracellular portion of MUC-16 and is the part that is retained by cells after cleavage of CA-125.","Cell|Pharmacologic Substance"]
["C977","4-Nitroestrone 3-Methyl Ether","4-Nitroestrone 3-Methyl Ether|4-Nitroestrone 3-methyl ether|4-Nitroestrone","A synthetic derivative of estradiol. 4-nitroestrone 3-methyl ether inhibits estrogen sulfotransferase (EST), a progesterone-induced secretory endometrial enzyme which affects estrogen receptor levels.  This agent has been shown to be an effective growth inhibitor of some chemically induced animal mammary tumors. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C91722","4-Peptide Melanoma Vaccine","4-Peptide Melanoma Vaccine","An emulsion of 4 melanoma peptides with potential immunomodulating and antineoplastic activities. Upon vaccination, 4-peptide melanoma vaccine may stimulate an immune response against 4 different melanoma associated antigens. This may lead to a reduction in tumor cell proliferation of cancer cells expressing these antigens.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C121828","4-Thio-2-deoxycytidine","4'-Thio-2'-deoxycytidine|4-Thio-2-deoxycytidine|T-dCyd|TdCyd","An orally bioavailable 4-thio modified 2-deoxycytidine analog, with potential antineoplastic activity. Upon administration of 4-thio-2-deoxycytidine (TdCyd), this cytidine analog gets incorporated into DNA during replication and inhibits the activity of DNA methyltransferase 1 (DNMT1), which blocks DNA hypermethylation. This results in DNMT1 depletion, hypomethylation of DNA, and the reactivation of tumor suppressor genes that were silenced by hypermethylation; this results in antitumor activity and an inhibition of tumor cell proliferation.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C62785","5-Fluoro-2-Deoxycytidine","5-FLUORO-2'-DEOXYCYTIDINE|5-Fluoro-2-Deoxycytidine|5-fluoro-2-deoxycytidine|Cytidine, 2'-deoxy-5-fluoro-|FdCyd|Ro 5-1090","An antimetabolite consisting of a fluorinated pyrimidine analog with potential antineoplastic activity. As a prodrug, 5-fluoro-2-deoxycytidine is converted by intracellular deaminases to the cytotoxic agent 5-Fluorouracil (5-FU). 5-FU is subsequently metabolized to active metabolites including 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). FdUMP binds to and inhibits thymidylate synthase, thereby reducing the production of thymidine monophosphate, which leads to depletion of thymidine triphosphate. This inhibits DNA synthesis and cell division. FUTP competes with uridine triphosphate for incorporation into the RNA strand thus leading to an inhibition of RNA and protein synthesis. Other fluorouracil metabolites also get incorporated into both DNA and RNA, thereby further hampering cellular growth.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C80039","6,8-Bis(benzylthio)octanoic Acid","6,8-BIS(BENZYLTHIO)OCTANOIC ACID|6,8-Bis(benzylthio)octanoic Acid|Alpha-Lipoic Acid Analogue CPI-613|CPI 613|CPI-613","A racemic mixture of the enantiomers of a synthetic alpha-lipoic lipoic acid analogue with potential chemopreventive and antineoplastic activities. Although the exact mechanism of action is unknown, 6,8-Bis(benzylthio)octanoic acid has been shown to inhibit metabolic and regulatory processes required for cell growth in solid tumors. Both enantiomers in the racemic mixture exhibit antineoplastic activity.","Organic Chemical|Pharmacologic Substance"]
["C113787","6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatases Isoform 3 Inhibitor ACT-PFK-158","6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatases Isoform 3 Inhibitor ACT-PFK-158|ACT-PFK-158|PFK-158|PFKFB3 Inhibitor PFK-158","An inhibitor of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFK-2/FBPase) isoform 3 (PFKFB3) and derivative of 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO), with potential antineoplastic activity. Upon administration, PFKFB3 inhibitor PFK-158 binds to and inhibits the activity of PFKFB3, which leads to the inhibition of both the glycolytic pathway in and glucose uptake by cancer cells. This prevents the production of macromolecules and energy that causes the enhanced cellular proliferation in cancer cells as compared to that of normal, healthy cells. Depriving cancer cells of nutrients and energy leads to the inhibition of cancer cell growth. PFKFB3, an enzyme that catalyzes the conversion of fructose-6-phosphate to fructose-2,6-bisphosphate, is highly expressed and active in human cancer cells; it plays a key role in increasing both glycolytic flux in and proliferation of cancer cells.","Pharmacologic Substance"]
["C1730","714-X","714-X|Camphorminium Chloride|Trimethylbicyclonitraminoheptane Chloride","A product elaborated and marketed by the private Canadian laboratory. 714-X contains trimethylbicyclonitraminoheptane chloride, a nitrogenated camphor-derivative, and mineral salts in ethanol. It is claimed to cure cancer, multiple sclerosis, fibromyalgia, AIDS and other diseases by improving the body's immune function. Few inconclusive animal studies and no human trials were conducted with the product. There is no scientific evidence that 714-X is effective in treating any type of disease. It has not been proven to be safe or effective for any use. 714-X is banned by FDA for use in the USA. In Canada 714-X is legally available on compassionate grounds only through a licensed physician.","Organic Chemical|Pharmacologic Substance"]
["C1611","7-Cyanoquinocarcinol","(+)-DX 52-1|7-Cyanoquinocarcinol|DX 52-1|DX-52-1","A semisynthetic analogue of the Streptomyces melanovinaceus-derived tetracyclic antitumor antibiotic quinocarmycin with potential antineoplastic activity. Quinocarmycin belongs to the naphthyridinomycin/saframycin class of antitumor antibiotics. These antibiotics appear to act through DNA alkylation.","Antibiotic|Organic Chemical"]
["C61618","7-Ethyl-10-Hydroxycamptothecin","7-ETHYL-10-HYDROXYCAMPTOTHECIN|7-Ethyl-10-Hydroxycamptothecin|7-Ethyl-10-hydroxy-20(S)-camptothecin|SN 38|SN-38",null,"Pharmacologic Substance"]
["C1271","7-Hydroxystaurosporine","(+)-UCN-01|2,3,9,10,11,12-Hexahydro-3-hydroxy-9-methoxy-8-methyl-10-(methylamino)-8,12-epoxy-1H,8H-2,7b,12a-triazadibenzo(a,g)cyclonona(cde)triinden-1-one|7-HYDROXYSTAUROSPORINE|7-Hydroxy-staurosporine|7-Hydroxystaurosporine|8,12-Epoxy-1H,8H-2,7b,12a-triazadibenzo[a, g]cyclonona[cde] Trinden-1-one, 2,3,9,10,11, 12-hexahydro-3-hydroxy-9-methoxy-8-methyl-10-(methylamino)|UCN-01","A synthetic derivative of staurosporine with antineoplastic activity. 7-hydroxystaurosporine inhibits many phosphokinases, including the serine/threonine kinase AKT, calcium-dependent protein kinase C, and cyclin-dependent kinases. This agent arrests tumor cells in the G1/S of the cell cycle and prevents nucleotide excision repair by inhibiting the G2 checkpoint kinase chk1, resulting in apoptosis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C28788","8-Azaguanine","5-Amino-1,4-dihydro-7H-1,2,3-triazolo(4,5-d)pyrimidin-7-one|5-Amino-1H-v-triazolo(d)pyrimidin-7-ol|5-Amino-7-hydroxy-1H-v-triazolo(d)pyrimidine|8 AG|8-AZAGUANINE|8-Azaguanine|Guanazolo|Pathocidin|SF-337|SK 1150|Triazologuanine","A purine analogue with potential antineoplastic activity.  8-Azaguanine interferes with the modification of transfer ribonucleic acid (tRNA) by competing with guanine for incorporation into tRNA catalyzed by the enzyme tRNA-guanine ribosyltransferase (tRNA-guanine transglycosylase).  Altered guanine modification of tRNA has been implicated in cellular differentiation and neoplastic transformation.  8-Azaguanine also inhibits the formation of 43S and 80S initiation complexes, thereby interfering with initiation of translation and inhibiting protein synthesis.  This agent inhibits tumor cell growth and stimulates cell differentiation. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C28789","9-Ethyl 6-Mercaptopurine","9-Ethyl 6-MP|9-Ethyl 6-Mercaptopurine","A synthetic alkyl derivative prodrug of the antineoplastic agent 6-mercaptopurine (6-MP).  In vivo, 9-ethyl 6-mercaptopurine appears to be converted to 6-MP, which substitutes for the normal nucleoside and fraudulently incorporates into DNA and inhibits de novo purine synthesis, thereby inducing cell death. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C28793","9H-Purine-6Thio-98D","9H-Purine-6Thio-98D","An antimetabolite analogue of purine with antineoplastic and immuno-suppressant properties.  9H-Purine-6Thio-98D substitutes for the normal nucleoside and fraudulently incorporates into DNA and inhibits de novo purine synthesis, thereby inducing cell death. In vivo, this agent, also known as 6MP-arabinoside, may occur as a metabolite of the antineoplastic agent mercaptopurine. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C2048","A-65","A-65","An amide analogue of Trichostatin A studied for potential antineoplastic activity.  A-65 inhibits zinc-dependent histone deacetylase, inducing terminal cell differentiation and anti-angiogenic activity. (NCI04)","Pharmacologic Substance"]
["C26449","Abagovomab","ABAGOVOMAB|Abagovomab|Monoclonal Antibody ACA125 Anti-Idiotype Vaccine|VaccinOvar","A murine IgG1 monoclonal anti-idiotype antibody, containing a variable antigen-binding region that functionally mimics the three-dimensional structure of a specific epitope on the ovarian cancer tumor-associated antigen CA-125, with potential antineoplastic activity. With a variable antigen-binding region that acts as a surrogate antigen for CA-125, abagovomab may stimulate the host immune system to elicit humoral and cellular immune responses against CA-125-positive tumor cells, resulting in inhibition of tumor cell proliferation.","Immunologic Factor|Pharmacologic Substance"]
["C2015","Abarelix","ABARELIX|Abarelix|PPI-149|Plenaxis|R-3827|abarelix","A synthetic decapeptide and antagonist of naturally occurring gonadotropin-releasing hormone (GnRH). Abarelix directly and competitively binds to and blocks the gonadotropin releasing hormone receptor in the anterior pituitary gland, thereby inhibiting the secretion and release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone.  As a result, this may relieve symptoms associated with prostate hypertrophy or prostate cancer, since testosterone is required to sustain prostate growth.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C120556","ABBV-221","ABBV-221","An intravenously-administered agent capable of modulating the activity of epidermal growth factor receptor (EGFR), with potential antineoplastic activity.","Pharmacologic Substance"]
["C97660","Abemaciclib","2-Pyrimidinamine, N-(5-((4-ethyl-1-piperazinyl)methyl)-2-pyridinyl)-5-fluoro-4-(4-fluoro-2-methyl-1-(1-methylethyl)-1H-benzimidazol-6-yl)|ABEMACICLIB|Abemaciclib|LY-2835219|LY2835219","An orally available cyclin-dependent kinase (CDK) inhibitor that targets the CDK4 (cyclin D1) and CDK6 (cyclin D3) cell cycle pathway, with potential antineoplastic activity. Abemaciclib specifically inhibits CDK4 and 6, thereby inhibiting retinoblastoma (Rb) protein phosphorylation in early G1. Inhibition of Rb phosphorylation prevents CDK-mediated G1-S phase transition, thereby arresting the cell cycle in the G1 phase, suppressing DNA synthesis and inhibiting cancer cell growth. Overexpression of the serine/threonine kinases CDK4/6, as seen in certain types of cancer, causes cell cycle deregulation.","Pharmacologic Substance"]
["C68920","Abexinostat","2-benzofurancarboxamide, 3-((dimethylamino)methyl)-n-(2-(4-((hydroxyamino)carbonyl)phenoxy)ethyl)-|3-((dimethylamino)methyl)-N-(2-(4-(hydroxycarbamoyl)phenoxy)ethyl)-1-benzofuran-2-carboxamide|ABEXINOSTAT|Abexinostat|CRA-024781|HDAC Inhibitor PCI-24781|PCI-24781","A broad-spectrum phenyl hydroxamic acid inhibitor of histone deacetylase (HDAC) with potential antineoplastic activity. Abexinostat inhibits several isoforms of HDAC, resulting in an accumulation of highly acetylated histones, followed by the induction of chromatin remodeling; the selective transcription of tumor suppressor genes; and the tumor suppressor protein-mediated inhibition of tumor cell division and induction of tumor cell apoptosis. In addition, this agent has been shown to inhibit homologous recombination (HR) activity by inhibiting the expression of RAD51. RAD51, a homologue of bacterial RecA, assists in the repair of DNA double-strand breaks (DSBs).","Organic Chemical|Pharmacologic Substance"]
["C77333","Abiraterone","17-(3-Pyridyl)androsta-5,16-dien-3beta-ol|ABIRATERONE|Abiraterone|CB 7598","A steroidal compound with antiandrogen activity. Abiraterone inhibits the enzymatic activity of steroid 17alpha-monooxygenase (17alpha-hydrolase/C17,20 lyase complex; CYP17A1), a member of the cytochrome p450 family that catalyzes the 17alpha-hydroxylation of steroid intermediates involved in testosterone synthesis. Administration of this agent may suppress testosterone production by both the testes and the adrenals to castrate-range levels.","Pharmacologic Substance"]
["C68845","Abiraterone Acetate","17-(3-Pyridyl)-5,16-androstadien-3beta-acetate|ABIRATERONE ACETATE|Abiraterone Acetate|Androsta-5,16-dien-3-ol, 17-(3-pyridinyl)-, acetate (ester), (3beta)-|CB7630|Zytiga|abiraterone acetate","An orally active acetate salt of the steroidal compound abiraterone with antiandrogen activity. Abiraterone inhibits the enzymatic activity of steroid 17alpha-monooxygenase (17alpha-hydrolase/C17,20 lyase complex), a member of the cytochrome p450 family that catalyzes the 17alpha-hydroxylation of steroid intermediates involved in testosterone synthesis. Administration of this agent may suppress testosterone production by both the testes and the adrenals to castrate-range levels.","Organic Chemical|Pharmacologic Substance"]
["C37447","ABT-510","ABT-510","A synthetic peptide that mimics the anti-angiogenic activity of the endogenous protein thrombospondin-1 (TSP-1).  ABT-510 inhibits the actions of several pro-angiogenic growth factors important to tumor neovascularization; these pro-angiogenic growth factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF)), hepatocyte growth factor (HGF), and interleukin 8 (IL-8). (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2679","ABT-751","ABT-751|E7010|N-[2-[(4-Hydroxyphenyl)amino]-3-pyridinyl]-4-methoxybenzenesulfonamide","An orally bioavailable antimitotic sulfonamide. ABT- 751 binds to the colchicine-binding site on beta-tubulin and inhibits the polymerization of microtubules, thereby preventing tumor cell replication. This agent also disrupts tumor neovascularization, reducing tumor blood flow and so inducing a cytotoxic effect. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C99901","Acai Berry Juice","Acai Berry Juice|Acai Juice|Açai Berry Juice|Açai Juice","A juice product obtained from the fruit of the acai palm tree (Euterpe oleracea) with anti-inflammatory, antioxidant and potential chemopreventive activities. Besides high amounts of vitamins, minerals and fatty acids, acai berry is rich in phytonutrients such as anthocyanins and flavones which are potent scavengers of reactive oxygen species. The fruit also contains high amounts of the flavone velutin which exhibits potent anti-inflammatory properties. Velutin is able to inhibit the degradation of the inhibitor of nuclear factor kappa-B (NF-kB), thereby blocking the activation of NF-kB, as well as inhibiting phosphorylation of mitogen-activated protein kinase p38 and JNK. Inhibition of these processes results in suppression of the production of proinflammatory cytokines, such as tumor necrosis factor alpha and interleukin 6.","Pharmacologic Substance"]
["C113442","Acalabrutinib","ACALABRUTINIB|ACP-196|Acalabrutinib|Benzamide, 4-(8-Amino-3-((2S)-1-(1-oxo-2-butyn-1-yl)-2-pyrrolidinyl)imidazo(1,5-a)pyrazin-1-yl)-N-2-pyridinyl-|Bruton Tyrosine Kinase Inhibitor ACP-196","An orally available inhibitor of Bruton's tyrosine kinase (BTK) with potential antineoplastic activity. Upon administration, acalabrutinib inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.","Pharmacologic Substance"]
["C984","Aceglatone","ACEGLATONE|Aceglatone|Glucaron","A derivative of D-glucaro-1, 4-lactone with chemopreventive and anti-tumor activities. One of the key processes in which human body eliminates toxic chemicals as well as hormones (such as estrogen) is by glucuronidation. When beta-glucuronidase deconjugates these glucuronides, it prolongs the stay of the hormone or toxic chemical in the body. Elevated beta-glucuronidase activity has been implicated to be associated with an increased risk for hormone-dependent cancers like breast, prostate, and colon cancers. Thereby, aceglatone may suppress the developments of hormone-dependent cancers mediated through beta-glucuronidase inhibition.","Organic Chemical|Pharmacologic Substance"]
["C200","Acetylcysteine","ACETYLCYSTEINE|Acetadote|Acetylcysteine|Airbron|Broncholysin|Brunac|Fabrol|Fluatox|Fluimucetin|Fluimucil|Fluprowit|L-Alpha-acetamido-beta-mercaptopropionic Acid|Muco Sanigen|Mucocedyl|Mucolator|Mucolyticum|Mucomyst|Mucosolvin|Mucret|N-Acetyl Cysteine|N-Acetyl-L-cysteine|N-Acetylcysteine|N-acetyl-3-mercaptoalanine|N-acetyl-L-cysteine|N-acetylcysteine|NAC|Neo-Fluimucil|Parvolex|Respaire|Tixair|acetylcysteine","A synthetic N-acetyl derivative of the endogenous amino acid L-cysteine, a precursor of the antioxidant enzyme glutathione.  Acetylcysteine regenerates liver stores of glutathione. This agent also reduces disulfide bonds in mucoproteins, resulting in liquification of mucus.  Some evidence suggests that acetylcysteine may exert an anti-apoptotic effect due to its antioxidant activity, possibly preventing cancer cell development or growth.  In addition, acetylcysteine has inhibited viral stimulation by reactive oxygen intermediates, thereby producing antiviral activity in HIV patients. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C985","Acitretin","(All-E)-9-(4-Methoxy-2,3,6-trimethylphenyl)-3,7-dimethyl-2,4,6,8-nonatetraenoic Acid|ACITRETIN|Acitretin|Etretin|Neotigason|Ro 10-1670|Ro-10-1670|Soriatane|Trimethylmethoxyphenyl-retinoic acid|acitretin","An orally-active metabolite of the synthetic aromatic retinoic acid agent etretinate with potential antineoplastic, chemopreventive, anti-psoratic, and embryotoxic properties.  Acitretin activates nuclear retinoic acid receptors (RAR), resulting in induction of cell differentiation, inhibition of cell proliferation, and inhibition of tissue infiltration by inflammatory cells.  This agent may also inhibit tumor angiogenesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C986","Acivicin","(S-(R*,R*))-4,5-Dihydro-alpha-amino-3-chloro-5-isoxazoleacetic Acid|ACIVICIN|AT-125|Acivicin|U-42126","A modified amino acid and structural analog of glutamine.  Acivicin inhibits glutamine amidotransferases in the purine and pyrimidine biosynthetic pathways, thereby inhibiting tumor growth in cell lines dependent on glutamine metabolism. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1861","Aclacinomycin B","1-Naphthacenecarboxylic acid, 2-ethyl-1,2,3,4,6,11-hexahydro-2,5,7-trihydroxy-6,11-dioxo-4-((2,3,6-trideoxy-3-(dimethylamino)-alpha-L-lyxo-hexapyranosyl)oxy)-, methyl ester,(1R-(1-alpha,2-beta,4-beta))-|Aclacinomycin B|Aclarubicin B|Antibiotic MA 144B1","An antineoplastic oligosaccharide anthracycline antibiotic isolated from the bacterium Streptomyces galilaeus.  Aclacinomycin B intercalates into DNA and inhibits both the topoisomerase I and II enzymes, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis.","Antibiotic|Organic Chemical"]
["C202","Aclarubicin","(1R,2R,4S)-2-ethyl-1,2,3,4,6,11-hexahydro-2,5,7-trihydroxy-6,11-dioxo-4-[[2,3,6-trideoxy-4-O-[2,6-dideoxy-4-O-[(2R,trans)-tetrahydro-6-methyl-5-oxo-2H-pyran-2-yl]-alpha-L-lyxo-hexopyranosyl]-3-(dimethylamino)-alpha-L-lyxo-hexopyranosyl]oxy]-1-naphthacenecarboxylic acid methyl ester|1-naphthacenecarboxylic acid, 2-ethyl-1,2,3,4,6,11-hexahydro-2,5, 7-trihydroxy-6,11-dioxo-4-[[2,3,6-trideoxy-4-O-[2,6-dideoxy-4-O-((2R-trans)-tetrahydro-6-methyl-5-oxo-2H-pyran-2-yl) -alpha-L-lyxo-hexopyranosyl]-3-(dimethylamino)-alpha-L-lyxo-hexopyranosyl]oxy]-, methyl ester,(1R-(1alpha,2beta,4beta))-(9CI)|ACLARUBICIN|ACM-A|Aclacinomycin A|Aclacinomycin-A|Aclacinomycin|Aclarubicin|Antibiotic MA144-A1|MA144-A1","An oligosaccharide anthracycline antineoplastic antibiotic isolated from the bacterium Streptomyces galilaeus. Aclarubicin intercalates into DNA and interacts with topoisomerases I and II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. Aclarubicin is antagonistic to other agents that inhibit topoisomerase II, such as etoposide, teniposide and amsacrine. This agent is less cardiotoxic than doxorubicin and daunorubicin.","Antibiotic|Organic Chemical"]
["C988","Acodazole","1H-imidazo[4,5-f]quinoline, acetamide deriv|ACODAZOLE|Acodazole|acetamide, N-methyl-N-[4-[(7-methyl-1H-imidazo[4, 5-f]quinolin-9-yl)amino]phenyl]-","A synthetic imidazoquinoline with antineoplastic activity. Acodazole intercalates into DNA, resulting in disruption of DNA replication.  Use of this agent has been associated with significant cardiotoxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C71627","Acodazole Hydrochloride","ACODAZOLE HYDROCHLORIDE|Acetamide, N-methyl-N-[4-[(7-methyl-1H-imidazo[4, 5-f]quinolin-9-yl)amino]phenyl]-, monohydrochloride (9CI)|Acodazole Hydrochloride|acetamide, N-methyl-N-[4-[(7-methyl-1H-imidazo[4, 5-f]quinolin-9-yl)amino]phenyl]-, monohydrochloride (9CI)","The hydrochloride salt of acodazole, a synthetic imidazoquinoline with antineoplastic activity. Acodazole intercalates into DNA, resulting in disruption of DNA replication.  Use of this agent has been associated with significant cardiotoxicity.","Organic Chemical|Pharmacologic Substance"]
["C65213","Acolbifene Hydrochloride","ACOLBIFENE HYDROCHLORIDE|Acolbifene Hydrochloride|acolbifene hydrochloride","The hydrochloride salt form of acolbifene, a fourth-generation estrogen receptor modulator (SERM) with potential lipid lowering and antineoplastic activity. Acolbifene specifically binds to estrogen receptors in responsive tissue, including liver, bone, breast, and endometrium. The resulting ligand-receptor complex is translocated to the nucleus where, depending on the tissue type, it promotes or suppresses the transcription of estrogen-regulated genes, thereby exerting its agonistic or antagonistic effects. Acolbifene acts as an estrogen antagonist in uterine and breast tissue, thereby blocking the effects of estrogen in these tissues. This may inhibit tumor cell proliferation in ER-positive tumor cells. This agent functions as an estrogen agonist in lipid metabolism, thereby decreasing total and LDL cholesterol levels. In bone, it decreases bone resorption and bone turnover and increases bone mineral density.","Pharmacologic Substance"]
["C203","Acridine","Acridine","A polycyclic aromatic dye with antineoplastic, antimicrobial and imaging activities. Acridine and its derivatives intercalate within DNA and RNA by forming hydrogen-bonds and stacking between base pairs resulting in DNA crosslinks and strand breaks. In addition, acridine and its derivatives are a potent inhibitor of topoisomerase II enzyme. This results in the inhibition of DNA and RNA synthesis, predominantly occurring during S phase of the cell cycle and ultimately leads to cell death.","Organic Chemical|Pharmacologic Substance"]
["C2203","Acridine Carboxamide","Acridine Carboxamide|DACA|N-(2-(Dimehtylamino)ethyl)acridine-4-carboxamide|NSC-601316|SN 22995|XR5000|acridine carboxamide","A tricyclic acridine-based (or carboxamide-based) drug with dual topoisomerase inhibitor and potential antineoplastic activities. Acridine carboxamide inhibits both topoisomerases I and II and intercalates into DNA, resulting in DNA damage, the disruption of DNA repair and replication, the inhibition of RNA and protein synthesis, and cell death.","Organic Chemical|Pharmacologic Substance"]
["C75297","Acronine","ACRONINE|Acronine|Acronycine","A natural alkaloid with an acridine structure isolated from the bark of the plant Acronychia baueri (Australian scrub ash) with antineoplastic properties.  Acronycine appears to alkylate DNA and interfere with DNA replication. (NCI04)","Pharmacologic Substance"]
["C82414","Actinium Ac 225 Lintuzumab","225Ac-HuM195|Actinium Ac 225 Lintuzumab|Actinium-225-Labeled Humanized Anti-CD33 Monoclonal Antibody HuM195","A radioimmunoconjugate consisting of the humanized monoclonal antibody lintuzumab conjugated to the alpha-emitting radioisotope actinium Ac 225 with potential antineoplastic activity. The monoclonal antibody moiety of actinium Ac 225 lintuzumab specifically binds to the cell surface antigen CD33 antigen, delivering a cytotoxic dose of alpha radiation to cells expressing CD33. CD33 is a cell surface antigen expressed on normal non-pluripotent hematopoietic stem cells and overexpressed on myeloid leukemia cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C95198","Actinomycin C2","ACTINOMYCIN C2|Actinomycin C2|Actinomycin D, 2a-D-Alloisoleucine-","A natural analogue of actinomycin, a chromopeptide antineoplastic antibiotic isolated from the bacterial genus Streptomyces. Actinomycin C2 inhibits DNA replication as well as RNA and protein synthesis by various mechanisms including, intercalating into the minor groove of DNA and interfering with the function of topoisomerase II. In addition, actinomycin C2 appears to block the interaction between the SH2 domain of growth factor receptor-bound protein-2 (GRB2) and the Src homology 2 domain containing transforming protein 1 adaptor protein SHC, which plays a key role in the Ras signaling pathway thereby halting cellular differentiation and proliferation.","Amino Acid, Peptide, or Protein|Antibiotic"]
["C99564","Actinomycin C3","2104-L-I|ACTINOMYCIN C3|AY 3|Actinomycin AY1|Actinomycin C3|Actinomycin I3|Actinomycin VII|Aurathin-A3","A natural analogue of actinomycin, a chromopeptide antineoplastic antibiotic isolated from the bacterial genus Streptomyces. Actinomycin C3 inhibits DNA replication as well as RNA and protein synthesis by various mechanisms such as intercalating into the minor groove of DNA and interfering with the function of topoisomerase II.","Amino Acid, Peptide, or Protein|Antibiotic"]
["C2844","Actinomycin F1","Actinomycin F1|Actinomycin KS4|KS4","A chromopeptide antineoplastic antibiotic isolated from the bacterium Streptomyces chrysomallus.  Actinomycin F1 intercalates into the minor groove of DNA and binds to topoisomerase II, leading to the inhibition of DNA replication and RNA and protein synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C111759","Activated Marrow Infiltrating Lymphocytes","Activated Marrow Infiltrating Lymphocytes|aMIL","A preparation of cells, which consists of autologous marrow infiltrating lymphocytes (MILs), that are manipulated in vitro, with potential antitumor and immune stimulating activities. MILs are harvested from autologous bone marrow from multiple myeloma patients and, in vitro, are exposed to and activated by anti-CD3/anti-CD28 monoclonal antibodies covalently attached to super-paramagnetic microbeads. After removal of the beads and expansion of the cells in culture, the activated MILs (aMILs) are re-introduced into the patient. The aMILs possess enhanced myeloma specificity, and are able to infiltrate the tumor microenvironment and initiate tumor cell lysis. CD3 and CD28, co-stimulatory molecules expressed on the surface of T-lymphocytes, play a key role in the activation of T-cells.","Pharmacologic Substance"]
["C118625","Activin Type 2B Receptor Fc Fusion Protein STM 434","Activin Inhibitor STM 434|Activin Type 2B Receptor Fc Fusion Protein STM 434|STM 434","A soluble fusion protein containing the extracellular domain of the activin receptor type 2B (ACVR2B or ActRIIB) fused to a human Fc domain, with potential antineoplastic activity. Upon intravenous administration, STM 434 selectively binds to the growth factor activin A, thereby preventing its binding to and the activation of endogenous ActRIIB. This prevents activin A/ActRIIB-mediated signaling and inhibits the proliferation of activin A-overexpressing tumor cells. Activin A, a member of the transforming growth factor beta (TGF-beta) superfamily, is overexpressed in a variety of cancers and plays a key role in promoting cancer cell proliferation, migration, and survival.","Pharmacologic Substance"]
["C88261","Ad5.SSTR/TK.RGD","Ad5.SSTR/TK.RGD|RGD-Modified Adenoviral Vector Encoding SSTR/TK","An RGD-4C-modified, infectivity-enhanced, bicistronic type 5 adenovirus expressing herpes simplex virus thymidine kinase (HSV-tk) gene, a therapeutic suicide gene, and the somatostatin receptor type 2 (SSTR2) gene with potential antineoplastic activity. Modification with the double cyclic peptide RGD-4C allows the virus to bind to cellular integrins, frequently expressed on the surfaces of ovarian cancer cells, instead of the coxsackie and adenovirus (CAR) receptor, which is often nonfunctional in ovarian cancer cells. Upon intratumoral administration, Ad5.SSTR/TK.RGD transfects tumor cells and expresses the HSV-tk gene. After subsequent administration of a synthetic acyclic guanosine analogue prodrug like ganciclovir (GCV), expressed HSV-tk phosphorylates and activates the prodrug, which may result in inhibition of DNA synthesis and apoptosis in HSV-tk-expressing cancer cells. Additionally, as a bystander effect, adjacent non-transfected cells may be killed by the activated antiviral drug. SSTR2 expression allows imaging of gene transfer into tumor cells using a radiolabeled somatostatin analogue.","Pharmacologic Substance"]
["C79800","Ad5-CMV-NIS","Ad5-CMV-NIS","A recombinant type 5 adenovirus (Ad5), encoding the gene for the human sodium-iodide symporter (NIS) linked to the cytomegalovirus (CMV) promoter, with potential gene transfection activity. Upon intratumoral injection, Ad5-CMV-NIS is taken up by tumor cells, resulting in the cellular expression of NIS. Subsequently, orally administered iodine 131 is taken up by NIS-expressing tumor cells, which may result in the selective accumulation of a cytotoxic dose of beta and gamma radiation in non-thyroidal tumor cells, sparing adjacent normal tissue. NIS, an intrinsic membrane glycoprotein, is an ion pump that actively transports iodide into cells which concentrate iodine; in addition to thyroid epithelial cells, it is found in non-thyroidal tissues including the salivary glands, the gastric mucosa, and lactating mammary glands.","Pharmacologic Substance|Virus"]
["C2471","Ad5CMV-p53 Gene","Ad-p53|Ad5CMV p53 Gene|Ad5CMV-p53 Gene|Adeno-p53|Adenovirus p53|Advexin|INGN-201|RPR/INGN-201|p53 Gene, Ad5CMV","A replication-defective adenoviral-CMV vector that encodes a wild-type p53 gene. Ad5CMV-p53 induces tumor cells that have been transfected with the vector to produce wild-type p53, a tumor suppressor gene that is deleted or mutated in a significant number of cancers. In transfected tumor cells, the wild-type p-53 gene product exerts an antitumor effect by blocking cell cycle progression at the G1/S regulation point, activating DNA repair proteins in the presence of DNA damage, and initiating apoptosis when DNA damage is irreparable.  (NCI04)","Pharmacologic Substance|Virus"]
["C73995","Ad5F35-LMP1/LMP2-Transduced Autologous Dendritic Cells","Ad5F35-LMP1/LMP2-Transduced Autologous Dendritic Cells","Autologous dendritic cells (DCs) transduced with the replication-deficient adenoviral vector Ad5F53 encoding the Epstein-Barr virus (EBV) transmembrane latent membrane proteins 1 and 2 (LMP1/LMP2) with potential immunostimulatory activity. Vaccination with Ad5F35-LMP1/LMP2-transduced autologous dendritic cells may stimulate a specific cytotoxic T-lymphocyte (CTL) response against LMP1- and LMP2-expressing tumor positive cells, resulting in tumor cell lysis and inhibition of tumor cell proliferation. LMP1 and LMP2 are expressed in various malignancies including nasopharyngeal cancer and EBV-positive Hodgkins disease.","Pharmacologic Substance"]
["C94205","Ad5-SGE-REIC/Dkk-3","Ad5-SGE-REIC/Dkk-3|Ad5-SGE-REIC/Dkk3","A replication incompetent adenoviral vector type 5 (Ad5) encoding the tumor suppressor gene dickkopf-3 (DKK3; Reduced Expression in Immortalized Cells; REIC; Dickkopf WNT signaling pathway inhibitor 3), and containing the super gene expression (SGE) system, composed of the triple tandem enhancer sequences of human telomerase reverse transcriptase (hTERT), simian virus 40 (SV40) and cytomegalovirus (CMV), with potential antineoplastic activity. Upon intratumoral injection and transfection of Ad5-SGE-REIC/Dkk-3, tumor cells express REIC/DKK3 protein. This may result in the activation of c-Jun-NH2-kinase (JNK) and ultimately lead to apoptosis via Bcl2 suppression and caspase-3 activation. REIC/DKK3 is expressed by healthy cells, but expression is reduced or absent in many cancer cells due to REIC/DKK3 gene defects, and this prevents tumor cell apoptosis.  Increased expression of REIC/DKK3 in cancer cells may lead to an induction of tumor cell apoptosis and a reduction in tumor cell growth, while sparing normal, healthy cells expressing endogenous REIC/DKK3. The SGE system, also called C-TSC (CMV promoter driving the triple tandem enhancer sequences of hTERT, SV40 and CMV), enhances gene expression compared to more conventional adenoviral vectors.","Pharmacologic Substance|Virus"]
["C128860","Ad5-survivin-transduced Autologous Dendritic Cell Vaccine","Ad5-survivin-transduced Autologous DC Vaccine|Ad5-survivin-transduced Autologous Dendritic Cell Vaccine|Autologous DC:AdmS|Autologous Dendritic Cell Adenovirus Type 5-Survivin Vaccine","A cell-based cancer vaccine containing autologous dendritic cells (DCs) that are transduced with a replication-deficient adenovirus type 5 vector (Ad5) encoding a mutated form of the tumor-associated antigen (TAA) survivin, with potential immunostimulatory and antineoplastic activities. Upon administration, Ad5-survivin-transduced autologous DC vaccine may elicit an immune response against cancer cells expressing survivin by activating cytotoxic T-cells (CTLs). This leads to an induction of cell death in survivin-positive tumor cells. Survivin, a member of the inhibitor of apoptosis (IAP) family of proteins, may be upregulated in certain tumor cell types and plays a key role in tumor cell growth and survival.","Cell|Pharmacologic Substance"]
["C88330","Ad5-yCD/mutTK(SR39)rep-ADP","Ad5-yCD/mutTK(SR39)rep-ADP","A second generation, replication-competent adenovirus type 5 containing a yeast cytosine deaminase(yCD)/mutant sr39 herpes simplex virus thymidine kinase fusion (yCD/mutTKsr39) gene and the 11.6 kDa adenovirus death protein (ADP) gene with potential oncolytic activity. Upon intratumoral administration and transduction of Ad5-yCD/mutTK(SR39)rep-ADP into tumor cells and subsequent expression of cytosine deaminase and viral thymidine kinase, administered prodrugs 5-fluorocytosine (5-FC) and ganciclovir are converted into their respective metabolites 5-fluorouracil (5-FU) and ganciclovir-5-monophosphate (ganciclovir-MP); 5-FU is subsequently metabolized to cytotoxic active metabolites 5-fluoroxyuridine monophosphate (F-UMP) and 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate (F-dUMP); ganciclovir-TP subsequently is converted by mammalian thymidine kinase to cytotoxic ganciclovir-triphosphate (ganciclovir -TP). Tumor cells adjacent to tumor cells transduced with this agent may be killed through a 'bystander effect'. ADP may enhance spread and oncolytic activity of replication-competent adenoviruses. In addition to its oncolytic activity, Ad5-yCD/mutTK(SR39)rep-ADP may exhibit radiosensitizing activity.","Pharmacologic Substance"]
["C123930","Ad5-yCD/mutTKSR39rep-hIL12","Ad5-yCD/mutTKSR39rep-hIL12|Oncolytic Adenovirus Ad5-yCD/mutTKSR39rep-hIL12","A replication-competent oncolytic adenovirus encoding the murine pro-inflammatory cytokine interleukin-12 (IL-12) gene and two suicide fusion genes, a yeast cytosine deaminase (yCD) and a mutant form of herpes simplex virus type 1 thymidine kinase (HSV-1 TKSR39), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration of Ad5-yCD/mutTKSR39rep-hIL12, the adenovirus selectively infects and replicates in tumor cells, which results in direct tumor cell lysis. Synergistically, IL-12 expressed by the adenovirus may activate the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma (IFN-g) and inducing cytotoxic T-lymphocyte (CTL) responses against tumor cells, which may result in immune-mediated tumor cell death, inhibition of tumor cell proliferation and inhibition of tumor angiogenesis. In addition, Ad5-yCD/mutTKSR39rep-hIL12-infected cancer cells express yCD and TKSR39; upon administration of the prodrugs 5-fluorocytosine (5-FC) and valganciclovir (vGCV), the yCD and HSV-1 TKSR39 activate these prodrugs to form 5-fluorouracil (5-FU) and ganciclovir, respectively. 5-FU gets converted to 5-fluoro-uridine monophosphate (5-FUMP) and subsequently to 5-fluoro-deoxyuridine monophosphate (5-FdUMP); 5-FdUMP irreversible inhibits thymidylate synthase, inhibits deoxythymidine triphosphate (dTTP) formation and halts DNA synthesis. Once phosphorylated intracellularly, ganciclovir triphosphate competitively inhibits deoxyguanosine triphosphate (dGTP) incorporation into DNA and inhibits DNA synthesis.","Pharmacologic Substance"]
["C82358","Adecatumumab","Adecatumumab|Anti-EpCAM Monoclonal Antibody MT201|MT201","A recombinant human IgG1 monoclonal antibody (MoAb) directed against the tumor associated antigen (TAA) epithelial cell adhesion molecule (EpCAM) with potential antitumor activity. Adecatumumab binds to EpCAM, which may result in antibody-dependent cellular cytotoxicity (ADCC) directed against EpCAM-expressing tumor cells. EpCAM (CD326), a cell surface protein upregulated on many tumor cell types, promotes the proliferation, migration and invasiveness of tumor cells; for some cancers, overexpression has been correlated with decreased survival.","Pharmacologic Substance"]
["C121664","Adenosine A2A Receptor Antagonist PBF-509","A2AR Antagonist PBF-509|Adenosine A2A Receptor Antagonist PBF-509|PBF-509","An orally bioavailable adenosine A2A receptor (A2AR) antagonist, with potential antineoplastic activity. Upon administration, A2AR antagonist PBF-509 selectively binds to and inhibits A2AR expressed on T-lymphocytes. This abrogates the adenosine/A2AR-mediated inhibition of T-lymphocytes and activates a T-cell-mediated immune response against tumor cells, thereby reducing proliferation of susceptible tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T-cells and, upon activation by adenosine, inhibits their proliferation and activation. Adenosine is often produced in excess by cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C79826","Adenosine A3 Receptor Agonist CF102","2-Chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide|2-Cl-IB-MECA|A3AdR Agonist CF102|Adenosine A3 Receptor Agonist CF102|Adenosine Receptor A3 Agonist CF102|C-Ibza-MU|CF102","An orally bioavailable, synthetic, highly selective adenosine A3 receptor (A3AR) agonist with potential antineoplastic activity. Adenosine A3 receptor agonist CF102 selectively binds to and activates the cell surface-expressed A3AR, deregulating Wnt and NF-kB signal transduction pathways downstream, which may result in apoptosis of A3AR-expressing tumor cells. A3AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of various solid tumor cell types, including hepatocellular carcinoma (HCC) cells, and plays an important role in cellular proliferation.","Pharmacologic Substance"]
["C125659","Adenosine-A2A Receptor Antagonist CPI-444","Adenosine-A2A Receptor Antagonist CPI-444|Adenosine-A2A Receptor-Targeting Agent CPI-444|CPI-444","A small molecule immune checkpoint inhibitor of the adenosine A2A receptor (ADORA2A) with potential antineoplastic activity. Upon oral administration, adenosine-A2A receptor antagonist CPI-444 binds to adenosine A2A receptors expressed on the surface of immune cells, including T-lymphocytes, natural killer (NK) cells, macrophages and dendritic cells (DCs). This prevents tumor-released adenosine from interacting with the A2A receptors on these key immune surveillance cells, thereby abrogating adenosine-induced immunosuppression in the tumor microenvironment. This may stimulate anti-tumor immune responses, resulting in tumor regression.","Pharmacologic Substance"]
["C48368","Adenovector Encoding MDA7","Adenovector Encoding MDA7","A nonreplicating adenoviral vector (adenovector) encoding the melanoma differentiation-associated 7 gene (MDA7) with potential antineoplastic activity. After intratumoral injection and adenovector-mediated gene transfer of MDA7 into tumor cells, the expressed MDA7 transgene may inhibit tumor cell proliferation and induce tumor cell apoptosis.","Pharmacologic Substance"]
["C106242","Adenovector-transduced AP1903-inducible MyD88/CD40-expressing Autologous PSMA-specific Prostate Cancer Vaccine BPX-201","Adenovector-transduced AP1903-inducible MyD88/CD40-expressing Autologous PSMA-specific Prostate Cancer Vaccine BPX-201|Adenovector-transduced AP1903-inducible iMC-expressing Autologous PSMA-specific Prostate Cancer Vaccine BPX-201|BPX-201","A genetically-modified, dendritic cell-based (DCs) vaccine in which the autologous cells are transduced with an adenoviral vector expressing the tumor antigen prostate-specific membrane antigen (PSMA) and a fusion protein composed of synthetic ligand inducible adjuvant iMC composed of a drug-inducible costimulatory CD40 receptor (iCD40) and the adaptor protein MyD88, with potential immunomodulating and antineoplastic activities. The iCD40 contains a membrane-localized cytoplasmic CD40 domain fused to the FK506 modified drug-binding protein 12 (FKBP12). Upon intradermal administration of BPX-201, these DCs accumulate in local draining lymph nodes. Twenty-four hours after vaccination, the dimerizing agent AP1903 is administered. AP1903 binds to the drug binding domain, leading to iMC oligomerization and activation of iCD40 and MyD88-mediated signaling in iMC-expressing DCs. This signaling pathway activates the DCs and stimulates a cytotoxic T-lymphocyte (CTL) response against host tumor cells that express PSMA. PSMA, a glycoprotein secreted by prostatic epithelial and ductal cells, is overexpressed in prostate cancer cells and is used as a tumor marker for both diagnosis and treatment evaluation. MyD88 is involved in interleukin 1 receptor (IL1R) and toll-like receptor (TLR) signaling.","Cell|Pharmacologic Substance"]
["C101789","Adenoviral Transduced hIL-12-expressing Autologous Dendritic Cells INXN-3001 Plus Activator Ligand INXN-1001","Adenoviral Transduced hIL-12-expressing Autologous Dendritic Cells INXN-3001 Plus Activator Ligand INXN-1001|DC-RTS-IL-12|INXN-3001/1001","Autologous dendritic cells tranduced with a replication incompetent adenovirus encoding human pro-inflammatory cytokine interleukin-12 (IL-12) (INXN-3001) in combination with the proprietary orally bioavailable, small molecule activator ligand INXN-1001, with potential immunomodulating and antineoplastic activities. Production of IL-12 is controlled by an inducible DNA element that allows transcription initiation only in the presence of the ligand inducer INXN-1001. Upon intratumoral injection of INXN-3001 and subsequent oral administration of activator ligand, INXN-1001 is able to induce expression of IL-12 in INXN-3001. IL-12 expressed by the adenovirus may activate the immune system by promoting the activation of natural killer cells, inducing the secretion of interferon-gamma and inducing a cytotoxic T lymphocyte response against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation. As INXN-1001 regulates both the timing and the levels of IL-12 expression, IL-12 toxicity can be reduced.","Pharmacologic Substance"]
["C91373","Adenoviral Vector Ad5-CEA(6D) Vaccine","Ad5 CEA Vaccine|Adenoviral Vector Ad5-CEA(6D) Vaccine|ETBX-011","A replication-defective, E1- and E2b-deleted oncolytic adenoviral serotype 5 (Ad5) encoding an epitope of human carcinoembryonic antigen (CEA) with potential antineoplastic activity. Adenoviral vector Ad5-CEA(6D) vaccine expresses a highly immunogenic analogue of CEA [CAP1-(6D)]. Upon administration, this vaccine may induce both humoral and cellular immune responses against tumor cells expressing the CEA antigen, thereby resulting in the immune-mediated inhibition of tumor cell proliferation and tumor cell death. CEA, a tumor-associated antigen, is overexpressed in various tumor cell types. Deletion of early genes E1 and E2b in Ad5 potentially circumvent pre-existing anti-adenovirus immunity and is capable of inducing strong immune responses.","Pharmacologic Substance|Virus"]
["C112005","Adenovirus 5-Human Guanylyl Cyclase C-PADRE Vaccine","Ad5-hGCC-PADRE Vaccine|Adenovirus 5-Human Guanylyl Cyclase C-PADRE Vaccine","A replication-defective, recombinant adenoviral serotype 5 (Ad5) encoding human guanylyl cyclase C (hGCC) and the synthetic Pan DR epitope (PADRE), with potential antineoplastic and immunomodulating activities. Upon intramuscular administration, the Ad5-hGCC-PADRE vaccine expresses hGCC, which may induce both humoral and cellular immune responses against tumor cells expressing the hGCC antigen. This results in the immune-mediated inhibition of tumor cell proliferation, and leads to tumor death. The hGCC protein is normally restricted to intestinal epithelial cells but is overexpressed by metastatic colorectal tumors. PADRE is a helper T-lymphocyte epitope that is able to augment the magnitude and duration of the cytotoxic T-lymphocyte (CTL) response.","Pharmacologic Substance"]
["C2204","Adenovirus B7-1","Adenovirus B7-1","A gene-viral vector complex comprised of an adenovirus vector and B7-1 gene targeting the CD80 antigen.  Adenovirus B7-1 is used as a component in antineoplastic vaccines to elicit a cytotoxic T-cell response. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C62527","Adenovirus Encoding Rat HER-2/neu","Adenovirus Encoding Rat HER-2/neu","A replication-defective oncolytic adenovirus, encoding rat Her-2/neu (ErbB-2), with potential antineoplastic activity. Upon administration, adenovirus encoding rat HER-2/neu may induce an immune response against tumor cells expressing the HER-2/neu antigen, which may result in the immune-mediated inhibition of tumor cell proliferation and tumor cell death. Her-2/neu, a tumor-associated antigen and member of the epidermal growth factor receptor (EGFR) family of tyrosine kinases, is overexpressed in various tumor cell types.","Pharmacologic Substance"]
["C61492","Adenovirus Encoding Recombinant Human Endostatin","Ad-rhENDO|Adenovirus Encoding Recombinant Human Endostatin|E10A","A replication-defective, recombinant oncolytic adenovirus encoding human endostatin with potential antineoplastic activity. Endostatin, a 20 kDa C-terminal proteolytic fragment of collagen XVIII, is an important angiogenesis inhibitor. Upon intratumoral administration, the adenovirus infects and replicates in tumor cells. The expressed endostatin may inhibit endothelial cell proliferation and angiogenesis which may result in a reduction of tumor growth.","Pharmacologic Substance"]
["C102753","Adenovirus Encoding Tyrosinase/MART-1/MAGEA6-transduced Autologous Dendritic Cell Vaccine","AdVTMM2-transduced Dendritic Cell Vaccine|Adenovirus Encoding Tyrosinase/MART-1/MAGEA6-transduced Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) transduced with a recombinant adenoviral vector encoding three full length human melanoma associated antigens (MAAs), tyrosinase, melan-A (MART-1) and the melanoma antigen A6 (MAGEA6), with potential antineoplastic activity. Upon intradermal administration, adenovirus encoding tyrosinase/MART-1/MAGEA6-transduced autologous DC vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tyrosinase/MART-1/MAGEA6-positive tumor cells, which may result in tumor cell death and decreased tumor growth. Tyrosinase, a melanoma-specific differentiation antigen, catalyzes the first step of melanin synthesis in melanocytes. Vaccination with multi-antigen modified DC may improve the efficacy of the DC immunotherapy.","Pharmacologic Substance"]
["C61098","Adenovirus HER2-Transduced Autologous Dendritic Cell Vaccine","AdHer2/DC|Adenovirus HER2-Transduced Autologous Dendritic Cell Vaccine|Autologous Dendritic Cell-Adenovirus HER2 Vaccine|HER-2 pulsed DC vaccine|autologous dendritic cell/adenovirus HER-2 vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) transduced with a replication-deficient adenovirus vector encoding HER-2 with potential antineoplastic activity. Upon administration, adenovirus HER2-transduced autologous dendritic cell vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against HER-2-positive tumor cells, which may result in tumor cell death and decreased tumor growth. HER-2, a tyrosine kinase receptor for epidermal growth factor (EGF) (also known as neu and ErbB2), is overexpressed by some breast, ovarian, and gastric cancers.","Immunologic Factor|Pharmacologic Substance"]
["C96221","Adenovirus-Encoding E.coli PNP","Ad/PNP|Adenovirus Encoding Purine Nucleoside Phosphorylase|Adenovirus-Encoding E.coli PNP","A replication-incompetent adenovirus encoding E. coli purine nucleoside phosphorylase (Ad/PNP) used as a prodrug activating agent. Administered intratumorally, Ad/PNP expresses the enzyme PNP, which may catalyze systematically administrated fludarabine phosphate prodrug into its active form 2-fluoroadenine (F-Ade). F-Ade inhibits DNA polymerase alpha, ribonucleotide reductase and DNA primase, thereby interrupting DNA synthesis and inhibiting tumor cell growth. Localized prodrug activation provides targeted chemotherapy, thereby potentially reducing systemic side effects.","Pharmacologic Substance"]
["C37515","Adenovirus-mediated Human Interleukin-12","Ad.hIL-12|Adenovirus-interleukin-12|Adenovirus-mediated Human Interleukin-12","A replication incompetent adenovirus encoding human pro-inflammatory cytokine interleukin-12 (IL-12) (Ad.hIL-12), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration, the adenovirus selectively infects and replicates in tumor cells, which may result in tumor cell lysis. Synergistically, IL-12 expressed by the adenovirus may activate the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma and inducing cytotoxic T cell responses against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation.","Therapeutic or Preventive Procedure"]
["C97959","Adenovirus-mediated Human Interleukin-12 INXN-2001 Plus Activator Ligand INXN-1001","Ad-RTS-IL-12 Plus AL|Adenovirus-mediated Human Interleukin-12 INXN-2001 Plus Activator Ligand INXN-1001|INXN-2001/1001|ZIN ATI-001","A replication incompetent adenovirus encoding the human pro-inflammatory cytokine interleukin-12 (IL-12) (INXN-2001) in combination with the proprietary activator ligand INXN-1001, with potential immunomodulating and antineoplastic activities. Production of IL-12 is controlled by an inducible DNA element that allows transcription initiation only in the presence of the ligand inducer. Upon intratumoral administration of INXN-2001 and oral administration of INXN-1001, INXN-1001 is able to induce expression of IL-12 from INXN-2001. IL-12 expressed by the adenovirus may activate the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma and inducing cytotoxic T cell responses against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation.","Pharmacologic Substance"]
["C90542","Adenovirus-p53 Transduced Dendritic Cell Vaccine","Adenovirus-p53 Transduced Dendritic Cell Vaccine","A cancer vaccine consisting of autologous dendritic cells (DCs) transduced with a recombinant adenovirus encoding p53 peptide, with potential immunomodulating activity. Intradermal vaccination with adenoviral-p53 transduced dendritic cell vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing mutant p53, resulting in tumor cell lysis. p53, a tumor suppressor gene, is mutated in many tumor cells, resulting in the loss of apoptosis regulation and abnormal cell proliferation.","Immunologic Factor|Pharmacologic Substance"]
["C102541","Adenovirus-PSA Prostate Cancer Vaccine","Ad/PSA Vaccine|Adenovirus-PSA Prostate Cancer Vaccine|Adenovirus/PSA Vaccine","A cancer vaccine composed of a genetically engineered, replication-deficient type 5 adenovirus carrying the human prostate-specific antigen (PSA), with potential immunostimulating and antineoplastic activities. Upon subcutaneous vaccination with the adenovirus-PSA prostate cancer vaccine, the adenovirus infects cells and expresses PSA. In turn, PSA may activate the immune system and may induce a cytotoxic T-lymphocyte response against PSA-expressing tumor cells. PSA, a tumor associated antigen, is expressed by prostate epithelial cells and is overexpressed in prostate cancer.","Pharmacologic Substance"]
["C105809","AdGMCAIX-transduced Autologous Dendritic Cells","AdGMCAIX-transduced Autologous Dendritic Cells|DC-AdGMCAIX|DCs expressing CMCA9 Gene","Autologous dendritic cells (DCs) transduced with a recombinant, replication-defective adenoviral vector expressing the fusion gene granulocyte-macrophage colony-stimulating factor (GM-CSF) and carbonic anhydrase IX (CA-IX or CA9) (GMCA-9), with potential immunomodulating activity. The autologous DCs are transduced ex vivo and express the GMCA-9 fusion protein on the cell surface. Upon intradermal administration of the AdGMCAIX-transduced autologous DCs back into the patient, the DCs activate the immune system to both mount a cytotoxic T lymphocyte-mediated response against tumor cells positive for the CA9 antigen, and generate memory T cells. This may result in decreased tumor growth. CA9, also known as G250, is a renal cell carcinoma (RCC)-associated antigen and a member of the carbonic anhydrase family that contains a human leukocyte antigen (HLA)-A2.1-restricted epitope; it is found in a majority of renal cell carcinomas while absent in most normal tissues. The cytokine GM-CSF enhances the immunogenicity of CA9-based DC vaccines.","Pharmacologic Substance"]
["C53399","ADH-1","ADH-1|Exherin","A small, cyclic pentapeptide vascular-targeting agent with potential antineoplastic and antiangiogenic activities. ADH-1 selectively and competitively binds to and blocks N-cadherin, which may result in disruption of tumor vasculature, inhibition of tumor cell growth, and the induction of tumor cell and endothelial cell apoptosis. N-cadherin, a cell- surface transmembrane glycoprotein of the cadherin superfamily of proteins involved in calcium-mediated cell-cell adhesion and signaling mechanisms; may be upregulated in some aggressive tumors and the endothelial cells and pericytes of some tumor blood vessels.","Organic Chemical|Pharmacologic Substance"]
["C105813","Ad-hCMV-Flt3L","Ad-hCMV-Flt3L","A human serotype 5, replication-defective, first generation adenoviral vector, with the viral E1a and E3 protein encoding regions deleted, which is engineered to express the soluble, immune-mediated stimulatory gene human fms-like tyrosine kinase 3 ligand (Flt3L), under the transcriptional control of the CMV promoter, with potential immunostimulating activity. Upon administration, Ad-hCMV-Flt3L is transduced into tumor cells and Flt3L is expressed. Flt3L stimulates both the proliferation of dendritic cells (DCs) and their migration to the tumor site. Upon exposure to the tumor-associated antigens (TAA) released from dying glioma cells, which were killed by thymidine kinase-mediated valacyclovir-induced tumor cell death, the DCs initiate a specific immune response against any remaining TAA-expressing tumor cells. Flt3L is a hematopoietic growth factor and ligand for the Flt3 tyrosine kinase receptor.","Pharmacologic Substance"]
["C105811","Ad-hCMV-TK","Ad-hCMV-TK","A human serotype 5, replication-defective, first generation adenoviral vector, with the viral E1a and E3 protein encoding regions deleted, which is engineered to express the herpes simplex virus thymidine kinase (HSV-tk) gene under the transcriptional control of the CMV promoter. This agent, when administered in conjunction with a synthetic acyclic guanosine analogue, possesses potential antineoplastic activity. Upon administration into the peritumoral region after tumor resection, adenoviral vector encoding HSV thymidine kinase is transduced into tumor cells, and HSV-tk is expressed. Tumor cells expressing HSV-tk are sensitive to synthetic acyclic guanosine analogues. Subsequent administration of a synthetic acyclic guanosine analogue, such as valacyclovir (VCV) or ganciclovir (GCV), kills the tumor cells expressing HSV-tk. The release of tumor-associated antigens (TAA) by dying tumor cells may then stimulate an antitumor cytotoxic T lymphocyte (CTL) response, directed aganst any remaining tumor cells.","Pharmacologic Substance"]
["C127154","Ad-ISF35","Ad-CD154 ISF35|Ad-CD40L ISF35|Ad-ISF35","A replication-defective adenovirus vector (Ad-ISF35), which encodes a membrane-stabilized, chimeric human-mouse CD40 binding protein (CD40 ligand; CD40L; CD154), with potential immunomodulatory and antineoplastic activities. Upon intratumoral administration, Ad-ISF135 preferentially transduces tumor cells and immunoregulatory cells in the tumor microenvironment. This increases the expression of CD154 in tumor cells, activates CD40 and stimulates signaling and immunoactivation, which are both mediated by CD40. This increases the expression of co-stimulatory molecules on these cells, which enhances their ability to function as antigen presenting cells (APCs) and increases their apoptotic potential. This leads to an increase in the infiltration of macrophages and neutrophils, which promote direct cytotoxicity, enhances the production of pro-inflammatory cytokines in the tumor microenvironment, and induces a specific cytotoxic T-lymphocyte (CTL) response against the tumor cells. In addition, transduction with Ad-ISF35 induces direct tumor cell death, probably through an anti-viral immune response. Ad-ISF35 also exerts a strong bystander effect in non-transduced cells thereby further inducing tumor cell death. Altogether, this will eradicate tumor cells. CD154, the main ligand for CD40, plays a key role in the activation of APCs, promotes immunoactivation, and increases apoptotic potential. The protein encoded by Ad-ISF35 does not contain the mouse antibody binding domains and does not induce human neutralizing antibodies. The metalloprotease cleavage site is deleted in this chimeric CD154 and thus it resists cleavage; the encoded protein also contains amino acid substitutions within the carboxy-terminal. Both sets of engineered mutations promote cell surface expression.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C64785","AdRTVP-1-Transduced Prostate Cancer Cell-Based Vaccine","AdRTVP-1-Transduced Prostate Cancer Cell-Based Vaccine|Adenoviral Vector-Mediated RTVP-1 Gene-modified Prostate Cancer Cell-based Vaccine","A cell-based vaccine comprised of prostate cancer cells transduced with an adenoviral vector encoding human RTVP-1 (AdRTVP-1), with potential antineoplastic and immunostimulating activities. RTVP-1, also referred to as glioma pathogenesis-related protein 1 (GLIP1), is down-regulated in prostate tumors. Regulated by tumor suppressor p53, the expression of RTVP-1 functions as a tumor suppressor, and is abundant in normal human prostate epithelial cells as well as in differentiated macrophages. Administration of this vaccine leads to an induction of apoptosis through the expression of RTVP-1 and results in a reduction in cellular proliferation in prostate cancer cells. In addition, this cancer-cell based vaccine may induce a cytotoxic T lymphocyte (CTL) response against prostate specific tumor associated antigens, resulting in an immune-mediated prostate cancer cell death. Furthermore, RTVP-1 stimulates CTL and natural killer (NK) cell activities.","Immunologic Factor|Pharmacologic Substance"]
["C77910","Ad-sig-hMUC-1/ecdCD40L Vaccine","Ad-sig-hMUC-1/ecdCD40L Adenoviral Vector Vaccine|Ad-sig-hMUC-1/ecdCD40L Vaccine","A cancer vaccine consisting of a recombinant adenoviral vector encoding the tumor-associated antigen (TAA) human MUC-1 (hMUC-1) linked to the extracellular domain (ecd) of the co-stimulatory molecule CD40 ligand (CD40L) and an adenovirus signal sequence that encodes a secretory signal peptide (Ad-sig) with potential immunostimulating and antineoplastic activities. Due to the presence of the secretory signal peptide expressed by Ad-sig in the vaccine construct, transfected cells may secrete a fusion protein composed of hMUC-1 and the CD40L ecd. The CD40L moiety part of the fusion protein binds to CD40 receptors on dendritic cells (DCs). Subsequently, DCs may be activated and migrate, T-cells may expand, and a cytotoxic T lymphocyte (CTL) response against tumor cells that overexpress hMUC-1 may follow. MUC-1 is a hypoglycosylated TAA overexpressed by epithelial cancer cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C91719","AE37 Peptide/GM-CSF Vaccine","AE37 Peptide/GM-CSF Vaccine","A vaccine containing HER2/Neu-derived epitope (amino acids 776-790) linked to li-Key peptide (li-Key/HER2/neu hybrid peptide or AE37), and combined with granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential antineoplastic and immunoadjuvant activities. Upon vaccination, AE37 may activate the immune system and stimulate T-helper cells against HER2/Neu expressing cancer cells. GM-CSF may potentiate the immune response against cancer cells expressing the HER2/Neu antigen. The Ii-Key moiety, a 4-amino acid (LRMK) epitope from the MHC class II-associated invariant chain (Ii protein), increases T-helper cell stimulation against HER2/neu antigen when compared to unmodified class II epitopes. HER2/neu, a tumor associated antigen (TAA), is overexpressed in a variety of tumor cell types and is highly immunogenic.","Immunologic Factor|Pharmacologic Substance"]
["C48369","AEE788","AEE 788|AEE-788|AEE788","An orally bioavailable multiple-receptor tyrosine kinase inhibitor. AEE788 inhibits phosphorylation of the tyrosine kinases of epidermal growth factor receptor (EGFR), human epidermal growth factor receptor 2 (HER2), and vascular endothelial growth factor receptor 2 (VEGF2), resulting in receptor inhibition, the inhibition of cellular proliferation, and induction of tumor cell and tumor-associated endothelial cell apoptosis. (NCI05)","Pharmacologic Substance"]
["C49180","AEG35156","AEG35156|GEM640","A second-generation synthetic antisense oligonucleotide with potential antineoplastic activity. AEG35156 selectively blocks the cellular expression of X-linked inhibitor of apoptosis protein (XIAP), a pivotal inhibitor of apoptosis that is overexpressed in many tumors. This agent reduces total levels of XIAP in tumor cells, working synergistically with cytotoxic drugs to overcome tumor cell resistance to apoptosis. XIAP interferes with both the intrinsic and extrinsic program-death signaling pathways, which may render tumor cells resistant to apoptosis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C101794","Aerosolized Aldesleukin","Aerosolized Aldesleukin|Aerosolized Recombinant IL-2","An aerosol formulation of aldesleukin, a recombinant form of interleukin-2 (IL-2), with potential immunostimulating activity. Upon IL-2 inhalation, this cytokine activates lymphokine-activated killer cells and natural killer cells, and induces expression of cytotoxic cytokines, such as interferon-gamma and transforming growth factor-beta. This may eventually halt tumor cell growth. Localized administration of IL-2 may decrease toxicity and increase efficacy.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C61071","Aerosolized Liposomal Rubitecan","Aerosolized Liposomal Rubitecan|Aerosolized liposomal 9-nitro-20(S)-camptothecin","An aerosolized liposomal preparation of rubitecan, a water-insoluble derivative of camptothecin with potential antineoplastic activity. Rubitecan (or 9-nitro-20 (S)-camptothecin) and its active metabolite 9-aminocamptothecin (9-AC) selectively stabilize topoisomerase I-DNA covalent complexes during S-phase, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. This agent is formulated with dilauroylphosphatidylcholine and nebulized in particle sizes of 1.2-1.6 micrometer mass median aerodynamic diameter.","Chemical Viewed Functionally"]
["C66940","Afatinib","(2e)-N-(4-(3-Chloro-4-Fluoroanilino)-7-(((3s)-Oxolan-3-yl)Oxy)Quinoxazolin-6-yl)-4-(Dimethylamino)But-2-Enamide|AFATINIB|Afatinib|BIBW 2992","An orally bioavailable anilino-quinazoline derivative and inhibitor of the receptor tyrosine kinase (RTK) epidermal growth factor receptor (ErbB; EGFR) family, with antineoplastic activity. Upon administration, afatinib selectively and irreversibly binds to and inhibits the epidermal growth factor receptors 1 (ErbB1; EGFR), 2 (ErbB2; HER2), and 4 (ErbB4; HER4), and certain EGFR mutants, including those caused by EGFR exon 19 deletion mutations or exon 21 (L858R) mutations. This may result in the inhibition of tumor growth and angiogenesis in tumor cells overexpressing these RTKs. Additionally, afatinib inhibits the EGFR T790M gatekeeper mutation which is resistant to treatment with first-generation EGFR inhibitors. EGFR, HER2 and HER4 are RTKs that belong to the EGFR superfamily; they play major roles in both tumor cell proliferation and tumor vascularization and are overexpressed in many cancer cell types.","Pharmacologic Substance"]
["C97273","Afatinib Dimaleate","(2E)-N-(4-((3-Chloro-4-fluorophenyl)amino)-7-(((3S)-tetrahydrofuran-3-yl)oxy)quinazolin- 6-yl)-4-(dimethylamino)but-2-enamide bis(hydrogen (2Z)-but-2-enedioate)|2-Butenamide, N-[4-[(3-chloro-4-fluorophenyl)amino]7-[[(3S)-tetrahydro-3-furanyl]oxy]-6-quinazolinyl]-4-(dimethylamino)-,(2E)-, (2Z)-2-Butenedioate (1:2)|AFATINIB DIMALEATE|Afatinib Dimaleate|BIBW 2992MA2|BIBW2992 MA2|Gilotrif","The dimaleate salt form of afatinib, an orally bioavailable anilino-quinazoline derivative and inhibitor of the receptor tyrosine kinase (RTK) epidermal growth factor receptor (ErbB; EGFR) family, with antineoplastic activity. Upon administration, afatinib selectively and irreversibly binds to and inhibits the epidermal growth factor receptors 1 (ErbB1; EGFR), 2 (ErbB2; HER2), and 4 (ErbB4; HER4), and certain EGFR mutants, including those caused by EGFR exon 19 deletion mutations or exon 21 (L858R) mutations. This may result in the inhibition of tumor growth and angiogenesis in tumor cells overexpressing these RTKs. Additionally, afatinib inhibits the EGFR T790M gatekeeper mutation which is resistant to treatment with first-generation EGFR inhibitors. EGFR, HER2 and HER4 are RTKs that belong to the EGFR superfamily; they play major roles in both tumor cell proliferation and tumor vascularization and are overexpressed in many cancer cell types.","Pharmacologic Substance"]
["C975","Afimoxifene","4-(1-(4-(2-(Dimethylamino)ethoxy)phenyl)-2-phenylbut-1-enyl)phenol|4-Hydroxy-Tamoxifen|4-Hydroxytamoxifen|4-OHT|4-hydroxytamoxifen|AFIMOXIFENE|Afimoxifene","A tamoxifen metabolite with both estrogenic and anti-estrogenic effects.  Afimoxifene has a higher affinity for the estrogen receptor than tamoxifen, and functions as an antagonist in breast cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C2512","AFP Gene Hepatocellular Carcinoma Vaccine","AFP Gene Hepatocellular Carcinoma Vaccine|vaccine, AFP gene hepatocellular carcinoma","A cancer vaccine composed of naked plasmid DNA of the gene for the tumor-associated antigen alpha-fetoprotein (AFP), a macromolecule that acts as a specific immunologic target for hepatocellular carcinoma. This agent exerts an antitumor effect by inducing cytotoxic T-lymphocytes to attack AFP-expressing tumor cells. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C48370","AFP464","AFP464","A synthetic lysyl prodrug of the amino-substituted flavone derivate aminoflavone with antiproliferative and antineoplastic activities. AFP464 is rapidly converted to aminoflavone in plasma. Aminoflavone activates the aryl hydrocarbon receptor (AhR) signaling pathway leading to an increase in cytochrome P450 1A1 (CYP1A1) and cytochrome P450 1A2 (CYP1A2) expression and, to a lesser extent, an increase in cytochrome P450 1B1 (CYP1B1) expression. Subsequently, aminoflavone is metabolized to toxic metabolites by the cytochromome P450 enzymes that it induces; these toxic metabolites covalently bind to DNA, resulting in the phosphorylation of p53, the induction of the p53 downstream target p21Waf1/Cip1, and apoptosis. Pulmonary toxicity may be dose-limiting.","Pharmacologic Substance"]
["C82390","Afuresertib","Afuresertib|GSK2110183","An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Afuresertib binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C52182","AG-024322","AG-024322","A cyclin-dependent kinase (CDK) inhibitor with antineoplastic activity. AG-024322 selectively inhibits cyclin-dependent kinases (particularly CDK1,2 and 4), enzymes that regulate cell cycle progression. Inhibition of CDK may result in cell cycle arrest, induction of apoptosis, and inhibition of DNA replication and tumor cell proliferation.","Pharmacologic Substance"]
["C88268","Agaricus blazei Murill Extract","Agaricus blazei Murill Extract","A dietary supplement containing an extract of the Basidiomycete fungus Agaricus blazei Murill with potential chemopreventive, antineoplastic and immunopotentiating activities. Agaricus blazei Murill extract contains high levels of phytochemicals, especially beta-D-glucans. Beta-D-glucans may promote dendritic cell (DC) maturation; increase interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) and immunoglobulin levels; and may enhance natural killer (NK) cell activity, potentially boosting anti-tumor host immune responses.","Pharmacologic Substance"]
["C28580","Agatolimod Sodium","(3'-5')d(P-thio)(T-C-G-T-C-G-T-T-T-T-G-T-C-G-T-T-T-T-G-T-C-G-T-T) Tricosasodium Salt|Agatolimod Sodium|CpG 7909|PF-3512676|ProMune","The tricosasodium salt of a synthetic 24-mer oligonucleotide containing 3 CpG motifs with potential antineoplastic and immunostimulatory activity. Agatolimod selectively targets Toll-like receptor 9 (TLR9), thereby activating dendritic and B cells and stimulating cytotoxic T cell and antibody responses against tumor cells bearing tumor antigens.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C73996","Aglatimagene Besadenovec","ADV-tk|AGLATIMAGENE BESADENOVEC|Aglatimagene Besadenovec|GliAtak|ProstAtak|Virafir","An adenoviral vector engineered to express the herpes simplex virus thymidine kinase (HSV-tk) gene, which, when administered in conjunction with a synthetic acyclic guanosine analogue, possesses potential antineoplastic activity. Aglatimagene besadenovec is transduced into tumor cells, sensitizing tumor cells that overexpress HSV-tk to synthetic acyclic guanosine analogues. Subsequently, a low dose of a synthetic acyclic guanosine analogue such as valacyclovir (VCV) or ganciclovir (GCV) is given, which may preferentially kill tumor cells containing the adenoviral vector and overexpressing HSV-tk. Release of tumor-associated antigens (TAAs) by dying tumor cells may then stimulate an antitumor cytotoxic T lymphocyte (CTL) response.","Pharmacologic Substance"]
["C121538","Agonistic Anti-CD40 Monoclonal Antibody ADC-1013","ADC-1013|Agonistic Anti-CD40 Monoclonal Antibody ADC-1013","A human immunoglobulin (Ig) G1 monoclonal antibody directed against the cell surface receptor CD40 with potential immunostimulatory and antineoplastic activities. Upon intratumoral administration, agonistic anti-CD40 monoclonal antibody ADC-1013 binds to CD40 on antigen-presenting dendritic cells, which leads to the activation and proliferation of effector and memory T-cells, and enhances the immune response against tumor cells. In addition, this agent binds to the CD40 antigen present on the surfaces of tumor cells, which induces antibody-dependent cytotoxicity (ADCC). This eventually inhibits the proliferation of CD40-expressing tumor cells. CD40, a stimulatory receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells, such as macrophages, dendritic cells and various tumor cell types; it plays a key role in the activation of the immune system.","Immunologic Factor|Pharmacologic Substance"]
["C118282","Agonistic Anti-OX40 Monoclonal Antibody MEDI6383","Agonistic Anti-OX40 Monoclonal Antibody MEDI6383|MEDI6383","An agonistic monoclonal antibody against receptor OX40 (CD134), with potential immunostimulatory activity. Upon administration, anti-OX40 monoclonal antibody MEDI6383 selectively binds to and activates the OX40 receptor, by mimicking the action of endogenous OX40 ligand (OX40L). OX40 receptor activation induces proliferation of memory and effector T lymphocytes. In the presence of tumor-associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor family, is expressed on T-lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C117293","Agonistic Anti-OX40 Monoclonal Antibody MEDI6469","Agonistic Anti-CD134 Monoclonal Antibody MEDI6469|Agonistic Anti-OX40 Monoclonal Antibody MEDI6469|MEDI6469","An agonistic monoclonal antibody against the co-stimulatory receptor OX40 (CD134), with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, anti-OX40 monoclonal antibody MEDI6469 selectively binds to and activates OX40. OX40 activation induces proliferation of effector T-lymphocytes. In the presence of tumor-associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on T-lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T-cells.","Pharmacologic Substance"]
["C99129","AIM2(-1)/HT001(-1)/TAF1B(-1) Frameshift Peptide Vaccine","AIM2(-1)/HT001(-1)/TAF1B(-1) FSP Vaccine|AIM2(-1)/HT001(-1)/TAF1B(-1) Frameshift Peptide Vaccine","A cancer vaccine containing the three frame shift peptides (FSP) AIM2(-1), HT001(-1) and TAF1B(-1), with potential immunomodulating activity. Upon administration, the AIM2(-1)/HT001(-1)/TAF1B(-1) FSP vaccine may induce an immune response against microsatellite instability (MSI) colorectal cancer-associated antigens. Frame shift mutations of AIM2 (absent in melanoma 2, an interferon-inducible protein), HT001 (asteroid homolog 1 or ASTE1, with an unknown function) and TAF1B (TATA box-binding protein-associated RNA polymerase I B, a transcription factor) are seen in MSI-positive colorectal cancers and may be associated with malignant transformation, tumor progression and the presence of tumor-infiltrating lymphocytes. These FSPs all have one-base deletions.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C111575","AKT 1/2 Inhibitor BAY1125976","AKT 1/2 Inhibitor BAY1125976|BAY1125976","An orally bioavailable inhibitor of the serine/threonine protein kinase AKT (protein kinase B) isoforms 1 and 2 (AKT1/2) with potential antineoplastic activity. AKT1/2 inhibitor BAY1125976 selectively binds to and inhibits the phosphorylation and activity of AKT1/2 in a non-ATP competitive manner, which may result in the inhibition of the phosphatidylinositol 3 (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway. This may lead to both the reduction of cell proliferation and the induction of cell apoptosis in AKT-overexpressing tumor cells. The AKT signaling pathway is often deregulated in cancer and is associated with tumor cell proliferation, survival and migration.","Organic Chemical|Pharmacologic Substance"]
["C99172","AKT Inhibitor ARQ 092","AKT Inhibitor ARQ 092|ARQ 092","An orally bioavailable inhibitor of the serine/threonine protein kinase AKT (protein kinase B) with potential antineoplastic activity. AKT inhibitor ARQ 092 binds to and inhibits the activity of AKT in a non-ATP competitive manner, which may result in the inhibition of the PI3K/AKT signaling pathway. This may lead to the reduction in tumor cell proliferation and the induction of tumor cell apoptosis. The AKT signaling pathway is often deregulated in cancer and is associated with tumor cell proliferation, survival and migration.","Organic Chemical|Pharmacologic Substance"]
["C102564","Akt inhibitor AZD5363","AZD5363|Akt inhibitor AZD5363","A novel pyrrolopyrimidine derivative, and an orally available inhibitor of the serine/threonine protein kinase AKT (protein kinase B) with potential antineoplastic activity. AKT inhibitor AZD5363 binds to and inhibits all AKT isoforms. Inhibition of AKT prevents the phosphorylation of AKT substrates that mediate cellular processes, such as cell division, apoptosis, and glucose and fatty acid metabolism. A wide range of solid and hematological malignancies show dysregulated PI3K/AKT/mTOR signaling due to mutations in multiple signaling components. By targeting AKT, the key node in the PIK3/AKT signaling network, this agent may be used as monotherapy or combination therapy for a variety of human cancers.","Organic Chemical|Pharmacologic Substance"]
["C84870","Akt Inhibitor GSK2141795","Akt Inhibitor GSK2141795|GSK2141795|Oral Akt Inhibitor GSK2141795","An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Akt inhibitor GSK2141795 binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C95737","Akt Inhibitor LY2780301","Akt Inhibitor LY2780301|LY2780301","An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Akt inhibitor LY2780301 binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway, thereby leading to inhibition of cell proliferation and the induction of apoptosis in tumor cells. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C90581","Akt Inhibitor MK2206","Akt Inhibitor MK2206|Akt inhibitor MK2206|MK2206","An orally bioavailable allosteric inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Akt inhibitor MK2206 binds to and inhibits the activity of Akt in a non-ATP competitive manner, which may result in the inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C85448","Akt Inhibitor SR13668","Akt Inhibitor SR13668|SRI13668","An orally bioavailable indole-3-carbinol (I3C) analogue inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic and antiangiogenic activities. Akt inhibitor SR13668 binds to and inhibits the activity of Akt, which may result in inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation, and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C113792","Akt/ERK Inhibitor ONC201","Akt/ERK Inhibitor ONC201|ONC201|TIC10","A water soluble, orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) and extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon administration, Akt/ERK inhibitor ONC201 binds to and inhibits the activity of Akt and ERK, which may result in inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt signal transduction pathway as well as the mitogen-activated protein kinase (MAPK)/ERK-mediated pathway. This may lead to the induction of tumor cell apoptosis mediated by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)/TRAIL death receptor type 5 (DR5) signaling in AKT/ERK-overexpressing tumor cells. The PI3K/Akt signaling pathway and MAPK/ERK pathway are upregulated in a variety of tumor cell types and play a key role in tumor cell proliferation, differentiation and survival by inhibiting apoptosis. In addition, ONC201 is able to cross the blood-brain barrier.","Pharmacologic Substance"]
["C123720","Akt-1/2 Inhibitor-treated Tumor Infiltrating Lymphocytes","AKTi-treated TIL|AKTi-treated TILs|Akt-1/2 Inhibitor-treated Tumor Infiltrating Lymphocytes|Akti-1/2-treated Tumor Infiltrating Lymphocytes","Autologous tumor infiltrating lymphocytes (TILs) harvested directly from the infiltrate of a patient's tumor and treated with an inhibitor of the serine/threonine kinases Akt-1 and -2 (Akti-1/2) during ex vivo expansion, with potential antineoplastic activity. Upon reintroduction into the patient, the Akti-1/2-treated TILs recognize and kill cancer cells. Akt inhibition promotes the immunologic memory of the TILs and enhances their expansion, in vivo long-term persistence and antitumor activity.","Cell|Pharmacologic Substance"]
["C994","Alanosine","3-(Hydroxynitrosoamino)-L-alanine|ALANOSINE|Alanosine|L-2-Amino-3-(hydroxynitrosoamino)propionic Acid|L-2-Amino-3-[(N-nitroso)hydroxylamino]propionic Acid|L-2-Amino-3-[(N-nitroso)hydroxylamino]propionic acid|L-Alanosine Sodium|L-Alanosine|SDX-102|alanosine","An amino acid analogue and antibiotic derived from the bacterium Streptomyces alanosinicus with antimetabolite and potential antineoplastic activities. L-alanosine inhibits adenylosuccinate synthetase, which converts inosine monophospate (IMP) into adenylosuccinate, an intermediate in purine metabolism. L-alanosine-induced disruption of de novo purine biosynthesis is potentiated by methylthioadenosine phosphorylase (MTAP) deficiency. The clinical use of this agent may be limited by its toxicity profile. MTAP is a key enzyme in the adenine and methionine salvage pathways.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1498","Aldesleukin","125-L-Serine-2-133-interleukin 2|ALDESLEUKIN|Aldesleukin|Proleukin|Recombinant Human IL-2|Recombinant Human Interleukin-2|aldesleukin|r-serHuIL-2|recombinant human interleukin-2","A recombinant analog of the endogenous cytokine interleukin-2 (IL-2) with immunoregulatory and antineoplastic activities. Aldesleukin binds to and activates the IL-2 receptor, followed by heterodimerization of the cytoplasmic domains of the IL-2R beta and gamma(c) chains; activation of the tyrosine kinase Jak3; and phosphorylation of tyrosine residues on the IL-2R beta chain, resulting in an activated receptor complex. Various cytoplasmic signaling molecules are recruited to the activated receptor complex and become substrates for regulatory enzymes that are associated with the receptor complex. This agent enhances lymphocyte mitogenesis; stimulates long-term growth of human IL-2 dependent cell lines; enhances lymphocyte cytotoxicity; induces lymphokine-activated killer (LAK) cell and natural killer (NK) cell activities; and induces expression of interferon-gamma. Aldesleukin may induce T cell-mediated tumor regression in some tumor types.","Organic Chemical|Pharmacologic Substance"]
["C131019","Aldesleukin Prodrug NKTR-214","Aldesleukin Prodrug NKTR-214|NKTR-214","A recombinant form of the endogenous cytokine interleukin-2 (IL-2) conjugated to six releasable polyethylene glycol (PEG) chains, with potential immunostimulating activity. Upon administration of the aldesleukin prodrug NKTR-214, the IL-2 moiety binds to the IL-2 receptor beta subunit (IL2Rb; IL2Rbeta; CD122). The binding of IL-2 to IL2Rb activates IL2Rb-mediated signaling, which activates cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells, and induces expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). The specific induction of T-cell-mediated cytotoxic immune responses against tumor cells primarily causes tumor cell destruction. IL2Rb plays a key role in the proliferation and activation of effector T-cells. PEG conjugation prevents IL-2 binding to the IL2Ralpha subunit (IL2Ra) because signaling through IL2Ra activates CD4-positive regulatory, immunosuppressive T-cells (Tregs), which would suppress tumor cell killing.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C68921","Aldoxorubicin","Aldoxorubicin|DOXO-EMCH|Doxorubicin-EMCH|INNO-206","A 6-maleimidocaproyl hydrazone derivative prodrug of the anthracycline antibiotic doxorubicin (DOXO-EMCH) with antineoplastic activity. Following intravenous administration, aldoxorubicin binds selectively to the cysteine-34 position of albumin via its maleimide moiety. Doxorubicin is released from the albumin carrier after cleavage of the acid-sensitive hydrazone linker within the acidic environment of tumors and, once located intracellularly, intercalates DNA, inhibits DNA synthesis, and induces apoptosis. Albumin tends to accumulate in solid tumors as a result of high metabolic turnover, rapid angiogenesis, hypervasculature, and impaired lymphatic drainage. Because of passive accumulation within tumors, this agent may improve the therapeutic effects of doxorubicin while minimizing systemic toxicity.","Pharmacologic Substance"]
["C101790","Alectinib","5H-benzo(b)carbazole-3-carbonitrile, 9-Ethyl-6,11-dihydro-6,6-dimethyl-8-(4-(4-morpholinyl)-1-piperidinyl)-11-oxo-|AF-802|AF802|ALECTINIB|Alecensa|Alectinib|CH5424802|RG7853|RO5424802","An orally available inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) with antineoplastic activity. Upon administration, alectinib binds to and inhibits ALK kinase, ALK fusion proteins as well as the gatekeeper mutation ALKL1196M known as one of the mechanisms of acquired resistance to small-molecule kinase inhibitors. The inhibition leads to disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a series of tumors.","Pharmacologic Substance"]
["C1681","Alemtuzumab","ALEMTUZUMAB|Alemtuzumab|Anti-CD52 Monoclonal Antibody|Campath-1H|Campath|LDP-03|Lemtrada|MabCampath|Monoclonal Antibody Campath-1H|alemtuzumab","A recombinant DNA-derived humanized monoclonal antibody directed against the cell surface glycoprotein, CD52. Alemtuzumab is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions derived from a rat monoclonal antibody. This agent selectively binds to CD52, thereby triggering a host immune response that results in lysis of CD52 + cells. CD52 is a glycoprotein expressed on the surface of essentially all normal and malignant B and T cells, a majority of monocytes, macrophages and natural killer (NK) cells, a subpopulation of granulocytes, and tissues of the male reproductive system. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C77370","Alestramustine","ALESTRAMUSTINE|Alestramustine","The l-alanine ester form of estramustine, a combination of the nitrogen mustard normustine coupled via a carbamate to estradiol, with antineoplastic activity. Upon conversion of alestramustine to estramustine, estramustine binds to microtubule-associated proteins (MAPs) and beta tubulin, thereby interfering with microtubule dynamics and leading to microtubule disassembly and cell cyle arrest. Due to the estrogen moiety, this agent is able to selectively bind to and be taken up by estrogen receptor-positive cells.","Pharmacologic Substance"]
["C61082","Algenpantucel-L","Algenpantucel-L|Alpha (1,3) Galactosyltransferase Tumor Vaccine|Alpha-1,3-Galactosyltransferase-expressing Allogeneic Pancreatic Tumor Cell Vaccine|HAPa|HyperAcute-Pancreas Immunotherapy|Hyperacute Pancreatic Cancer Vaccine","A cancer vaccine comprised of irradiated allogeneic pancreatic cancer cells transfected to express murine alpha-1,3-galactosyltransferase with potential antitumor activity. Vaccination is associated with the expression of murine alpha-1,3-galactosyl (alpha-gal) carbohydrate residues on cell membrane glycoproteins and glycolipids of the vaccine pancreatic cancer cell allograft; murine alpha-gal epitopes, not present on human cells, then induce a hyperacute rejection of the vaccine pancreatic cancer cell allograft. The hyperacute rejection involves the binding of pre-existing human anti-alpha-gal antibodies (which naturally occur against gut flora) to murine alpha-gal epitopes, resulting in the rapid activation of antibody-dependent cell-mediated cytotoxicity (ADCC) towards allograft cells. The host immune system then attacks endogenous pancreatic cancer cells, resulting in ADCC towards endogenous pancreatic cancer cells.","Pharmacologic Substance"]
["C71717","Alisertib","ALISERTIB|Alisertib|Aurora A Kinase Inhibitor MLN8237|Benzoic Acid, 4-((9-Chloro-7-(2-Fluoro-6-Methoxyphenyl)-5H-Pyrimido(5,4-d)(2)Benzazepin-2-yl)Amino)-2-Methoxy-|MLN-8237|MLN8237","A second-generation, orally bioavailable, highly selective small molecule inhibitor of the serine/threonine protein kinase Aurora A kinase with potential antineoplastic activity. Alisertib binds to and inhibits Aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cell proliferation. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis, and is thought to regulate spindle assembly. Aberrant expression of Aurora kinases occurs in a wide variety of cancers, including colon and breast cancers.","Chemical Viewed Functionally"]
["C1574","Alitretinoin","3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)2-trans-4-trans-6-cis-8-trans-nonatetraenoic Acid|9-Cis-Retinoic Acid|9-cRA|9-cis Retinoic Acid|9-cis retinoic acid|9-cis-RA|9-cis-Retinoic Acid|ALITRETINOIN|ALRT1057|Alitretinoin|LGD1057|Panretin|Panretyn|Panrexin|Retinoicacid-9-cis","An orally- and topically-active naturally-occurring retinoic acid with antineoplastic, chemopreventive, teratogenic, and embryotoxic activities. Alitretinoin binds to and activates nuclear retinoic acid receptors (RAR) and retinoid X receptors (RXR); these activated receptors act as transcription factors, regulating gene expression that results in the inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C116727","ALK Inhibitor ASP3026","ALK Inhibitor ASP3026|ASP-3026|ASP3026|N2-[2-Methoxy-4-[4-(4-methyl-1-piperazinyl)-1-piperidinyl]phenyl]-N4-[2-[(1-methylethyl)sulfonyl]phenyl]-1,3,5-triazine-2,4-diamine","An orally available, small molecule inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon oral administration, ASP3026 binds to and inhibits ALK tyrosine kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to the disruption of ALK-mediated signaling and the inhibition of cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a series of tumors. Additionally, ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.","Pharmacologic Substance"]
["C105615","ALK Inhibitor RO5424802","ALK Inhibitor RO5424802|RO5424802","An orally available inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) with antineoplastic activity. Upon administration, ALK inhibitor RO5424802 binds to and inhibits ALK kinase, which leads to a disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a series of tumors. Additionally, ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.","Pharmacologic Substance"]
["C102754","ALK Inhibitor X-396","ALK Inhibitor X-396|Anaplastic Lymphoma Kinase Inhibitor X-396|X-396","An orally available small molecule inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) with potential antineoplastic activity. Upon oral administration, X-396 binds to and inhibits ALK kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to the disruption of ALK-mediated signaling and eventually inhibits tumor cell growth in ALK-expressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK is not expressed in healthy adult human tissue but ALK dysregulation and gene rearrangements are associated with a series of tumors; ALK mutations are associated with acquired resistance to small molecule tyrosine kinase inhibitors.","Pharmacologic Substance"]
["C126648","ALK/FAK/Pyk2 Inhibitor CT-707","ALK/FAK/Pyk2 Inhibitor CT-707|CT 707|CT-707","An orally available inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK), focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2), with potential antineoplastic activity. Upon administration, ALK/FAK/Pyk2 inhibitor CT-707 selectively binds to and inhibits ALK , FAK and Pyk2. The inhibition leads to disruption of ALK- , FAK- and Pyk2-mediated signal transduction pathways and eventually inhibits tumor cell growth in ALK-, FAK- and Pyk2-overexpressing tumor cells. Expression of these tyrosine kinases is dysregulated in various tumor types; they play a key role in tumor cell migration, proliferation, survival, and tumor angiogenesis.","Pharmacologic Substance"]
["C114287","ALK/TRK Inhibitor TSR-011","ALK/TRK Inhibitor TSR-011|TSR-011","An orally available inhibitor of both the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and the tropomyosin-related kinases (TRK) TRKA, TRKB, and TRKC, with potential antineoplastic activity. Upon administration, ALK/TRK inhibitor TSR-011 binds to and inhibits both ALK and TRK kinases. The inhibition leads to disruption of ALK- and TRK-mediated signaling and impedes tumor cell growth in ALK/TRK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development; ALK dysregulation and gene rearrangements are associated with a series of tumors. TRK, a family of receptor tyrosine kinases activated by neurotrophins, is mutated in a variety of cancer cell types and plays an important role in tumor cell growth and survival.","Pharmacologic Substance"]
["C116357","ALK5 Inhibitor TEW-7197","ALK5 Inhibitor TEW-7197|TEW-7197|TEW7197|TGFBR1 Inhibitor TEW-7197","An orally bioavailable inhibitor of the serine/threonine kinase, transforming growth factor (TGF)-beta receptor type 1 (TGFBR1), also known as activin receptor-like kinase 5 (ALK5), with potential antineoplastic activity. Upon oral administration, ALK5 inhibitor TEW-7197 inhibits the activity of TGFBR1 and prevents TGF-beta/TGFBR1-mediated signaling. This suppresses tumor growth in TGFBR1-overexpressing tumor cells. TGFBR1, which is overexpressed in a variety of tumor cell types, plays a key role in tumor cell proliferation. Expression of TGF-beta promotes tumor cell proliferation, enhances the migration of tumor cells and suppresses the response of the host immune system to tumor cells.","Pharmacologic Substance"]
["C111685","ALK-FAK Inhibitor CEP-37440","ALK-FAK Inhibitor CEP-37440|CEP-37440","An orally available dual kinase inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and focal adhesion kinase (FAK), with potential antineoplastic activity. Upon administration, ALK-FAK inhibitor CEP-37440 selectively binds to and inhibits ALK kinase and FAK kinase. The inhibition leads to disruption of ALK- and FAK-mediated signal transduction pathways and eventually inhibits tumor cell growth in ALK- and FAK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development; its dysregulation and gene rearrangements are associated with a variety of tumors. The cytoplasmic tyrosine kinase FAK, a signal transducer for integrins, is upregulated and constitutively activated in various tumor types; it plays a key role in tumor cell migration, proliferation, survival, and tumor angiogenesis.","Pharmacologic Substance"]
["C123911","Allodepleted T Cell Immunotherapeutic ATIR101","ATIR101|Allodepleted T Cell Immunotherapeutic ATIR101|Allodepleted T-cell ImmunotheRapeutics|Theralux-ATIR","A cell-based immunotherapeutic product containing T-lymphocyte-enriched leukocytes that are devoid of alloreactive T-lymphocytes, that can potentially be used to restore lymphocyte levels after stem cell transplantations and are derived from partially matched (haploidentical) family donors for blood cancer patients who do not have a matching stem cell donor available. Host alloreactive T-cells, which can cause graft-versus-host disease (GVHD), are eliminated from the donor lymphocytes ex vivo using photodynamic therapy. After allogeneic hematopoietic stem cell transplantation (HSCT), allodepleted T cell immunotherapeutic ATIR101 is administered. This maintains a T-cell-mediated immune response against tumor cells and the donor T-cells can prevent opportunistic infections. ATIR101 does not cause severe, acute GVHD. In addition, administration of ATIR101 eliminates the need for immunosuppressants.","Cell|Pharmacologic Substance"]
["C97265","Allogeneic AML Antigen-expressing Dendritic Cell Vaccine","Allogeneic AML Antigen-expressing Dendritic Cell Vaccine|Allogeneic Acute Myeloid Leukemia Antigen-expressing Dendritic Cell Vaccine|DCOne|DCP-001","A cancer vaccine consisting of allogeneic, immortalized dendritic precursor cells derived from a patient with acute myelogenous leukemia (AML), with potential immunostimulatory and antineoplastic activities. Upon ex vivo stimulation and expansion of the precursor cells into mature, fully functional dendritic cells (DCs) and subsequent administration, the allogeneic AML antigen-expressing DC vaccine may elicit a potent cytotoxic T-cell (CTL) and antibody response against AML antigen-expressing cells, resulting in tumor cell death.","Pharmacologic Substance"]
["C70985","Allogeneic B7.1/HLA-A1 Transfected Tumor Cell Vaccine","Allogeneic B7.1/HLA-A1 Transfected Tumor Cell Vaccine","An allogeneic whole cell vaccine, derived from irradiated allogenic tumor cells manipulated to express human B7.1 (CD80 antigen) and human leukocyte antigen (HLA) A1, with potential antitumor activity. Vaccination with allogeneic B7.1/HLA-A1 transfected tumor cell vaccine may elicit a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor cell proliferation.","Pharmacologic Substance"]
["C99215","Allogeneic CD19-specific CAR-modified CD8 Plus Central Memory-derived Virus-specific T Cells","Allogeneic CD19-specific CAR-modified CD8 Plus Central Memory-derived Virus-specific T Cells|Allogeneic CD19CAR-TCM Cells","A preparation of allogeneic Epstein-Barr virus (EBV)- and human cytomegalovirus (CMV)-specific CD8+ central memory-derived T effector-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) anti-CD19/CD3 zeta chain fusion protein coupled to the intracellular signal domain of CD28 antigen, with potential immunostimulating, anti-viral and antineoplastic activities. Upon infusion, allogeneic CD19-specific CAR-modified CD8+ central memory-derived virus-specific T cells directs the T-lymphocytes to CD19-expressing tumor cells, stimulating a selective toxicity to tumor cells which may eventually result in tumor cell lysis. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The viral specific T-cells exert antiviral immunity.","Pharmacologic Substance"]
["C71540","Allogeneic CD4+ Memory Th1-like T Cells/Microparticle-bound Anti-CD3/anti-CD28","AlloStim|Allogeneic CD4+ Memory Th1-like T Cells/Microparticle-bound Anti-CD3/anti-CD28","A preparation consisting of allogeneic, differentiated Th1-like T cells bound to T cell-stimulating monoclonal antibodies with potential antitumor activity. More specifically, allogeneic CD4+ memory Th1-like T cells/microparticle-bound anti-CD3/anti-CD28 are composed of a proprietary preparation of mismatched, allogeneic differentiated CD4+ memory Th1-like T cells bound to paramagnetic, epoxy-covered 4.5 micron microparticles with covalently bound anti-CD3/anti-CD28 monoclonal antibodies at a 2:1 bead:cell ratio. The CD4+ memory Th1-like T cells are derived from precursors found in the circulation of a normal donor. Stimulated by the microparticle-bound monoclonal antibodies, the infused T cells produce pro-inflammatory, anti-tumor cytokines such as like IFN-gamma, TNF-beta, and IL-2, disabling tumor immune avoidance mechanisms and stimulating the host immune system to both reject the infused T cells and kill tumor cells.","Cell|Pharmacologic Substance"]
["C96741","Allogeneic CD56-positive CD3-negative Natural Killer Cells","Allogeneic CD56-positive CD3-negative Natural Killer Cells","A population of allogeneic lymphocytes expressing the CD56 surface antigen and exhibiting a lack of CD3, with immunomodulating activity. Upon infusion of allogeneic CD56-positive CD3-negative natural killer (NK) cells, these cells are able to secrete cytokines and recognize and kill tumor cells as well as virally-infected cells. CD56 is a transmembrane glycoprotein also known as NCAM (Neural Cell Adhesion Molecule).","Cell|Pharmacologic Substance"]
["C99902","Allogeneic Dendritic Cell Vaccine COMBIG-DC","Allogeneic Dendritic Cell Vaccine COMBIG-DC|COMBIG-DC","A cancer vaccine consisting of allogeneic, immortalized dendritic cells (DCs) loaded with tumor specific antigens and activated, with potential immunostimulatory and antineoplastic activities. Upon intratumoral administration of the allogeneic dendritic cell vaccine COMBIG-DC, these activated DCs attract natural killer (NK) cells, induce an anti-inflammatory response leading to the induction of NK-cell-mediated tumor cell death. Upon release of tumor associated antigens (TAAs) from the lysed tumor cells, these antigens are taken up by antigen presenting cells which activate the immune system to elicit a potent cytotoxic T-cell (CTL) response against the TAAs, resulting in the death of TAAs-expressing tumor cells.","Pharmacologic Substance"]
["C61434","Allogeneic Dendritic Cell-Myeloma Idiotype Vaccine","Allogeneic Dendritic Cell-Myeloma Idiotype Vaccine","A cell-based vaccine composed of allogeneic dendritic cells pulsed ex-vivo with an autologous myeloma idiotype with potential antineoplastic activity. Upon administration, allogeneic dendritic cell-myeloma idiotype vaccine may stimulate the host immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against myeloma cells, resulting in cell lysis.","Cell|Pharmacologic Substance"]
["C62769","Allogeneic Epstein-Barr Virus-Specific Cytotoxic T-Lymphocytes","Allogeneic EBV-Specific CTL|Allogeneic Epstein-Barr Virus-Specific Cytotoxic T-Lymphocytes","A preparation of allogeneic Epstein-Barr virus (EBV) specific cytotoxic T-lymphocytes (CTL) with potential antineoplastic activity. The allogeneic EBV-specific CTLs are either harvested from a donor with an EBV-positive tumor or are donor CTLs activated against EBV-specific antigens ex vivo. Adm inistration into a patient exerts a CTL response against EBV-positive tumor cells or EBV-infected cells. This results in cell lysis and inhibition of cancer cell proliferation. EBV, a ubiquitous human herpes virus, is associated with various malignancies, including nasopharyngeal carcinoma, Hodgkin's disease, non-Hodgkin's lymphoma, and other lymphomas.","Cell|Pharmacologic Substance"]
["C113296","Allogeneic Glioblastoma Stem-like Cell Line Lysate-pulsed Autologous Dendritic Cell Vaccine","Allogeneic Glioblastoma Stem-like Cell Line Lysate-pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysates from an allogeneic glioblastoma (GBM) stem-like cell line, with potential immunostimulatory and antineoplastic activities. Upon administration allogeneic glioblastoma stem-like cell line lysate-pulsed autologous dendritic cell vaccine exposes the immune system to GBM stem cell antigens, which may result in cytotoxic T lymphocyte (CTL) and antibody responses against GBM cells. This leads to GBM cell lysis. GBM stem-like cells contain a specific range of antigens that are essential for the neoplastic growth and survival of GBM cells.","Cell|Pharmacologic Substance"]
["C90540","Allogeneic GM-CSF-Based Myeloma Cell Vaccine","Allogeneic GM-CSF-Based Myeloma Cell Vaccine|Allogeneic Granulocyte Macrophage Colony-Stimulating Factor-Based Myeloma Cellular Vaccine","An allogeneic tumor cell vaccine containing myeloma cancer cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene with potential antineoplastic activity. Upon vaccination, allogeneic GM-CSF-based myeloma cellular vaccine secretes GM-CSF, which may potentiate a tumor-specific cytotoxic T-lymphocyte (CTL) response against myeloma cancer cell-associated antigens.","Immunologic Factor|Pharmacologic Substance"]
["C48371","Allogeneic GM-CSF-Secreting Breast Cancer Vaccine","Allogeneic GM-CSF-Secreting Breast Cancer Vaccine|GM-CSF BREAST VAC|GM-CSF-secreting breast tumor vaccine","An allogenic vaccine consisting of irradiated breast cancer cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene. Upon vaccination, the genetically modified cells secrete GM-CSF, thereby potentiating a tumor-specific T cell response against breast cancer cell-asociated antigens.","Pharmacologic Substance"]
["C98282","Allogeneic GM-CSF-secreting Lethally Irradiated Whole Melanoma Cell Vaccine","Allogeneic GM-CSF-secreting Lethally Irradiated Whole Melanoma Cell Vaccine|GVAX Melanoma Vaccine","An allogeneic cancer vaccine composed of lethally irradiated whole melanoma cancer cells that are genetically modified to secrete the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon intradermal injections, allogeneic GM-CSF-secreting lethally irradiated whole melanoma cell vaccine secretes GM-CSF. In turn, GM-CSF may stimulate the body's immune system against tumor cells by enhancing the activation of dendritic cells (DCs) and promoting antigen presentation to both B- and T-lymphocytes. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.","Pharmacologic Substance"]
["C101892","Allogeneic GM-CSF-secreting Tumor Vaccine PANC 10.05 pcDNA-1/GM-Neo","Allogeneic GM-CSF-secreting Tumor Vaccine PANC 10.05 pcDNA-1/GM-Neo|PANC 10.05 pcDNA-1/GM-Neo","An allogeneic cancer vaccine composed of lethally irradiated, whole pancreatic cancer cells transfected with a plasmid carrying the gene for cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Allogeneic GM-CSF-secreting tumor vaccine PANC 10.05 pcDNA-1/GM-Neo secretes GM-CSF thereby activating dendritic cells, promoting antigen presentation to B- and T-cells, and promoting a cytotoxic T-lymphocyte (CTL) response. This may eventually kill tumor cells. The pancreatic tumor cells are derived from the PANC 10.05 tumor cell line.","Cell|Pharmacologic Substance"]
["C101891","Allogeneic GM-CSF-secreting Tumor Vaccine PANC 6.03 pcDNA-1/GM-Neo","Allogeneic GM-CSF-secreting Tumor Vaccine PANC 6.03 pcDNA-1/GM-Neo|PANC 6.03 pcDNA-1/GM-Neo","An allogeneic cancer vaccine composed of lethally irradiated, whole pancreatic cancer cells transfected with a plasmid carrying the gene for cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Allogeneic GM-CSF-secreting tumor vaccine PANC 6.03 pcDNA-1/GM-Neo secretes GM-CSF thereby activating dendritic cells, promoting antigen presentation to B- and T-cells, and promoting a cytotoxic T-lymphocyte (CTL) response. This may eventually kill tumor cells. The pancreatic tumor cells are derived from the PANC 6.03 tumor cell line.","Cell|Pharmacologic Substance"]
["C107169","Allogeneic HLA-A2/4-1BB ligand-expressing Melanoma Vaccine","Allogeneic HLA-A2/4-1BB ligand-expressing Melanoma Vaccine","An allogeneic melanoma cell vaccine derived from a cell line with high expression of melanoma associated antigens and genetically modified to express both HLA-A2 and 4-1BB ligand, with potential immunostimulating and antineoplastic activities. Upon administration, the 4-1BB ligand of the allogeneic HLA-A2/4-1BB ligand-expressing melanoma vaccine binds to 4-1BB on activated T-lymphocytes, which induces a strong immune response against HLA-A2 positive melanoma cells.","Cell|Pharmacologic Substance"]
["C90577","Allogeneic IL13-Zetakine/HyTK-Expressing-Glucocorticoid Resistant Cytotoxic T Lymphocytes GRm13Z40-2","Allogeneic IL13-Zetakine/HyTK-Expressing-Glucocorticoid Resistant Cytotoxic T Lymphocytes GRm13Z40-2|GRm13Z40-2","A preparation of glucocorticoid receptor (GR) negative, allogeneic cytotoxic T-lymphocytes (CTLs) expressing a membrane-tethered interleukin 13 (IL13) cytokine chimeric T-cell antigen receptor (zetakine), with potential antineoplastic activity. Upon transfection of donor T-lymphocytes with a plasmid encoding a fusion protein of the IL13-zetakine and the selection-suicide expression enzyme HyTK, these modified CTLs are expanded and introduced into a patient with glioblastoma multiforme (GBM). This agent specifically targets IL13 receptor alpha2, a glioma-restricted cell-surface epitope; the CTLs exert their cytolytic effect thereby killing IL13Ra2-expressing glioma cells. In addition, IL13-zetakine redirected CTLs induce production of certain cytokines. Furthermore, due to the fact that these CTLs are GR negative, they can be used concomitantly with glucocorticoid therapy. The IL13-zetakine consists of an extracellular IL-13 E13Y mutein-human IgG4 hinge-Fc chimera fused to human cytoplasmic CD3-zeta via the transmembrane domain of human CD4.","Cell|Pharmacologic Substance"]
["C103862","Allogeneic Irradiated Melanoma Cell Vaccine CSF470","Allogeneic Irradiated Melanoma Cell Vaccine CSF470|CSF 470 Vaccine|CSF470 Vaccine","An allogeneic cancer vaccine composed of a mixture of lethally irradiated whole melanoma cancer cells obtained from four different melanoma cell lines, with potential immunostimulating and antineoplastic activities. Upon intradermal injections, allogeneic irradiated melanoma cell vaccine may stimulate the body's immune system to exert a cytotoxic T-lymphocyte response and antibody-dependent cellular cytotoxicity (ADCC) against the melanoma cancer cells.","Pharmacologic Substance"]
["C79799","Allogeneic Large Multivalent Immunogen Breast Cancer Vaccine","Allogeneic LMI Breast Cancer Vaccine|Allogeneic Large Multivalent Immunogen Breast Cancer Vaccine","A cancer vaccine, containing human-specific large multivalent immunogens (LMIs) isolated from the membrane fraction of cells from a breast cancer cell line, with potential immunostimulatory and antineoplastic activities. Upon administration, allogeneic large multivalent immunogen breast cancer vaccine may stimulate a cytotoxic T lymphocyte (CTL) immune response against tumor cells that express the breast cancer cell-specific LMIs.","Immunologic Factor|Pharmacologic Substance"]
["C78862","Allogeneic Large Multivalent Immunogen Melanoma Vaccine LP2307","Allogeneic LMI Melanoma Vaccine LP2307|Allogeneic Large Multivalent Immunogen Melanoma Vaccine LP2307|LP2307","A cancer vaccine, containing human-specific large multivalent immunogen (LMI) isolated from plasma membrane fractions of the melanoma cell lines MSM-M1 and MSM-M2, with potential immunostimulating and antineoplastic activities. Upon administration, allogeneic large multivalent immunogen melanoma vaccine LP2307 may stimulate a CD8+ cytotoxic T lymphocyte (CTL) response against melanoma tumor cells that express melanoma-specific LMI.","Immunologic Factor|Pharmacologic Substance"]
["C78201","Allogeneic LMP1/LMP2-Specific Cytotoxic T-Lymphocytes","Allogeneic LMP1/LMP2-Specific Cytotoxic T-Lymphocytes","A preparation of cytotoxic T-lymphocytes (CTL), specifically reactive to the Epstein-Barr virus (EBV) latent membrane proteins (LMP) 1 and 2, with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMC) are collected from a donor and are exposed ex vivo to dendritic cells (DCs) transfected with a replication-deficient adenovirus encoding EBV LMP1/2 to generate LMP1/2-specific CTL which are subsequently expanded. Administration of allogeneic LMP1-/LMP2- specific CTL to patients with LMP1/2-positive tumors may result in a specific CTL response against tumor cells expressing LMP1 and LMP2, resulting in cell lysis and inhibition of tumor cell proliferation. As tumor associated antigens (TAAs), LMP1 and LMP2 are expressed in various malignancies including nasopharyngeal cancer and EBV-positive Hodgkin lymphoma.","Cell|Pharmacologic Substance"]
["C78861","Allogeneic Melanoma Vaccine AGI-101H","AGI-101H|Allogeneic Melanoma Vaccine AGI-101H","A cancer vaccine derived from two gentically modified human melanoma cell lines with potential antineoplastic activity. Allogeneic melanoma vaccine AGI-101H consists of a 1:1 mixture of cells from two genetically modified human melanoma cell lines, designated as Mich1H6 and Mich2H6, that have been gamma-irradiated to render the cells non-proliferative. Upon administration, this vaccine may stimulate a cytotoxic immune response against melanoma tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C121640","Allogeneic Mesothelioma Tumor Lysate-pulsed Autologous Dendritic Cell Vaccine","Allogeneic Mesothelioma Tumor Lysate-pulsed Autologous DC Vaccine|Allogeneic Mesothelioma Tumor Lysate-pulsed Autologous Dendritic Cell Vaccine|MesoCancerVac","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with a mixture of lysates from five allogeneic mesothelioma tumor cell lines, with potential immunostimulatory and antineoplastic activities. Upon leukapheresis, DCs are loaded with allogeneic mesothelioma tumor cell lysates. Upon re-administration of the allogeneic mesothelioma tumor lysate-pulsed autologous DC vaccine, the immune system is exposed to an undefined amount of mesothelioma-associated antigens, which stimulates the induction of a specific cytotoxic T-lymphocyte (CTL) response against mesothelioma tumor cells and leads to tumor cell lysis.","Cell|Pharmacologic Substance"]
["C94209","Allogeneic Natural Killer Cell Line MG4101","Allogeneic NK Cell Line MG4101|Allogeneic Natural Killer Cell Line MG4101|MG4101","A population of allogeneic, cytotoxic natural killer (NK) cells with potential antitumor activity. Allogeneic natural killer cell line MG4101 is derived from cells of a normal, healthy donor upon leukapheresis and activation.","Cell|Pharmacologic Substance"]
["C117231","Allogeneic Natural Killer Cell Line NK-92","Allogeneic Natural Killer Cell Line NK-92|NK-92 Cells|NK-92","A proprietary, human cytotoxic cell line composed of allogeneic, activated, interleukin-2 (IL-2) dependent-natural killer cells derived from a 50-year old male patient with rapidly progressive non-Hodgkin's lymphoma, with potential antineoplastic activity. As NK-92 cells are devoid of killer inhibitory receptors (KIRs; also called killer cell immunoglobulin-like receptors), which are negative regulators of NK cell activity, cancer cells are unable to suppress the cancer cell killing ability of the NK-92 cells. Upon infusion of the allogeneic NK cell line NK-92, the NKs recognize and bind to tumor cells. This leads to the secretion and release of perforins, granzymes, cytokines and chemokines, which results in cancer cell lysis and apoptosis. In addition, NK-92 cells express high affinity Fc receptors, which bind to therapeutic antibodies; therefore, this agent can enhance antibody dependent cellular cytotoxicity (ADCC) of co-administered therapeutic antibodies.","Cell|Pharmacologic Substance"]
["C95213","Allogeneic Renal Cell Carcinoma Vaccine MGN1601","Allogeneic Renal Cell Carcinoma Vaccine MGN1601|IL-7/GM-CSF/CD80/CD154-encoding Synthetic dSLIM-30L1 Allogeneic Renal Cell Carcinoma Vaccine MGN1601|MGN1601","A whole cell vaccine comprised of irradiated allogeneic renal cell carcinoma (RCC) with potential immunostimulating and antineoplastic activities. Allogeneic renal cell carcinoma vaccine MGN1601 contains two active ingredients: 1) genetically modified allogeneic RCC cells that are transiently transfected with four different MIDGE (Minimalistic Immunogenically Defined Gene Expression) vectors encoding IL-7, GM-CSF, CD80 and CD154 and 2) the synthetic DNA-based immunomodulator dSLIM-30L1, a TLR9 agonist.. Vaccination results in expression of IL-7, GM-CSF, CD80 and CD154, which all contribute to the activation or enhancement of immune responses. Furthermore, administration of this RCC vaccine may elicit a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor growth. TLR9 is a member of the TLR family, which plays a fundamental role in pathogen recognition and activation of innate immunity.","Cell|Pharmacologic Substance"]
["C1983","Allogeneic Tumor Cell Vaccine","Allogeneic Tumor Cell Vaccine|allogenic cell vaccine","A vaccine composed of tumor cells isolated from the tumor of one patient, killed and processed, and administered to another patient to stimulate cytotoxic immune responses to a similar tumor cell type. The cells found in this type of whole-cell vaccine express many cell-surface tumor-associated antigens. This vaccine is frequently administered with an adjuvant immunostimulant. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C114494","Allosteric Bcr-Abl Tyrosine Kinase Inhibitor ABL001","ABL001|Allosteric Bcr-Abl Tyrosine Kinase Inhibitor ABL001","An orally bioavailable, allosteric Bcr-Abl tyrosine kinase inhibitor with potential antineoplastic activity. Designed to overcome resistance, ABL001 binds to the Abl portion of the Bcr-Abl fusion protein at a location that is distinct from the ATP-binding domain. This binding results in the inhibition of Bcr-Abl-mediated proliferation and enhanced apoptosis of Philadelphia chromosome-positive (Ph+) hematological malignancies. The Bcr-Abl fusion protein tyrosine kinase is an abnormal enzyme produced by leukemia cells that contain the Philadelphia chromosome.","Pharmacologic Substance"]
["C81667","Almurtide","2-Acetamido-3-O-((((1S)-1-(((1R)-1-carbamoyl-3- carboxypropyl)carbamoyl)ethyl)carbamoyl)methyl)-2-deoxy-D- glucopyranose|ALMURTIDE|Almurtide|Cgp-11637|N-Acetyl-nor-muramyl-L-alanyl-D-isoglutamine|nor-MDP|norMDP","A synthetic muramyl dipeptide (MDP) analogue with potential immunostimulating and antineoplastic activity. As a derivative of the mycobacterial cell wall component MDP, almurtide activates both monocytes and macrophages. This results in the secretion of cytokines and induces the recruitment and activation of other immune cells, which may result in indirect tumoricidal or cytostatic effects.","Pharmacologic Substance"]
["C94214","Alpelisib","Alpelisib|BYL719|Phosphoinositide 3-kinase Inhibitor BYL719","An orally bioavailable phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. Alpelisib specifically inhibits PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway, thereby inhibiting the activation of the PI3K signaling pathway. This may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C48372","Alpha Fetoprotein Adenoviral Vector Vaccine","AdVhAFP|Alpha Fetoprotein Adenoviral Vector Vaccine","A vaccine consisting of a recombinant adenoviral vector encoding alpha fetoprotein. After vaccination, expressed alpha fetoprotein may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells that express alpha fetoprotein, resulting in tumor cell lysis. (NCI05)","Pharmacologic Substance"]
["C48373","Alpha Fetoprotein Plasmid DNA Vaccine","Alpha Fetoprotein Plasmid DNA Vaccine|phAFP","A vaccine consisting of plasmid DNA encoding alpha fetoprotein. After vaccination, expressed alpha fetoprotein may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells that express alpha fetoprotein, resulting in tumor cell lysis. (NCI05)","Pharmacologic Substance"]
["C1720","Alpha Galactosylceramide","Alpha Galactosylceramide|KRN-7000|KRN7000|a-GalCer","A potent alpha galactosylceramide modified from marine-sponge that stimulates the immune system to exhibit antitumor activity.","Organic Chemical|Pharmacologic Substance"]
["C113647","Alpha-1,3-galactosyltransferase-expressing Allogeneic Renal Cell Carcinoma Vaccine","Alpha-1,3-galactosyltransferase-expressing Allogeneic Renal Cell Carcinoma Vaccine|HAR|HyperAcute Renal","An allogeneic renal cell cancer (RCC) vaccine composed of cell line-derived RCCs that are genetically engineered to express the murine alpha-1,3-galactosyltransferase (GalT), with potential immunostimulatory and antineoplastic activities. Not naturally occurring in humans, GalT catalyzes the expression of foreign alpha-1,3-galactosyl (alpha-gal) carbohydrate epitopes on the cell membranes of the allogeneic RCCs present in the vaccine. This induces a hyperacute rejection reaction involving pre-existing human anti-alpha-gal antibodies, which bind to the foreign alpha-gal epitopes expressed by the allogeneic RCCs. This results in complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) towards endogenous RCCs with unmodified carbohydrate epitopes.","Cell|Pharmacologic Substance"]
["C82258","Alpha-1-Proteinase Inhibitor Human",".ALPHA.1-PROTEINASE INHIBITOR HUMAN|A1AT|A1PI|AAT|Alpha 1 Antitrypsin|Alpha-1 Antitrypsin|Alpha-1-Antiproteinase|Alpha-1-Proteinase Inhibitor Human|Aralast|Prolastin-C","Human serum-derived alpha-1 proteinase inhibitor (alpha-1-antitrypsin or AAT) with immunomodulating and anti-inflammatory activity. Upon administration, AAT reduces the production of proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-32, IL-6, and proteinase 3, and induces the production of anti-inflammatory cytokines, such as IL-10 and the IL-1 receptor antagonist IL-1RN. This agent also downregulates heparan sulfate and reduces the expansion of cytotoxic effector T cells, interferes with the maturation of dendritic cells and increases T regulatory cells. Altogether, AAT may attenuate acute graft-versus-host disease (GvHD) and may facilitate graft acceptance and survival. In addition, AAT enhances levels of cAMP and activation of cAMP-dependent protein kinase A. AAT, a 52kD protein and serine protease inhibitor, belongs to the serpin superfamily.","Pharmacologic Substance"]
["C91378","Alpha-fetoprotein Peptide-Pulsed Autologous Dendritic Cell Vaccine","Alpha-fetoprotein Peptide-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine comprised of autologous dendritic cells pulsed with four alpha-fetoprotein (AFP) peptides, with potential immunostimulatory and antineoplastic activities. Upon administration, AFP peptide-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against AFP-expressing cancer cells, resulting in tumor cell lysis. AFP is overexpressed in a variety of cancer cells.","Immunologic Factor|Pharmacologic Substance"]
["C120550","alpha-Folate Receptor-targeting Thymidylate Synthase Inhibitor ONX-0801","BGC 945|N-[4-[2-Propyn-1-yl[(6S)-4,6,7,8-tetrahydro-2-(hydroxymethyl)-4-oxo-3H-cyclopenta[g]quinazolin-6-yl]amino]benzoyl]-l-gamma-glutamyl-d-glutamic Acid|ONX 0801|ONX-0801|alpha-Folate Receptor-targeting Thymidylate Synthase Inhibitor ONX-0801","An alpha-folate receptor (aFR)-mediated inhibitor of thymidylate synthase (TS), with potential antineoplastic activity. Upon intravenous infusion, ONX-0801 selectively targets and binds to aFR-expressing tumor cells. Upon uptake by aFR, this agent binds to and inhibits TS. This reduces thymine nucleotide synthesis, inhibits both DNA synthesis and cell division, and leads to tumor cell apoptosis. TS catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), an essential precursor for DNA synthesis, and plays a key role in cell growth and division. aFR, a cell-surface receptor glycoprotein, is overexpressed on various tumor cell types, but is minimally expressed by normal, healthy tissue.","Pharmacologic Substance"]
["C78200","Alpha-Gal Glycosphingolipids","Alpha-Gal Glycosphingolipids|GSL alpha-GAL|Galactose(alpha1,3,)galactose Glycosphingolipids","A preparation of glycosphingolipids (GSL), containing the disaccharide epitope galactose-alpha-1,3-galactose (alpha-Gal), with potential antineoplastic activity. Upon intratumoral injection, alpha-Gal glycosphingolipids may stimulate the immune system to mount complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) responses against alpha-Gal GSL, which may result in tumor cell death; these responses involve natural anti-alpha-Gal immunoglobulins (Igs).  As antibodies that occur naturally due to sensitization to alpha-Gal present on symbiotic bacterial flora, anti-alpha-Gal Igs are present in unusually high amounts in human sera.  GSL represent a glycolipid subtype containing the amino alcohol sphingosine; tumor-associated GSL antigens contain various oligosaccharide residues.","Organic Chemical|Pharmacologic Substance"]
["C78489","Alpha-Galactosylceramide-Pulsed Autologous Dendritic Cells","Alpha-Galactosylceramide-Pulsed Autologous Dendritic Cells|DC-KRN7000|KRN7000-Pulsed Autologous Dendritic Cells","A cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with the marine sponge glycolipid alpha-galactosylceramide (alpha-GalCer) with potential immunostimulatory and antimetastatic activities. Upon administration, alpha-galactosylceramide-pulsed autologous dendritic cells may result in the activation and proliferation of a subset of endogenous natural killer T (NKT) cells, B cells, and CD4+ and CD8+ T cells, and the production of interferon-gamma and interleukin-12; these cascade events may result in a T helper-1 cell-biased proinflammatory antitumor immune response. The NKT cell ligand alpha-GalCer was originally isolated from the marine sponge Agelas mauritianusis.","Cell|Pharmacologic Substance"]
["C106371","Alpha-lipoic Acid-Palladium/Vitamin/Mineral Supplement","Alpha-lipoic Acid-Palladium/Vitamin/Mineral Supplement|LAPd|Palladium Lipoic Complex|PolyMVA","A proprietary water- and lipid-soluble polymer-based nutritional supplement composed of a complex mixture of alpha-lipoic acid bound to palladium (Palladium Lipoic Acid Complex (PdLA)) and other minerals, vitamins and amino acids, including vitamins B1, B2 and B12, formylmethionine, acetyl cysteine, and trace amounts of molybdinum, rhodium, and ruthenium, with potential anti-oxidant and cytoprotective activities. Upon oral administration, the alpha-lipoic acid-palladium/vitamin/mineral supplement acts as a free radical scavenger, crosses the cell membrane and is able to transfer electrons from fatty acids to DNA via the electron transport chain in mitochondria, which protects against DNA damage. This could protect non-cancerous cells from the oxidative damage caused by radiation and chemotherapy. In addition, in the hypoxic conditions found within tumors, the excess electrons can generate free radicals within mitochondria and could induce both cytochrome c release and apoptosis.","Pharmacologic Substance"]
["C28795","Alpha-Thioguanine Deoxyriboside","6H-Purine-6-thione, 2-amino-9-(2-deoxy-alpha-D-erythro-pentofuranosyl)-1,9-dihydro- (9CI)|9H-Purine-6-thiol, 2-amino-9-(2-deoxy-alpha-D-erythro-pentofuranosyl)-|A-TGDR|Alpha-Thioguanine Deoxyriboside|Thioguanine 9-alpha-D-2'-deoxyriboside|alpha-2'-Deoxy-6-thioguanosine|alpha-2'-Deoxythioguanosine|alpha-Thiodeoxyguanosine","A purine analog with potential antineoplastic activity. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C117234","Alpha-tocopheryloxyacetic Acid","2,5,7,8-Tetramethyl-(2R-(4R,8R,12-trimethyltridecyl) chroman-6-yloxy) Acetic Acid|Alpha-tocopheryloxyacetic Acid|a-TEA|alpha-TEA","An orally bioavailable vitamin E derivative with potential antineoplastic and immunostimulating activities. Upon administration, alpha-tocopheryloxyacetic acid (alpha-TEA) induces tumor autophagy; the autophagosomes formed, which carry tumor associated antigens (TAAs), allow for increased cross-presentation of TAAs by professional antigen-presenting cells (APCs). This activates a T cell-mediated T helper type 1 (TH1) response, generates a cytotoxic T-lymphocyte (CTL) response against cancer cells, and reduces the frequency of regulatory T-cell (Treg) differentiation. In addition, alpha-TEA modulates the release of various cytokines and chemokines and induces tumor cell apoptosis. Altogether, this results in decreased tumor cell proliferation.","Pharmacologic Substance"]
["C64846","Alpha-type-1 Polarized Dendritic Cells","Alpha-type-1 Polarized Dendritic Cells|alphaDC1","A mature polarized dendritic cell with potent immunostimulating activity. Treating dendritic cells (DCs) with interferon-alpha (IFN-a) and polyinosinic:polycytidylic acid (p-I:C) in addition to a cytokine cocktail (tumor necrosis factor alpha/Interleukin-1beta/IFN-gamma) produces mature but not exhausted alpha type-1 polarized DCs (alphaDC1) that are capable of: 1) high responsiveness to other lymphoid chemokines, and 2) producing high level of interleukin-12p70 (IL-12p70). Therefore, alphaDC1 has a much more significant capability of inducing helper T cell (CD4+ T-cell) responses in comparison with the \"gold standard\" DCs. When pulsed with specific tumor associated antigens (TAAs), alphaDC1 is able to induce a potent cytotoxic T lymphocyte (CTL) response against TAAs; as a result it can be used as a cancer vaccine.","Cell|Pharmacologic Substance"]
["C118290","Altiratinib","Altiratinib|DCC-2701","An orally bioavailable inhibitor of c-Met/hepatocyte growth factor receptor (HGFR), vascular endothelial growth factor receptor type 2 (VEGFR2), Tie2 receptor tyrosine kinase (TIE2), and tropomyosin receptor kinase (Trk), with potential antiangiogenic and antineoplastic activities. Upon administration, altiratinib selectively binds to c-Met, VEGFR2, Tie2 and Trk tyrosine kinases, which may lead to the inhibition of endothelial cell migration, proliferation and survival. This also results in both an inhibition of tumor cell proliferation and increased tumor cell death in c-Met/VEGFR2/Tie2/Trk-expressing cells. These receptor tyrosine kinases (RTKs), frequently overexpressed or mutated by a variety of tumor cell types, play crucial roles in the regulation of angiogenesis, tumor cell growth and survival.","Pharmacologic Substance"]
["C544","Altretamine","2,4,6-Tris(dimethylamino)-s-triazine|2,4,6-tris(dimethylamino)-s-triazine|ALTRETAMINE|Altretamine|ENT 50852|ENT-50852|HMM|HXM|Hemel|Hexalen|Hexaloids|Hexamethylamine|Hexamethylmelamine|Hexastat|Hexinawas|N,N,N',N',N\",N\"-hexamethyl-1,3,5-triazine-2,4,6-triamine|N,n,n',N\"N\"-hexamethyl-1,3,5,-triazine-2,4,6,-triamine|RB-1515|WR-95704|altretamine|s-Triazine, 2,4,6-tris(dimethylamino)-","A synthetic cytotoxic s-triazine derivative similar in structure to alkylating agent triethylenemelamin with antineoplastic activity.  Although the precise mechanism by which altretamine exerts its cytotoxic effect is unknown, N-demethylation of altretamine may produce reactive intermediates which covalently bind to DNA, resulting in DNA damage. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C73998","ALVAC(2) Melanoma Multi-antigen Vaccine","ALVAC(2) Melanoma Multi-antigen Vaccine","A therapeutic cancer vaccine, based on a replication-defective recombinant canarypox virus (ALVAC) encoding multiple melanoma antigens, with potential immunostimulatory and antineoplastic activities. Vaccination with ALVAC(2) melanoma multi-antigen therapeutic vaccine may stimulate the host immune system to mount an immune response against antigen-expressing melanoma cells, resulting in inhibition of tumor growth and/or metastasis.","Pharmacologic Substance"]
["C79832","ALVAC(2)-NY-ESO-1 (M)/TRICOM Vaccine","ALVAC(2)-NY-ESO-1 (M)/TRICOM Vaccine|vCP2292","A cancer vaccine consisting of a replication-defective recombinant canarypox virus [ALVAC(2)] encoding the cancer-testis antigen NY-ESO and the TRIad of COstimulatory Molecules (B7-1, ICAM-1 and LFA-3; also called TRICOM), with potential immunostimulatory and antineoplastic activities. Upon administration, ALVAC(2)/NY-ESO (M)/TRICOM vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against NY-ESO-expressing cancer cells, which may result in the inhibition of tumor cell proliferation. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cells, including bladder, breast, hepatocellular, melanoma, and prostate tumor cells. TRICOM may enhance antigen presentation and activate cytotoxic T-cells. In addition, ALVAC(2) encodes the vaccinia virus (vv) E3L ad K3L genes, which may potentiate the translation of the NY-ESO and TRICOM genes.","Pharmacologic Substance"]
["C1977","ALVAC-CEA B7.1 Vaccine","ALVAC CEA B7.1 Vaccine|ALVAC-CEA B7.1 Vaccine","A cancer vaccine that uses a viral vector system derived from the canarypox virus engineered to target the carcinoembryonic antigen (CEA). It causes infected cells to temporarily display CEA and activates the immune system to attack the tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C1648","ALVAC-CEA Vaccine","ALVAC-CEA Vaccine|ALVAC-CEA vaccine|ALVAC-CEA","A cancer vaccine consisting of ALVAC, a highly attenuated poxvirus strain derived from the canarypox virus, encoding for the tumor associated antigen (TAA) carcinoembryonic antigen (CEA), with potential antineoplastic activity. Upon administration, ALVAC-CEA vaccine expresses CEA and may stimulate a host immune response against tumor cells expressing CEA. This may result in the inhibition of tumor growth and/or metastasis. CEA is overexpressed in a variety of tumor cell types.","Immunologic Factor|Pharmacologic Substance"]
["C90558","ALVAC-ESO-1 Vaccine","ALVAC-ESO-1 Vaccine","A cancer vaccine consisting of a replication-defective recombinant canarypox virus (ALVAC) encoding the cancer-testis antigen NY-ESO-1, with potential immunostimulatory and antineoplastic activities. Upon administration, ALVAC-ESO-1 vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against NY-ESO-1-expressing cancer cells, which may result in the inhibition of tumor cell proliferation. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C2485","ALVAC-hB7.1","ALVAC-hB7.1","A vaccine comprise of a canarypox viral vector that carries the gene for human B7.1 (CD80 antigen) with potential use as an autologous therapeutic cancer vaccine.  Tumor cells harvested from a patient are infected with ALVAC-hB7 1, thereby producing an autologous cell line that exhibits increased expression of HLA class I and class II, CD54 (ICAM), and CD80. Increased expression of these proteins by this autologous cell line may activate an antitumor T-cell response when the modified cells are administered to the patient. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C73999","ALVAC-MART-1 Vaccine","ALVAC-MART-1 Vaccine","A cancer vaccine containing a replication-defective recombinant canarypox virus (ALVAC), encoding an epitope of MART-1 (melanoma antigen recognized by T-cells), with potential immunostimulatory and antineoplastic activities. Upon administration, the MART-1 epitope is expressed by the ALVAC vector in ALVAC-MART-1 vaccine; a host cytotoxic T lymphocyte (CTL) response against MART-1-expressing tumor cells may follow, resulting in tumor cell lysis and decreased tumor cell proliferation.","Pharmacologic Substance"]
["C38142","Alvespimycin","17-(Dimethylaminoethylamino)-17-Demethoxygeldanamycin|17-DMAG|17-dimethylaminoethylamino-17-demethoxygeldanamycin|ALVESPIMYCIN|Alvespimycin|Geldanamycin,17-demethoxy-17-((2-(dimethylamino)ethyl)amino)-","An analogue of the antineoplastic benzoquinone antibiotic geldanamycin. Alvespimycin binds to HSP90, a chaperone protein that aids in the assembly, maturation and folding of proteins. Subsequently, the function of Hsp90 is inhibited, leading to the degradation and depletion of its client proteins such as kinases and transcription factors involved with cell cycle regulation and signal transduction.","Antibiotic|Organic Chemical|Pharmacologic Substance"]
["C76665","Alvespimycin Hydrochloride","17-DMAG HCl|ALVESPIMYCIN HYDROCHLORIDE|Alvespimycin Hydrochloride|BMS-826476|Geldanamycin,17-demethoxy-17-((2-(dimethylamino)ethyl)amino)-, Monohydrochloride|KOS-1022","The hydrochloride salt of alvespimycin, an analogue of the antineoplastic benzoquinone antibiotic geldanamycin. Alvespimycin binds to HSP90, a chaperone protein that aids in the assembly, maturation and folding of proteins. Subsequently, the function of Hsp90 is inhibited, leading to the degradation and depletion of its client proteins such as kinases and transcription factors involved with cell cycle regulation and signal transduction.","Pharmacologic Substance"]
["C62483","Amatuximab","AMATUXIMAB|Amatuximab|Anti-Mesothelin Monoclonal Antibody MORAb-009|Immunoglobulin G1, Anti-(mesothelin) (Human-Mouse Monoclonal MORAb-009 Heavy Chain), Disulfide with Human-Mouse Monoclonal MORAb-009 Kappa-Chain, Dimer|MORAb-009|anti-mesothelin monoclonal antibody MORAb-009","A chimeric IgG1 monoclonal antibody against human mesothelin with potential anti-tumor activity. Amatuximab specifically targets mesothelin, a cell surface glycoprotein involved in cell adhesion and overexpressed on many epithelial-derived cancer cells. Upon binding to the mesothelin antigen, amatuximab triggers an antibody dependent cellular cytotoxicity (ADCC)-mediated host immune response against mesothelin-expressing cells, resulting in cell lysis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C73320","Ambamustine","AMBAMUSTINE|Ambamustine|N-(3-(m-(Bis(2-chloroethyl)amino)phenyl)-N-(3-(p-fluorophenyl)-L-alanyl)-L-alanyl)-L-methionine, Ethyl Ester|PTT-119","A tripeptidic nitrogen mustard compound and bifunctional alkylating agent with antineoplastic activity.","Pharmacologic Substance"]
["C72627","Ambazone","AMBAZONE|Ambazone|Faringosept|p-Benzoquinone Amidinohydrazone Thiosemicarbazone","An antiseptic agent with potential antibacterial and antileukemic activity. Although the exact mechanism of action remains to be fully elucidated, ambazone appears to interfere with the membrane-bound nucleotide system by increasing the intracellular concentration of cAMP in leukemia cells and macrophages, which potentially contributes to this agent's antineoplastic activity. Furthermore, this agent's affinity for various cellular targets, i.e. membranes, nucleic acids and proteins, may contribute to the overall antibacterial effect.","Pharmacologic Substance"]
["C1342","Ametantrone","1,4-bis[[2-[(2-Hydroxyethyl)amino]ethyl]amino]9,10-anthracenedione|9, 10-Anthracenedione, 1, 4-bis[[2-[(2-hydroxyethyl)amino]ethyl]amino]-|AMETANTRONE|Ametantrone","A topoisomerase II inhibitor of the anthrapyrazole family that causes covalent cross-links in DNA of tumor cells.","Antibiotic|Organic Chemical"]
["C488","Amifostine","2-[(3-Aminopropyl)amino]ethanethiol Dihydrogen Phosphate Ester Trihydrate|AMIFOSTINE|APAETP|Amifostine Trihydrate|Amifostine|Aminopropylaminoethylthiophosphoric Acid Trihydrate|Cytofos|Ethiofos|Ethyol|Gammaphos|S-(N-(3-Aminopropyl)-2-aminoethyl)thiophosphoric Acid Trihydrate|S-2-(3-Aminopropylamino)ethylphosphorothioic Acid Trihydrate|WR 2721|WR-2721|WR2721|YM-08310","The trihydrate form of a phosphorylated aminosulfhydryl compound. After dephosphorylation of amifostine by alkaline phosphatase to an active free sulfhydryl (thiol) metabolite, the thiol metabolite binds to and detoxifies cytotoxic platinum-containing metabolites of cisplatin and scavenges free radicals induced by cisplatin and ionizing radiation. The elevated activity of this agent in normal tissues results from both the relative abundance of alkaline phosphatase in normal tissues and the greater vascularity of normal tissues compared to tumor tissues.","Organic Chemical|Pharmacologic Substance"]
["C1488","Aminocamptothecin","9-AC|9-AMINOCAMPTOTHECIN|9-Amino-20-(S)-camptothecin|9-amino-20(S)-camptothecin|9-amino-20-camptothecin|9-amino-CPT|9-amino-camptothecin|9-aminocamptothecin|Aminocamptothecin|aminocamptothecin","A water-insoluble camptothecin derivative.  Aminocamptothecin binds to the nuclear enzyme topoisomerase I, thereby inhibiting repair of single-strand DNA breakages.  Because the terminal lactone ring of aminocamptothecin required for the agent's antitumor activity spontaneously opens under physiological conditions to an inactive carboxy form, the drug must be administered over an extended period of time to achieve effective cytotoxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2452","Aminocamptothecin Colloidal Dispersion","9-aminocamptothecin colloidal dispersion|9AC colloidal dispersion|Aminocamptothecin Colloidal Dispersion","A colloidal dispersion formulation of 9-Aminocamptothecin, a water-insoluble camptothecin derivative. Aminocamptothecin binds to the nuclear enzyme topoisomerase I, thereby inhibiting repair of single-strand DNA breakages. Because the terminal lactone ring of aminocamptothecin required for the agent's antitumor activity spontaneously opens under physiological conditions to an inactive carboxy form, the drug must be administered over an extended period of time to achieve effective cytotoxicity.","Pharmacologic Substance"]
["C235","Aminopterin","4-Amino-PGA|4-Aminofolic Acid|4-Aminofolic acid|4-Aminopteroylglutamic Acid|4-Aminopteroylglutamic acid|AMINOPTERIN|APGA|Aminopterin|Aminopteroylglutamic Acid|aminopterin","A synthetic derivative of pterins with antineoplastic and immunosuppressive properties.  As a folate analogue, aminopterin competes for the folate binding site of the enzyme dihydrofolate reductase, thereby blocking tetrahydrofolate synthesis, and resulting in depletion of nucleotide precursors and inhibition of DNA, RNA and protein synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C74554","Aminopterin Sodium","AMINOPTERIN SODIUM|Aminopterin Sodium|Sodium Aminopterin","The sodium salt of a pterin derivative with antineoplastic and immunosuppressive properties.  As a folate analogue, aminopterin competes for the folate binding site of the enzyme dihydrofolate reductase, thereby blocking tetrahydrofolate synthesis, and resulting in depletion of nucleotide precursors and inhibition of DNA, RNA and protein synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C74000","AML mRNA Positive Lysate Loaded Autologous Dendritic Cell Vaccine","AML mRNA Positive Lysate Loaded Autologous Dendritic Cell Vaccine|Acute Myelogenous Leukemia mRNA Plus Lysate Loaded Autologous Dendritic Cell Vaccine","A cancer vaccine consisting of autologous dendritic cells loaded with separate preparations of acute myelogenous leukemia (AML) cell lysate and AML-specific messenger RNA (mRNA) with potential immunostimulatory and antineoplastic activities. Upon administration, AML mRNA plus lysate loaded autologous dendritic cell vaccine may elicit a potent cytotoxic T-cell (CTL) response against AML cells, resulting in tumor cell death. Autologous dendritic cells doubly-loaded with AML cell lysate and AML-specific mRNA may elicit superior primary, recall, and effector lytic immune responses compared to autologous dendritic cells loaded with tumor lysate or tumor mRNA alone.","Pharmacologic Substance"]
["C79714","Ammonia N-13","AMMONIA N-13|Ammonia N 13|Ammonia N-13|Ammonia-(sup 13)N","A radiopharmaceutical composed of ammonia labeled with the radioisotope nitrogen N 13 that can be used, during positron emission tomography (PET), as a blood flow imaging agent and potentially as a tumor imaging agent. Upon intravenous administration, ammonia N 13 distributes to various organs in the body, such as the myocardium, liver, kidneys and brain. This agent is taken up by cells and is retained following conversion to glutamine N 13 by glutamine synthetase (GS). Upon PET, organ perfusion and the presence of cancer cells can be assessed. GS, an enzyme that catalyzes the synthesis of glutamine from glutamate and ammonia, is overexpressed in a variety of cancers and plays a key role in cancer cell proliferation.","Pharmacologic Substance"]
["C90592","Amolimogene Bepiplasmid","Amolimogene Bepiplasmid|Amolimogene|Bacterially Derived DNA and Microparticles Made of Poly(D,L-lactide-co-glydolide)|DNA (synthetic Plasmid p3kDRalphaHPV16-18)|ZYC101a","A plasmid DNA-based vaccine consisting of small biodegradable poly(lactide-co-glicolide) polymer microparticles encapsulating plasmid-DNA vector encoding a chimeric protein comprising epitopes derived from the E6 and E7 oncoproteins of the human papillomavirus (HPV) types 16 and 18, with potential antineoplastic activity. Upon intramuscular vaccination, amolimogene bepiplasmid may elicit the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells positive for HPV-16 and -18 E6 and E7 and may result in a reduction in tumor cell growth. HPV types 16 and 18 oncoproteins E6 and E7 are most commonly involved in cervical cancer.","Pharmacologic Substance"]
["C61306","Amonafide L-Malate","5-amino-2-[2-(dimethylamino)ethyl]-1H-benz[de]isoquinoline-1,3(2H)-dione (2S)-2-ydroxybutanedioate|AMONAFIDE L-MALATE|AS1413|Amonafide L-Malate|Butanedioic Acid, 2-hydroxy-, (2S)-, compd. with 5-amino-2-(2-(dimethylamino)ethyl)-1h-benz[de]isoquinoline-1,3(2h)-dione (1:1)|XAN-02|Xanafide","The malate salt of amonafide, an imide derivative of naphthalic acid, with potential antineoplastic activity. Amonafide intercalates into DNA and inhibits topoisomerase II, resulting in DNA double-strand breaks (DSB) and inhibition of DNA replication and RNA synthesis.","Pharmacologic Substance"]
["C80089","Amrubicin","(+)-(7S,9S)-9-Acetyl-9-amino-7-((2-deoxy-beta-D-erythro-pentopyranosyl)oxy)- 6,11-dihydroxy-7,8,9,10-tetrahydrotetracene-5,12-dione|AMRUBICIN|Amrubicin|amrubicin","A synthetic 9-amino-anthracycline with antineoplastic activity. Amrubicin intercalates into DNA and inhibits the activity of topoisomerase II, resulting in inhibition of DNA replication, and RNA and protein synthesis, followed by cell growth inhibition and cell death. This agent has demonstrated a higher level of anti-tumor activity than conventional anthracycline drugs without exhibiting any indication of the cumulative cardiac toxicity common to this class of compounds.","Antibiotic|Organic Chemical"]
["C47948","Amrubicin Hydrochloride","(+)-(7S,9S)-9-Acetyl-9-amino-7-((2-deoxy-beta-D-erythro-pentopyranosyl)oxy)- 6,11-dihydroxy-7,8,9,10-tetrahydrotetracene-5,12-dione hydrochloride|AMRUBICIN HYDROCHLORIDE|Amrubicin Hydrochloride|Calsed|SM-5887|SMP-5887","The hydrochloride salt of a third-generation synthetic 9-amino-anthracycline with antineoplastic activity. Amrubicin intercalates into DNA and inhibits the activity of topoisomerase II, resulting in inhibition of DNA replication, and RNA and protein synthesis, followed by cell growth inhibition and cell death. This agent has demonstrated a higher level of anti-tumor activity than conventional anthracycline drugs without exhibiting any indication of the cumulative cardiac toxicity common to this class of compounds.","Antibiotic|Organic Chemical"]
["C240","Amsacrine","4'-(9-Acridinylamino)methane-sulfon-m-anisidide|AMSA|AMSACRINE|Acridinyl Anisidide|Amekrin|Amsa P-D|Amsacrine|Amsidine|Amsidyl|CI-880|Cain's Acridine|Lamasine|N-[4-(9-Acridinylamino)-3-methoxyphenyl]methanesulfonamide|SN 11841|SN-11841|SN-21429|amsacrine|m-AMSA","An aminoacridine derivative with potential antineoplastic activity. Although its mechanism of action is incompletely defined, amsacrine may intercalate into DNA and inhibit topoisomerase II, resulting in DNA double-strand breaks, arrest of the S/G2 phase of the cell cycle, and cell death. This agent's cytotoxicity is maximal during the S phase of the cell cycle when topoisomerase levels are greatest. In addition, amsacrine may induce transcription of tumor promoter p53 protein and block p53 ubiquitination and proteasomal degradation, resulting in p53-dependent tumor cell apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C96771","Amsacrine Lactate","AMSACRINE LACTATE|Amsacrine Lactate|Methanesulfon-m-anisidide, 4'-(9-acridinylamino)-, compd. with Lactic Acid|N-(4-(9-Acridinylamino)-3-methoxyphenyl)methanesulfonamide compd. with Lactic Acid|m-AMSA lactate","The lactate form of amsacrine, an aminoacridine analog and topoisomerase II inhibitor, with antineoplastic activity. Although the exact relationship between DNA binding and its activity has yet to be fully elucidated, amsacrine intercalates DNA through its acridine moiety, and its nonintercalative headgroup impedes topoisomerase II activity, augmenting enzyme-mediated DNA cleavage and resulting in DNA double-strand breaks. This ultimately induces programmed cell death.","Organic Chemical|Pharmacologic Substance"]
["C38684","Amsilarotene","AMSILAROTENE|Amsilarotene|TAC 101|TAC-101","A retinobenzoic acid with potential antineoplastic activity. Amsilarotene inhibits retinoblastoma-gene product (RB) phosphorylation and increases the presence of 2 cyclin-dependent kinase (CDK) inhibitors, resulting in cell cycle arrest.  This agent also causes a cytotoxic decline in cyclin A and thymidylate synthase expression.","Pharmacologic Substance"]
["C75926","Amustaline","(N,N-bis(2-chloroethyl))-2-aminoethyl-3-((acridin-9-yl)amino)propionate|AMUSTALINE|Amustaline|S-303","A quinacrine mustard compound with potential antineoplastic activity. Amustaline binds to, intercalates and crosslinks DNA and RNA. This agent is mainly used for ex vivo purposes, specifically for the inactivation of pathogens such as viruses, protozoa and bacteria in red blood cells (RBCs).","Pharmacologic Substance"]
["C75035","Amustaline Dihydrochloride","AMUSTALINE DIHYDROCHLORIDE|Amustaline Dihydrochloride","The hydrochloride salt form of amustaline, a quinacrine mustard compound with potential antineoplastic activity. Amustaline binds to, intercalates and crosslinks DNA and RNA. This agent is mainly used for ex vivo purposes, specifically for the inactivation of pathogens such as viruses, protozoa and bacteria in red blood cells (RBCs).","Pharmacologic Substance"]
["C71750","Amuvatinib","AMUVATINIB|Amuvatinib|HPK56|MP470|Receptor Tyrosine Kinase Inhibitor MP470","An orally bioavailable synthetic carbothioamide with potential antineoplastic activity. Multitargeted receptor tyrosine kinase inhibitor MP470 binds to mutant forms of the stem cell factor receptor (c-Kit; SCFR), inhibiting clinically relevant mutants of this receptor tyrosine kinase that may be associated with resistance to therapy. In addition, MP470 inhibits activities of other receptor tyrosine kinases, such as c-Met, Ret oncoprotein, and mutant forms of Flt3 and PDGFR alpha, which are frequently dysregulated in variety of tumors. This agent also suppresses the induction of DNA repair protein Rad51, thereby potentiating the activities of DNA damage-inducing agents. Mutant forms of c-Kit are often associated with tumor chemoresistance.","Pharmacologic Substance"]
["C95776","Amuvatinib Hydrochloride","1-Piperazinecarbothioamide, N-(1,3-Benzodioxol-5-Ylmethyl)-4-Benzofuro(3,2-D)Pyrimidin-4-Yl-, Hydrochloride (1:1)|AMUVATINIB HYDROCHLORIDE|Amuvatinib Hydrochloride|HPK56 HCl|MP-470 HCI|MP470 HCl|N-(1,3-Benzodioxol-5-Ylmethyl)-4-(Benzofuro(3,2-D)Pyrimidin-4-Yl)Piperazine-1- Carbothioamide Monohydrochloride","The hydrochloride salt of an orally bioavailable synthetic carbothioamide with potential antineoplastic activity. Multitargeted receptor tyrosine kinase inhibitor MP470 binds to mutant forms of the stem cell factor receptor (c-Kit; SCFR), inhibiting clinically relevant mutants of this receptor tyrosine kinase that may be associated with resistance to therapy. In addition, MP470 inhibits activities of other receptor tyrosine kinases, such as c-Met, Ret oncoprotein, and mutant forms of Flt3 and PDGFR alpha, which are frequently dysregulated in variety of tumors. This agent also suppresses the induction of DNA repair protein Rad51, thereby potentiating the activities of DNA damage-inducing agents. Mutant forms of c-Kit are often associated with tumor chemoresistance.","Pharmacologic Substance"]
["C38717","Anakinra","ANAKINRA|Anakinra|Kinaret|Kineret|anakinra|rIL-1ra|rIL1RN","A recombinant human nonglycosylated interleukin-1 (IL-1) receptor antagonist with potential antineoplastic activity. Anakinra binds to the IL-1 receptor, thereby blocking the binding of the IL-1 to and activation of its receptor. Blockade of IL-1 activity may inhibit the cascade of downstream pro-angiogenic factors such as vascular endothelial cell growth factor, tumor necrosis factor-alpha, and IL-6, resulting in inhibition of tumor angiogenesis. (NCI04)","Pharmacologic Substance"]
["C1607","Anastrozole","2,2'-[5-(1H-1,2,4-Triazol-1-ylmethyl)-1,3-phenylene]di(2-methylpropionitrile)|ANASTROZOLE|Alpha,alpha,alpha', alpha'-tetramethyl-5-(1H-1,2,4-triazol-1-ylmethyl)-1,3-benzenediacetonitrile|Anastrazole|Anastrozole|Arimidex|ICI D1033|ICI-D1033|ZD-1033|anastrozole","A nonsteroidal inhibitor of estrogen synthesis that resembles paclitaxel in chemical structure.  As a third-generation aromatase inhibitor, anastrozole selectively binds to and reversibly inhibits aromatase, a cytochrome P-450 enzyme complex found in many tissues including those of the premenopausal ovary, liver, and breast; aromatase catalyzes the aromatization of androstenedione and testosterone into estrone and estradiol, the final step in estrogen biosynthesis.  In estrogen-dependent breast cancers, ananstrozole may inhibit tumor growth. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C950","Anaxirone","1,2,4-triglycidylurazol|ANAXIRONE|Anaxirone|TGU|Triglycidylurazol","A synthetic triepoxide alkylating agent with potential antineoplastic activity. Anaxirone alkylates DNA via actual or derived epoxide groups, resulting in inhibition of DNA synthesis. This agent has been shown to exhibit a broad spectrum of antineoplastic activity against experimental tumors, including those resistant to other alkylating agents.","Organic Chemical|Pharmacologic Substance"]
["C80636","Ancitabine","ANCITABINE|Ancitabine","A cytarabine congener prodrug with antineoplastic activity. Upon administration, ancitabine is slowly hydrolyzed into cytarabine, which is converted to the active triphosphate form and competes with deoxycytidine triphosphate for incorporation into DNA. Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle. This agent also inhibits DNA and RNA polymerases, resulting in a decrease in cell growth. Compared to cytarabine, a more prolonged, consistent cytarabine-mediated therapeutic effect may be achieved with ancitabine because of the slow hydrolytic conversion of ancitabine to cytarabine.","Pharmacologic Substance"]
["C403","Ancitabine Hydrochloride","6H-furo(2',3':4,5)oxazolo(3,2-a)pyrimidine-2-methanol,2,3,3a,9a-tetrahydro-3-hydroxy-6-imino-,(2R(2alpha,3beta,3a beta,9a beta))|ANCITABINE HYDROCHLORIDE|Ancid|Ancitabine Hydrochloride|Ancitabine hydrochloride|Ancytabine Hydrochloride|CycloCMP Hydrochloride|CycloCMP hydrochloride|Cyclocytidine HCL|Cyclocytidine Hydrochloride|Cyclocytidine hydrochloride|Cyclocytidine|U-33, 624A","The hydrochloride salt of a cytarabine congener prodrug with antineoplastic activity. Upon administration, ancitabine is slowly hydrolyzed into cytarabine. Subsequently, cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA. Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle. Cytarabine agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Compared to cytarabine, a more prolonged, consistent cytarabine-mediated therapeutic effect may be achieved with ancitabine because of the slow hydrolytic conversion of ancitabine to cytarabine.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C98290","Androgen Antagonist APC-100","APC-100|Androgen Antagonist APC-100","An orally available, vitamin E derivative and androgen receptor (AR) antagonist with potential anti-oxidant, chemopreventative and antineoplastic activity. APC-100 binds to ARs in target tissues thereby inhibiting androgen-induced receptor activation and facilitating the formation of inactive complexes that cannot be translocated to the nucleus. By inhibiting the formation of the complex between androgen activated AR- and the AP1 transcription factor JunD, the expression of androgen-responsive genes are blocked. One of such gene is spermidine/spermine N1-acetyl transferase gene (SSAT) that is responsible for the breakdown of polyamines, which are produced in high levels by prostatic epithelial cells, into reactive oxygen species (ROS) that cause cellular damage. APC-100 may ultimately lead to an inhibition of growth in both AR-dependent and AR-independent prostate tumor cells.","Pharmacologic Substance"]
["C92574","Androgen Receptor Antagonist ARN-509","ARN-509|Androgen Receptor Antagonist ARN-509","A small molecule and androgen receptor (AR) antagonist with potential antineoplastic activity. ARN-509 binds to AR in target tissues thereby preventing androgen-induced receptor activation and facilitating the formation of inactive complexes that cannot be translocated to the nucleus. This prevents binding to and transcription of AR-responsive genes. This ultimately inhibits the expression of genes that regulate prostate cancer cell proliferation and may lead to an inhibition of cell growth in AR-expressing tumor cells.","Pharmacologic Substance"]
["C126335","Androgen Receptor Antagonist SHR3680","Androgen Receptor Antagonist SHR3680|SHR 3680|SHR3680","An orally bioavailable androgen receptor (AR) antagonist with potential antineoplastic activity. Upon administration, SHR3680 competitively binds to AR in target tissues, which both prevents androgen-induced receptor activation and facilitates the formation of inactive complexes that cannot be translocated to the nucleus. This prevents binding to and transcription of AR-responsive genes, inhibits the expression of genes that regulate prostate cancer cell proliferation, and may lead to an inhibition of cell growth of AR-expressing tumor cells. ARs are overexpressed in prostate cancer and play a key role in prostate cancer cell proliferation.","Pharmacologic Substance"]
["C116326","Androgen Receptor Antisense Oligonucleotide AZD5312","AZD5312|Androgen Receptor Antisense Oligonucleotide AZD5312|ISIS-ARRx|ISIS-AZ1Rx","An antisense oligonucleotide targeting the androgen receptor (AR) mRNA, with potential antineoplastic activity. Upon intravenous administration, AZD5312 hybridizes with AR mRNA, which blocks translation of the AR protein. This both inhibits AR-induced tumor cell growth and promotes apoptosis in AR-overexpressing tumor cells. AR is overexpressed in certain breast and prostate cancers and is involved in tumor cell proliferation and survival.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C96742","Androgen Receptor Antisense Oligonucleotide EZN-4176","Androgen Receptor Antisense Oligonucleotide EZN-4176|EZN-4176","A locked nucleic acid (LNA)-based antisense oligonucleotide targeting the androgen receptor (AR) mRNA, with potential antineoplastic activity. Upon administration, EZN-4176 is hybridized and releases the complementary sequences of AR mRNA, thereby blocking translation of the AR protein and inhibiting AR-induced tumor cell growth and promoting tumor cell apoptosis in AR-overexpressing tumor cells. AR is overexpressed in certain breast and prostate cancers and is involved in tumor cell proliferation and survival. LNAs contain a methylene bridge linking 2'-oxygen and 4'-carbon of ribose sugar rings, thereby increasing their thermal stability and decreasing degradation.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C116726","Androgen Receptor Downregulator AZD3514","AZD3514|Androgen Receptor Downregulator AZD3514|SARD AZD3514","An orally available selective androgen receptor (AR) downregulator (SARD), with potential antineoplastic activity. Upon oral administration, AZD3514 binds to the AR ligand binding domain and inhibits the binding of androgen, thereby preventing androgen-dependent AR signaling. AZD3514 also causes downregulation of AR expression, which further prevents AR-mediated signaling. This results in an inhibition of proliferation in AR-overexpressing tumor cells. AR plays a key role in the proliferation of castration-resistant prostate cancer cells.","Pharmacologic Substance"]
["C124654","Androgen Receptor Inhibitor EPI-506","AR Inhibitor EPI-506|Androgen Receptor Inhibitor EPI-506|EPI-506","An orally bioavailable, small molecule inhibitor of the N-terminal domain (NTD) of the androgen receptor (AR), with potential antineoplastic activity. Upon oral administration, AR inhibitor EPI-506 specifically binds to the NTD of AR, thereby inhibiting both AR activation and the AR-mediated signaling pathway. This inhibits cell growth in AR-overexpressing tumor cells. AR is overexpressed in prostate cancers and is involved in proliferation, survival and chemoresistance of tumor cells.","Pharmacologic Substance"]
["C121777","Androgen Receptor Ligand-binding Domain-encoding Plasmid DNA Vaccine MVI-118","AR LBD-encoding Plasmid DNA Vaccine MVI-118|Androgen Receptor Ligand-binding Domain-encoding Plasmid DNA Vaccine MVI-118|MVI-118|pTVG-AR Vaccine|pTVG-AR","A cancer vaccine containing pTVG4 plasmid DNA encoding the human androgen receptor (AR) ligand-binding domain (LBD) (pTVG-AR), with potential immunostimulating and antineoplastic activities. Upon intradermal administration of AR LBD-encoding plasmid DNA vaccine MVI-118, the plasmid DNA vaccine expresses AR LBD and may stimulate the host immune system to generate a cytotoxic T-lymphocyte (CTL) response against AR LBD-expressing prostate cancer cells. This reduces proliferation of AR-expressing tumor cells. AR, a tumor-associated antigen (TAA) overexpressed in prostate cancer cells, plays a key role in the development and progression of prostate cancer; its expression is correlated with poor prognosis.","Pharmacologic Substance"]
["C61637","Andrographolide","(1R-(1-alpha(E(S)),4a-beta,5alpha,6alpha,8a-alpha))-3-(2-(decahydro-6-hydroxy-5-(hydroxymethyl)-5,8a-dimethyl-2-methylene-1-naphthalenyl)ethylidene)dihydro-4-hydroxy-2(3H)-furanone|(3E,4S)-3-[2-[(1R,4aS,5R,6R,8aS)-6-hydroxy-5-(hydroxymethyl)-5,8a-dimethyl-2-methylidene-3,4,4a,6,7,8-hexahydro-1H-naphthalen-1-yl]ethylidene]-4-hydroxyoxolan-2-one|(3E,4S)-4-hydroxy-3-{2-[(1R,4aS,5R,6R,8aS)-6-hydroxy-5-(hydroxymethyl)-5,8a-dimethyl-2-methylidenedecahydronaphthalen-1-yl]ethylidene}dihydrofuran-2(3H)-one|2(3H)-Furanone, 3-(2-(decahydro-6-hydroxy-5-(hydroxymethyl)-5,8a-dimethyl-2-methylene-1-naphthalenyl)ethylidene)dihydro-4-hydroxy-, (1R-(1-alpha(E(S*)),4a-beta,5-alpha,6-alpha,8a-alpha))-|3-(2-(decahydro-6-hydroxy-5-(hydroxymethyl)-5,8a-dimethyl-2-methylenenaphthyl)ethylidene)dihydro-4-hydroxyfuran-2(3H)-one|3alpha,14,15,18-tetrahydroxy-5b,9bH,10a-labda-8(20),12-dien-16-oic acid gamma-Lactone|ANDROGRAPHOLIDE|Andrographis|Andrographolide","A labdane diterpenoid that is produced by the Andrographis paniculata plant, which has a broad range of therapeutic applications including anti-inflammatory and anti-platelet aggregation activities and potential antineoplastic properties. Since andrographolide has multiple therapeutic activities there are several proposed mechanisms of action for this agent. The anti-inflammatory effects of this agent appear to be related to the inhibition of nitric oxide (NO) production by macrophages. This agent may activate the NO/cyclic GMP pathway and inhibit both the phospholipase C gamma 2 (PLC gamma2)/protein kinase C (PKC) and PI3K/AKT-MAPK signaling pathways in activated platelets to inhibit platelet aggregation. In activated platelets, these three signaling pathways are downstream of integrin activation mediated by collagen binding and influence the association of fibrinogen with its receptors. Additionally, andrographolide may exert its anti-cancer activity through the induction of cell cycle arrest at G0/G1 phase and the stimulation of lymphocyte proliferation and activation. These processes could result in decreased proliferation of and increased immunocytotoxicity against tumor cells.","Pharmacologic Substance"]
["C78831","Androstane Steroid HE3235","17Alpha-ethynyl-5alpha-androstane-3alpha, 17Beta-diol|APOPTONE|Androstane Steroid HE3235|HE3235","An orally bioavailable adrenal steroid analogue with potential antineoplastic activity. Androstane steroid HE3235 appears to bind the androgen receptor (AR), down-regulating anti-apoptotic genes, such as Bcl-2, while increasing the expression of pro-apoptotic genes, such as caspases. In vitro and in vivo studies indicate that this agent inhibits androstenediol-dependent LNCaP cell tumor growth. In addition, HE3235 may potentiate chemotherapeutic agents by down-regulating ABCG2, the gene encoding the multi-drug resistant (MDR) protein MDR2.","Pharmacologic Substance"]
["C98293","Anetumab Ravtansine","ANETUMAB RAVTANSINE|Anetumab Ravtansine|BAY 94-9343","A fully human IgG1 monoclonal antibody directed against the cell surface glycoprotein mesothelin and conjugated to the maytansinoid DM4 with potential antineoplastic activity. The monoclonal antibody moiety of anetumab ravtansine targets and binds to the tumor associated antigen mesothelin; upon internalization, the DM4 moiety binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of mesothelin-expressing tumor cells. Mesothelin is overexpressed on all mesotheliomas as well as many ovarian and pancreatic cancers while minimally expressed on normal tissue.","Pharmacologic Substance"]
["C88301","Ang2/VEGF-Binding Peptides-Antibody Fusion Protein CVX-241","Ang2/VEGF-Binding Peptides-Antibody Fusion Protein CVX-241|CVX-241|PF-05057459","A fusion protein containing angiopoietin-2 (Ang2) and vascular endothelial growth factor (VEGF) derived peptides covalently attached, via a proprietary diketone linker, to a proprietary humanized catalytic aldolase monoclonal antibody, with potential antiangiogenic and antineoplastic activities. The Ang2/VEGF peptide moieties of Ang2/VEGF-binding peptides-antibody fusion protein CVX-241 bind to Ang2 and VEGF receptors, which may inhibit tumor angiogenesis and tumor cell proliferation. The proprietary humanized catalytic IgG1 monoclonal aldolase antibody contains reactive lysine residues in its binding sites, which react covalently with compounds having a diketone function; the Ang2 and VEGFR peptide moieties are then covalently attached to the diketone linkers via a proprietary spacer. Both VEGF and Ang2 are upregulated in a variety of cancer cell types and play a crucial role in angiogenesis. This agent possesses an enhanced half-life compared to the naked peptides.","Pharmacologic Substance"]
["C60817","Angelica sinensis Root Extract","Angelica Root|Angelica root|Angelica sinensis Root Extract|Angelicae sinensis Radix Extract|Chinese Angelica|Dang qui|Dong quai|Female Ginseng|Tanggwi|Toki|dong quai","An herbal extract derived from the root of the plant Angelica sinensis with possible antiinflammatory, antispasmodic, vasodilatory, estrogenic, and antitumor activities. Angelica sinensis contains volatile oils, including safrole, isosafrole, and n-butylphthalide; coumarin derivatives, including psoralens, bergapten, osthol, imperatorin, and oxypeucedanin; and ferulic acid. The coumarin derivatives in this agent may vasodilate and relax smooth muscle and may exhibit additive anticoagulant effects. Ferulic acid, a phenolic phytochemical present in plant cell walls, may neutralize free radicals such as reactive oxygen species. In addition, Angelica sinensis extract has been shown to inhibit the growth and induce apoptosis of glioblastoma mutltiforme brain tumor cells through p53-dependent and p53-independent pathways.","Pharmacologic Substance|Plant"]
["C71539","Angiogenesis Inhibitor GT-111","Angiogenesis Inhibitor GT-111|GT-111","An adenovirus encoding an endothelial cell-specific, murine pre-proendothelin-1 (PPE-1) promoter and a Fas-based chimeric death receptor with potential anti-angiogenic activity. Endothelial cell-specific transcriptional control of the adenoviral vector is achieved by the use of a modified murine PPE-1 promoter that is specifically activated in PPE-1-expressing angiogenic endothelial cells residing in the tumor microvasculature. Subsequently, the Fas-c (Fas-chimeric) death receptor, containing Fas and tumor necrosis factor (TNF) receptor 1 (TNFR1) moieties, is expressed in angiogenic endothelial cells; endothelial cell-specific Fas-mediated apoptosis is initiated by the binding of TNF-alpha, abundant in the tumor microenvironment, to the TNFR1 moiety of the expressed Fas-c death receptor.","Pharmacologic Substance"]
["C82413","Angiogenesis Inhibitor JI-101","Angiogenesis Inhibitor JI-101|JI-101","An orally active inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor beta (PDGFRb), and the ephrin B4 receptor B4 (EphB4) with potential antiangiogenic and antineoplastic activities. Angiogenesis inhibitor JI-101 binds to and inhibits VEGFR2, PDGFRb and EphB4, which may inhibit tumor angiogenesis and, so, cellular proliferation in tumor cells overexpressing VEGFR2, PDGFRb and EphB4. The receptor tyrosine kinases VEGFR2, PDGFRb and EphB4 may be overexpressed in a number of different cancer cell types and may play crucial roles in tumor angiogenesis.","Pharmacologic Substance"]
["C95202","Angiogenesis/Heparanase Inhibitor PG545","Angiogenesis/Heparanase Inhibitor PG545|PG545","A synthetic heparan sulfate mimetic with potential anti-angiogenic and antineoplastic activity. PG545 inhibits the cleavage of heparan sulfate from cell surface proteoglycan by heparanase and thus inhibits the neovascularization induced by interaction between heparan sulfate and other extracellular matrix proteins. In this manner, this agent may have the potential to slow the progression of growth of solid tumors.","Pharmacologic Substance"]
["C116625","Angiopoietin-2-specific Fusion Protein PF-04856884","Angiopoietin-2-specific Fusion Protein PF-04856884|CVX-060|PF-04856884","A humanized monoclonal antibody fused to two peptides that bind to angiopoietin 2 (Ang2; ANGPT2), with potential anti-angiogenic and antineoplastic activities. Upon intravenous administration, Ang2-targeting PF-04856884 CovX body specifically binds to Ang2 and prevents the binding of Ang2 to its receptor Tie2 expressed on endothelial cells. This inhibits Tie2-mediated signaling, prevents angiogenesis and inhibits tumor cell proliferation.  Ang2, a proangiogenic cytokine and ligand for the Tie2 receptor, plays a key role in the regulation of tumor angiogenesis and tumor cell proliferation; its expression is upregulated by tumor endothelial cells.","Pharmacologic Substance"]
["C2526","Anhydrovinblastine","AVLB|Anhydrovinblastine|anhydrovinblastine","A semisynthetic derivative of the vinca alkaloid vinblastine, with potential antineoplastic activity. Like vinblastine, anhydrovinblastine targets and binds to tubulin and inhibits microtubule formation, resulting in disruption of mitotic spindle assembly and causing tumor cell cycle arrest in the M phase.","Organic Chemical|Pharmacologic Substance"]
["C249","Aniline Mustard",".beta.,.beta.'-Dichlorodiethylaniline|A 14489|Aniline Mustard|Aniline mustard|Benzenamine, N, N-bis(2-chloroethyl)- (9CI)|Benzenamine, N, N-bis(2-chloroethyl)-(9CI)|CB 1074|Lymphochin|Lymphocin|Lymphoquin|Mesylerythrol|N, N-Bis(2-chloroethyl)aniline|N,N-bis(2-chloroethyl)aniline|N,N-bis(2-chloroethyl)benzenamine|Phenylbis(2-chloroethylamine)|SK 592|TL 476|beta, beta'-dichlorodiethylaniline|mesylerythrol|phenylbis[2-chloroethylamine]","An alkylating mustard with antineoplastic activity. Aniline mustard forms covalent linkages with nucleophilic centers, resulting in depurination, base miscoding and strand scission, and crosslinking of DNA strands, all of which contribute to its cytotoxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C106428","Anlotinib Hydrochloride","ALTN HCl|Anlotinib Hydrochloride","The hydrochloride salt form of anlotinib, a receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic and anti-angiogenic activities. Upon administration, anlotininib targets multiple RTKs, including vascular endothelial growth factor receptor type 2 (VEGFR2) and type 3 (VEGFR3). This agent may both inhibit angiogenesis and halt tumor cell growth.","Pharmacologic Substance"]
["C2632","Annamycin","2'-iodo-3'-hydroxy-4'-epi-4-demethoxydoxorubicin|5,12-naphthacenedione, 7-((2,6-dideoxy-2-iodo-alpha-l-mannopyranosyl)oxy)-7,8,9,10-tetrahydro-6,9,11-trihydroxy-9-(hydroxyacetyl)-, (7S-cis)-|ANNAMYCIN|Annamycin|annamycin","A lipophilic, anthracycline antineoplastic antibiotic. Annamycin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and repair as well as inhibiting RNA and protein synthesis.  This agent appears to not be a substrate for the p-glycoprotein associated multidrug-resistance (MDR) transporter; therefore, overcoming the resistance pattern seen with other anthracycline compounds.","Antibiotic|Organic Chemical"]
["C25838","Annamycin Liposomal","Annamycin Liposomal","A liposome-encapsulated form of the semi-synthetic doxorubicin analogue annamycin with antineoplastic activity. Annamycin intercalates into DNA and inhibits topoisomerase II, resulting in the inhibition of DNA replication and repair and RNA and protein synthesis. This agent circumvents multidrug-resistance (MDR) transporters, including P-glycoprotein (P-gp). Liposomal annamycin is less toxic and shows improved antitumor activity compared to annamycin.","Antibiotic|Organic Chemical"]
["C118972","Annonaceous Acetogenins","Acetogenins|Annonaceous Acetogenins","A family of naturally occurring polyketides that consist of C32 or C34 long chain fatty acids and combined with a propan-2-ol unit at C-2 to form a gamma-lactone, which are isolated from various species of the plant family Annonaceae, with potential antineoplastic and antimicrobial activity. Annonaceous acetogenins bind to the ubiquinone catalytic site(s) within the mitochondrial NADH:ubiquinone oxidoreductase (complex I), and block the electron transport chain in mitochondria. In addition, the acetogenins bind to and block the activity of ubiquinone-linked NADH oxidase, an enzyme overexpressed in the plasma membranes of cancer cells. This inhibits adenosine triphosphate (ATP) production, decreases intracellular ATP levels, and induces tumor cell apoptosis. Compared to normal cells, cancer cells have higher ATP demands. The Annonaceous acetogenins also inhibit microbial glucose dehydrogenase 6.","Organic Chemical|Pharmacologic Substance"]
["C97710","Ansamitomicin P-3","ANSAMITOMICIN P-3|Ansamitomicin P-3|Maytansine, 3-o-de(2-(acetylmethylamino)-1-oxopropyl)-3-o-(1-oxobutyl)-","An ansamacrolide and maytansine analogue originally isolated from the Ethiopian shrub Maytenus serrata with antineoplastic activity. Ansamitomicin P-3 binds to tubulin at the maytansine-binding site, thereby inhibiting microtubule assembly, inducing microtubule disassembly, and disrupting mitosis.","Pharmacologic Substance"]
["C117239","Anthocyanin-rich Corn Extract","Anthocyanin-rich Corn Extract","A corn-based, water-soluble extract rich in the polyphenol anthocyanin, with potential antioxidant, anti-inflammatory and chemoprotective activities. Upon administration of the anthocyanin-rich corn extract, the anthocyanins scavenge reactive oxygen species (ROS), which protects healthy cells from radiation-induced oxidative stress and DNA damage. In addition, anthocyanins modulate the expression of various genes and proteins involved in inflammation, tumor cell proliferation, angiogenesis, tumor cell invasion and differentiation. This agent also chelates metals and induces the expression of enzymes involved in Phase II antioxidant and detoxification pathways, which may further protect cells against oxidative stress induced by toxins and carcinogens.","Pharmacologic Substance"]
["C78863","Anthracycline Analogue GPX-150","5-Imino-13-deoxydoxoubicin|Anthracycline Analogue GPX-150|GPX-150","A synthetic non-cardiotoxic analogue of the anthracycline antibiotic doxorubicin with potential antineoplastic activity. Anthracycline analogue GPX-150 intercalates DNA and impedes the activity of topoisomerase II, inducing single and double-stranded breaks in DNA; inhibiting DNA replication and/or repair, transcription, and protein synthesis; and activating tumor cell apoptosis.","Pharmacologic Substance"]
["C252","Anthramycin","3-(5,10,11,11a-tetrahydro-9,11-dihydroxy-8-methyl-5-oxo-1h-pyrrolo(2,1-c)(1,4)benzodiazepin-2-yl)-2-propenamide|ANTHRAMYCIN|Anthramycin","A pyrrolo(1,4)benzodiazepine antineoplastic antibiotic isolated from the bacterium Streptomyces refuineus var. thermotolerans.  Anthramycin binds covalently to guanine in the minor groove of DNA, thereby inhibiting DNA replication and RNA and protein synthesis. (NCI04)","Antibiotic|Organic Chemical"]
["C2706","Anthrapyrazole","Anthra[1, 9-cd]pyrazol-6(2H)-one, 7, 10-dihydroxy-2-[2-[(2-hydroxyethyl)amino]ethyl]-5-[[2-(methylamino )ethyl]amino]-acetate (salt) hydrobromide (10:5:21)|Anthra[1, 9-cd]pyrazol-6(2H)-one, 7, 10-dihydroxy-2-[2-[(2-hydroxyethyl)amino]ethyl]-5-[[2-(methylamino )ethyl]amino]-acetate (salt) hydrobromide(10:5:21)|Anthra[1,9-cd]pyrazol-6(2H)-one, 7, 10-dihydroxy-2-[2-[(2-hydroxyethyl)amino]ethyl]-5-[[2-(methylamino )ethyl]amino]-, acetate (salt) hydrobromide (10:5:21)|Anthra[1,9-cd]pyrazol-6(2H)-one, 7, 10-dihydroxy-2-[2-[(2-hydroxyethyl)amino]ethyl]-5-[[2-(methylamino )ethyl]amino]-, acetate (salt) hydrobromide(10:5:21)|Anthrapyrazole","An antineoplastic antibiotic that intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.  Anthrapyrazoles may also block cell cycle division.  In the presence of electron donors, some anthrapyrazole antibiotics cause single-strand breaks in DNA via photosensitization by visible light.  These agents are less cardiotoxic than doxorubicin. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C117735","Anti c-KIT Antibody-drug Conjugate LOP628","Anti c-KIT ADC LOP628|Anti c-KIT Antibody-drug Conjugate LOP628|LOP628","An antibody-drug conjugate (ADC) consisting of a humanized monoclonal antibody against the stem cell factor receptor c-Kit (SCFR) and conjugated, via a non-cleavable linker, to the cytotoxic agent maytansine, with potential antineoplastic activity. The monoclonal antibody moiety of anti c-KIT ADC LOP628 targets and binds to the cell surface antigen c-Kit. After antibody-antigen interaction followed by internalization, the maytansine moiety binds to tubulin, inhibits microtubule assembly, and induces microtubule disassembly. This leads to a disruption of mitosis and the inhibition of cell proliferation in cancer cells expressing c-Kit. c-Kit, a transmembrane protein and receptor tyrosine kinase, is overexpressed in solid tumors and hematological malignancies; it plays a key role in the regulation of cell differentiation and proliferation.","Pharmacologic Substance"]
["C107388","Anti-5T4 Antibody-Drug Conjugate PF-06263507","Anti-5T4 Antibody-Drug Conjugate PF-06263507|PF-06263507","An antibody-drug conjugate composed of an antibody directed against 5T4 and conjugated, via the stable linker maleimidocaproyl (mc), to the microtubule inhibitor monomethyl auristatin phenylalanine (MMAF), with potential antineoplastic activity. Upon administration, the antibody moiety of PF-06263507 selectively binds to cells expressing the 5T4 oncofetal antigen. After internalization and enzymatic cleavage of the immunoconjugate within the tumor cell cytosol, free MMAF binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.","Pharmacologic Substance"]
["C90583","Anti-A33 Monoclonal Antibody KRN330","Anti-A33 Monoclonal Antibody KRN330|KRN330","A recombinant fully human monoclonal antibody directed against the human A33 antigen, with potential immunomodulatory and antineoplastic activity. Anti-A33 monoclonal antibody KRN330 recognizes and binds to the human A33 antigen, which may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against A33-positive colorectal cancers. A33 antigen, a 43 kDa transmembrane glycoprotein of the immunoglobulin superfamily, is highly and homogenously expressed in 95% of colorectal cancer cancers with only restricted expression in normal colonic mucosa and small bowel epithelia.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C85478","Anti-A5B1 Integrin Monoclonal Antibody PF-04605412","Anti-A5B1 Integrin Monoclonal Antibody PF-04605412|Anti-alpha5beta1 Integrin Monoclonal Antibody PF-04605412|PF-04605412","A monoclonal antibody directed against the human alpha5beta1 integrin with potential antiangiogenic and antineoplastic activities. Anti-alpha5beta1 integrin monoclonal antibody PF-04605412 selectively binds to alpha5beta1 integrin, preventing the binding of integrin ligands. This may result in the inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, and integrin-mediated tumor angiogenesis and metastasis in alpha5beta1-expressing tumor cells. Alpha5beta1 integrin, a cell adhesion and signaling receptor, is often overexpressed on the surface of tumor vessel endothelial cells and plays a crucial role in endothelial cell adhesion and migration.","Pharmacologic Substance"]
["C129715","Anti-ACTR/4-1BB/CD3zeta-Viral Vector-transduced Autologous T-Lymphocytes ACTR087","ACTR-087|ACTR087|Anti-ACTR Viral Vector-transduced Autologous T-lymphocytes ACTR087|Anti-ACTR/4-1BB/CD3zeta-Viral Vector-transduced Autologous T-Lymphocytes ACTR087|CD16-41BB-CD3zeta ACTR Autologous T-cells|Virally-delivered Antibody-coupled TCR ACTR087","Autologous T-lymphocytes that are genetically modified and transfected with a viral vector expressing the ACTR gene, a proprietary gene encoding for an antibody-coupled T-cell receptor (ATCR), with potential antineoplastic activity. The ACTR contains the extracellular Fc receptor CD16 domain, normally found on certain immune cells, such as natural killer (NK) cells, coupled to the co-immunostimulatory signaling domain 4-1BB, normally expressed on T-cells, and linked to the intracellular CD3 zeta domain (CD3z), which is needed for TCR signaling. Upon reintroduction into the patient and co-administration of a cancer-specific antibody, the co-administered antibody targets and binds to the tumor-associated antigen (TAA) expressed on the tumor cell. In turn, this induces the activation of the ACTR087 cells and destruction of the tumor cells by a) releasing cytotoxins that directly kill cancer cells; b) releasing cytokines that trigger an immune response and recruit other immune-mediated killer cells to kill the tumor cells; b) targeting and killing adjacent tumor cells that are not bound to the antibody; c) inducing T-cell proliferation and thereby further enhancing the T-cell mediated tumor cell attack. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex; it enhances the survival and persistence of T-lymphocytes. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of the TAA.","Cell|Pharmacologic Substance"]
["C82685","Anti-AGS-16 Monoclonal Antibody AGS-16M18","AGS-16M18|Anti-AGS-16 Monoclonal Antibody AGS-16M18","A humanized monoclonal antibody directed against the activator of g-proteins signaling (AGS) cell surface protein AGS-16 with potential antineoplastic activity. Anti-AGS-16 monoclonal antibody AGS-16M18 selectively binds to AGS-16, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) in tumor cells expressing AGS-16. While normally expressed at low levels in the proximal tubules of the kidney, AGS-16 has been found to be overexpressed in more than 95% of kidney and 40% of liver neoplasms.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C92590","Anti-AGS-5 Antibody-Drug Conjugate ASG-5ME","ASG-5ME|Anti-AGS-5 Antibody-Drug Conjugate ASG-5ME","An antibody drug conjugate (ADC) containing the fully human IgG2k monoclonal antibody targeting an epitope of SLC44A4 (AGS-5) linked, via a valine-citrulline (vc) maleimidocaproyl (mc) linker, to the antimicrotubulin drug monomethyl auristatin E (MMAE), with potential antineoplastic activity. The monoclonal antibody moiety of ASG-5ME selectively binds to AGS-5. After internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and tumor cell apoptosis. SLC44A4, potentially a sodium-dependent transmembrane transport protein, is overexpressed on more than 80 percent of samples derived from patients with pancreatic, prostate and gastric cancers.","Pharmacologic Substance"]
["C82686","Anti-AGS-8 Monoclonal Antibody AGS-8M4","AGS-8M4|Anti-AGS-8 Monoclonal Antibody AGS-8M4","A humanized monoclonal antibody directed against the activator of g-proteins signaling (AGS) cell surface protein AGS-8 with potential antineoplastic activity. Anti-AGS-8 monoclonal antibody AGS-8M4 selectively binds to AGS-8, triggering complement-dependent cell lysis and antibody-dependent cell-mediated cytotoxicity in tumor cells expressing AGS-8. While normally expressed at low levels in the heart in response to ischemia, AGS-8 has been found to be expressed in more than 70% of ovarian neoplasms.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C91073","Anti-ALK-1 Monoclonal Antibody PF-03446962","Anti-ALK-1 Monoclonal Antibody PF-03446962|Anti-Activin Receptor-like Kinase 1 Monoclonal Antibody PF-03446962|PF-03446962","A fully human, IgG2 monoclonal antibody directed against activin-like receptor kinase 1 (ALK-1) with potential antineoplastic activity. Anti-ALK-1 monoclonal antibody PF-03446962 binds to and neutralizes ALK-1. This may disrupt tumor endothelial cell function and inhibit tumor angiogenesis, eventually leading to an inhibition of tumor cell proliferation. ALK-1, a member of the transforming growth factor beta (TGF-b) type I receptor family, is overexpressed on endothelial cells in a variety of tumor cell types and increases endothelial cell proliferation and migration.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116865","Anti-alpha5beta1 Integrin Antibody MINT1526A","Anti-a5b1 Antibody MINT1526A|Anti-alpha5beta1 Integrin Antibody MINT1526A|MINT1526A","An antibody directed against the human alpha5beta1 integrin (a5b1) with potential antiangiogenic and antineoplastic activities. Anti-a5b1 antibody MINT1526A selectively binds to a5b1, thereby preventing the binding of integrin ligands. This may result in the inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, and integrin-mediated tumor angiogenesis and metastasis in a5b1-expressing tumor cells. a5b1, a cell adhesion and signaling receptor, is often overexpressed on the surface of tumor vessel endothelial cells and plays a crucial role in both endothelial cell adhesion and migration.","Pharmacologic Substance"]
["C82422","Anti-alphaVbeta3 Monoclonal Antibody EMD 525797","Anti-alphaVbeta3 Monoclonal Antibody EMD 525797|EMD 525797","A humanized monoclonal antibody directed against the human alpha v integrin subunit with potential antiangiogenic and antineoplastic activities. Anti-human integrin alpha v subunit monoclonal antibody EMD 525797, a chimeric antibody which includes the antigen binding sites of the anti-integrin mouse antibody 17E6, binds to and inhibits the activity of alphaVbeta3 integrin (vitronectin receptor); this may result in the inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, and integrin-mediated tumor angiogenesis and metastasis in alphavbeta3-expressing tumor cells. AlphaVbeta3 integrin, a cell adhesion and signaling receptor, is expressed on the surface of tumor vessel endothelial cells and plays a crucial role in endothelial cell adhesion and migration.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C95704","Anti-ANG2 Monoclonal Antibody MEDI-3617","Anti-ANG2 MoAb MEDI-3617|Anti-ANG2 Monoclonal Antibody MEDI-3617|MEDI-3617","A fully human IgG1 monoclonal antibody against angiopoietin 2 (ANG2), with potential antiangiogenic activity. Anti-ANG2 monoclonal antibody MEDI-3617 binds to Ang2 and interferes with the interaction between Ang2 and its receptor TEK tyrosine kinase (Tie2), thereby resulting in the disruption of vascular remodeling. This may inhibit angiogenesis and may eventually lead to an inhibition of tumor cell proliferation.","Immunologic Factor|Pharmacologic Substance"]
["C99761","Antiangiogenic Drug Combination TL-118","Antiangiogenic Drug Combination TL-118|Hamsa-1|TL-118","A proprietary, oral suspension containing a combination of agents comprised of a nonsteroidal anti-inflammatory agent, an alkylating agent, a histamine H2 antagonist and a sulfonamide with potential anti-angiogenic and antineoplastic activities. Antiangiogenic drug combination TL-118 is administrated as a specific dosing regimen and may result in a synergistic effect and reduce angiogenesis and inhibit tumor cell proliferation.","Pharmacologic Substance"]
["C116627","Anti-angiopoietin Monoclonal Antibody AMG 780","AMG 780|Anti-angiopoietin Monoclonal Antibody AMG 780","An immunoglobulin (Ig) G2 monoclonal antibody targeting the proangiogenic cytokines angiopoietin 1 (Ang1) and 2 (Ang2), with potential anti-angiogenic and antineoplastic activities. Upon administration, anti-angiopoietin monoclonal antibody AMG 780 binds to Ang1 and Ang2. This prevents the binding of the angiopoietin ligands to their receptor Tie2 (TEK), an endothelial cell-specific receptor tyrosine kinase. This prevents Tie2-mediated signaling and results in an inhibition of Tie2-expressing, tumor-stimulated endothelial cell proliferation, which prevents angiogenesis and inhibits tumor cell proliferation.","Pharmacologic Substance"]
["C122924","Anti-B7-H3 Antibody DS-5573a","Anti-B7-H3 Antibody DS-5573a|DS-5573a","An antibody directed against the immunoregulatory protein B7-homologue 3 (B7-H3, CD276), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, anti-B7-H3 antibody DS-5573a binds to the cell surface antigen B7-H3, thereby blocking B7-H3-mediated signaling. This abrogates the inhibitory effect on T-cell activation and may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against B7-H3-expressing tumor cells. B7-H3, a type I transmembrane protein and a member of the B7 co-stimulatory protein superfamily, is overexpressed on certain tumor cell types and on various immune cells. It is a negative regulator of the T-cell activation and and its overexpression plays a key role in tumor cell invasion and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C114299","Anti-BCMA Antibody-drug Conjugate GSK2857916","Anti-BCMA ADC GSK2857916|Anti-BCMA Antibody-drug Conjugate GSK2857916|GSK2857916|J6M0-mcMMAF","An antibody-drug conjugate (ADC) consisting of an afucosylated, humanized monoclonal antibody, directed against the B-cell maturation antigen (BCMA), conjugated to the auristatin analogue and microtubule inhibitor monomethyl auristatin phenylalanine (MMAF), with potential antineoplastic activity. The anti-BCMA antibody moiety of anti-BCMA ADC GSK2857916 selectively binds to the BCMA on tumor cell surfaces. Upon internalization, the MMAF moiety binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces tumor cell apoptosis. In addition, GSK2857916 induces antibody-dependent cellular cytotoxicity (ADCC). Altogether, this results in the inhibition of cellular proliferation in tumor cells that overexpress BCMA. BCMA, a receptor for a proliferation-inducing ligand and B-cell activating factor, is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells. Afucosylation of the antibody moiety increases ADCC.","Pharmacologic Substance"]
["C124134","Antibody-drug Conjugate ABBV-085","ABBV-085|ADC ABBV-085|Antibody-drug Conjugate ABBV-085","An antibody-drug conjugate (ADC) composed of a proprietary monoclonal antibody against a tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of ABBV-085 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.","Pharmacologic Substance"]
["C125549","Antibody-drug Conjugate ADCT-402","ADC ADCT-402|ADCT-402|Anti-CD19 PBD-conjugate ADCT-402|Antibody-drug Conjugate ADCT-402","An antibody-drug conjugate (ADC) consisting of an anti-CD19 humanized monoclonal antibody conjugated, via a cleavable linker comprised of valine-alanine and maleimide, to a cytotoxic, cross-linking agent pyrrolobenzodiazepine (PBD) dimer, which targets DNA minor grooves, with potential antineoplastic activity. Upon administration, the monoclonal antibody portion of anti-CD19-PBD conjugate ADCT-402 targets the cell surface antigen CD19 on various cancer cells. Upon antibody/antigen binding and internalization, the cytotoxic PBD moiety is released. The imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces interstrand cross-links in the minor groove of DNA and inhibits DNA replication, which inhibits the proliferation of CD19-overexpressing tumor cells. CD19, a transmembrane receptor and tumor-associated antigen (TAA), is expressed on a number of B-cell-derived cancers.","Pharmacologic Substance"]
["C129401","Antibody-drug Conjugate Anti-TIM-1-vcMMAE CDX-014","ADC Anti-TIM-1-vcMMAE CDX-014|ADC CDX-014|Antibody-drug Conjugate Anti-TIM-1-vcMMAE CDX-014|Antibody-drug Conjugate CDX-014|CDX-014|CR014-vc-MMAE|CR014-vcMMAE","A monoclonal antibody-drug conjugate (ADC) comprised of human immunoglobulin G1 (IgG1) clone CR014, which targets the extracellular domain of T-cell immunoglobulin mucin-1 (TIM-1; HAVCR1), that is linked, via a valine-citrulline (VC) peptide linker, to the potent cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration of ADC anti-TIM-1-vcMMAE CDX-014, the monoclonal antibody moiety targets and binds to TIM-1. Upon internalization and proteolytic cleavage, MMAE is released into the cytosol of TIM-1-expressing tumor cells, binds to tubulin, and inhibits microtubule polymerization, which induces both G2/M phase arrest and tumor cell apoptosis. TIM-1 is upregulated in a variety of cancer cell types while only minimally expressed in healthy tissue. The linkage system in CDX-014 is highly stable in plasma, resulting in increased specificity and cytotoxic efficacy towards TIM-1-positive cells.","Pharmacologic Substance"]
["C106256","Antibody-Drug Conjugate DFRF4539A","ADC DFRF4539A|Antibody-Drug Conjugate DFRF4539A|DFRF4539A","An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against a specific myeloma antigen and conjugated to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DFRF4539A selectively binds to a specific protein expressed on the surface of myeloma cells. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and tumor cell apoptosis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C123828","Antibody-drug Conjugate PF-06647020","ADC PF-06647020|Antibody-drug Conjugate PF-06647020|PF-06647020","An antibody-drug conjugate (ADC) composed of a proprietary monoclonal antibody against an unnamed tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of PF-06647020 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.","Pharmacologic Substance"]
["C123284","Antibody-drug Conjugate SC-002","ADC SC-002|Antibody-drug Conjugate SC-002|SC-002","An antibody-drug conjugate (ADC) composed of an as of yet publicly unknown monoclonal antibody against a tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of SC-002 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.","Pharmacologic Substance"]
["C124133","Antibody-drug Conjugate SC-003","ADC SC-003|Antibody-drug Conjugate SC-003|SC 003|SC-003|SC003","An antibody-drug conjugate (ADC) composed of a proprietary monoclonal antibody against a tumor-associated antigen (TAA) linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of SC-003 targets and binds to the TAA expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills the TAA-expressing cancer cells, through an as of yet unknown mechanism of action.","Pharmacologic Substance"]
["C107678","Antibody-Drug Conjugate SC16LD6.5","Anti-SC16 ADC SC16LD6.5|Antibody-Drug Conjugate SC16LD6.5|SC16LD6.5","An antibody-drug conjugate (ADC) containing an antibody directed against the scr-like kinase Fyn3 (SC-16), conjugated to the cytotoxic agent D6.5, with potential antineoplastic activity. The anti-Fyn3 antibody moiety of the ADC SC16LD6.5 selectively binds to Fyn3 on tumor cell surfaces. Upon internalization, the D6.5 moiety is released and causes DNA damage, which may result in the inhibition of proliferation of tumor cells that overexpress Fyn3. Fyn3, a tyrosine protein kinase involved in tyrosine phosphorylation, cytoskeleton remodeling and signal transduction, is upregulated in certain cancers and plays a key role in cancer cell invasion and survival.","Pharmacologic Substance"]
["C116070","Anti-C4.4a Antibody-Drug Conjugate BAY1129980","Anti-C4.4a ADC BAY1129980|Anti-C4.4a Antibody-Drug Conjugate BAY1129980|BAY112-9980|BAY1129980","An antibody-drug conjugate (ADC) composed of an antibody against a structural homolog of the urokinase-type plasminogen activator receptor (uPAR) and tumor-associated antigen, C4.4a, and conjugated with a cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, anti-C4.4a antibody-drug conjugate BAY1129980 targets and binds to C4.4a-expressing tumor cells. Upon binding and cell entry, the cytotoxic agent kills the tumor cell. C4.4a, a glycolipid-anchored membrane protein and a member of the Ly-6 family, is overexpressed by a variety of cancer cell types whereas it is minimally expressed on healthy cells.","Pharmacologic Substance"]
["C125900","Anti-CA19-9 Monoclonal Antibody 5B1","5B1|Anti-CA19-9 Monoclonal Antibody 5B1|HuMab 5B1|HuMab-5B1|MVT-5873","A human monoclonal antibody against the carbohydrate antigen sialyl-Lewis A (carbohydrate antigen 19-9; CA19-9), with potential antineoplastic activity. Upon administration, monoclonal antibody 5B1 binds to CA19-9 and kills CA19-9-expressing tumor cells, possibly through the induction of both complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC). CA19-9 is overexpressed on a number of different tumor cell types, and plays a key role in tumor cell survival and metastasis.","Immunologic Factor|Pharmacologic Substance"]
["C95764","Anti-CA6-DM4 Immunoconjugate SAR566658","Anti-CA6-DM4 Immunoconjugate SAR566658|SAR566658|huDs6-DM4","An immunoconjugate consisting of a humanized monoclonal antibody against the tumor-associated sialoglycotope CA6 (huDS6) conjugated to the cytotoxic maytansinoid DM4, with potential antineoplastic activity. The anti-CA6 monoclonal antibody moiety of SAR566658 targets and binds to the cell surface antigen CA6. Upon antibody/antigen binding and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CA6-expressing tumor cells. The CA6 epitope is found on a variety of solid tumors, including breast, ovarian, cervical, lung and pancreatic tumors.","Pharmacologic Substance"]
["C91093","Anti-CD123 Monoclonal Antibody CSL360","Anti-CD123 Monoclonal Antibody CSL360|CSL360","A chimeric IgG1 monoclonal antibody against CD123 (Interleukin-3 receptor alpha chain) with potential antineoplastic activity. Derived from mouse monoclonal antibody 7G3, anti-CD123 monoclonal antibody CSL360 binds to and neutralizes CD123 which is upregulated on leukemic stem cells (LSC) in acute myeloid leukemia (AML). This may inhibit IL-3-dependent signalling and proliferation and may prevent the uncontrolled growth and differentiation of mutated LSC.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C102784","Anti-CD123 Monoclonal Antibody CSL362","Anti-CD123 Monoclonal Antibody CSL362|Anti-IL-3 Receptor Alpha Monoclonal Antibody CSL362|CSL362","A humanized IgG1 monoclonal antibody against CD123 (Interleukin-3 receptor alpha chain or IL3RA) with potential antineoplastic activity. Upon intravenous administration, anti-CD123 monoclonal antibody CSL362 binds to and neutralizes CD123. This may inhibit IL-3-dependent signaling and may inhibit proliferation and differentiation in CD123-positive tumor cells. CSL362 contains an engineered Fc region which increases its binding affinity to Fc-gamma receptors on the surface of natural killer (NK) cells thereby initiating antibody-dependent cellular cytotoxicity (ADCC). CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C123380","Anti-CD123 Monoclonal Antibody KHK2823","Anti-CD123 Monoclonal Antibody KHK2823|KHK2823","A fully humanized monoclonal antibody against CD123 (interleukin-3 receptor alpha chain) with potential antineoplastic activity. Anti-CD123 monoclonal antibody KHK2823 binds to and neutralizes CD123, which is upregulated on leukemic stem cells (LSC) found in myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). This agent may inhibit IL-3-dependent signaling and proliferation and may prevent the uncontrolled growth and differentiation of mutated LSC.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C127120","Anti-CD123 x Anti-CD3 Bispecific Antibody XmAb1404","Anti-CD123 x Anti-CD3 Bispecific Antibody XmAb1404|Anti-CD123/Anti-CD3 Bispecific Antibody XmAb1404|XmAb14045","An anti-CD123/anti-CD3 bispecific monoclonal antibody, in which most of the naturally-occurring Fc domain is maintained, with potential immunostimulatory and antineoplastic activities. Anti-CD123/CD3 monoclonal antibody XmAb14045 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for CD123, a tumor-associated antigen (TAA) overexpressed on the surface of certain tumor cells. Upon administration of XmAb14045, this bispecific antibody simultaneously binds to both CD3-expressing T-cells and CD123-expressing cancer cells, thereby crosslinking CD123-expressing tumor cells and cytotoxic T-lymphocytes (CTLs). This may result in potent CTL-mediated cell lysis of CD123-expressing tumor cells. CD123, the interleukin-3 receptor alpha chain, is overexpressed in a variety of hematological malignancies; its expression is low or absent in normal hematopoietic progenitors and stem cells. The Fc domain on the antibody prolongs the half-life of the bispecific antibody and enhances T-cell mediated tumor cell killing through its binding to the Fc receptors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C117238","Anti-CD123/CD3 Monoclonal Antibody MGD006","Anti-CD123/CD3 Monoclonal Antibody MGD006|CD123 x CD3 DART Bi-Specific Antibody MGD006|CD123 x CD3 Dual Affinity Re-Targeting Bi-Specific Antibody MGD006|MGD006","An anti-CD123/anti-CD3 bispecific humanized monoclonal antibody with potential immunostimulatory and antineoplastic activities. Anti-CD123/CD3 monoclonal antibody MGD006 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for CD123, a tumor-associated antigen (TAA) overexpressed on the surface of certain tumor cells. Upon administration of MGD006, this bispecific antibody simultaneously binds to both CD3-expressing T-cells and CD123-expressing cancer cells, thereby crosslinking CD123-expressing tumor cells and cytotoxic T-lymphocytes (CTLs). This may result in potent CTL-mediated cell lysis of CD123-expressing tumor cells. CD123, the interleukin-3 receptor alpha chain, is overexpressed in a variety of hematological malignancies; its expression is low or absent in normal hematopoietic progenitors and stem cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C129457","Anti-CD123-Pyrrolobenzodiazepine Dimer Antibody Drug Conjugate SGN-CD123A","ADC SGN-CD123A|Anti-CD123 ADC SGN-CD123A|Anti-CD123-PBD ADC SGN-CD123A|Anti-CD123-Pyrrolobenzodiazepine Dimer Antibody Drug Conjugate SGN-CD123A|Antibody-drug Conjugate SGN-CD123A|SGN CD123A|SGN-CD123A","An antibody-drug conjugate (ADC) consisting of an anti-CD123 humanized monoclonal antibody conjugated, via a stable maleimidocaproyl-valine-alanine dipeptide protease-cleavable linker, to the cytotoxic, DNA minor-groove crosslinking agent pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-CD123 ADC SGN-CD123A, the antibody moiety targets the cell surface antigen CD123. Upon antibody/antigen binding, internalization, and lysosome uptake, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of CD123-overexpressing tumor cells. CD123, the alpha subunit of the IL-3 receptor, regulates the proliferation, survival and differentiation of hematopoietic cells. CD123 is overexpressed on a variety of cancers, including myeloid leukemia, and increased expression of CD123 on leukemic stem cells is associated with poor prognosis. Cysteine engineering of the monoclonal antibody (EC-mAb) allows for a site-specific, stable conjugation and uniform loading of the PBD agent to the antibody.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C124132","Anti-CD133-CAR Vector-transduced Allogeneic T Lymphocytes","Allogeneic Anti-CD133 CAR T Cells|Allogeneic CART133|Anti-CD133-CAR Vector-transduced Allogeneic T Lymphocytes","A preparation of allogeneic peripheral blood T-lymphocytes (PBTL) that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the chimeric CD (cluster of differentiation) 133 antigen receptor, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD133-CAR vector-transduced allogeneic T-lymphocytes specifically recognize and kill CD133-expressing tumor cells. CD133, a tumor associated antigen (TAA), is overexpressed on a variety of tumor cell types.","Cell|Pharmacologic Substance"]
["C120317","Anti-CD157 Monoclonal Antibody MEN1112","Anti-CD157 Monoclonal Antibody MEN1112|MEN1112","A humanized, Fc engineered, de-fucosylated monoclonal immunoglobulin G1 (IgG1) antibody directed against the bone marrow stromal cell antigen 1 (BST1/CD157), with potential antineoplastic activity. Upon intravenous infusion, anti-CD157 monoclonal antibody MEN1112 specifically binds to and induces an antibody dependent cell cytotoxic (ADCC) response against CD157-expressing tumor cells. CD157, also known as ADP-ribosyl cyclase 2, is a glycosyl-phosphatidylinositol (GPI)-anchored transmembrane protein belonging to the ADP-ribosyl-cyclase family and is overexpressed on certain cancer cell types. Fc-optimization of MEN1112, which involves the removal of fucose residues from its Fc domain, allows for enhanced Fc-gamma receptor binding on effector cells, such as natural killer (NK) cells, and further enhances tumor cell lysis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C105805","Anti-CD19 Monoclonal Antibody DI-B4","Anti-CD19 Monoclonal Antibody DI-B4|DI-B4|anti-CD19 MoAb DI-B4","A low-fucosylated, humanized, IgG1 isotype, monoclonal antibody directed against the B-cell-specific membrane protein CD19 with potential immunostimulating and antineoplastic activities. Anti-CD19 monoclonal antibody DI-B4 binds to CD19, which may result in a strong antibody-dependent cellular cytotoxicity (ADCC) directed at CD19-expressing B-cells but with minimal complement dependent cytotoxicity. DI-B4 contains low levels of fucose, which contributes to its enhanced ADCC activity. CD19 is a B-cell specific membrane antigen that is widely expressed during B-cell development and in all B-cell lineage malignancies.","Pharmacologic Substance"]
["C74003","Anti-CD19 Monoclonal Antibody MDX-1342","Anti-CD19 Monoclonal Antibody MDX-1342|MDX-1342","A fully human anti-CD19 monoclonal antibody directed against the B-cell-specific membrane protein CD-19 with potential antineoplastic activity. Anti-CD19 monoclonal antibody MDX-1342 binds to CD19, depleting and eliminating CD19-expressing B-cells. CD19 is widely expressed during B-cell development, from pro-B-cell to early plasma cell stages.","Pharmacologic Substance"]
["C88283","Anti-CD19 Monoclonal Antibody MEDI-551","Anti-CD19 Monoclonal Antibody MEDI-551|MEDI-551","A humanized immunoglobulin IgG1 kappa monoclonal antibody directed against the B-cell-specific membrane protein CD-19 with potential immunostimulating and antineoplastic activities. Anti-CD19 monoclonal antibody MEDI-551 binds to CD19, which may result in a cytotoxic T-lymphocyte (CTL) response and antibody-dependent cellular cytotoxicity (ADCC) to CD19-expressing B-cells. The Fc portion of MEDI-551 does not contain a fucose sugar moiety, which may contribute to its enhanced ADCC activity. CD19 is a membrane antigen that is widely expressed during B-cell development, from pro-B-cell to early plasma cell stages.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C95768","Anti-CD19 Monoclonal Antibody XmAb5574","Anti-CD19 Monoclonal Antibody XmAb5574|MOR208|XmAb5574","An Fc engineered, humanized anti-CD19 monoclonal antibody directed against the B-cell-specific membrane protein CD19 with potential immunostimulating and antineoplastic activities. Anti-CD19 monoclonal antibody XmAb5574 targets and binds to CD19, thereby depleting and eliminating CD19-expressing B-cells. The modified Fc region of XmAb5574 increases binding affinity to Fc-gamma receptors of effector cells and thereby enhances antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cell-mediated phagocytosis (ADCP). CD19 is widely expressed during B-cell development, from pro-B-cell to early plasma cell stages.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82375","Anti-CD19/Anti-CD22 Bispecific Immunotoxin DT2219ARL","Anti-CD19/Anti-CD22 Bispecific Immunotoxin DT2219ARL|Anti-CD19/CD22 BLT DT2219ARL|DT2219ARL immunotoxin|DT2219ARL","An immunotoxin consisting of two scFv ligands recognizing human CD19 and CD22 linked to the first 389 amino acids of diphtheria toxin (DT), DT 390, with potential antineoplastic activity. The VH and VL regions of anti-CD22 (sFv) and anti-CD19 are reversed and linked by an aggregration stabilizing linker (ARL) consisting of a 20 amino acid segment of human muscle aldolase (hma) and an Xho1-compatible restriction site; the CDR3 region of the VH of anti-CD22 sFv is mutated to enhance its affinity. The anti-CD19 and anti CD-22 portions of the immunotoxin specifically bind to CD19 and CD22 receptors on tumor B cells. Upon internalization, DT catalyzes ADP ribosylation of elongation factor 2 (EF-2) which may result in the irreversible inhibition of protein synthesis and cell death in CD19- and CD22-expressing tumor cells. CD19 and CD22 are transmembrane proteins upregulated on malignant B cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C120309","Anti-CD19/CD28/CD3zeta CAR Gammaretroviral Vector-transduced Autologous T Lymphocytes KTE-C19","Anti-CD19/CD28/CD3zeta CAR Gammaretroviral Vector-transduced Autologous T Lymphocytes KTE-C19|KTE-C19 CAR|KTE-C19","A preparation of autologous peripheral blood T-lymphocytes (PBTL) that have been transduced with a gammaretoviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv) coupled to the costimulatory signaling domain CD28 and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3 zeta), with potential immunostimulating and antineoplastic activities. Upon intravenous infusion and re-introduction of the anti-CD19/CD28/CD3zeta CAR gammaretroviral vector-transduced autologous T lymphocytes KTE-C19 into the patient, these cells bind to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen that is expressed in all B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex; it regulates both the assembly and cell surface expression of TCR complexes. CD28 is essential for CD4+ T-cell proliferation, interleukin-2 production, and T-helper type-2 (Th2) development.","Cell|Pharmacologic Substance"]
["C115101","Anti-CD19/CD3 Tetravalent Antibody AFM11","AFM11|Anti-CD19/CD3 Tetravalent Antibody AFM11","An anti-CD19/anti-CD3 bispecific tetravalent antibody with potential immunostimulatory and antineoplastic activities. Anti-CD19/CD3 tetravalent antibody AFM11 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B-cells. Upon bolus infusion of AFM11, this bispecific antibody binds to CD3-expressing T-cells and CD19-expressing cancer cells, thereby crosslinking CD19-expressing tumor B-cells and cytotoxic T-lymphocytes (CTLs). This may result in a potent CTL-mediated cell lysis of CD19-expressing B-lymphocytes. CD19, a B-cell specific membrane antigen, is expressed during both B-cell development and B-cell malignant growth.","Cell|Pharmacologic Substance"]
["C111041","Anti-CD19-CAR FMC63-28Z Retroviral Vector-transduced Allogeneic T-lymphocytes","Anti-CD19-CAR FMC63-28Z Retroviral Vector-transduced Allogeneic T-lymphocytes|FMC63-28Z CAR-transduced Allogeneic T-lymphocytes|MSGV1-FMC63-28Z Anti-CD19 CAR-transduced Allogeneic T-lymphocytes","Allogeneic T-lymphocytes derived from peripheral blood mononuclear cells (PBMC) transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of both the light and heavy chain variable regions of anti-CD19 monoclonal antibody FMC63, coupled to the molecule CD28 and the signaling domain of the zeta chain of the T-cell receptor (TCR) (FMC63-28Z), with potential immunomodulating and antineoplastic activities. Upon transfusion, the anti-CD19-CAR FMC63-28Z retroviral vector-transduced allogeneic T lymphocytes specifically recognize and kill CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies and normal B-cells.","Cell|Pharmacologic Substance"]
["C88055","Anti-CD19-CAR Retroviral Vector-Transduced Autologous T Cells","Anti-CD19-CAR Retroviral Vector-Transduced Autologous T Cells","A preparation of autologous peripheral blood T-lymphocytes (PBTL) that have been genetically modified to express a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to the costimulatory signaling domain CD28 and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3 zeta), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD19-CAR retroviral vector-transduced autologous T cells direct the T-lymphocytes to CD19-expressing tumor cells, thereby inducing selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the TCR/CD3 complex, which regulates both the assembly of complete TCR complexes and their expression on the cell surface. CD28 is essential for CD4+ T-cell proliferation, interleukin-2 production, and T-helper type-2 (Th2) development.","Cell|Pharmacologic Substance"]
["C112179","Anti-CD19-CAR-CD3zeta-4-1BB-Expressing Allogenic Natural Killer Cells","Anti-CD19 Redirected NK Cells|Anti-CD19-CAR-CD3zeta-4-1BB-Expressing Allogenic NK Cells|Anti-CD19-CAR-CD3zeta-4-1BB-Expressing Allogenic Natural Killer Cells|Anti-CD19-CAR-CD3zeta-4-1BB-Expressing Donor NK Cells|Anti-CD19-CAR-CD3zeta-4-1BB-Expressing Donor Natural Killer Cells|Anti-CD19-CAR-CD3zeta-4-1BB-Expressing NK Cells|Anti-CD19-CAR-CD3zeta-4-1BB-Expressing Natural Killer Cells|NKCARCD19","Allogeneic natural killer (NK) cells transduced with an mRNA expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), coupled to the signaling domain of 4-1BB (CD137), with potential immunomodulating and antineoplastic activities. NK cells from haploidentical donors are expanded in culture and electroporated with the CAR mRNA. Upon transfusion of the transduced cultured cells, CD19CAR-CD3zeta-4-1BB-expressing allogeneic NK cells bind to and induce selective cytotoxicity in CD19-expressing tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. Its inclusion may also increase antitumor activity, when compared to the inclusion of the CD3-zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.","Cell|Pharmacologic Substance"]
["C71009","Anti-CD19-DM4 Immunoconjugate SAR3419","Anti-CD19-DM4 Immunoconjugate SAR3419|SAR3419","An immunoconjugate consisting of an anti-CD19 monoclonal antibody conjugated to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. Anti-CD19-DM4 conjugate SAR3419 targets the cell surface antigen CD19, found on a number of B-cell-derived cancers. Upon antibody/antigen binding and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CD19-expressing tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C121167","Anti-CD20 B9E9 scFv-Streptavidin Fusion Protein","Anti-CD20 B9E9 scFv-SA Fusion Protein|Anti-CD20 B9E9 scFv-Streptavidin Fusion Protein|Anti-CD20 B9E9-SA Fusion Protein|B9E9 scFvSA Fusion Protein|Recombinant Anti-CD20 B9E9 scFvSA Fusion Protein|scFv B9E9-streptavidin Fusion Protein","An Escherichia coli periplasm-expressed tetrameric fusion protein composed of four single-chain variable regions (scFv) of the murine immunoglobulin (Ig) G2a anti-CD20 monoclonal antibody B9E9 fused to the streptavidin (SA) gene of Streptomyces avidinii (scFv-SA), with potential use in pretargeted radioimmunotherapy (PRIT). Upon intravenous administration of the anti-CD20 B9E9 scFv-SA fusion protein, this agent targets and binds to CD20-expressing tumor cells. Subsequently, a biotinylated N-acetylgalactosamine-containing clearing agent is administered, which binds to the streptavidin moiety of the unbound fusion protein and promotes its hepatic excretion. In turn, radiolabeled DOTA (1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid)-biotin is administered and, due to its small size, quickly distributes. The biotin moiety efficiently binds to the SA moiety of the bound fusion protein, which localizes the biotin-conjugated radionuclide to the tumor site. CD20, a tumor-associated antigen (TAA), is overexpressed on B-cell malignancies. PRIT increases both tumor uptake and renal elimination of the radionuclide conjugate as compared to conventional radioimmunotherapy (RIT), where the radioisotope is bound to the antibody before administration; this increases the dose of radionuclide delivered to the tumor while limiting radiation exposure for normal, healthy tissues.","Pharmacologic Substance"]
["C90590","Anti-CD20 Monoclonal Antibody PRO131921","Anti-CD20 Monoclonal Antibody PRO131921|PRO131921","A third-generation, humanized monoclonal antibody directed against human CD20 with potential antineoplastic activity. Anti-CD20 monoclonal antibody PRO131921 specifically binds to the B cell-specific cell surface antigen CD20. This may result in the induction of a B cell-directed complement dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC) against CD20-expressing B cells leading to B cell apoptosis. CD20 is a non-glycosylated cell surface phosphoprotein which is exclusively expressed on B cells during most stages of B cell development and which is often overexpressed in B-cell malignancies.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C122680","Anti-CD20 Monoclonal Antibody SCT400","Anti-CD20 Monoclonal Antibody SCT400|SCT400","A chimeric monoclonal antibody directed against human CD20, with potential antineoplastic activity. Anti-CD20 monoclonal antibody SCT400 binds to the B-cell-specific cell surface antigen CD20, which triggers an immune response against CD20-positive B-cells, leading to apoptosis. CD20, a non-glycosylated cell surface phosphoprotein, is exclusively expressed on B-cells during most stages of B-cell development and is often overexpressed in B-cell malignancies.","Immunologic Factor|Pharmacologic Substance"]
["C94206","Anti-CD20 Monoclonal Antibody TL011","Anti-CD20 Monoclonal Antibody TL011|TL011","A monoclonal antibody directed against human CD20 with potential antineoplastic activity. Anti-CD20 monoclonal antibody TL011 specifically binds to the B cell-specific cell surface antigen CD20 antigen (MS4A1; membrane-spanning 4-domains, subfamily A, member 1), thereby potentially triggering an immune response against CD20-positive B cells, leading to B cell apoptosis. CD20 is a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B cell development and is often overexpressed in B-cell malignancies.","Immunologic Factor|Pharmacologic Substance"]
["C123915","Anti-CD20 Monoclonal Antibody-Interferon-alpha Fusion Protein IGN002","Anti-CD20 Monoclonal Antibody-IFN-a Fusion Protein IGN002|Anti-CD20 Monoclonal Antibody-Interferon-alpha Fusion Protein IGN002|IGN002","A humanized monoclonal antibody directed against the human B-cell-specific cell surface antigen CD20 and fused to the recombinant cytokine, interferon-alpha (IFN-a), with potential antineoplastic and immunomodulating activities. Upon administration of anti-CD20 monoclonal antibody-interferon alpha fusion protein IGN002, the antibody moiety specifically targets and binds to CD20. In turn, the IFN-a moiety binds to the IFN receptor, and activates IFN-mediated signal transduction, which induces the transcription and translation of genes whose protein products mediate anticancer effects. This results in the induction of both G2 cell cycle arrest and apoptosis in CD20-expressing tumor cells. In addition, IGN002 causes the induction of complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC) against CD20-expressing B-cells, which leads to B-cell apoptosis and the inhibition of tumor cell proliferation. CD20, a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B-cells during most stages of B-cell development, is often overexpressed in B-cell malignancies.","Pharmacologic Substance"]
["C129691","Anti-CD20 x Anti-CD3 Bispecific Monoclonal Antibody BTCT4465A","Anti-CD20 x Anti-CD3 Bispecific Monoclonal Antibody BTCT4465A|BTCT 4465A|BTCT-4465A|BTCT4465A|CD20/CD3 BiMAb BTCT4465A|RG 7828|RG7828","A bispecific, humanized monoclonal antibody with potential antineoplastic activity. Anti-CD20/CD3 bispecific monoclonal antibody BTCT4465A contains two antigen-recognition sites: one for human CD3, a T-cell surface antigen, and one for human CD20, a tumor-associated antigen (TAA) that is exclusively expressed on B-cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. Upon administration, BTCT4465A binds to both T-cells and CD20-expressing tumor B-cells; this cross-links T-cells to tumor cells, and may result in a potent cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor B-cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C119615","Anti-CD20/CD3 Monoclonal Antibody REGN1979","Anti-CD20 x Anti-CD3 Bispecific Monoclonal Antibody REGN1979|Anti-CD20/CD3 Monoclonal Antibody REGN1979|REGN1979","A bispecific, human monoclonal antibody with potential antineoplastic activity. Anti-CD20/CD3 monoclonal antibody REGN1979 contains two antigen-recognition sites: one for human CD3, a T cell surface antigen, and one for human CD20, a tumor-associated antigen that is exclusively expressed on B-cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. Upon administration, REGN1979 binds to both T-cells and CD20-expressing tumor B-cells, which cross-links the T-cells to tumor cells, and may result in a potent cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor B-cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C130050","Anti-CD20/CD3 Monoclonal Antibody XmAb13676","Anti-CD20 x Anti-CD3 Bispecific Monoclonal Antibody XmAb13676|Anti-CD20/CD3 Monoclonal Antibody XmAb13676|XmAb13676","A bispecific, Fc domain-containing, monoclonal antibody with potential antineoplastic activity. Anti-CD20/CD3 monoclonal antibody XmAb13676 contains two antigen-recognition sites: one for human CD3, a T cell surface antigen, and one for human CD20, a tumor-associated antigen (TAA) that is exclusively expressed on B-cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. Upon administration, XmAb13676 binds to both T-cells and CD20-expressing B-lineage tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the CD20-expressing tumor B-cells. Inclusion of an Fc domain on the antibody prolongs the half-life of the bispecific antibody and enhances T-cell-mediated tumor cell killing because the agent is able to bind to Fc receptors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77891","Anti-CD200 Monoclonal Antibody ALXN6000","ALXN6000|Anti-CD200 Monoclonal Antibody ALXN6000","A humanized monoclonal antibody directed against the human immunosuppressive molecule CD200 (OX-2) with potential immunomodulating and antineoplastic activities. Anti-CD200 monoclonal antibody ALXN6000 binds to CD200, blocking the binding of CD200 to its receptor, CD200R, present on cells of the macrophage lineage; inhibition of CD200 may augment the cytotoxic T-lymphocyte (CTL) mediated immune response against CD200-expressing tumor cells.  CD200 is a type 1a transmembrane protein, related to the B7 family of co-stimulatory receptors, and is upregulated on the surface of multiple hematologic malignant cells; this transmembrane protein appears to be involved in the downregulation of a Th1 (helper T cell) immune response.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C104006","Anti-CD20-CAR-CD3zeta-4-1BB-expressing Autologous T-lymphocyte Cells","Anti-CD20-CAR-CD3zeta-4-1BB-expressing Autologous T-lymphocyte Cells","A preparation of autologous blood T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) consisting of an anti-CD20 scFv (single chain variable fragment); the cytoplasmic portion of the human TCR-[zeta] molecule; and the co-stimulatory molecule 4-1BB (CD137), with potential immunostimulating and antineoplastic activities. Upon transfusion, anti-CD20-CAR-CD3zeta-4-1BB-expressing autologous T-lymphocyte cells direct T-cells to CD20-expressing tumor cells. This results in cytotoxic T lymphocyte (CTL) and antibody responses against CD20-expressing tumor cells, causing tumor cell lysis. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen expressed in B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the T-cell receptor (TCR)/CD3 complex and regulates the assembly of complete TCR complexes and their expression on the cell surface. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD20; the inclusion of this signaling domain may increase the antitumor activity compared to the inclusion of the CD3-zeta chain alone.","Pharmacologic Substance"]
["C120546","Anti-CD20-engineered Toxin Body MT-3724","Anti-CD20-engineered Toxin Body MT-3724|MT-3724","An engineered toxin body (ETB) composed of the single-chain variable fragment (ScFv) from an antibody targeting CD20 that is linked to a modified form of the ribosome-inactivating alpha subunit of Shiga-like toxin 1 (Shiga-like Toxin-1 A or SLT-1A), with antineoplastic activity. Upon administration, the ScFv moiety of anti-CD20-engineered toxin body MT-3724 targets and binds to the CD20 antigen expressed on tumor cells. Upon internalization, the SLT-1A moiety is released and acts as an N-glycosidase, which binds to and cleaves an adenine nucleobase in the 28S RNA component of the 60S subunit of ribosomes and prevents ribosome activity. This inhibits protein synthesis and eventually leads to apoptosis of CD20-expressing tumor cells. CD20, a B-cell specific transmembrane protein and tumor-associated antigen (TAA), is expressed during most stages of B-cell development and is often overexpressed in B-cell malignancies.","Pharmacologic Substance"]
["C104167","Anti-CD22 Monoclonal Antibody-MMAE Conjugate DCDT2980S","ADC DCDT2980S|Anti-CD22 Monoclonal Antibody-MMAE Conjugate DCDT2980S|Antibody-Drug Conjugate DCDT2980S|DCDT2980S","An antibody-drug conjugate (ADC) composed of MCDT2219A, a humanized IgG1 anti-CD22 monoclonal antibody covalently linked, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DCDT2980S binds to B cell-specific CD22 receptors and is rapidly internalized, thereby delivering MMAE intracellularly. Upon proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. CD22, a cell surface glycoprotein, is expressed on mature B-cells and on most malignant B-cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C124656","Anti-CD22 scFv TCRz:41BB-CAR Lentiviral Vector-transduced Autologous T-lymphocytes","Anti-CD22 scFv TCRz:41BB-CAR Lentiviral Vector-transduced Autologous T-lymphocytes|Autologous T-lymphocytes-expressing CD22 CARs-expressing Tandem TCR-zeta/4-1BB|TCRzeta/4-1BB CART22 Cells","Autologous human T-lymphocytes transduced with a recombinant lentiviral vector encoding a chimeric T-cell receptor consisting of an anti-CD22 single chain variable fragment (scFv) and the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunostimulating and antineoplastic activities. Autologous peripheral blood lymphocytes (PBLs) from a patient with CD22-positive cancer are transduced with this lentiviral vector that encodes the CAR gene specific for CD22. After isolation, transduction, expansion in culture and reintroduction into the patient, the anti-CD22 scFv TCRz:41BB-CAR lentiviral vector-transduced autologous T-lymphocytes express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces. Subsequently, CD22-expressing tumor cells are lysed. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B-cells.","Cell|Pharmacologic Substance"]
["C120035","Anti-CD22-CAR m971-BBz Lentiviral Vector-transduced Autologous T Lymphocytes","Anti-CD22-CAR m971-BBz Cells|Anti-CD22-CAR m971-BBz Lentiviral Vector-transduced Autologous T Lymphocytes","Autologous human T-lymphocytes transduced with a recombinant lentiviral vector encoding a chimeric T-cell receptor (chimeric antigen receptor or CAR) consisting of an anti-CD22 single chain variable fragment (scFv) derived from the monoclonal antibody (moAb) 971 (m971), and the co-stimulatory domain 4-1BB (CD137) coupled to the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunostimulating and antineoplastic activities. Autologous peripheral blood lymphocytes (PBLs) from a patient with CD22-positive cancer are transduced with this lentiviral vector that encodes the CAR gene specific for CD22. After expansion in culture and reintroduction into the patient, the anti-CD22-CAR m971-BBz lentiviral vector-transduced autologous T-lymphocytes express anti-CD22-CAR on their cell surfaces and bind to the CD22 antigen on tumor cell surfaces. Subsequently, CD22-expressing tumor cells are lysed. CD22, a B-lineage-restricted, transmembrane phosphoglycoprotein, is expressed on malignant B-cells. m971 binds to a membrane proximal epitope on CD22 and has a higher binding affinity compared to other anti-CD22 moAb.","Cell|Pharmacologic Substance"]
["C121949","Anti-CD25-PBD Antibody-drug Conjugate ADCT-301","ADC ADCT-301|ADCT-301|Anti-CD25-PBD Antibody-drug Conjugate ADCT-301","An immunoconjugate consisting of a human immunoglobulin (Ig) G1 monoclonal antibody directed against the alpha subunit of the interleukin-2 receptor (IL-2R alpha or CD25) and conjugated, via a cleavable linker, to a synthetic, cross-linking agent pyrrolobenzodiazepine (PBD) dimer that targets DNA minor grooves, with potential antineoplastic activity. The monoclonal antibody portion of the anti-CD25 antibody-drug conjugate (ADC) ADCT-301 specifically binds to the cell surface antigen CD25. This causes the internalization of ADCT-301 and the subsequent release of the cytotoxic PBD moiety. The imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces interstrand cross-links in the minor groove of DNA and inhibits DNA replication, which inhibits the proliferation of CD25-overexpressing tumor cells. CD25, a transmembrane receptor and tumor-associated antigen (TAA), is expressed on certain cancer cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C106266","Anti-CD27L Antibody-Drug Conjugate AMG 172","AMG 172|Anti-CD27L Antibody-Drug Conjugate AMG 172","An immunoconjugate consisting of a human IgG1 monoclonal antibody directed against CD27L conjugated, via a non-cleavable linker, to the cytotoxic agent maytansinoid DM1, with potential antineoplastic activity. The monoclonal antibody moiety of this immunoconjugate binds to CD27L on tumor cell surfaces. After internalization, the DM1 moiety binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics and inhibiting both cell division and proliferation of cancer cells that express CD27L. CD27L, a type II transmembrane protein and member of the tumor necrosis factor family, is a co-stimulatory molecule constitutively expressed on a subset of activated T-cells, B-cells, and dendritic cells, which is overexpressed in certain tumor cell types.","Pharmacologic Substance"]
["C74004","Anti-CD3 Immunotoxin A-dmDT390-bisFv(UCHT1)","A-dmDT390-bisFv(UCHT1)|Anti-CD3 Immunotoxin A-dmDT390-bisFv(UCHT1)|Resimmune","A bivalent recombinant fusion protein immunotoxin derived from the anti-CD3 monoclonal antibody UCHT1 with potential antineoplastic activity. Anti-CD3 immunotoxin A-dmDT390-bisFv(UCHT1) consists of 1-390 amino acid residues of chain A diphtheria toxin (DT) joined via a spacer to the Fv fragment of UCHT1, which is connected to a second UCHT1 Fv fragment via a disulfide bond (hence the \"bisFv\" designation); the addition of the second Fv fragment overcomes the steric hindrance of immunotoxin binding due to the large N-terminal DT domain. Once inside target T cells, the DT moiety catalyzes the transfer of the ADP-ribose moiety of NAD to diphthamide, a posttranslationally modified histidine residue found in elongation factor 2 (EF-2); inactivation of EF-2, disruption of polypeptide chain elongation, and cell death ensue. CD3 is a complex of five cell-surface polypeptides associated with the T cell receptor (TCR) complex.","Pharmacologic Substance"]
["C116330","Anti-CD3 OKT3/Humanized Anti-GD2 3F8 Bispecific Antibody-activated T Lymphocytes","Anti-CD3 OKT3/Humanized Anti-GD2 3F8 Bispecific Antibody-activated T Lymphocytes|Anti-CD3 x hu3F8 Bispecific Antibody Armed ATC|GD2Bi-aATC|Hu3F8Bi Armed ATC|OKT3/Humanized 3F8 Bispecific Antibody-activated T Lymphocytes","Autologous activated T cells that have been coated with bispecific antibodies (BiAb) comprised of anti-CD3 murine monoclonal antibody OKT3 heteroconjugated to anti-GD2 humanized monoclonal antibody 3F8 (hu3F8), with potential antineoplastic and immunomodulating activities. In vitro, T cells are exposed to OKT3, which binds to the T cell receptor-CD3 complex on the T cell surface, crosslinks the CD3 receptors and leads to T cell activation. In turn, the hu3F8 monoclonal antibody is heteroconjugated to OKT3. Upon administration, anti-CD3 x anti-GD2 bispecific antibody-armed activated T cells attach to GD2-expressing tumor cells, thereby selectively cross-linking T cells and tumor cells. This results in selective cytotoxicity towards the GD2-expressing tumor cells. In addition, cytokine and chemokine secretion by the T cells further activates the immune system, which leads to the recruitment and activation of cytotoxic T lymphocytes (CTLs), and additional CTL-mediated tumor-specific cell lysis. GD2, a disialoganglioside and tumor-associated antigen, is overexpressed in a variety of tumor cell types. CD3 is part of the functional T cell receptor (TCR) complex, which is necessary for antigen recognition by T cells, and is required for signal transduction.","Cell|Pharmacologic Substance"]
["C95751","Anti-CD3 x Anti-CD20 Bispecific Antibody-Armed Activated T Cells","Anti-CD3 x Anti-CD20 Bispecific Antibody-Armed Activated T Cells|Anti-CD3 x CD20Bi-Armed ATC","Autologous activated T cells that have been coated with bispecific antibodies (BiAb), with potential antineoplastic and immunomodulating activities. In vitro, T cells are activated through exposure to the anti-CD3 murine monoclonal antibody OKT3 and low-dose interleukin 2 (Il-2) for 6-14 days and then armed with anti-CD3 x anti-CD20 bispecific antibody (CD20Bi). Upon administration, anti-CD3 x anti-CD20 bispecific antibody-armed activated T cells (AATC) attach to CD3-expressing T cells and CD20-expressing tumor cells, selectively cross-linking T cells and tumor cells. This may result in the recruitment and activation of cytotoxic T lymphocyte (CTLs), CTL-mediated specific tumor cell lysis, and the secretion of antitumor cytokines and chemokines. CD20, a cell surface phosphoprotein, is found on normal B cells and most B-cell tumors.","Cell|Pharmacologic Substance"]
["C95760","Anti-CD3/Anti-CD20 Trifunctional Bispecific Monoclonal Antibody FBTA05","Anti-CD3/Anti-CD20 Trifunctional Bispecific Monoclonal Antibody FBTA05|FBTA05","A trifunctional bispecific monoclonal antibody with potential antineoplastic activity. FBTA05 contains two antigen-recognition sites: one for human CD3, a T cell surface antigen; and one for human CD20, a tumor-associated antigen that is exclusively expressed on B cells during most stages of B cell development and often overexpressed in B-cell malignancies. In addition, the modified Fc portion of this antibody binds Fc receptors on antigen presenting cells (APCs) such as macrophages and dendritic cells (DCs). FBTA05 brings T cells, CD20-expressing tumor B-cells and APCs together into tricellular complexes, which may result in a potent cytotoxic T-lymphocyte (CTL) response against CD20-expressing tumor B-cells. Fc-mediated binding of APCs in the tricellular complex potentiates CD20 antigen presentation to T cells and the activation of anti-tumor cytotoxic T cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C125185","Anti-CD3/Anti-EGFR-bispecific Monoclonal Antibody-armed Activated Autologous T-lymphocytes","Anti-CD3 x Anti-EGFR AATCs|Anti-CD3 x Anti-EGFR BATs|Anti-CD3 x Anti-EGFR-bispecific Antibody Armed Activated Autologous T-cells|Anti-CD3/Anti-EGFR-bispecific Monoclonal Antibody-armed Activated Autologous T-lymphocytes","Autologous activated T-cells that have been coated with bispecific antibodies (BiAb) comprised of an anti-CD3 monoclonal antibody heteroconjugated to an anti-epidermal growth factor receptor (EGFR) monoclonal antibody, with potential antineoplastic and immunomodulating activities. Upon administration, anti-CD3 x anti-EGFR bispecific antibody-armed activated T-cells (AATC) attach to and selectively cross-link CD3-expressing T-cells and EGFR-expressing tumor cells. This results in the activation of cytotoxic T-lymphocytes (CTLs) and selective cytotoxicity towards the EGFR-expressing tumor cells. In addition, cytokine and chemokine secretion by the T-cells further activates the immune system, which leads to the recruitment and activation of CTLs, and additional CTL-mediated tumor-specific cell lysis. CD3 is part of the functional T-cell receptor (TCR) complex, which is necessary for antigen recognition by T-cells, and is required for signal transduction. EGFR, a receptor tyrosine kinase, is overexpressed on the surfaces of various tumor cell types.","Cell|Pharmacologic Substance"]
["C77886","Anti-CD30 Monoclonal Antibody MDX-1401","Anti-CD30 Monoclonal Antibody MDX-1401|MDX-1401","A fully human, second-generation, nonfucosylated monoclonal antibody directed against the cell surface receptor CD30 with potential immunomodulating and antineoplastic activities. Anti-CD30 monoclonal antibody MDX-1401 specifically binds to the CD30 antigen, which may result in a cytotoxic T lymphocyte (CTL) response against CD30-expressing tumor cells. CD30, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on activated lymphocytes transiently and is constitutively expressed in hematologic malignancies including Hodgkin's disease and some T-cell non-Hodgkin's lymphomas. Compared to conventional antibodies, deletion of fucose molecules on the antibody backbone, as is done in MDX-1401, may result in an increased affinity for Fc receptors and an enhanced antibody-dependent cellular cytotoxicity (ADCC).","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C74005","Anti-CD30 Monoclonal Antibody XmAb2513","Anti-CD30 Monoclonal Antibody XmAb2513|XmAb2513","A humanized monoclonal antibody directed against the cell surface receptor CD30 with potential immunotherapeutic activity. Anti-CD30 monoclonal antibody XmAb2513 specifically binds to the CD30 antigen, which may result in a cytotoxic T lymphocyte (CTL) response against CD30-expressing tumor cells. CD30, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on activated lymphocytes transiently and is constitutively expressed in hematologic malignancies including Hodgkin's disease and some T-cell non-Hodgkin's lymphomas.","Pharmacologic Substance"]
["C94219","Anti-CD30/CD16A Monoclonal Antibody AFM13","AFM13|Anti-CD30/CD16A Monoclonal Antibody AFM13","A tetravalent bispecific antibody directed against human CD30 and the human low affinity IgG Fc region receptor (FCGR3A; CD16A), with potential immunomodulating and antineoplastic activities. Anti-CD30/CD16A monoclonal antibody AFM13 binds to the CD16A expressed on natural killer (NK) cells with two of its binding sites and to CD30 on CD30-expressing tumor cells with the other two binding sites, thereby selectively cross-linking tumor and NK cells. This may result in NK cell activation, antibody-dependent cellular cytotoxicity (ADCC) and eventually tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is overexpressed in hematologic malignancies; CD16A is specifically expressed on the surface of NK cells.","Immunologic Factor|Pharmacologic Substance"]
["C125717","Anti-CD33 Antibody-drug Conjugate IMGN779","ADC IMGN779|Anti-CD33 ADC IMGN779|Anti-CD33 Antibody-drug Conjugate IMGN779|IMGN779","An antibody-drug conjugate (ADC) consisting of the humanized monoclonal antibody Z4681A conjugated, via a cleavable disulfide linker, to the cytotoxic DNA alkylating agent DGN462, which is an indolino-benzodiazepine dimer containing a mono-imine moiety, with potential antineoplastic activity. The monoclonal antibody portion of anti-CD33 monoclonal antibody-DGN462 conjugate IMGN779 specifically binds to the cell surface antigen CD33 expressed on myeloid leukemia cells; upon internalization, the DGN462 moiety is released, and covalently binds to and alkylates DNA, thereby causing cell cycle arrest, apoptosis and inhibition of cell growth in myeloid leukemia cells that express CD33. CD33 is expressed on normal non-pluripotent hematopoietic stem cells and myeloid leukemia cells.","Pharmacologic Substance"]
["C116737","Anti-CD33 Monoclonal Antibody BI 836858","Anti-CD33 Monoclonal Antibody BI 836858|BI 836858","An engineered, fully human, immunoglobulin (Ig) G1 anti-CD33 monoclonal antibody, with potential antineoplastic activity. Upon administration, anti-CD33 monoclonal antibody BI 836858 induces an antibody-dependent cellular cytotoxicity (ADCC) against CD33-expressing tumor cells, leading to cell death. CD33, a cell surface antigen expressed on normal non-pluripotent hematopoietic stem cells, is overexpressed on myeloid leukemia cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C71523","Anti-CD33 Monoclonal Antibody-DM4 Conjugate AVE9633","Anti-CD33 Monoclonal Antibody-DM4 Conjugate AVE9633","An immunoconjugate consisting of the humanized monoclonal antibody huMy9-6 conjugated to the cytotoxic maytansinoid DM4 with potential antineoplastic activity. The monoclonal antibody portion of anti-CD33 monoclonal antibody-DM4 conjugate AVE9633 specifically binds to the cell surface antigen CD33 expressed on myeloid leukemia cells; upon internalization, the DM4 moiety is released, binds tubulin, and disrupts microtubule assembly/disassembly dynamics, resulting in the inhibition of cell division and cell growth in myeloid leukemia cells that express CD33. CD33 is expressed on normal non-pluripotent hematopoietic stem cells as well as on myeloid leukemia cells.","Immunologic Factor|Pharmacologic Substance"]
["C123332","Anti-CD33/CD3 BiTE Antibody AMG 330","AMG 330|AMG330|Anti-CD33/CD3 BiTE Antibody AMG 330|BiTE Antibody AMG 330|Bispecific T-cell Engager Antibody AMG 330|CD33/CD3-directed Bispecific T-cell Engager Antibody AMG 330","A proprietary recombinant bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) CD33 fused to one that is directed against the CD3 antigen found on T-lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of anti-CD33/CD3 BiTE antibody AMG 330, this bispecific antibody binds to both the CD3 antigen on cytotoxic T-lymphocytes (CTLs) and the CD33 antigen found on CD33-expressing tumor cells. This activates and redirects CTLs to CD33-expressing tumor cells, which results in the CTL-mediated cell death of CD33-expressing tumor cells. CD33, a myeloid differentiation antigen, is expressed on normal non-pluripotent hematopoietic stem cells and overexpressed on neoplastic cells in patients with acute myeloid leukemia.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C131174","Anti-CD352 Antibody-drug Conjugate SGN-CD352A","ADC SGN-CD352A|Anti-CD352 Antibody-drug Conjugate SGN-CD352A|PBD Dimer ADC SGN-CD352A|PBD-based Anti-CD352 ADC SGN-CD352A|PBD-based Anti-CD352 Antibody-drug Conjugate SGN-CD352A|SGN-CD352A","An antibody-drug conjugate (ADC) consisting of an engineered cysteine humanized monoclonal antibody (EC-mAb) targeting CD352 (SLAM family member 6; SLAM6) that is conjugated to the cytotoxic, DNA minor-groove crosslinking agent pyrrolobenzodiazepine (PBD) dimer, with potential antineoplastic activity. Upon administration of anti-CD352 ADC SGN-CD352A, the antibody moiety targets the cell surface antigen CD352. Upon antibody/antigen binding, internalization, and lysosome uptake, the cytotoxic PBD moiety is released. In turn, the imine groups of the PBD moiety bind to the N2 positions of guanines on opposite strands of DNA. This induces DNA strand breaks, inhibits DNA replication, leads to G2/M cell cycle arrest, induces cell death, and inhibits the proliferation of CD352-overexpressing tumor cells. CD352, a tumor-associated antigen (TAA), is overexpressed on a variety of cancers. Cysteine engineering of the monoclonal antibody allows for a site-specific, stable conjugation and uniform loading of the PBD agent to the antibody.","Pharmacologic Substance"]
["C100101","Anti-CD37 Antibody-Drug Conjugate IMGN529","Anti-CD37 Antibody-Drug Conjugate IMGN529|IMGN529","An immunoconjugate that consists of a humanized IgG1 antibody K7153A against the cell-surface antigen CD37 and covalently linked via the uncleavable, maleimide-derived thioether-based linker SMCC to the maytansinoid DM1, with potential pro-apoptotic and cytotoxic activities. The antibody moiety of IMGN529 binds to CD37 on tumor B-cells and induces an antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), thereby showing pro-apoptotic activity. In addition, after the internalization of this agent and lysosomal degradation, the DM1 moiety binds to tubulin and inhibits tubulin polymerization and microtubule assembly, resulting in a disruption of microtubule activity and cell division, and eventually causing cell death in CD37-positive B-cells. CD37, a transmembrane glycoprotein, is overexpressed in B-cell malignancies. Compared to reducible, cleavable linkers, the non-reducible SMCC linker shows increased stability in plasma.","Pharmacologic Substance"]
["C122833","Anti-CD37 Monoclonal Antibody BI 836826","Anti-CD37 Monoclonal Antibody BI 836826|BI 836826|MAb 37.1","An Fc-engineered, chimeric immunoglobulin (Ig) G1 monoclonal antibody against the tumor-associated antigen (TAA) CD37, with potential antineoplastic activity. Upon administration, the anti-CD37 monoclonal antibody BI 836826 both activates the immune system to induce an antibody-dependent cell-mediated cytotoxicity (ADCC) against CD37-overexpressing tumor cells and induces apoptosis in these tumor cells. BI 836826 is Fc-engineered to improve ADCC activity and enhance affinity for the receptor Fc-gamma-RIIIa, which is expressed on human natural killer (NK) cells. CD37, a member of the tetraspanin superfamily of cell surface antigens, is overexpressed on a variety of cancer cell types and plays a key role in tumor cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C97954","Anti-CD38 Monoclonal Antibody MOR03087","Anti-CD38 Monoclonal Antibody MOR03087|MOR03087|MOR202","A fully human monoclonal antibody directed against the cell surface glycoprotein CD-38 with potential antineoplastic activity. Anti-CD38 monoclonal antibody MOR03087 specifically binds to CD38 on CD38-positive tumor cells. This may trigger antitumoral antibody-dependent cellular cytotoxicity (ADCC) and may eventually lead to cell lysis in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis.","Pharmacologic Substance"]
["C90578","Anti-CD38 Monoclonal Antibody SAR650984","Anti-CD38 Monoclonal Antibody SAR650984|SAR650984","A humanized IgG1 monoclonal antibody directed against the cell surface glycoprotein CD-38 with potential antineoplastic activity. Anti-CD38 monoclonal antibody SAR650984 specifically binds to CD38 on CD38-positive tumor cells. This may trigger antitumoral antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC) and apoptosis eventually leading to cell lysis in CD38-expressing tumor cells. CD38, a type II transmembrane glycoprotein, is present on various immune cells and hematologic malignancies, and its expression has been correlated with poor prognosis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C101366","Anti-CD40 Monoclonal Antibody Chi Lob 7/4","Anti-CD40 Monoclonal Antibody Chi Lob 7/4|Chi Lob 7/4","An IgG1 chimeric monoclonal antibody agonist of the cell surface receptor CD40 with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, anti-CD40 monoclonal antibody Chi Lob 7/4 binds to CD40 on a variety of immune cell types, triggering the cellular proliferation and activation of antigen-presenting cells (APCs), activating B cells and T cells, and enhancing the immune response; in addition, this agent binds to the CD40 antigen present on the surfaces of some solid tumor cells, resulting in complement-dependent cytotoxicity (CDC) and antibody-dependent cytotoxicity (ADCC) eventually resulting in decreased tumor growth. CD40, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells, many B-cell malignancies, and many solid tumors, mediating both indirect tumor cell death through the activation of the immune system and direct tumor cell apoptosis.","Immunologic Factor|Pharmacologic Substance"]
["C121217","Anti-CD40 Monoclonal Antibody SEA-CD40","Anti-CD40 Monoclonal Antibody SEA-CD40|SEA-CD40","A proprietary, non-fucosylated monoclonal antibody directed against the cell surface receptor CD40 with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, anti-CD40 monoclonal antibody SEA-CD40 binds to CD40 on a variety of immune cell types, triggering both cellular proliferation and activation of antigen-presenting cells (APCs), which activates B-cells and T-cells, and enhances the immune response against tumor cells. In addition, this agent binds to the CD40 antigen present on the surfaces of tumor cells, which induces antibody-dependent cytotoxicity (ADCC), and eventually inhibits the proliferation of CD40-expressing tumor cells. CD40, a stimulatory receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells, such as macrophages, dendritic cells and various tumor cell types; it plays a key role in the activation of the immune system. The non-fucosylated antibody shows increased efficacy as compared to its fucosylated counterpart.","Immunologic Factor|Pharmacologic Substance"]
["C120140","Anti-CD40L Fc-Fusion Protein BMS-986004","Anti-CD40L Fc-Fusion Protein BMS-986004|BMS-986004|BMS986004|Fc-Fusion Protein BMS986004","A dimeric fusion protein composed of the C-terminus of the domain antibody (dAb) BMS2h-572-633 targeting the CD40 ligand (CD40L or CD154) linked to a modified Fc fragment of immunoglobulin G1 (IgG1), with potential immunomodulatory activity. Upon intravenous administration, the peptide moiety of anti-CD40L antibody BMS-986004 specifically targets and binds to CD40L expressed on T-lymphocytes. This prevents the binding of CD40L to its cognate receptor CD40 expressed on B-lymphocytes, macrophages, and dendritic cells (DCs). This prevents T-cell mediated proliferation and differentiation of B-cells, and prevents the production of antibodies. By inhibiting both the production of anti-glycoprotein (GP) IIb/IIIa antibodies by B-cells and GPIIb/IIIa-dependent T-cell proliferation, BMS-986004 may prevent platelet destruction and may increase platelet counts in idiopathic thrombocytopenic purpura (ITP). The direct binding of BMS-986004 to CD40L on platelets further prevents CD40L/CD40-mediated destruction by macrophages and DCs in ITP. The modified Fc domain prevents the binding of BMS-986004 to the Fc receptor FcgammaRIIA on platelets, thereby preventing FcgammaRIIA-dependent platelet activation and anti-CD40L-induced thromboembolism. CD40L, a transmembrane protein of the tumor necrosis factor (TNF) superfamily, is primarily expressed on activated T-cells, but is also expressed on eosinophils, basophils, natural killer (NK) cells, mast cells, platelets and activated endothelial cells.","Pharmacologic Substance"]
["C116881","Anti-CD44 Monoclonal Antibody RO5429083","Anti-CD44 Monoclonal Antibody RO5429083|RG 7356|RO5429083","A recombinant, humanized monoclonal antibody targeting the cancer stem cell (CSC) antigen CD44, with potential immunomodulating and antineoplastic activities. Upon administration, RO5429083 binds to the constant region of the extracellular domain of CD44, thereby preventing the activation of various CD44-mediated signal transduction pathways. This may lead to a reduction in the proliferation of CD44-expressing tumor stem cells. CD44, a transmembrane glycoprotein and hyaluronic acid receptor, is expressed in healthy tissue and overexpressed in numerous cancer cell types; it plays a key role in tumor cell proliferation, migration and survival.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C88287","Anti-CD45 BC8 Monoclonal Antibody-Streptavidin Conjugate","Anti-CD45 BC8 Antibody-Streptavidin Fusion Protein|Anti-CD45 BC8 Monoclonal Antibody-Streptavidin Conjugate|BC8 scFv4SA Fusion Protein","An immunoconjugate containing a monoclonal antibody directed against the CD45 antigen BC8, conjugated to streptavidin, a nonglycosylated homotetrameric protein that has four high affinity binding sites for biotin. Anti-CD45 BC8 antibody-streptavidin conjugate binds to CD45, a transmembrane protein tyrosine phosphatase that is expressed on the surface of normal and malignant hematopoietic cells. Upon administration of a biotin-based radioconjugate, the biotin moiety of the radioconjugate binds to the streptavidin moiety of anti-CD45 BC8 antibody-streptavidin conjugate and, upon cellular internalization, specifically delivers cytotoxic radiation to CD45-expressing tumor cells.","Pharmacologic Substance"]
["C121211","Anti-CD47 Monoclonal Antibody CC-90002","Anti-CD47 Mab CC-90002|Anti-CD47 Monoclonal Antibody CC-90002|CC 90002|CC-90002","A monoclonal antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody CC-90002 selectively binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with signal regulatory protein alpha (SIRPa), a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor T-lymphocyte immune response and T cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C117730","Anti-CD47 Monoclonal Antibody Hu5F9-G4","Anti-CD47 Monoclonal Antibody Hu5F9-G4|Hu5F9-G4","A humanized monoclonal antibody targeting the human cell surface antigen CD47, with potential immunostimulating and antineoplastic activities. Upon administration, anti-CD47 monoclonal antibody Hu5F9-G4 selectively binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with its ligand signal regulatory protein alpha (SIRPa), a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling, allows the activation of macrophages, through the induction of pro-phagocytic signaling mediated by calreticulin, which is specifically expressed on the surface of tumor cells, and results in specific tumor cell phagocytosis. In addition, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-mediated cell killing. CD47, a tumor associated antigen expressed on normal, healthy hematopoietic stem cells (HSC), is overexpressed on the surface of a variety of cancer cells. Expression of CD47, and interaction with SIRP-alpha, leads to inhibition of macrophages and protects cancer cells from phagocytosis thereby allowing cancer cells to proliferate.","Immunologic Factor|Pharmacologic Substance"]
["C84855","Anti-CD70 Antibody-Drug Conjugate MDX-1203","Anti-CD70 ADC MDX-1203|Anti-CD70 Antibody-Drug Conjugate MDX-1203|MDX-1203","An antibody-drug conjugate (ADC) containing a fully human monoclonal antibody, directed against the extracellular domain of the human CD70 molecule, conjugated to a prodrug of a CC-1065 (rachelmycin) analogue via a stable peptide-based linker, with potential antineoplastic activity. The anti-CD70 antibody moiety of the anti-CD70 antibody-drug conjugate MDX-1203 selectively binds to the extracellular domain of CD70 on tumor cell surfaces. Upon internalization, the prodrug moiety is released and activated and binds to double-stranded B-DNA within the minor groove, thereby alkylating the -3 position of adenine, which may result in the inhibition of cellular proliferation of tumor cells that overexpress CD70. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. The antitumor antibiotic CC-1065, a DNA minor-groove-binding alkylating agent, was originally isolated from the bacterium Streptomyces zelensis.","Pharmacologic Substance"]
["C117732","Anti-CD70 Antibody-drug Conjugate SGN-CD70A","Anti-CD70 Antibody-drug Conjugate SGN-CD70A|SGN-CD70A","An antibody-drug conjugate (ADC) containing an engineered cysteine monoclonal antibody (EC-mAb), directed against the extracellular domain of the human CD70 molecule, conjugated to the synthetic, cytotoxic, DNA minor-groove crosslinking agent, pyrrolobenzodiazepine (PBD) dimer, via a stable, protease-cleavable, peptide-based linker, with potential antineoplastic activity. The anti-CD70 antibody moiety of the anti-CD70 antibody-drug conjugate SGN-CD70A selectively binds to the extracellular domain of CD70 on tumor cell surfaces. Upon internalization, the PBD dimer moiety is released and covalently binds, through its imine moieties, to the N2 positions of guanines on opposite strands of DNA. This induces DNA double strand breaks and inhibits DNA replication, which lead to the inhibition of cell growth of tumor cells that overexpress CD70. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. The cysteine moiety of the EC-mAb allows for the stable conjugation of the PBD to the antibody.","Immunologic Factor|Pharmacologic Substance"]
["C106116","Anti-CD70 Monoclonal Antibody ARGX-110","ARGX-110|Anti-CD70 Monoclonal Antibody ARGX-110","A defucosylated, humanized IgG1 monoclonal antibody directed against the extracellular domain of the human CD70 molecule with potential antineoplastic activity. Upon administration, anti-CD70 monoclonal antibody ARGX-110 selectively binds to, and neutralizes the activity of CD70, which may also induce an antibody-dependent cellular cytotoxicity (ADCC) response against CD70-expressing tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on a number of solid and hematological tumors. Its overexpression may play an important role in evasion of immune surveillance.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C78187","Anti-CD70 Monoclonal Antibody MDX-1411","Anti-CD70 Monoclonal Antibody MDX-1411|MDX-1411","A glycoengineered, fully humanized IgG1 monoclonal antibody directed against the extracellular domain of the human CD70 molecule with potential antineoplastic activity. Anti-CD70 fully human monoclonal antibody MDX-1411 selectivity binds to the extracellular domain of CD70, which may induce an antibody-dependent cellular cytotoxicity (ADCC) response against CD70-expressing tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on renal cell carcinoma (RCC) cells among other cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C123914","Anti-CD73 Monoclonal Antibody MEDI9447","Anti-CD73 Monoclonal Antibody MEDI9447|MEDI9447","A monoclonal antibody against the ectoenzyme CD73 (cluster of differentiation 73), also known as 5'-nucleotidase (5'-NT; ecto-5'-nucleotidase) with potential antineoplastic activity. Upon administration, anti-CD73 monoclonal antibody MEDI9447 targets and binds to CD73, leading to clustering of and internalization of CD73. This prevents CD73-mediated conversion of adenosine monophosphate (AMP) to adenosine and decreases the amount of free adenosine. This prevents adenosine-mediated lymphocyte suppression and increases the activity of CD8-positive effector cells. This also activates macrophages, and reduces both myeloid-derived suppressor cells (MDSCs) and regulatory T-lymphocytes. By abrogating the inhibitory effect on the immune system and enhancing the cytotoxic T-cell-mediated immune response against cancer cells, tumor cell growth decreases. In addition, clustering and internalization of CD73 decreases the migration of cancer cells and prevents metastasis. CD73, a plasma membrane protein upregulated on a number of cancer cell types, catalyzes the conversion of extracellular nucleotides, such as AMP, to membrane-permeable nucleosides, such as adenosine; it plays a key role in adenosine-mediated immunosuppression within the tumor microenvironment.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C113659","Anti-CD98 Monoclonal Antibody IGN523","Anti-CD98 Monoclonal Antibody IGN523|IGN523","A humanized, monoclonal antibody targeting the CD98 (gp125) antigen, with potential immunomodulatory and antineoplastic activities. Upon intravenous administration, IGN523 binds to CD98 expressed on the tumor cell surface and elicits both natural killer (NK)-cell mediated antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity towards CD98-expressing tumor cells. In addition, IGN523 inhibits essential amino acid uptake by rapidly proliferating tumor cells. CD98, a type II transmembrane glycoprotein, is involved in both integrin signaling and amino acid transport processes; it is overexpressed in certain cancer cells and plays a key role in the proliferation, survival and metastasis of tumor cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C95728","Anti-CEA BiTE Monoclonal Antibody AMG211","AMG211|Anti-CEA BiTE Monoclonal Antibody AMG211|MEDI-565|MT111","A recombinant, proprietary bispecific T-cell engagers (BiTE) antibody directed against human carcinoembryonic antigen (CEA), with potential immunostimulating and antineoplastic activities. Anti-CEA BiTE monoclonal antibody AMG211 possesses two antigen-recognition sites, one for CEA and one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR). This bispecific monoclonal antibody brings CEA-expressing tumor cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CEA-expressing cells. CEA, a tumor associated antigen, is overexpressed in many cancer types, including gastrointestinal, breast, non-small cell lung, and thyroid cancers.","Immunologic Factor|Pharmacologic Substance"]
["C77865","Anti-CEA IgCD28TCR-Transduced Autologous T Cells","Anti-CEA IgCD28TCR-Transduced Autologous T Cells","A population of autologous tumor infiltrating lymphocytes (TIL) transduced with a retroviral vector encoding the chimeric gene IgCD28TCR with potential immunostimulating and antineoplastic activities. The chimeric IgCD28TCR gene consists of portions of CD28, the zeta chain of the T-cell receptor (TCRzeta), and a single chain antibody domain (sFv) specific for the tumor-associated antigen CEA.  Upon administration, these gene-modified TIL bind to tumor cells expressing CEA, which may result in activation and proliferation of TIL and an enhanced cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. CEA may be overexpressed in various gastrointestinal and breast cancers. CD28, a T-cell surface-associated co-stimulatory molecule, is required for full T-cell activation, proliferation, and survival; expression of the CD28 fragment in this chimeric gene construct may impede activation-induced cell death (AICD) of TIL.","Cell|Pharmacologic Substance"]
["C79842","Anti-CEA TCR Retroviral Vector-Transduced Autologous Peripheral Blood Lymphocytes","Anti-CEA TCR Retroviral Vector-Transduced Autologous PBLs|Anti-CEA TCR Retroviral Vector-Transduced Autologous Peripheral Blood Lymphocytes|Anti-CEA TCR-Gene Engineered Autologous Lymphocytes","Autologous human peripheral blood lymphocytes (PBLs), transduced with a retroviral vector encoding both the alpha and beta chains of a T cell receptor (TCR) specific for the carcinoembryonic antigen (CEA), with potential immunostimulating and antineoplastic activities. After transduction, expansion in culture, and reintroduction into the patient, anti-CEA TCR retroviral vector-transduced autologous lymphocytes bind to tumor cells expressing CEA, which may result in cytokine expression, activation and proliferation of T-cells, and a specific cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. The tumor-associated antigen (TAA) CEA is overexpressed by a variety of cancer cell types, including those of the gastrointestinal tract, lung, and breast.","Cell|Pharmacologic Substance"]
["C68927","Anti-CEA/Anti-DTPA-In (F6-734) Bispecific Antibody","Anti-CEA/Anti-DTPA-In (F6-734) Bispecific Antibody|F6-734 BsMAb","A bispecific monoclonal antibody (BsMAb) consisting of the Fab fragment of an anti-CEA monoclonal antibody (F6) coupled to the Fab fragment of an anti-DTPA-In monoclonal antibody (734) with potential radioimmunotherapeutic activity. In a two-step pretargeted radioimmunotherapeutic approach, this BsMAb, localizing to CEA-expressing tumor cells via the F6 Fab fragment, is introduced into patient first, followed by injection of indium 131-radiolabeled DTPA, which is recognized by the 734 Fab fragment of the BsMAb. Accordingly, a potentially lethal dose of indium 131 is delivered specifically to CEA-expressing tumor cells while minimizing radiotoxicity to normal tissues. CEA (carcinoembryonic antigen) is a tumor antigen overexpressed in many cancer types, including gastrointestinal, breast, non-small cell lung, and thyroid cancers. DTPA (diethylenetriaminepentaacetic acid) is a bivalent hapten.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82355","Anti-CEA/Anti-HSG Bispecific Monoclonal Antibody TF2","Anti-CEA x Anti-Histamine-Succinyl-Glycine Bispecific Monoclonal Antibody TF2|Anti-CEA/Anti-HSG Bispecific Monoclonal Antibody TF2|TF2","A tri-Fab bispecific monoclonal antibody (BiMoAb) divalent for the carcinoembryonic antigen (CEA) and monovalent for histamine-succinyl-glycine (HSG) peptide-hapten. Anti-CEA/anti-HSG bispecific monoclonal antibody TF2 binds to the tumor associated antigen (TAA) CEA on CEA-expressing tumor cells. Subsequently, an HSG peptide-hapten carrying a radionuclide is administered, binding to the anti-HSG binding fragment on the BiMoAb. Depending on the characteristics of the radionuclide used, CEA-expressing tumor cells may then be radioimaged and/or treated radioimmunotherapeutically.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C120097","Anti-CEA/CD3 Bispecific Antibody RO6958688","Anti-CEA/CD3 Bispecific Antibody RO6958688|RO6958688","An anti-carcinoembryonic antigen (CEA)/anti-CD3 bispecific monoclonal antibody with potential antineoplastic activity. Anti-CEA/CD3 monoclonal antibody RO6958688 contains two antigen-recognition sites: one for human CD3, a T-cell surface antigen, and one for human CEA, a tumor-associated antigen that is specifically expressed on certain tumor cells. Upon intravenous administration, RO6958688 binds to both T-cells and CEA-expressing tumor cells, which cross-links the T-cells with the tumor cells. This may result in a potent cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. CEA is overexpressed in many cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C120305","Anti-CEACAM1 Monoclonal Antibody CM-24","Anti-CEACAM1 Monoclonal Antibody CM-24|CM-24","A humanized monoclonal immunoglobulin G4 (IgG4) antibody targeting the anti-carcinoembryonic antigen (CEA)-related cell adhesion molecule 1 (CEACAM1; CD66a), with potential immunomodulating and antineoplastic activities. Upon administration of anti-CEACAM1 monoclonal antibody CM-24, this agent binds to CEACAM1 on cancer cells and certain immune cells. This blocks the binding of CEACAM1-expressing cancer cells to CEACAM1-expressing immune cells and abrogates CEACAM1-mediated immunosuppression. This enhances the activation of cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells and increases CTL- and NK-mediated killing of CEACAM1-overexpressing cancer cells. CEACAM1, a member of the CEA family of proteins that plays a key role in cell migration, cell invasion, and cell adhesion, is overexpressed by a variety of cancer cell types. Its overexpression is correlated with both immunosuppression and poor prognosis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C117229","Anti-CEACAM5 Antibody-Drug Conjugate SAR408701","ADC SAR408701|Anti-CEACAM5 Antibody-Drug Conjugate SAR408701|SAR408701","An immunoconjugate consisting of anti-carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) conjugated to a cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-CEACAM5 antibody-drug conjugate SAR408701, the antibody moiety targets CEACAM5 on tumor cells. Upon antibody/antigen binding and internalization, the immunoconjugate releases the cytotoxic agent, which results in tumor cell death. CEACAM5, a member of the CEA family of proteins that plays a key role in cell migration, cell invasion, and cell adhesion, is overexpressed by a variety of cancer cell types.","Pharmacologic Substance"]
["C121784","Anti-CEA-CAR Autologous T Lymphocytes","Anti-CEA-CAR Autologous T Lymphocytes|Autologous Anti-CEA CAR-T Cells","Autologous lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen human carcinoembryonic antigen (CEA), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CEA-CAR autologous T-lymphocytes target and bind to tumor cells expressing CEA, which results in the cytotoxic T-lymphocyte (CTL)-mediated cell killing of CEA-expressing tumor cells. CEA is overexpressed in various tumor cell types.","Pharmacologic Substance"]
["C98295","Anti-c-fms Monoclonal Antibody AMG 820","AMG 820|Anti-c-fms Monoclonal Antibody AMG 820","A fully human IgG2 monoclonal antibody against the colony-stimulating factor-1 (CSF-1 or M-CSF) receptor c-fms (or CSFR1), with potential antineoplastic activity. Upon administration, anti-c-fms monoclonal antibody AMG 820 binds to and blocks c-fms, thereby blocking CSF-1 binding to its receptor and suppressing CSF-1-induced c-fms signaling. This results in the suppression of recruitment and activation of tumor associated macrophages (TAM) within the tumor microenvironment. This eventually leads to a decrease in tumor growth. c-fms, a transmembrane protein belonging to the tyrosine kinase family, is overexpressed in certain tumor cell types and plays an essential role in macrophage differentiation and regulation of cell proliferation. The presence of TAM is correlated with tumor proliferation, invasion and a poor prognosis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C125620","Anti-c-KIT Monoclonal Antibody KTN0158","Anti-c-KIT Monoclonal Antibody KTN0158|KTN0158","A humanized immunoglobulin (Ig) G1 monoclonal antibody against the stem cell factor receptor c-Kit (SCFR; KIT; CD117), with potential antineoplastic and anti-allergic activities. Upon administration, the anti-c-KIT monoclonal antibody KTN0158 binds to and inhibits the activation of the cell surface antigen c-Kit. This leads to an inhibition of the activation of c-KIT-mediated signal transduction pathways and inhibits cell proliferation in cancer cells expressing c-Kit. In mast cells, inhibition of c-KIT and c-KIT-mediated signaling prevents mast cell activation, degranulation and subsequent cytokine release. c-Kit, a transmembrane protein and receptor tyrosine kinase, is overexpressed in various cell types, including certain cancer cells and mast cells; it plays a key role in the regulation of cell differentiation and proliferation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C114286","Anti-CLDN6 Monoclonal Antibody IMAB027","Anti-CLDN6 Monoclonal Antibody IMAB027|IMAB027","A monoclonal antibody directed against the cell surface protein claudin 6 (CLDN6), with potential immunostimulating and antineoplastic activities. Upon administration, the anti-CLDN6 monoclonal antibody IMAB027 binds to CLDN-6 and may stimulate the immune system to exert both an antibody-dependent cellular cytotoxicity (ADCC) and a complement-dependent cytotoxicity (CDC) mediated immune response against CLDN-6-expressing tumor cells. This may inhibit tumor cell growth. CLDN-6, a tight-junction protein and embryonic antigen, is expressed on a variety of tumor cells but is not expressed on normal, healthy adult cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C106262","Anti-c-Met Monoclonal Antibody ABT-700","ABT-700|Anti-c-Met Monoclonal Antibody ABT-700","A monoclonal antibody directed against human hepatocyte growth factor receptor (HGFR or c-Met), with potential antineoplastic activity. Anti-c-Met monoclonal antibody ABT-700 binds to c-Met, thereby preventing both c-Met binding to its ligand, HGF and the subsequent activation of the HGF/c-Met signaling pathway. This may cause cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C113802","Anti-c-Met Monoclonal Antibody ARGX-111","ARGX-111|Anti-c-Met Monoclonal Antibody ARGX-111","A human monoclonal antibody targeting c-Met, with potential antineoplastic activity. Anti-c-Met monoclonal antibody ARGX-111 binds to c-Met, and blocks both ligand-dependent and -independent activation of c-Met-mediated signaling pathways. In addition, this agent enhances antibody dependent cellular cytotoxicity (ADCC). This leads to a reduction in cell proliferation of c-Met-expressing cancer cells. c-Met, a receptor tyrosine kinase overexpressed in certain cancer cell types, is involved in cell proliferation, angiogenesis and metastasis in multiple solid tumors. Compared to other c-Met targeting monoclonal antibodies, ARGX-111 shows increased antibody circulation time, enhanced tissue distribution and increased efficacy. ARGX-111 is obtained through active immunization with C-met antigen in Camelids and utilizes the Camelid V-domains fused with human antibody backbones.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C95732","Anti-c-MET Monoclonal Antibody LY2875358","Anti-c-MET Monoclonal Antibody LY2875358|LY2875358","A humanized IgG4 monoclonal antibody directed against human hepatocyte growth factor receptor (HGFR or c-MET) with potential antineoplastic activity. Anti-c-MET monoclonal antibody LY2875358 binds to c-MET, thereby preventing the binding of HGF to its receptor c-Met and subsequent activation of the HGF/c-Met signaling pathway. This may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.","Immunologic Factor|Pharmacologic Substance"]
["C119619","Anti-C-met Monoclonal Antibody SAIT301","Anti-C-met Monoclonal Antibody SAIT301|SAIT301","A humanized monoclonal antibody targeting the alpha chain of the extracellular domain of human hepatocyte growth factor receptor (HGFR or c-Met), with potential antineoplastic activity. Anti-c-Met monoclonal antibody SAIT301 binds to c-Met, thereby preventing both binding of its ligand, HGF, and the subsequent activation of the HGF/c-Met signaling pathway. In addition, SAIT301 induces c-MET internalization and subsequent degradation, which further inhibits c-Met-mediated signaling. This leads to a reduction in the proliferation of c-Met-expressing cancer cells. c-Met, a proto-oncogene receptor tyrosine kinase overexpressed in certain cancer cell types, is involved in various tumors.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C123831","Anti-CSF1R Monoclonal Antibody FPA008","Anti-CSF1 Receptor Antibody FPA008|Anti-CSF1R FPA008|Anti-CSF1R Monoclonal Antibody FPA008|Anti-Colony Stimulating Factor 1 Receptor Antibody FPA008|FPA008","A humanized monoclonal antibody directed against the tyrosine kinase receptor colony stimulating factor 1 receptor (CSF1R; CSF-1R), also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), with potential antineoplastic activity. Upon administration, anti-CSF1R monoclonal antibody FPA008 binds to CSF1R expressed on monocytes, macrophages, and osteoclasts and inhibits the binding of the CSF1R ligands colony-stimulating factor-1 (CSF-1) and interleukin-34 (IL-34), to CSF1R. This prevents CSF1R activation and CSF1R-mediated signaling in these cells. This blocks the production of inflammatory mediators by macrophages and monocytes and reduces inflammation. By blocking the recruitment to the tumor microenvironment and activity of CSF1R-dependent tumor-associated macrophages (TAMs), FPA008 enhances T-cell infiltration and antitumor T-cell immune responses, which inhibits the proliferation of tumor cells. Additionally, FPA008 prevents the activation of osteoclasts and blocks bone destruction. TAMs play key roles in immune suppression and promoting inflammation, tumor cell proliferation and survival.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C96801","Anti-CSF1R Monoclonal Antibody IMC-CS4","Anti-CSF1R Monoclonal Antibody IMC-CS4|IMC-CS4|LY3022855","A monoclonal antibody directed against colony stimulating factor 1 receptor (CSF1R) with potential antineoplastic activity. CSF1R monoclonal antibody IMC-CS4 binds to CSF1R which may trigger antitumoral antibody-dependent cell-mediated cytotoxicity (ADCC) in tumor cells overexpressing CSF1R. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (Cluster of Differentiation 115), is a cell-surface receptor for its ligand colony stimulating factor 1 (CSF1); this receptor is overexpressed or mutated in certain tumor cell types and plays major roles in tumor cell proliferation and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C92577","Anti-CTGF Monoclonal Antibody FG-3019","Anti-CTGF Monoclonal Antibody FG-3019|Anti-Connective Tissue Growth Factor Monoclonal Antibody FG-3019|FG-3019","A human monoclonal antibody targeting connective tissue growth factor (CTGF) with potential anti-fibrotic and antineoplastic activities. FG-3019 binds to CTGF thereby preventing the binding of the ligand to the receptor and subsequent receptor activation. As CTGF enhances the production of collagen and fibronectin, FG-319 may prevent and reverse fibrosis. In addition, FG-3019 may prevent tumor cell proliferation in CTGF-expressing tumor cells. CTGF, a member of the CCN family (CTGF, CYR61/CEF and NOV), is expressed in a variety of tumor cell types and is involved in processes such as cell proliferation, cell migration, cell adhesion, differentiation and angiogenesis.","Immunologic Factor|Pharmacologic Substance"]
["C94218","Anti-CTLA4 MoAb RNA/GITRL RNA-transfected Autologous Dendritic Cell Vaccine","Anti-CTLA4 MoAb RNA/GITRL RNA-transfected Autologous Dendritic Cell Vaccine|GITRL/antiCTLA4 RNA DC|anti-CTLA-4 mAb Heavy and Light Chain RNA/GITRL RNA-transfected Autologous DC","An autologous dendritic cell (DC) cancer vaccine with potential immunostimulatory activity. Anti-CTLA4 MoAb RNA/GITRL RNA-transfected DC vaccine is prepared by transfecting DCs with RNAs encoding humanized heavy and light chains of the anti-CTLA4 (cytotoxic T-Lymphocyte-Associated Antigen 4) monoclonal antibody and tumor necrosis factor (ligand) superfamily, member 18 (TNFSF18 or GlTRL); expression of anti-CTLA4 blocks the inhibitory effect of CTLA4 on the activation of T-lymphocytes, while expression of GlTRL modulates T lymphocyte survival in peripheral tissues. Co-vaccination of this vaccine with melanoma antigen specific vaccine may eliminate the adverse effects associated with systemic administration of immune modulators, while also enhancing vaccine-induced immune responses.","Cell|Pharmacologic Substance"]
["C94217","Anti-CTLA4 MoAb RNA-transfected Autologous Dendritic Cell Vaccine","Anti-CTLA4 MoAb RNA-transfected Autologous Dendritic Cell Vaccine|anti-CTLA-4 mAb Heavy and Light Chain RNA-transfected Autologous DC|antiCTLA4 RNA DC","An autologous dendritic cell (DC) cancer vaccine with potential immunostimulatory activity. Anti-CTLA4 MoAb RNA-transfected autologous DC vaccine is prepared by transfecting DCs with RNAs encoding humanized heavy and light chains of the anti-CTLA4 (cytotoxic T-Lymphocyte-Associated Antigen 4); expression of anti-CTLA4 blocks the inhibitory effect of CTLA4 on the activation of T-lymphocytes. Co-vaccination of this vaccine with melanoma antigen specific vaccine may eliminate the adverse effects associated with systemic administration of immune modulators, while also enhancing vaccine-induced immune responses.","Cell|Pharmacologic Substance"]
["C126113","Anti-CTLA-4 Monoclonal Antibody AGEN1884","AGEN-1884|AGEN1884|Anti-CTLA-4 Monoclonal Antibody AGEN1884","A recombinant human monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody AGEN1884 binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","Immunologic Factor|Pharmacologic Substance"]
["C71749","Anti-Denatured Collagen Monoclonal Antibody TRC093","Anti-Denatured Collagen Monoclonal Antibody TRC093|D93|MT293|TRC093","A humanized, affinity-matured IgG1k antibody directed against denatured collagens (I-IV) with potential antiangiogenic and antineoplastic activities. Anti-denatured collagen recombinant monoclonal antibody TRC093 binds to multiple epitopes on denatured collagens, inhibiting proteolytic collagen-mediated signaling in the extracellular matrix (ECM) that is important to tumor angiogenesis, tumor growth, and metastasis. The epitopes on denatured collagen bound by this antibody are considered cryptic because, in vivo, they are accessible only on the subendothelial basement membrane of tumors or in normal tissues undergoing neovascularization.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C80040","Anti-DKK1 Monoclonal Antibody BHQ880","Anti-DKK1 Monoclonal Antibody BHQ880|BHQ880","A humanized monoclonal antibody directed against Wnt antagonist Dickkopf-1 (DKK1) with potential anti-osteolytic activity. Anti-DKK1 monoclonal antibody BHQ880 binds to and inhibits DKK1, enhancing signaling through the Wnt pathway, which may result in osteoblast differentiation and activation within the bone matrix and the reversal of tumor-induced osteolytic disease. DKK1 is a potent Wnt signaling pathway antagonist.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C99123","Anti-DKK-1 Monoclonal Antibody LY2812176","Anti-DKK-1 Monoclonal Antibody LY2812176|LY-2812176|LY2812176","A human monoclonal antibody directed against the WNT antagonist dickkopf homolog 1 (DKK1), with potential anti-osteolytic activity. Anti-DKK1 monoclonal antibody LY2812176 binds to and inhibits DKK1, thereby restoring signaling through the WNT pathway, which may result in osteoblast differentiation and activation within the bone matrix and the reversal of tumor-induced osteolytic disease. DKK1, overexpressed by myeloma cells, is an inhibitor of the WNT signaling pathway and prevents the mediated formation of bone.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C101521","Anti-DLL4 Monoclonal Antibody MEDI0639","Anti-DLL4 Monoclonal Antibody MEDI0639|MEDI0639","An immunoglobulin G1 lambda monoclonal antibody directed against the Notch ligand delta-like 4 (DLL4) with potential antineoplastic activity. Anti-DLL4 monoclonal antibody MEDI0639 specifically binds to DLL4 and prevents its interaction with Notch receptors, thereby inhibiting Notch-mediated signaling and gene transcription, which may block tumor angiogenesis and eventually the inhibition of tumor cell growth. Activation of Notch receptors by DLL4 stimulates proteolytic cleavage of the Notch intracellular domain (NICD); after cleavage, NICD is translocated to the nucleus and mediates the transcriptional regulation of a variety of genes involved in vascular development. The expression of DLL4 is highly restricted to the vascular endothelium; DLL4/Notch signaling is required for the development of functional tumor blood vessels.","Immunologic Factor|Pharmacologic Substance"]
["C82367","Anti-Dll4 Monoclonal Antibody REGN421","Anti-Delta-Like 4 Monoclonal Antibody REGN421|Anti-Dll4 Monoclonal Antibody REGN421|REGN421","A human monoclonal antibody directed against Delta-like ligand-4 (DLL4) with potential antineoplastic activity.  Anti-DLL4 monoclonal antibody REGN421 specifically binds to human DLL4, preventing its binding to Notch receptors and inhibiting Notch signaling, which may result in defective tumor vascularization and, so, the inhibition of tumor cell growth. DLL4 is the only Notch ligand selectively expressed on endothelial cells; DLL4/Notch signaling is required for the development of functional tumor blood vessels.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C119620","Anti-DLL4/VEGF Bispecific Monoclonal Antibody OMP-305B83","Anti-DLL4/VEGF Bispecific Monoclonal Antibody OMP-305B83|OMP-305B83","A bispecific monoclonal antibody directed against both the Notch ligand delta-like 4 (DLL4) and the human tyrosine kinase vascular endothelial growth factor (VEGF), with potential anti-angiogenic and antineoplastic activities. The anti-DLL4 moiety of anti-DLL4/VEGF monoclonal antibody OMP-305B83 specifically binds to DLL4, prevents its interaction with Notch receptors, and inhibits Notch-mediated signaling and gene transcription, which may both block tumor angiogenesis and inhibit tumor cell growth. The anti-VEGF moiety binds to VEGF and prevents the binding of VEGF to its receptor, which blocks VEGF-mediated signaling and further inhibits the growth and maintenance of tumor blood vessels. The expression of DLL4 is highly restricted to the vascular endothelium; DLL4/Notch signaling is required for the development of functional tumor blood vessels. The expression of the pro-angiogenic growth factor VEGF is associated with tumor angiogenesis and tumor cell proliferation and invasion.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C78826","Anti-DR5 Agonist Monoclonal Antibody TRA-8","Anti-DR5 Agonist Monoclonal Antibody TRA-8|Anti-death Receptor 5 Agonist Monoclonal Antibody TRA-8|TRA-8","An agonist mouse monoclonal antibody directed against TRAIL death receptor type 5 (DR5) with potential antineoplastic activity. Anti-DR5 agonist monoclonal antibody TRA-8 binds DR5, which may induce apoptosis in DR5-expressing tumor cells. DR5 is a tumor cell surface ligand that crosslinks with death receptor type 4 (DR4) when bound by TRAIL [Tumor necrosis (TNF)-related apoptosis-inducing ligand], triggering apoptosis via a death receptor signaling pathway. The apoptotic activity of this antibody may not require DR4/DR5 crosslinking.","Pharmacologic Substance"]
["C120316","Anti-EGFR Monoclonal Antibody GC1118","Anti-EGFR Monoclonal Antibody GC1118|GC1118","A recombinant, human monoclonal antibody directed against the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Upon intravenous administration, GC1118 binds to and blocks the ligand binding site of EGFR, which prevents receptor dimerization and activation. This may lead to an inhibition of both EGFR-dependent downstream pathways and EGFR-dependent tumor cell proliferation and metastasis. EGFR, a receptor tyrosine kinase, may be overexpressed on the surfaces of various tumor cell types.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C94221","Anti-EGFR Monoclonal Antibody GT-MAB 5.2-GEX","Anti-EGFR Monoclonal Antibody GT-MAB 5.2-GEX|CetuGEX","A glycoengineered form of a human monoclonal antibody directed against the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Anti-EGFR monoclonal antibody GT-MAB 5.2-GEX specifically binds to the extracellular domain of EGFR, thereby potentially inducing an antibody-dependent cell-mediated cytotoxicity (ADCC) against EGFR-expressing tumor cells, eventually leading to tumor cell apoptosis and an inhibition of tumor cell growth. EGFR, a member of the epidermal growth factor family of extracellular protein ligands, is overexpressed on the cell surfaces of various solid tumors. This antibody has a specific glycosylation profile that may enhance its ADCC response against EGFR-expressing tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C99899","Anti-EGFR Monoclonal Antibody Mixture MM-151","Anti-EGFR Monoclonal Antibody Mixture MM-151|MM-151","An oligoclonal therapeutic composed of three fully human monoclonal antibodies targeting epidermal growth factor receptor (EGFR or ErbB1), with potential antineoplastic activity. Upon administration of MM-151, the three antibodies bind to distinct, non-overlapping epitopes of EGFR, thereby preventing the binding of a full range of both high and low affinity EGFR ligands and inhibiting EGFR-ERK-mediated signaling. This eventually inhibits tumor cell proliferation in EGFR-overexpressing tumor cells. Furthermore, multi antibody-antigen bindings cause crosslinking of EGFR and downregulate receptor signalings that are mediated via heterodimerization of EGFR with other members of the EGFR family. EGFR, a receptor tyrosine kinase overexpressed in a variety of cancer cell types, is a key regulator of cancer cell proliferation, apoptosis, invasion, and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C91381","Anti-EGFR Monoclonal Antibody Mixture Sym004","Anti-EGFR Monoclonal Antibody Mixture Sym004|Futuximab/Zatuximab|Sym004","A mixture of two recombinant IgG1 antibodies directed against different epitopes in the epidermal growth factor receptor (EGFR) extracellular domain III, with potential antineoplastic activity. Anti-EGFR monoclonal antibody mixture Sym004 binds to the extracellular domain of EGFR, thereby preventing ligand binding. This may prevent activation and subsequent dimerization of the receptor; the decrease in receptor activation may result in an inhibition of downstream ERK and JNK signaling pathways and thus inhibition of EGFR-dependent tumor cell proliferation and metastasis. In addition, binding of Sym004 to EGFRs causes EGFR internalization and degradation. EGFR, a receptor tyrosine kinase, often is overexpressed on the cell surfaces of various solid tumor cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C78838","Anti-EGFR Monoclonal Antibody RO5083945","Anti-EGFR Monoclonal Antibody RO5083945|Anti-Epidermal Growth Factor Receptor Monoclonal Antibody RO5083945","A glycoengineered monoclonal antibody directed against the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Anti-EGFR monoclonal antibody RO5083945 binds to the extracellular domain of EGFR, preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization may result in an inhibition of downstream ERK and JNK signaling pathways and so inhibition of EGFR-dependent tumor cell proliferation and metastasis.  EGFR, a member of the epidermal growth factor family of extracellular protein ligands, may be overexpressed on the cell surfaces of various solid tumor cell types.","Pharmacologic Substance"]
["C117726","Anti-EGFR Monoclonal Antibody SCT200","Anti-EGFR Monoclonal Antibody SCT200|SCT200","A recombinant monoclonal antibody against human epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Upon administration, anti-EGFR monoclonal antibody SCT200 targets EGFR, prevents the activation and subsequent dimerization of this receptor and inhibits both EGFR-mediated signal transduction and cellular proliferation of EGFR-expressing tumor cells. In addition, SCT200 may induce antibody-dependent cell-mediated cytotoxicity (ADCC) against EGFR-expressing tumor cells. EGFR, a member of the epidermal growth factor receptor family, is overexpressed on the cell surfaces of various solid tumors.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C121550","Anti-EGFR Monoclonal Antibody SYN004","Anti-EGFR Monoclonal Antibody SYN004|SYN004","A glyco-engineered monoclonal antibody directed against the receptor tyrosine kinase epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon administration, anti-EGFR monoclonal antibody SYN004 binds to the extracellular domain of EGFR, which prevents ligand binding and the subsequent activation and dimerization of the receptor. This inhibits the activation of EGFR-mediated signaling pathways and inhibits EGFR-dependent tumor cell proliferation. EGFR, a member of the EGFR receptor tyrosine kinase family, may be overexpressed on the cell surfaces of various tumor cell types.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C111906","Anti-EGFR TAP Antibody-drug Conjugate IMGN289","Anti-EGFR TAP Antibody-drug Conjugate IMGN289|Anti-EGFR-SMCC-DM1|IMGN289","A targeted antibody payload (TAP)-based immunoconjugate consisting of a human monoclonal antibody directed against the epidermal growth factor receptor (EGFR) conjugated, via a nonreducible thioether linker (succinimidyl trans-4-(maleimidylmethyl)cyclohexane-1-carboxylate or SMCC), to the cytotoxic agent maytansinoid mertansine (DM1), with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of immunoconjugate IMGN289 binds to and inhibits EGFR on tumor cell surfaces. Inhibition of EGFR prevents EGFR-mediated signaling and may inhibit tumor cell proliferation. After internalization, the mertansine moiety binds to tubulin and interferes with microtubule assembly/disassembly dynamics. This inhibits both cell division and the proliferation of cancer cells that express EGFR. EGFR, overexpressed by a variety of cancers, plays a key role in tumor cell proliferation and survival. Linkage of the antibody and drug, through a nonreducible linker, appears to contribute to the improved efficacy and reduced toxicity of this antibody-drug conjugate (ADC) compared to similar ADCs constructed with reducible linkers.","Pharmacologic Substance"]
["C124993","Anti-EGFR/c-Met Bispecific Antibody JNJ-61186372","Anti-EGFR/c-Met Bispecific Antibody JNJ-61186372|JNJ-61186372","A human bispecific antibody targeting both epidermal growth factor receptor EGFR and hepatocyte growth factor receptor (HGFR; cMet), with potential antineoplastic activity. Upon administration, anti-EGFR/c-Met bispecific antibody JNJ-61186372 simultaneously targets and binds to wild-type or certain mutant forms of both EGFR and cMet expressed on cancer cells, thereby preventing receptor phosphorylation. This prevents the activation of both EGFR- and cMet-mediated signaling pathways. In addition, binding results in receptor degradation, which further inhibits EGFR- and cMet-mediated signaling. JNJ-61186372 also causes antibody-dependent cellular cytotoxicity (ADCC). Altogether, this results in the inhibition of tumor cell proliferation. EGFR and cMet, both upregulated or mutated in a variety of tumor cell types, play key roles in tumor cell proliferation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C131175","Anti-EGFR/HER2/HER3 Monoclonal Antibody Mixture Sym013","Anti-EGFR/HER2/HER3 Monoclonal Antibody Mixture Sym013|Pan-HER mAb Mixture Sym013|Sym-013|Sym013|pan-HER Antibody Mixture Sym013","An antibody mixture composed of six humanized, immunoglobulin G1 (IgG1) monoclonal antibodies directed against three members of the human epidermal growth factor receptor (EGFR; HER) family: EGFR (HER1; ErbB1), HER2 (ErbB2) and HER3 (ErbB3), with potential antineoplastic activity. Upon administration of anti-EGFR/HER2/HER3 monoclonal antibody mixture Sym013, the six antibodies bind to non-overlapping epitopes on EGFR, HER2 and HER3, which prevents both ligand binding and receptor activation, and induce simultaneous down-modulation of EGFR, HER2 and HER3.  This inhibits the activation of HER-dependent signaling pathways and HER-dependent tumor cell proliferation. Overexpression of the HER family plays a key role in many cancers; targeting multiple HER family members simultaneously may increase therapeutic efficacy.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C99222","Anti-EGFRvIII Antibody Drug Conjugate AMG 595","AMG 595|Anti-EGFRvIII Antibody Drug Conjugate AMG 595|Anti-EGFRvIII-DM1 Immunoconjugate AMG 595","An immunoconjugate consisting of a human monoclonal antibody directed against the deletion-mutant of epidermal growth factor receptor, EGFRvIII, conjugated via a non-cleavable linker to the cytotoxic agent maytansinoid DM1, with potential antineoplastic activity. The monoclonal antibody moiety of this immunoconjugate binds to EGFRvIII on tumor cell surfaces. After internalization, the DM1 moiety binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics and inhibiting cell division and the proliferation of cancer cells that express the EGFRvIII mutant. EGFRvIII, a deletion mutation of exons 2-7 in the epidermal growth factor receptor gene, is overexpressed by a variety of cancers, including glioblastoma multiforme, non-small lung carcinoma, and breast carcinoma.","Pharmacologic Substance"]
["C111565","Anti-EGFRvIII CAR-transduced Allogeneic T-lymphocytes","Anti-EGFRvIII CAR PG13-139-CD8-CD28BBZ- transduced T-lymphocytes|Anti-EGFRvIII CAR-transduced Allogeneic T-lymphocytes","Allogeneic human T-lymphocytes transduced with a retroviral vector encoding an anti-epidermal growth factor receptor (EGFR) variant III (EGFRvIII) mutant chimeric T cell receptor (chimeric antigen receptor or CAR) gene coupled to the signaling domains from CD8, CD28, 4-1BB (CD137) and CD3 zeta, with potential immunostimulatory and antineoplastic activities. Upon administration, the anti-EGFRvIII CAR-transduced allogeneic T lymphocytes bind to the EGFRvIII antigen on tumor cell surfaces; subsequently, EGFRvIII-expressing tumor cells may be lysed. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types and absent in normal, healthy cells; it plays a key role in tumor cell proliferation, tumor angiogenesis and radio- and chemoresistance.","Cell|Pharmacologic Substance"]
["C88307","Anti-EGFRvIII Immunotoxin MR1-1","Anti-EGFRvIII Immunotoxin MR1-1|MR1-1|MR1-1KDEL|MR1scFvPE38KDEL","A recombinant immunotoxin consisting of single-chain variable domain fragment antibody directed against the tumor-specific antigen EGFRvIII (MR1scFv) fused to domains II and III of the Pseudomonas exotoxin (PE38KDEL), with potential antineoplastic activity. Upon administration, the antibody moiety of anti-EGFRvIII immunotoxin MR1-1 binds to EGFRvIII; upon internalization, the exotoxin portion inhibits protein synthesis, resulting in a reduction in tumor cell proliferation of EGFRvIII- expressing tumor cells. EGFRvIII, a type III in-frame deletion mutation of the epidermal growth factor receptor (EGFR) gene, is expressed by a variety of cancers, including glioblastoma multiforme, non-small lung carcinoma, and breast carcinoma. Compared to intact IgG antibodies, single-chain antibodies such as MR1scFv are smaller and may penetrate tumors better. Pseudomonas exotoxin PE38KDEL was modified to remove the natural cell binding domain.","Pharmacologic Substance"]
["C90551","Anti-EGP-2 Immunotoxin MOC31-PE","Anti-EGP-2 Immunotoxin MOC31-PE|Anti-Epithelial Glycoprotein-2 Immunotoxin MOC31-PE|MOC31-PE","An immunotoxin consisting of a monoclonal antibody directed against epithelial glycoprotein-2 (EP-2, or epithelial cell adhesion molecule (EpCAM)) conjugated to the bacterial toxin Pseudomonas exotoxin A (PE) with potential antineoplastic activity. Upon administration of anti-EGP-2 immunotoxin MOC31-PE, the monoclonal antibody moiety targets and binds to EP-2. Upon internalization, the Pseudomonas exotoxin A moiety then inactivates elongation factor 2 (EF-2) through ADP ribosylation, resulting in inhibition of protein synthesis in EP-2-expressing cells. EP-2, a tumor-associated antigen, is overexpressed in a variety of cancer cell types.","Pharmacologic Substance"]
["C74010","Anti-Endoglin Chimeric Monoclonal Antibody TRC105","Anti-Endoglin Chimeric Monoclonal Antibody TRC105|TRC105","A human/murine chimeric monoclonal antibody directed against endoglin (CD105) with potential antiangiogenic and antineoplastic activities. Anti-endoglin monoclonal antibody TRC105 binds to endoglin, which may result in inhibition of tumor angiogenesis and decreased tumor cell proliferation. The glycoprotein endoglin is a transforming growth factor beta-1 (TGF beta-1) accessory receptor that is highly expressed on tumor vessel endothelial cells and appears to be essential for angiogenesis.","Pharmacologic Substance"]
["C82406","Anti-Endosialin Monoclonal Antibody MORAb-004","Anti-Endosialin Monoclonal Antibody MORAb-004|MORAb-004","A humanized IgG1 monoclonal antibody directed against human endosialin/TEM1 (tumor endothelial marker;CD248) with potential anti-angiogenic and antineoplastic activities. Anti-endosialin/TEM1 monoclonal antibody MORAb-004 binds to and inhibits the activity of cell surface protein endosialin/TEM1, which may result in the inhibition of angiogenesis, tumor cell proliferation and metastasis. Endosialin/TEM1 plays a key role in angiogenesis and may be overexpressed on tumor stromal cells and endothelial cells.","Pharmacologic Substance"]
["C102980","Anti-ENPP3 Antibody-Drug Conjugate AGS-16C3F","ADC AGS-16C3F|AGS-16C3F|Anti-ENPP3 Antibody-Drug Conjugate AGS-16C3F","An antibody-drug conjugate (ADC) containing a fully human monoclonal antibody (AGS-16C) directed to the ectonucleotide pyrophosphatase/phosphodiesterase family member 3 (ENPP3), conjugated via a non-cleavable linker to monomethyl auristatin F (MMAF), an auristatin derivative and a potent microtubule inhibitor, that has potential antineoplastic activity. Upon intravenous administration of ADC AGS-16C3F, the monoclonal antibody moiety of this conjugate selectively binds to ENPP3 then is internalized and undergoes proteolytic cleavage to release MMAF. MMAF binds to and inhibits tubulin polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. While normally expressed at low levels in the proximal tubules of the kidney, the type II transmembrane glycoprotein ENPP3 has been found to be overexpressed in renal neoplasms.","Pharmacologic Substance"]
["C116626","Anti-ENPP3/MMAF Antibody-Drug Conjugate AGS-16M8F","AGS-16M8F|Anti-ENPP3/MMAF Antibody-Drug Conjugate AGS-16M8F","An antibody-drug conjugate (ADC) containing a human immunoglobulin (Ig) G2k monoclonal antibody (AGS-16C) directed against the ectonucleotide pyrophosphatase/phosphodiesterase family member 3 (ENPP3, NPP3, B10, PDNP3 CD203c, or PD-IBETA ), conjugated, via the non-cleavable maleimidocaproyl (mc) linker, to monomethyl auristatin F (MMAF), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. Upon intravenous administration of anti-ENPP3/MMAF ADC AGS-16M8F, the monoclonal antibody moiety selectively binds to ENPP3 expressed on tumor cells; upon internalization, the ADC is degraded by lysosomal proteases and MMAF is released. In turn, MMAF binds to and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis. While normally expressed at low levels in the proximal tubules of the kidney, the type II transmembrane glycoprotein ENPP3 is overexpressed in most renal neoplasms and some liver cancers.","Pharmacologic Substance"]
["C61307","Anti-EpCAM Antibody Fragment-Pseudomonas-exotoxin Fusion Protein","Anti-EpCAM Antibody Fragment-Pseudomonas-exotoxin Fusion Protein|Proxinium|VB4-845|anti-EpCAM-Pseudomonas-exotoxin fusion protein","A fusion protein immunotoxin consisting of a humanized, single-chain monoclonal antibody fragment specific for the epithelial cell adhesion molecule (EpCAM) conjugated with a truncated form of Pseudomonas exotoxin A with potential antineoplastic activity. Anti-EpCAM-Pseudomonas-exotoxin fusion protein binds to Ep-CAM-positive tumor cells, thereby delivering the Pseudomonas exotoxin A moiety specifically; the Pseudomonas exotoxin A moiety then inactivates elongation factor 2 (EF-2) through ADP ribosylation, resulting in inhibition of protein synthesis in target cells. EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers.","Pharmacologic Substance"]
["C118447","Anti-EphA2 Monoclonal Antibody DS-8895a","Anti-EphA2 Monoclonal Antibody DS-8895a|DS-8895a","A monoclonal antibody directed against the ephrin receptor A2 (EphA2), with potential antineoplastic activity. Upon administration, anti-EphA2 monoclonal antibody DS-8895a selectively binds to cells expressing the EphA2 receptor. This blocks EphA2 activation and EphA2-mediated signaling. In addition, DS-8895a may activate an immune response against EphA2-expressing tumor cells. The cell-surface receptor EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) that are involved in mammalian development, is overexpressed by a variety of cancer cell types and plays an important role in tumor growth.","Immunologic Factor|Pharmacologic Substance"]
["C79836","Anti-EphA2 Monoclonal Antibody-MMAF Immunoconjugate MEDI-547","1C1-mcMMAF|Anti-EphA2 Monoclonal Antibody-MMAF Immunoconjugate MEDI-547|Medi-547","An auristatin analogue immunoconjugate directed against Eph receptor A2 (EphA2)-positive cancer cells with potential antineoplastic activity. Anti-EphA2 monoclonal antibody-MMAF immunoconjugate MEDI-547 is generated by conjugating the fully human IgG1 anti-EphA2 monoclonal antibody (1C1) to the small-molecule microtubule inhibitor monomethyl auristatin phenylalanine (MMAF) via the stable linker maleimidocaproyl (mc) (1C1-mcMMAF). The monoclonal antibody moiety of this agent selectively binds to cells expressing the EphA2 receptor. After internalization and enzymatic cleavage of the immunoconjugate within the tumor cell cytosol, free MMAF binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. The cell-surface receptor EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) involved in mammalian development, is overexpressed by a variety of different cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116629","Anti-EphA3 Monoclonal Antibody KB004","Anti-EphA3 Monoclonal Antibody KB004|KB004","A non-fucosylated monoclonal antibody directed against the ephrin receptor A3 (EphA3), with potential antineoplastic activity. Upon administration, anti-EphA3 monoclonal antibody KB004 selectively binds to tumor cells expressing EphA3. This blocks both EphA3 activation and EphA3-mediated signaling, and induces apoptosis in EphA3-expressing tumor cells. In addition, KB004 can stimulate antibody dependent cell-mediated cytotoxicity (ADCC) against EphA3-expressing tumor cells. This agent also prevents tumor cell proliferation by inhibiting both EphA3 signaling and proliferation of endothelial cells in the tumor vasculature. The cell-surface receptor EphA3, a member of the ephrin family of receptor tyrosine kinases (RTKs) that are involved in mammalian development, is overexpressed by a variety of tumor types but is not expressed in normal healthy adult tissues. It plays an important role in tumor cell proliferation. Non-fucosylation of the antibody enhances its ADCC activity.","Pharmacologic Substance"]
["C125633","Anti-Epidermal Growth Factor Receptor 2 Antibody Expressing Pluripotent Killer T-Lymphocytes","Anti-ERBB2 Antibody Expressing Pluripotent Killer T-Cells|Anti-ERBB2 Antibody Expressing Pluripotent Killer T-Lymphocytes|Anti-Epidermal Growth Factor Receptor 2 Antibody Expressing Pluripotent Killer T-Cells|Anti-Epidermal Growth Factor Receptor 2 Antibody Expressing Pluripotent Killer T-Lymphocytes|Anti-HER2 Antibody Expressing Pluripotent Killer T-Cells|Anti-HER2 Antibody Expressing Pluripotent Killer T-Lymphocytes|PIK-HER2","A specific population of pluripotent killer (PIK) T-cells that have been induced to express high levels of antibodies against human epidermal growth factor receptor 2 (ERBB2; HER2), with potential antitumor activity. Although the exact mechanism(s) of action through which PIK-HER2 cells exert their effects has yet to be elucidated, upon infusion, these cells secrete antibodies targeting HER2 expressed on the surface of tumor cells. This may inhibit HER2-dependent signaling, which may lead to inhibition of cellular proliferation and differentiation. Additionally, these cells may stimulate the host immune system to mount both a highly-specific cytotoxic T-lymphocyte (CTL) response and antibody-dependent cell cytotoxicity (ADCC) directed against HER2-overexpressing tumors, which leads to tumor cell lysis. HER2 is a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases and is frequently overexpressed in solid tumors.","Cell|Pharmacologic Substance"]
["C85486","Anti-ErbB2/Anti-ErbB3 Bispecific Monoclonal Antibody MM-111","Anti-ErbB2/Anti-ErbB3 Bispecific Monoclonal Antibody MM-111|MM-111","A bispecific monoclonal antibody directed against the human epidermal growth factor receptors ErbB2 (Her2) and ErbB3 (Her3) with potential antineoplastic activity. The anti-ErB2 targeting arm of anti-ErbB2/anti-ErbB3 bispecific monoclonal antibody MM-111 binds to ErbB2 on tumor cells with high affinity while the anti-Erb3 therapeutic arm binds to ErbB3, which may result in the inhibition of cellular proliferation and differentiation in ErbB2-overexpressing tumor cells via inhibition of ErbB3-dependent signal transduction pathways. ErbB2 and ErB3 are members of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases and are frequently overexpressed in solid tumors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C102535","Anti-ErbB3 Monoclonal Antibody AV-203","AV-203|Anti-ErbB3 MoAb AV-203|Anti-ErbB3 Monoclonal Antibody AV-203","A humanized monoclonal antibody (MoAb) directed against the human receptor tyrosine-protein kinase ErbB-3 (HER3) with potential antineoplastic activity. Anti-ErbB3 MoAb AV-203 binds to and inhibits both ligand neuregulin-1 (NRG-1)-dependent and ligand-independent ErbB3 activation, which may result in inhibition of ErbB3-dependent PI3K/Akt signaling and may lead to inhibition of cellular proliferation and differentiation. ErbB3, a member of the epidermal growth factor receptor (EGFR) family, is frequently overexpressed in solid tumors and its overexpression generally correlates with poor prognosis and tumor resistance; it has no active kinase domain itself but is activated through heterodimerization with other members of the EGFR receptor family that do.","Pharmacologic Substance"]
["C113333","Anti-ErbB3 Monoclonal Antibody KTN3379","Anti-ErbB3 Monoclonal Antibody KTN3379|KTN3379","A monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (Her3) with potential antineoplastic activity. Anti-ErbB3 monoclonal antibody KTN3379 binds to and prevents ligand binding to ErbB3, which may inhibit ErbB3-dependent phosphatidylinositol-3 kinase (PI3K)/Akt signaling and may lead to the inhibition of cellular proliferation and differentiation. ErbB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in a variety of solid tumors and its overexpression generally correlates with poor prognosis and tumor resistance.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C103859","Anti-ErbB3 Monoclonal Antibody REGN1400","Anti-ErbB3 Monoclonal Antibody REGN1400|REGN1400","A human monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (Her3) with potential antineoplastic activity. Anti-ErbB3 receptor monoclonal antibody REGN1400 binds to ErbB3 and prevents neuregulin 1 ligand binding to ErbB3, which may result in an inhibition of ErbB3-dependent phosphatidylinositol-3 kinase (PI3K)/Akt signaling. This eventually leads to the inhibition of cellular proliferation and differentiation. ErbB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in a variety of solid tumors and its overexpression generally correlates with poor prognosis and tumor resistance.","Pharmacologic Substance"]
["C103863","Anti-ErbB3/Anti-IGF-1R Bispecific Monoclonal Antibody MM-141","Anti-ErbB3/Anti-IGF-1R Bispecific Monoclonal Antibody MM-141|MM-141","A bispecific monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (Her3) and the human insulin-like growth factor-1 receptor (IGF-1R), with potential antineoplastic activity. The anti-IGF-1R targeting arm of anti-IGF-1R/anti-ErbB3 bispecific monoclonal antibody MM-141 binds to IGF-1R on tumor cells thereby preventing the binding of the natural ligands IGF-1, 2 and heregulin (HRG) to IGF-1R; the anti-ErbB3 therapeutic arm prevents the binding of neuregulin (NRG) to ErbB3. This prevents the activation of the PI3K/AKT signal transduction pathway and may result in both the induction of apoptosis and a decrease in cellular proliferation in IGF-1R and ErbB3-overexpressing tumor cells. IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily, and ErB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, are frequently overexpressed in solid tumors.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C116742","Anti-ETBR/MMAE Antibody-Drug Conjugate DEDN6526A","ADC DEDN6526A|Anti-ETBR/MMAE Antibody-Drug Conjugate DEDN6526A|DEDN6526A","An antibody-drug conjugate (ADC) composed of a humanized immunoglobulin (Ig) G1 monoclonal antibody against anti-endothelin B receptor (ETBR) and covalently linked to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DEDN6526A binds to ETBR-expressing tumor cells and is internalized, thereby delivering MMAE intracellularly. Proteolytic cleavage releases MMAE, which then binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. ETBR, a G-protein coupled receptor that can activate RAF/MEK signaling, is overexpressed in a variety of tumor cell types and plays a key role in tumor cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and angiogenesis.","Pharmacologic Substance"]
["C129383","Anti-FAP/Interleukin-2 Fusion Protein RO6874281","Anti-FAP/Interleukin-2 Fusion Protein RO6874281|FAP-IL2v FP RO6874281|FAP-IL2v RO6874281|RG 7461|RG-7461|RG7461|RO 6874281|RO-6874281|RO6874281|aFAP-IL2v RO6874281","A recombinant fusion protein comprised of a human monoclonal antibody directed against fibroblast activation protein-alpha (FAP) linked to an engineered, variant form of interleukin-2 (IL-2v), with potential immunostimulating and antineoplastic activities. Upon administration of RO6874281, the monoclonal antibody moiety recognizes and binds to FAP, thereby concentrating IL-2 in FAP-expressing tumor tissue. Subsequently, the IL-2 moiety of this fusion protein may stimulate a local immune response and activate natural killer (NK) cells and cytotoxic T-cells. FAP is a cell surface protein that is expressed on a wide variety of cancer cells. IL-2v cannot bind to IL-2 receptor-alpha (CD25, IL2Ra) and does not activate regulatory T-cells (Tregs).","Pharmacologic Substance"]
["C119744","Anti-FGF23 IgG1 Monoclonal Antibody KRN23","Anti-FGF23 IgG1 Monoclonal Antibody KRN23|KRN23|UX023","An orally bioavailable recombinant human immunoglobulin G1 monoclonal antibody directed against human fibroblast growth factor 23 (FGF23), that can be used to increase serum phosphate levels. Upon subcutaneous administration, anti-FGF23 IgG1 monoclonal antibody KRN23 binds to and inhibits FGF23, thereby interfering with FGF23 signaling. This increases tubular phosphate reabsorption, decreases excretion of phosphate, and increases serum phosphate levels, resulting in enhanced bone mineralization. FGF23, a member of the fibroblast growth factor (FGF) family produced by osteocytes, plays a key role in hypophosphatemic rickets/osteomalacia, such as X-linked hypophosphatemia (XLH) and tumor-induced rickets/osteomalacia. Increased FGF23 levels lead to decreased expression of the sodium-phosphate co-transporters in the proximal tubules, reduced renal phosphate reabsorption, increased excretion by the kidneys, and low serum phosphate concentration.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C107683","Anti-FGFR2 Antibody BAY1179470","Anti-FGFR2 Antibody BAY1179470|BAY1179470","An antibody against the fibroblast growth factor receptor type 2 (FGFR2), with potential antineoplastic activity. Upon administration, the anti-FGFR2 antibody BAY1179470 binds to and inhibits FGFR2, which may result in the inhibition of both FGFR2 phosphorylation and FGFR2-mediated signal transduction pathways. This results in the inhibition of cell proliferation and the induction of cell death of FGFR2-expressing tumor cells. FGFR2, upregulated in many tumor cell types, is a receptor tyrosine kinase, which is essential to tumor cellular proliferation, differentiation and survival.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C121212","Anti-FGFR2 Antibody-drug Conjugate BAY1187982","ADC BAY1187982|Anti-FGFR2 Antibody-drug Conjugate BAY1187982|BAY 1187982|BAY1187982","An antibody-drug conjugate (ADC) directed against the fibroblast growth factor receptor type 2 (FGFR2) and conjugated to an as of yet unidentified toxin, with potential antineoplastic activity. Upon intravenous administration, the anti-FGFR2 ADC BAY1187982 binds to FGFR2. Upon binding, the toxin selectively induces cell death, through an as of yet undisclosed mechanism of action, in FGFR2-expressing tumor cells. FGFR2, a receptor tyrosine kinase upregulated in many tumor cell types, plays an essential role in tumor cell proliferation, differentiation and survival.","Pharmacologic Substance"]
["C120040","Anti-FGFR2 Monoclonal Antibody FPA144","Anti-FGFR2 Monoclonal Antibody FPA144|FPA144","A glycoengineered, humanized monoclonal antibody directed against the fibroblast growth factor receptor type 2b (FGFR2b), with potential antineoplastic activity. Upon administration, the anti-FGFR2 antibody FPA144 specifically binds to and inhibits FGFR2b on tumor cell surfaces, which prevents FGFR2 from binding to its ligands, FGFR2b activation and the activation of FGFR2b-mediated signal transduction pathways. The binding of FPA144 to FGFR2b protein also induces antibody-dependent cell-mediated cytotoxicity (ADCC) against FGFR2b-expressing tumor cells. This results in the inhibition of cell proliferation and the induction of cell death of FGFR2-expressing tumor cells. FGFR2b, a specific isoform of the receptor tyrosine kinase FGFR2 upregulated in many tumor cell types, is essential to tumor proliferation, differentiation and survival. Glycoengineering enhances the FPA144-mediated ADCC.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C123829","Anti-FGFR3 Antibody-drug Conjugate LY3076226","ADC LY3076226|Anti-FGFR3 ADC LY3076226|Anti-FGFR3 Antibody-drug Conjugate LY3076226|Anti-fibroblast Growth Factor Receptor 3 Antibody-Drug Conjugate LY3076226|LY3076226","An antibody-drug conjugate (ADC) composed of a human monoclonal antibody against the fibroblast growth factor receptor type 3 (FGFR3) that is conjugated to an undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration, the antibody moiety of anti-FGFR3 ADC LY3076226 binds to FGFR3. Upon internalization, the cytotoxic moiety causes cell death in FGFR3-expressing tumor cells. FGFR3, a receptor tyrosine kinase upregulated or mutated in many tumor cell types, plays a key role in tumor cell proliferation.","Pharmacologic Substance"]
["C121649","Anti-FGFR3 Monoclonal Antibody B-701","Anti-FGFR3 Monoclonal Antibody B-701|B-701","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the fibroblast growth factor receptor type 3 (FGFR3), with potential antineoplastic activity. Upon intravenous administration, the anti-FGFR3 monoclonal antibody B-701 specifically binds to and inhibits both wild-type and mutated forms of FGFR3. This may result in the inhibition of FGFR3 phosphorylation, and thereby preventing its activation and FGFR3-mediated signal transduction pathways. This results in the inhibition of cell proliferation and the induction of cell death in FGFR3-expressing tumor cells. FGFR3, a receptor tyrosine kinase upregulated or mutated in many tumor cell types, plays a key role in tumor cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116863","Anti-FGFR3 Monoclonal Antibody MFGR1877S","Anti-FGFR3 Monoclonal Antibody MFGR1877S|MFGR1877S","A human monoclonal antibody against the fibroblast growth factor receptor type 3 (FGFR3), with potential antineoplastic activity. Upon administration, the anti-FGFR3 antibody MFGR1877S binds to and inhibits FGFR3, which may result in the inhibition of both FGFR3 phosphorylation and FGFR3-mediated signal transduction pathways. This results in the inhibition of cell proliferation and the induction of cell death in FGFR3-expressing tumor cells. FGFR3, upregulated or mutated in many tumor cell types, is a receptor tyrosine kinase, and plays a key role in tumor cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C126334","Anti-FGFR4 Monoclonal Antibody U3-1784","Anti-FGFR4 Monoclonal Antibody U3-1784|U3 1784|U3-1784","A human monoclonal antibody against human fibroblast growth factor receptor 4 (FGFR4), with potential antineoplastic activity. Upon administration, U3-1784 specifically binds to and blocks FGFR4. This prevents the activation of FGFR4, inhibits FGFR4-mediated signaling and leads to an inhibition of cell proliferation in FGFR4-overexpressing tumor cells. FGFR4, a receptor tyrosine kinase overexpressed by certain tumor cell types, is involved in tumor cell proliferation, differentiation, angiogenesis, and survival.","Pharmacologic Substance"]
["C129937","Anti-FLT3 Antibody-drug Conjugate AGS62P1","ADC AGS62P1|AGS62P1|Anti-FLT3 Antibody-drug Conjugate AGS62P1","An antibody-drug conjugate (ADC) composed of a human monoclonal antibody directed against the extracellular domain of receptor-type tyrosine-protein kinase FLT3 (FLT-3; FMS-like tyrosine kinase 3; CD135; fetal-liver kinase 2; FLK2) and conjugated, via an oxime linker and the site-directed non-natural amino acid linker para-acetyl-phenylalanine (pAcF), to a microtubule-disrupting cytotoxic agent, with potential antineoplastic activity. Upon administration of ADC AGS62P1, the antibody moiety targets and binds to FLT3. Upon antibody/antigen binding and internalization, the microtubule-targeting agent binds to and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis. The site-specific conjugation of the cytotoxic agent to the antibody, through pAcF, improves the biophysical properties of AGS62P1, increases payload distribution and stability, and optimizes its efficacy. FLT3, a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage, acute lymphoblastic leukemias and acute myeloid leukemias.","Pharmacologic Substance"]
["C129376","Anti-FLT3 Monoclonal Antibody 4G8-SDIEM","4G8-SDIEM|Anti-FLT3 Monoclonal Antibody 4G8-SDIEM|FLYSYN","A human, Fc-optimized, immunoglobulin G1 (IgG1) monoclonal antibody directed against the FLT3 tyrosine kinase receptor (CD135), with potential antineoplastic activity. Upon binding to FLT3, anti-FLT3 monoclonal antibody 4G8-SDIEM blocks FLT3 ligand binding to FLT3 and subsequent phosphorylation of FLT3, which may result in the inhibition of FLT3-mediated signal transduction pathways. In addition, this agent may stimulate an anti-FLT3 antibody-dependent cell-mediated cytotoxicity (ADCC) against FLT3-expressing tumor cells, which may lead to the inhibition of cellular proliferation and decreased survival in FLT3-expressing cells. FLT3 (FLK2), a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C85453","Anti-FLT3 Monoclonal Antibody IMC-EB10","Anti-FLT3 Monoclonal Antibody IMC-EB10|IMC-EB10","A fully human, IgG1 monoclonal antibody directed against the FLT3 tyrosine kinase receptor (CD135) with potential antineoplastic activity. Upon binding to FLT3, anti-FLT3 monoclonal antibody IMC-EB10 blocks FLT3 ligand binding to FLT3 and subsequent FLT3 phosphorylation, which may result in the inhibition of FLT3-mediated signal transduction pathways. In addition, this agent may stimulate an anti-FLT3 antibody-dependent cell-mediated cytotoxicity (ADCC) against FLT3-expressing tumor cells, which may result in the inhibition of cellular proliferation and survival in FLT3-expressing cells. FLT3 (FLK2), a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C118443","Anti-fucosyl-GM1 Monoclonal Antibody BMS-986012","Anti-fucosyl-GM1 Monoclonal Antibody BMS-986012|BMS-986012","A monoclonal antibody directed against the ganglioside fucosyl-GM1, with potential antineoplastic and immunomodulating activities. Upon administration, anti-fucosyl-GM1 monoclonal antibody BMS-986012 binds to fucosyl-GM1 on cancer cells and may activate both antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity against the bound tumor cells. This may inhibit the proliferation of GM1-expressing tumor cells. Fucosyl-GM1, a sphingolipid monosialoganglioside and tumor associated antigen (TAA), is overexpressed on the surface of many cancer cells while its expression is minimal or non-existent in normal tissues.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C79795","Anti-Ganglioside GM2 Monoclonal Antibody BIW-8962","Anti-GM2 Monoclonal Antibody BIW-8962|Anti-Ganglioside GM2 Monoclonal Antibody BIW-8962|BIW-8962","A humanized anti-ganglioside GM2 (GM2) monoclonal antibody with potential antineoplastic and immunomodulating activities. Upon administration, anti-ganglioside GM2 monoclonal antibody BIW-8962 may activate an antibody dependent cellular cytotoxicity (ADCC) against GM2-expressing tumor cells. GM2 is a tumor associated antigen (TAA) overexpressed on the surface of many cancer cells, such as multiple myeloma (MM) cells and neuroblastoma cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C101524","Anti-GCC Antibody-Drug Conjugate MLN0264","Anti-GCC Antibody-Drug Conjugate MLN0264|MLN0264","An antibody-drug conjugate (ADC) containing a monoclonal antibody directed against guanylyl cyclase C (GCC or GUCY2C) conjugated to monomethylauristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. The monoclonal antibody moiety of MLN0264 selectively binds to GCC, a transmembrane receptor normally found on intestinal cells and dopamine neurons in the brain, but is also overexpressed on the surface of gastrointestinal cancers. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis in GCC-expressing tumor cells.","Pharmacologic Substance"]
["C80042","Anti-GD2 Monoclonal Antibody hu14.18K322A","Anti-GD2 Monoclonal Antibody hu14.18K322A|hu14.18K322A","A monoclonal antibody directed against human glycosphingolipid GD2 with potential antineoplastic activity. Upon binding to the GD2 antigen, anti-GD2 monoclonal antibody hu14.18K322A triggers a host immune response against GD2-expressing tumor cells, which may result in tumor cell death. GD2, an O-acetylated disialoganglioside with expression in normal tissues restricted primarily to the cerebellum and peripheral nerves, is commonly expressed at high levels on tumors of neuroectodermal origins such as melanomas and neuroblastomas.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C91383","Anti-GD2 Monoclonal Antibody MORAb-028","Anti-GD2 Monoclonal Antibody MORAb-028|MORAb-028","A human IgM monoclonal antibody directed against disialoganglioside GD2 with potential immunomodulating activity. Upon administration, anti-GD2 monoclonal antibody MORAb-028 may stimulate the immune system to exert a complement-mediated cytotoxic response against GD2-expressing tumor cells. The glycosphingolipid GD2 is a tumor associated antigen (TAA) overexpressed on the surface of many cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C120039","Antigen-targeted Personalized Breast Cancer Vaccine","Antigen-targeted Personalized Breast Cancer Vaccine|IVAC_W_bre1_uID","An individualized, therapeutic cancer vaccine (IVAC) composed of liposomes containing RNA encoding two or three tumor associated antigens (TAAs) that are specifically expressed in the patient's individual cancer selected from a warehouse (\"off the shelf\") and p53 RNA, with potential immunostimulatory and antineoplastic activities. Upon administration, the antigen-targeted personalized breast cancer vaccines are translated by antigen presenting cells (APCs) and the expressed protein is presented via major histocompatibility complex (MHC) molecules on the surface of the APCs. This leads to an induction of both cytotoxic T-lymphocyte (CTL) and memory T-cell immune responses against the TAAs. The RNAs in the vaccine are specifically selected for an individual patient after RNA profiling of the patient's tumor.","Pharmacologic Substance"]
["C126643","Anti-GITR Agonistic Monoclonal Antibody INCAGN01876","Anti-GITR Agonistic Monoclonal Antibody INCAGN01876|INCAGN01876","An anti-human glucocorticoid-induced tumor necrosis factor receptor (tumor necrosis factor superfamily, member 18; TNFRSF18; GITR; CD357) agonistic humanized monoclonal antibody, with potential immune checkpoint modulating activity. Anti-GITR antibody INCAGN01876 binds to and activates GITRs found on multiple types of T-cells. This stimulates the immune system, induces both the activation and proliferation of tumor-antigen-specific T effector cells (Teff), and suppresses the function of activated T regulatory cells (Tregs). This leads to tumor cell eradication. GITR, a member of the TNF receptor superfamily and T-cell receptor co-stimulator, is expressed on the surface of multiple immune cell types, including Tregs, Teffs, B-cells, and natural killer (NK) cells. Inappropriately activated Tregs suppress Teffs and suppress T-cell receptor (TCR) signaling.","Pharmacologic Substance"]
["C128028","Anti-GITR Monoclonal Antibody GWN 323","Anti-GITR Monoclonal Antibody GWN 323|GWN 323|GWN323","An anti-human glucocorticoid-induced tumor necrosis factor receptor (tumor necrosis factor superfamily, member 18; TNFRSF18; GITR; CD357) agonistic monoclonal antibody, with potential immune checkpoint modulating activity. Anti-GITR antibody GWN 323 binds to and activates GITRs found on multiple types of T-cells. This stimulates the immune system, induces both the activation and proliferation of tumor-antigen-specific T effector cells (Teff), and suppresses the function of activated T regulatory cells (Tregs). This leads to tumor cell eradication. GITR, a member of the TNF receptor superfamily and T-cell receptor co-stimulator, is expressed on the surface of multiple immune cell types, including Tregs, Teffs, B-cells, and natural killer (NK) cells. Inappropriately activated Tregs suppress both Teffs and T-cell receptor (TCR) signaling.","Pharmacologic Substance"]
["C116065","Anti-GITR Monoclonal Antibody MK-4166","Anti-GITR Monoclonal Antibody MK-4166|MK-4166","An anti-human glucocorticoid-induced tumor necrosis factor receptor (GITR) agonistic monoclonal antibody (MoAb) with potential immunomodulating activity. Anti-GITR monoclonal antibody MK-4166 binds to and activates GITRs found on multiple types of T-cells. This stimulates the immune system and induces both the activation and proliferation of tumor-antigen-specific T effector cells, and suppresses the function of activated T regulatory cells. This leads to tumor cell eradication. Also, this agent is shown to act synergistically with chemotherapeutic drugs in multiple cancer models. GITR, a member of the TNF receptor superfamily, is expressed on the surface of multiple types of immune cells, including regulatory T-cells, effector T-cells, B-cells, and natural killer (NK) cells.","Pharmacologic Substance"]
["C129936","Anti-Glypican 3/CD3 Bispecific Antibody ERY974","Anti-GPC3/CD3 BiAb ERY974|Anti-GPC3/CD3 Bispecific Antibody ERY974|Anti-Glypican 3/CD3 Bispecific Antibody ERY974|ERY974","An anti-glypican 3 (GPC3; GPC-3)/anti-CD3 bispecific monoclonal antibody, with potential immunostimulating and antineoplastic activities. Anti-GPC3/CD3 bispecific antibody ERY974 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for GPC3, a tumor-associated antigen (TAA) overexpressed on the surface of certain tumor cells. Upon administration of ERY974, this bispecific antibody simultaneously binds to both CD3-expressing and GPC3-expressing cells, thereby crosslinking GPC3-expressing tumor cells and cytotoxic T-lymphocytes (CTLs). This may result in potent CTL-mediated lysis of GPC3-expressing tumor cells. GPC3, a heparan sulfate proteoglycan and an oncofetal antigen protein, is overexpressed in a variety of cancers; it plays a role in cell division and growth regulation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C85464","Anti-GnRH Vaccine PEP223","Anti-GnRH Vaccine PEP223|PEP223","A peptide vaccine derived from the synthetic peptide pyroEHWSYGLRPG, corresponding to amino acids 22-31 of mouse gonadotropin releasing hormone (GnRH), with potential immunocastration activity. PEP223 is dimerized and contains a D-lysine (k) substitution at position 6 (pyroEHWSYkLRPG) to increase its immunogenicity. Anti-GnRH vaccine PEP223 may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against GnRH, neutralizing its activity. In turn, testosterone production and tumor cell growth may be inhibited in testosterone-sensitive tumors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C118442","Anti-gpA33/CD3 Monoclonal Antibody MGD007","Anti-gpA33/CD3 Monoclonal Antibody MGD007|Humanized gpA33 x CD3 DART (TM) Protein MGD007|MGD007","An anti-glycoprotein A33 (gpA33)/anti-CD3 bispecific humanized monoclonal antibody with potential immunostimulatory and antineoplastic activities. Anti-gpA33/CD3 monoclonal antibody MGD007 possesses two antigen-recognition sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for gpA33, a tumor-associated antigen (TAA) overexpressed on the surface of certain tumor cells. Upon administration of MGD007, this bispecific antibody simultaneously binds to both CD3-expressing T-cells and gpA33-expressing cancer cells, thereby crosslinking cytotoxic T-lymphocytes (CTLs) to gpA33-expressing tumor cells. This may result in CTL-mediated cell lysis of the crosslinked tumor cells. The gpA33 antigen, a member of the immunoglobulin superfamily, is expressed in certain malignancies, including colon and gastrointestinal cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C80043","Anti-GPC3 Monoclonal Antibody GC33","Anti-GPC3 Monoclonal Antibody GC33|Anti-Glypican 3 Monoclonal Antibody GC33|GC33","A humanized monoclonal antibody directed against the cell surface oncofetal protein glypican-3 (GPC3) with potential antineoplastic activity. Anti-GPC3 monoclonal antibody GC33 binds to GPC3 and triggers a host immune response against GPC3-expressing tumor cells, which may result in tumor cell death. GPC3, a heparin sulfate proteoglycan, is frequently upregulated in hepatocellular carcinoma and mesoderm-derived organs such as the liver, lungs, and kidney.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C121638","Anti-GPC3-CAR Autologous T Lymphocytes","Anti-GPC3 CAR Autologous T Cells|Anti-GPC3-CAR Autologous T Lymphocytes|GPC3-targeted CAR Autologous T Cells","A preparation of autologous T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for glypican-3 (GPC3), with potential immunostimulating and antineoplastic activities. Upon administration, anti-GPC3-CAR autologous T-lymphocytes specifically target and bind to GPC3-expressing tumor cells, resulting in tumor cell lysis. GPC3, a heparan sulfate proteoglycan and a member of the glypican family, is overexpressed on certain tumor cell types while minimally expressed in normal, healthy cells; GPC3 plays an important role in cellular proliferation and differentiation.","Cell|Pharmacologic Substance"]
["C103857","Anti-GRP78 Monoclonal Antibody PAT-SM6","Anti-GRP78 Monoclonal Antibody PAT-SM6|PAT-SM6","A IgM monoclonal antibody (MoAb) against 78-kDa glucose-regulated protein (GRP78; also called BiP or HSPA5), with potential proapoptotic and antineoplastic activities. Upon intravenous administration of the anti-GRP78 monoclonal antibody PAT-SM6, the MoAb strongly binds to GRP78, thereby preventing the activation of multiple GRP78-mediated pathways and blocking the GRP78-induced suppression of apoptotic pathways. This eventually leads to the induction of tumor cell apoptosis and a reduction in tumor cell proliferation. GRP78, the endoplasmic reticulum (ER) chaperone and unfolded protein response (UPR) regulator, is overexpressed on the surface of a variety of cancer cell types; its expression is associated with increased tumor cell survival and proliferation, as well as angiogenesis and resistance to chemotherapy.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C95721","Anti-HB-EGF Monoclonal Antibody KHK2866","Anti-HB-EGF MoAb KHK2866|Anti-HB-EGF Monoclonal Antibody KHK2866|KHK2866","A proprietary fucose-free monoclonal antibody directed against human heparin-binding EGF-like growth factor (HBEGF) with potential antineoplastic activity. Anti-HB-EGF Monoclonal Antibody KHK2866 binds to HBEGF, thereby blocking its binding to the EGF receptors. This prevents EGF receptor activation and the subsequent induction of cell growth signaling. HBEGF is mitogenic for fibroblasts and smooth muscle and may be involved in macrophage-mediated cellular proliferation. The fucose-free monoclonal antibodies enhance antigen dependent cellular cytotoxicity (ADCC), and increase binding affinity to the Fc Receptor to overcome genetic polymorphism.","Immunologic Factor|Pharmacologic Substance"]
["C95736","Anti-HBEGF Monoclonal Antibody U3-1565","Anti-HBEGF Monoclonal Antibody U3-1565|U3-1565","A humanized monoclonal antibody directed against human heparin-binding EGF-like growth factor (HBEGF) with potential antineoplastic activity. Anti-HBEGF monoclonal antibody U3-1565 binds to HBEGF and blocks the binding of HBEGF to the EGF receptors. This prevents EGF receptor activation and the subsequent induction of cell growth signaling. HBEGF is mitogenic for fibroblasts and smooth muscle and may be involved in macrophage-mediated cellular proliferation.","Immunologic Factor|Pharmacologic Substance"]
["C129593","Anti-hCD70-CAR Retroviral Vector-transduced Autologous PBLs","Anti-hCD70 Autologous CAR-transduced T Cells|Anti-hCD70 CAR autologous PBLs|Anti-hCD70-CAR Retroviral Vector-transduced Autologous PBLs|Anti-hCD70-CAR Retroviral Vector-transduced Autologous Peripheral Blood Lymphocytes","A preparation of autologous human peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding for a T-cell chimeric antigen receptor (CAR) gene specific for the human cluster of differentiation 70 (CD70), with potential immunostimulatory and antineoplastic activities. Autologous PBLs from a patient with CD70-positive cancer are transduced with a retroviral vector that encodes the CAR gene specific for CD70. After expansion in culture and reintroduction into the patient, anti-hCD70-CAR retroviral vector-transduced autologous PBLs bind to the CD70 antigen on tumor cell surfaces; subsequently, CD70-expressing tumor cells are lysed. CD70, the ligand for the costimulatory receptor CD27, is overexpressed on the surfaces of various cancer cell types.","Pharmacologic Substance"]
["C116630","Anti-hepcidin Monoclonal Antibody LY2787106","Anti-hepcidin Monoclonal Antibody LY2787106|LY2787106","A humanized monoclonal antibody (MoAb) targeting the peptide hormone hepcidin, with potential anti-anemic activity. Upon intravenous administration, anti-hepcidin MoAb LY2787106 binds to hepcidin and prevents it from binding to the iron exporting protein ferroportin, which is expressed on both the basolateral surface of gastrointestinal (GI) enterocytes and the plasma membrane of macrophages. This prevents hepcidin-induced internalization and degradation of ferroportin and increases ferroportin-mediated iron export, thus increasing iron export from macrophages and iron absorption by enterocytes. This normalizes plasma iron levels, increases erythropoiesis and may inhibit anemia. Hepcidin, produced in hepatocytes, plays a key role in the homeostasis of systemic iron; it is upregulated during acute and chronic inflammation in response to cytokines and, in certain cancers, may contribute to cancer-associated anemia.","Pharmacologic Substance"]
["C128799","Anti-HER2 ADC DS-8201a","ADC DS-8201a|Anti-HER2 ADC DS-8201a|Anti-HER2 Antibody-Drug Conjugate DS-8201a|Anti-HER2-DX-8951 Derivative ADC DS-8201a|DS-8201a","An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting human epidermal growth factor receptor 2 (ERBB2; EGFR2; HER2) conjugated to a derivative of the camptothecin analog exatecan (DXd; DX-8951 derivative), a DNA topoisomerase 1 (topoisomerase I; Top1) inhibitor, with potential antineoplastic activity. Upon administration of anti-HER2 ADC conjugate DS-8201a, the antibody moiety targets and binds to HER2 on tumor cells. Upon antibody/antigen binding and internalization, the DX-8951 derivative moiety binds to and inhibits Top1-DNA complexes, which results in an inhibition of DNA replication, cell cycle arrest and tumor cell apoptosis. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types. In addition, DS-8201a induces antibody-dependent cell-mediated cytotoxicity (ADCC) and causes a bystander killing effect, thereby killing neighboring HER2-expressing tumor cells.","Pharmacologic Substance"]
["C123917","Anti-HER2 Antibody-drug Conjugate ARX788","ADC ARX788|ARX788|Anti-HER2 ADC ARX788|Anti-HER2 Antibody-drug Conjugate ARX788","An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting human epidermal growth factor receptor 2 (EGFR2; HER2) site-specifically conjugated, via the non-natural amino acid linker para-acetyl-phenylalanine (pAcF), to the auristatin analog and potent microtubule inhibitor monomethyl auristatin F (MMAF), with potential antineoplastic activity. Upon administration of anti-HER2 ADC ARX788, the antibody moiety targets and binds to HER2 on tumor cells. Upon antibody/antigen binding and internalization, MMAF binds to and inhibits tubulin polymerization, which results in G2/M phase arrest and tumor cell apoptosis. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types. The site-specific conjugation of the cytotoxic agent to the antibody improves the biophysical properties of ARX788, increases payload stability and optimizes its efficacy.","Pharmacologic Substance"]
["C126355","Anti-HER2 Antibody-drug Conjugate MEDI4276","ADC MEDI4276|Anti-HER2 Antibody-drug Conjugate MEDI4276|MEDI-4276|MEDI4276","An antibody-drug conjugate (ADC) composed of a bispecific antibody against the extracellular domain of human epidermal growth factor receptor 2 (HER2; ERBB2) comprised of the single-chain variable fragment (scFv) of the anti- HER2 monoclonal antibody trastuzumab, which binds to domain IV of HER2, fused to the heavy chains of the anti-HER2 monoclonal antibody 39S, which binds to domain II of HER2, and conjugated, via a cleavable linker, to the cytotoxic anti-microtubule agent tubulysin, with potential antineoplastic activity. Upon administration of ADC MEDI4276, the anti-HER2 bispecific antibody specifically targets and binds to HER2 on the surface of certain cancer cells. Upon binding, crosslinking and internalization of antibody-HER2 complexes occurs and MEDI4276 is transported to the lysosome where the linker is cleaved, thereby delivering tubulysin inside HER2-expressing cancer cells. Tubulysin binds to tubulin and inhibits microtubule polymerization, which blocks cell division. This results in G2/M phase arrest, tumor cell apoptosis, and decreased proliferation of HER2-expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.","Pharmacologic Substance"]
["C130011","Anti-HER2 Antibody-drug Conjugate RC48","ADC RC48|Anti-HER2 ADC RC48|Anti-HER2 Antibody-drug Conjugate RC48|RC48","An antibody-drug conjugate (ADC) composed of a monoclonal antibody targeting human epidermal growth factor receptor 2 (EGFR2; HER2) and conjugated to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon administration of anti-HER2 ADC RC48, the antibody moiety targets and binds to HER2 on tumor cells. Upon antibody/antigen binding and internalization, the cytotoxic agent induces tumor cell apoptosis, through an as of yet not publicly known mechanism. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C130010","Anti-HER2 Bi-specific Monoclonal Antibody ZW25","Anti-HER2 Bi-specific Monoclonal Antibody ZW25|ZW25","An engineered bi-specific monoclonal antibody that targets two different epitopes of the human tumor-associated antigen (TAA) epidermal growth factor receptor 2 (HER2) with potential immunomodulating and antineoplastic activities. After binding to HER2 on the tumor cell surface, anti-HER2 bispecific monoclonal antibody ZW25 induces a cytotoxic T-lymphocyte (CTL) response and antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells that overexpress HER2. Antibody-dependent cellular phagocytosis. (ADCP) is also induced and further stimulates the immune system to kill HER2-overexpressing tumor cells. In addition, binding of ZW25 to HER2 induces receptor internalization, which inhibits HER2 activation, HER2-mediated signaling and HER2-mediated tumor cell growth. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C90579","Anti-HER2 Monoclonal Antibody CT-P6","Anti-HER2 Monoclonal Antibody CT-P6|CT-P06|CT-P6","A monoclonal antibody directed against the human epidermal growth factor receptor 2 (HER2) with potential immunomodulating and antineoplastic activity. After binding to HER2 on the tumor cell surface, anti-HER2 monoclonal antibody CT-P6 may induce a cytotoxic T-lymphocyte (CTL) as well as an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells that overexpress HER2. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C91091","Anti-HER2-CAR Autologous CMV-Specific Cytotoxic T-Lymphocytes","Anti-HER2-CAR Autologous CMV-Specific Cytotoxic T-Lymphocytes","Autologous human cytomegalovirus (CMV)-specific human cytotoxic T-lymphocytes (CTLs) transduced with a retroviral vector encoding a human anti-Her-2 (epidermal growth factor receptor 2) chimeric T cell receptor (CAR) gene with potential immunostimulatory and antineoplastic activities. Autologous CTLs from a patient with Her-2- and CMV-positive glioblastoma multiforme (GBM) are genetically modified to express CAR gene specific for Her-2 on their cell surfaces. After expansion in culture and reintroduction into the patient, the anti-HER2-CAR autologous CMV-specific CTLs bind to Her-2 antigen on tumor cell surfaces; subsequently, Her-2-positive tumor cells and stem cells may be lysed. Her-2 (ErbB-2), a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, plays key roles in tumor cell proliferation and tumor angiogenesis. CMV is present in the majority of GBM tumors.","Cell|Pharmacologic Substance"]
["C79834","Anti-Her-2-CAR Retroviral Vector-Transduced Autologous Peripheral Blood Lymphocytes","Anti-Her-2-CAR Retroviral Vector-Transduced Autologous Peripheral Blood Lymphocytes|Anti-Her-2-CAR-Engineered Autologous PBLs|Anti-Her-2-CAR-Engineered Autologous Peripheral Blood Lymphocytes|Anti-Her-2-Chimeric Antigen Receptor-Engineered Autologous Peripheral Blood Lymphocytes","Autologous human peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding an anti-Her-2 (epidermal growth factor receptor 2) chimeric T cell receptor (chimeric antigen receptor or CAR) gene with potential immunostimulatory and antineoplastic activities. Autologous PBLs from a patient with Her-2-positive cancer are pulsed with a retroviral vector that encodes the CAR gene specific for Her-2. After expansion in culture and reintroduction into the patient, anti-Her-2-CAR retroviral vector-transduced autologous peripheral blood lymphocytes, which express anti-Her-2-CAR on their cell surfaces, bind to Her-2 antigen on tumor cell surfaces. Subsequently, Her-2-expressing tumor cells may be lysed. Her-2 (ErbB-2), a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, belongs to the EGFR superfamily and plays key roles in both tumor cell proliferation and tumor angiogenesis.","Cell|Pharmacologic Substance"]
["C111997","Anti-HER3 Monoclonal Antibody GSK2849330","Anti-HER3 Monoclonal Antibody GSK2849330|GSK2849330","A monoclonal antibody directed against the human epidermal growth factor receptor 3 (HER3; ERBB3) with potential antineoplastic activity. Anti-HER3 monoclonal antibody GSK2849330 binds to HER3 and inhibits its activation. This may prevent HER3-mediated signaling and inhibit HER3-dependent tumor cell proliferation and differentiation. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors and is associated with poor prognosis and drug resistance; it has no active kinase domain but is activated through heterodimerization with other members of the EGFR receptor family, such as HER2.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C101895","Anti-HER3 Monoclonal Antibody LJM716","Anti-HER3 Monoclonal Antibody LJM716|LJM716","A human monoclonal antibody directed against the human epidermal growth factor receptor HER3 (ErbB3) with potential antineoplastic activity. Anti-HER3 monoclonal antibody LJM716 possesses a novel mechanism of action; LJM716 binds to and locks HER3 in the inactive conformation and does not interfere with its interaction with neuregulin (NRG). The inactivated form of HER3 blocks the PI3K/Akt signaling pathway, thereby inhibiting cellular proliferation in HER2 or NRG expressing tumor cells. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors; it has no active kinase domain but is activated through heterodimerization with other members of the EGFR receptor family, such as HER2.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C81939","Anti-HGF Monoclonal Antibody TAK-701","Anti-HGF MoAb TAK-701|Anti-HGF Monoclonal Antibody TAK-701|TAK-701","A humanized monoclonal antibody directed against human hepatocyte growth factor (HGF) with potential antineoplastic activity. Anti-HGF monoclonal antibody TAK-701 binds to the soluble ligand HGF, preventing HGF binding to and activation of the HGF receptor c-Met and so the activation of the c-Met signaling pathway; this may result in the induction of cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in a variety of tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.","Pharmacologic Substance"]
["C68930","Anti-HIF-1alpha LNA Antisense Oligonucleotide EZN-2968","Anti-HIF-1alpha LNA Antisense Oligonucleotide EZN-2968|EZN-2968|anti-HIF-1alpha LNA AS-ODN","A synthetic antisense oligodeoxynucleotide (AS ODN) targeting hypoxia-inducible factor-1alpha (HIF-1alpha) with potential antineoplastic activity. Anti-HIF-1alpha LNA antisense oligonucleotide EZN-2968 hybridizes with HIF-1alpha mRNA and blocks t HIF-1 alpha protein expression, which may result in the inhibition of angiogenesis, the inhibition of tumor cell proliferation, and apoptosis. HIF-1alpha, normally activated in response to hypoxia-induced stress, is a key transcription regulator of a large number of genes important in cellular adaptation to low-oxygen conditions, including angiogenesis, cell proliferation, apoptosis, and cell invasion.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C122679","Anti-HLA-A2/NY-ESO-1 TCR-transduced Autologous T Lymphocytes","Anti-HLA-A2/NY-ESO-1 TCR-transduced Autologous T Lymphocytes|Anti-HLA-A2/NY-ESO1 TCR-transduced Autologous T cells|Autologous Anti-HLA-A2/NY-ESO1 TCR-transduced T Lymphocytes|Autologous HLA-A2/NY-ESO-1-specific TCR Gene-transduced T-lymphocytes","Autologous human peripheral blood T-lymphocytes transduced with a lentiviral or retroviral vector encoding a human leukocyte antigen A2 (HLA-A2) restricted anti-cancer-testis antigen 1 (NY-ESO-1) T-cell receptor (TCR) gene, with potential antineoplastic activity. Following leukapheresis, isolation of lymphocytes, expansion ex vivo, transduction, and re-introduction into the patient, the anti-HLA-A2/NY-ESO-1 TCR-transduced autologous T lymphocytes recognize and bind to NY-ESO-1/HLA-A2-positive tumor cells. This results in cytotoxic T-lymphocyte (CTL)-mediated elimination of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types.","Cell|Pharmacologic Substance"]
["C103860","Anti-HLA-DR Monoclonal Antibody IMMU-114","Anti-HLA-DR MoAb L243|Anti-HLA-DR Monoclonal Antibody IMMU-114|IMMU-114|hL243gamma4P","A humanized IgG4 monoclonal antibody that targets the human leukocyte antigen HLA-DR, with potential antineoplastic activity. Upon administration, anti-HLA-DR monoclonal antibody IMMU-114 binds to HLA-DR on HLA-DR-expressing tumor cells and, although the exact mechanism has yet to be fully elucidated, appears to induce hyperactivation of ERK- and JNK-dependent mitogen activated protein kinase signaling pathways. This may lead to mitochondrial membrane depolarization and reactive oxygen species (ROS) generation. This eventually leads to an induction of tumor cell apoptosis and a reduction in tumor cell proliferation. IMMU-14 may be beneficial in the treatment of graft versus host disease (GVHD) as it appears to suppress T-lymphocyte proliferation and natural killer (NK) cell activation. As the Fc region of the orgnial IgG1 MoAb was replaced with the IgG4 isotype, IMMU-114 does not induce a complement cytotoxicity (CDC) or an antibody-dependent cell-mediated cytotoxicity (ADCC). HLA-DR, a MHC class II molecule, is found on various b-cell hematologic malignancies and in autoimmune diseases as well as on normal cells.","Pharmacologic Substance"]
["C129694","Anti-human GITR Monoclonal Antibody AMG 228","AMG 228|AMG-228|AMG228|Agonistic GITR Antibody AMG 228|Anti-human GITR Monoclonal Antibody AMG 228","An agonistic anti-human glucocorticoid-induced tumor necrosis factor receptor (tumor necrosis factor receptor superfamily, member 18; TNFRSF18; GITR; CD357) humanized monoclonal antibody, with potential immune checkpoint modulating activity. Anti-human GITR monoclonal antibody AMG 228 binds to and activates GITRs found on multiple types of T-cells. This stimulates the immune system, induces both the activation and proliferation of tumor-antigen-specific T effector cells (Teffs), and suppresses the function of activated T regulatory cells (Tregs). This leads to immune-mediated tumor cell eradication though a cytotoxic T-lymphocyte (CTL) response. GITR, a member of the TNF receptor superfamily and T-cell receptor co-stimulator, is expressed on the surface of multiple immune cell types, including Tregs, Teffs, B-cells, and natural killer (NK) cells. Inappropriately activated Tregs suppress Teffs and suppress T-cell receptor (TCR) signaling.","Pharmacologic Substance"]
["C95023","Anti-human GITR Monoclonal Antibody TRX518","Anti-huGITR MoAb TRX518|Anti-human GITR Monoclonal Antibody TRX518|TRX518","A humanized, Fc disabled anti-human glucocorticoid-induced tumor necrosis factor receptor (GITR) monoclonal antibody (MoAb) with immunomodulating activity. Anti-human GITR MoAb TRX518 blocks the interaction of GITR, found on multiple types of T cells, with its ligand, thereby inducing both the activation of tumor-antigen-specific T effector cells, as well as abrogating the suppression induced by inappropriately activated T regulatory cells. This agent is shown to act synergistically with chemotherapeutic drugs in multiple cancer models.","Immunologic Factor|Pharmacologic Substance"]
["C88327","Anti-ICAM-1 Monoclonal Antibody BI-505","Anti-ICAM-1 Monoclonal Antibody BI-505|BI-505","A fully human IgG1 monoclonal antibody directed against intercellular adhesion molecule-1 (ICAM-1 or CD54), with potential antineoplastic activity. Anti-ICAM-1 monoclonal antibody BI-505 selectively binds to the adhesion protein ICAM-1, which may result in antibody-dependent cellular cytotoxicity (ADCC), hyper-cross-linking-induced apoptosis, and a decrease in cellular proliferation of ICAM-1-expressing tumor cells. ICAM-1, normally expressed on leukocytes and endothelial cells, may be overexpressed in a variety of cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C126804","Anti-ICOS Agonist Antibody GSK3359609","Anti-ICOS Agonist Antibody GSK3359609|GSK3359609","An agonistic antibody for the inducible T-cell co-stimulator (ICOS; CD278), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-ICOS agonist antibody GSK3359609 targets and binds to ICOS expressed on tumor infiltrating CD4-positive T-cells. This stimulates ICOS-positive T-cell proliferation, enhances cytotoxic T-lymphocyte (CTL) survival and increases CTL-mediated immune responses against tumor cells. ICOS, a T-cell specific, CD28-superfamily costimulatory molecule and immune checkpoint protein, is normally expressed on certain activated T-cells and plays a key role in the proliferation and activation of T-cells.","Pharmacologic Substance"]
["C129876","Anti-ICOS Agonist Monoclonal Antibody JTX-2011","Anti-ICOS Agonist MAb JTX-2011|Anti-ICOS Agonist Monoclonal Antibody JTX-2011|ICOS Agonist Monoclonal Antibody JTX-2011|JTX-2011","An agonistic humanized monoclonal antibody that recognizes inducible T-cell co-stimulator (ICOS; CD278), with potential antineoplastic activity. Upon administration, anti-ICOS agonist monoclonal antibody JTX-2011 targets and binds to ICOS expressed on certain T-cells. This stimulates ICOS-mediated signaling, induces proliferation of ICOS-positive T-cells, enhances cytotoxic T-lymphocyte (CTL) survival and augments the CTL-mediated immune response against tumor cells. ICOS, a T-cell specific, CD28-superfamily co-stimulatory molecule and immune checkpoint protein, is normally expressed on certain activated T-cells and plays a key role in the proliferation and activation of T-cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C123267","Anti-ICOS Monoclonal Antibody MEDI-570","Anti-ICOS Monoclonal Antibody MEDI-570|MEDI-570","An Fc-optimized humanized immunoglobulin (Ig) G1 monoclonal antibody (MoAb) directed against the inducible T-cell co-stimulator (ICOS, CD278), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-ICOS MoAb MEDI-570 targets and binds to ICOS expressed on tumor infiltrating CD4-positive T-cells. This prevents the interaction between ICOS-positive T-cells and plasmacytoid dendritic cells (pDCs), which express the ICOS ligand (ICOSL). Blocking ICOS activation prevents the pDC-induced proliferation and accumulation of regulatory ICOS-positive T-cells (ICOS+ Tregs) and inhibits interleukin-10 (IL-10) secretion by CD4+ infiltrating T-cells. This may abrogate Treg-mediated immune suppression and may enhance cytotoxic T-lymphocyte (CTL)-mediated immune responses against tumor cells. Fc optimization enhances antibody-dependent cellular cytotoxicity (ADCC). ICOS, a T-cell specific, CD28-superfamily costimulatory molecule and immune checkpoint protein, plays a key role in the proliferation and activation of T-cells. It is normally expressed on both activated CD4+ T-cells, which is a subset of memory T-cells (Tm), and follicular helper T-cells (Tfh). ICOS is highly expressed on Tregs infiltrating various tumors and its expression is associated with a poor prognosis; ICOS-positive Tregs play a key role in immune suppression and tumor immune evasion.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C82683","Anti-IGF1/2 Monoclonal Antibody MEDI-573","Anti-IGF1/2 Monoclonal Antibody MEDI-573|Anti-Insulin-Like Growth Factor 1/2 Monoclonal Antibody MEDI-573|MEDI-573","A humanized monoclonal antibody directed against insulin-like growth factors 1 and 2 (IGF-1/2) with potential antineoplastic activity. Anti-IGF1/2 monoclonal antibody MEDI-573 inhibits IGF1- and IGF2-stimulated activation of membrane-bound IGF receptors and the subsequent triggering of proliferation and survival signaling pathways. This may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. IGF1/2 ligands stimulate cell proliferation, enable oncogenic transformation, and suppress apoptosis; IGF1/2 signaling has been highly implicated in tumorigenesis and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C79798","Anti-IGF-1R Monoclonal Antibody AVE1642","AVE1642|Anti-IGF-1R Monoclonal Antibody AVE1642|anti-CD122 monoclonal antibody AVE1642","A humanized monoclonal antibody directed against the human insulin-like growth factor-1 receptor (IGF-1R/CD221) with potential antineoplastic activity. Anti-IGF-1R monoclonal antibody AVE1642 specifically binds to and blocks membrane-bound IGF-1R, preventing the binding of the natural ligand IGF-1 and the subsequent activation of PI3K/AKT signal transduction, which may result in the induction of apoptosis and a decrease in cellular proliferation. Activation of IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily overexpressed by various cancer cell types, stimulates cell proliferation, promotes angiogenesis, enables oncogenic transformation, and suppresses apoptosis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C71530","Anti-IGF-1R Recombinant Monoclonal Antibody BIIB022","Anti-IGF-1R Recombinant Monoclonal Antibody BIIB022|BIIB-022|BIIB022","A recombinant, human monoclonal antibody directed against the insulin-like growth factor 1 receptor (IGF-1R) with potential antineoplastic activity. Anti-IGF-1R recombinant monoclonal antibody BIIB022 binds to membrane-bound IGF-1R, preventing binding of the ligand IGF-1 and the subsequent triggering of the PI3K/Akt signaling pathway; inhibition of this survival signaling pathway may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. The activation of IGF-1R, a tyrosine kinase and a member of the insulin receptor family, stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF-1R signaling has been highly implicated in tumorigenesis and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C95708","Anti-IL-1 alpha Monoclonal Antibody CA-18C3","Anti-IL-1 alpha Monoclonal Antibody CA-18C3|CA-18C3","A \"true human\" (cloned from human B lymphocytes) monoclonal antibody directed against interleukin-1 alpha (IL1a) with potential antineoplastic activity. Anti-IL-1 alpha monoclonal antibody CA-18C3 binds to IL1a and may block the activity of IL1a. IL1a, an inflammatory mediator, plays a key role in interleukin-mediated tumor cell activity such as angiogenesis, tissue matrix remodeling, metastasis and tumor cell invasion.","Immunologic Factor|Pharmacologic Substance"]
["C88325","Anti-IL-1 alpha Monoclonal Antibody MABp1","Anti-IL-1 Alpha Monoclonal Antibody|Anti-IL-1 alpha Monoclonal Antibody MABp1|Anti-IL1a Monoclonal Antibody|MABp1|Xilonix","A human IgG1 monoclonal antibody directed against interleukin-1 alpha (IL1a) with potential A human IgG1 monoclonal antibody targeting the inflammatory cytokine interleukin-1 alpha (IL1a) with potential antineoplastic, anti-cachectic and anti-angiogenic activities. Anti-IL1a monoclonal antibody MABp1 targets and binds to IL1a and prevents IL1a activity. This prevents IL1a-mediated tumorigenesis and angiogenesis. In addition, MABp1 abrogates IL1a-mediated cachexia. IL1a, an inflammatory mediator expressed on monocytes, platelets and overexpressed by certain tumors, plays a key role in the promotion of tumor cell growth, metastasis and invasion. In addition, IL1a stimulates metabolic activity in the central nervous system.","Pharmacologic Substance"]
["C66988","Anti-IL-13 Humanized Monoclonal Antibody TNX-650","Anti-IL-13 Humanized Monoclonal Antibody TNX-650|Monoclonal Antibody TNX-650|TNX-650","A humanized monoclonal antibody directed against interleukin-13 (IL-13) with potential antineoplastic activity. Anti-IL-13 humanized monoclonal antibody TNX-650 binds to and blocks the activity of IL-13, which may result in the inhibition of Hodgkin lymphoma cell proliferation. IL-13 cytokine, an important mediator in allergic inflammation, may be an autocrine growth factor for Hodgkin lymphoma cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C126841","Anti-IL-15 Monoclonal Antibody AMG 714","AMG 714|AMG714|Anti-IL-15 Monoclonal Antibody AMG 714|HuMab-IL15 AMG 714","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human pro-inflammatory cytokine interleukin-15 (IL-15), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, anti-IL-15 monoclonal antibody AMG 714 binds to and neutralizes IL-15, thereby preventing IL-15-mediated pro-inflammatory signaling. By inhibiting IL-15-mediated immune responses, AMG 714 decreases natural killer (NK) cell activation and proliferation, reduces T-cell infiltration, increases T-cell apoptosis, and may prevent the growth of IL-15-driven cancer cells. IL-15 plays a key role in inflammation and is associated with a variety of autoimmune and inflammatory disorders as well as with cell proliferation in certain cancer types, such as T-cell lymphomas. IL-15 is required for the proliferation of certain T-cells and NK cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C124227","Anti-IL-8 Monoclonal Antibody HuMax-IL8","Anti-IL-8 Monoclonal Antibody HuMax-IL8|HuMax-IL8|MDX 018|MDX-018","A human monoclonal antibody against the pro-inflammatory mediator interleukin-8 (IL-8; CXCL8), with potential antineoplastic activities. Upon administration, HuMax-IL8 directly binds to IL-8, thereby inhibiting the binding of IL-8 to its receptors CXCR1 and CXCR2. This inhibits activation of IL-8-mediated signaling transduction pathways, which decreases proliferation of susceptible tumor cells. Also, HuMax-IL8 effectively blocks binding of IL-8 to neutrophils and inhibits neutrophil activation and recruitment towards sites of inflammation, which reduces inflammation. IL-8, a member of the CXC chemokine family, is upregulated in a variety of cancer cell types and inflammatory diseases; it plays a key role in tumor cell proliferation, endothelial cell proliferation, and cancer stem cell (CSC) renewal.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C78839","Anti-Integrin Monoclonal Antibody-DM4 Immunoconjugate IMGN388","Anti-Integrin Monoclonal Antibody-DM4 Immunoconjugate IMGN388|IMGN388","An immunoconjugate consisting of an anti-integrin monoclonal antibody covalently attached to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. Integrin-targeted immunoconjugate IMGN388 binds to tumor cell surface integrins; upon internalization, the DM4 moiety is released from the immunoconjugate, binding to tubulin and disrupting microtubule assembly/disassembly dynamics, which may result in inhibition of cell division and cell growth of integrin-expressing tumor cells. Integrins, a class of transmembrane cell surface receptors, link the extracellular matrix (ECM) to intracellular signaling pathways that control cell proliferation and differentiation.","Pharmacologic Substance"]
["C78464","Anti-KIR Monoclonal Antibody IPH 2101","1-7F9|Anti-KIR Monoclonal Antibody IPH 2101|IPH 2101","A human monoclonal antibody directed against the human inhibitory killer IgG-like receptor (KIR) with potential immunostimulating and antineoplastic activities. Anti-KIR monoclonal antibody IPH 2101 binds to the KIR receptor expressed on human natural killer (NK) cells, which may prevent KIR-mediated inhibition of NK cells and permit NK cell-mediated anti-tumor cytotoxicity. KIRs are surface glycoproteins that bind to major histocompatibility complex (MHC)/human leukocyte antigen (HLA) class I subtypes on target cells; binding of KIRs inhibits NK cell-mediated cytotoxicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C124999","Anti-KIR3DL2 Monoclonal Antibody IPH4102","Anti-KIR3DL2 Monoclonal Antibody IPH4102|Anti-KIR3DL2 mAb IPH4102|IPH4102","A humanized monoclonal antibody against the immune receptor human killer cell immunoglobulin-like receptor, three domains, long cytoplasmic tail, 2 (KIR3DL2), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-KIR3DL2 monoclonal antibody IPH4102 binds to KIR3DL2 expressed on certain tumor cells. This recruits natural killer (NK) cells and leads to lysis of KIR3DL2-expressing tumor cells. In addition, IPH4102 induces antibody-dependent cellular cytotoxicity (ADCC), thereby further eliminating tumor cells. KIR3DL2, a tumor-associated antigen (TAA) and inhibitory receptor of the KIR family, is specifically expressed in most subtypes of cutaneous T-cell lymphomas (CTCL) and expressed only on a fraction of normal NK cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82391","Anti-KSP/Anti-VEGF siRNAs ALN-VSP02","ALN-VSP02|Anti-KSP/Anti-VEGF siRNAs ALN-VSP02","A lipid nanoparticle formulation containing two small interfering RNAs (siRNAs) for kinesin spindle protein (KSP) and vascular endothelial growth factor (VEGF) with potential antitumor activity. Upon intravenous administration, the siRNAs in KSP/VEGF siRNAs ALN-VSP02ALN bind to both KSP and VEGF messenger RNAs (mRNAs), preventing translation of KSP and VEGF proteins; this may result in growth inhibition of tumor cells that overexpress KSP and VEGF. VEGF and KSP are upregulated in many tumor cells and play an important role in tumor proliferation and survival.","Pharmacologic Substance"]
["C111999","Anti-LAG-3 Monoclonal Antibody BMS-986016","Anti-LAG-3 Monoclonal Antibody BMS-986016|BMS-986016|BMS986016","A monoclonal antibody directed against the inhibitor receptor lymphocyte activation gene-3 (LAG-3), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-LAG-3 monoclonal antibody BMS-986016 binds to LAG-3 on tumor infiltrating lymphocytes (TILs). This may activate antigen-specific T-lymphocytes and enhance cytotoxic T cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG-3 is a member of the immunoglobulin superfamily (IgSF) and binds to major histocompatibility complex (MHC) class II. LAG-3 expression on TILs is associated with tumor-mediated immune suppression.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C122683","Anti-LAG-3 Monoclonal Antibody LAG525","Anti-LAG-3 Monoclonal Antibody LAG525|LAG 525|LAG525","A humanized monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene-3 (LAG-3), with potential immunomodulating and antineoplastic activities. Upon administration, the anti-LAG-3 monoclonal antibody LAG525 binds to LAG-3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF) and expressed on various immune cells, negatively regulates cellular proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C126275","Anti-LAMP1 Antibody-drug Conjugate SAR428926","ADC SAR428926|Anti-LAMP1 ADC SAR428926|Anti-LAMP1 Antibody-drug Conjugate SAR428926|SAR428926","An antibody-drug conjugate (ADC) consisting of a monoclonal antibody against lysosome-associated membrane protein 1 (LAMP1) conjugated, via the disulfide-containing cleavable linker N-succinimidyl-4-(2-pyridyldithio)butyrate (SPDB), to the cytotoxic maytansinoid DM4, with potential antineoplastic activity. Upon administration of anti-LAMP1 ADC SAR428926, the anti-LAMP1 monoclonal antibody moiety targets and binds to the cell surface antigen LAMP1. After antibody-antigen interaction and internalization, the SPDB linker is selectively cleaved by proteases in the cytosol and the DM4 moiety is released. DM4 binds to tubulin and disrupts microtubule assembly/disassembly dynamics, thereby inhibiting both cell division and cell growth of LAMP1-expressing tumor cells. LAMP1, overexpressed on a variety of cancer cells, plays a key role in cell-cell adhesion and migration. The SPDB linker is resistant to cleavage in the bloodstream, which may increase stability and reduce toxicity.","Pharmacologic Substance"]
["C126794","Anti-LGR5 Monoclonal Antibody BNC101","Anti-LGR5 Monoclonal Antibody BNC101|BNC-101|BNC101|ET-101","A humanized monoclonal antibody targeting leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5), with potential antineoplastic activity. Upon administration, the anti-LGR5 humanized monoclonal antibody BNC101 targets and binds to LGR5, thereby inhibiting LRG5-mediated signal transduction pathways. This prevents proliferation of LRG5-expressing tumor cells. LGR5, a member of the Wnt signaling pathway, is a cancer stem cell (CSC) receptor overexpressed on certain cancer cells; it plays a key role in CSC proliferation and survival.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C112001","Anti-LIV-1 Monoclonal Antibody-MMAE Conjugate SGN-LIV1A","Anti-LIV-1 Antibody-drug Conjugate SGN-LIV1A|Anti-LIV-1 Monoclonal Antibody-MMAE Conjugate SGN-LIV1A|SGN-LIV1A","An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the anti-solute carrier family 39 zinc transporter member 6 (SLC39A6; LIV-1; ZIP6) protein that is conjugated, via a protease-cleavable linker, to the cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration and internalization by LIV-1-positive tumor cells, anti-LIV-1 antibody-drug conjugate SGN-LIV1A undergoes enzymatic cleavage to release MMAE into the cytosol. In turn, MMAE binds to and inhibits tubulin polymerization, which may result in G2/M phase cell cycle arrest and apoptosis in LIV-1-expressing tumor cells. LIV-1, a member of the zinc transporter family, is expressed in several types of solid tumors and plays a key role in tumor cell progression and metastasis. The linkage system in SGN-LIV1A is highly stable in plasma, resulting in cytotoxic specificity against LIV-1-positive cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116745","Anti-Ly6E Antibody-Drug Conjugate DLYE5953A","ADC DLYE5953A|Anti-Ly6E Antibody-Drug Conjugate DLYE5953A|DLYE5953A","An antibody-drug conjugate (ADC) composed of an antibody against the tumor-associated antigen (TAA) lymphocyte antigen 6 complex locus E (Ly6E) and linked to an as of yet undisclosed cytotoxic agent, with potential antineoplastic activity. Upon intravenous administration, the antibody moiety of DLYE5953A targets and binds to Ly6E expressed on tumor cells. Upon binding and internalization, the cytotoxic agent is released and kills, through an as of yet unknown mechanism of action, the Ly6E-expressing cancer cells. Ly6E, an interferon (IFN)-inducible glycosylphosphatidylinositol (GPI)-linked cell membrane protein, is expressed on a variety of tumor cell types.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C91092","Anti-Melanin Monoclonal Antibody PTI-6D2","Anti-Melanin Monoclonal Antibody PTI-6D2|PTI-6D2","A monoclonal antibody (MoAb) against extracellular melanin with tumor targeting activity. Anti-melanin monoclonal antibody PTI-6D2 binds to extracellular melanin, a melanocyte pigment which is released during tumor cell turnover from dead melanoma tumor cells, while avoiding the binding of melanin in normal, healthy tissue because of melanin's normal intracellular location. Upon labeling with the beta-emitting radioisotope rhenium Re 188 (PTI-188), this MoAb may target multiple melanoma (MM) cells, thereby delivering a cytotoxic dose of radiation specifically to the targeted tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C120303","Anti-mesothelin Antibody-drug Conjugate BMS-986148","Anti-mesothelin Antibody-drug Conjugate BMS-986148|BMS-986148","An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the cell surface glycoprotein mesothelin and conjugated to an as of yet undisclosed cytotoxic drug, with potential antineoplastic activity. The monoclonal antibody moiety of anti-mesothelin ADC BMS-986148 targets and binds to the tumor associated antigen mesothelin. Upon internalization, the cytotoxic agent kills or prevents cellular proliferation of mesothelin-expressing tumor cells through an as of yet undescribed mechanism of action. Mesothelin is overexpressed by all mesotheliomas and a variety of other cancers, while it is minimally expressed in normal tissue.","Pharmacologic Substance"]
["C124650","Anti-mesothelin CAR Vector-transduced Autologous T-lymphocytes","Anti-meso-CAR Vector-transduced Autologous T Cells|Anti-mesothelin CAR Vector-transduced Autologous T-lymphocytes","Genetically modified, autologous T-lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) consisting of an anti-human tumor-associated antigen (TAA) mesothelin single chain variable fragment (scFv), the intracellular CD3 zeta T-cell receptor domain and the 4-1BB (cd137) costimulatory domain, with potential immunomodulating and antineoplastic activities. After isolation, transduction, expansion in culture, and reintroduction into the patient, the anti-mesothelin CAR vector-transduced autologous T-lymphocytes specifically target and kill mesothelin-expressing tumor cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in a variety of cancer cell types.","Cell|Pharmacologic Substance"]
["C97038","Anti-mesothelin CIR mRNA-electroporated Autologous T Cells","Anti-mesothelin CIR mRNA-electroporated Autologous T Cells|Autologous Redirected RNA Meso-CIR T cells","Autologous chimeric immune receptor (CIR) T cells transfected with anti-mesothelin chimeric T cell receptor mRNA, with potential antineoplastic activity. The anti-mesothelin mRNA encodes a single chain antibody variable fragment (ScFv), the intracellular CD 3 zeta T cell receptor domain and the 4-1BB (cd137) costimulatory domain. Upon intravenous administration, the anti-mesothelin CIR mRNA-electroporated autologous T cells may attach to cancer cells expressing mesothelin. This may stimulate the secretion of multiple cytokines and may result in cell lysis of mesothelin-expressing cancer cells. Mesothelin is a cell surface glycoprotein involved in cell adhesion and is overexpressed in many epithelial-derived cancers.","Cell|Pharmacologic Substance"]
["C121782","Anti-mesothelin iCasp9M28z CAR-transduced Autologous T Lymphocytes","Anti-mesothelin iCasp9M28z CAR-transduced Autologous T Lymphocytes|iCasp9M28z T Cells","Genetically modified, autologous T-lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for mesothelin linked to the signaling domains for the co-stimulatory molecules CD28 and CD3 zeta, as well as the suicide gene inducible caspase 9 (iCasp9 or iC9), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, anti-mesothelin iCasp9M28z CAR-transduced autologous T lymphocytes specifically target and kill mesothelin-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T-cells lead to unacceptable side effects, a dimerizing agent can be administered, which binds to the FKBP12-F36V drug-binding domain and activates caspase 9, resulting in the apoptosis of the administered T-cells. Mesothelin, a tumor-associated antigen, is overexpressed in a variety of cancer cell types.","Cell|Pharmacologic Substance"]
["C116746","Anti-mesothelin/MMAE Antibody-Drug Conjugate DMOT4039A","Anti-mesothelin/MMAE Antibody-Drug Conjugate DMOT4039A|DMOT-4039A|DMOT4039A|RG 7600|RG7600","An antibody-drug conjugate (ADC) composed of MMOT0530A, a humanized immunoglobulin (Ig) G1 monoclonal antibody directed against the cell surface glycoprotein mesothelin (MSLN), and covalently linked, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DMOT4039A binds to MSLN-expressing tumor cells and is internalized, thereby delivering MMAE intracellularly. Proteolytic cleavage releases MMAE, which then binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. MSLN, a tumor-associated antigen (TAA), is overexpressed by all mesotheliomas and a variety of other cancers, while it is minimally expressed in normal tissue.","Pharmacologic Substance"]
["C121653","Anti-mesothelin-Pseudomonas Exotoxin 24 Cytolytic Fusion Protein LMB-100","Anti-MSLN-PE24 cFP LMB-100|Anti-mesothelin-Pseudomonas Exotoxin 24 Cytolytic Fusion Protein LMB-100|LMB-100|RG 7787|RG-7787|RG7787|RO 6927005|RO6927005","An anti-mesothelin (MSLN) recombinant cytolytic fusion protein (cFP) composed of a humanized Fab fragment of anti-MSLN monoclonal antibody SS1 linked to a truncated and de-immunized 24 kDa fragment of the Pseudomonas exotoxin (PE) (PE24), with potential antineoplastic activity. Upon intravenous administration of anti-MSLN-PE24 cFP LMB-100, the anti-MSLN moiety targets and binds to MSLN-expressing tumor cells. Upon binding and internalization through endocytosis, the toxin moiety ADP-ribosylates and inactivates eukaryotic elongation factor 2 (eEF2), preventing the elongation step of protein synthesis and leading to both an inhibition of protein synthesis and an induction of MSLN-expressing tumor cell apoptosis. MSLN, a tumor-associated antigen overexpressed in a variety of cancer cell types, plays a key role in tumor cell proliferation and migration. The engineered PE24 portion of LMB-100 does contain the targeting domain and furin cleavage site, which are needed for cytotoxicity, but most of the translocation domain II is deleted and the catalytic domain III contains point mutations, which result in the deletion and silencing of most T- and B-cell epitopes; therefore, the immunogenicity and toxicity is reduced compared to non-engineered PE toxin, which allows for the administration of larger doses of LMB-100.","Pharmacologic Substance"]
["C127906","Anti-Met Monoclonal Antibody Mixture Sym015","Anti-Met Monoclonal Antibody Mixture Sym015|Hu9006-Hu9338|Hu9006/Hu9338|Sym 015|Sym-015|Sym015","A mixture of two humanized immunoglobulin G1 (IgG1) monoclonal antibodies, Hu9006 and Hu9338, which recognize non-overlapping epitopes in the extracellular domain of the human hepatocyte growth factor receptor (MET; HGFR; c-Met), with potential antineoplastic activity. Upon administration, anti-MET monoclonal antibody mixture Sym015 targets and binds to the extracellular domain of MET, thereby preventing the binding of its ligand, hepatocyte growth factor (HGF). This may prevent activation of the receptor and MET-mediated signal transduction pathways. This inhibits MET-dependent tumor cell proliferation. MET, a receptor tyrosine kinase, is overexpressed on the cell surfaces of various solid tumor cell types; it plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C118281","Anti-Met/EGFR Monoclonal Antibody LY3164530","Anti-Met/EGFR Monoclonal Antibody LY3164530|LY3164530","A monoclonal antibody (MoAb) against human epidermal growth factor receptor (EGFR) and human hepatocyte growth factor receptor (HGFR or c-Met), with potential antineoplastic activity. Upon administration, anti-Met/EGFR MoAb LY3164530 targets and prevents the activation of EGFR and c-Met. This leads to a downstream inhibition of EGFR/c-Met-mediated signal transduction pathways, and prevents cellular proliferation in tumor cells overexpressing EGFR and c-Met. EGFR, a member of the epidermal growth factor family of extracellular protein ligands, may be overexpressed on the cell surface of various solid tumor cell types. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C125690","Antimetabolite FF-10502","Antimetabolite FF-10502|FF-10502-01|FF-10502","An antimetabolite with potential antineoplastic activity. Upon administration, FF-10502 is able to enter the nucleus where it inhibits DNA polymerases, thereby preventing DNA synthesis and halting tumor cell proliferation.","Pharmacologic Substance"]
["C105803","Anti-MMP-9 Monoclonal Antibody GS-5745","Anti-MMP-9 Monoclonal Antibody GS-5745|GS-5745","A humanized monoclonal antibody against matrix metalloproteinase 9 (MMP-9), with potential antineoplastic activity. Upon administration, anti-MMP-9 monoclonal antibody GS-5745 binds to MMP-9 and inhibits its enzymatic activity. This results in an inhibition of extracellular matrix protein degradation and, potentially, the inhibition of angiogenesis, tumor growth, invasion, and metastasis. MMP-9, a protein belonging to the MMP family, plays a key role in the degradation of collagens and proteoglycans; increased activity of MMP-9 has been associated with increased invasion and metastasis of cancer.","Pharmacologic Substance"]
["C124646","Anti-MUC1 CAR-transduced Autologous T-lymphocytes","Anti-MUC1 Autologous CAR T Cells|Anti-MUC1 CAR-transduced Autologous T Cells|Anti-MUC1 CAR-transduced Autologous T-lymphocytes|Anti-Mucin1 Autologous CAR T Cells","Autologous T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of a single chain variable fragment (scFv) against the human tumor-associated epithelial antigen mucin 1 (MUC1), with potential immunomodulating and antineoplastic activities. Autologous PBLs from a patient with MUC1-positive cancer are transduced with a retroviral vector that encodes the CAR gene specific for MUC1. After expansion in culture and reintroduction into the patient, anti-MUC1 CAR-transduced autologous T-lymphocytes target and induce selective toxicity in MUC1-expressing tumor cells. MUC-1 is a human, hypoglycosylated tumor-associated antigen (TAA) overexpressed by epithelial cancer cells.","Cell|Pharmacologic Substance"]
["C118362","Anti-MUC1 Monoclonal Antibody BTH1704","Anti-MUC1 Monoclonal Antibody BTH1704|BTH1704","A monoclonal antibody against the tumor associated antigen (TAA) mucin-1 (MUC1), with potential antineoplastic activity. Upon administration, anti-MUC1 monoclonal antibody BTH1704 targets and binds to MUC1 expressed on the surface of tumor cells, which can potentially activate the immune system to induce an antibody-dependent cellular cytotoxicity (ADCC) against MUC1-expressing tumor cells. MUC1, a glycoprotein overexpressed on the surface of a variety of cancer cells, plays a key role in tumor cell survival and proliferation.","Pharmacologic Substance"]
["C78840","Anti-Myeloma Monoclonal Antibody-DM4 Immunoconjugate BT-062","Anti-Myeloma Monoclonal Antibody-DM4 Immunoconjugate BT-062|BT-062|Maytansinoid-Conjugated Anti-Myeloma Monoclonal Antibody BT062","An immunoconjugate consisting of a monoclonal antibody directed against a highly-expressed myeloma cell surface antigen covalently attached to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. Anti-myeloma cell surface antigen immunoconjugate BT-062 binds to an unspecified cell surface antigen highly expressed on myeloma cells; upon internalization the DM4 moiety is released, binding to tubulin and disrupting microtubule assembly/disassembly dynamics, which may result in the inhibition of cell division and cell growth of myeloma tumor cells.","Pharmacologic Substance"]
["C99640","Anti-myostatin Monoclonal Antibody LY2495655","Anti-myostatin Monoclonal Antibody LY2495655|LY2495655","A monoclonal antibody against myostatin (MSTN) with potential anti-cachexia activity. Upon administration, anti-myostatin monoclonal antibody LY2495655 binds to and neutralizes the MSTN protein, thereby blocking the MSTN signalling pathway. This may help decrease muscle protein breakdown and muscle weakness and may attenuate cancer cachexia. MSTN, a member of the transforming growth factor-beta (TGF-beta) superfamily, is a negative regulator of muscle growth and development.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116747","Anti-NaPi2b/MMAE Antibody-Drug Conjugate DNIB0600A","ADC DNIB0600A|Anti-NaPi2b/MMAE Antibody-Drug Conjugate DNIB0600A|DNIB0600A","An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against the sodium-dependent phosphate transport protein 2B (NaPi2b), and covalently linked to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of DNIB0600A binds to NaPi2b-expressing tumor cells and is internalized, thereby delivering MMAE intracellularly. Proteolytic cleavage releases MMAE, which then binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. NaPi2b, a tumor-associated antigen (TAA), overexpressed in a variety of cancer cell types, plays a key role in transport of inorganic phosphate and the maintenance of phosphate homeostasis.","Pharmacologic Substance"]
["C114500","Anti-Nectin 4 Antibody-Drug Conjugate ASG-22CE","ASG-22CE|Anti-Nectin 4 ADC ASG-22CE|Anti-Nectin 4 Antibody-Drug Conjugate ASG-22CE","An antibody drug conjugate (ADC) containing a human monoclonal antibody AGS-22 targeting the cell adhesion molecule nectin-4 and conjugated to the cytotoxic agent monomethyl auristatin E (MMAE), via a proprietary enzyme-cleavable linker (AGS-22CE), with potential antineoplastic activity. The monoclonal antibody moiety of AGS-22CE selectively binds to nectin-4. After internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in nectin-4 overexpressing tumor cells. Nectin-4, a tumor associated antigen belonging to the nectin family, is overexpressed in a variety of cancers, including breast, bladder, lung and pancreatic cancer.","Pharmacologic Substance"]
["C97916","Anti-nectin-4 Monoclonal Antibody-Drug Conjugate AGS-22M6E","AGS-22M6E|Anti-nectin-4 Monoclonal Antibody-Drug Conjugate AGS-22M6E","An antibody drug conjugate (ADC) containing a fully human monoclonal antibody AGS-22 targeting the cell adhesion molecule nectin-4 and conjugated, via a proprietary enzyme-cleavable linker, to the cytotoxic agent monomethyl auristatin E (MMAE) (AGS-22M6E), with potential antineoplastic activity. The monoclonal antibody moiety of AGS-22M6E selectively binds to nectin-4. After internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and induces apoptosis in nectin-4 overexpressing tumor cells. Nectin-4, a tumor associated antigen belonging to the nectin family, is overexpressed in a variety of cancers, including breast, bladder, lung and pancreatic cancer.","Pharmacologic Substance"]
["C124051","Antineoplastic Agent Combination SM-88","Antineoplastic Agent Combination SM-88|SM-88","An orally bioavailable, proprietary combination of four agents with potential antineoplastic activity. Although the four agents and their exact mechanisms of action are not publicly known, the components of SM-88 appear, upon oral administration, to work synergistically to increase the amount of free radicals in cancer cells, thereby inducing oxidative stress and selective killing of the cancer cells.","Pharmacologic Substance"]
["C123824","Antineoplastic Agent TRX-818","Antineoplastic Agent TRX-818|TRX-818","An orally bioavailable agent with potential antineoplastic and anti-vasculogenic mimicry (VM) activities. Although the exact multiple mechanisms of action through which this agent exerts its effects have yet to be fully elucidated, TRX-818, upon oral administration appears to induce cancer cell apoptosis and inhibits cancer cell proliferation. This agent also prevents tumor cell VM by blocking the formation of vasculogenic-like tubular structures through an as of yet undetermined mechanism of action.","Pharmacologic Substance"]
["C129821","Antineoplastic Biological Agent","Anti-cancer Biological Agent|Anticancer Biological|Antineoplastic Biological Agent|Antineoplastic Biological|Antineoplastic Biotherapeutic","Any agent that has a biological nature, such as agents containing living organisms, derived from living organisms, or comprised of ex vivo synthesized analogs of substances derived from living organisms, and that exerts antineoplastic activity.","Pharmacologic Substance"]
["C129818","Antineoplastic Hormonal/Endocrine Agent","Antineoplastic Endocrinal Agent|Antineoplastic Hormonal Agent|Antineoplastic Hormonal Therapeutic|Antineoplastic Hormonal/Endocrine Agent","Any agent that affects hormone levels and exerts antineoplastic effects. Antineoplastic hormonal/endocrine agents treat either hormone-dependent or hormone-sensitive cancers by modulating hormone levels and manipulating the endocrine system.","Pharmacologic Substance"]
["C129820","Antineoplastic Immunomodulating Agent","Anti-cancer Immunotherapeutic|Antineoplastic BRM|Antineoplastic Biological Response Modifier|Antineoplastic Immunomodulating Agent|Antineoplastic Immunotherapeutic","Any agent that is capable of modulating the immune system in order to exert antineoplastic effects. Antineoplastic immunomodulating agents either activate the immune system, restore certain immune system activators or abrogate immunosuppression.","Pharmacologic Substance"]
["C129819","Antineoplastic Radiopharmaceutical Agent","Anti-cancer Radiopharmaceutical|Antineoplastic Radiopharmaceutical Agent|Antineoplastic Radiopharmaceutical","Any radiopharmaceutical agent that targets cancer cells and exerts an antineoplastic effect through radiotoxicity.","Pharmacologic Substance"]
["C1004","Antineoplaston A10","3-Phenylacetylamino-2, 6-piperidinedione|3-Phenylacetylamino-2,6-piperidinedione|A10|ANTINEOPLASTON A10|Antineoplaston A10|Atengenal|Benzeneacetamide, N-(2,6-dioxo-3-piperidinyl)-, (S)-","A piperidinedione antineoplaston with potential antineoplastic activity.  Antineoplaston A10 was originally isolated from human urine but is now synthetically derived.  This agent intercalates into DNA, resulting in cell cycle arrest in G1 phase, reduction of mitosis, and decreased protein synthesis.  Antineoplaston A10 may also inhibit ras-oncogene expression and activate tumor suppressor gene p53, leading to cell differentiation and apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1613","Antineoplaston AS2-1","AS2-1|Antineoplaston AS2-1|Astugenal|L-Glutamine, N2-(phenylacetyl)-, Monosodium Salt, Mixture with Sodium Benzeneacetate","A 4:1 mixture of phenylacetate and phenylacetylgluatmine, degradation products of the antineoplaston agent A10.  Antineoplaston AS2-1 inhibits the incorporation of L-glutamine into tumor-cell proteins, leading to cell cycle arrest in the G1 phase and inhibition of mitosis.  This agent may also inhibit RAS oncogene expression and activate tumor suppressor gene p53, resulting in cell differentiation and apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C91728","Anti-Neuropilin-1 Monoclonal Antibody MNRP1685A","Anti-Neuropilin-1 Monoclonal Antibody MNRP1685A|MNRP1685A","A human IgG1 monoclonal antibody directed against neuropilin-1 (NRP1), with potential antiangiogenic and antineoplastic activities. Upon intravenous administration, MNRP1685A specifically targets and binds to NRP1; the antibody-NRP1 complex prevents the subsequent coupling of NRP1 to VEGFR2, thereby potentially inhibiting VEGF-mediated signaling and potentially preventing angiogenesis. In combination with other anti-VEGF therapies, MNRP1685A may enhance their anti-angiogenic effect. NRP1 is a membrane-bound co-receptor normally expressed by endothelial cells and overexpressed by certain tumor cells, and plays a role in angiogenesis, cell survival, migration, and invasion.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C124647","Anti-nf-P2X7 Antibody Ointment BIL-010t","Anti-nf-P2X7 Antibody Ointment BIL-010t|BIL-010t|BSCT 10 % Ointment","An ointment formulation composed of a purified sheep immunoglobulin G (IgG) antibody against the non-functional form of the purinergic P2X7 receptor (nf-P2X7), with potential antineoplastic activity. Upon topical application of the anti-nf-P2X7 antibody ointment BIL-010t, the antibody binds to nf-P2X7 and inhibits its antiapoptotic activity. This may induce apoptosis and inhibit the growth of nf-P2X7-overexpressing cancer cells. P2X7, an ATP-gated cation-selective channel, plays a role in the induction of apoptosis; nf-P2X7, is upregulated in a variety of cancer cell types while not expressed on normal, healthy cells and is unable to form a large transmembrane, apoptotic pore upon exposure to ATP and prevents apoptosis.","Pharmacologic Substance"]
["C91721","Anti-Nucleolin Aptamer AS1411","AS1411|Anti-Nucleolin Aptamer AS1411","A 26-base guanine-rich oligodeoxynucleotide aptamer with potential apoptotic induction activity. Upon administration, anti-nucleolin aptamer AS1411 targets and binds to nucleolin, a nucleolar phosphoprotein which is overexpressed on the surface of certain cancer cells. Via binding to cell surface nucleolin, AS1411 is internalized and may prevent nucleolin from binding to and stabilizing mRNA of the anti-apoptotic BCL2, thereby destabilizing BCL2 mRNA, leading to a reduction in BCL2 protein synthesis. This may lead to the induction of apoptosis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C116847","Anti-NY-ESO-1 Immunotherapeutic GSK-2241658A","Anti-NY-ESO-1 Immunotherapeutic GSK-2241658A|CTAG1A ASCI|GSK-2241658A|GSK2241658A Antigen-Specific Cancer Immunotherapeutic|GSK2241658A","An immunotherapeutic agent targeting the tumor-associated antigen (TAA), cancer/testis antigen NY-ESO-1, with potential antineoplastic activity.","Pharmacologic Substance"]
["C114295","Anti-NY-ESO1 TCR-transduced Autologous CD62L+-derived T-Lymphocytes","Anti-NY-ESO1 TCR-transduced Autologous CD62L+-derived T-Lymphocytes|Autologous CD62L+-derived T Lymphocytes Transduced With NY-ESO-1-specific TCR","Human autologous CD62L-positive T-lymphocytes transduced with a retroviral vector encoding a T cell receptor (TCR) specific for the cancer-testis antigen NY-ESO-1, with potential antineoplastic activity. Following leukapheresis, isolation of lymphocytes, expansion ex vivo, transduction, and reintroduction into the patient, the anti-NY-ESO1 TCR-transduced autologous CD62L+-derived T-Lymphocytes bind to NY-ESO-1-overexpressing tumor cells. This may result in cytotoxic T-lymphocyte (CTL)-mediated elimination of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types. CD62L, also called L-selectin, is a lymphoid homing receptor and differentiation marker and is expressed on a subset of CD8-positive T-lymphocytes; it is involved in the migration of T-lymphocytes to lymph nodes and may improve the efficacy for ex vivo-expanded T-cells following adoptive cell therapy.","Cell|Pharmacologic Substance"]
["C118368","Anti-OFA Immunotherapeutic BB-MPI-03","Anti-OFA Immunotherapeutic BB-MPI-03|BB-MPI-03|BBMPI03","A cancer vaccine composed of 3 different cytotoxic T-cell epitopes derived from the tumor-associated antigen oncofetal antigen (OFA), with potential immunostimulating and antineoplastic activities. Upon intradermal administration, anti-OFA immunotherapeutic vaccine BB-MPI-03 activates the immune system to elicit a specific cytotoxic T-lymphocyte (CTL) response against tumor cells expressing OFA. OFA, also called immature laminin receptor protein (iLRP), is expressed in fetal tissues and is overexpressed in various cancers; its expression is correlated with cancer cell survival.","Immunologic Factor|Pharmacologic Substance"]
["C128026","Anti-OX40 Antibody BMS 986178","Anti-OX40 Antibody BMS 986178|BMS 986178|BMS-986178","An agonistic monoclonal antibody against the co-stimulatory receptor OX40 (CD134; TNFRSF4), with potential immunostimulatory activity. Upon administration, anti-OX40 monoclonal antibody BMS 986178 selectively binds to and activates the OX40 receptor, by mimicking the action of the endogenous OX40 ligand (OX40L). OX40 receptor activation induces proliferation of memory and effector T-lymphocytes. In the presence of tumor-associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor receptor family (TNFRSF), is expressed on T-lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T-cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C96040","Anti-OX40 Monoclonal Antibody","Anti-OX40 Monoclonal Antibody|anti-OX40 MoAb","An agonistic monoclonal antibody against receptor OX40 (CD134), with potential immunostimulatory activity. Mimicking the natural OX4 ligand (OX40L), anti-OX40 monoclonal antibody selectively binds to and activates the OX40 receptor. Receptor activation induces proliferation of memory and effector T lymphocytes. In the presence of tumor associated antigens (TAAs), this may promote an immune response against the TAA-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor family, is expressed by CD4 T cells and provides a costimulatory signal for T cell activation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C120041","Anti-OX40 Monoclonal Antibody MEDI0562","Anti-OX40 Monoclonal Antibody MEDI0562|MEDI-0562|MEDI0562","An agonistic, humanized monoclonal antibody against receptor OX40 (CD134), with potential immunostimulatory activity. Upon administration, anti-OX40 monoclonal antibody MEDI0562 selectively binds to and activates the OX40 receptor. OX40 receptor activation induces proliferation of memory and effector T-lymphocytes. In the presence of tumor-associated antigens (TAAs), this agent may promote an immune response against TAAs-expressing tumor cells. OX40, a cell surface glycoprotein and member of the tumor necrosis factor (TNF) receptor family, is expressed on T-lymphocytes and provides a co-stimulatory signal for the proliferation and survival of activated T-cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C64773","Anti-p53 T-Cell Receptor-Transduced Peripheral Blood Lymphocytes","Anti-p53 T-Cell Receptor Retroviral Vector-Transduced Peripheral Blood Lymphocytes|Anti-p53 T-Cell Receptor-Transduced Peripheral Blood Lymphocytes|Anti-p53 TCR Retroviral Vector-Transduced PBL|Anti-p53 TCR-Transduced PBL","Human autologous peripheral blood lymphocytes (PBLs) transduced with an anti-p53 T cell receptor gene with potential antineoplastic activity. PBLs are harvested from a patient and pulsed with a retroviral vector that encodes the T-cell receptor gene specific for a mutated form of p53. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these modified PBLs express the anti-p53 T cell receptor which binds to mutant p53-overexpressing tumor cells; PBL-mediated tumor growth inhibition may follow. Many tumor cell types overexpress mutant p53 proteins, which are associated with the loss of apoptosis regulation and abnormal cell proliferation.","Cell|Pharmacologic Substance"]
["C124058","Anti-PD-1 Checkpoint Inhibitor PF-06801591","Anti-PD-1 Checkpoint Inhibitor PF-06801591|PF-06801591","An inhibitor of the human inhibitory receptor programmed cell death 1 (PD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 checkpoint inhibitor PF-06801591 targets and binds to PD-1 and blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs) against tumor cells. PD-1, an inhibitory receptor belonging to the B7-receptor family, is expressed on activated T-lymphocytes, B-cells and NK cells; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity.","Pharmacologic Substance"]
["C97039","Anti-PD-1 Fusion Protein AMP-224","AMP-224|Anti-PD-1 Fusion Protein AMP-224","A recombinant B7-DC Fc-fusion protein composed of the extracellular domain of the PD-1 ligand programmed cell death ligand 2 (PD-L2, B7-DC) and the Fc region of human immunoglobulin (Ig) G1, with potential immune checkpoint inhibitory and antineoplastic activities. Anti-PD-1 fusion protein AMP-224 specifically binds to PD-1 on chronically stimulated T-cells and reduces their proliferation. This may restore immune function and may result in the activation of cytotoxic T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein of Ig superfamily and inhibitor receptor expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity. AMP-224 does not bind normal activated T-cells.","Pharmacologic Substance"]
["C121775","Anti-PD-1 Monoclonal Antibody BGB-A317","Anti-PD-1 Monoclonal Antibody BGB-A317|BGB-A317","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody BGB-A317 binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C113332","Anti-PD-1 Monoclonal Antibody MEDI0680","AMP-514|Anti-PD-1 Monoclonal Antibody MEDI0680|MEDI0680","A humanized immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody MEDI0680 binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C121625","Anti-PD1 Monoclonal Antibody PDR001","Anti-PD1 Monoclonal Antibody PDR001|PDR001","A fully humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD1 monoclonal antibody PDR001 binds to PD-1 expressed on activated T-cells and blocks the interaction with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1) and PD-1 ligand 2 (PD-L2, PD-1L2). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C121540","Anti-PD-1 Monoclonal Antibody REGN2810","Anti-PD-1 Monoclonal Antibody REGN2810|REGN2810","A human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1) protein, with potential immune checkpoint inhibitory and antineoplastic activity. Upon administration, anti-PD-1 monoclonal antibody REGN2810 binds to PD-1, inhibits its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C123816","Anti-PD-1 Monoclonal Antibody SHR-1210","Anti-PD-1 Monoclonal Antibody SHR-1210|HR-301210|SHR-1210|SHR1210","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1,) with immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SHR-1210 binds to and blocks the binding of PD-1, expressed on activated T-lymphocytes, B-cells and natural killer (NK) cells, to its ligands programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen presenting cells (APCs). This prevents the activation of PD-1 and its downstream signaling pathways. This restores immune function through the activation of cytotoxic T-lymphocytes (CTLs) and cell-mediated immune responses against tumor cells or pathogens. Activated PD-1 negatively regulates T-cell activation and plays a key role in tumor evasion from host immunity.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C126799","Anti-PD-1 Monoclonal Antibody TSR-042","ANB011|Anti-PD-1 Monoclonal Antibody TSR-042|TSR-042","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; programmed death-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody TSR-042 binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T-cells, functions as an immune checkpoint protein that negatively regulates T-cell activation and T-cell-mediated immune responses when activated by its ligands programmed cell death receptor ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C82684","Anti-PDGFR Alpha Monoclonal Antibody MEDI-575","Anti-PDGFR Alpha Monoclonal Antibody MEDI-575|Anti-Platelet-Derived Growth Factor Receptor Alpha Monoclonal Antibody MEDI-575|MEDI-575","A humanized monoclonal antibody directed against the platelet-derived growth factor receptor (PDGFR) alpha with potential antineoplastic activity. Anti-PDGFR alpha monoclonal antibody MEDI-575 inhibits activation of the cell-surface tyrosine kinase PDGFR alpha subunit and subsequent triggering of mitogenic signaling pathways, including the JAK/STAT, PI3K/Akt, and MAP kinase pathways. PDGFR alpha acts as a mitogenic signaling receptor for cells of mesenchymal origin and inhibition of receptor activity may inhibit tumor cell proliferation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C129714","Anti-PD-L1 Monoclonal Antibody KN035","Anti-PD-L1 MoAb KN035|Anti-PD-L1 Monoclonal Antibody KN035|KN 035|KN035","An injectable formulation of a monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with immune checkpoint inhibitory and potential antineoplastic activities. Upon subcutaneous administration, anti-PD-L1 monoclonal antibody KN035 binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.","Pharmacologic Substance"]
["C128138","Anti-PD-L1 Monoclonal Antibody LY3300054","Anti-PD-L1 Checkpoint Antibody LY3300054|Anti-PD-L1 Monoclonal Antibody LY3300054|Anti-Programmed Cell Death Ligand 1 Checkpoint Antibody LY3300054|LY3300054","A monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1) with immune checkpoint inhibitory and potential antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody LY3300054 binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T-cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C78852","Anti-PD-L1 Monoclonal Antibody MDX-1105","Anti-PD-L1 Monoclonal Antibody MDX-1105|BMS 936559|MDX-1105","A fully human monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1) with immune checkpoint inhibitory and potential antineoplastic activities. Anti-PD-L1 monoclonal antibody MDX-1105 binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.","Pharmacologic Substance"]
["C91386","Anti-PGF Monoclonal Antibody RO5323441","Anti-PGF Monoclonal Antibody RO5323441|RO5323441","A humanized IgG1 monoclonal antibody directed against the placenta growth factor (PGF), with potential anti-angiogenic and antineoplastic activities. Anti-PGF monoclonal antibody RO5323441 binds to both PGF-1 and -2, thereby inhibiting the binding of PGF-1 and -2 to the vascular endothelial growth factor receptor-1 (VEGFR-1) and subsequent VEGFR-1 phosphorylation. This may result in the inhibition of tumor angiogenesis and tumor cell proliferation. PGF, a member of the VEGF sub-family and a key molecule in angiogenesis and vasculogenesis, is upregulated in many cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C84847","Anti-PKN3 siRNA Atu027","Anti-PKN3 siRNA Atu027|Atu027","A lipoplexed formulation consisting of short-interfering RNAs (siRNAs) directed against protein kinase N3 (PKN3) encapsulated in catiogenic and fusiogenic lipids with potential antineoplastic activity. Upon administration, catiogenic and fusiogenic lipids promote anti-PKN3 siRNA Atu02 uptake by tumor cells; the siRNAs moieties are subsequently released once inside the cell. The siRNAs bind to PKN3 mRNAs, which may result in the inhibition of translation and expression of the PKN3 protein and, so, growth inhibition of tumor cells that overexpress PKN3. The protein kinase C-related molecule PKN3, downstream in the phosphoinositide-3-kinase (PI3K) signaling pathway, is upregulated in many tumor cells and plays an important role in invasive cell growth and metastasis.","Pharmacologic Substance"]
["C78486","Anti-PLGF Monoclonal Antibody TB-403","Anti-PLGF Monoclonal Antibody TB-403|Anti-Placental Growth Factor Monoclonal Antibody TB-403|RG7334|TB-403","A humanized monoclonal antibody directed against placental growth factor (PLGF) with potential anti-angiogenic and antineoplastic acivities. Anti-PLGF monoclonal antibody TB-403 binds to PLGF, inhibiting the binding of PLGF to the vascular endothelial growth factor receptor, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation. PLGF is a protein that belongs to the family of vascular endothelial growth factors (VEGFs).","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C123924","Anti-PR1/HLA-A2 Monoclonal Antibody Hu8F4","Anti-PR1/HLA-A2 Monoclonal Antibody Hu8F4|Hu8F4","A T-cell receptor (TCR)-like monoclonal antibody against PR1, a 9 amino-acid (VLQELNVTV) human leukocyte antigen (HLA)-A2-restricted leukemia-associated antigen (LAA) derived from the myeloid leukemia-associated antigens proteinase 3 (P3) and neutrophil elastase (NE), with potential immunostimulating and antineoplastic activities. Upon administration, anti-PR1/HLA-A2 monoclonal antibody Hu8F4 selectively binds to a combined epitope of the PR1/HLA-A2 complex expressed on acute myeloid leukemia (AML) blasts and leukemic stem cells (LSC), and prevents PR1/HLA-A2-mediated signaling. This induces complement-dependent cytotoxicity (CDC), to a lesser extent, antibody-dependent cell-mediated cytotoxicity (ADCC), and CDC/ADCC-independent cytolysis of myeloid leukemia cells. This results in a reduction of cellular proliferation in PR1/HLA-A2-overexpressing leukemic cells. PR1 in combination with the HLA-A2 molecule is highly expressed on AML blasts and LSCs.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C116848","Anti-PRAME Immunotherapeutic GSK2302032A","Anti-PRAME Immunotherapeutic GSK2302032A|GSK-2302032A|GSK2302032A|PRAME ASCI","An immunotherapeutic agent targeting the tumor-associated antigen (TAA), preferentially expressed antigen of melanoma (PRAME), with potential antineoplastic activity.","Pharmacologic Substance"]
["C125654","Anti-Programmed Cell Death Protein 1 Antibody Expressing Pluripotent Killer T-Lymphocytes","Anti-PD-1 Antibody Expressing Pluripotent Killer T-Cells|Anti-PD-1 Antibody Expressing Pluripotent Killer T-Lymphocytes|Anti-PDCD1 Antibody Expressing Pluripotent Killer T-Cells|Anti-PDCD1 Antibody Expressing Pluripotent Killer T-Lymphocytes|Anti-Programmed Cell Death Protein 1 Antibody Expressing Pluripotent Killer T-Cells|Anti-Programmed Cell Death Protein 1 Antibody Expressing Pluripotent Killer T-Lymphocytes|PIK-PD-1","A specific population of pluripotent killer (PIK) T-cells that have been induced to express high levels of antibodies against the negative immunoregulatory human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential antitumor activity. Although the exact mechanism(s) of action through which PIK-PD-1 cells exert their effects has yet to be elucidated, upon infusion, these cells secrete antibodies that target PD-1 expressed on the surface of activated T-cells and tumor cells. This may block the interaction of PD-1 with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) and PD-1 ligand 2 (PD-L2, PD-1L2; CD273). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation; PD-L1 is overexpressed on certain cancer cells, and PD-L2 is primarily expressed on antigen presenting cells (APCs).","Cell|Pharmacologic Substance"]
["C96744","Anti-prolactin Receptor Antibody LFA102","Anti-prolactin Receptor Antibody LFA102|LFA102","A neutralizing antibody against the prolactin receptor (PRLR) with potential antineoplastic activity. Upon administration, anti-prolactin receptor antibody LFA102 binds to PRLR and prevents the binding of the peptide hormone prolactin (PRL) to its receptor. This binding induces an antibody-dependent cellular cytotoxicity (ADCC) and may eventually prevent tumor cell proliferation in PRLR-positive cancer cells. PRLR/PRL signaling pathway is frequently overexpressed in breast and prostate cancer.","Pharmacologic Substance"]
["C71157","Anti-PSCA Monoclonal Antibody AGS-1C4D4","AGS-1C4D4|Anti-PSCA Monoclonal Antibody AGS-1C4D4|MK4721","An IgG1k fully human monoclonal antibody directed against the human prostate stem cell antigen (PSCA) with potential antineoplastic activity. Anti-PSCA fully human monoclonal antibody MK4721 selectively targets and binds to PSCA, triggering complement-dependent cell lysis and antibody-dependent cell-mediated cytotoxicity in tumor cells expressing PSCA. PSCA is a glycosyl-phosphatidylinositol (GPI)-linked cell surface antigen found in cancers of the bladder, pancreas, and prostate.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C113439","Anti-PSMA Monoclonal Antibody MDX1201-A488","Anti-PSMA Monoclonal Antibody MDX1201-A488|MDX1201-A488","A recombinant, human monoclonal antibody targeting an extracellular epitope of human prostate specific membrane antigen (PSMA) that is conjugated with a fluorescent dye A488, with potential imaging activity. Upon intravenous administration, the MDX1201 moiety of anti-PSMA monoclonal antibody MDX1201-A488 targets PSMA expressed on cancer cells. Subsequently, the A488 moiety can then be visualized by fluorescence-based imaging and the amount of PSMA-expressing tumor cells can be assessed. A488 is a photostable fluorescent dye with a high quantum yield. PSMA, a tumor-associated antigen and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C95707","Anti-PSMA Monoclonal Antibody-MMAE Conjugate","Anti-PSMA Monoclonal Antibody-MMAE Conjugate|Anti-PSMA Monoclonal Antibody-Monomethylauristatin E Conjugate|Anti-PSMA-MMAE-ADC|PSMA ADC|Prostate-specific Membrane Antigen Antibody-Drug Conjugate","An antibody-drug conjugate (ADC) containing a fully human monoclonal antibody directed against prostate-specific membrane antigen (PSMA), conjugated via a stable, enzyme-cleavable linker to monomethylauristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity.  The monoclonal antibody moiety of this conjugate selectively binds to PSMA, a protein which is abundantly expressed on the surface of metastatic and hormone-refractory prostate cancer cells. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis.","Immunologic Factor|Pharmacologic Substance"]
["C103827","Anti-PSMA/CD3 BiTE Monoclonal Antibody MT112","Anti-PSMA/CD3 BiTE Monoclonal Antibody MT112|BAY2010112|MT112","A recombinant T-cell engaging bispecific monoclonal antibody (BiTE) directed against human prostate specific membrane antigen (PSMA) and the CD3 epsilon subunit of the T cell receptor complex, with potential immunostimulating and antineoplastic activities.  Anti-PSMA/CD3 BiTE monoclonal antibody MT112 possesses two antigen-recognition sites, one for PSMA, and one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR). This bispecific monoclonal antibody brings PSMA-expressing tumor cells and cytotoxic T lymphocytes (CTLs) together, which may result in the CTL-mediated cell death of PSMA-expressing cells. PSMA, a tumor associated antigen, is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.","Immunologic Factor|Pharmacologic Substance"]
["C118626","Anti-PSMA/CD3 Monoclonal Antibody MOR209/ES414","Anti-PSMA/CD3 Monoclonal Antibody MOR209/ES414|MOR209/ES414","An anti-prostate specific membrane antigen (PSMA)/anti-CD3 bispecific humanized monoclonal antibody, with potential immunostimulatory and antineoplastic activities. Anti-PSMA/CD3 monoclonal antibody MOR209/ES414 possesses two antigen-recognition sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for PSMA, a tumor-associated antigen (TAA) overexpressed on the surface of prostate tumor cells. Upon intravenous administration of MOR209/ES414, this bispecific antibody simultaneously binds to both CD3-expressing T-cells and PSMA-expressing cancer cells, thereby crosslinking PSMA-expressing tumor cells and cytotoxic T-lymphocytes (CTLs). This results in CTL-mediated cancer cell lysis of prostate cancer cells expressing PSMA.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C121778","Anti-sCLU Monoclonal Antibody AB-16B5","AB-16B5|Anti-sCLU Monoclonal Antibody AB-16B5","A humanized, immunoglobulin (Ig) G2 monoclonal antibody against the secreted form of human clusterin (sCLU) expressed by tumor cells, with potential antineoplastic and anti-metastatic activities. Upon administration, anti-sCLU monoclonal antibody AB-16B5 specifically binds to tumor-associated sCLU and inhibits its activity. This inhibits both the sCLU-mediated signal transduction pathways and epithelial-to-mesenchymal transition (EMT), which leads to the inhibition of tumor cell migration and invasion. In addition, AB-16B5 enhances chemo-sensitivity. sCLU, a heterodimeric disulfide-linked glycoprotein overexpressed by various types of cancer cells, contributes to proliferation and survival of cancer cells, and stimulates tumor cell EMT.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C96222","Anti-SEMA4D Monoclonal Antibody VX15/2503","Anti-SEMA4D Monoclonal Antibody VX15/2503|VX15/2503|moAb VX15/2503","A humanized IgG4 monoclonal antibody against the semaphorin 4D (SEMA4D; CD100) with potential immunomodulating and antineoplastic activities. Upon administration, anti-SEMA4D monoclonal antibody VX15/2503 binds to and neutralizes SEMA4D, thereby preventing binding of SEMA4D to its receptor plexin-B1 (PLXNB1). By blocking the interaction of SEMA4D and PLXNB1, VX15/2503 may cause an inhibition of endothelial cell activation and migration, eventually leading to an inhibition of angiogenesis and tumor cell proliferation. Semaphorin 4D, a large cell surface antigen found on the resting T-cell and overexpressed in a variety of tumor cell types, plays an important role in vascular growth, tumor progression, invasion and immune cell regulation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C111995","Anti-SLITRK6 Monoclonal Antibody-MMAE Conjugate AGS15E","AGS15E|ASG-15ME|Anti-SLITRK6 ADC AGS15E|Anti-SLITRK6 Antibody-drug Conjugate AGS15E|Anti-SLITRK6 Monoclonal Antibody-MMAE Conjugate AGS15E","An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against SLIT and NTRK-like protein 6 (SLITRK6), covalently linked to the cytotoxic agent monomethyl auristatin E (MMAE), an auristatin derivative and a potent inhibitor of microtubule polymerization, with potential antineoplastic activity. Upon intravenous administration, the monoclonal antibody moiety of AGS15E binds to SLITRK6 expressed on tumor cells, which facilitates both AGS15E internalization and the intracellular delivery of MMAE. Upon cleavage, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and tumor cell apoptosis.  SLITRK6, a member of the Slitrk family of leucine-rich repeat (LRR) neuronal transmembrane proteins, is minimally expressed in normal tissue but overexpressed in a variety of cancers, including bladder cancer, some forms of lung cancer, breast cancer and glioblastoma.","Pharmacologic Substance"]
["C94220","Anti-TA-MUC1 Monoclonal Antibody PankoMab","Anti-TA-MUC1 Monoclonal Antibody PankoMab|PankoMab-GEX|PankoMab","A humanized monoclonal antibody recognizing the tumor-specific epitope of mucin-1 (TA-MUC1), with potential antineoplastic activity. Anti-TA-MUC1 monoclonal antibody PankoMab targets and binds to the TA-MUC1 epitopes expressed on the cell surface of tumor cells, thereby potentially activating the immune system to induce an antibody-dependent cellular cytotoxicity (ADCC) against the TA-MUC1-expressing tumor cells. TA-MUC1 is designated to MUC1 epitopes with O-glycosylated carbohydrate-induced conformational structures that are tumor-specific, thereby enabling PankoMab to differentiate between tumor MUC1 and non-tumor MUC1 epitopes.","Immunologic Factor|Pharmacologic Substance"]
["C96430","Anti-TF Monoclonal Antibody ALT-836","ALT-836|Anti-TF MoAb ALT-836|Anti-TF Monoclonal Antibody ALT-836","A recombinant human-mouse chimeric monoclonal antibody against human tissue factor (TF), with potential antiangiogenic, anticoagulant and anti-inflammatory activities. Upon administration, anti-TF monoclonal antibody ALT-836 binds to TF or the TF-Factor VIIa (FVIIa) complex preventing binding and activation of Factor X (FX) and Factor IX (FIX). This may prevent thrombin formation and cancer-associated venous thromboembolism, and may inhibit angiogenesis and tumor cell proliferation. TF, a transmembrane protein and procoagulant, is overexpressed in many tumor cell types, and is correlated with metastasis, angiogenesis, tumor growth and tumor-associated thrombosis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C113164","Anti-TF Monoclonal Antibody-MMAE Conjugate","Anti-TF Monoclonal Antibody-MMAE Conjugate|HuMax-TF-ADC","An antibody-drug conjugate (ADC) comprised of a monoclonal antibody against human tissue factor (TF) covalently coupled, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and potent microtubule disrupting agent, with potential antiangiogenic, anticoagulant and antineoplastic activities. Upon administration, anti-TF monoclonal antibody-MMAE conjugate binds to cell surface TF and is internalized. The antibody moiety prevents binding of TF to factor VIIa (FVIIa) and interferes with the activation of factor X (FX) into FXa. This may prevent thrombin formation and cancer-associated venous thromboembolism, and may inhibit angiogenesis and tumor cell proliferation. After internalization of the agent, the MMAE moiety is released by proteolytic cleavage. It then binds to tubulin and inhibits its polymerization, which results in G2/M phase arrest and apoptosis. TF, a transmembrane protein and initiator of the coagulation cascade, is overexpressed in many tumor cells and tumor-resident endothelial cells. Expression of TF is correlated with metastasis, angiogenesis, tumor cell growth and tumor-associated thrombosis.","Pharmacologic Substance"]
["C102853","Anti-TGF-beta RII Monoclonal Antibody IMC-TR1","Anti-TGF-beta RII Monoclonal Antibody IMC-TR1|IMC-TR1|LY3022859","A monoclonal antibody directed against transforming growth factor-beta receptor type II (TGF-beta RII) with potential antineoplastic activity. Anti-TGF-beta RII monoclonal antibody IMC-TR1 specifically targets and binds to TGF-beta R11, thereby preventing the activation of TGF-beta RII-mediated signaling pathways. TGF-beta RII is mutated in a number of cancer cell types and is involved in cancer cell proliferation and tumor progression.","Pharmacologic Substance"]
["C121552","Anti-thyroglobulin mTCR-transduced Autologous Peripheral Blood Lymphocytes","Anti-thyroglobulin mTCR-transduced Autologous PBL|Anti-thyroglobulin mTCR-transduced Autologous Peripheral Blood Lymphocytes","Peripheral blood lymphocytes (PBLs) transduced with a gene encoding for a thyroglobulin (TG)-specific murine T-cell receptor (mTCR), with potential antineoplastic activity. PBLs are harvested from a thyroid cancer patient, and transfected with a retroviral vector that encodes the mTCR gene specific for the human TG antigen. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these anti-TG mTCR-expressing PBLs target and bind to TG-overexpressing tumor cells, which results in both cytokine secretion and tumor cell lysis. TG is a thyroid-specific protein.","Cell|Pharmacologic Substance"]
["C124850","Anti-TIM-3 Monoclonal Antibody MBG453","Anti-TIM-3 Monoclonal Antibody MBG453|Anti-TIM3 Checkpoint Inhibitor MBG453|MBG 453|MBG453","An inhibitor of the inhibitory T-cell receptor T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-TIM-3 checkpoint inhibitor MBG453 binds to TIM-3 expressed on certain immune cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis resulting in a reduction in tumor growth. TIM-3, a transmembrane protein expressed on certain T-cells, is associated with tumor-mediated immune suppression.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C128627","Anti-TIM-3 Monoclonal Antibody TSR-022","Anti-TIM-3 Monoclonal Antibody TSR-022|Anti-TIM3 Checkpoint Inhibitor TSR-022|Anti-TIM3 Monoclonal Antibody TSR-022|TSR-022","A monoclonal antibody against the inhibitory T-cell receptor, T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3; TIM3; hepatitis A virus cellular receptor 2; HAVCR2), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the anti-TIM-3 monoclonal antibody TSR-022 binds to TIM-3 expressed on certain T-cells, including tumor infiltrating lymphocytes (TILs). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which results in a reduction in tumor growth. TIM-3, a transmembrane protein and immune checkpoint receptor, is associated with tumor-mediated immune suppression.","Pharmacologic Substance"]
["C104291","Anti-Tissue Factor Monoclonal Antibody MORAb-066","Anti-TF Monoclonal Antibody MORAb-066|Anti-Tissue Factor Monoclonal Antibody MORAb-066|MORAb-066","A humanized monoclonal antibody against human tissue factor (TF), with potential antiangiogenic, anticoagulant and anti-inflammatory activities. Upon administration, anti-TF monoclonal antibody MORAb-066 binds to TF and prevents Factor VIIa (FVIIa) from binding, thereby interfering with the activation of Factor X (FX) into FXa. This may prevent thrombin formation and cancer-associated venous thromboembolism, and may inhibit angiogenesis and tumor cell proliferation. TF, a transmembrane protein and initiator of the coagulation cascade, is overexpressed in many tumor cells and tumor endothelial cells; its expression is correlated with metastasis, angiogenesis, tumor cell growth and tumor-associated thrombosis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C120554","Anti-TLR2 Monoclonal Antibody OPN-305","Anti-TLR2 Monoclonal Antibody OPN-305|OPN-305","A humanized immunoglobulin (Ig) G4 monoclonal antibody directed against toll-like receptor type 2 (TLR2), with potential anti-inflammatory and antineoplastic activities. Upon intravenous administration, OPN-305 binds to the ligand-binding site on the TLR2 receptor and blocks the activation of TLR2-mediated innate immunity signaling. This prevents the TLR2-mediated production of pro-inflammatory mediators and prevents inflammation. TLR2, a member of the TLR family primarily found on leukocytes, plays a key role in the activation of innate immunity; it is overexpressed in various inflammatory diseases and in certain types of cancer.","Immunologic Factor|Pharmacologic Substance"]
["C97337","Anti-TWEAK Monoclonal Antibody RO5458640","Anti-TWEAK Monoclonal Antibody RO5458640|RO5458640","A humanized monoclonal antibody directed against the apoptotic ligand TNF-like weak inducer of apoptosis (TWEAK) with potential antineoplastic activity. Anti-TWEAK monoclonal antibody RO5458640 binds to TWEAK and prevents the binding of TWEAK to its receptor, FGF-inducible molecule 14 (Fn14), thereby blocking the TWEAK/Fn14 signaling. This may prevent tumor cell proliferation, invasion, migration and angiogenesis. TWEAK has pleiotropic effects, mediating proinflammatory and pro-angiogenic activity as well as stimulation of invasion, migration, and survival mediated via its receptor Fn14; Fn14 is expressed at relatively low levels in normal tissues, but is elevated in tumor cells and locally in injured and diseased tissues.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C91376","Anti-VEGF Anticalin PRS-050-PEG40","Anti-VEGF Anticalin PRS-050-PEG40|PRS-050-PEG40","A pegylated, proprietary lipocalin that targets human vascular endothelial growth factor (VEGF), with potential antineoplastic activity. Pegylated anti-VEGF anticalin PRS-050 specifically targets and binds to VEGF receptor 2 (VEGFR2 or KDR), thereby preventing its activity. This may inhibit angiogenesis and eventually reduce tumor cell growth.","Pharmacologic Substance"]
["C126644","Anti-VEGF/ANG2 Nanobody BI 836880","Anti-VEGF/ANG2 BI 836880|Anti-VEGF/ANG2 Nanobody BI 836880|BI 836880|Bi-specific Anti-VEGF/Ang2 Nanobody BI 836880","A nanobody directed against angiopoietin-2 (Ang2; ANGPT2)- and vascular endothelial growth factor (VEGF)-derived peptides, with potential antiangiogenic and antineoplastic activities. Anti-VEGF/ANG2 nanobody BI 836880 binds to Ang2 and VEGF and inhibits receptor binding; this prevents Ang2- and VEGF-mediated signaling and inhibits both tumor angiogenesis and tumor cell proliferation. Both VEGF and Ang2 are upregulated in a variety of cancer cell types and play a crucial role in angiogenesis. The nanobody is based on functional fragments of single-chain antibodies.","Pharmacologic Substance"]
["C99765","Anti-VEGFC Monoclonal Antibody VGX-100","Anti-VEGFC Monoclonal Antibody VGX-100|VEGF-C mAb VGX-100|VGX-100","A fully human monoclonal antibody directed against the human vascular endothelial growth factor C (VEGFC or Flt4 ligand) with potential antiangiogenic activity. Anti-VEGFC monoclonal antibody VGX-100 specifically binds to and inhibits VEGFC protein, thereby preventing its binding to VEGFR3 (FLT4) or VEGFR2 (KDR or FLK1). This may prevent VEGFC-mediated signaling and may lead to the inhibition of vascular and lymphatic endothelial cell proliferation. The inhibition of tumor angiogenesis and lymphangiogenesis may eventually decrease tumor cell proliferation and prevent metastasis. VEGFC is overexpressed in a variety of cancer cells, and is associated with increased invasiveness and decreased survival.","Immunologic Factor|Pharmacologic Substance"]
["C111038","Anti-VEGFR2-CAR Retroviral Vector-transduced Autologous T-lymphocytes","Anti-VEGFR2 Gene Engineered CD8+ Lymphocytes|Anti-VEGFR2-CAR Retroviral Vector-transduced Autologous T-lymphocytes","Autologous human CD8-positive T-lymphocytes transduced with a recombinant retroviral vector encoding a chimeric T cell receptor (chimeric antigen receptor or CAR) consisting of an anti-vascular endothelial growth factor receptor type 2 (VEGFR2) scFv (single chain variable fragment), linked to the transmembrane domain of human CD8alpha and coupled to the costimulatory signaling domains of both CD28 and 4-1BB (CD137), and the CD3 zeta chain of the T-cell receptor (TCR), with potential immunostimulating and antineoplastic activities. Autologous peripheral blood lymphocytes (PBLs) from a patient with VEGFR2-positive cancer are pulsed with a retroviral vector that encodes the CAR gene specific for VEGFR2. After expansion in culture and reintroduction into the patient, the anti-VEGFR2 CAR-gene engineered CD8+ lymphocytes express anti-VEGFR2-CAR on their cell surfaces and bind to the VEGFR2 antigen on tumor cell surfaces. Subsequently, VEGFR2-expressing tumor cells are lysed. VEGFR2, a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, belongs to the VEGFR superfamily and plays key roles in tumor cell proliferation, survival, invasion and tumor angiogenesis. The co-stimulatory molecules are required for optimal T-cell activation.","Cell|Pharmacologic Substance"]
["C95734","Anti-VEGFR3 Monoclonal Antibody IMC-3C5","Anti-VEGFR3 MoAb IMC-3C5|Anti-VEGFR3 Monoclonal Antibody IMC-3C5|IMC-3C5","A fully-human monoclonal antibody directed against human vascular endothelial growth factor receptor 3 (VEGFR-3; Flt-4) with antiangiogenic activity. Anti-VEGFR-3 monoclonal antibody IMC-3C5 specifically binds to and inhibits VEGFR-3, which may result in inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR-3 plays a critical role in the embryonic vascular system development but is restricted postnatally to endothelial cells of lymphatic vessels and found to be expressed in many solid and hematologic malignancies.","Immunologic Factor|Pharmacologic Substance"]
["C127124","Anti-VISTA Monoclonal Antibody JNJ 61610588","Anti-VISTA Monoclonal Antibody JNJ 61610588|JNJ 61610588|JNJ-61610588","A human monoclonal antibody against the protein V-domain immunoglobulin (Ig) suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative checkpoint regulatory and antineoplastic activities. Upon administration, JNJ 61610588 targets and binds to VISTA. This inhibits VISTA signaling, abrogates the VISTA-induced suppression of T-lymphocyte-mediated immune responses, enhances cytotoxic T-cell responses against tumor cells and inhibits tumor cell growth. VISTA, mainly expressed on hematopoietic cells, plays a key role in immunosuppression.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C95731","Antrodia cinnamomea Supplement","Antrodia cinnamomea Supplement","A dietary supplement containing extract from the medicinal fungus Antrodia cinnamomea with potential antiangiogenic, hepatoprotective and antioxidant activities. The components in Antrodia cinnamomea supplement are rather complex, however, rich in triterpenoids, polysaccharides, nucleosides (adenosine) nucleic acids, superoxide dismutase, other small molecular weight proteins and steroid like compounds. Neutral sugars in this supplement show inhibitory activity on endothelial tube formation, while maleimide and maleic anhydride derivative components in the extract, such as antrodin B and antrodin C and their metabolites, exhibit significant cytotoxic effects on tumor cells and hepatitis C virus.","Pharmacologic Substance"]
["C74012","Apatinib","3-Pyridinecarboxamide, N-(4-(1-cyanocyclopentyl)phenyl)-2-((4-pyridinylmethyl)amino)-, methanesulfonate (1:1)|APATINIB|Aitan|Apatinib|YN-968D1|YN968D1","An orally bioavailable, small-molecule receptor tyrosine kinase inhibitor with potential antiangiogenic and antineoplastic activities. Apatinib selectively binds to and inhibits vascular endothelial growth factor receptor 2, which may inhibit VEGF-stimulated endothelial cell migration and proliferation and decrease tumor microvessel density. In addition, this agent mildly inhibits c-Kit and c-SRC tyrosine kinases.","Pharmacologic Substance"]
["C71740","Apatorsen","Apatorsen|ISIS 306053|OGX-427","A second-generation antisense oligonucleotide targeting heat shock protein 27 (Hsp27) with potential antitumor and chemosensitizing activities. Apatorsen suppresses tumor cell expression of Hsp27, which may induce tumor cell apoptosis and enhance tumor cell sensitivity to cytotoxic agents. Hsp27, a chaperone belonging to the small heat shock protein (sHsp) group of proteins, is a cytoprotective protein that supports cell survival under conditions of stress; it has been found to be over-expressed in a variety of human cancers.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1087","Apaziquone","3-hydroxymethyl-5-aziridinyl-1-methyl-2-(1H-indole-4,7-dione) prop-beta-en-alpha-ol|APAZIQUONE|Apaziquone|E O9|EO9|Eoquin|Neoquin","An indolequinone bioreductive prodrug and analog of mitomycin C with potential antineoplastic and radiosensitization activities. Apaziquone is converted to active metabolites in hypoxic cells by intracellular reductases, which are present in greater amounts in hypoxic tumor cells. The active metabolites alkylate DNA, resulting in apoptotic cell death. This agent displays selectivity activity towards both hypoxic solid tumors, which exhibits higher expression of cytochrome P450 reductase, and well-oxygenated malignant cells that overexpress the bioreductive enzyme NQO1 (NAD(P)H: quinone oxidoreductase). Apaziquone may selectively sensitize hypoxic tumor cells to radiocytotoxicity.","Organic Chemical|Pharmacologic Substance"]
["C48640","APC8015F","APC 8015F|APC8015F","A cell-based vaccine composed of previously frozen autologous antigen-presenting peripheral blood mononuclear cells (enriched for a dendritic cell fraction) that have been exposed to a recombinant protein consisting of granulocyte-macrophage colony-stimulating factor (GM-CSF) fused to prostatic-acid phosphatase (PAP), a protein expressed by prostate cancer cells.  Upon administration, the vaccine may stimulate an antitumor T-cell response against tumor cells expressing PAP.","Immunologic Factor|Pharmacologic Substance"]
["C28802","Aphidicoline Glycinate","Aphidicoline Glycinate","A tetracyclic diterpene antibiotic isolated from the fungus Cephalosporium aphidicola and other fungal species with potential antineoplastic activity.  Aphidicoline glycinate blocks the cell cycle at early S-phase by specifically inhibiting DNA polymerases in eukaryotic cells, induces apoptosis, and stops the growth of eukaryotic cells and certain viruses by selectively inhibiting DNA polymerase II or viral-induced DNA polymerases. (NCI04)","Pharmacologic Substance"]
["C126661","Apilimod Dimesylate Capsule","Apilimod Dimesylate Capsule|LAM 002A|LAM-002A","A capsule containing the dimesylate salt form of apilimod, an inhibitor of the class III PI kinase phosphatidylinositol-3-phosphate 5-kinase (PIKfyve), with potential antineoplastic and immunomodulatory activities. Upon oral administration of apilimod dimesylate capsule, apilimod selectively binds to and inhibits PIKfyve. The inhibition leads to disruption of PIKfyve-mediated signal transduction pathways and eventually inhibits tumor cell growth in PIKfyve-overexpressing tumor cells. Also, PIKfyve inhibition by apilimod inhibits the toll-like receptor (TLR)-induced production of various cytokines, including interleukin-12 (IL-12) and IL-23, thereby preventing IL-12/IL-23-mediated immune responses. PIKfyve, a lipid kinase dysregulated in various tumor types, plays a key role in TLR signaling and tumor cell migration, proliferation and survival.","Pharmacologic Substance"]
["C71693","Apomab","APOMAB|Apomab","A fully human monoclonal antibody directed against human death receptor 5 (DR5; TRAIL-R2; TNFRSF10B) with potential pro-apoptotic and antineoplastic activities. Mimicking the natural ligand TRAIL (tumor necrosis factor-related apoptosis inducing ligand), apomab binds to DR5, which may directly activate the extrinsic apoptosis pathway and indirectly induce the intrinsic apoptosis pathway in tumor cells. DR5 is a cell surface receptor of the TNF-receptor superfamily and is expressed in a broad range of cancers.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1873","Apomine","Apomine|Phosphonic acid, (2-(3,5-bis(1,1-dimethylethyl)-4-hydroxyphenyl)ethylidene)bis-, tetrakis(1-methylethyl) Ester|SKF 99085|SR-45023A (Apomine)|SR-45023A|TETRAISOPROPYL 2-(3,5-DI-TERT-BUTYL-4-HYDROXYPHENYL)ETHYL-1,1-BIPHOSPHONATE|Tetraisopropyl-2-(3,5-di-tert-butyl-4-hydroxyphenyl)ethylidene-1,1-diphosphonate","A 1,1-bisphosphonate ester with potential antineoplastic and hypocholesterolemic activities. SR-45023A binds to hydroxyapatite crystals in the bone matrix where it inhibits enzymatic activity of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which is required for the formation of mevalonate, the precursor of cholesterol. Consequently, shortage of mevalonate impedes the synthesis of downstream isoprenoids that are essential for protein prenylation. This leads to the loss of activity of proteins involved in osteoclast function and cellular proliferation, such as Ras and Rho, leading to an inhibition of cellular proliferation, and induction of osteoclasts apoptosis. In addition, SR-45023A activates the farnesoid X activated receptor (FXR), a member of the nuclear hormone superfamily implicated in cholesterol metabolism and bile acid transport and may play a role in this agent's antineoplastic effect.","Organic Chemical|Pharmacologic Substance"]
["C69134","Apoptosis Inducer BZL101","Apoptosis Inducer BZL101|BZL101","An orally active aqueous extract derived from the plant Scutellaria barbata with potential antineoplastic activity. Sparing normal cells, apoptosis inducer BZL101 specifically facilitates translocation of the protein apoptosis-inducing factor (AIF) from the mitochondrial membrane into the nucleus in tumor cells, thereby causing tumor cell-specific chromatin condensation and DNA degradation followed by the induction of caspase-independent apoptosis. AIF is both a mitochondrial intermembrane flavoprotein with oxidoreductase activity and a caspase-independent death effector that, similar to cytochrome c, is released from mitochondria early in the apoptotic process.","Pharmacologic Substance"]
["C70984","Apoptosis Inducer GCS-100","Apoptosis Inducer GCS-100|GCS-100","A galectin-binding polysaccharide derived from citrus pectin with potential antineoplastic activity. Apoptosis inducer GCS-100 binds to the carbohydrate-binding domain of the lectin galectin-3, which may result in apoptosis mediated through mitochondria/caspase activation cascades; this agent may overcome tumor growth mediated through anti-apoptotic protein Bcl-2, heat-shock protein 27 (Hsp27), and nuclear factor-kappa B (NF-kB). Galectin-3, a chimeric molecule consisting of both carbohydrate recognition and collagen-like domains, interacts with a variety of carbohydrate and protein ligands to form pentamers with unique crosslinking abilities; this lectin also exhibits anti-apoptotic properties, perhaps, in part, through the regulation of intracellular signaling pathways.","Pharmacologic Substance"]
["C64781","Apoptosis Inducer MPC-2130","Apoptosis Inducer MPC-2130|MPC-2130","A broad-acting, apoptosis-inducing, small molecule with potential antineoplastic activity. Although the exact mechanism of action has yet to be fully elucidated, apoptosis inducer MPC-2130 exhibits proapoptotic activities in tumor cells, including membrane phosphatidylserine externalization, release of cytochrome C from mitochondria, caspase activation, cell condensation, and DNA fragmentation. In addition, because this agent is not a substrate for several types of multidrug resistance (MDR) ABC superfamily transporters, such as P-glycoprotein 1 (MDR-1), multidrug resistance-associated protein 1 (MRP1), and breast cancer resistance protein 1 (BCRP1/ABCG2), it may be useful in treating MDR tumors that express these particular MDR efflux pumps.","Pharmacologic Substance"]
["C102978","Apoptotic Autologous Tumor Cells-pulsed Alpha-type-1 Polarized Dendritic Cells","Apoptotic Autologous Tumor Cells-pulsed Alpha-type-1 Polarized Dendritic Cells","A cell based cancer vaccine composed of mature polarized dendritic cells (DCs) and pulsed with apoptotic autologous tumor cells that has potential immunostimulating and antineoplatic activities. Dendritic cells (DCs) were treated with interleukin-1beta, tumor necrosis factor alpha, interferon-alpha (IFN-a), IFN-gamma and polyinosinic:polycytidylic acid (p-I:C) to produce mature alpha type-1 polarized DCs (alphaDC1) that are capable of producing high levels of interleukin-12p70 (IL-12p70). The alphaDC1 are subsequently pulsed with apoptotic autologous tumor cells. Upon administration, these DCs are able to induce a potent cytotoxic T lymphocyte (CTL) response against tumor associated antigens (TAAs), resulting in tumor cell lysis and inhibition of tumor cell growth. Apoptotic tumor cells contain an array of TAAs.","Pharmacologic Substance"]
["C74021","Apricoxib","APRICOXIB|Apricoxib|COX-2 Inhibitor TG01|CS-706|R-109339|TG01|TP2001","An orally bioavailable nonsteroidal anti-inflammatory agent (NSAID) with potential antiangiogenic and antineoplastic activities. Apricoxib binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), thereby inhibiting the conversion of arachidonic acid into prostaglandins. Apricoxib-mediated inhibition of COX-2 may induce tumor cell apoptosis and inhibit tumor cell proliferation and tumor angiogenesis. COX-related metabolic pathways may represent crucial regulators of cellular proliferation and angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C62522","AR Antagonist BMS-641988","AR Antagonist BMS-641988|BMS-641988","An androgen receptor (AR) antagonist with potential antineoplastic and anti-androgenic activities. BMS-641988 binds to the androgen receptor in target tissues, thereby preventing androgen-induced receptor activation, and facilitates the formation of inactive complexes that cannot be translocated to the nucleus. This may inhibit androgen-dependent gene expression, subsequently leading to an inhibition of cell growth and apoptosis in AR-expressing cells.","Pharmacologic Substance"]
["C104748","AR Antagonist ODM-201","AR Antagonist ODM-201|Antiandrogen ODM-201|BAY 1841788|ODM 201|ODM-201","A formulation containing an androgen receptor (AR) antagonist with potential antineoplastic activity. AR antagonist ODM-201 binds to ARs in target tissues; subsequently, inhibiting androgen-induced receptor activation and facilitating the formation of inactive complexes that cannot translocate to the nucleus. This prevents binding to and transcription of AR-responsive genes that regulate prostate cancer cell proliferation. This ultimately leads to an inhibition of growth in AR-expressing prostate cancer cells.","Pharmacologic Substance"]
["C88335","Archexin","ARCHEXIN|Akt-1 Antisense Oligonucleotide RX-0201|Archexin|RX-0201","A 20-mer antisense oligodeoxynucleotide (ODN) against the proto-oncogene Akt with potential antineoplastic activity. Akt-1 antisense oligonucleotide RX-0201 binds to Akt-1 mRNA, inhibiting translation of the transcript; suppression of Akt-1 expression may result in the inhibition of cellular proliferation and the induction of apoptosis in tumor cells that overexpress Akt-1. Akt-1 is a serine-threonine protein kinase that stimulates proliferation and inhibits apoptosis of tumor cells.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1494","Arcitumomab","ARCITUMOMAB|Arcitumomab|CEA-Scan|IMMU-4|Immunoglobulin G 1 (mouse monoclonal IMMU-4 Fab' fragment gamma-chain anti-human antigen CEA), disulfide with mouse Monoclonal IMMU-4 Light Chain","A murine IgG monoclonal Fab' fragment antibody directed against carcinoembryonic antigen (CEA), a protein that is overexpressed by many tumor cell types. For tumors that overexpress CEA, technetium-99m labeled arcitumomab may be used as an adjunct diagnostic imaging tool to obtain prognostic information following resection and to monitor for recurrent disease. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2570","Arginine Butyrate","ARGININE BUTYRATE|Arginine Butyrate|L-Arginine, Butanoate (3:4)|VX-105|arginine butyrate","The butyric acid salt of the amino acid arginine.  In EBV-related lymphomas, arginine butyrate induces EBV thymidine kinase transcription and may act synergistically with the antiviral agent ganciclovir to inhibit cell proliferation and decrease cell viability. In addition, the butyrate moiety inhibits histone deacetylase, which results in hyperacetylation of histones H3 and H4. Acetylated histones have a reduced affinity for chromatin; this reduced histone-chromatin affinity may allow chromosomal unfolding, potentially enhancing the expression of genes related to tumor cell growth arrest and apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C74013","Arnebia Indigo Jade Pearl Topical Cream","AIJP|Arnebia Indigo Jade Pearl Topical Cream","A proprietary multiherbal topical cream based on Chinese herbal medicine with potential antineoplastic, antiviral, antibacterial and immunostimulatory activities. Arnebia Indigo Jade Pearl topical cream contains 12 ingredients including 9 herbs infused in sesame oil, with an additional three powdered ingredients and beeswax added to the infused oil to create the salve. The purported mechanism(s) of action is unclear due to the complexity of the herbal mixture.","Pharmacologic Substance"]
["C1005","Arsenic Trioxide","ARSENIC TRIOXIDE|Arsenic (III) Oxide|Arsenic Sesquioxide|Arsenic Trioxide|Arsenous Acid Anhydride|Arsenous Acid|Arsenous Oxide|Trisenox|White Arsenic|arsenic trioxide","A small-molecule arsenic compound with antineoplastic activity.  The mechanism of action of arsenic trioxide is not completely understood. This agent causes damage to or degradation of the promyelocytic leukemia protein/retinoic acid receptor-alpha (PML/RARa) fusion protein; induces apoptosis in acute promyelocytic leukemia (APL) cells and in many other tumor cell types; promotes cell differentiation and suppresses cell proliferation in many different tumor cell types; and is pro-angiogenic. (NCI04)","Inorganic Chemical|Pharmacologic Substance"]
["C118504","Artemether Sublingual Spray","Artemether Sublingual Spray|LON002|Sublingual Artemether Spray","A sublingual spray containing artemether, a semisynthetic derivative of artemisinin, an endoperoxide extracted from the Chinese herb qinghaosu (Artemisia annua or annual wormwood), with antiparasitic and potential antineoplastic activity. Upon sublingual application of the spray, artemether exerts its antineoplastic activity through as of yet not fully elucidated mechanism(s) of action. This agent binds to heme molecules inside cells, thereby inducing reactive oxygen species (ROS)-mediated damage which selectively kills cancer cells. In addition, artemether appears to target and modulate the expression of various proteins involved in cancer cell proliferation, angiogenesis, invasion and metastasis. Also, this agent depletes T regulatory cells, and modulates the production of inflammatory cytokines, such as interleukin-4 and interferon-gamma. Altogether, this inhibits tumor cell proliferation. The sublingual spray allows faster absorption of a higher percentage of the artemether dose, when compared to the oral form, as it avoids first pass metabolism; this results in an increased efficacy.","Pharmacologic Substance"]
["C60769","Artemisinin Dimer","Artemisinin Dimer","A sesquiterpene lactone peroxide and dimerized plant product derived from Artemisia annua L with anti-malarial, anti-proliferative and anti-angiogenic effects. Artemisinin contains an endoperoxide moiety which forms free radicals when it reacts with iron. The resultant carbon-based radical can lead to cellular damage and cell death by reacting with cellular macromolecules such as proteins and membrane lipids. Malaria parasites contain large amounts of heme-iron, a product from the digestion of hemoglobin. However, recently it has been suggested that activation of artemisinin inside the parasite is by ferrous iron. Furthermore, due to their rapid rate of division, cancer cells require and uptake a large amount of iron to proliferate, therefore they are more susceptible to the cytotoxic effect of artemisinin than non-cancerous cells. The dimer configuration has been shown to increase compound stability and reduce general toxicity.","Pharmacologic Substance"]
["C131020","Arugula Seed Powder","Arugula Seed Powder|Eruca sativa Seed Powder","A dietary supplement containing an extract powder derived from the seeds of the cruciferous vegetable arugula (Eruca sativa), with potential chemopreventive and antioxidant activities. Arugula seed powder contains numerous vitamins and minerals, and is rich in phytonutrients, such as sulforaphane and indole-3-carbinol. Although the exact mechanism of action through which arugula seed powder may exert its anti-tumor effect has yet to be fully elucidated, the effects of this powder on cancer cells may be attributable to the antioxidant and pro-apoptotic activities of the phytonutrients.","Pharmacologic Substance"]
["C1346","Asaley","Asalex|Asaley|Ethyl ester of N-acetyl-DL-sarcolysyl-L-leucine|L-Leucine, N-[N-acetyl-4-[bis(2-chloroethyl)amino]-DL-phenylalanyl]-, ethyl ester (9CI)|L-Leucine, N-[N-acetyl-4-[bis-(2-chloroethyl)amino]-DL-phenylalanyl]-, ethylester|L-leucine, N-[N-acetyl-4-[bis(2-chloroethyl)amino]-DL-phenylalanyl]-, ethyl ester (9CI)|L-leucine, N-[N-acetyl-4-[bis-(2-chloroethyl)amino]-DL-phenylalanyl]-, ethylester|Leucine, N-[N-acetyl-3-[p-[bis(2-chloroethyl)amino]phenyl]-DL-alanyl]-, ethyl ester, L- (8CI)|ethyl ester of N-acetyl-DL-sarcolysyl-L-leucine|leucine, N-[N-acetyl-3-[p-[bis(2-chloroethyl)amino]phenyl]-DL-alanyl]-, ethyl ester, L- (8CI)","An L-leucine derivative of melphalan with antineoplastic activity. Asaley alkylates and crosslinks DNA, resulting in disruption of DNA synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77883","Ashwagandha Root Powder Extract","Ashwagandha Root Powder Extract","A dietary supplement containing an extract powder derived from the root of the ashwagandha shrub with potential antineoplastic, antioxidant, immunostimulating and anti-angiogenic activities. Ashwagandha root powder extract contains numerous alkaloids, including withanine as the primary alkaloid, and steroidal lactone withanolides. The withanolides in this agent may suppress nuclear factor-kappaB activation and nuclear factor-kappaB-regulated gene expression, potentiating apoptosis and inhibiting tumor cell invasion. Cultivated in India and North America, ashwagandha (Withania somnifera Dunal or Indian ginseng) belongs to the Solanaceae (nightshade) family.","Organic Chemical|Pharmacologic Substance"]
["C121943","ASK1 Inhibitor GS-4997","ASK1 Inhibitor GS-4997|GS-4997","An orally bioavailable inhibitor of apoptosis signal-regulating kinase 1 (ASK1), with potential anti-inflammatory, antineoplastic and anti-fibrotic activities. Upon oral administration, ASK1 inhibitor GS-4997 targets and binds to the catalytic kinase domain of ASK1 in an ATP-competitive manner, thereby preventing its phosphorylation and activation. This prevents the phosphorylation of downstream kinases, such as c-Jun N-terminal kinases (JNKs) and p38 mitogen-activated protein kinase (p38 MAPK). By preventing the activation of ASK1-dependent signal transduction pathways, GS-4997 prevents the production of inflammatory cytokines, down-regulates the expression of genes involved in fibrosis, suppresses excessive apoptosis and inhibits cellular proliferation. ASK1, also called mitogen-activated protein kinase kinase kinase 5 (MAP3K5), is activated in response to oxidative and endoplasmic reticulum (ER) stress, calcium influx and infection. It plays a key role in the development of certain cardiovascular and neurodegenerative diseases, diabetes, as well as certain types of cancer.","Pharmacologic Substance"]
["C122720","ASP4132","ASP4132","A molecule with potential antineoplastic activity. Upon oral administration, ASP4132 affects oxidative phosphorylation in mitochondria of metabolically-active tumor cells, which reduces both energy production and tumor cell proliferation. Mitochondrial oxidative phosphorylation is hyperactivated in tumor cells and plays a key role in the promotion of tumor cell proliferation.","Pharmacologic Substance"]
["C116728","ASP9853","ASP9853","An orally bioavailable small molecule, with potential antineoplastic activity.","Pharmacologic Substance"]
["C286","Asparaginase","ASP-1|ASPARAGINASE|Asparaginase II|Asparaginase-E.Coli|Asparaginase|Colaspase|Elspar|Kidrolase|L-ASP|L-Asnase|L-Asparaginase|L-Asparagine Amidohydrolase|L-Asparagine amidohydrolase|L-asparaginase|Laspar|Lcf-ASP|Leucogen|Leunase|MK-965|Paronal|Re-82-TAD-15|Serasa|asparaginase","An enzyme isolated from the bacterium Escherichia coli or the bacterium Erwinia carotovora with antileukemic activity. Asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia in leukemic cells, resulting in the depletion of asparagine, inhibition of protein synthesis, cell cycle arrest in the G1 phase, and apoptosis in susceptible leukemic cell populations. Asparagine is critical to protein synthesis in leukemic cells; some leukemic cells cannot synthesize this amino acid de novo due to the absent or deficient expression of the enzyme asparagine synthase. The E. carotovora-derived form of asparaginase is typically reserved for cases of asparaginase hypersensitivity.","Enzyme|Pharmacologic Substance"]
["C64260","Asparaginase Erwinia chrysanthemi","ASPARAGINASE ERWINIA CHRYSANTHEMI|Asparaginase Erwinia chrysanthemi|Crisantaspasum|Cristantaspase|Erwinase|Erwinaze|L-asparginase (Erwinia )","An enzyme isolated from the bacterium Erwinia chrysanthemi (E. carotovora). Asparagine is critical to protein synthesis in leukemic cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. Asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting leukemic cells of asparagine and blocking protein synthesis and tumor cell proliferation, especially in the G1 phase of the cell cycle.  This agent also induces apoptosis in tumor cells. The Erwinia-derived product is often used for those patients who have experienced a hypersensitivity reaction to the E. Coli formulation.","Enzyme|Pharmacologic Substance"]
["C78478","Astuprotimut-R","ASTUPROTIMUT-R|Astuprotimut-R|GSK1203486A|MAGE-A3|Recombinant MAGE-A3 ASCI GSK1203486A","A cancer vaccine consisting of a recombinant form of human melanoma antigen A3 (MAGE-A3) combined with a proprietary adjuvant with potential immunostimulatory and antineoplastic activities. Upon administration, astuprotimut-R may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing the MAGE-A3 antigen, resulting in tumor cell death. MAGE-A3, a tumor-associated antigen (TAA) originally discovered in melanoma cells, is expressed by various tumor types. The proprietary immunostimulating adjuvant in this agent is composed of a specific combination of immunostimulating compounds selected to increase the anti-tumor immune response to MAGE-A3.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C91758","Asulacrine","4-Acridinecarboxamide,9-((2-methoxy-4-((methylsulfonyl)amino)phenyl)amino)-N,5-dimethyl|ASULACRINE|Amsalog|Asulacrine","An amsacrine analogue with antineoplastic properties. Asulacrine inhibits the enzyme topoisomerase ll, thereby blocking DNA replication and RNA and protein synthesis.","Organic Chemical|Pharmacologic Substance"]
["C1050","Asulacrine Isethionate","9-(2-Methoxy-4-(methylsulfonylamino)phenylamino)-N,5-dimethyl-4-acridinecarboxamide 2-hydroxyethanesulfonate|Asulacrine Isethionate|CI-921","The isethionate salt of an amsacrine analogue with antineoplastic properties. Asulacrine inhibits the enzyme topoisomerase ll, thereby blocking DNA replication and RNA and protein synthesis.","Organic Chemical|Pharmacologic Substance"]
["C2490","At 211 Monoclonal Antibody 81C6","Astatine 211 Conjugated 81C6 Anti-Tenascin Monoclonal Antibody|Astatine At 211 MOAB 81C6|Astatine At 211 Monoclonal Antibody 81C6|Astatine-211 Labelled Anti-Tenascin Monoclonal Antibody 81C6|At 211 Monoclonal Antibody 81C6","A radioimmunoconjugate of a human-murine chimeric IgG2 monoclonal antibody (MoAb) 81C6 labeled with an alpha-emitting radionuclide Astatine 211 (At-211), with imaging and radioimmunotherapeutic properties. MoAb 81C6 recognizes the extracellular matrix antigen tenascin (hexabrachion), which is up-regulated in gliomas and other cancers. Using MoAb 81C6 as a carrier for At-211 results in the targeted imaging and/or destruction of cells expressing tenascin.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1224","Atamestane","ATAMESTANE|Atamestane|atamestane","A synthetic steroidal substance with antineoplastic activity.  Atamestane binds irreversibly to and inhibits the enzyme aromatase, thereby blocking the conversion of cholesterol to pregnenolone and the peripheral aromatization of androgenic precursors into estrogens. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C106250","Atezolizumab","ATEZOLIZUMAB|Atezolizumab|Immunoglobulin G1, Anti-(human CD Antigen cd274) (Human Monoclonal MPDL3280A Heavy Chain), Disulfide with Human Monoclonal MPDL3280A Kappa-chain, Dimer|MPDL 3280A|MPDL 328OA|MPDL-3280A|MPDL3280A|MPDL328OA|RG7446|RO5541267|Tecentriq","A human, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1) expressed on activated T-cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, MPDL3280A also prevents binding of this ligand to B7.1 expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of MPDL3280A is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC).","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C52184","Atiprimod","ATIPRIMOD|Atiprimod|Azaspirane SK&F106615|N,N-Diethyl-8,8-dipropyl-2-azaspiro(4.5)decane-2-propanamine|SK&F106615|atiprimod|azaspirane","An orally bioavailable small molecule belonging to the azaspirane class of cationic amphiphilic agents with anti-inflammatory, antineoplastic, and antiangiogenic properties. Atiprimod inhibits the phosphorylation of signal transducer and activator of transcription 3 (STAT3), blocking the signalling pathways of interleukin-6 and vascular endothelial growth factor (VEGF) and downregulating the anti-apoptotic proteins Bcl-2, Bcl-XL, and Mcl-1, thereby inhibiting cell proliferation, inducing cell cycle arrest, and inducing apoptosis.","Pharmacologic Substance"]
["C76969","Atiprimod Dihydrochloride","ATIPRIMOD DIHYDROCHLORIDE|Atiprimod Dihydrochloride","The dihydrochloride salt form of atiprimod, an orally bioavailable small molecule belonging to the azaspirane class of cationic amphiphilic agents with anti-inflammatory, antineoplastic, and anti-angiogenic activities. Atiprimod inhibits the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and AKT, blocking the signaling pathways of interleukin-6, vascular endothelial growth factor (VEGF) and downregulating the anti-apoptotic proteins Bcl-2, Bcl-XL, and Mcl-1. This results in the inhibition of cell proliferation, induction of cell cycle arrest, and apoptosis.","Pharmacologic Substance"]
["C76970","Atiprimod Dimaleate","ATIPRIMOD DIMALEATE|Atiprimod Dimaleate","The dimaleate salt form of atiprimod, an orally bioavailable small molecule belonging to the azaspirane class of cationic amphiphilic agents with anti-inflammatory, antineoplastic, and antiangiogenic activities. Atiprimod inhibits the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and AKT, blocking the signaling pathways of interleukin-6 and vascular endothelial growth factor (VEGF) and downregulating the anti-apoptotic proteins Bcl-2, Bcl-XL, and Mcl-1. This results in the inhibition of cell proliferation, induction of cell cycle arrest, and apoptosis.","Pharmacologic Substance"]
["C124648","ATM Kinase Inhibitor AZD0156","ATM Kinase Inhibitor AZD0156|AZD0156","An orally bioavailable ataxia telangiectasia mutated (ATM) kinase inhibitor, with potential chemo-/radio-sensitizing and antineoplastic activities. Upon oral administration, AZD0156 targets and binds to ATM, thereby inhibiting the kinase activity of ATM and ATM-mediated signaling. This prevents DNA damage checkpoint activation, disrupts DNA damage repair, induces tumor cell apoptosis, and leads to cell death of ATM-overexpressing tumor cells. In addition, AZD0156 sensitizes tumor cells to chemo- and radiotherapy. ATM, a serine/threonine protein kinase, is upregulated in a variety of cancer cell types; it is activated in response to DNA damage and plays a key role in DNA-strand repair.","Pharmacologic Substance"]
["C52185","ATN-161","ATN-161","A small peptide antagonist of integrin alpha5beta1 with potential antineoplastic activity. ATN-161 selectively binds to and blocks the receptor for integrin alpha5beta1, thereby preventing integrin alpha5beta1 binding. This receptor blockade may result in inhibition of endothelial cell-cell interactions, endothelial cell-matrix interactions, angiogenesis, and tumor progression. Integrin alpha5beta1 is expressed on endothelial cells and plays a crucial role in endothelial cell adhesion and migration.","Pharmacologic Substance"]
["C28837","Atorvastatin Calcium","ATORVASTATIN CALCIUM|Atorvastatin Calcium|CI-981|Lipitor|atorvastatin calcium","The calcium salt of atorvastatin, a synthetic lipid-lowering agent. Atorvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent increases the number of LDL receptors on hepatic cell surfaces, enhancing the uptake and catabolism of LDL and reducing LDL production and the number of LDL particles, and lowers plasma cholesterol and lipoprotein levels. Like other statins, atorvastatin may also display direct antineoplastic activity, possibly by inhibiting farnesylation and geranylgeranylation of proteins such as small GTP-binding proteins, which may result in the arrest of cells in the G1 phase of the cell cycle. This agent may also sensitize tumor cells to cyctostatic drugs, possibly through the mTOR-dependent inhibition of Akt phosphorylation.","Organic Chemical|Pharmacologic Substance"]
["C78676","Atorvastatin Sodium","ATORVASTATIN SODIUM|Atorvastatin Sodium","The sodium salt of atorvastatin, a synthetic lipid-lowering agent. Atorvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent increases the number of LDL receptors on hepatic cell surfaces, enhancing the uptake and catabolism of LDL and reducing LDL production and the number of LDL particles, and lowers plasma cholesterol and lipoprotein levels. Like other statins, atorvastatin may also display direct antineoplastic activity, possibly by inhibiting farnesylation and geranylgeranylation of proteins such as small GTP-binding proteins, which may result in the arrest of cells in the G1 phase of the cell cycle. This agent may also sensitize tumor cells to cyctostatic drugs, possibly through the mTOR-dependent inhibition of Akt phosphorylation.","Pharmacologic Substance"]
["C111993","ATR Kinase Inhibitor AZD6738","ATR Kinase Inhibitor AZD6738|AZD-6738|AZD6738","An orally available morpholino-pyrimidine-based inhibitor of ataxia telangiectasia and rad3 related (ATR) kinase, with potential antineoplastic activity. Upon oral administration, ATR kinase inhibitor AZD6738 selectively inhibits ATR activity by blocking the downstream phosphorylation of the serine/threonine protein kinase CHK1. This prevents ATR-mediated signaling, and results in the inhibition of DNA damage checkpoint activation, disruption of DNA damage repair, and the induction of tumor cell apoptosis. In addition, AZD6738 sensitizes tumor cells to chemo- and radiotherapy. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival; it is activated by DNA damage caused during DNA replication-associated stress.","Pharmacologic Substance"]
["C129693","ATR Kinase Inhibitor VX-803","ATR Kinase Inhibitor VX-803|VX 803|VX-803|VX803","An orally available inhibitor of ataxia telangiectasia and Rad3 related (ATR) kinase, with potential antineoplastic activity. Upon oral administration, ATR kinase inhibitor VX-803 selectively inhibits ATR activity and blocks the downstream phosphorylation of the serine/threonine protein kinase CHK1. This prevents ATR-mediated signaling, which results in the inhibition of DNA damage checkpoint activation, the disruption of DNA damage repair, and the induction of tumor cell apoptosis. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression and survival; it is activated by DNA damage caused during DNA replication-associated stress.","Organic Chemical|Pharmacologic Substance"]
["C116355","ATR Kinase Inhibitor VX-970","ATR Kinase Inhibitor VX-970|VX-970","An inhibitor of ataxia telangiectasia and rad3-related (ATR) kinase, a DNA damage response kinase, with potential antineoplastic activity. ATR kinase inhibitor VX-970 selectively inhibits ATR kinase activity and prevents ATR-mediated signaling in the ATR-checkpoint kinase 1 (Chk1) signaling pathway. This prevents DNA damage checkpoint activation, disrupts DNA damage repair, and induces tumor cell apoptosis. In addition, VX-970 sensitizes tumor cells to chemo- and radiotherapy. ATR, a serine/threonine protein kinase upregulated in a variety of cancer cell types, plays a key role in DNA repair, cell cycle progression, and survival; it is activated by DNA damage caused during DNA replication-associated stress.","Pharmacologic Substance"]
["C111758","ATR-101","ATR-101","An orally bioavailable agent that is selective towards adrenal cortex cells with potential antitumor activity. Upon administration, ATR-101 selectively kills adrenal and adrenal cancer cells, through an unknown mechanism.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1779","Atrasentan Hydrochloride","(+)-A 127722|(2R,3R,4S)-4-(1,3-Benzodioxo-5-yl)-1-(2-(dibutylamino)-2-oxoethyl)-2-(4-methoxyphenyl)-3-pyrrolidinecarboxylic Acid Monohydrochloride|ABT-627|ATRASENTAN HYDROCHLORIDE|Atrasentan Hydrochloride|Xinlay","The orally available hydrochloride salt of pyrrolidine-3-carboxylic acid with potential antineoplastic activity.  As a selective antagonist of the endothelin-A (ETA) receptor, atrasentan binds selectively to the ETA receptor, which may result in inhibition of endothelin-induced angiogenesis and tumor cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C121544","Attenuated Chimpanzee Adenovirus 5T4 Vaccine","Attenuated Chimpanzee Adenovirus 5T4 Vaccine|ChAdOx.5T4 Vaccine|ChAdOx1.5T4 Vaccine","A cancer vaccine comprised of a recombinant, attenuated, replication-defective simian adenovirus vector (ChAdOx1) encoding the human 5T4 fetal oncoprotein (ChAdOx1.5T4), with potential immuno-activating and antineoplastic activities. Upon administration of the recombinant attenuated chimpanzee adenovirus 5T4 vaccine, the viral vector expresses 5T4 and stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing 5T4, which results in tumor cell lysis. 5T4, a transmembrane glycoprotein, is overexpressed by a variety of cancer cell types; its expression is correlated with increased invasiveness.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C780","Attenuated Corynebacterium Parvum","Attenuated Corynebacterium Parvum|C. parvum|CPAR|Coparvax|Corynebacterium parvum, Burroughs|Corynebacterium parvum, Merieux|Corynebacterium parvum|Propionibacterium acnes|Therapeutic Corynebacterium Parvum","A heat-inactivated preparation of Corynebacterium parvum with immunoadjuvant properties. Therapeutic Corynebacterium parvum may stimulate host antitumor immune responses when added to cancer vaccines. (NCI04)","Bacterium|Pharmacologic Substance"]
["C62409","Attenuated Listeria monocytogenes CRS-100","Attenuated Listeria monocytogenes CRS-100|CRS-100","A live-attenuated strain of the Gram-positive bacterium Listeria monocytogenes (Lm) with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, attenuated Listeria monocytogenes CRS-100 may accumulate in and infect liver cells where it may activate a potent innate immune response and an adaptive immune response involving the by recruitment and activation of T lymphocytes. This agent may potentiate the immune response to vaccines against various liver neoplasms.","Bacterium"]
["C74595","Attenuated Live Listeria Encoding HPV 16 E7 Vaccine ADXS11-001","ADXS11-001 Vaccine|ADXS11-001|Attenuated Live Listeria Encoding HPV 16 E7 Vaccine ADXS11-001|Attenuated Live Listeria Encoding HPV 16 E7 Vaccine|Attenuated Live Listeria Encoding Human Papilloma Virus 16 E7 Vaccine|Lm-LLO-E7|Lovaxin-C","A cancer vaccine containing a live-attenuated strain of the bacterium Listeria monocytogenes (Lm) encoding human papillomavirus (HPV) type 16 E7 fused to a non-hemolytic listeriolysin O protein with potential immunostimulatory and antineoplastic activities. Upon vaccination, Listeria expresses the HPV 16 E7 antigen and activates the immune system to mount a cytotoxic T-lymphocyte (CTL) response against cancer cells expressing HPV 16 E7. This may result in tumor cell lysis. In addition, the Listeria vector itself may induce a potent immune response. HPV 16 E7, a cell surface glycoprotein and tumor associated antigen, is overexpressed in the majority of cervical cancer cells.","Pharmacologic Substance"]
["C65242","Auranofin","AURANOFIN|Auranofin|Ridaura","An orally available, lipophilic, organogold compound, used to treat rheumatoid arthritis, with anti-inflammatory and potential antineoplastic activities. Auranofin interacts with selenocysteine residue within the redox-active domain of mitochondrial thioredoxin reductase (TrxR), thereby blocking the activity of TrxR. As a result, this agent induces mitochondrial oxidative stress leading to the induction of apoptosis. Furthermore, this agent strongly inhibits the JAK1/STAT3 signal transduction pathway, thereby suppressing expression of immune factors involved in inflammation. TrxR, overexpressed in many cancer cell types, inhibits apoptosis, promotes cell growth and survival and plays a role in resistance to chemotherapy; TrxR catalyzes the reduction of oxidized thioredoxin (Trx) and plays a central role in regulating cellular redox homeostasis.","Pharmacologic Substance"]
["C90585","Aurora A Kinase Inhibitor MK5108","Aurora A Kinase Inhibitor MK5108|MK5108","An orally bioavailable, highly selective small molecule inhibitor of the serine/threonine protein kinase Aurora A, with potential antimitotic and antineoplastic activity. Aurora A kinase inhibitor MK5108 binds to and inhibits Aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and eventually inhibition of cell division, proliferation and an induction of apoptosis in cells overexpressing Aurora A kinase. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis, and is thought to regulate spindle assembly. Aurora kinases are overexpressed in a wide variety of cancers.","Pharmacologic Substance"]
["C116068","Aurora A Kinase Inhibitor TAS-119","Aurora A Kinase Inhibitor TAS-119|TAS-119|TAS-2104","An orally bioavailable inhibitor of the serine/threonine protein kinase aurora A, with potential antimitotic and antineoplastic activities. Upon intravenous administration, aurora A kinase inhibitor TAS-119 binds to and inhibits aurora A kinase, which may result in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, inhibition of cell division and the induction of apoptosis in cells overexpressing aurora A kinase. Aurora A kinase localizes to the spindle poles and to spindle microtubules during mitosis; it plays an essential role in the regulation of spindle assembly. Aurora kinase A is overexpressed in a wide variety of cancers.","Pharmacologic Substance"]
["C78190","Aurora A Kinase/Tyrosine Kinase Inhibitor ENMD-2076","Aurora A Kinase/Tyrosine Kinase Inhibitor ENMD-2076|ENMD-2076","An orally bioavailable synthetic small molecule with potential antiangiogenic and antineoplastic activities. Aurora A kinase/tyrosine kinase inhibitor ENMD-2076 selectively binds to and inhibits non-specified tyrosine kinases and Aurora kinases (AKs). The inhibition of AKs may result in the inhibition of cell division and proliferation and may induce apoptosis in tumor cells that overexpress AKs; antiangiogenic activity is related to the inhibition of angiogenic tyrosine kinases. AKs are serine-threonine kinases that play an essential role in mitotic checkpoint control during mitosis and are important regulators of cell division and proliferation.","Organic Chemical|Pharmacologic Substance"]
["C82674","Aurora B Serine/Threonine Kinase Inhibitor TAK-901","Aurora B Serine/Threonine Kinase Inhibitor TAK-901|TAK-901","A small-molecule inhibitor of the serine-threonine kinase Aurora B with potential antineoplastic activity. Aurora B kinase inhibitor TAK-901 binds to and inhibits the activity of Aurora B, which may result in a decrease in the proliferation of tumor cells that overexpress Aurora B. Aurora B is a positive regulator of mitosis that functions in the attachment of the mitotic spindle to the centromere; the segregation of sister chromatids to each daughter cell; and the separation of daughter cells during cytokinesis. This serine/threonine kinase may be amplified and overexpressed by a variety of cancer cell types.","Pharmacologic Substance"]
["C91081","Aurora B/C Kinase Inhibitor GSK1070916A","Aurora B/C Kinase Inhibitor GSK1070916A|GSK1070916A","An ATP-competitive inhibitor of the serine/threonine kinases Aurora B and C with potential antineoplastic activity. Aurora B/C kinase inhibitor GSK1070916A binds to and inhibits the activity of Aurora B and C, which may result in inhibition of cellular division and a decrease in the proliferation of tumor cells that overexpress the Aurora kinases B and C. Aurora kinases play essential roles in mitotic checkpoint control during mitosis, and are overexpressed by a wide variety of cancer cell types.","Pharmacologic Substance"]
["C82349","Aurora Kinase Inhibitor AMG 900","AMG 900|Aurora Kinase Inhibitor AMG 900","A small-molecule inhibitor of Aurora kinases A, B and C with potential antineoplastic activity. Aurora kinase inhibitor AMG 900 selectively binds to and inhibits the activities of Aurora kinases A, B and C, which may result in inhibition of cellular division and proliferation in tumor cells that overexpress these kinases. Aurora kinases are serine-threonine kinases that play essential roles in mitotic checkpoint control during mitosis and are overexpressed by a wide variety of cancer cell types.","Pharmacologic Substance"]
["C74014","Aurora Kinase Inhibitor BI 811283","Aurora Kinase Inhibitor BI 811283|BI 811283","A small molecule inhibitor of the serine/threonine protein kinase Aurora kinase with potential antineoplastic activity. Aurora kinase inhibitor BI 811283 binds to and inhibits Aurora kinases, resulting in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cell proliferation.","Pharmacologic Substance"]
["C61075","Aurora Kinase Inhibitor MLN8054","Aurora Kinase Inhibitor MLN8054","An orally bioavailable, highly selective small molecule inhibitor of the serine/threonine protein kinase Aurora A kinase with potential antineoplastic activity. Auora kinase inhibitor MLN8054 binds to and inhibits Aurora kinase A, resulting in disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cell proliferation. Aurora A localizes in mitosis to the spindle poles and to spindle microtubules and is thought to regulate spindle assembly. Aberrant expression of Aurora kinases occurs in a wide variety of cancers, including colon and breast cancers.","Chemical Viewed Functionally"]
["C66946","Aurora Kinase Inhibitor PF-03814735","Aurora Kinase Inhibitor PF-03814735|PF-03814735","An aurora kinase inhibitor with potential antineoplastic activity. PF-03814735 binds to and inhibits aurora kinases, serine-threonine kinases that play essential roles in mitotic checkpoint control during mitosis. Inhibition of aurora kinases may result in an inhibition of cellular division and proliferation in tumor cells that overexpress aurora kinases.","Pharmacologic Substance"]
["C70655","Aurora Kinase Inhibitor SNS-314","Aurora Kinase Inhibitor SNS-314|SNS-314","A synthetic small molecule Aurora kinase (AK) inhibitor with potential antineoplastic activity. Aurora kinase inhibitor SNS-314 selectively binds to and inhibits AKs A and B, which may result in the inhibition of cellular division and proliferation in tumor cells that overexpress AKs. AKs are serine-threonine kinases that play essential roles in mitotic checkpoint control during mitosis.","Pharmacologic Substance"]
["C84846","Aurora Kinase Inhibitor TTP607","Aurora Kinase Inhibitor TTP607|TTP607","A small-molecule pan-Aurora kinase inhibitor with potential antineoplastic activity. Aurora kinase inhibitor TTP607 selectively binds to and inhibits Aurora kinases A, B and C, which may result in the disruption of the assembly of the mitotic spindle apparatus, disruption of chromosome segregation, and inhibition of cellular division and proliferation in Aurora kinase-overexpressing tumor cells. Aurora kinases A, B and C, are serine/threonine kinases that play essential roles in mitotic checkpoint control and are overexpressed by a wide variety of tumor cell types.","Pharmacologic Substance"]
["C70983","Aurora Kinase/VEGFR2 Inhibitor CYC116","Aurora Kinase/VEGFR2 Inhibitor CYC116|CYC116","An orally bioavailable small molecule multi-kinase inhibitor with antineoplastic activity. Aurora kinase/VEGFR 2 inhibitor CYC116 inhibits Aurora kinases A and B and vascular endothelial growth factor receptor 2 (VEGFR2), resulting in disruption of the cell cycle, rapid cell death, and the inhibition of angiogenesis. Aurora kinases are serine/threonine protein kinases that are only expressed in actively dividing cells and are critical in division or mitosis. VEGFR2 is a receptor tyrosine kinase that appears to account for most of the mitogenic and chemotactic effects of vascular endothelial growth factor (VEGF) on adult endothelial cells.","Pharmacologic Substance"]
["C68842","Autologous Ad-CD154-Transduced CLL B Cells","Autologous Ad-CD154-Transduced CLL B Cells|L-Vax","An autologous tumor cell vaccine containing chronic lymphocytic leukemia (CLL) B cells transduced with an adenoviral vector carrying chimeric CD154 (ad-CD154) with potential antineoplastic activity. Administration of autologous ad-CD154 transduced CLL B cells may result in increases in the numbers of leukemia-specific CD4+ T cells and high serum-levels of IL-12 and IFN-gamma. Due to ligation of CD154 to CD40 on CLL cells, this agent may induce CLL cells to express the proapoptotic molecule BID and death receptors CD95 (Fas) and DR5, rendering CLL B cells first resistant and then sensitive to Fas-mediated apoptosis. In addition, autologous ad-CD154 transduced CLL B cells may induce MHC class I-dependent cytotoxic T lymphocyte (CTL) responses against autologous leukemia cells. CD154 is a type II membrane glycoprotein and ligand for CD40; both molecules are important in cognate co-stimulatory cell-cell interactions.","Immunologic Factor"]
["C125101","Autologous Anti-CD123 CAR TCR/4-1BB-expressing T-lymphocytes","Anti-CD123 CAR mRNA-electroporated Autologous T-lymphocytes|Autologous Anti-CD123 CAR TCR/4-1BB-expressing T Lymphocytes|Autologous Anti-CD123 CAR TCR/4-1BB-expressing T-lymphocytes|Autologous RNA CART123 Cells|RNA Anti-CD123 CAR T Cells|RNA CART123 Cells","Autologous, genetically engineered T-lymphocytes that have been electroporated with a messenger RNA (mRNA) encoding a chimeric antigen receptor (CAR) consisting of an anti-human interleukin-3 receptor alpha chain (IL3RA; CD123) single chain variable fragment (scFv) coupled to the co-stimulatory signaling domains of 4-1BB (CD137) and the zeta chain of the T-cell receptor (TCR) CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities.  Upon transfusion, the mRNA-electroporated autologous anti-CD123 CAR TCR/4-1BB expressing T-lymphocytes attach to cancer cells expressing CD123. This induces selective toxicity in and causes lysis of CD123-expressing tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances T-cell activation and signaling after recognition of CD123. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with both increased leukemic cell proliferation and aggressiveness.","Cell|Pharmacologic Substance"]
["C125691","Autologous Anti-CD19 CAR-expressing T Lymphocytes","Autologous Anti-CD19 CAR-expressing T Lymphocytes|Autologous Anti-CD19-CAR T Cells","A preparation of autologous T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) that targets the human tumor associated antigen (TAA) CD19, with potential immunostimulating and antineoplastic activities. Upon administration, autologous anti-CD19 CAR-expressing T lymphocytes bind to and induce selective toxicity against CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.","Cell|Pharmacologic Substance"]
["C126639","Autologous Anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ Central Memory T-lymphocytes JCAR014","Autologous Anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ CM T-lymphocytes JCAR014|Autologous Anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ Central Memory T-lymphocytes JCAR014|JCAR014","A defined preparation of CD4+ and CD8+ central memory (CM) autologous T-lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) containing an anti-CD19 single chain variable fragment (scFv) fused to the signaling domains of CD28, 4-1BB (CD137), the zeta chain of the TCR/CD3 complex (CD3-zeta), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+CM T-lymphocytes JCAR014 are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T-cells and can promote elimination of those cells through a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response. The 4-1BB costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity.","Cell|Pharmacologic Substance"]
["C125192","Autologous Anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ T-lymphocytes JCAR017","Anti-CD19-CAR Genetically Engineered Autologous T Lymphocytes JCAR017|Anti-CD19-CAR Genetically Engineered Autologous T-lymphocytes JCAR017|Autologous Anti-CD19-EGFRt-4-1BB-zeta-modified CAR CD8+ and CD4+ T-lymphocytes JCAR017|Autologous Anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ T-lymphocytes JCAR017|JCAR017","A preparation of a defined ratio of CD4+ and CD8+ autologous T-lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) containing an anti-CD19 single chain variable fragment (scFv) fused to the signaling domain of 4-1BB (CD137), the zeta chain of the TCR/CD3 complex (CD3-zeta), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing CD4+/CD8+ T-lymphocytes JCAR017 are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T-cells and can promote elimination of those cells through a cetuximab-induced antibody dependent cellular cytotoxicity (ADCC) response. The 4-1BB costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity.","Cell|Pharmacologic Substance"]
["C116914","Autologous Anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing T Lymphocytes","Autologous Anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing T Lymphocytes","A preparation of genetically modified CD8+ central memory (Tcm) and CD4+ autologous T-lymphocytes (1:1) transduced with a replication incompetent, self-inactivating (SIN) lentiviral vector expressing a chimeric antigen receptor (CAR) containing an anti-CD19 single chain variable fragment (scFv) derived from the murine IgG1 monoclonal antibody (mAb) FMC63, fused to the signaling domain of 4-1BB (CD137), the zeta chain of the TCR/CD3 complex (CD3-zeta), and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous anti-CD19CAR-4-1BB-CD3zeta-EGFRt-expressing T lymphocytes are directed to and induce selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Devoid of both ligand binding domains and tyrosine kinase activity, the expressed EGFRt both facilitates in vivo detection of the administered, transduced T-cells and can promote elimination of those cells through a cetuximab-induced antibody dependent cellular cytotoxicity response. The 4-1BB costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity.","Pharmacologic Substance"]
["C71748","Autologous Anti-gp100:154-162 T-Cell Receptor Gene-Engineered Peripheral Blood Lymphocytes","Anti-p53 TCR-Transduced PBL|Autologous Anti-gp100:154-162 T-Cell Receptor Gene-Engineered Peripheral Blood Lymphocytes|Autologous Anti-gp100:154-162 TCR Gene-Engineered PBL","Human autologous peripheral blood lymphocytes (PBLs) transduced with a glycoprotein 100 (gp100) epitope-determined T cell receptor (TCR) gene, with potential antineoplastic activity. PBLs are isolated from a melanoma patient and pulsed with a viral vector encoding the TCR specific for amino acid residues 154-162 of gp100 (KTWGQYWQV). After expansion ex vivo, the transduced autologous PBLs, expressing this specific TCR, are reintroduced into the patient and bind to melanoma cells expressing the gp100 protein, which may result in specific cytotoxic T-lymphocyte (CTL) killing of gp100-expressing melanoma cells. gp100 is a melanocyte lineage-specific antigen overexpressed in melanomas.","Cell|Pharmacologic Substance"]
["C38587","Autologous Anti-MART-1 F5 T-Cell Receptor Gene-Engineered Peripheral Blood Lymphocytes","Anti-MART-1 TCR Retroviral Vector-Transduced Autologous PBL|Autologous Anti-MART-1 F5 T-Cell Receptor Gene-Engineered Peripheral Blood Lymphocytes|MSGV1AIB (Anti-MART-1 TCR) Retroviral Vector-Transduced Autologous PBL","Human autologous peripheral blood lymphocytes (PBLs) transduced with a melanoma antigen MART-1 epitope-determined T cell receptor (TCR) gene, with potential antineoplastic activity. PBLs are isolated from a melanoma patient and pulsed with a viral vector that encodes the TCR specific for an epitope of MART-1 (F5 TCR). After expansion ex vivo, the transduced autologous PBLs, expressing this specific TCR, are reintroduced into the patient, and bind to melanoma cells expressing the MART-1 antigen, which may result in specific cytotoxic T-lymphocyte (CTL) killing of MART-1-expressing melanoma cells. MART-1 (melanoma antigen recognized by T cells 1), also known as Melan-A, is a melanocyte lineage-specific transmembrane protein.","Cell|Pharmacologic Substance"]
["C78197","Autologous Anti-PSMA Gene-Modified T-Lymphocytes","Autologous Anti-PSMA Gene-Modified T-Lymphocytes|Autologous Anti-Prostate-Specific Membrane Antigen Gene-Modified T-Cells","Autologous prostate specific membrane antigen (PSMA) gene-modified T lymphocytes with potential antineoplastic activity. Human autologous T-lymphocytes are isolated and transduced ex vivo with a retrovirus encoding a chimeric immune receptor (CIR) consisting of an antibody fragment against PSMA fused with signaling domains of the T cell. Upon reintroduction into the patient, autologous anti-PSMA gene-modified T-cells bind to PSMA-expressing prostate cancer cells, which may result in specific cytotoxic T-lymphocyte (CTL) tumor cell killing.","Cell|Pharmacologic Substance"]
["C129522","Autologous Bladder Cell Carcinoma RNAs/CD40L RNA Electroporated Autologous Matured Dendritic Cells","); Bladder Cell Carcinoma RNAs/CD40L RNA-transfected Autologous Dendritic Cells|AGS-003-BLD|Autologous Bladder Cell Carcinoma RNAs/CD40L RNA Electroporated Autologous Matured Dendritic Cells|Autologous DCs Electroporated with Autologous Tumor-derived IVT RNAs/CD40L IVT RNA|Autologous DCs Electroporated with Autologous Tumor-derived RNAs/CD40L RNA","A cell-based preparation in which autologous, mature dendritic cells (DCs) are electroporated with in vitro transcribed (IVT) RNAs encoding for a synthetic form of T-cell protein CD40 ligand (CD40L) and IVT RNA encoding for autologous tumor-associated antigens (TAAs) derived from patient-specific bladder cell carcinoma (BCC) cells, with potential immunostimulatory and antineoplastic activities. Upon electroporation into autologous DCs, the RNA is translated and processed. BCC-specific antigenic peptides are subsequently presented via major histocompatibility complex (MHC) Class I molecules on the DCs surface. When AGS-003-BLD is reintroduced to the patient, the MHC-presented peptides interact with and activate CD8-positive T-cells, which elicits a highly specific cytotoxic T-cell (CTL) response against tumor cells expressing the patient-specific BCC TAAs. The signal cascade initiated by expression of the co-stimulatory molecule CD40L results in the secretion of the inflammatory cytokine IL-12, which further stimulates CTLs.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C103865","Autologous Bone Marrow-derived CD34/CXCR4-positive Stem Cells AMR-001","AMR-001|Autologous Bone Marrow-derived CD34/CXCR4-positive Stem Cells AMR-001","A cell-based product containing autologous bone marrow derived CD34 positive and C-X-C chemokine receptor type 4 (CXCR4) positive stem cells with potential antiapoptotic and proangiogenic activities. Upon intracoronary infusion after a myocardial infarction (MI), autologous bone marrow-derived CD34/CXCR4-positive stem cells may preserve cardiac muscle cells and prevent apoptosis; thus improving myocardial perfusion. CD34/CXCR4-positive stem cells are naturally mobilized upon cell injury through signaling by hypoxia inducing factor (HIF), which is secreted in response to hypoxia. In turn, HIF induces the synthesis of stromal-derived factor 1 (SDF-1) and vascular endothelial growth factor (VEGF) which mobilize CD34/CXCR4 positive stem cells; CXCR4 is the receptor for stromal-derived factor 1 (SDF-1).","Pharmacologic Substance"]
["C116329","Autologous CD123CAR-CD28-CD3zeta-EGFRt-expressing T Lymphocytes","Anti CD123-CAR/CD28-costimulatory Lentiviral Vector-transduced Autologous T Lymphocytes|Autologous CD123CAR-CD28-CD3zeta-EGFRt-expressing T Lymphocytes|CD123R(EQ)28zeta/EGFRt+ T Cells","A preparation of genetically modified autologous T-cells transduced with a replication incompetent, self-inactivating lentiviral vector expressing a hinge-optimized, chimeric antigen receptor (CAR), containing a CD28 co-stimulatory signaling domain fused to CD3 zeta, the single-chain variable fragment of CD123 (Interleukin-3 receptor alpha chain or IL3RA) antigen, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous CD123CAR-CD28-CD3zeta-EGFRt-expressing T Lymphocytes are directed to and induce selective toxicity in CD123-expressing tumor cells. CD123 is normally expressed on committed blood progenitor cells in the bone marrow; its overexpression is associated with increased leukemic cell proliferation and aggressiveness. Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates detection of the administered T-cells in vivo and can promote elimination of those cells following a cetuximab-induced antibody-dependent cellular cytotoxicity response. The costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity. Hinge optimization prevents recognition of the CAR by Fc receptors (FcRs).","Pharmacologic Substance"]
["C85445","Autologous CD133-Positive BTSC mRNA-Pulsed Autologous Dendritic Cell Vaccine","Autologous CD133-Positive BTSC mRNA-Pulsed Autologous Dendritic Cell Vaccine|Autologous CD133-Positive Brain Tumor Stem Cell mRNA-Pulsed Autologous Dendritic Cell Vaccine","A cancer vaccine consisting of autologous dendritic cells (DCs) loaded with CD133-positive autologous brain tumor stem cells (BTSCs) -derived mRNA with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, autologous CD133-positive BTSC mRNA-pulsed autologous dendritic cell vaccine may elicit a cytotoxic T-lymphocyte (CTL) response against the CD133-positive BTSCs from which the autologous tumor mRNA is derived. CD133, a tumor-associated antigen (TAA) and neural stem cell marker, has been found on a specific subset of glioblastoma multiforme (GBM) stem cells; its presence has been correlated with resistance to conventional chemotherapy and radiotherapy.","Cell|Pharmacologic Substance"]
["C119746","Autologous CD171-specific CAR-CD28 zeta-4-1-BB-EGFRt-expressing T Lymphocytes","Autologous CD171-specific CAR-CD28 zeta-4-1-BB-EGFRt-expressing T Lymphocytes|CD171 CAR+ T Cells|CE7R CAR T Cells","A preparation of genetically modified autologous human T-lymphocytes transduced with a lentiviral vector expressing a chimeric antigen receptor (CAR) specific for the L1 cell adhesion molecule (L1-CAM/CD171) antigen, and the co-stimulatory signaling domains CD28, 4-1BB (CD137) and CD3 zeta, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon re-infusion into the patient, the autologous L1-CAM-specific CAR-CD28 zeta-4-1-BB-EGFRt-expressing T-lymphocytes are directed to and induce selective toxicity in L1-CAM-expressing tumor cells. L1-CAM, a neuronal cell adhesion molecule and member of the L1 protein family, plays a key role in the development of the nervous system; it is overexpressed in various tumor cell types and is associated with increased chemoresistance, tumor progression, migration and metastasis. Devoid of both ligand-binding domains and tyrosine kinase activity, EGFRt facilitates both the detection of the administered T-cells in vivo and the elimination of the modified T-cells following a cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) response. The co-stimulatory signaling domains enhance both proliferation of T-cells and antitumor activity.","Cell|Pharmacologic Substance"]
["C106247","Autologous CD19-28z Chimeric Antigen Receptor-expressing T-lymphocytes","Autologous CD19-28z Chimeric Antigen Receptor-expressing T-lymphocytes|CAR 19-28z T Cells","Genetically modified autologous T-lymphocytes transduced with a replication incompetent retroviral vector expressing a chimeric T cell antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment), fused to the extracellular, transmembrane and intracellular signaling domains of the T cell co-stimulatory receptor CD28 and the cytoplasmic signaling domain of the zeta chain of the TCR/CD3 complex (CD3-zeta) (CAR19-28z), with potential antineoplastic activities. Upon intravenous administration, autologous CD19-28z CAR-expressing T-lymphocytes are directed to CD19-expressing tumor cells, which induces selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The CD28 co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. The inclusion of the CD28 signaling domain may increase proliferation of T-cells and antitumor activity compared to the inclusion of the CD3-zeta chain alone.","Cell|Pharmacologic Substance"]
["C105614","Autologous CD19CAR-CD28-CD3zeta-EGFRt-expressing Tcm-enriched T Cells","Autologous CD19CAR-CD28-CD3zeta-EGFRt-expressing Tcm-enriched T Cells|CD19R:CD28:lentiviral/EGFRt+ T Cells","A preparation of genetically modified autologous central memory (Tcm) enriched T-cells transduced with a replication incompetent lentiviral vector expressing a chimeric antigen receptor (CAR), containing a CD28 signaling domain fused to both CD3 zeta, which targets the CD19 antigen, and a truncated form of the human epidermal growth factor receptor (EGFRt), with potential immunostimulating and antineoplastic activities. Upon intravenous administration, autologous CD19CAR-CD28-CD3zeta-EGFRt-expressing Tcm-enriched T cells are directed to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.  Devoid of both ligand binding domains and tyrosine kinase activity, EGFRt both facilitates in vivo detection of the administered T-cells and can promote elimination of those cells upon a cetuximab-induced antibody dependent cellular cytotoxicity response. The costimulatory signaling domain enhances proliferation of T cells and antitumor activity.","Pharmacologic Substance"]
["C95715","Autologous CD8 Positive PBL Sensitized to Drosophila Cell-Presented Melanoma Peptides","Autologous CD8 Positive PBL Sensitized to Drosophila Cell-Presented Melanoma Peptides|Autologous CD8+ PBL Sensitized To Drosophila Cell-Presented Melanoma Peptides","A preparation of autologous CD8+ (cytotoxic) human peripheral blood lymphocytes (PBLs) sensitized to Drosophila cell-presented melanoma peptides, with potential immunostimulating and antineoplastic activities. Autologous CD8+ T-lymphocytes, isolated from a melanoma patient, are exposed in vitro to melanoma peptide-pulsed HLA-A2-expressing Drosophila cells, expanded, and reintroduced into the patient; these tumor-reactive T-cells may stimulate a host immune response against tumor cells expressing the melanoma antigens, resulting in tumor cell lysis. Drosophila cells, which do not express any native MHC molecules, have been shown to potently stimulate tumor-reactivity in vitro from human peripheral blood lymphocytes (PBL) when stably transfected with human MHC molecules and appropriate adhesion and costimulatory molecules.","Cell|Pharmacologic Substance"]
["C116072","Autologous CD8+ Melanoma Specific T Cells","Autologous CD8+ Melanoma Specific T Cells|Autologous Melanoma Specific Cytotoxic T Lymphocytes","Autologous CD8 T-lymphocytes against melanoma-associated antigens, with potential immunomodulating and antineoplastic activities. Following leukapheresis and the ex vivo expansion of cytotoxic T-lymphocytes, the autologous CD8+ melanoma specific T-cells are re-introduced into the melanoma patient. These cytotoxic T-cells recognize and kill the patient's own melanoma cells.","Cell|Pharmacologic Substance"]
["C123822","Autologous CEA-specific Cytotoxic T-lymphocytes","Autologous CEA-specific Cytotoxic T-lymphocytes|CEA-specific AAV-DC-CTLs|CEA-specific CTLs","Autologous cytotoxic T-lymphocytes (CTLs) specifically reactive to the tumor-associated antigen (TAA) human carcinoembryonic antigen (CEA), with potential antineoplastic activity. Dendritic cells (DCs) isolated from the patient's blood are infected with recombinant adeno-associated virus (AAV) expressing the CEA gene. Exposure of T-lymphocytes to DCs creates CEA-specific CTLs which are expanded. Upon reintroduction of these CTLs into the patient, these cells recognize and kill CEA-expressing tumor cells. CEA, a tumor-associated antigen and a member of the CEA family of proteins, plays a key role in cell migration, cell invasion, and cell adhesion and is overexpressed by a variety of cancer types.","Cell|Pharmacologic Substance"]
["C1984","Autologous Colon Cancer Cell Vaccine","Autologous Colon Cancer Cell Vaccine|OncoVAX","A personalized, proprietary cancer vaccine composed of sterile, irradiated, non-dividing, live colon cancer cells obtained from an individual after tumor resection, with potential immunoactivating and antineoplastic activities. Upon intradermal administration, the autologous colon cancer cell vaccine activates the immune system and elicits a cytotoxic T-lymphocytic (CTL) response against the residual colon cancer cells, which results in tumor cell death. This may prevent cancer recurrence. According to the vaccination schedule, the first two out of the four doses are co-administered with the immunoadjuvant bacillus Calmette-Guerin (BCG), which is an attenuated strain of Mycobacterium bovis that non-specifically enhances the immune response.","Immunologic Factor|Pharmacologic Substance"]
["C123918","Autologous Colorectal Tumor Antigen-pulsed Dendritic Cell Vaccine","APDC Vaccine|Autologous Colorectal Tumor Antigen-pulsed DC Vaccine|Autologous Colorectal Tumor Antigen-pulsed Dendritic Cell Vaccine","A dendritic cell (DC)-based cancer vaccine composed of autologous DCs pulsed with tumor cell lysates from a colorectal cancer patient containing tumor-associated antigens (TAAs), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous colorectal tumor antigen-pulsed DC vaccine exposes the immune system to colorectal tumor cell antigens, which may result in cytotoxic T-lymphocyte (CTL)-mediated immune responses against the colorectal cancer cells. This leads to cancer cell lysis. The tumor cell lysate contains a range of antigens that are essential for the neoplastic growth and survival of the cancer cells.","Cell|Pharmacologic Substance"]
["C113174","Autologous CT7/MAGE-A3/WT1 mRNA-Electroporated Langerhans-Type Dendritic Cells","Autologous CT7/MAGE-A3/WT1 mRNA-Electroporated Langerhans-Type Dendritic Cells|CT7/MAGE-A3/WT1 mRNA-Electroporated LCs","An autologous tumor cell vaccine containing CD34+ hematopoietic progenitor cell (HPC)-derived Langerhans-type dendritic cells (LCs) electroporated with mRNA encoding the full-length cancer-testis antigens, CT7 and melanoma-associated antigen 3 (MAGE-A3), and the self-differentiation tumor antigen, Wilms tumor 1 (WT1) with potential immunomodulating and antineoplastic activity. The autologous CT7/MAGE-A3/WT1 mRNA-electroporated Langerhans-type dendritic cells are prepared by drawing a blood sample containing the CD34+ HPCs from a cancer patient. The CD34+ HPCs are treated with a combination of cytokines which specifically support LC development, and the LC population is enriched and expanded ex vivo. The cultured LCs are allowed to mature for one day and then electroporated separately with CT7, MAGE-A3 or WT1 mRNA before final maturation. Upon intradermal administration into the patient, the mature LCs may activate cell-mediated immunity and induce both cytotoxic CD8+ T cells and CD4+ helper T cells against cancer cells expressing CT7, MAGE-A3 and WT1 tumor antigens. This may result in the immune-mediated inhibition of tumor cell proliferation, leading to tumor cell death. CT7 and MAGE-A3 are tumor-specific proteins overexpressed in a number of cancers but not in healthy tissues other than testis and placenta. WT1 is a transcription factor important in development and cancer pathogenesis, which is overexpressed in a variety of cancers, including multiple myeloma, leukemia, ovarian cancer, malignant mesothelioma, neural tumors and renal carcinoma.","Cell|Pharmacologic Substance"]
["C111996","Autologous Cultured Acute Myeloid Leukemia-specific Cytotoxic T Lymphocytes","Autologous AML-reactive Cultured CTL|Autologous AML-specific CTLs|Autologous Cultured Acute Myeloid Leukemia-specific Cytotoxic T Lymphocytes","A preparation of cytotoxic, autologous acute myelogenous leukemia (AML)-reactive T lymphocytes (CTL), with potential immunomodulating and antineoplastic activities. The autologous cultured AML-specific CTLs are prepared using a specific AML-CTL culture method. Autologous peripheral blood lymphocytes are taken from an AML patient and the autologous AML blasts are treated with granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4), both of which promote ex vivo differentiation of AML blasts into dendritic cells (DCs). In the same culture, T cells are treated and activated by low-dose interleukin 2 (IL-2), and expanded using anti-CD3. This results in cultured AML-reactive CTLs which are administered back into the patient after autologous hematopoietic stem cell transplant (AHSCT). The autologous cultured AML-specific CTLs may eradicate residual AML cells.","Cell|Pharmacologic Substance"]
["C124997","Autologous Cytotoxic T-lymphocytes Induced with MUC1 Gene-transfected Dendritic Cells","Autologous Cytotoxic T-lymphocytes Induced with MUC1 Gene-transfected Dendritic Cells|MUC1-DC-CTL|MUC1-Gene-DC-CTL","A preparation of autologous cytotoxic T-lymphocytes (CTL), specifically reactive to the tumor-associated antigen (TAA) mucin-1 (MUC1), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are collected from the patient with MUC1-positive tumors and are exposed ex vivo to dendritic cells (DCs) transfected with a replication-deficient adenovirus encoding MUC1 to generate MUC1-specific CTLs, which are subsequently expanded in vitro. Upon re-infusion of autologous CTLs induced with MUC1 gene-transfected DCs to the patient, the CTLs target and lyse the MUC1-expressing tumor cells. This inhibits tumor cell proliferation. MUC1 is expressed by a variety of tumor cell types.","Cell|Pharmacologic Substance"]
["C124998","Autologous Cytotoxic T-lymphocytes Induced with MUC1 Peptide-pulsed Dendritic Cells","Autologous Cytotoxic T-lymphocytes Induced with MUC1 Peptide-pulsed Dendritic Cells|MUC1-Peptide-DC-CTL","A preparation of autologous cytotoxic T-lymphocytes (CTL), specifically reactive to the tumor-associated antigen (TAA) mucin-1 (MUC1), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are collected from the patient with MUC1-positive tumors and are exposed ex vivo to dendritic cells (DCs) that are pulsed with a MUC1 peptide to generate MUC1-specific CTLs, which are subsequently expanded in vitro. Upon re-infusion of autologous CTLs induced with MUC1 peptide-pulsed DCs to the patient, the CTLs target and lyse the MUC1-expressing tumor cells. This inhibits tumor cell proliferation. MUC1 is expressed by a variety of tumor cell types.","Cell|Pharmacologic Substance"]
["C121856","Autologous Dendritic Cell Vaccine ACT2001","ACT2001|Autologous DC Vaccine ACT2001|Autologous Dendritic Cell Vaccine ACT2001","A cell-based cancer vaccine composed of autologous, immature dendritic cells (DCs), with potential immunostimulating and antineoplastic activities. Upon leukapheresis, immature DCs are isolated and re-administered intra-tumorally. The immature DCs internalize and process the tumor-associated antigens (TAAs), migrate to the lymphatic system, and then expose the immune system to the TAAs. This induces a specific cytotoxic T-lymphocyte (CTL) response against the cancer cells leading to tumor cell lysis.","Immunologic Factor|Pharmacologic Substance"]
["C74015","Autologous Dendritic Cell-Adenovirus CCL21 Vaccine","Autologous Dendritic Cell-Adenovirus CCL21 Vaccine","A cancer vaccine comprised of autologous dendritic cells (DCs) that have been transduced ex vivo with an adenoviral vector containing the CCL21 gene with potential immunostimulatory and antineoplastic activities. Upon intratumoral administration, autologous dendritic cell-adenovirus CCL21 vaccine expresses the chemokine CCL21, which may induce an antitumoral cytotoxic immune response in the tumor microenvironment. CCL21 [chemokine (C-C motif) ligand 21] has been shown to attract antigen presenting cells (APCs), like leukocytes and DCs, and natural killer (NK) cells and their T-cell effectors to induce a cytotoxic immune response.","Pharmacologic Substance"]
["C26445","Autologous Dendritic Cell-Adenovirus P53 Vaccine","Autologous Dendritic Cell-Adenovirus P53 Vaccine","An autologous vaccine composed of dendritic cells (DC) that have been transduced with a p53 tumor suppressor gene-modified virus. When the autologous dendritic cell-adenovirus p53 vaccine is administered, the host cytotoxic T lymphocytes (CTL) are directed against p53-positive tumor cells, which may result in tumor cell death and decreased tumor growth. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C48376","Autologous Dendritic Cell-Allogeneic Melanoma Tumor Cell Lysate Vaccine","Allogeneic Melanoma Cell-Loaded Dendritic Cell Vaccine|Autologous Dendritic Cell-Allogeneic Melanoma Tumor Cell Lysate Vaccine|IDD-3","A cell-based vaccine composed of autologous dendritic cells (DCs) pulsed with lysates from heat-treated allogeneic melanoma tumor cells. Upon administration, this vaccine may stimulate anti-tumoral cytotoxic T-cell and antibody responses to melanoma cells bearing shared melanoma antigens such as MelanA/MART-1, gp100, MAGE3, resulting in tumor cell lysis.","Pharmacologic Substance"]
["C61077","Autologous Dendritic Cell-Autologous Tumor mRNA-Human CD40L Vaccine","Autologous Dendritic Cell-Autologous Tumor mRNA-Human CD40L Vaccine","A cancer vaccine consisting of autologous dendritic cells transfected with autologous tumor mRNA and the human CD40 ligand (CD40L) gene with immunostimulatory and antitumor activities. Vaccination with autologous dendritic cell-autologous tumor mRNA-human CD40L vaccine may elicit a cytotoxic T cell response against tumor cells from which the autologous tumor mRNA was derived. When expressed by dendritic cells, tumor antigens and the co-stimulatory molecule CD40L, which binds to CD40 receptors on antigen presenting cells (APC), facilitate both humoral and cellular immune responses against tumor cells.","Pharmacologic Substance"]
["C123928","Autologous Dendritic Cell-based Immunotherapeutic AV0113","AV0113 DC-CIT|AV0113 Dendritic Cell Cancer Immunotherapeutic|AV0113|Autologous DC-based Immunotherapeutic AV0113|Autologous Dendritic Cell-based Immunotherapeutic AV0113","A therapeutic interleukin-12 (IL-12)-expressing dendritic cell (DC)-based vaccine composed of autologous monocyte-derived DCs loaded with autologous tumor cell lysate and exposed to the microbial cell wall component lipopolysaccharide (LPS), with potential immunomodulating and antineoplastic activities. The monocyte-derived immature DCs are loaded with autologous tumor cell lysates and are subsequently exposed to LPS and interferon-gamma (IFN-gamma). Upon administration of autologous DC-based immunotherapeutic AV0113, the mature DCs migrate into the lymph nodes, express the immune stimulatory cytokine interleukin-12 (IL-12) and activate the immune system by promoting the activation of natural killer (NK) cells and induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, which may result in immune-mediated tumor cell death and inhibition of tumor cell proliferation. Exposure to LPS and IFN-gamma allows the maturation of DCs and optimizes the presentation of tumor-associated antigens (TAAs) by DCs to T-lymphocytes.","Cell|Pharmacologic Substance"]
["C74016","Autologous Dendritic Cell-Tumor Fusion Vaccine","Autologous Dendritic Cell-Tumor Fusion Vaccine","A therapeutic cancer vaccine consisting of autologous dendritic cells (DCs) fused with autologous tumor cells with potential immunostimulatory and antineoplastic activities. Autologous dendritic cell-tumor fusion vaccine is generated in vitro by mixing DCs and irradiated tumor cells harvested from individual patients and treating them with polyethylene glycol (PEG) to produce DC-tumor cell fusion hybrid cells. Upon administration, autologous dendritic cell-tumor fusion vaccine may elicit antitumor humoral and cellular immune responses.","Pharmacologic Substance"]
["C78193","Autologous Dinitrophenyl-Modified Ovarian Cancer Vaccine","Autologous Dinitrophenyl-Modified Ovarian Cancer Vaccine","A cancer vaccine consisting of autologous ovarian cancer cell peptide antigens conjugated to the hapten 2,4-dinitrophenol (DNP) with potential immunostimulating and antineoplastic activities. Administration of autologous dinitrophenyl-modified ovarian cancer vaccine may induce a cytotoxic T-lymphocyte (CTL) response against ovarian cancer cells. DNP conjugation may enhance the immunogenicity of weakly immunogenic antigens.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C78824","Autologous EBV-CTL CD19CAR zeta","Autologous EBV-CTL CD19CAR zeta","Autologous Epstein-Barr virus (EBV)-specific cytotoxic T-lymphocytes (CTL) that have been genetically modified to express a T-cell chimeric antigen receptor (CAR) targeting the CD19 antigen, with potential immunotherapeutic activity. The CAR consists of a single chain Fv of anti-CD19 IgG1 coupled with an intracellular signaling region of the zeta-chain of the TCR/CD3 complex (CD3 zeta). Autologous EBV-CTL CD19CAR zeta directs the T-lymphocytes to CD19-expressing tumor cells, stimulating a selective toxicity to tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.","Pharmacologic Substance"]
["C48377","Autologous EBV-Transformed B Lymphoblastoid-Tumor Fusion Cell Vaccine","Autologous EBV-Transformed B Lymphoblastoid-Tumor Fusion Cell Vaccine","A cell-based vaccine composed of autologous tumor cells fused with Epstein-Barr virus-transformed B-lymphoblastoid cells. Upon administration, this vaccine may stimulate a cytotoxic T cell response against tumor cells, resulting in tumor cell lysis. (NCI05)","Pharmacologic Substance"]
["C28842","Autologous Epstein-Barr Virus-Specific Cytotoxic T Lymphocytes","Autologous Epstein-Barr Virus-Specific Cytotoxic T Lymphocytes|EBV-Specific Cytotoxic T-Lymphocytes|Epstein-Barr Virus-Specific Cytotoxic T Lymphocytes","A preparation of lymphocytes harvested from a patient with an Epstein-Barr virus (EBV)-positive tumor.  Ex vivo, the lymphocytes are activated against EBV-specific antigens and then returned to the patient, where they mount a specific immune response against EBV-positive tumor cells. (NCI04)","Cell|Pharmacologic Substance"]
["C71036","Autologous Follicular Lymphoma-Derived Idiotype Vaccine","Autologous Follicular Lymphoma-Derived Idiotype Vaccine","A patient-specific cancer vaccine directed against the soluble protein idiotype of an individual follicular lymphoma with potential antineoplastic activity. A patient-specific follicular lymphoma-derived anti-idiotype vaccine may be composed of a patient-specific, synthetic idiotype-related peptide (such as one corresponding to a hypervariable region of an IgG heavy chain) conjugated to the immunostimulant carrier protein keyhole limpet hemocyanin (KLH). Upon administration, this vaccine may induce an idiotype-specific cytotoxic T-lymphocyte (CTL) response against follicular lymphoma cells expressing the idiotype, resulting in tumor cell lysis.","Pharmacologic Substance"]
["C105810","Autologous Glioma Cell Lysate","Autologous Glioma Cell Lysate","A cell lysate derived from glioma cells with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, the autologous glioma cell lysate exposes the immune system to an undefined amount of glioma-type tumor associated antigens (TAA), which may result in the induction of both specific anti-tumoral cytotoxic T lymphocytes (CTL) and antibody-dependent responses against the glioma TAA-expressing cells, resulting in glioma cell lysis.","Pharmacologic Substance"]
["C82388","Autologous GM-CSF-Secreting Breast Cancer Vaccine","Autologous GM-CSF-Secreting Breast Cancer Vaccine","An autologous tumor cell vaccine containing irradiated breast cancer cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene with potential antineoplastic activity. Autologous breast cancer cells are transduced ex vivo with an adenovirus vector encoding the GM-CSF gene and irradiated and then reintroduced into the patient. Upon repeated subcutaneous administration of the vaccine, autologous GM-CSF-secreting breast cancer cells secrete GM-CSF, which may stimulate a tumor-specific cytotoxic T-lymphocyte (CTL) response.","Pharmacologic Substance"]
["C111991","Autologous GM-CSF-secreting Lethally Irradiated Colorectal Cancer Cell Vaccine","Autologous GM-CSF-secreting Lethally Irradiated Colorectal Cancer Cell Vaccine|GVAX Colorectal Cancer Vaccine","A lethally irradiated, autologous colorectal cancer vaccine consisting of patient-specific colorectal cancer cells genetically modified to secrete the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon vaccination, the autologous GM-CSF-secreting lethally irradiated colorectal cancer cell vaccine releases GM-CSF. In turn, GM-CSF may increase the body's immune response against tumor cells by promoting the maturation and activation of dendritic cells (DCs), and enhancing tumor-specific antigen presentation to both B- and T-cells, which leads to better recognition of tumors by the immune system. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.","Immunologic Factor|Pharmacologic Substance"]
["C104419","Autologous GM-CSF-Secreting Lethally Irradiated Leukemia Cell Vaccine","Autologous GM-CSF-Secreting Lethally Irradiated Leukemia Cell Vaccine|GVAX Leukemia Vaccine","An autologous cancer vaccine composed of lethally irradiated leukemia cells that are genetically modified to secrete the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon intradermal injection, the autologous GM-CSF-secreting lethally irradiated leukemia cell vaccine secretes GM-CSF. In turn, GM-CSF may stimulate the immune system to attack tumor cells by enhancing the activation of dendritic cells (DCs) and promoting antigen presentation to both B- and T-lymphocytes. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.","Immunologic Factor|Pharmacologic Substance"]
["C126270","Autologous HBV-specific TCR-redirected T-Lymphocytes","Autologous HBV Antigen-specific TCR-redirected T-Cells|Autologous HBV-specific TCR-redirected T-Lymphocytes|Autologous HBV/TCR-T-Cells","A preparation of human autologous T-lymphocytes transduced with a viral vector encoding for a T-cell receptor (TCR) specific for a human hepatitis B virus (HBV) surface antigen (HBsAg), with potential antineoplastic activity. Following administration, the autologous HBV antigen specific TCR-redirected autologous T-lymphocytes recognize and bind to the HBV antigen-positive cells, which induces cytotoxic T-lymphocyte (CTL)-mediated elimination of HBV antigen-positive cancer cells. HBV antigens are found on HBV-positive cells and HPV-induced hepatocellular carcinoma (HCC).","Pharmacologic Substance"]
["C37448","Autologous Heat-Shock Protein 70 Peptide Vaccine AG-858","AG-858|Autologous Heat-Shock Protein 70 Peptide Vaccine AG-858","A recombinant cancer vaccine made with tumor-derived heat shock protein 70 (HSP70) peptide complexes.  HSP70 associates with antigenic peptides, transporting them into antigen presenting cells (APC) for processing. Tumor-derived HSP70-peptide complexes used in vaccine preparations have been shown to prime tumor immunity and tumor-specific T cells in animal models. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C117725","Autologous HNSCC DNA-transfected Semi-allogeneic Fibroblasts MRC-5 Vaccine","Autologous HNSCC DNA-transfected Semi-allogeneic Fibroblasts MRC-5 Vaccine","A vaccine consisting of lethally irradiated human fetal lung fibroblasts (Medical Research Council 5 or MRC-5) transfected with autologous tumor DNA derived from a head and neck squamous cell carcinoma (HNSCC), with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, the autologous HNSCC DNA-transfected semi-allogeneic fibroblasts MRC-5 vaccine expresses HNSCC tumor-associated antigens (TAAs), which may activate the immune system to induce a cytotoxic T-lymphocyte (CTL) response against HNSCC cells. The MRC-5 cell line, established in 1966, is a human diploid lung fibroblast cell line derived from the human lung tissue of a 14-week-old male fetus.","Pharmacologic Substance"]
["C121537","Autologous HPV-16/18 E6/E7-specific TGF-beta-resistant T Lymphocytes","Anti-VEGFR2-CAR Retroviral Vector-transduced Autologous T-lymphocytes|Autologous HPV-16/18 E6/E7-specific TGF-beta-resistant T Lymphocytes|HPVST Cells","A preparation of autologous transforming growth factor-beta (TGF-beta)-resistant cytotoxic T-lymphocytes (CTL) reactive to human papilloma virus (HPV) types 16 and 18 E6/E7 antigens, with potential antineoplastic activity. Autologous T-lymphocytes from a HPV-positive cancer patient are exposed to and stimulated with dendritic cells (DCs) loaded with the HPV-16/18 proteins E6 and E7. In turn, the HPV-16/18 E6/E7-specific T-lymphocytes are transduced with a retroviral vector expressing a dominant-negative mutant of type II transforming growth factor (TGF)-beta receptor, which blocks signaling mediated by all three TGF-beta isoforms. Following re-administration to patients with HPV-positive tumors, the HPV-16/18 E6/E7-specific TGF-beta-resistant T lymphocytes target HPV16/18 E6/E7-positive cells, which may result in a specific cytotoxic T-lymphocyte (CTL) response, followed by cell lysis and the inhibition of tumor cell proliferation. Tumors expressing TGF-beta inhibit T-lymphocyte activation and expansion.","Cell|Pharmacologic Substance"]
["C111989","Autologous iC9-GD2-CAR-expressing VZV-specific T Lymphocytes","Autologous iC9-GD2-CAR-VZV-CTLs|Autologous iC9-GD2-CAR-expressing VZV-specific T Lymphocytes","Genetically modified, autologous varicella zoster virus (VZV)-specific T-lymphocytes transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for the disialoganglioside GD2, which contains the signaling domains for the co-stimulatory molecules CD28 and CD134 (OX-40), and the suicide gene, inducible caspase 9 (iCasp9 or iC9), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, iC9-GD2-CD28-OX40-expressing T lymphocytes target the GD2 antigen on tumor cells for selective toxicity against GD2-expressing tumor cells. iCasp9 consists of a full-length caspase 9, including its caspase recruitment domain, linked to a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V). If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered, which binds to the FKBP12-F36V drug binding domain, activates caspase 9, and results in apoptosis of the administered T-cells. Expression of the iCasp9 gene in T cells for adoptive transfer increases safety and broadens the scope for their clinical applications. The tumor associated antigen GD2 is overexpressed on the surface of almost all tumors of neuroectodermal origin. OX40 and CD28, both T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation. An additional VZV vaccine can be administered to increase T-cell activity.","Cell|Pharmacologic Substance"]
["C131214","Autologous ICASP9-CD19-expressing T-Lymphocytes","Autologous ICASP9-CD19-expressing T-Lymphocytes|Autologous Inducible Caspase 9-CD19-expressing Autologous T-Lymphocytes|Autologous iC9.2A.deltaNGFR.2A.CAR.CD19 T Cells","A preparation of autologous T-lymphocytes that are transduced with a retroviral vector encoding a chimeric antigen receptor (CAR) specific for the CD19 antigen, the suicide gene, inducible human caspase 9 (iCasp9 or iC9), and a truncated low-affinity nerve growth factor receptor (deltaNGFR), with potential immunomodulating and antineoplastic activities. The iCasp9 construct consists of the entire coding sequence for the human FK506-drug binding protein (FKBP12) with an F36V mutation (FKBP12-F36V) that is linked to the gene encoding human caspase 9, which is deleted of its endogenous caspase activation and recruitment domains. Upon intravenous administration, autologous iCASP9-CD19-expressing T-lymphocytes are selectively toxic to CD19-expressing tumor cells. If the administered T-cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered, which binds to the FKBP12-F36V drug binding domain, activates caspase 9, and results in apoptosis of the administered CAR19 T-cells. The CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. Prior to administration, deltaNGFR, is used to select the CAR19-transduced T-cells for further enrichment by flow cytometry using an anti-NGFR antibody.","Cell|Pharmacologic Substance"]
["C91088","Autologous IL-21-Modulated CD8+ MART1-Specific T Cells","Autologous IL-21-Modulated CD8+ MART1-Specific T Cells","A preparation of interleukin 21 (IL-21) stimulated, CD8+ T-lymphocytes sensitized to MART-1 (melanoma antigen recognized by T-cells) antigen with potential immunostimulating and antineoplastic activities. CD8+ T-lymphocytes are exposed ex vivo to autologous dendritic cells (DCs) pulsed with MART-1 antigen peptide and grown in the presence of IL-21. These tumor-reactive T-cells may stimulate a host immune response against tumor cells expressing the MART-1 antigen, resulting in tumor cell lysis. MART-1 is expressed by certain types of melanoma cells. IL-21, a cytokine involved in the regulation of cellular immune responses, may play a key role during priming of antigen-specific CD8+ T cells and may enhance proliferation of the CTLs.","Cell|Pharmacologic Substance"]
["C38715","Autologous Immunoglobulin Idiotype-KLH Conjugate Vaccine","Autologous Immunoglobulin Idiotype-KLH Conjugate Vaccine|Autologous Immunoglobulin Idiotype-Keyhole Limpet Hemocyanin Conjugate Vaccine","A cancer vaccine composed of tumor-specific idiotype determinants derived from an individual's tumor cells which are conjugated to keyhole limpet hemocyanin, an immunostimulant carrier protein. When injected into the individual from whom the tumor cells were isolated, this vaccine may stimulate an antitumoral cytotoxic T-lymphocytic immune response. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C125667","Autologous Interferon-producing Killer Dendritic Cells","Autologous IKDC-like Cells|Autologous IKDC|Autologous Interferon-producing Killer Dendritic Cells","A preparation of autologous dendritic cells (DC) with a molecular expression profile similar to both natural killer (NK) cells and DCs, with potential antineoplastic activity. Autologous interferon-producing killer dendritic cells (IKDCs) are characterized by double-negative expression of CD3 and CD19; these cells also express low levels of CD11 and are positive for B220. They are distinguished from plasmacytoid DCs (pDCs) by the absence of lymphocyte antigen 6C (Ly6C, Gr-1) expression. IKDCs produce interferon gamma (IFN-gamma) and interleukin (IL) -12, and are able to kill typical NK target cells using NK receptors while retaining DC-like antigen-presenting activity. Upon administration of the autologous IKDCs, these cells secrete high levels of IFN-gamma and, when in contact with tumor cells, mediate TNF-related apoptosis-inducing ligand (TRAIL)-dependent direct lysis of tumor cells. The resulting apoptotic tumor antigens may be presented by the IKDCs, thus activating the immune system to exert a cytotoxic T-lymphocyte (CTL) response to further eliminate tumor cells.","Cell|Pharmacologic Substance"]
["C70836","Autologous LMP1-/LMP2- Specific Cytotoxic T-Lymphocytes","Autologous LMP1-/LMP2- Specific Cytotoxic T-Lymphocytes","A preparation of cytotoxic T-lymphocytes (CTL), specifically reactive to the Epstein-Barr virus (EBV) latent membrane proteins (LMP) 1 and 2, with potential antineoplastic activity. Autologous dendritic cells and EBV-infected lymphoblastoid cell lines (LCL) from patients with EBV-positive nasopharyngeal carcinoma (NPC) are transduced with an LMP1/LMP2-expressing adenoviral vector, are irradiated, and then are used to stimulate and expand autologous CTL to produce autologous LMP1-/LMP2-specific CTL ex vivo. Administration of autologous LMP1-/LMP2- specific cytotoxic T-lymphocytes may result in a specific CTL response against tumor cells expressing LMP1 and LMP2, resulting in cell lysis and inhibition of tumor cell proliferation in vivo. Among a limited set of viral antigens expressed by NPC cells, LMP1 and LMP2 are weak immunogens which, nevertheless, are capable of inducing a T-lymphocyte response.","Cell|Pharmacologic Substance"]
["C112495","Autologous Lymphoid Effector Cells Specific Against Tumor Cells","ALECSAT|Autologous Activated Cytotoxic T Lymphocytes/Natural Killer Cells|Autologous Lymphoid Effector Cells Specific Against Tumor Cells","A preparation of cytotoxic, autologous lymphoid effector cells specifically targeted towards tumor cells, with potential immunomodulating and antineoplastic activities. The autologous lymphoid effector cells are prepared by drawing a blood sample containing the required precursors for CD4+ helper T-cells, CD8+ cytotoxic T-cells, and natural killer (NK) cells from a cancer patient. The precursor cells are activated, selected and expanded to generate mature autologous lymphoid effector cells with the potential for enhanced tumor recognition. Upon readministration into the patient, the autologous lymphoid effector cells may induce both humoral and cellular immune responses against tumor cells. This may result in the immune-mediated inhibition of tumor cell proliferation, which leads to tumor cell death.","Cell|Pharmacologic Substance"]
["C85452","Autologous Lymphoma Cell Lysate-Pulsed Autologous Dendritic Cell Vaccine","Autologous Lymphoma Cell Lysate-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysate from autologous lymphoma cells with potential immunostimulatory and antineoplastic activities. Upon intranodal administration, autologous lymphoma cell lysate-pulsed autologous DC vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against lymphoma cells, which may result in lymphoma cell lysis.","Cell|Pharmacologic Substance"]
["C85451","Autologous Lymphoma Cell/Allogeneic Dendritic Cell Electrofusion Hybrid Vaccine","Autologous Lymphoma Cell/Allogeneic Dendritic Cell Electrofusion Hybrid Vaccine","A cell-based cancer vaccine consisting of hybrid cells created by electrofusing allogeneic dendritic cells (DCs) and autologous lymphoma cells with potential immunostimulating and antitumor activities. Upon administration, autologous lymphoma cell/allogeneic dendritic cell electrofusion hybrid vaccine may stimulate the immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against specific autologous lymphoma-associated antigens, resulting in lymphoma cell apoptosis.","Cell|Pharmacologic Substance"]
["C85450","Autologous Lymphoma Cell/Autologous Dendritic Cell Electrofusion Hybrid Vaccine","Autologous Lymphoma Cell/Autologous Dendritic Cell Electrofusion Hybrid Vaccine","A cell-based cancer vaccine consisting of hybrid cells created by electrofusing autologous dendritic cells (DCs) and autologous lymphoma cells with potential immunostimulating and antitumor activities. Upon administration, autologous lymphoma cell/autologous dendritic cell electrofusion hybrid vaccine may stimulate the immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against specific autologous lymphoma-associated antigens, resulting in lymphoma cell apoptosis.","Cell|Pharmacologic Substance"]
["C116733","Autologous Lymphoma Immunoglobulin-derived scFv-chemokine DNA Vaccine","Autologous Lymphoma Immunoglobulin-derived scFv-chemokine DNA Vaccine","A plasmid DNA vaccine encoding an autologous lymphoma-derived idiotype-targeting immunoglobulin (Ig)-derived single chain variable fragment (scFv) fused to the chemokine macrophage inflammatory protein 3 alpha (MIP3a), with potential immunostimulating and antineoplastic activities. Upon intramuscular vaccination, the autologous lymphoma immunoglobulin-derived scFv-chemokine DNA vaccine is taken up by antigen-presenting cells (APCs) and stimulates the immune system to exert a cytotoxic T-lymphocyte (CTL) response against the idiotype expressed on the surface of B lymphoma cells. MIP3a, also called chemokine (C-C motif) ligand 20 (CCL20), is a chemotactic cytokine able to enhance the immune response through binding to chemokine receptors expressed on APCs.","Gene or Genome|Pharmacologic Substance"]
["C116711","Autologous MAGE-A3-specific HLA-A*01-Restricted T Cell Receptor Gene Engineered Lymphocytes","Anti-MAGE-A3 HLA-A*01 Restricted TCR-Gene Engineered Lymphocytes|Autologous MAGE-A3-specific HLA-A*01-Restricted T Cell Receptor Gene Engineered Lymphocytes","Human autologous T-lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-A*01-restricted, human melanoma-associated antigen A3 (MAGE-A3), with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with an anti-MAGE-A3-HLA-A*01 restricted TCR, expanded ex vivo, and reintroduced into the HLA-A*01-positive patient. Then, the autologous MAGE-A3-specific, HLA-A*01-restricted TCR gene engineered lymphocytes bind to tumor cells expressing the MAGE-A3 antigen, which may increase cell death and halt the growth of MAGE-A3-expressing cancer cells. The tumor-associated antigen MAGE-A3 is overexpressed by a variety of cancer cell types.","Cell|Pharmacologic Substance"]
["C90572","Autologous Melanoma Lysate/KLH-Pulsed Autologous Dendritic Cell Vaccine","Autologous Melanoma Lysate/KLH-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysate from autologous melanoma cells containing tumor associated antigens (TAAs) and conjugated to the immunostimulant Keyhole limpet hemocyanin (KLH), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous melanoma lysate/KLH-pulsed autologous dendritic cell vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against melanoma cells, which may result in melanoma cell lysis. KLH is an immunogenic carrier and serves as an immunostimulant to improve antigenic immune recognition and T-cell responses and can be used to evaluate vaccine efficacy.","Immunologic Factor|Pharmacologic Substance"]
["C111900","Autologous Melanoma Lysate/NY-ESO-1-pulsed Autologous Dendritic Cell Vaccine","Autologous Melanoma Lysate/NY-ESO-1-pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with both a lysate from autologous melanoma cells containing tumor associated antigens (TAAs) and a synthetic peptide derived from the tumor associated antigen human cancer-testis antigen NY-ESO-1, with potential immunostimulatory and antineoplastic activities. Upon administration, autologous melanoma lysate/NY-ESO-1-pulsed autologous DC vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody-mediated immune responses against melanoma cells, which may result in melanoma cell lysis. NY-ESO-1 is expressed in normal testes and on the surfaces of various tumor cells, and plays a key role in tumor cell proliferation and survival.","Immunologic Factor|Pharmacologic Substance"]
["C90571","Autologous Melanoma Lysate-Pulsed Autologous Dendritic Cell Vaccine","Autologous Melanoma Lysate-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysate from autologous melanoma cells containing tumor associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, autologous melanoma lysate-pulsed autologous DC vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against melanoma cells, which may result in melanoma cell lysis.","Immunologic Factor|Pharmacologic Substance"]
["C113803","Autologous Mesenchymal Stem Cells Apceth_101","Agenmestencel-T|Autologous MSC_Apceth_101|Autologous Mesenchymal Stem Cells Apceth_101","Human autologous mesenchymal stem cells (MSCs) harvested from the bone marrow of a patient and genetically modified with a self-inactivating retroviral vector expressing the suicide gene herpes simplex virus thymidine kinase (HSV-TK), that can be used to activate synthetic acyclic guanosine analogues when co-administered. Upon intravenous administration of autologous mesenchymal stem cells apceth_101, the cells are actively recruited to the tumor stroma, differentiate into more mature mesenchymal cells, and become part of the tumor microenvironment. When a synthetic acyclic guanosine analogue, such as ganciclovir, is co-administered, the HSV-TK within the HSV-TK-transduced MSCs will monophosphorylate this prodrug. Subsequently the monophosphate form is further converted to the diphosphate form and then to its active triphosphate form by cellular kinases. The active form of ganciclovir kills the HSV-TK-transduced MSCs and leads to a bystander effect, which eliminates neighboring cancer cells. Therefore, synthetic acyclic guanosine analogues are activated only at the tumor site, which increases their local efficacy and reduces systemic toxicity.","Pharmacologic Substance"]
["C127115","Autologous Neuroblastoma Lysate/KLH-pulsed Dendritic Cell Vaccine","Autologous Neuroblastoma Lysate/KLH-pulsed DC Vaccine|Autologous Neuroblastoma Lysate/KLH-pulsed Dendritic Cell Vaccine|Keyhole Limpet Hemocyanin-pulsed Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with a cell lysate from an autologous neuroblastoma containing tumor-associated antigens (TAAs) and the immunostimulant keyhole limpet hemocyanin (KLH), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous neuroblastoma lysate/KLH-pulsed DC vaccine may stimulate the immune system to mount an anti-tumoral cytotoxic T-lymphocyte (CTL) response against neuroblastoma cells, which may result in tumor cell lysis. KLH is an immunogenic carrier and serves as an immunostimulant to improve antigenic immune recognition and T-cell responses.","Cell|Pharmacologic Substance"]
["C82416","Autologous NSCLC DNA-Transfected Semi-Allogeneic Fibroblasts MRC-5 Vaccine","Autologous NSCLC DNA-Transfected Semi-Allogeneic Fibroblasts MRC-5 Vaccine","A vaccine consisting of irradiated human fetal lung fibroblasts (Medical Research Council 5 or MRC-5) transfected with autologous non-small cell lung cancer (NSCLC)-derived DNA with potential immunostimulatory and antineoplastic activities. Upon administration, autologous NSCLC DNA-transfected semi-allogeneic fibroblasts MRC-5 vaccine expresses NSCLC tumor-associated antigens (TAAs) in addition to MHC class I-determinants and the co-stimulatory molecule B7.1, which may induce a cytotoxic T-lymphocyte (CTL) response against NSCLC cells. The MRC-5 cell line is a human diploid lung fibroblast cell line extablished in 1966.","Pharmacologic Substance"]
["C121848","Autologous NSCLC Peptide-specific Dendritic Cell Vaccine","Autologous NSCLC Peptide-specific DC Vaccine|Autologous NSCLC Peptide-specific Dendritic Cell Vaccine","A personalized cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with immunogenic peptides derived from autologous non-small cell lung cancer (NSCLC) cells, with potential immunostimulating and antineoplastic activities. During leukapheresis, mature DCs are loaded with autologous NSCLC-derived peptides. Upon re-administration of the NSCLC peptide-specific DC vaccine, the immune system is exposed to NSCLC-associated antigens. This results in the induction of a specific cytotoxic T-lymphocyte (CTL) response against NSCLC cells and tumor cell lysis.","Pharmacologic Substance"]
["C82350","Autologous NY-ESO-1-Melanoma-Specific CD8+ T-lymphocytes","Autologous NY-ESO-1-Melanoma-Specific CD8+ T-lymphocytes","A preparation of autologous CD8+ (cytotoxic) T-lymphocytes sensitized to cancer-testis antigen NY-ESO-1 antigen with potential immunostimulating and antineoplastic activities. Autologous CD8+ T-lymphocytes, isolated from a melanoma patient, are exposed to an NY-ESO-1 peptide ex vivo, expanded, and reintroduced into the patient; these tumor-reactive T-cells may stimulate a host immune response against tumor cells expressing the NY-ESO-1 antigen, resulting in tumor cell lysis. NY-ESO-1, an antigen found in normal testis, may be upregulated in various cancers, including bladder, breast, hepatocellular, melanoma, and prostate cancers.","Cell|Pharmacologic Substance"]
["C78830","Autologous OFA-iLRP RNA-Transfected Dendritic Cell Vaccine","Autologous OFA-iLRP RNA-Transfected Dendritic Cell Vaccine","A cancer vaccine consisting of autologous, mature monocyte-derived dendritic cells (DCs) transfected with oncofetal antigen immature laminin receptor protein (OFA-iLRP) RNA, with potential antineoplastic activity. Upon administration, DCs in the OFA-iLRP RNA-transfected autologous dendritic cell vaccine express, process, and present OFA-iLRP to the host immune system, which may mount a potent cytotoxic T-cell (CTL) response against OFA-iLRP-expressing tumor cells. As a highly conserved protein, OFA-iLRP is preferentially expressed in fetal tissues and in many types of cancer, including hematopoietic malignancies, but is not detectable in normal differentiated adult cells.","Pharmacologic Substance"]
["C95759","Autologous Ovarian Tumor Cell Lysate-Pulsed Dendritic Cell Vaccine","Autologous Ovarian Tumor Cell Lysate-Pulsed Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous, irradiated dendritic cells (DCs) pulsed with ovarian tumor cell lysate containing tumor associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, autologous ovarian tumor cell lysate-pulsed dendritic cell vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against ovarian tumor cells expressing the patients ovarian tumor cell-specific TAAs, which may result in ovarian tumor cell lysis.","Pharmacologic Substance"]
["C122402","Autologous Oxidized Ovarian Tumor Cell Lysate Vaccine","Autologous OC-L Vaccine|Autologous Oxidized Ovarian Tumor Cell Lysate Vaccine","An autologous cancer vaccine composed of oxidized ovarian tumor cell lysate, with potential immunostimulatory and antineoplastic activities. Upon administration, the autologous oxidized ovarian tumor cell lysate vaccine exposes the immune system to an undefined amount of tumor-associated antigens (TAAs), which may result in the induction of both anti-tumor cytotoxic T-lymphocytes (CTLs) and antibody-dependent responses against TAA-expressing cells, leading to tumor cell lysis. Compared to non-oxidized tumor cell lysate vaccines, oxidized tumor cell lysate vaccines induce necrotic cell death, increase the immunogenicity of the TAAs and may enhance the anti-tumor immune response.","Immunologic Factor|Pharmacologic Substance"]
["C78823","Autologous PBTL CD19CAR-28 zeta","Autologous PBTL CD19CAR-28 zeta|Autologous Peripheral Blood T-Lymphocytes CD19CAR-28 zeta","A preparation of autologous peripheral blood T-lymphocytes (PBTL) that have been genetically modified to express the chimeric antigen receptor (CAR) anti-CD19/CD3 zeta chain fusion protein coupled to the intracellular signal domain of CD28 antigen, with potential immunostimulating and antineoplastic activities. Upon administration, autologous PBTL CD19CAR-28 zeta may stimulate host cytotoxic T lymphocyte (CTL) and antibody responses against CD19-expressing tumor cells, resulting in tumor cell lysis. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD3 zeta is one of several membrane-bound polypeptides found in the T-cell receptor (TCR)/CD3 complex and regulates the assembly of complete TCR complexes and their expression on the cell surface. CD28 is essential for CD4+ T-cell proliferation, interleukin-2 production, and T-helper type-2 (Th2) development.","Pharmacologic Substance"]
["C113161","Autologous Peripheral Blood Lymphocytes Cotransduced with Retroviral Vectors Encoding Inducible IL-12 and Anti-NY-ESO-1 TCR","Autologous Lymphocytes Cotransduced with Genes Encoding IL-12 and Anti-NY-ESO-1 TCR|Autologous PBL Cotransduced with Retroviral Vectors Encoding Inducible IL-12 and Anti-NY-ESO-1 TCR|Autologous Peripheral Blood Lymphocytes Cotransduced with Retroviral Vectors Encoding Inducible IL-12 and Anti-NY-ESO-1 TCR|IL-12 Plus anti-ESO-1 TCR PBL|IL-12/Anti-NY-ESO-1 TCR-Expressing Autologous PBL|IL-12/Anti-NY-ESO-1 TCR-Expressing Autologous Peripheral Blood Lymphocytes|Inducible IL-12/Anti-NY-ESO-1 TCR-Expressing Autologous PBL|Inducible IL-12/Anti-NY-ESO-1 TCR-Expressing Autologous Peripheral Blood Lymphocytes","Human autologous peripheral blood lymphocytes (PBLs) transduced with two retroviral vectors, one encoding a T-cell receptor (TCR) specific for the cancer-testis antigen NY-ESO-1 and a second that encodes an inducible single chain form of interleukin-12 (IL-12) driven by a nuclear factor of activated T-cells (NFAT)-responsive promoter, with potential immunomodulating and antineoplastic activities. Following isolation of lymphocytes, retroviral vector transduction, and expansion of the cells ex vivo, the inducible IL-12/anti-NY-ESO-1 TCR-expressing autologous PBLs are re-administered into the patient by intravenous injection. As the transduced PBLs traverse the patient's circulation, they can bind to NY-ESO-1-overexpressing tumor cells. This binding activates the TCR signaling pathway in the transduced PBLs, which promotes NFAT-dependent gene transcription and induces expression of the cotransduced IL-12. IL-12 expression activates the immune system by promoting the secretion of interferon-gamma, activating natural killer cells (NKs), and inducing cytotoxic T-cell responses, which may result in both decreased cell proliferation and increased cell death for the NY-ESO-1-overexpressing tumor cells. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types. NFAT, a family of transcription factors involved in immune responses, is activated by calcium signaling, which can occur downstream of TCR activation. Use of a retroviral vector to express an inducible IL-12 may remove the requirement for concomitant administration of interleukin-2 (IL-2) as is the case for conventional cell transfer immunotherapies.","Cell|Pharmacologic Substance"]
["C82361","Autologous Prostate Cancer Antigen-expressing Dendritic Cell Vaccine BPX-101","Autologous Prostate Cancer Antigen-expressing Dendritic Cell Vaccine BPX-101|BP-GMAX-CD1|BPX-101","A genetically-modified autologous dendritic cell-based vaccine expressing a drug-inducible costimulatory CD40 receptor (iCD40) with potential immunomodulating and antineoplastic activities. Autologous dendritic cells (DCs) are genetically modified to express the iCD40 receptor and are pulsed with the tumor antigen prostate-specific membrane antigen (PSMA). Upon intradermal administration, these DCs accumulate in local draining lymph nodes. Twenty-four hours after vaccination, the dimerizer agent AP1903 is administered; AP1903 binds to and activates iCD40 receptors presented on DC surfaces, thus activating the DCs and stimulating a cytotoxic T-lymphocyte (CTL) response against host tumor cells that express PSMA.  This delayed activation strategy optimizes DC accumulation in local draining lymph nodes prior to DC activation. iCD40 contains a membrane-localized cytoplasmic CD40 domain fused to a drug-binding domain.","Cell|Pharmacologic Substance"]
["C128031","Autologous Prostate Stem Cell Antigen-specific CAR T Cells BPX-601","Autologous PSCA-Specific Chimeric Antigen Receptor Engineered T Cells BPX-601|Autologous PSCA-specific CAR T Cells BPX-601|Autologous Prostate Stem Cell Antigen-specific CAR T Cells BPX-601|BPX-601|GoCART BPX-601|iMC/PSCA-zeta CAR BPX-601","A preparation of autologous T-lymphocytes expressing a chimeric antigen receptor (CAR) consisting of an anti-human prostate stem cell antigen (PSCA) scFv (single chain variable fragment) coupled to the zeta chain of the T-cell receptor (TCRzeta) and a drug-induced co-stimulatory molecule, composed of an inducible, chimeric MyD88/CD40 (inducible MC; iMC) co-stimulatory domain, in which both the MyD88 and CD40 lack their extracellular domains, with potential antineoplastic activity. Upon administration of BPX-601, the T-cells target and bind to PSCA-expressing cancer cells. Upon subsequent administration of the chemical inducer of dimerization (CID) agent rimiducid, this agent targets and binds to the drug binding domain, which leads to iMC expression, activation of both CD40- and MyD88-mediated signal transduction pathways, and an induction of selective cytotoxicity in, and eradication of PSCA-expressing cancer cells. iMC activation by rimiducid increases T-cell survival and anti-tumor activity of the administered T-cells, compared to T-cells without the drug iMC activation-switch. As these T-cells are engineered to only be fully activated by binding to both antigen and rimiducid, T-cell proliferation, activity and toxicity can be controlled by adjusting the dose of rimiducid, thereby preventing uncontrolled T-cell activation which increases the safety of the administered T-cells. PSCA is a glycosylphosphatidylinositol (GPI)-anchored cell surface antigen overexpressed in many cancer cell types.","Pharmacologic Substance"]
["C85479","Autologous Renal Cell Carcinoma Tumor Lysate-Pulsed Dendritic Cell Vaccine","Autologous RCC Tumor Lysate-DC Vaccine|Autologous Renal Cell Carcinoma Tumor Lysate-Pulsed Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with renal cell carcinoma (RCC) tumor cell lysate containing tumor associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, autologous renal cell carcinoma tumor lysate-dendritic cell vaccine may stimulate anti-tumoral cytotoxic T-lymphocyte (CTL) and antibody responses against RCC tumor cells expressing RCC TAAs, resulting in RCC tumor cell lysis.","Cell|Pharmacologic Substance"]
["C105807","Autologous Sarcoma Cell Lysate","Autologous Sarcoma Cell Lysate","A cell lysate derived from sarcoma cells with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, the autologous sarcoma cell lysate exposes the immune system to an undefined amount of sarcoma-type tumor associated antigens (TAA), which may result in the induction of both specific anti-tumoral cytotoxic T lymphocytes (CTL) and antibody-dependent responses against the sarcoma TAA-expressing cells, resulting in sarcoma cell lysis.","Pharmacologic Substance"]
["C105806","Autologous Sarcoma Lysate-pulsed Dendritic Cell Vaccine","Autologous Sarcoma Lysate-pulsed Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysates from sarcoma cells with potential immunostimulatory and antineoplastic activities. Upon administration, the autologous sarcoma lysate-pulsed dendritic cell vaccine exposes the immune system to an undefined amount of sarcoma-type tumor associated antigens (TAA), which may result in the induction of both specific anti-tumoral cytotoxic T lymphocytes (CTL) and antibody-dependent responses against the sarcoma TAA-expressing cells, resulting in sarcoma cell lysis.","Pharmacologic Substance"]
["C85470","Autologous TARP Peptide-Pulsed Dendritic Cell Vaccine","Autologous TARP Peptide-Pulsed Dendritic Cell Vaccine","A cell-based cancer vaccine comprised of autologous dendritic cells pulsed with autologous T cell receptor gamma-chain alternate reading frame protein (TARP) peptide with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, autologous TARP peptide-pulsed dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against TARP-expressing cancer cells, resulting in tumor cell lysis. The highly immunogenic nuclear protein TARP is commonly expressed in breast and prostate cancer cells.","Cell|Pharmacologic Substance"]
["C85459","Autologous TGFbeta-Resistant HER2/EBV-Specific Cytotoxic T Lymphocytes","Autologous TGFbeta-Resistant HER2/EBV-Specific Cytotoxic T Lymphocytes","A preparation of transforming growth factor-beta (TGF-beta)-resistant Epstein-Barr virus (EBV)-specific cytotoxic T-lymphocytes (CTLs) directed to EBV through their native receptor and HER2 through a retrovirally transduced HER2 chimeric antigen receptor (CAR) with potential antineoplastic activity. Autologous EBV-specific CTLs are produced by exposing autologous CTLs to \"stimulator\" autologous EBV-transformed lymphoblastoid cell lines (EBV-LCLs). Subsequently, autologous EBV-specific CTLs are transduced with retroviral vectors expressing the mutant type II TGF-beta dominant-negative receptor (DNR), which blocks signaling by all three TGF-beta isoforms, and the HER2 CAR. After transduction, transgenic EBV-CTLs are expanded on EBV-LCLs. Upon administration, autologous HER2 chimeric receptor/TGFbeta dominant negative receptor-expressing EBV-specific cytotoxic T lymphocytes may bind to HER2-expressing tumors cells, which may result in CTL-mediated cell lysis and inhibition of tumor cell proliferation. Tumor-expressed TGF-beta inhibits T lymphocyte activation and expansion.","Cell|Pharmacologic Substance"]
["C124655","Autologous T-lymphocytes-expressing NY-ESO-1-C259-specific Enhanced T-cell Receptors","Autologous T-lymphocytes-expressing NY-ESO-1-C259-specific Enhanced T-cell Receptors|NY-ESO-1/C259T|NY-ESO-1C259T|NY-ESOc259T","Human autologous lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the cancer/testis antigen NY-ESO-1, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the autologous T-lymphocytes expressing NY-ESO-1-C259-specific enhanced T-cell receptors bind to NY-ESO-1-overexpressing tumor cells. This may result in the specific cytotoxic T-lymphocyte (CTL) killing of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types; the TCR is specific for SLLMWITQC, an NY-ESO-1-derived peptide, in a complex with human leukocyte antigen (HLA) A2 peptide.","Cell|Pharmacologic Substance"]
["C112206","Autologous Tumor Cell Proteoliposome Chronic Lymphocytic Leukemia Vaccine","Autologous Tumor Cell Proteoliposome Chronic Lymphocytic Leukemia Vaccine|Oncoquest-CLL Vaccine|Oncoquest-L Vaccine","An autologous chronic lymphocytic leukemia cancer vaccine consisting of patient-specific membrane proteins directly extracted from patient autologous tumor cells and incorporated into liposomes along with Interleukin 2 (IL-2) to produce membrane-patched proteoliposomes, with potential immunostimulating and antineoplastic activities. After subcutaneous injection of the autologous tumor cell proteoliposomes chronic lymphocytic leukemia vaccine, liposomes deliver the encapsulated tumor antigens into the cytosol of antigen presenting cells (APCs). Subsequently, the APCs process the antigens and present antigen-derived peptides to the immune system. This may enhance recognition of tumors by the immune system, and activate both cytotoxic CD8+ T cells and CD4+ helper T cells against tumor cells. IL-2 is incorporated into the vaccine to leverage its ability to expand activated T cells.","Immunologic Factor"]
["C1980","Autologous Tumor Cell Vaccine","AC vaccine|Autologous Cell Vaccine|Autologous Tumor Cell Vaccine","A therapeutic agent produced by isolating tumor cells from an individual and processing these tumor cells into a vaccine formulation in vitro; the vaccine is then administered to the individual from whom the tumor cells were isolated. Typically combined with an adjuvant immunostimulant, an autologous cell vaccine may elicit a cytotoxic T-lymphocytic immune response to cell surface-expressed tumor-associated antigens (TAAs), resulting in tumor cell death. (NCI04)","Cell|Immunologic Factor|Pharmacologic Substance"]
["C120552","Autologous Tumor Infiltrating Lymphocytes LN-144","Autologous TIL LN-144|Autologous Tumor Infiltrating Lymphocytes LN-144|Contego|LN-144","A preparation of autologous tumor infiltrating lymphocytes (TILs), with potential antineoplastic activity. TILs are isolated from a patient's tumor tissue, cultured in vitro with high-dose interleukin-2 (lL-2), further selected based on antigen specificity and tumor reactivity, and the selected TILs are subsequently expanded. Upon re-introduction of LN-144 into the patient, the TILs re-infiltrate the tumor, specifically recognize the tumor-associated antigens (TAAs), and initiate tumor cell lysis. IL-2 induces the proliferation and expansion of TILs in vitro.","Cell|Pharmacologic Substance"]
["C126797","Autologous Tumor-associated Peptide Antigen-pulsed Dendritic Cell Vaccine","Autologous TAPA loaded DC Vaccine|Autologous TAPA-pulsed DC Vaccine KiroVAX|Autologous Tumor Associated Peptide Antigen-pulsed DC Vaccine KiroVAX|Autologous Tumor-associated Peptide Antigen-pulsed Dendritic Cell Vaccine|KiroVAX","A dendritic cell (DC)-based cancer vaccine composed of autologous DCs pulsed with specific tumor-associated peptide antigens (TAPA), with potential immunostimulatory and antineoplastic activities. Upon administration, autologous TAPA-pulsed DC vaccine exposes the immune system to the specific TAPAs, which may result in cytotoxic T-lymphocyte (CTL)-mediated immune responses against the TAPA-expressing cancer cells. This leads to cancer cell lysis. This vaccine is specific towards peptides derived from the following proteins: sperm autoantigenic protein 17 (SP17), ropporin, A-kinase anchor protein 4 (AKAP4), pituitary tumor-transforming 1 (PTTG1) and SPANX family member B (SPANX-B).","Pharmacologic Substance"]
["C121308","Autologous WT1-TCRc4 Gene-transduced CD8-positive Tcm/Tn Lymphocytes","Autologous WT1-TCRc4 Gene-transduced CD8-positive Tcm/Tn Lymphocytes","Autologous, human CD8 T-lymphocytes, comprised of both central memory T-cells (Tcm) and naïve T-cells (Tn), that are transduced, ex vivo, with a self-inactivating (SIN) lentiviral vector encoding a high-affinity T-cell receptor (TCRc4) specific for the human tumor antigen Wilms tumor 1 (WT1) epitope 126-134 (RMFPNAPYL), with potential antineoplastic activity. Upon isolation of peripheral blood lymphocytes (PBLs), transduction, expansion ex vivo, priming of the Tn subset, but not the Tcm subset, with interleukin-21 (IL-21) and reintroduction of equal amounts of Tcm and Tn cells into the patient, WT1-TCRc4 gene-transduced CD8-positive Tcm/Tn lymphocytes redirect T-lymphocytes to WT1-expressing tumor cells and specifically bind to and lyse those cells. This inhibits proliferation of WT1-expressing tumor cells. WT1 protein, a zinc finger DNA-binding transcriptional regulator, is overexpressed in most leukemias and various solid tumors, while expression in normal, healthy tissues is very limited; its expression is correlated with aggressiveness and poor prognosis.","Cell|Pharmacologic Substance"]
["C116870","Avelumab","Avelumab|MSB0010718C","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human immunosuppressive ligand programmed death-ligand 1 (PD-L1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, avelumab binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-lymphocytes (CTLs) targeted to PD-L1-overexpressing tumor cells. In addition, avelumab induces an antibody-dependent cellular cytotoxic (ADCC) response against PD-L1-expressing tumor cells. PD-1, a cell surface receptor belonging to the immunoglobulin superfamily expressed on T-cells, negatively regulates T-cell activation and effector function when activated by its ligand, and plays an important role in tumor evasion from host immunity. PD-L1, a transmembrane protein, is overexpressed on a variety of tumor cell types and is associated with poor prognosis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C118671","Avitinib Maleate","Avitinib Maleate","The maleate salt form of avitinib, an orally available, irreversible, epidermal growth factor receptor (EGFR) mutant-selective inhibitor, with potential antineoplastic activity. Upon oral administration, avitinib covalently binds to and inhibits the activity of mutant forms of EGFR, including the drug-resistant T790M EGFR mutant, which prevents signaling mediated by mutant forms of EGFR. This may both induce cell death and inhibit tumor growth in EGFR-mutated tumor cells. EGFR, a receptor tyrosine kinase that is mutated in a variety of cancers, plays a key role in tumor cell proliferation and tumor vascularization. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced when compared to non-selective EGFR inhibitors, which also inhibit wild-type EGFR.","Pharmacologic Substance"]
["C49181","AVN944","AVN-944|AVN944","An orally available, synthetic small molecule with potential antineoplastic activity. AVN944 inhibits inosine monosphosphate dehydrogenase (IMPDH), an enzyme involved in the de novo synthesis of guanosine triphosphate (GTP), a purine molecule required for DNA and RNA synthesis.  Inhibition of IMPDH deprives cancer cells of GTP, resulting in disruption of DNA and RNA synthesis, inhibition of cell proliferation, and the induction of apoptosis. AVN944 appears to have a selective effect on cancer cells in that deprivation of GTP in normal cells results in a temporary slowing of cell growth only. IMPDH is overexpressed in some cancer cells, particularly in hematological malignancies.","Pharmacologic Substance"]
["C38718","Axitinib","AG-013736|AG013736|AXITINIB|Axitinib|Inlyta|N-methyl-2-((3-((1E)-2-(pyridin-2-yl)ethenyl)-1H-indazol-6-yl)sulfanyl)benzamide|axitinib","An orally bioavailable tyrosine kinase inhibitor. Axitinib inhibits the proangiogenic cytokines vascular endothelial growth factor (VEGF) and platelet-derived growth factor receptor (PDGF), thereby exerting an anti-angiogenic effect.","Pharmacologic Substance"]
["C121854","AXL Inhibitor BGB324","AXL Inhibitor BGB324|BGB324","An orally available and selective inhibitor of the AXL receptor tyrosine kinase (UFO), with potential antineoplastic activity. Upon administration, BGB324 targets and binds to the intracellular catalytic kinase domain of AXL and prevents its activity. This blocks AXL-mediated signal transduction pathways and inhibits the epithelial-mesenchymal transition (EMT), which, in turn, inhibits tumor cell proliferation and migration. In addition, BGB324 enhances chemo-sensitivity. AXL, a member of the TAM (TYRO3, AXL and MER) family of receptor tyrosine kinases overexpressed by many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis.","Pharmacologic Substance"]
["C127116","AXL Inhibitor TP-0903","2-((5-Chloro-2-((4-((4-methylpiperazin-1-yl)methyl)phenyl)amino)pyrimidin-4-yl)amino)-N,N-dimethylbenzenesulfonamide|AXL Inhibitor TP-0903|TP 0903|TP-0903|TP0903","An orally available and selective inhibitor of the receptor tyrosine kinase AXL (UFO), with potential antineoplastic activity. Upon administration, TP-0903 targets and binds to AXL and prevents its activity. This blocks AXL-mediated signal transduction pathways and inhibits the epithelial-mesenchymal transition (EMT), which, in turn, inhibits tumor cell proliferation and migration. In addition, TP-0903 enhances chemo-sensitivity to certain other chemotherapeutic agents. AXL, a member of the Tyro3, AXL and Mer (TAM) family of receptor tyrosine kinases and overexpressed by many tumor cell types, plays a key role in tumor cell proliferation, survival, invasion and metastasis; its expression is associated with drug resistance and poor prognosis","Pharmacologic Substance"]
["C288","Azacitidine","4-Amino-1-beta-D-ribofuranosyl-1,3,5-triazin-2(1H)-one|5 AZC|5-AC|5-AZC|5-Aza-cytidine|5-Azacytidine|AZACITIDINE|Azacitidine|Azacytidine, 5-|Azacytidine|Ladakamycin|Mylosar|U-18496|Vidaza|azacitidine","A pyrimidine nucleoside analogue of cytidine with antineoplastic activity. Azacitidine is incorporated into DNA, where it reversibly inhibits DNA methyltransferase, thereby blocking DNA methylation.  Hypomethylation of DNA by azacitidine may activate tumor suppressor genes silenced by hypermethylation, resulting in an antitumor effect. This agent is also incorporated into RNA, thereby disrupting normal RNA function and impairing tRNA cytosine-5-methyltransferase activity. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1007","Azapicyl","1-Acetyl-2-picolinoylhydrazine|1-acetyl-2-picolinoylhydrazine|2-acetylhydrazide-2-pyridinecarboxylic acid|Azapicyl|P-2292","A hydrazine compound that has been investigated for antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1008","Azaribine","1,2,4-Triazine-3,5(2H,4H)-dione, 2-Beta-D-ribofuranosyl-|2',3',4'-azauridine triacetate|2-(2,3,5-Tri-O-acetyl-beta-D-ribofuranosyl)-as-triazine-3,5(2H,4H)-dione|6-Azauridine Triacetate|6-Azauridine triacetate|AZARIBINE|Azaribine|Azauridine Triacetate|Azauridine triacetate|CB 304|SKI 28426|Triacetyl 6-azauridine|Triacetyl 6-azuridine|Triacetyl-6-azuridine|Triazure","The triacetate salt of azauridine, a synthetic triazine nucleoside derivative possessing antineoplastic and anti-psoriatic activity. After metabolism to 6-azauridine-5-prime monophosphate, 6-Azauridine inhibits de novo pyrimidine biosynthesis and its 5-prime triphosphate metabolite gets incorporated into RNA, thereby preventing RNA synthesis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C289","Azaserine","AZASERINE|AZS|Azaserine|CL-337|CN 15757|CN-15757|Cl 337|Diazoacetate (Ester) L-Serine|Diazoacetate(ester) L-serine|Diazoacetic Acid Ester with Serine|Diazoacetylserine|L-Azaserine|L-Diazoacetate(ester) serine|L-diazoacetate (ester) serine|L-serine diazoacetate (ester)|O-diazoacetyl-L-serine|P-165|Serine Diazoacetate|o-Diazoacetyl-L-serine","A naturally occurring serine derivative diazo compound with antineoplastic properties, Azaserine functions as a purine antagonist and glutamine analogue (glutamine amidotransferase inhibitor) that competitively inhibits pathways in which glutamine is metabolized. An antibiotic and antitumor agent, Azaserine is used in clinical studies as a potential antineoplastic agent. (NCI04)","Antibiotic|Nucleic Acid, Nucleoside, or Nucleotide"]
["C1347","Azimexon","2-Aziridinecarboxamide, 1-[1-(2-cyano-1-aziridinyl)-1-methylethyl]|2-Cyanaziridinyl-2-carbamoyl-aziridinyl-1-propane|AZ|AZIMEXON|Azimexon|Azimexone|BM 12.531|BM12531","Azimexon (2-cyanaziridinyl-2-carbamoyl-aziridinyl-1-propane) is a derivative of 2-cyanaziridine. Immunostimulant which shows therapeutic effects in tumor models and experimental infections in vitro, enhancing T lymphocyte transformation and phagocytosis. The mode of action of azimexon is unknown. It has been suggested that azimexon may alkylate DNA. In cancer patients it increases leukocytosis, blood active T rosettes, T4/T8 ratio, and is used as an adjuvant to chemotherapy in the treatment of melanoma and myeloma.","Organic Chemical|Pharmacologic Substance"]
["C29404","Aziridinylbenzoquinone RH1","2,5-Diaziridinyl-3-(hydroxymethyl)-6-methyl-1,4-benzoquinone|Aziridinylbenzoquinone RH1|RH1","A water-soluble, synthetic aziridinylbenzoquinone with potential antineoplastic activity. Bioactivation of aziridinylbenzoquinone RH1 occurs through the two-electron reduction of the quinone to the hydroquinone by the two-electron quinone reductase DT-diaphorase (DTD). The resultant hydroquinone selectively alkylates and cross-links DNA at the 5'-GNC-3' sequence, inihibiting DNA replication, inducing apoptosis, and inhibiting tumor cell proliferation. DTD is over-expressed in many tumors relative to normal tissue, including lung, colon, breast and liver tumors.","Organic Chemical|Pharmacologic Substance"]
["C28803","Azotomycin","A 10270B|AZOTOMYCIN|Azotomycin|Diazomycin B|Duazomycin B|L-Norleucine, 6-diazo-N-(6-diazo-N-L-gamma-glutamyl-5-oxo-L-norleucyl)-5-oxo- (8CI 9CI)","An antineoplastic-antibiotic diazo analog of L-glutamine isolated from the bacterium Streptomyces ambofaciens.  Azotomycin inhibits glutamine-dependent enzymes involved in purine and pyrimidine biosynthesis, resulting in inhibition of DNA synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C85480","Azurin:50-77 Cell Penetrating Peptide p28","Azurin-Derived Cell Penetrating Peptide p28|Azurin:50-77 CPP p28|Azurin:50-77 Cell Penetrating Peptide p28","A water-soluble, amphipathic, 28 amino acid (amino acids 50-77), 2.9 kD fragment peptide (p28) derived from the protein azurin with potential antineoplastic and antiangiogenic activities. Although the mechanism has yet to be fully elucidated, the preferential cellular uptake of azurin-derived cell-penetrating peptide p28 by tumor cells and endothelial cells is likely via caveolae-mediated endocytosis; the C-terminal 18 amino acid residues (50-67) appear to be responsible for this preferential uptake. After cell entry, the first 12 amino acid residues interact with tumor suppressor p53 and form a p28:p53 complex, which may result in a reduction of proteasomal degradation of p53, increased p53 levels, and p53-mediated cell cycle inhibition and apoptosis. Azurin is a cupredoxin secreted by the bacterium Pseudomonas aeruginosa. Cell penetrating peptides (CPPs) are cationic and/or amphipathic peptides, typically less than 30 amino acids in length, that can penetrate cell membranes easily and may transport molecular cargo.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C80046","B16alphaGal Melanoma Vaccine","B16alphaGal Melanoma Vaccine|Hyperacute Melanoma","A whole cell melanoma cancer vaccine with potential immunostimulating and antineoplastic activities. B16alphaGal melanoma vaccine contains three types of human melanoma cell lines that are genetically engineered to express the alpha(1,3)-galactosyl (alphaGal) epitope on cell surfaces. The agent stimulates a hyperacute rejection of whole melanoma cancer cells expressing alphaGal epitopes, initiated by opsonization by anti-alphaGal antibodies and followed by antibody-dependent cell-mediated cytotoxicity (ADCC) and cell lysis. This results in the stimulation of a broader cytotoxic T-lymphocyte response (CTL) directed against tumor antigens on melanoma cells that do not express alphaGal. AlphaGal is not normally expressed in humans because alpha(1,3)-galactosyltransferase (Alpha-GT), the enzyme that catalyzes the synthesis of alphaGal epitopes on glycoproteins and glycolipids, is not naturally present in humans and other primates.","Immunologic Factor|Pharmacologic Substance"]
["C2745","B7 Transfected Melanoma Cell Vaccine","B7 Transfected Allogenic Melanoma Cell Vaccine|B7 Transfected Melanoma Cell Vaccine","An allogenic whole tumor cell vaccine with potential antineoplastic activity.  B7 transfected melanoma cell vaccine consists of melanoma cells that have been induced to express the human leukocyte antigen (HLA) B7.  Vaccination with these altered cells may elicit an anti-tumor immune response via CD8+ cytotoxic T lymphocytes (CTL). (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C28850","Bactobolin","(-)-Bactobolin|2-Amino-N-[3-(dichloromethyl)-3,4,4a,5,6,7- hexahydro-5,6,8-trihydroxy-3-methyl-1-oxo-1H-2- benzopyran-4-yl], Propanamide|Antibiotic BN 183B|BN 183B|Bactobolin|Y 12278","A 3-dichloromethylactinobolin antineoplastic antibiotic isolated from various Pseudomonas bacterial species.  BN-183 induces apoptosis via a caspase-dependent pathway.  This agent also has immunomodulatory properties. (NCI04)","Antibiotic|Organic Chemical"]
["C28851","Baculovirus CEA Protein Vaccine","Baculovirus CEA Protein Vaccine|CEA Vaccine","A vaccine consisting of recombinant carcinoembryonic antigen (CEA) produced by a baculovirus expression system with potential antineoplastic activity. Vaccination with baculovirus CEA protein vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against CEA positive cells, resulting in decreased tumor growth.  CEA is overexpressed in several cancer cell types, including gastrointestinal, breast, and non-small cell lung cancers. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C62516","Bafetinib","BAFETINIB|Bafetinib|Benzamide, N-[3-([4,5'-bipyrimidin]-2-ylamino)-4-methylphenyl]-4-[[(3S)-3- (dimethylamino)-1-pyrrolidinyl]methyl]-3-(trifluoromethyl)-|CNS-9|Dual Bcr-Abl/Lyn Tyrosine Kinase Inhibitor INNO-406|INNO-406|NS-187","An orally active 2-phenylaminopyrimidine derivative with potential antineoplastic activity. INNO-406 specifically binds to and inhibits the Bcr/Abl fusion protein tyrosine kinase, an abnormal enzyme produced by Philadelphia chromosomal translocation associated with chronic myeloid leukemia (CML). Furthermore, this agent also inhibits the Src-family member Lyn tyrosine kinase, upregulated in imatinib-resistant CML cells and in a variety of solid cancer cell types. The inhibitory effect of INNO-406 on these specific tyrosine kinases decreases cellular proliferation and induces apoptosis. A high percentage of CML patients are refractory to imatinib, which sometimes results from point mutations occurring in the kinase domain of the Bcr/Abl fusion product. Due to its dual inhibitory activity, INNO-406 has been shown to overcome this particular drug resistance and to be a potent and effective agent in the treatment of imatinib-resistant CML.","Pharmacologic Substance"]
["C129374","Baltaleucel-T","Baltaleucel T|Baltaleucel-T|CMD-003|Epstein Barr Virus-specific LMP1/LMP2/EBNABARF1-targeting Autologous Cytotoxic T-lymphocytes","A preparation of autologous Epstein-Barr virus (EBV)-specific cytotoxic T-lymphocytes (CTLs), which have specific reactivity to the EBV antigens, latent membrane proteins (LMP) 1 (LMP1) and 2 (LMP2), EBV nuclear antigen (EBNA) and BamHI-A rightward frame-1 (BARF1), with potential immunomodulating and antineoplastic activities. Upon administration, baltaleucel-T targets and binds to EBV-expressing cancer cells specifically expressing the targeted antigens. This may kill LMP1/LMP2/EBNA/BARF1-expressing EBV-associated cancer cells. LMP1, LMP2, EBNA and BARF1 are tumor-associated antigens (TAAs) that are specifically associated with EBV infection, and play key roles in the proliferation of a variety of tumors.","Cell|Pharmacologic Substance"]
["C79528","Banoxantrone","9,10-Anthracenedione, 1,4-bis((2-(dimethylamino)ethyl)amino)-5,8-dihydroxy-, N,N'-dioxide|AQ 4N|Aq4N|BANOXANTRONE|Banoxantrone","A bioreductive, alkylaminoanthraquinone prodrug with antineoplastic activity. Under hypoxic conditions, often seen in solid tumors, banoxantrone (AQ4N) is converted and activated by cytochrome P450 enzymes, which are upregulated in certain tumors, to the cytotoxic DNA-binding agent AQ4. Banoxantrone intercalates into and crosslinks DNA, and inhibits topoisomerase II. This results in an inhibition of DNA replication and repair in tumor cells. Combined with conventional therapeutic agents, both oxygenic and hypoxic regions of tumors can be targeted.","Pharmacologic Substance"]
["C62502","Barasertib","1h-pyrazole-3-acetamide, 5-((7-(3-(ethyl(2-(phosphonooxy)ethyl)amino)propoxy)-4-quinazolinyl)amino)-n-(3-fluorophenyl)-|AZD-1152|AZD1152|Aurora Kinase Inhibitor AZD1152|BARASERTIB|Barasertib","An orally bioavailable, small-molecule, dihydrogen phosphate prodrug of the pyrazoloquinazoline Aurora kinase inhibitor AZD1152-hydroxyquinazoline pyrazol anilide (AZD1152-HQPA) with potential antineoplastic activity. Upon administration and rapid conversion from the prodrug form in plasma, AZD1152-HQPA specifically binds to and inhibits Aurora kinase B, which results in the disruption of spindle checkpoint functions and chromosome alignment and, so, the disruption of chromosome segregation and cytokinesis. Consequently, cell division and cell proliferation are inhibited and apoptosis is induced in Aurora kinase B-overexpressing tumor cells. Aurora kinase B, a serine/threonine protein kinase that functions in the attachment of the mitotic spindle to the centromere, is overexpressed in a wide variety of cancer cell types.","Pharmacologic Substance"]
["C48382","Bardoxolone","2-Cyano-3,12-dioxoolean-1,9-dien-28-oic Acid|2-Cyano-3,12-dioxooleana-1,9(11)-dien-28-oic Acid|BARDOXOLONE|Bardoxolone|CDDO|Oleana-1,9(11)-dien-28-oic acid, 2-cyano-3,12-dioxo-|RTA 401","A synthetic triterpenoid compound with potential antineoplastic and anti-inflammatory activities. Bardoxolone blocks the synthesis of inducible nitric oxide synthase (iNOS) and inducible cyclooxygenase (COX-2), two enzymes involved in inflammation and carcinogenesis. This agent also inhibits the interleukin-1 (IL-1)-induced expression of the pro-inflammatory proteins matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-13 (MMP-13) and the expression of Bcl-3; Bcl-3 is an IL-1-responsive gene that preferentially contributes to MMP-1 gene expression.","Pharmacologic Substance"]
["C127012","Baricitinib","3-Azetidineacetonitrile, 1-(Ethylsulfonyl)-3-(4-(7H-pyrrolo(2,3-d)pyrimidin-4-yl)-1H-pyrazol-1-yl)-|BARICITINIB|Baricitinib|INCB 028050|INCB028050|LY 3009104|LY3009104","An orally bioavailable inhibitor of Janus kinases 1 and 2 (JAK1/2), with potential anti-inflammatory, immunomodulating and antineoplastic activities. Upon administration, baricitinib binds to JAK1/2, which inhibits JAK1/2 activation and leads to the inhibition of the JAK-signal transducers and activators of transcription (STAT) signaling pathway. This decreases the production of inflammatory cytokines and may prevent an inflammatory response. In addition, baricitinib may induce apoptosis and reduce proliferation of JAK1/2-expressing tumor cells. JAK kinases are intracellular enzymes involved in cytokine signaling, inflammation, immune function and hematopoiesis; they are also upregulated and/or mutated in various tumor cell types.","Pharmacologic Substance"]
["C72716","Batabulin","2-Fluoro-1-methoxy-4-pentafluorophenylsulfonamidobenzene|BATABULIN|Batabulin|T138067","A synthetic pentafluorophenylsulfonamide with potential antineoplastic activity. Batabulin covalently binds to beta tubulin, resulting in a disruption of microtubule polymerization, collapse of the cytoskeleton, cell cycle arrest, and tumor cell apoptosis.","Pharmacologic Substance"]
["C1835","Batabulin Sodium","2-Fluoro-1-methoxy-4-(pentafluorophenyl-sulfonamido)benzene, Sodium Salt|BATABULIN SODIUM|Batabulin Sodium|T138067 Sodium","The sodium salt form of batabulin, a synthetic pentafluorophenylsulfonamide with potential antineoplastic activity. Batabulin covalently binds to and selectively modifies the beta 1, beta 2, beta 3, and beta 4 isotypes of beta tubulin at a conserved cysteine residue, resulting in disruption of microtubule polymerization, collapse of the cytoskeleton, an increase in chromosomal ploidy, cell cycle arrest, and tumor cell apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C1529","Batimastat","(2R,3S)-N{4}-Hydroxy-N{1}-[(1S)-2-(methylamino)-2-oxo-1-(phenylmethyl)ethyl]-2-(2-methylpropyl)-3-[(2-thienylthio)methyl]butanediamide|BATIMASTAT|BB-94|BB94|Batimastat|Butanediamide, N4-hydroxy-N1-(2-(methylamino)-2-oxo-1-(phenylmethyl)ethyl)-2-(2-methylpropyl)-3-((2-thienylthio)methyl)-, (2R-(1(S*),2R*,3S*))-|[4-(N-Hydroxyamino)-2R-isobutyl-3S-(2-thienylthiomethyl)-succinyl]-L-phenylalanine-N-methylamide|[4-(N-Hydroxyamino)-2R-isobutyl-3S-(thiophen-2-ylthiomethyl)-succinyl]-L-phenylalanine-N-methylamide|batimastat","A synthetic hydroxamate with potential antineoplastic activity.  Batimastat binds covalently to the zinc ion in the active site of matrix metalloproteinases (MMPs), thereby inhibiting the action of MMPs, inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C49088","Bavituximab","BAVITUXIMAB|Bavituximab|Chimeric Anti-Phosphotidylserine Monoclonal Antibody|Tarvacin","A chimeric, IgG1 monoclonal antibody directed against anionic phospholipids with potential antineoplastic activity. Bavituximab binds to anionic phospholipids in a beta 2-glycoprotein I-dependent manner, inhibiting tumor growth by stimulating antibody-dependent cellular cytotoxicity (ADCC) to tumor vessels.","Pharmacologic Substance"]
["C1886","BAY 56-3722","BAY 38-3441|BAY 56-3722","A water-soluble camptothecin derivative conjugated to a carbohydrate moiety exhibiting antineoplastic activity. BAY 56-3722 stabilizes the topoisomerase I-DNA covalent complex and forms an enzyme-drug-DNA ternary complex. As a consequence of the formation of this complex, both the initial cleavage reaction and religation steps are inhibited and subsequent collision of the replication fork with the cleaved strand of DNA results in inhibition of DNA replication, double strand DNA breakage and triggering of apoptosis. The peptide carbohydrate moiety of this agent stabilizes the lactone form of camptothecin in blood.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C73598","Bazedoxifene","1H-Indol-5-ol, 1-((4-(2-(hexahydro-1H-azepin-1-yl)ethoxy)phenyl)methyl)-2-(4-hydroxyphenyl)-3-methyl-|BAZEDOXIFENE|Bazedoxifene|TSE-424|WAY 140424","An indole derivative and third-generation selective estrogen receptor modulator (SERM) with potential antineoplastic activity. Upon administration, bazedoxifene specifically binds to estrogen receptors in responsive tissues, including liver, bone, breast, and endometrium. The resulting ligand-receptor complex is translocated to the nucleus where, depending on the tissue type, it either promotes or suppresses the transcription of estrogen-regulated genes. Bazedoxifene acts as an estrogen antagonist in uterine and breast tissue, thereby blocking the proliferative effects of estrogen-binding to ER-positive cells in these tissues. Bazedoxifene functions as an estrogen agonist in lipid metabolism, thereby decreasing total and LDL cholesterol levels. In bone, it decreases bone resorption and bone turnover and increases bone mineral density.","Pharmacologic Substance"]
["C1827","BBR 3464","BBR 3464","A cationic tri-nuclear platinum complex related to cisplatin.  BBR 3464 binds to and forms DNA crosslinks and platinum-DNA adducts, preventing DNA replication and tumor cell division.","Organic Chemical|Pharmacologic Substance"]
["C107685","BC-819 Plasmid/Polyethylenimine Complex","BC-819 Plasmid/Polyethylenimine Complex|BC-819/PEI|DTA-H19/PEI","A plasmid DNA encoding for the A fragment of Diphtheria Toxin (DTA) under the control of the H19 gene promoter (BC-819 or DTA-H19) and mixed with the transfectant polyethylenimine (PEI), with potential antineoplastic activity. Upon administration, the PEI moiety enhances the entry of the agent into rapidly dividing cells. Upon cell entry, activation of the H19 gene promoter-containing plasmids and DTA expression are limited to tumor cells, as high levels of H19 expression are only found in tumor cells. DTA disrupts protein synthesis. Tumor-cell selective expression of this toxin leads to the selective destruction of the tumor while sparing healthy, normal cells. H19, an oncofetal, regulatory RNA, is overexpressed in certain cancer cells while its expression in normal cells is minimal or absent; it plays a key role in cancer progression, angiogenesis and metastasis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C83496","BCG Solution","BCG Solution|BCG solution|Bacillus Calmette-Guerin Solution|TICE BCG Solution","A solution containing an attenuated, live culture preparation of the Bacillus Calmette Guerin (BCG) strain of Mycobacterium bovis with potential immunostimulating activity. Although the precise mechanism of action is unknown, upon intravesical administration, attenuated, live BCG bacteria in the solution come into direct contact with the bladder wall, inciting an antitumor granulomatous inflammatory reaction.","Pharmacologic Substance"]
["C298","BCG Vaccine","BCG (Pasteur)|BCG TICE|BCG Tice|BCG Vaccine|BCG|Bacille Calmette-Guerin Live|Bacillius Calmette-Guerin Vaccine|Bacillus Calmette Guerin|Bacillus Calmette-Guerin|Bacillus Calmette-Guérin Vaccine|Cultivo BCG|ImmuCyst|Imovax BCG|Live Intravesical BCG|Monovax|Mycobacterium bovis (Strain BCG)|Oncotice|Pacis|Pastimmun|TICE BCG","A vaccine containing bacillus Calmette-Guerin (BCG), an attenuated strain of Mycobacterium bovis, with non-specific immunoadjuvant and immunotherapeutic activities. Although the mechanism of its anti-tumor activity is unclear, immunization with BCG vaccine likely activates a Th1 cytokine response that includes the induction of interferon. Vaccination with BCG vaccine may be immunoprotective against infection with Mycobacterium tuberculosis.","Bacterium|Immunologic Factor|Pharmacologic Substance"]
["C125603","Bcl-2 Inhibitor BCL201","BCL-201|BCL201|Bcl-2 Inhibitor BCL201|S-55746|S55746|Servier 1|Servier-1","A selective inhibitor of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), with potential pro-apoptotic and antineoplastic activities. Upon administration, Bcl-2 inhibitor BCL201 binds to and inhibits the activity of Bcl-2. This restores apoptotic processes in tumor cells. Bcl-2 protein is overexpressed in many cancers and plays an important role in the negative regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival.","Pharmacologic Substance"]
["C28860","Bcl-Xs Adenovirus Vaccine","Bcl-Xs Adenovirus Vaccine","A vaccine consisting of replication-defective recombinant adenovirus that encodes for Bcl-Xs with potential antineoplastic activity.  Vaccination with Bcl-Xs adenovirus vaccine induces apoptosis in Bcl-2 and Bcl-XL positive cancer cells, resulting in decreased tumor growth while leaving normal cells unaffected.  Bcl-Xs block the function of the protooncogenes Bcl-2 and Bcl-XL which are overexpressed in a variety of solid tumors and promote cancer cell survival by inhibiting apoptosis. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C117729","BCMA-specific CAR-expressing T Lymphocytes","Anti-BCMA CAR T Cells|Anti-BCMA-CAR-transduced T Cells|BB2121|BCMA-specific CAR-expressing T Lymphocytes","A preparation of autologous peripheral blood T-lymphocytes (PBTL) that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the B-cell maturation antigen (BCMA), with potential immunostimulating and antineoplastic activities. Upon administration, BCMA-specific CAR-expressing T-lymphocytes specifically recognize and kill BCMA-expressing tumor cells. BCMA, a tumor specific antigen and a receptor for both a proliferation-inducing ligand and B-cell activating factor, is a member of the tumor necrosis factor (TNF) receptor superfamily and plays a key role in plasma survival; it is found on the surfaces of plasma cells and overexpressed on malignant plasma cells.","Pharmacologic Substance"]
["C61309","Bcr-Abl (b2a2)-Derived Peptide Vaccine","Bcr-Abl (b2a2)-Derived Peptide Vaccine|CML-VAX B2","A peptide vaccine consisting of the bcr-abl b2a2 fusion oncoprotein, frequently expressed in chronic myelogenous leukemia (CML), with potential antineoplastic activity. Vaccination with the bcr-abl (b2a2)-derived peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl b2a2 fusion protein. Fusion genes in CML typically result from the fusion of either BCR exon b2 or BCR exon b3 to ABL exon a2, a 'b3a2' or a 'b2a2' fusion.","Pharmacologic Substance"]
["C61310","Bcr-Abl (b3a2)-Derived Peptide Vaccine","Bcr-Abl (b3a2)-Derived Peptide Vaccine|CML-VAX B3","A peptide vaccine consisting of the bcr-abl b3a2 fusion oncoprotein, frequently expressed in chronic myelogenous leukemia (CML), with potential antineoplastic activity. Vaccination with the bcr-abl (b3a2)-derived peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl b3a2 fusion protein. Fusion genes in CML typically result from the fusion of either BCR exon b2 or BCR exon b3 to ABL exon a2, a 'b3a2' or a 'b2a2' fusion.","Pharmacologic Substance"]
["C130033","Bcr-Abl Kinase Inhibitor PF-114","Bcr-Abl Inhibitor PF-114|Bcr-Abl Kinase Inhibitor PF-114|PF-114","An orally bioavailable, Bcr-Abl tyrosine kinase inhibitor, with potential antineoplastic activity. Designed to overcome resistance of tumor cells to second generation Bcr-Abl inhibitors, PF-114 targets and binds to the Bcr-Abl fusion oncoprotein, including those fusion proteins with the 'gatekeeper' resistance mutation T315I, an amino acid substitution at position 315 in Bcr-Abl from a threonine (T) to an isoleucine (I). This inhibits Bcr-Abl-mediated proliferation of, and enhances apoptosis in, Philadelphia chromosome-positive (Ph+) hematologic malignancies. The Bcr-Abl fusion protein is an aberrantly activated tyrosine kinase produced by leukemia cells that contain the Philadelphia chromosome.","Pharmacologic Substance"]
["C69082","BCR-ABL p210-b3a2 Breakpoint-derived Pentapeptide Vaccine","BCR-ABL p210-b3a2 Breakpoint-derived Pentapeptide Vaccine|CML-VAX100|p210-B3A2 Derived Peptide Vaccine","A multipeptide vaccine consisting of five peptides derived from the bcr-abl p210-b3a2 breakpoint fusion protein with potential antineoplastic activity. Vaccination with bcr-abl p210-b3a2 breakpoint-derived multipeptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the bcr-abl p210-b3a2 breakpoint fusion protein. In chronic myelogenous leukemia (CML), fusion genes typically result from the fusion of either bcr exon b2 or exon b3 to abl exon a2, resulting in either a b3a2 or a b2a2 gene fusion product.","Pharmacologic Substance"]
["C2205","BCR-ABL Peptide Vaccine","BCR-ABL Peptide Vaccine|bcr-abl vaccine","A multivalent antineoplastic vaccine comprised of the bcr-abl oncogene breakpoint fusion peptide that elicits a bcr-abl specific T-cell immune response.  (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C1011","Beauvericin","Beauvericin","A cyclic hexadepsipeptide antibiotic and mycotoxin isolated from the fungus Beauveria bassiana and various Fusarium fungal species.  As a potassium-specific ionophore, beauvericin A increases intracellular calcium concentrations and triggers DNA fragmentation and apoptosis through a calcium dependent caspase 3-sensitive pathway.  This agent has been studied as a potential antineoplastic agent. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C1620","Becatecarin","1,11-Dichloro-6-[2-(diethylamino)ethyl]-12,13-dihydro-12-(4-O-methyl-beta-D-glucopyranosyl)-5H-indolo[2,3-a]pyrrolo[3,4-c]carbazole-5,7(6H)-dione|5H-Indolo(2,3-a)pyrrolo(3,4-c)carbazole-5,7(6H)-dione, 1,11-dichloro-6-(2-(diethylamino)ethyl)-12,13-dihydro-12-(4-O-methyl-beta-D-glucopyranosyl)-|BECATECARIN|BMS-181176|BMY-27557-14|Becatecarin|DEAE-Rebeccamycin|NSC 655649|Rebeccamycin Analogue, Tartrate Salt|Rebeccamycin Analogue|Rebeccamycin analog|XL119|rebeccamycin analog","A synthetic diethylaminoethyl analogue of the indolocarbazole glycoside antineoplastic antibiotic rebeccamycin.  Becatecarin intercalates into DNA and stabilizes the DNA-topoisomerase I complex, thereby interfering with the topoisomerase I-catalyzed DNA breakage-reunion reaction and initiating DNA cleavage and apoptosis.  (NCI04)","Antibiotic|Organic Chemical"]
["C73438","Belagenpumatucel-L","Belagenpumatucel-L|Lucanix","A transforming growth factor beta2 (TGF-beta2) antisense gene-modified allogeneic tumor cell vaccine with potential immunostimulatory and antineoplastic activities. Belagenpumatucel-L is prepared by transfecting allogeneic non-small cell lung cancer (NSCLC) cells with a plasmid containing a TGF-beta2 antisense transgene, expanding the cells, and then irradiating and freezing them. Upon administration, this agent may elicit a cytotoxic T lymphocyte (CTL) response against host NSCLC cells, resulting in decreased tumor cell proliferation; vaccine immunogenicity may be potentiated by suppression of tumor TGF-beta2 production by antisense RNA expressed by the vaccine plasmid TGF-beta2 antisense transgene. Elevated levels of TGF-beta2 are frequently linked to immunosuppression in cancer patients and may be inversely correlated with prognosis in patients with NSCLC.","Cell|Pharmacologic Substance"]
["C48812","Belinostat","BELINOSTAT|Beleodaq|Belinostat|PXD 101|PXD101|belinostat","A novel hydroxamic acid-type histone deacetylase (HDAC) inhibitor with antineoplastic activity. Belinostat targets HDAC enzymes, thereby inhibiting tumor cell proliferation, inducing apoptosis, promoting cellular differentiation, and inhibiting angiogenesis. This agent may sensitize drug-resistant tumor cells to other antineoplastic agents, possibly through a mechanism involving the down-regulation of thymidylate synthase.","Organic Chemical|Pharmacologic Substance"]
["C66954","Belotecan Hydrochloride","BELOTECAN HYDROCHLORIDE|Belotecan Hydrochloride|CKD602 HCl|belotecan hydrochloride","The hydrochloride salt of the semi-synthetic camptothecin analogue belotecan with potential antitumor activity. Belotecan binds to and inhibits the activity of topoisomerase I, stabilizing the cleavable complex of topoisomerase I-DNA, which inhibits the religation of single-stranded DNA breaks generated by topoisomerase I; lethal double-stranded DNA breaks occur when the topoisomerase I-DNA complex is encountered by the DNA replication machinery, DNA replication is disrupted, and the tumor cell undergoes apoptosis. Topoisomerase I is an enzyme that mediates reversible single-strand breaks in DNA during DNA replication.","Pharmacologic Substance"]
["C73231","Benaxibine","4-Aminobenzoic acid-N-xyloside|BENAXIBINE|Benaxibine","A cyclophosphamide synergizer with antineoplastic, antidiabetic, antihypertensive and immunopotentiating activity. Benaxibine is active against integrin alph-4 precursor.","Pharmacologic Substance"]
["C73261","Bendamustine","5-(Bis(2-chloroethyl)amino)-1-methyl-2-benzimidazolebutyric Acid|BENDAMUSTINE|Bendamustine|SDX-105|bendamustine","A bifunctional mechlorethamine derivative with alkylating and antimetabolite activities. Although the exact mechanism of action of bendamustine is unknown, this agent appears to alkylate and crosslink macromolecules, resulting in DNA, RNA and protein synthesis inhibition, and eventually the induction of apoptosis.","Pharmacologic Substance"]
["C61565","Bendamustine Hydrochloride","2-Benzimidazolinebutryric acid, 1-methyl-5-bis(2-chloroethyl)amino-, hydrochloride|BENDAMUSTINE HYDROCHLORIDE|Bendamustin Hydrochloride|Bendamustine Hydrochloride|Cytostasan Hydrochloride|Levact|Ribomustin|SyB L-0501|Treanda|bendamustine hydrochloride","The hydrochloride salt of bendamustine, a bifunctional mechlorethamine derivative with alkylator and antimetabolite activities. Bendamustine possesses three active moieties: an alkylating group; a benzimidazole ring, which may act as a purine analogue; and a butyric acid side chain. Although its exact mechanism of action is unknown this agent appears to act primarily as an alkylator. Bendamustine metabolites alkylate and crosslink macromolecules, resulting in DNA, RNA and protein synthesis inhibition, and, subsequently, apoptosis. Bendamustine may differ from other alkylators in that it may be more potent in activating p53-dependent stress pathways and inducing apoptosis; it may induce mitotic catastrophe; and it may activate a base excision DNA repair pathway rather than an alkyltransferase DNA repair mechanism. Accordingly, this agent may be more efficacious and less susceptible to drug resistance than other alkylators.","Nucleic Acid, Nucleoside, or Nucleotide"]
["C124053","Bendamustine-containing Nanoparticle-based Formulation RXDX-107","Bendamustine-containing Nanoparticle-based Formulation RXDX-107|CEP-40125|RXDX 107|RXDX-107","A nanoparticle-based formulation containing the alkyl ester of bendamustine, a bifunctional mechlorethamine derivative, encapsulated in human serum albumin (HSA), with potential alkylating and antineoplastic activities. Upon administration of the alkyl ester bendamustine-containing nanoparticle formulation RXDX-107, the nanoparticle formulation permits high concentrations of the alkyl ester of bendamustine be localized at the tumor site. The modified bendamustine alkylates and crosslinks macromolecules, resulting in DNA, RNA and protein synthesis inhibition, and, subsequently, apoptosis.","Pharmacologic Substance"]
["C126105","Bendamustine-Vorinostat Fusion Molecule EDO-S101","7-(5-(Bis(2-chloroethyl)amino)-1-methyl-1H-benzo[d]imidazol-2-yl)-N-hydroxyheptanamide|Bendamustine-Vorinostat Fusion Molecule EDO-S101|EDO-S 101|EDO-S-101|EDO-S101","An alkylating histone-deacetylase inhibitor (HDACi) fusion molecule composed of the alkylating agent bendamustine fused to the pan-HDACi vorinostat, with potential bi-functional antineoplastic activity. Upon administration of the bendamustine-vorinostat fusion molecule EDO-S101, the vorinostat moiety targets and binds to HDACs. This leads to an accumulation of highly acetylated histones, which results in an induction of chromatin remodeling, a modulation of gene expression, an inhibition of tumor cell division and the induction of tumor cell apoptosis. The bendamustine moiety binds to, alkylates and crosslinks macromolecules, inhibiting DNA, RNA and protein synthesis, which also results in tumor cell apoptosis. Thus, EDO-S101 shows superior efficacy compared to the activity of either agent alone. In addition, the inhibition of HDAC6 activity by EDO-S101 induces the activation of inositol-requiring enzyme 1 (IRE-1), the key regulatory protein for the unfolded protein response (UPR). Induction of the UPR increases the sensitivity of certain cancer cell types to certain chemotherapeutic agents, such as proteasome inhibitors. Therefore, EDO-S101 may work synergistically with proteasome inhibitors. HDACs, enzymes that deacetylate chromatin histone proteins, are overexpressed in various cancers and play a key role in proliferation and resistance of tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C107164","Benzaldehyde Dimethane Sulfonate","BEN|Benzaldehyde Dimethane Sulfonate|DMS-612|DMS612|NSC 281612","A dimethane sulfonate derivative and alkylating agent with a structure similar to other alkylating agents such as chlorambucil, busulfan and melphalan, with potential antineoplastic activity. Although the exact mechanism of action has yet to be fully elucidated, benzaldehyde dimethane sulfonate alkylates DNA, which results in DNA double strand breaks, inhibition of DNA replication, cell cycle arrest and cell death. In addition, this agent is metabolized by the enzyme aldehyde dehydrogenase (ALDH) into the active carboxylic acid metabolite benzoic acid dimethane sulfonate (BA), which further contributes to its alkylating activity. Unlike other alkylating agents, benzaldehyde dimethane sulfonate has demonstrated antitumor activity in renal cell carcinoma.","Organic Chemical|Pharmacologic Substance"]
["C2618","Benzoylphenylurea","BPU|Benzoylphenylurea|benzoylphenylurea","A low molecular weight agent with antineoplastic activity. Benzoylphenylurea binds to the colchicine binding site on tubulin, thereby blocking tubulin polymerization and disrupting mitotic function.  This agent also inhibits DNA polymerase, and has been shown to arrest leukemia cells in the G1-S transition phase of the cell cycle. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C87331","Berberine Chloride","5,6-Dihydro-9,10-Dimethoxybenzo(G)-1,3-Benzodioxolo(5,6-A)Quinolizinium Chloride|BERBERINE CHLORIDE|Berberine Chloride Dihydrate|Berberine Chloride|Berberine Hydrochloride|Berberinum Chloride","The orally bioavailable, hydrochloride salt form of berberine, a quaternary ammonium salt of an isoquinoline alkaloid and active component of various Chinese herbs, with potential antineoplastic, radiosensitizing, anti-inflammatory, anti-lipidemic and antidiabetic activities. Although the mechanisms of action through which berberine exerts its effects are not yet fully elucidated, upon administration this agent appears to suppress the activation of various proteins and/or modulate the expression of a variety of genes involved in tumorigenesis and inflammation, including, but not limited to transcription factor nuclear factor-kappa B (NF-kB), myeloid cell leukemia 1 (Mcl-1), B-cell lymphoma 2 (Bcl-2), B-cell lymphoma-extra large (Bcl-xl), cyclooxygenase (COX)-2, tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1), E-selectin, monocyte chemoattractant protein-1 (MCP-1), C-X-C motif chemokine 2 (CXCL2), cyclin D1, activator protein (AP-1), hypoxia-inducible factor 1 (HIF-1), signal transducer and activator of transcription 3 (STAT3), peroxisome proliferator-activated receptor (PPAR), arylamine N-acetyltransferase (NAT), and DNA topoisomerase I and II. The modulation of gene expression may induce cell cycle arrest and apoptosis, and inhibit cancer cell proliferation.  In addition, berberine modulates lipid and glucose metabolism.","Pharmacologic Substance"]
["C61568","Berubicin Hydrochloride","(8S,10S)-10-((3-amino-4-O-benzyl-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy)- 6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-7,8,9,10-tetrahydrotetracene-5,12-dione Hydrochloride|BERUBICIN HYDROCHLORIDE|Berubicin Hydrochloride|RTA 744|WP744|topoisomerase II inhibitor RTA 744","The hydrochloride salt of the anthracycline derivative berubicin with potential antineoplastic activity. Berubicin intercalates into DNA and interrupts topoisomerase II activity, resulting in the inhibition of DNA replication and repair, and RNA and protein synthesis. Unlike other anthracycline derivatives, this agent crosses the blood-brain barrier (BBB).","Pharmacologic Substance"]
["C126805","BET Bromodomain Inhibitor ZEN-3694","BET Bromodomain Inhibitor ZEN-3694|BETi ZEN-3694|ZEN 3694|ZEN-3694|ZEN003694","An orally bioavailable inhibitor of the bromodomain and extra-terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor ZEN-3694 binds to the acetylated lysine recognition motifs in the bromodomains of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of proliferation in BET-overexpressing tumor cells. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.","Pharmacologic Substance"]
["C103298","BET Bromodomains 2/3/4 Inhibitor MK-8628","6H-Thieno(3,2-f)(1,2,4)triazolo(4,3-a)(1,4)diazepine-6-acetamide, 4-(4-Chlorophenyl)-N-(4-hydroxyphenyl)-2,3,9-trimethyl-, (6S)-|BET Bromodomains 2/3/4 Inhibitor MK-8628|BRD 2/3/4 Inhibitor OTX015|MK-8628|OTX015","A synthetic, small molecule inhibitor of the BET (Bromodomain and Extra-Terminal) family of bromodomain-containing proteins 2, 3 and 4 with potential antineoplastic activity. Upon administration, the BET bromodomains 2, 3 and 4 inhibitor MK-8628 binds to the acetylated lysine recognition motifs on the bromodomain of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histone peptides. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes, including c-Myc-dependent target genes, may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomain at the N-terminus, the BET proteins BRD2, BRD3, BRD4 are transcriptional regulators that play an important role in cellular growth.","Pharmacologic Substance"]
["C121213","BET Inhibitor BAY1238097","BAY 1238097|BAY1238097|BET Inhibitor BAY1238097","An inhibitor of the Bromodomain (BRD) and Extra-Terminal domain (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor BAY1238097 binds to the acetylated lysine recognition motifs on the BRD of BET proteins, thereby preventing the interaction between BET proteins and histones. This disrupts chromatin remodeling and prevents the expression of certain growth-promoting genes. This leads to an inhibition of tumor cell growth. BET proteins (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that bind to acetylated lysines on the tails of histones H3 and H4, and regulate chromatin structure and function; they play an important role in the modulation of gene expression during development and cellular growth.","Pharmacologic Substance"]
["C121849","BET Inhibitor BMS-986158","BET Inhibitor BMS-986158|BMS-986158","An inhibitor of the Bromodomain (BRD) and Extra-Terminal domain (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor BMS-986158 binds to the acetyl-lysine binding site in the BRD of BET proteins, thereby preventing the interaction between BET proteins and acetylated histones. This disrupts chromatin remodeling and prevents the expression of certain growth-promoting genes, resulting in an inhibition of tumor cell growth. BET proteins (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that bind to acetylated lysines on the tails of histones H3 and H4, and regulate chromatin structure and function; they play an important role in the modulation of gene expression during development and cellular growth.","Pharmacologic Substance"]
["C111901","BET Inhibitor CPI-0610","BET Inhibitor CPI-0610|CPI-0610","A small molecule inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor CPI-0610 binds to the acetylated lysine recognition motifs on the bromodomain of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histone peptides. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of two bromodomains at the N-terminus, the BET proteins (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that play an important role during development and cellular growth.","Pharmacologic Substance"]
["C123733","BET Inhibitor FT-1101","BET Inhibitor FT-1101|FT-1101|FT1101","An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon administration, the BET inhibitor FT-1101 binds to the acetylated lysine recognition motifs in the bromodomain sites of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to the inhibition of tumor cell growth. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.","Pharmacologic Substance"]
["C125391","BET Inhibitor GSK2820151","BET Inhibitor GSK2820151|GSK 2820151|GSK2820151","An orally bioavailable inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon oral administration, the BET inhibitor GSK2820151 binds to the acetylated lysine recognition motifs in the bromodomains of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.","Pharmacologic Substance"]
["C101538","BET Inhibitor GSK525762","BET Inhibitor GSK525762|GSK525762","A small molecule inhibitor of the BET (Bromodomain and Extra-Terminal) family of bromodomain-containing proteins with potential antineoplastic activity. Upon administration, the BET inhibitor GSK525762 binds to the acetylated lysine recognition motifs on the bromodomain of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histone peptides. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomain at the N-terminus, BET proteins, comprising of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during development and cellular growth.","Pharmacologic Substance"]
["C121948","BET Inhibitor INCB054329","BET Inhibitor INCB054329|INCB054329","An inhibitor of the Bromodomain and Extra-Terminal (BET) family of bromodomain-containing proteins with potential antineoplastic activity. Upon administration, the BET inhibitor INCB054329 binds to the acetylated lysine recognition motifs on the bromodomain of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomain at the N-terminus, BET proteins, BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular growth.","Pharmacologic Substance"]
["C112500","BET Inhibitor TEN-010","BET Inhibitor TEN-010|TEN-010","A small molecule inhibitor of the BET (Bromodomain and Extra-Terminal) family of bromodomain-containing proteins with potential antineoplastic activity. Upon administration, the BET inhibitor TEN-010 binds to the acetylated lysine recognition motifs found in the bromodomain of BET proteins, which prevents the interaction between BET proteins and acetylated histones. This interaction disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of bromodomains at the N-terminus, BET proteins, comprised of BRD2, BRD3, BRD4 and BRDT, are transcriptional regulators that play an important role during cellular development and growth.","Pharmacologic Substance"]
["C2605","Beta Alethine","ALETHINE|Alethine|Beta Alethine|Beta-alanyl-cysteamine Disulfide|BetaLT|Betathine|N,N'-(Dithiodiethylene)bis(3-aminopropionamide)|beta alethine","A disulfide agent that stimulates T and B-cell functions and exhibits anti-tumor and immunostimulant activity. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C1016","Beta-Carotene",".BETA.-CAROTENE|.beta.-Carotene|3,7,12,16-tetramethyl-1,18-bis(2,6,6-trimethyl-1-cyclohexenyl)-octadeca-1,3,5,7,9,11,13,15,17-nonaene|Beta Carotene|Beta-Carotene|Beta-carotene|CAROTENE, BETA|Lumitene|Solatene|beta carotene|beta-Carotene","A naturally-occurring retinol (vitamin A) precursor obtained from certain fruits and vegetables with potential antineoplastic and chemopreventive activities.  As an anti-oxidant, beta carotene inhibits free-radical damage to DNA.  This agent also induces cell differentiation and apoptosis of some tumor cell types, particularly in early stages of tumorigenesis, and enhances immune system activity by stimulating the release of natural killer cells, lymphocytes, and monocytes. (NCI04)","Pharmacologic Substance|Vitamin"]
["C103177","Beta-elemene","(1S,2S,4R)-2,4-diisopropenyl-1-methyl-1-vinylcyclohexane|(1alpha,2beta,4beta)-1-Methyl-2,4-bis(methylvinyl)-1- vinylcyclohexane|Beta-elemene","One of the isomers of elemene, a lipid soluble sesquiterpene and the active component isolated from the Chinese medicinal herb Rhizoma zedoariae with potential antineoplastic and chemopreventive activities. Although the exact mechanism of action through which beta-elemene exerts its effect has yet to be fully elucidated, this agent appears to induce apoptosis through different mechanisms of action and induces cell cycle arrest at different stages based on the tumor cell type involved. Beta-elemene may sensitize cancer cells to other chemotherapeutic agents.","Pharmacologic Substance"]
["C2678","Beta-Glucan","Beta-Glucan|beta-glucan","A polysaccharide isolated from the cell walls of bacteria, plants, and fungi with immunostimulant and antineoplastic activities. In a solubilized form, beta-glucan binds to a lectin site within complement receptor 3 (CR3) on leukocytes, priming the receptor to trigger cytotoxic degranulation of leukocytes when leukocyte CR3 binds to complement 3 (iC3b)-coated tumors. Thus, the attachment of beta-glucan to CR3 of circulating leukocytes simulates leukocytes to kill iC3b-coated tumor cells in the same way as they kill iC3b-coated yeast. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C82657","Beta-Glucan MM-10-001","Beta-Glucan MM-10-001|MM-10-001","A powder formulation containing a triple helix beta-glucan, isolated from the cell walls of the shiitake mushroom (Lentinula edodes), with potential immunostimulating activity. The beta-glucan in beta-glucan MM-10-001 binds to a lectin site within the complement receptor 3 (CR3 or iC3b receptor) on leukocytes, priming the receptor to trigger cytotoxic degranulation of leukocytes when leukocyte CR3 binds to iC3b-opsonized tumor cells. iC3b is the proteolyticly inactive product of the complement cleavage fragment C3b.","Organic Chemical|Pharmacologic Substance"]
["C99146","Beta-lapachone Prodrug ARQ 761","ARQ 761|Beta-lapachone Prodrug ARQ 761","A synthetic, soluble prodrug of beta-lapachone, a poorly soluble, ortho-naphthoquinone with potential antineoplastic and radiosensitizing activity. ARQ 761 is converted to beta-lapachone (b-lap) in vivo. When b-lap is activated by NAD(P)H:quinone oxidoreductase-1 (NQO1) this agent creates a futile oxidoreduction, generating highly reactive oxygen species (ROS) that results in DNA damage. The activation of b-lap also causes hyperactivation of poly (ADP-ribose) polymerase-1 (PARP-1), an enzyme that facilitates DNA repair, accompanied by rapid depletion of NAD+/ATP nucleotide levels. As a result, a caspase-independent and endoplasmic reticulum (ER) stress-induced mu-calpain-mediated cell death occurs in NQO1-overexpressing tumor cells. In addition, b-lap induces expression of the checkpoints activator E2F transcription factor 1 (E2F1) and thereby activates the E2F1-mediated checkpoint pathway that directly triggers apoptosis. As ARQ 761 is soluble and requires less solvent, this formulation may cause less hemolytic anemia associated with administration of the synthetic b-lap ARQ 501.","Organic Chemical|Pharmacologic Substance"]
["C1350","Beta-Thioguanine Deoxyriboside",".beta.-2'-Deoxy-6-thioguanosine|.beta.-2'-Deoxythioguanosine|.beta.-2'-Deoxythiol guanosine|.beta.-Thioguanine deoxyriboside|1,9-dihydro-6H-purine-6-thione, 2-amino-9-(2-deoxy-beta-D-erythro-pentofuranosyl)|2'-Deoxythioguanosine|2'-Desoxy-6-thioguanosine|2'-deoxythioguanosine|2'-desoxy-6-thioguanosine|6-Mercaptoguaninedeoxyriboside|6H-Purine-6-thione, 2-amino-9-(2-deoxy-.beta.-D-erythro-pentofuranosyl)-1,9-dihydro-|9H-Purine-6-thiol, 2-amino-9-(2-deoxy-.beta.-D-erythro-pentofuranosyl)-, monohydrate|9H-purine-6-thiol, 2-amino-9-(2-deoxy-beta-D-erythro-pentofuranosyl) monohydrate|B-TGDR|BTG|Beta Thioguanine Deoxyriboside|Beta-Thioguanine Deoxyriboside|Thioguanine 9.beta.D-2'-deoxyriboside|beta-2'-deoxy-6-thioguanosine|beta-2'-deoxythioguanosine|beta-2'-deoxythiol guanosine|thioguanine 9-beta-D-2'-deoxyriboside","A thiopurine nucleoside derivative with antineoplastic activity. After conversion to the triphosphate, beta-thioguanine deoxyriboside is incorporated into DNA, resulting in inhibition of DNA replication.  This agent is cytotoxic against leukemia cell lines and has demonstrated some activity against leukemia cells in vivo.  Beta-thioguanine deoxyriboside demonstrates antineoplastic activity against 6-thioguanine-resistant tumor cells. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C38126","Betulinic Acid","(3beta)-3-Hydroxy-lup-20(29)-en-28-oic Acid|ALS-357|BETULINIC ACID|Betulinic Acid|Mairin","A pentacyclic lupane-type triterpene derivative of betulin (isolated from the bark of Betula alba, the common white birch) with antiinflammatory, anti-HIV and antineoplastic activities. Betulinic acid induces apoptosis through induction of changes in mitochondrial membrane potential, production of reactive oxygen species, and opening of mitochondrial permeability transition pores, resulting in the release of mitochondrial apogenic factors, activation of caspases, and DNA fragmentation. Although originally thought to exhibit specific cytotoxicity against melanoma cells, this agent has been found to be cytotoxic against non-melanoma tumor cell types including neuroectodermal and brain tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C2039","Bevacizumab","Anti-VEGF Humanized Monoclonal Antibody|Anti-VEGF rhuMAb|Anti-VEGF|Avastin|BEVACIZUMAB|Bevacizumab Biosimilar BEVZ92|Bevacizumab Biosimilar BI 695502|Bevacizumab Biosimilar FKB238|Bevacizumab|Immunoglobulin G1 (Human-Mouse Monoclonal rhuMab-VEGF Gamma-Chain Anti-Human Vascular Endothelial Growth Factor), Disulfide With Human-Mouse Monoclonal rhuMab-VEGF Light Chain, Dimer|Recombinant Humanized Anti-VEGF Monoclonal Antibody|bevacizumab|rhuMab-VEGF","A recombinant humanized monoclonal antibody directed against the vascular endothelial growth factor (VEGF), a pro-angiogenic cytokine.  Bevacizumab binds to VEGF and inhibits VEGF receptor binding, thereby preventing the growth and maintenance of tumor blood vessels.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C101261","Bevacizumab-IRDye 800CW","Bevacizumab-IRDye 800CW","An immunoconjugate and a fluorescent tracer consisting of the recombinant humanized anti-vascular endothelial growth factor (VEGF) monoclonal antibody bevacizumab conjugated to the N-hydroxysuccinamide (NHS) ester form of the near-infrared (NIR) fluorescent dye IRDye 800CW, that may be used for VEGF-specific tumor imaging. Upon administration, the bevacizumab moiety of bevacizumab-IRDye 800CW binds to VEGF and the fluorescent signal can be visualized using NIR fluorescence imaging (700-1,000 nm).","Pharmacologic Substance"]
["C1635","Bexarotene","3-methyl TTNEB|4-[1-(5,6,7,8-Tetrahydro-3,5,5,8,8-pentamethyl-2-naphthalenyl)ethenyl]benzoic Acid|BEXAROTENE|Bexarotene|LGD1069|Targretin|bexarotene","A synthetic retinoic acid agent with potential antineoplastic, chemopreventive, teratogenic and embryotoxic properties.  Bexarotene selectively binds to and activates retinoid X receptors (RXRs), thereby inducing changes in gene expression that lead to cell differentiation, decreased cell proliferation, apoptosis of some cancer cell types, and tumor regression. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C114384","BH3 Mimetic ABT-737","ABT-737|BH3 Mimetic ABT-737|Benzamide, 4-(4-((4'-Chloro(1,1'-biphenyl)-2-yl)methyl)-1-piperazinyl)-n-((4-(((1r)-3-(dimethylamino)-1-((phenylthio)methyl)propyl)amino)-3-nitrophenyl)sulfonyl)-","An orally bioavailable, selective small molecule B-cell lymphoma 2 (Bcl-2) Homology 3 (BH3) mimetic, with potential pro-apoptotic and antineoplastic activities. ABT-737 binds to the hydrophobic groove of multiple members of the anti-apoptotic Bcl-2 protein family, including Bcl-2, Bcl-xl and Bcl-w. This inhibits the activity of these pro-survival proteins and restores apoptotic processes in tumor cells, via activation of Bak/Bax-mediated apoptosis. The pro-survival Bcl-2 proteins are overexpressed in many cancers and play important roles in the regulation of apoptosis. Their expression is associated with increased drug resistance and tumor cell survival. ABT-737 does not inhibit the pro-survival proteins Mcl-1, Bcl-B, Bfl-1 (A1); therefore, tumors that overexpress these Bcl-2 family proteins are resistant to ABT-737.","Pharmacologic Substance"]
["C49091","BI 2536","BI 2536","A small molecule compound with potential antineoplastic activities. BI 2536 binds to and inhibits Polo-like kinase 1 (Plk1), resulting in mitotic arrest, disruption of cytokinesis, and apoptosis in susceptible tumor cell populations. Plk1, a serine/threonine-protein kinase, is a key regulator of multiple processes fundamental to mitosis and cell division.","Pharmacologic Substance"]
["C2539","BIBX 1382","BIBX 1382|BIBX1382","A pyrimido-pyrimidine with antitumor activity. BIBX 1382 inhibits the intracellular tyrosine kinase domain of the Epidermal Growth Factor Receptor (EGFR) thus specifically reversing the aberrant enzymatic activity from overexpressed and constitutively activated EGFR, and subsequently inhibiting cell proliferation and inducing cell differentiation.","Organic Chemical|Pharmacologic Substance"]
["C1599","Bicalutamide","(+/-)-N-[4-Cyano-3-(trifluoromethyl)phenyl]-3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanamide|4'-Cyano-alpha,alpha,alpha-trifuloro-3-[(p-fluorophenyl)sulfonyl]-2-methyl-m-lactotoluidide|4-Cyano-3-trifluoromethyl-N-(3-p-fluorophenylsulfonyl-2-hydroxy-2-methylpropionyl)aniline|BICALUTAMIDE|Bicalutamide|Casodex|Cosudex|ICI 176,334|ICI 176334|N-[4-Cyano-3-(trifluoromethyl)phenyl]3-3[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methyl-propanamide|bicalutamide","A synthetic, nonsteroidal antiandrogen.  Bicalutamide competitively binds to cytosolic androgen receptors in target tissues, thereby inhibiting the receptor binding of androgens. This agent does not bind to most mutated forms of androgen receptors. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C99224","Bi-functional Alkylating Agent VAL-083","Bi-functional Alkylating Agent VAL-083|VAL-083|VAL083","A bi-functional alkylating agent, with potential antineoplastic activity. Upon administration, VAL-083 crosses the blood brain barrier (BBB) and appears to be selective for tumor cells. This agent alkylates and crosslinks DNA which ultimately leads to a reduction in cancer cell proliferation. In addition, VAL-083 does not show cross-resistance to other conventional chemotherapeutic agents and has a long half-life in the brain.","Organic Chemical|Pharmacologic Substance"]
["C127121","Bifunctional Expression Vector Plasmid DNA-bi-shRNA EWS/FLI1 Type 1 Lipoplex","Bifunctional Expression Vector Plasmid DNA-bi-shRNA EWS/FLI1 Type 1 Lipoplex|Pbi-functional Short Hairpin RNA EWS/FLI1 Type 1 Lipoplex|Pbi-functional shRNA EWS-FLI1 Type 1 Lipoplex|Pbi-shRNA EWS/FLI1 Type 1 Lipoplex|pbi-shRNA EWS/FLI1 Type 1 LP|pbi-shRNA EWS/FLI1 Type 1 LPX","A proprietary plasmid DNA expression vector encoding bi-functional short hairpin RNAs (bi-shRNAs) targeting the identical type 1 translocation junction region of the human fusion oncogene Ewing sarcoma (EWS)/Ets family transcription factor Friend leukemia virus integration 1 (FLI1) and are encapsulated in liposomal delivery vehicle (lipoplex; LPX), with potential antineoplastic activity. pbi-shRNA EWS/FLI1 type 1 contains 2 stem-loop structures encoded by a plasmid vector: one cleavage-dependent unit with perfectly matched passenger- and guide-strand, which is the small interfering RNA (siRNA)-like component, and one cleavage-independent unit composed of a strategically mismatched double strand, which is the microRNA (miRNA)-like component. Upon intratumoral administration and transcription into tumor cells, one shRNA unit with an imperfectly matched sequence causes inhibition of EWS/FLI1 messenger RNA (mRNA) translation (through mRNA sequestration and cleavage-independent degradation) while the other unit with a perfectly matched sequence promotes EWS/FLI1 mRNA degradation (through cleavage-dependent mRNA silencing). This prevents EWS/FLI1 expression in tumor cells, which results in a reduction of tumor cell proliferation. The EWS/FLI1 type 1 fusion gene product is overexpressed in type 1 Ewing's sarcoma and correlates with increased tumor proliferation and poor prognosis.","Pharmacologic Substance"]
["C589","Binetrakin","B Cell Proliferating Factor|B-Cell Growth Factor|B-Cell Stimulating Factor|B-Cell Stimulatory Factor 1|BCGF|BCSF 1|BINETRAKIN|Binetrakin|IL-4|Interleukin-4|MCGF 2|Mast Cell Growth Factor-2|RHIL-4|Recombinant Human IL-4|T-Cell Growth Factor 2","A recombinant agent chemically identical to or similar to the endogenous cytokine interleukin-4 (IL-4). Produced primarily by activated T-cells, IL-4 binds to and activates its cell-surface receptor, stimulating the proliferation and differentiation of activated B-cells and enhancing their ability to present antigens to T-cells. As a potential immunotherapeutic agent, recombinant IL-4 also augments the effects of other cytokines on dendritic cells (DC), cytotoxic T lymphocytes (CTL), and tumor-infiltrating lymphocytes (TIL).","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C84865","Binimetinib","ARRY-162|ARRY-438162|Binimetinib|MEK162","An orally available inhibitor of mitogen-activated protein kinase kinase 1 and 2 (MEK1/2) with potential antineoplastic activity. Binimetinib, noncompetitive with ATP, binds to and inhibits the activity of MEK1/2. Inhibition of MEK1/2 prevents the activation of MEK1/2 dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling. This may eventually lead to an inhibition of tumor cell proliferation and an inhibition in production of various inflammatory cytokines including interleukin-1, -6 and tumor necrosis factor. MEK1/2 are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C2206","Biomed 101","Biomed 101","An agent binding to the leukotriene B4 receptor, leading to reduced interleukin-2 mediated hypoxia. Biomed 101 does not affect interleukin-2 antitumor activity.  (NCI04)","Pharmacologic Substance"]
["C88295","Birinapant","Birinapant|Propanamide, N,N'-[(6,6'-difluoro[2,2'-bi-1H-indole]-3,3'-diyl)bis[methylene[(2R,4S)-4-hydroxy-2,1-pyrrolidinediyl][(1S)-1-ethyl-2-oxo-2,1-ethanediyl]]]bis[2-(methylamino)-,(2S,2'S)-|TL32711","A synthetic small molecule that is both a peptidomimetic of second mitochondrial-derived activator of caspases (SMAC) and inhibitor of IAP (Inhibitor of Apoptosis Protein) family proteins, with potential antineoplastic activity. As a SMAC mimetic and IAP antagonist, birinapant selectively binds to and inhibits the activity of IAPs, such as X chromosome-linked IAP (XIAP) and cellular IAPs 1 (cIAP1) and 2 (cIAP2), with a greater effect on cIAP1 than cIAP2. Since IAPs shield cancer cells from the apoptosis process, this agent may restore and promote the induction of apoptosis through apoptotic signaling pathways in cancer cells and inactivate the nuclear factor-kappa B (NF-kB)-mediated survival pathway. IAPs are overexpressed by many cancer cell types. They are able to suppress apoptosis by binding to, via their baculoviral lAP repeat (BIR) domains, and inhibiting active caspases-3, -7 and -9. IAP overexpression promotes both cancer cell survival and chemotherapy resistance.","Pharmacologic Substance"]
["C62514","Bis(choline)tetrathiomolybdate","ATN-224|BIS(CHOLINE)TETRATHIOMOLYBDATE|Bis(choline)tetrathiomolybdate|Ethanaminium, 2-Hydroxy-N,N,N-Trimethyl-, (T-4)-Tetrathioxomolybdate(2-) (2:1)|SOD1 Inhibitor ATN-224|SOD1 inhibitor ATN-224","An orally active second generation tetrathiomolybdate analog with anti-angiogenic and antineoplastic activities. ATN-224 selectively chelates the copper ion in superoxide dismutase 1 (SOD1) in endothelial cells, thereby depleting SOD1 of copper and inhibiting its activity. Inhibition of SOD1 interferes with the activation of several signal transduction pathways required for cellular proliferation and angiogenesis, including those mediated by ERK1/2 and FAK and Src kinases. This results in an inhibition of cell proliferation and angiogenesis as well as induction of apoptosis.","Pharmacologic Substance"]
["C1019","Bisantrene","9,10-Anthracenedicarboxakdehyde Bis[(4,5-dihydro-1H-imidazol-2-yl)hydrazone]|9,10-Anthracenedicarboxaldehyde Bis(2-imidazolin-2-yl)hydrazone|BISANTRENE|Bisantrene","An anthracenyl bishydrazone with antineoplastic activity. Bisantrene intercalates with and disrupts the configuration of DNA, resulting in DNA single-strand breaks, DNA-protein crosslinking, and inhibition of DNA replication.  This agent is similar to doxorubicin in activity, but unlike doxorubicin, does not exhibit cardiotoxicity. (NCI04)","Antibiotic|Organic Chemical"]
["C77218","Bisantrene Hydrochloride","9,10,Anthracenedicarboxaldehyde Dihydrochloride|9,10-Anthracenedicarboxakdehyde Bis[(4,5-dihydro-1H-imidazol-2-yl)hydrazone] Dihydrochloride|9,10-Anthracenedicarboxaldehyde Bis(2-imidazolin-2-yl)hydrazone Dihydrochloride|BISANTRENE HYDROCHLORIDE|Bisantrene Dihydrochloride|Bisantrene Hydrochloride|CL 216942|CL-216942|Orange Crush|Zantrene","The hydrochloride salt of an anthracenyl bishydrazone with antineoplastic activity. Bisantrene intercalates with and disrupts the helical structure of DNA, resulting in DNA single-strand breaks, DNA-protein crosslinking, and inhibition of DNA replication. This agent is similar to doxorubicin in activity, but unlike doxorubicin, does not exhibit cardiotoxicity.","Antibiotic|Organic Chemical"]
["C90552","bi-shRNA-Furin/GM-CSF-Expressing Autologous Tumor Cell Vaccine","FANG Vaccine|Vigil|bi-shRNA-Furin and Granulocyte Macrophage Colony Stimulating Factor Augmented Autologous Tumor Cell Vaccine|bi-shRNA-Furin/GM-CSF-Expressing Autologous Tumor Cell Vaccine","Autologous tumor cells transfected with a plasmid expressing recombinant human granulocyte macrophage-colony stimulating factor (rhGM-CSF) and bifunctional short hairpin RNA (bi-shRNA) against furin, with potential immunostimulatory and antineoplastic activities. Upon intradermal vaccination of bi-shRNA-furin/GM-CSF-expressing autologous tumor cell vaccine, expressed GM-CSF protein, a potent stimulator of the immune system, recruits immune effectors to the site of injection and promotes antigen presentation. The furin bifunctional shRNA blocks furin protein production. Decreased levels of furin lead to a reduction in the conversion of transforming growth factor (TGF) beta into TGF beta1 and beta2 protein isoforms. In turn, as part of the negative feedback mechanism, reduced furin protein levels inhibit TGFbeta1 and TGFbeta2 gene expression, thereby further decreasing TGF levels. As TGFs are potent immunosuppressive cytokines, reducing their levels may activate the immune system locally and this may eventually cause a cytotoxic T-lymphocyte (CTL) response against the tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C73611","Bisnafide","BISNAFIDE|Bisnafide|DMP 840","A bis-naphthalimide compound with anticancer activity. Bisnafide selectively intercalates guanine-cytosine (GC) rich regions of DNA, thereby interfering with DNA replication machinery and activity of topoisomerase II. As a result, this agent causes potent cytotoxicity.","Pharmacologic Substance"]
["C73307","Bisnafide Dimesylate","BISNAFIDE DIMESYLATE|Bisnafide Dimesylate","The dimesylate salt form of bisnafide, a bis-naphthalimide compound with anticancer activity. Bisnafide selectively intercalates guanine-cytosine (GC) rich regions of DNA, thereby interfering with DNA replication machinery and activity of topoisomerase II. As a result, this agent causes potent cytotoxicity.","Pharmacologic Substance"]
["C2399","Bispecific Antibody 2B1","2B1 Antibody, Bispecific|2B1 Bispecific MAb|2B1 Bispecific Murine MAb|2B1|Bispecific Antibody 2B1|MoAb 2B1 Bispecific|bsAb 2B1","A monoclonal antibody with potential antineoplastic activity.  Specific for both the immunoglobulin G (IgG) receptor CD16 and c-erbB-2, bispecific antibody 2B1 may enhance cellular immune responses against c-erbB-2-positive cells, resulting in increased tumor cell lysis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2207","Bispecific Antibody MDX447","Bispecific Antibody MDX447|BsAb MDX447|EMD 82633|MDX-447","An antibody with potential antineoplastic activity. Specific for both the high-affinity immunoglobulin G (IgG) receptor CD64 and epidermal growth factor receptor (EGFR), bispecific antibody MDX447 may enhance cellular immune responses against EGFR positive cells, resulting in increased tumor cell lysis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1578","Bispecific Antibody MDX-H210","520C9x22 Bispecific Antibody|520C9xH22 Bispecific Antibody|Antibody, Bispecific 520C9xH22|Bispecific Antibody 520C9 x H22|Bispecific Antibody MDX-H210|Bispecific Antibody MDXH210|BsAb 520C9x22|BsAb 520C9xH22|MDX-210|MDX-H210","A humanized bivalent antibody directed against both cytotoxic effector cells expressing Fc gamma receptor type I (Fc gammaRI, or CD64) and HER2/neu-overexpressing tumor cells with potential antineoplastic activity. Bispecific antibody MDX-H210 was constructed by chemically linking Fab' fragments of the anti-HER2/neu-specific monoclonal antibody 520C9 and the Fab' fragments of the anti-Fc gammaRI-specific monoclonal antibody H22. This agent selectively binds to both HER2/neu-expressing tumor cells and Fc gammaRI-expressing cytotoxic effector cells, which may trigger antibody-dependent cell-mediated cytotoxicity (ADCC) and cell lysis of HER2/neu-expressing tumor cells. While HER2/neu is overexpressed in a variety of epithelial malignancies, expression of Fc gammaRI is primarily found in cytotoxic immune cells, including monocytes, macrophages, and cytokine-activated polymorphonuclear (PMN) cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C112207","Bivalent HPV16/18 Therapeutic Cervical Cancer Vaccine","Bivalent HPV16/18 Therapeutic Cervical Cancer Vaccine|ProCervix","A bivalent human papillomavirus (HPV) therapeutic vaccine containing recombinant inactivated adenylate cyclase (CyaA) from Bordetella pertussis carrying a sequence encoding the E7 antigen of both HPV16 and 18, with potential immunostimulatory and antiviral properties. Upon administration of bivalent HPV16/18 therapeutic cervical cancer vaccine, the expressed proteins may activate cell-mediated immunity and induce both cytotoxic CD8+ T cells and CD4+ helper T cells against the target antigens HPV16-E7 and HPV18-E7, which leads to HPV viral clearance. Adenylate cyclase is a virulence factor of Bordetella pertussis. Its ability to bind to CD11b-expressing dendritic cells and deliver antigens directly to the cytosol allows the activation and induction of T-cell immunity. CyaA may also induce a B cell response.","Pharmacologic Substance"]
["C1472","Bizelesin","BIZELESIN|Benzo(1,2-b:4,3-b')dipyrrol-4-ol, 6,6'-(carbonylbis(imino-1H-indole-5,2-diylcarbonyl))bis(8-(chloromethyl)-3,6,7,8-tetrahydro-1-methyl-, (S-(R*,R*)))-|Benzo[1,2-b:4,3-b']dipyrrol-4-ol, 6, 6'-[carbonylbis(imino- 1H-indole-5, 2-diylcarbonyl)]bis[8-(chloromethyl)-3,6,7,8-tetrahydro-1-methyl-, (S-(R*,R*))]|Bizelesin|U-77779|bizelesin","A synthetic cyclopropylpyrroloindole antineoplastic antibiotic.  Bizelesin binds to the minor groove of DNA and induces interstrand cross-linking of DNA, thereby inhibiting DNA replication and RNA synthesis.  Bizelesin also enhances p53 and p21 induction and triggers G2/M cell-cycle arrest, resulting in cell senescence without apoptosis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1842","BL22 Immunotoxin","Anti-CD22 Recombinant Immunotoxin BL22|BL22 Immunotoxin [RFB4(dsFv)-PE38]|BL22 Immunotoxin|BL22 immunotoxin|BL22|Immunotoxin BL22|RFB4(dsFv)-PE38 Immunotoxin","A recombinant immunotoxin consisting of the Fv portion of the anti-CD22 antibody RFB4 fused to a fragment of Pseudomonas exotoxin-A with potential antineoplastic activity.  BL22 immunotoxin binds to CD22, an antigen expressed in B-cell malignancies, thereby delivering its toxin directly to tumor cells.  The toxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also blocks translational elongation via binding to elongation factor-2 in eukaryotic cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C26647","Black Cohosh","Actaea racemosa Root|BLACK COHOSH|Black Cohosh|Cimicifuga racemosa Root|Cimicifugae racemosae Rhizoma|Fariy Candle Root|Remifemin|black cohosh|black snakeroot|bugbane|bugwort|rattlesnake root","A triterpene-containing herb isolated from the roots and rhizomes of the plant Cimicifuga racemosa (also known as Actaea racemosa). While the mechanism of action of black cohosh is not completely understood, it appears to act as a selective estrogen receptor modulator.  In vitro, this preparation has been shown to induce cell cycle arrest and caspase-dependent apoptosis of estrogen-sensitive breast cancer cells. (NCI04)","Plant"]
["C122398","Black Raspberry Nectar","BRB Nectar|Black Raspberry Nectar","A concentrated fruit juice containing black raspberries, with potential antioxidant, pro-apoptotic, anti-angiogenic and chemopreventive activities. In addition to vitamins, minerals and phytosterols, black raspberries are rich in phenolic acids, such as gallic acid, ellagic acid, anthocyanidins, and flavonoids. Upon oral administration, the phytochemicals in the black raspberry nectar inhibit the activation of several signal transduction pathways involved in carcinogenesis and the expression of downstream target genes that are upregulated in a variety of cancer cell types. In addition, the phytochemicals in black raspberry may protect the oral microbiome and may enhance the bacterial defense against pathogens.","Pharmacologic Substance"]
["C29871","Black Tea","Black Tea|Tea, Black Extract","Black tea is an infusion of dried leaves from plants of the Theaceae family. Due to the alkaloid caffeine, its main effect is stimulation. Black teas also contain other phytochemicals such as flavonoid and flavonoid-related compounds with strong antioxidant effects. They also attenuate atherosclerotic inflammation, reduce thrombosis, promote normal endothelial function, and block expression of cellular adhesion molecules. Black tea may reduce the risk of cancer, heart diseases, infectious diseases, and degenerative diseases. (NCI04)","Food"]
["C313","Bleomycin","BLEO|BLEOMYCIN|BLM|Bleo|Bleomycin|bleomycin","A mixture of glycopeptide antineoplastic antibiotics isolated from the bacterium Streptomyces verticillus. Bleomycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.","Antibiotic|Organic Chemical"]
["C311","Bleomycin A2","BLEOMYCIN A2|Bleomycin A2|N1-(3-(Dimethylsulfonio)propyl)bleomycinamide|Pingyangmycin A2|Zhengguangmycin A2","The primary bleomycin species in bleomycin sulfate, a mixture of the sulfate salts of several basic glycopeptide antineoplastic antibiotics isolated from Streptomyces verticillus.  Bleomycin A2 forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C81672","Bleomycin B2","BLEOMYCIN B2|Bleomycin B2|Bleomycinamide, N1-(4-((aminoiminomethyl)amino)butyl)-|Dehydrophleomycin D1|N1-(4-((Aminoiminomethyl)amino)butyl)bleomycinamide|Phleomycin D2","One of the primary bleomycin species in bleomycin sulfate, a mixture of the sulfate salts of glycopeptide bleomycin A2 and B2 isolated from Streptomyces verticillus with potential antineoplastic activity. Bleomycin B2 forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.","Pharmacologic Substance"]
["C312","Bleomycin Sulfate","BLEOMYCIN SULFATE|Blanoxan|BleMomycine|Blenoxane|Bleo-S|Bleo-cell|Bleocin|Bleolem|Bleomycin Sulfas|Bleomycin Sulfate|Bleomycin Sulphate|Bleomycin sulfate|Bleomycini Sulfas|Blexane|Oil Bleo|bleomycin sulfate","A mixture of the sulfate salts of basic glycopeptide antineoplastic antibiotics isolated from Streptomyces verticillus. Bleomycin sulfate forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals which cause single- and double-stranded breaks in DNA; these reactive oxygen species also induce lipid peroxidation, carbohydrate oxidation, and alterations in prostaglandin synthesis and degradation.","Amino Acid, Peptide, or Protein|Antibiotic"]
["C62528","Blinatumomab","Anti-CD19 x Anti-CD3 Bispecific Monoclonal Antibody|Anti-CD19/Anti-CD3 Recombinant Bispecific Monoclonal Antibody MT103|BLINATUMOMAB|Blinatumomab|Blincyto|MEDI-538|MT-103","A recombinant, single-chain, anti-CD19/anti-CD3 bispecific monoclonal antibody with potential immunostimulating and antineoplastic activities. Blinatumomab possesses two antigen-recognition sites, one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B cells. This bispecific monoclonal antibody brings CD19-expressing tumor B-cells and cytotoxic T lymphocytes (CTLs) and helper T lymphocytes (HTLs) together, which may result in the CTL- and HTL-mediated cell death of CD19-expressing B-lymphocytes.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C98108","Blueberry Powder Supplement","Blueberry Powder Supplement","An orally available, dietary supplement consisting of lyophilized blueberry powder, with antioxidant and potential chemopreventive and chemosensitizing activity. In addition to vitamins and minerals, blueberries are rich in phytonutrients, such as proanthocyanidins, anthocyanins (e.g. malvidin, delphinidin, pelargonidin, cyanidin, petunidin, and peonidin), hydroxycinnamic acids, hydroxybenzoic acids, pterostilbene, resveratrol, and flavonols (e.g. kaempferol, quercetin and myricetin). Although the exact mechanism of action through which blueberries may exert their anti-tumor effect has yet to be fully elucidated, the effects of blueberry powder on cancer cells may be attributable to the phytonutrient's antioxidant and pro-apoptotic activities.","Pharmacologic Substance"]
["C121645","BMI1 Inhibitor PTC596","BMI1 Inhibitor PTC596|PTC596|Polycomb Ring Finger Oncogene Inhibitor PTC596","An orally active inhibitor of the polycomb ring finger oncogene BMI1 (B-cell-specific Moloney murine leukemia virus integration site 1), with potential antineoplastic activity. Upon oral administration, BMI1 inhibitor PTC596 targets BMI1 expressed by both tumor cells and cancer stem cells (CSCs), and induces hyper-phosphorylation of BMI1 leading to its degradation. This inhibits BMI1-mediated signal transduction pathways and results in a reduction of proliferation of BMI1-expressing tumor cells.  BMI1, a key protein in the polycomb repressive complex 1 (PRC1), is overexpressed in certain tumor cell types, and plays a key role in CSC survival, proliferation and resistance to chemotherapeutics; its expression is associated with increased tumor aggressiveness and a poor prognosis.","Pharmacologic Substance"]
["C1843","BMS-184476","7-O-[(Methylthio)methyl]paclitaxel|BMS-184476|beta-(Benzoylamino)-a-hydroxybenzenepropanoic Acid (aR,bS)-(2aR,4S,4aS,6R,9S,11S,12S,12aR,12bS)-6,12b-Bis(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-11-hydroxy-4a,8,13,13-tetramethyl-4-[(methylthio)methoxy]-5-oxo-7,11-methano-1H|beta-(Benzoylamino)-alpha-hydroxybenzenepropanoic Acid (aR,bS)-(2aR,4S,4aS,6R,9S,11S,12S,12aR,12bS)-6,12b-Bis(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-11-hydroxy-4a,8,13,13-tetramethyl-4-[(methylthio)methoxy]-5-oxo-7,11-methano-1H","A 7-methylthiomethyl ether derivative of paclitaxel with antineoplastic activity.  BMS-184476 binds to and stabilizes the resulting microtubules, thereby inhibiting microtubule disassembly which results in cell- cycle arrest at the G2/M phase and apoptosis. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C1859","BMS-188797","BMS-188797","An analog of paclitaxel with antineoplastic activity.  BMS-188797 binds to and stabilizes the resulting microtubules, thereby inhibiting microtubule disassembly which results in cell- cycle arrest at the G2/M phase and apoptosis. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C1856","BMS-214662","7-Cyano-2,3,4,5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3-(phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-Benzodiazepine|BMS-214662|FTI BMS 214662","A nonsedating benzodiazepine derivative with potential antineoplastic activity. Farnesyltransferase inhibitor BMS-214662 inhibits the enzyme farnesyltransferase and the post-translational farnesylation of number of proteins involved in signal transduction, which may result in the inhibition of Ras function and apoptosis in susceptible tumor cells. This agent may reverse the malignant phenotype of H-Ras-transformed cells and has been shown to be active against tumor cells with and without Ras mutations.","Organic Chemical|Pharmacologic Substance"]
["C62639","BMS-275183","BMS-275183","An orally available, C-4 methyl carbonate analog of paclitaxel with potential antineoplastic activity. Like paclitaxel, BMS-275183 binds to tubulin and stabilizes microtubules, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and an induction of apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C102878","Boanmycin Hydrochloride","BAM HCl|Bleomycin A6 Hydrochloride|Boanmycin Hydrochloride","The hydrochloride salt form of boanmycin (aka bleomycin A6), a component of the antibiotic bleomycin produced by Streptomyces species, with potential antineoplastic activity. Upon administration, boanmycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals. This causes single- and double-stranded DNA breaks which eventually leads to cell death. Compared to bleomycin, boanmycin appears to have a more favorable toxicity profile.","Antibiotic"]
["C82370","Bone Metastasis Targeting Peptide-11","BMTP-11|Bone Metastasis Targeting Peptide-11","A peptide that mimics naturally occurring interleukin-11 (IL-11) with interleukin receptor binding activity. Upon administration, bone metastasis targeting peptide-11 (BMTP-11) binds to interleukin-11 receptor alpha (IL-11Ra) BMTP-11. This agent might be used to deliver therapeutic agents specifically to IL-11Ra-expressing tumor cells while sparing normal cells. IL-11Ra is a cell surface receptor that may be overexpressed by osteosarcoma cells and by prostate cancer cells in prostate cancer bone metastases.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2405","Boronophenylalanine-Fructose Complex","BPA-F|Boronophenylalanine-Fructose Complex|boronophenylalanine-fructose complex|p-Boronophenylalanine-Fructose Complex","A boronated phenylalanine complexed with fructose to increase its solubility. When exposed to neutron irradiation, boronophenylalanine absorbs neutrons and self-destructs releasing short-range alpha radiation and 'recoil' lithium in tumor cells, resulting in alpha radiation-induced tumor cell death. This highly selective, localized radiotargeting of tumor cells, known as boron neutron capture therapy (BNCT), spares adjacent normal tissues.","Organic Chemical|Pharmacologic Substance"]
["C1851","Bortezomib","BORTEZOMIB|Bortezomib|LDP 341|MLN341|PS-341|PS341|Velcade|[(1R)-3-Methyl-1-[[(2S)-1-oxo-3-phenyl-2-[(pyrazinylcarbonyl)amino]propyl]amino]butyl]boronic Acid|bortezomib|velcade","A dipeptide boronic acid analogue with antineoplastic activity. Bortezomib reversibly inhibits the 26S proteasome, a large protease complex that degrades ubiquinated proteins. By blocking the targeted proteolysis normally performed by the proteasome, bortezomib disrupts various cell signaling pathways, leading to cell cycle arrest, apoptosis, and inhibition of angiogenesis. Specifically, the agent inhibits nuclear factor (NF)-kappaB, a protein that is constitutively activated in some cancers, thereby interfering with NF-kappaB-mediated cell survival, tumor growth, and angiogenesis. In vivo, bortezomib delays tumor growth and enhances the cytotoxic effects of radiation and chemotherapy.","Organic Chemical|Pharmacologic Substance"]
["C60809","Bosutinib","4-Anilino-3-quinolinecarbonitrile|4-Anilinobenzo(g)quinoline-3-carbonitrile|4-[(2,4-dichloro-5-methoxyphenyl)amino]-6-methoxy-7-[3-(4-methylpiperazin-1-yl)propoxy]quinoline-3-carbonitrile|BOSUTINIB|Bosulif|Bosutinib|SKI 606|SKI-606","A synthetic quinolone derivative and dual kinase inhibitor that targets both Abl and Src kinases with potential antineoplastic activity. Unlike imatinib, bosutinib inhibits the autophosphorylation of both Abl and Src kinases, resulting in inhibition of cell growth and apoptosis. Because of the dual mechanism of action, this agent may have activity in resistant CML disease, other myeloid malignancies and solid tumors. Abl kinase is upregulated in the presence of the abnormal Bcr-abl fusion protein which is commonly associated with chronic myeloid leukemia (CML). Overexpression of specific Src kinases is also associated with the imatinib-resistant CML phenotype.","Organic Chemical|Pharmacologic Substance"]
["C129711","Botanical Agent LEAC-102","Botanical Agent LEAC-102|LEAC 102|LEAC-102","A botanical-based formulation derived from the Taiwanese mushroom Antrodia cinnamomea, with potential antineoplastic activity, Upon administration, the components in LEAC-102 may exert cytotoxic effects against cancer cells.","Pharmacologic Substance"]
["C2418","Bovine Cartilage","Bovine Cartilage","Cartilage extracted from various parts of a cow and is proposed to stimulate the immune system and inhibit tumor cell growth.  It was used in the 1950s and 60s to enhance wound healing. (NCI)","Pharmacologic Substance"]
["C107387","BP-Cx1-Platinum Complex BP-C1","BP-C1|BP-Cx1-Platinum Complex BP-C1","A combination agent composed of the benzo-poly-carbonic-acid polymer BP-Cx1 chelated to platinum with potential antineoplastic activity. Upon intramuscular injection, the polymer moiety of BP-Cx1-Platinum Complex BP-C1 (BP-C1) alters the permeability of the cell membranes, which allows for increased penetration of platinum into tumor cells. In turn, platinum binds to nucleophilic groups such as GC-rich sites in DNA and induces intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition. In addition, the BP-Cx1 ligand is able to stimulate the innate immune system and upregulates a variety of cytokines including interferon, tumor necrosis factor-alpha (TNF-alpha), granulocyte macrophage-colony stimulating factor (GM-CSF), and various interleukins (ILs) such as IL-6 and IL-25. In comparison to cisplatin and other platinum-based compounds, treatment with BP-C1 allows for less platinum administration, which reduces platinum-associated systemic toxicity and side effects, and enhances the safety profile while maintaining or improving its efficacy.","Pharmacologic Substance"]
["C1617","BR96-Doxorubicin Immunoconjugate","BMS-182248-01|BR96-DOX immunoconjugate|BR96-DOX|BR96-Doxorubicin Conjugate|BR96-Doxorubicin Immunoconjugate|SGN-15|cBR96-Doxorubicin Immunoconjugate","An antibody-drug conjugate composed of the chimeric monoclonal antibody BR96 chemically linked to the cytotoxic drug doxorubicin.  The antibody moiety of BMS-182248-1 binds to Lewis Y, a cell surface antigen expressed on many solid tumor types.  Thus, the doxorubicin conjugate is targeted specifically to Lewis Y-expressing tumor cells, where it intercalates with DNA, thereby inhibiting DNA replication and repair, RNA synthesis and protein synthesis. (NCI)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116777","Brachyury-expressing Modified Vaccinia Ankara-TRICOM Vaccine","Brachyury-expressing Modified Vaccinia Ankara-TRICOM Vaccine|MVA Brachyury-TRICOM","A cancer vaccine composed of a replication-deficient, attenuated derivative of the vaccinia virus strain Ankara expressing both a CD8+ T-cell epitope from the brachyury protein and a triad of T-cell co-stimulatory molecules (MVA Brachyury-TRICOM), with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration of the brachyury-expressing modified vaccinia Ankara (MVA)-TRICOM vaccine, the expressed brachyury protein induces specific CD8+ and CD4+ T-cell responses against brachyury-expressing tumor cells. This causes both tumor cell lysis and a decrease in the growth of brachyury-expressing tumor cells. Brachyury, a member of the T-box family of transcription factors that is overexpressed in numerous cancer cell types, is correlated with increased epithelial-mesenchymal transition (EMT), cancer resistance and cancer progression. TRICOM, a triad of three human T-cell co-stimulatory molecules, B7.1, ICAM-1 and LFA-3, enhances antigen-specific T-cell activation.","Pharmacologic Substance|Virus"]
["C106267","Brachyury-expressing Yeast Vaccine GI-6301","Brachyury-expressing Yeast Vaccine GI-6301|GI-6301","A cancer vaccine composed of a heat-killed, recombinant form of the yeast Saccharomyces cerevisiae that is genetically modified to express the transcription factor brachyury protein, with potential antineoplastic activity. Upon subcutaneous administration, the brachyury-expressing yeast vaccine GI-6301 is recognized by dendritic cells, processed, and presented by Class I and II MHC molecules on the dendritic cell surface. This elicits a targeted CD4+ and CD8+ T-lymphocyte-mediated immune response. This process kills brachyury-expressing tumor cells. Brachyury is overexpressed in a variety of tumor types and plays an important role in cancer progression and metastasis.","Immunologic Factor|Pharmacologic Substance"]
["C94224","BRAF Inhibitor ARQ 736","AQ 736|BRAF Inhibitor ARQ 736","An orally bioavailable, highly soluble phosphate prodrug of B-raf (BRAF) protein kinase with potential antineoplastic activity. BRAF inhibitor ARQ 736 is converted into its active form ARQ 680 in the presence of phosphatases. In turn, ARQ 680 selectively binds to and inhibits the activity of oncogenic B-raf, which may inhibit the proliferation of tumor cells expressing mutated B-raf gene. B-raf belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway, which may be constitutively activated due to BRAF gene mutations. The valine to glutamic acid substitution at residue 600 (V600E) accounts for about 90% of BRAF gene mutations.","Pharmacologic Substance"]
["C113330","BRAF Inhibitor PLX8394","BRAF Inhibitor PLX8394|PLX8394","An orally bioavailable inhibitor of serine/threonine-protein kinase B-raf (BRAF) protein with potential antineoplastic activity. BRAF inhibitor PLX8394 appears to selectively bind to and inhibit the activity of both wild-type and mutated forms of BRAF, which may subsequently inhibit the proliferation of tumor cells which express mutated forms of BRAF. This inhibitor appears to be effective against tumors that express multiple mutated forms of the kinase and may be an effective therapeutic agent for tumors that are resistant to other BRAF inhibitor therapies that are specific for the BRAF V600E mutant. BRAF, a member of the raf family of serine/threonine protein kinases, plays a role in the regulation of MAP kinase/ERK signaling pathways, which may be constitutively activated due to BRAF gene mutations. Mutated forms of BRAF are associated with a number of neoplastic diseases.","Pharmacologic Substance"]
["C107245","BRAF(V600E) Inhibitor CEP-32496","1-(3-(6,7-Dimethoxyquinazolin-4-yloxy)phenyl)-3-(5-(1,1,1-trifluoro-2-methylpropan-2-yl)isoxazol-3-yl)urea Hydrochloride|AC013773|BRAF(V600E) Inhibitor CEP-32496|CEP-32496","An orally available v-raf murine sarcoma viral oncogene homolog B1 (B-raf) serine/threonine protein kinase inhibitor with potential antineoplastic activity. CEP-32496 specifically and selectively inhibits the activity of the mutated form (V600E) of B-raf kinase. This inhibits the activation of the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway and may result in a decrease in the proliferation of tumor cells expressing the mutated B-raf gene. The Raf mutation BRAF V600E, in which valine is substituted for glutamic acid at residue 600, is frequently found in a variety of human tumors and results in the constitutive activation of the RAF/MEK/ERK signaling pathway that regulates cellular proliferation and survival.","Pharmacologic Substance"]
["C92591","BRAF(V600E) Kinase Inhibitor RO5212054","B-Raf Inhibitor RO5212054|BRAF(V600E) Kinase Inhibitor RO5212054|PLX3603|RO5212054","An orally available small-molecule inhibitor of mutant (V600E) v-raf murine sarcoma viral oncogene homolog B1 (BRAF) with potential antineoplastic activity. BRAF(V600E) kinase inhibitor RO5212054 selectively binds to the ATP-binding site of BRAF(V600E) kinase and inhibits its activity, which may result in an inhibition of an over-activated MAPK signaling pathway downstream in BRAF(V600E) kinase-expressing tumor cells and a reduction in tumor cell proliferation. The valine to glutamic acid substitution at residue 600 accounts for about 90% of BRAF gene mutations; the oncogenic product, BRAF(V600E) kinase, exhibits a markedly elevated activity that over-activates the MAPK signaling pathway. The BRAF(V600E) mutation has been found to occur in approximately 60% of melanomas, and in about 8% of all solid tumors.","Organic Chemical|Pharmacologic Substance"]
["C124995","BRAF/EGFR Inhibitor BGB-283","BEIGENE-283|BGB 283|BGB-283|BRAF/EGFR Inhibitor BGB-283|Begeine-283","An inhibitor of the serine/threonine protein kinase B-raf (BRAF) and epidermal growth factor receptor (EGFR), with potential antineoplastic activity. BRAF/EGFR inhibitor BGB-283 selectively binds to and inhibits the activity of BRAF and certain BRAF mutant forms, and EGFR. This prevents BRAF- and EGFR-mediated signaling and inhibits the proliferation of tumor cells that either contain a mutated BRAF gene or express over-activated EGFR. In addition, BGB-283 inhibits mutant forms of the Ras proteins K-RAS and N-RAS. BRAF and EGFR are mutated or upregulated in many tumor cell types.","Pharmacologic Substance"]
["C61311","B-Raf/VEGFR-2 Inhibitor RAF265","B-Raf/VEGFR-2 Inhibitor RAF265|CHIR-265|RAF-265|RAF265","An orally bioavailable small molecule with potential antineoplastic activity. CHIR-265 binds and inhibits Raf kinases, which may result in a reduction of tumor cell growth and proliferation, and tumor cell death. In addition, this agent inhibits vascular endothelial growth factor receptor type 2 (VEGFR-2), thereby disrupting tumor angiogenesis. Raf kinases are critical enzymes in the Ras/Raf/MEK/ERK signaling pathway and are frequently upregulated in neoplasms.","Pharmacologic Substance"]
["C97666","Brain Tumor Initiating Cell Vaccine","BTIC Vaccine|Brain Tumor Initiating Cell Vaccine","A cell-based cancer vaccine comprised of brain tumor initiating cells (BTICs), with potential immunostimulating and antineoplastic activity. BITCs are from the glioblastoma multiforme (GBM) cell line GBM-6 and contain glioma stem-like cell-associated antigens. Upon administration, the BITC vaccine may stimulate a specific anti-tumoral cytotoxic T-lymphocyte (CTL) response against brain tumor cancer cells and brain tumor stem like cells, resulting in tumor cell lysis. BITC have unique antigenicity and have the ability to self-renew; vaccination against BITC antigens may kill these cells and may prevent tumor recurrences.","Immunologic Factor|Pharmacologic Substance"]
["C120121","Branched-chain Amino Acid Supplement","BCAA Supplement|Branched-chain Amino Acid Supplement","A nutritional supplement containing essential branched-chain amino acids (BCAAs), including leucine, isoleucine and valine, with potential anti-cachectic, antiangiogenic, hepatocellular carcinoma (HCC) inhibiting and hepatoprotective activities. Upon oral administration, BCAAs inhibit the expression of both hypoxia-inducible factor 1-alpha subunit (HIF-1a) and vascular endothelial growth factor (VEGF), which prevents VEGF-mediated angiogenesis in HCC cells. In addition, BCAAs inhibit proliferation and induce apoptosis of HCC cells by both suppressing the expression of insulin-like growth factor (IGF), and inhibiting the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. BCAAs also correct the plasma amino acid imbalance and promote protein metabolism, including the synthesis of albumin and glycogen. They reduce oxidative stress by inducing the activation of genes involved in antioxidant defenses, which prevent the production of reactive oxygen species (ROS). BCAAs also strengthen the immune system by increasing hepatic lymphocytes and stimulating natural killer (NK) cell activity. This supplement is able to improve insulin resistance and promote ammonia detoxification through increased glutamine (Gln) production.","Pharmacologic Substance"]
["C125739","BRD4 Inhibitor PLX51107","BRD4 Inhibitor PLX51107|PLX 51107|PLX-51107|PLX51107","An inhibitor of the bromodomain-containing protein 4 (BRD4), with potential antineoplastic activity. Upon administration, the BRD4 inhibitor PLX51107 binds to the acetylated lysine recognition motifs in the bromodomains of the BRD4 protein, thereby preventing the binding of BRD4 to acetylated lysines on histones. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an induction of apoptosis and an inhibition of proliferation in BRD4-overexpressing tumor cells. BRD4, a member of the human bromodomain and extra-terminal (BET) family of proteins, is a transcriptional regulator that is overexpressed in certain tumor cells and plays an important role in cellular proliferation.","Pharmacologic Substance"]
["C28855","Breflate","13-(N,N-Dimethylglycyl)brefeldin A|Breflate","A water soluble analogue of the antineoplastic agent brefeldin A (BFA). (NCI04)","Pharmacologic Substance"]
["C66944","Brentuximab Vedotin","ADC SGN-35|Adcetris|Anti-CD30 Antibody-Drug Conjugate SGN-35|Anti-CD30 Monoclonal Antibody-MMAE SGN-35|Anti-CD30 Monoclonal Antibody-Monomethylauristatin E SGN-35|BRENTUXIMAB VEDOTIN|Brentuximab Vedotin|SGN-35|cAC10-vcMMAE","An antibody-drug conjugate (ADC) directed against the tumor necrosis factor (TNF) receptor CD30 with potential antineoplastic activity. Brentuximab vedotin is generated by conjugating the chimeric anti-CD30 monoclonal antibody SGN-30 to the cytotoxic agent monomethyl auristatin E (MMAE) via a valine-citrulline peptide linker. Upon administration and internalization by CD30-positive tumor cells, brentuximab vedotin undergoes enzymatic cleavage, releasing MMAE into the cytosol; MMAE binds to tubulin and inhibits tubulin polymerization, which may result in G2/M phase arrest and tumor cell apoptosis. Transiently activated during lymphocyte activation, CD30 (tumor necrosis factor receptor superfamily, member 8;TNFRSF8) may be constitutively expressed in hematologic malignancies including Hodgkin lymphoma and some T-cell non-Hodgkin lymphomas. The linkage system in brentuximab vedotin is highly stable in plasma, resulting in cytotoxic specificity for CD30-positive cells.","Pharmacologic Substance"]
["C1560","Brequinar","6-Fluoro-2-(2'-fluoro[1,1'-biphenyl]-4-yl)-3-methyl-4-quinolinecarboxylic Acid|BREQUINAR|Bipenquinate|Brequinar","A synthetic quinolinecarboxylic acid analogue with antineoplastic properties.  Brequinar inhibits the enzyme dihydroorotate dehydrogenase, thereby blocking de novo pyrimidine biosynthesis.  This agent may also enhance the in vivo antitumor effect of antineoplastic agents such as 5-FU. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1078","Brequinar Sodium","BREQUINAR SODIUM|Brequinar Sodium|Brequinar sodium|DUP-785|DUP785|Sodium 6-Fluoro-2-(2'-fluoro-4-biphenylyl)-3-methyl-4-quinolinecarboxylate","The sodium salt form of Brequinar.  Brequinar inhibits the enzyme dihydroorotate dehydrogenase, thereby blocking de novo pyrimidine biosynthesis.  This agent may also enhance the in vivo antitumor effect of antineoplastic agents such as 5-FU. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C90541","Briciclib Sodium","Briciclib Sodium|ON 013105","A benzyl styryl sulfone analog, and a disodium phosphate ester prodrug of ON 013100, with potential antineoplastic activity. Upon hydrolysis, briciclib is converted to ON 013100, which blocks cyclin D mRNA translation and decreases protein expression of cyclin D. This may induce cell cycle arrest and apoptosis in cancer cells overexpressing cyclin D and eventually decrease tumor cell proliferation. This agent may exhibit synergistic antitumor activity in combination with other chemotherapeutic agents. Cyclin D, a member of the cyclin family of cell cycle regulators, plays a key role in cell cycle division and is often overexpressed in a variety of hematologic and solid tumors and is correlated with poor prognosis.","Pharmacologic Substance"]
["C98831","Brigatinib","(2-((5-Chloro-2-((2-methoxy-4-(4-(4-methylpiperazin-1-yl)piperidin-1-yl)phenyl)amino)pyrimidin-4-yl)amino)phenyl)dimethyl-,delta5-phosphanone|AP26113|BRIGATINIB|Brigatinib","An orally available inhibitor of receptor tyrosine kinases anaplastic lymphoma kinase (ALK) and the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Brigatinib binds to and inhibits ALK kinase and ALK fusion proteins as well as EGFR and mutant forms. This leads to the inhibition of ALK kinase and EGFR kinase, disrupts their signaling pathways and eventually inhibits tumor cell growth in susceptible tumor cells. In addition, AP26113 appears to overcome mutation-based resistance. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development; ALK dysregulation and gene rearrangements are associated with a series of tumors. EGFR is overexpressed in a variety of cancer cell types.","Pharmacologic Substance"]
["C67040","Brivanib","(R)-1-(4-(4-Fluoro-2-methyl-1H-indol-5-yloxy)-5- methylpyrrolo[2,1-f][1,2,4]triazin-6-yloxy)propan- 2-ol|BMS-540215|BRIVANIB|Brivanib|VEGFR2 Inhibitor BMS-540215|brivanib","A pyrrolotriazine-based compound and an inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antineoplastic activity. BMS-540215 specifically targets and binds strongly to human VEGFR-2, a tyrosine kinase receptor and pro-angiogenic growth factor expressed almost exclusively on vascular endothelial cells. Blockade of VEGFR-2 by this agent may lead to an inhibition of VEGF-stimulated endothelial cell migration and proliferation, thereby inhibiting tumor angiogenesis.","Pharmacologic Substance"]
["C53397","Brivanib Alaninate","BMS 582664|BMS-582664|BRIVANIB ALANINATE|Brivanib Alaninate|brivanib alaninate","The alaninate salt of a vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor with potential antineoplastic activity. Brivanib strongly binds to and inhibits VEGFR2, a tyrosine kinase receptor expressed almost exclusively on vascular endothelial cells; inhibition of VEGFR2 may result in inhibition of tumor angiogenesis, inhibition of tumor cell growth, and tumor regression.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C67088","Brivudine","(E)-5-(2-Bromovinyl)-deoxyuridine|BRIVUDINE|BVDU|Brivudine|Bromovinyl-Deoxyuridine|Helpin|RP101|Trans-5-(2-Bromovinyl)-2'-deoxyuridine|brivudine","A uridine derivative and nucleoside analog with pro-apoptotic and chemosensitizing properties. In vitro, bromovinyl-deoxyuridine (BVDU) has been shown to downregulate the multifunctional DNA repair enzyme APEX nuclease 1, resulting in the inhibition of DNA repair and the induction of apoptosis. In addition, this agent may inhibit the expression of STAT3 (signal transducer and activator of transcription 3), which may result in the downregulation of vascular endothelial growth factor (VEGF). BVDU has also been found to inhibit the upregulation of chemoresistance genes (Mdr1 and DHFR) during chemotherapy. Overall, the gene expression changes associated with BVDU treatment result in the decrease or prevention of chemoresistance. In addition, this agent has been shown to enhance the cytolytic activity of NK-92 natural killer cells towards a pancreatic cancer cell line in vitro.","Chemical Viewed Functionally"]
["C1882","Brivudine Phosphoramidate","(E)-5-(2-Bromovinyl)-2'-deoxy-5'-uridyl Phenyl L-methoxyalaninylphosphoramidate|BVDU Prodrug|BVdU Phosphoramidate|Brivudine Phosphoramidate|NB101.1|NB1011|Thymectacin","A small molecule phosphoramidate derivative of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVdU) with potential antineoplastic activity. Selectively active against tumor cells expressing high levels of thymidylate synthase (TS), brivudine is converted intracellularly by TS to bromovinyldeoxyuridine monophosphate (BVdUMP) which competes with the natural substrate, deoxyuridine monophosphate, for binding to TS. Unlike TS inhibitors, this agent is a reversible substrate for TS catalysis. Thus, TS retains activity and converts BVdUMP into cytotoxic metabolites. As key enzyme in the de novo synthesis of dTMP, TS is an enzyme critical to DNA biosynthesis and is overexpressed in many solid tumors.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C70598","Broad-Spectrum Human Papillomavirus Vaccine V505","Broad-Spectrum Human Papillomavirus Vaccine V505|V505","A non-infectious recombinant cancer vaccine prepared from the human papillomavirus (HPV) with potential immunoprophylactic activity. Vaccination with broad-spectrum human papillomavirus vaccine V505 may stimulate the host immune system to mount humoral and cytotoxic T lymphocyte (CTL) responses against HPV-infected cells. HPV infection, the cause of genital warts, is a risk factor for the development of cancers of the cervix, vagina, vulva, anus, and penis.","Immunologic Factor"]
["C128293","Broccoli Sprout/Broccoli Seed Extract Supplement","Avmacol|Broccoli Sprout/Broccoli Seed Extract Supplement","A tablet-based nutritional supplement composed of a mixture of sprout and seed extracts of the cruciferous vegetable broccoli, with potential chemopreventive and antioxidant activities. Broccoli sprout/broccoli seed extract contains a high amount of both the glycosinolate glucoraphanin and the enzyme myrosinase, which catalyzes the production of glucoraphanin to sulforaphane. Upon administration of the broccoli sprout/broccoli seed extract, sulforaphane activates the transcription factor NF-E2-related factor 2 (Nrf2), a member of the basic leucine zipper family, which binds to and activates antioxidant-response elements (AREs). Subsequently, activated AREs promote the transcription of antioxidant and detoxifying enzymes, particularly glutathione-S-transferase and NAD(P)H dehydrogenase [quinone] 1 (NAD(P)H:quinone oxidoreductase; NQO1), resulting in the detoxification of highly reactive carcinogens. This accelerates the elimination of carcinogens, may protect against cellular damage, and prevents cancer formation. AREs are cis-acting regulatory enhancer elements found in the 5' flanking region of many phase II detoxification enzymes.","Pharmacologic Substance"]
["C73259","Bromacrylide","BROMACRYLIDE|Bromacrylide","A propenamide-based agent with antineoplastic activity. Bromacrylide has been shown to decrease tumor growth in animal models, but is accompanied with severe toxicity, including severe bone marrow suppression and weight loss.","Pharmacologic Substance"]
["C72089","Bromebric Acid","(E)-3-p-Anisoyl-3-bromoacrylic Acid|BROMEBRIC ACID|Bromebric Acid","A derivative of bromoacrylic acid with cytostatic and antineoplastic activity. Bromebric acid appears to inhibit purine synthesis, oxidative phosphorylation and DNA synthesis. This agent inhibits tumor cell growth and causes cell cycle arrest. This agent may also have some use in the phrophylaxis of migraine.","Pharmacologic Substance"]
["C317","Bromocriptine Mesylate","2-Bromo-alpha-ergocryptine Mesylate|BROMOCRIPTINE MESYLATE|Bromocriptine Mesylate|Ergotaman-3',6',18-trione, 2-bromo-12'-hydroxy-2'-(1-methylethyl)-5'-(2-methylpropyl)-, monomethanesulfonate (salt), (5'alpha)-|Parlodel","The mesylate salt of bromocriptine, a semisynthetic ergot alkaloid with dopaminergic, antidyskinetic, and antiprolactinemic activities. Bromocriptine selectively binds to and activates postsynaptic dopamine D2 receptors in the corpus striatum of the central nervous system (CNS). Activation of these D2 receptors activate inhibitory G-proteins, which inhibit adenylyl cyclase, preventing signal transduction mediated via cAMP and resulting in the inhibition of neurotransmission and an antidyskinetic effect. This agent also stimulates dopamine D2 receptors in the anterior pituitary gland, which results in the inhibition of prolactin secretion and lactation and may inhibit the proliferation of prolactin-dependent breast cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C103274","Brontictuzumab","BRONTICTUZUMAB|Brontictuzumab|Immunoglobulin G2-lambda, Anti-(homo Sapiens Notch1 (Notch 1, Translocation-associated Notch-1, TAN-1,Tan1)), Humanized Monoclonal Antibody|OMP-52M51","A humanized monoclonal antibody directed against the Notch-1 receptor with potential antineoplastic activity. Upon administration, brontictuzumab binds to Notch-1 on the cell surface, thereby inhibiting Notch-mediated signaling and tumor cell proliferation. Notch 1, a type 1 transmembrane protein belonging to the Notch family, functions as a receptor for membrane bound ligands and has various roles during development; dysregulated Notch signaling is associated with increased cell growth and chemoresistance in cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C128040","Brostacillin Hydrochloride","4-(2-Bromoacrylamido)-N'''-(2-guanidinoethyl)-1,1',1',1'''-tetramethyl-N,4':N',4':N',4'''-quater(pyrrole-2-carboxamide) Hydrochloride|BROSTALLICIN HYDROCHLORIDE|Brostacillin Hydrochloride|PNU-166196 Hydrochloride|brostallicin hydrochloride","The hydrochloride salt form of brostacillin, a synthetic, alpha-bromoacrylic, second-generation minor groove binder (MGB), related to distamycin A, with potential antineoplastic activity. Brostallicin binds to DNA minor groove DNA, after having formed a highly reactive glutathione (GSH)-brostallicin complex in the presence of the enzyme glutathione S-transferase (GST), which is overexpressed in cancer cells; DNA replication and cell division are inhibited, resulting in tumor cell death. Compared to typical MGBs, this agent appears to bind covalently to DNA in a different manner and its activity does not depend on a functional DNA mismatch repair (MMR) mechanism. Accordingly, brostallicin may be effective against MMR-defective tumors that are refractory to various anticancer agents.","Organic Chemical|Pharmacologic Substance"]
["C1889","Brostallicin","4-(2-Bromoacrylamido)-N'''-(2-guanidinoethyl)-1,1',1',1'''-tetramethyl-N,4':N',4':N',4'''-quater(pyrrole-2-carboxamide)|BROSTALLICIN|Brostallicin|PNU-166196","A synthetic, alpha-bromoacrylic, second-generation minor groove binder (MGB), related to distamycin A, with potential antineoplastic activity. Brostallicin binds to DNA minor groove DNA, after having formed a highly reactive glutathione (GSH)-brostallicin complex in the presence of the enzyme glutathione S-transferase (GST), which is overexpressed in cancer cells; DNA replication and cell division are inhibited, resulting in tumor cell death. Compared to typical MGBs, this agent appears to bind covalently to DNA in a different manner and its activity does not depend on a functional DNA mismatch repair (MMR) mechanism. Accordingly, brostallicin may be effective against MMR-defective tumors that are refractory to various anticancer agents.","Organic Chemical|Pharmacologic Substance"]
["C318","Broxuridine","5-BrdU|5-Bromo-2'-deoxyuridine|5-Bromodeoxyuridine|5-Bromouracil Deoxyriboside|5-Bromouracil deoxyriboside|5-Bromouracil-2-deoxyriboside|5-Budr|BRDU|BROXURIDINE|BrdU|Bromodeoxyuridine|Bromouracil Deoxyriboside|Bromouracil deoxyriboside|Bromouridine|Broxine|Broxuridine|Neomark-BU|Neomark|broxuridine","A halogenated thymidine analogue with potential antineoplastic and radiosensitizing activities. Bromodeoxyuridine competes with thymidine for incorporation into DNA, resulting in DNA mutation and the inhibition of cell proliferation. As a radiosensitizer, this agent is associated with the inhibition of repair of radiation-induced DNA double-strand breaks.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1765","Bruceanol A","Bruceanol A|Picras-3-en-21-oic Acid, 15-(benzoyloxy)-13,20-epoxy-1,11,12-trihydroxy-2,16-dioxo-, Methyl Ester, (1beta,11beta,12alpha,15beta)-","A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1764","Bruceanol B","Bruceanol B|Picras-3-en-21-oic Acid, 13,20-epoxy-1,11,12-trihydroxy-2,16-dioxo-15-((1-oxopentyl)oxy)-, Methyl Ester, (1beta,11beta,12alpha,15beta)-","A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1768","Bruceanol C","Bruceanol C|Picras-3-en-21-oic Acid, 15-((4-(acetyloxy)-3,4-dimethyl-1-oxo-2-pentenyl)oxy)-13,20-epoxy-1,11,12-trihydroxy-2,16-dioxo-, Methyl Ester, (1beta,11beta,12alpha,15beta(E))-","A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1535","Bruceanol D","Bruceanol D|Picras-3-en-21-oic Acid, 15-((3,4-dimethyl-1-oxo-2-pentenyl)oxy)-13,20-epoxy-1,11,12-trihydroxy-2,16-dioxo-, Methyl Ester, (1beta,11beta,12alpha,15beta(E))-","A quassinoid phytochemical isolated form the plant Brucea antidysenterica with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1536","Bruceanol E","Bruceanol E|Picrasan-21-oic Acid, 15-((3,4-dimethyl-1-oxo-2-pentenyl)oxy)-13,20-epoxy-1,11,12-trihydroxy-2,16-dioxo-, Methyl Ester, (1beta,11beta,12alpha,15beta(E))-","A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1537","Bruceanol F","Bruceanol F|Picras-2-en-21-oic Acid, 15-((3,4-dimethyl-1-oxo-2-pentenyl)oxy)-13,20-epoxy-2,11,12-trihydroxy-1,16-dioxo-, Methyl Ester, (11beta,12alpha,15beta(E))-","A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1694","Bruceanol G","Bruceanol G","A natural quassinoid agent extracted from Brucea antidysenterica with potential antineoplastic activity that is cytotoxic to certain cancer cell lines. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1695","Bruceanol H","Bruceanol H","A quassinoid phytochemical isolated from the plant Brucea antidysenterica with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1025","Bruceantin","2H-3, 11c-(Epoxymethano)phenanthro[10,1-bc]pyran, Picras-3-en-21-oic Acid Derivative|BRUCEANTIN|Bruceantin|Picras-3-en-21-oic Acid, 15-[(3,4-dimethyl-1-oxo-2-pentenyl)oxy]-13,20-epoxy-3,11, 12-trihydroxy-2,16-dioxo-, Methyl Ester, (11beta,12alpha,15beta(E))|Picras-3-en-21-oic acid, 15-[(3, 4-dimethyl-1-oxo-2-pentenyl)oxy]-13,20-epoxy-3,11,12-trihydroxy-2, 16-dioxo-, methyl ester [11.beta.,12.alpha.,15.beta.(E)]-|Picras-3-en-21-oic acid, 15-[(3, 4-dimethyl-1-oxo-2-pentenyl)oxy]-13,20-epoxy-3,11,12-trihydroxy-2, 16-dioxo-, methyl ester, [11.beta.,12.alpha.,15.beta.(E)]-|[11Beta,12alpha,15beta(E)]-15-[(3,4-dimethyl-1-oxo-2-pentenyl)oxy]-13,20-epoxy-3,11,12-trihydroxy-2,16-dioxopicras-3-en-21-oic Acid Methyl Ester","A triterpene quassinoid antineoplastic antibiotic isolated from the plant Brucea antidysenterica.  Bruceantin inhibits the peptidyl transferase elongation reaction, resulting in decreased protein and DNA synthesis.  Bruceantin also has antiamoebic and antimalarial activity. (NCI04)","Antibiotic|Organic Chemical"]
["C1026","Bryostatin 1","B705008K112|BRYOSTATIN 1|Bryostatin 1|Bryostatin I|bryostatin 1","A macrocyclic lactone isolated from the bryozoan Bugula neritina with antineoplastic activity.  Bryostatin 1 binds to and inhibits the cell-signaling enzyme protein kinase C, resulting in the inhibition of tumor cell proliferation, the promotion of tumor cell differentiation, and the induction of tumor cell apoptosis. This agent may act synergistically with other chemotherapeutic agents. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C120215","BTK Inhibitor BGB-3111","BGB-3111|BTK Inhibitor BGB-3111|BTK-InhB","An orally available inhibitor of Bruton tyrosine kinase (BTK) with potential antineoplastic activity. Upon administration, BGB-3111 selectively binds to and inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B-cells that overexpress BTK. BTK, a member of the TEC family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B-lymphocytes.","Pharmacologic Substance"]
["C130001","BTK Inhibitor DTRMWXHS-12","BTK Inhibitor DTRMWXHS-12|DTRMWXHS 12|DTRMWXHS-12","An orally available inhibitor of Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon administration, DTRMWXHS-12 inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways. This leads to an inhibition of the growth of malignant B-cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B-lymphocytes.","Pharmacologic Substance"]
["C116844","BTK Inhibitor GDC-0853","BTK Inhibitor GDC-0853|Bruton Tyrosine Kinase Inhibitor GDC-0853|GDC-0853","An orally available inhibitor of Bruton's tyrosine kinase (BTK) with potential antineoplastic activity. Upon administration, GDC-0853 inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents both B-cell activation and BTK-mediated activation of downstream survival pathways, which leads to the inhibition of the growth of malignant B-cells that overexpress BTK. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed in B-cell malignancies; it plays an important role in B-lymphocyte development, activation, signaling, proliferation and survival.","Pharmacologic Substance"]
["C102876","BTK Inhibitor ONO-4059","BTK Inhibitor ONO-4059|Bruton's Tyrosine Kinase Inhibitor ONO-4059|ONO-4059","An orally available formulation containing an inhibitor of Bruton agammaglobulinemia tyrosine kinase (BTK), with potential antineoplastic activity. Upon administration, ONO-4059 covalently binds to BTK within B cells, thereby preventing B cell receptor signaling and impeding B cell development. As a result, this agent may inhibit the proliferation of B cell malignancies. BTK, a cytoplasmic tyrosine kinase and member of the Tec family of kinases, plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.","Pharmacologic Substance"]
["C81555","Budotitane","BUDOTITANE|Budotitane","A titanium metal complex, coordinated with asymmetric beta-diketonate ligands, with antineoplastic activity. Although the exact mechanism of action remains to be elucidated, budotitane potentially binds either to macromolecules via coordinative covalent bonds, or via intercalation between nucleic acids strands by the aromatic ring of the beta-diketonate. In addition, this agent appears to cause cardiac arrhythmias and is toxic to the liver and kidneys at higher doses. The development of budotitane was halted due to the rapid loss of its labile groups under physiological conditions.","Pharmacologic Substance"]
["C107555","Bufalin","3,14-Dihydroxy-Bufa-20,22-Dienolide|3-Beta,14-Dihydroxy-5-Beta-Bufa-20,22-Dienolide|3beta,14beta-Dihydroxy-5beta-Bufa-20,22-Dienolide|5-Beta-Bufa-20,22-Dienolide, 3-Beta,14-Dihydroxy-|5beta-Bufa-20,22-Dienolide, 3beta,14-Dihydroxy- (8CI)|Bufa-20,22-Dienolide, 3,14-Dihydroxy-, (3-Beta,5-Beta)- (9CI)|Bufa-20,22-Dienolide, 3,14-Dihydroxy-, (3beta,5beta)- (9CI)|Bufalin","An active ingredient and one of the glycosides in the traditional Chinese medicine ChanSu; it is also a bufadienolide toxin originally isolated from the venom of the Chinese toad Bufo gargarizans, with potential cardiotonic and antineoplastic activity. Although the mechanism of action of bufalin is still under investigation, this agent is a specific Na+/K+-ATPase inhibitor and can induce apoptosis in cancer cell lines through the activation of the transcription factor AP-1 via a mitogen activated protein kinase (MAPK) pathway.","Pharmacologic Substance"]
["C90565","Buparlisib","BKM120|Buparlisib|PI3K Inhibitor BKM120","An orally bioavailable specific oral inhibitor of the pan-class I phosphatidylinositol 3-kinase (PI3K) family of lipid kinases with potential antineoplastic activity. Buparlisib specifically inhibits class I PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway in an ATP-competitive manner, thereby inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate and activation of the PI3K signaling pathway. This may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C88323","Burixafor","BURIXAFOR|Burixafor|Phosphonic Acid, p-(2-(4-(6-Amino-2-(((trans-4-(((3-(cyclohexylamino)propyl)amino)methyl)cyclohexyl)methyl)amino)-4-pyrimidinyl)-1-piperazinyl)ethyl)-|TG-0054","An orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with receptor binding and hematopoietic stem cell-mobilization activities. Burixafor binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation; this may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into blood. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.","Pharmacologic Substance"]
["C130049","Burixafor Hydrobromide","Burixafor HBr|Burixafor Hydrobromide|TG-0054 HBr|TG-0054 Hydrobromide","The hydrobromide salt form of burixafor, an orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with hematopoietic stem cell (HSC)-mobilization and chemosensitizing activities. Upon administration, burixafor binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal cell-derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation. This may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into the peripheral circulation. Additionally, burixafor-mediated mobilization of disseminated tumor cells (DTCs) from the bone marrow into the blood may make these metastatic tumor cells more susceptible to the actions of chemotherapeutic agents. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types. CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.","Pharmacologic Substance"]
["C321","Busulfan","1, 4-Bis[methanesulfonoxy]butane|1,4-Bis(methanesulfonoxy)butane|1,4-Bitanediol Dimethanesulfonate Esters|1,4-Butanediol Dimethylsulfonate|1,4-Di(methanesulfonyloxy)butane|1,4-Di(methylsulfonyloxy)butane|BUS|BUSULFAN|Bussulfam|Busulfan|Busulfanum|Busulfex|Busulphan|CB 2041|CB-2041|GT 41|GT-41|Glyzophrol|Joacamine|Methanesulfonic Acid Tetramethylene Ester|Methanesulfonic acid, tetramethylene ester|Mielucin|Misulban|Misulfan|Mitosan|Myeleukon|Myeloleukon|Myelosan|Mylecytan|Myleran|Sulfabutin|Tetramethylene Bis(methanesulfonate)|Tetramethylene bis[methanesulfonate]|WR-19508|busulfan","A synthetic derivative of dimethane-sulfonate with antineoplastic and cytotoxic properties.  Although its mechanism of action is not fully understood, busulfan appears to act through the alkylation of DNA.  Following systemic absorption of busulfan, carbonium ions are formed, resulting in DNA alkylation and DNA breaks and inhibition of DNA replication and RNA transcription. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1029","Buthionine Sulfoximine","2-Amino-4-(S-butylsulfonimidoyl) Butanoic Acid|BSO|BUTHIONINE SULFOXIMINE, L-|Butanoic Acid, 2-Amino-4-(S-butylsulfonimidoyl)-|Butanoic acid, 2-amino-4-(S-butylsulfonimidoyl)-|Buthionine Sulfoximine|Buthionine Sulphoximine|L-Buthionine Sulfoximine|L-Buthionine sulfoximine|S-(3-Amino-3-carboxypropyl)-S-butylsulfoximine|S-(n-Butyl)homocysteine Sulfoximine|buthionine sulfoximine","A synthetic amino acid. Buthionine sulfoximine irreversibly inhibits gamma-glutamylcysteine synthase, thereby depleting cells of glutathione, a metabolite that plays a critical role in protecting cells against oxidative stress, and resulting in free radical-induced apoptosis. Elevated glutathione levels are associated with tumor cell resistance to alkylating agents and platinum compounds. By depleting cells of glutathione, this agent may enhance the in vitro and in vivo cytotoxicities of various chemotherapeutic agents in drug-resistant tumors. Buthionine sulfoximine may also exhibit antiangiogenesis activity. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C66937","Cabazitaxel","1-hydroxy-7beta,10beta-dimethoxy-9-oxo-5beta,20-epoxytax-11-ene-2alpha,4,13alpha-triyl 4-acetate 2-benzoate 13-[(2R,3S)-3-{[(tertbutoxy)carbonyl]amino}-2-hydroxy-3-phenylpropanoate]|CABAZITAXEL|Cabazitaxel|Jevtana|RPR-116258A|Taxoid XRP6258|XRP-6258|cabazitaxel|taxoid XRP6258","A semi-synthetic derivative of the natural taxoid 10-deacetylbaccatin III with potential antineoplastic activity. Cabazitaxel binds to and stabilizes tubulin, resulting in the inhibition of microtubule depolymerization and cell division, cell cycle arrest in the G2/M phase, and the inhibition of tumor cell proliferation. Unlike other taxane compounds, this agent is a poor substrate for the membrane-associated, multidrug resistance (MDR), P-glycoprotein (P-gp) efflux pump and may be useful for treating multidrug-resistant tumors. In addition, cabazitaxel penetrates the blood-brain barrier (BBB).","Organic Chemical|Pharmacologic Substance"]
["C52200","Cabozantinib","1,1-Cyclopropanedicarboxamide, N'-[4-[(6,7-dimethoxy-4-quinolinyl)oxy]phenyl]-N-(4- fluorophenyl)-|CABOZANTINIB|Cabozantinib|N-{4-[(6,7-dimethoxyquinolin-4-yl)oxy]phenyl}-N'-(4-fluorophenyl)cyclopropane-1,1- dicarboxamide","An orally bioavailable, small molecule receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Cabozantinib strongly binds to and inhibits several RTKs, which are often overexpressed in a variety of cancer cell types, including hepatocyte growth factor receptor (MET), RET (rearranged during transfection), vascular endothelial growth factor receptor types 1 (VEGFR-1), 2 (VEGFR-2), and 3 (VEGFR-3), mast/stem cell growth factor (KIT), FMS-like tyrosine kinase 3 (FLT-3), TIE-2 (TEK tyrosine kinase, endothelial), tropomyosin-related kinase B (TRKB) and AXL. This may result in an inhibition of both tumor growth and angiogenesis, and eventually lead to tumor regression.","Pharmacologic Substance"]
["C97938","Cabozantinib S-malate","BMS-907351|Butanedioic acid, 2-hydroxy-, (2S)-, compd. with N-[4-[(6,7-dimethoxy-4-quinolinyl)oxy]phenyl]-N'-(4-fluorophenyl)-1,1-cyclopropanedicarboxamide (1:1)|CABOZANTINIB S-MALATE|Cabometyx|Cabozantinib S-malate|Cometriq|XL184","The s-malate salt form of cabozantinib, an orally bioavailable, small molecule receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Cabozantinib strongly binds to and inhibits several RTKs, which are often overexpressed in a variety of cancer cell types, including hepatocyte growth factor receptor (MET), RET (rearranged during transfection), vascular endothelial growth factor receptor types 1 (VEGFR-1), 2 (VEGFR-2), and 3 (VEGFR-3), mast/stem cell growth factor (KIT), FMS-like tyrosine kinase 3 (FLT-3), TIE-2 (TEK tyrosine kinase, endothelial), tropomyosin-related kinase B (TRKB) and AXL. This may result in an inhibition of both tumor growth and angiogenesis, and eventually lead to tumor regression.","Pharmacologic Substance"]
["C1032","Cactinomycin","ACTINOMYCIN C|Actinomycin C|CACTINOMYCIN|Cactinomycin","A chromopeptide antineoplastic antibiotic isolated from the bacterium Streptomyces chrysomallus.  Cactinomycin binds to DNA by intercalating between guanine and cytosine, forming stable antibiotic-DNA complexes that inhibit RNA and protein synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C63756","Caffeic Acid Phenethyl Ester","2-Phenylethyl 3-(3,4-dihydroxyphenyl)-2-propenoate|3-(3,4-Dihydroxyphenyl)-2-propenoic Acid, 2-Phenylethyl Ester|CAFFEIC ACID PHENETHYL ESTER|CAPE|Caffeic Acid Phenethyl Ester","The phenethyl alcohol ester of caffeic acid and a bioactive component of honeybee hive propolis, with antineoplastic, cytoprotective and immunomodulating activities. Upon administration, caffeic acid phenethyl ester (CAPE) inhibits the activation of nuclear transcription factor NF-kappa B and may suppress p70S6K and Akt-driven signaling pathways. In addition, CAPE inhibits PDGF-induced proliferation of vascular smooth muscle cells through the activation of p38 mitogen-activated protein kinase (MAPK) and hypoxia-inducible factor (HIF)-1alpha and subsequent induction of heme oxygenase-1 (HO-1).","Organic Chemical|Pharmacologic Substance"]
["C117731","CAIX Inhibitor DTP348","2-(2-Methyl-5-nitro-1H-imidazol-1-yl)ethylsulfamide|CAIX Inhibitor DTP348|DTP348","An orally bioavailable, nitroimidazole-based sulfamide, carbonic anhydrase IX (CAIX) inhibitor with potential antineoplastic activity. Upon administration, CAIX inhibitor DTP348 inhibits tumor-associated CAIX, a hypoxia-inducible transmembrane glycoprotein that catalyzes the reversible reaction and rapid interconversion of carbon dioxide and water to carbonic acid, protons, and bicarbonate ions. This prevents the acidification of the tumor's extracellular microenvironment and decreases the intracellular pH. This results in increased cell death in CAIX-expressing, hypoxic tumors. In addition, DTP348, through its nitroimidazole moiety, is able to sensitize hypoxic tumor cells to irradiation. CAIX is overexpressed in various tumors and plays a key role in intra- and extracellular pH regulation, cancer cell progression, survival, migration and invasion.","Pharmacologic Substance"]
["C117728","CAIX Inhibitor SLC-0111","CAIX Inhibitor SLC-0111|SLC-0111","A sulfonamide carbonic anhydrase inhibitor with potential antineoplastic activity. Upon administration, CAIX inhibitor SLC-0111 inhibits tumor-associated carbonic anhydrase IX (CAIX), an hypoxia-inducible transmembrane glycoprotein that catalyzes the reversible reaction and rapid interconversion of carbon dioxide and water to carbonic acid, protons, and bicarbonate ions. This prevents both the acidification of the tumor's extracellular microenvironment and cytoplasmic alkalization. This increases cell death in CAIX-expressing, hypoxic tumors. CAIX is overexpressed in various tumors and plays a key role in intra- and extracellular pH regulation, cancer cell progression, survival, migration and invasion; it is also involved in resistance to both chemo- and radiotherapy.","Pharmacologic Substance"]
["C78198","Calaspargase Pegol","Calaspargase Pegol|EZN-2285|Oncaspar-IV|SC-PEG E. Coli L-Asparaginase|SC-PEG E. coli L-asparaginase|Succinimidyl Carbonate Monomethoxypolyethylene Glycol E. coli L-Asparaginase","An intravenous formulation containing E.coli-derived L-asparaginase II conjugated with succinimidyl carbonate monomethoxypolyethylene glycol (SC-PEG), with potential antineoplastic activity. L-asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting cells of asparagine; asparagine depletion blocks protein synthesis and tumor cell proliferation, especially in the G1 phase of the cell cycle and ultimately induces tumor cell death. Asparagine is critical to protein synthesis in acute lymphoblastic leukemia (ALL) cells which, unlike normal cells, cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. Pegylation decreases enzyme antigenicity and increases its half life. SC is used as a PEG linker to facilitate attachment to asparaginase and enhances the stability of the formulation.","Pharmacologic Substance"]
["C330","Calcitriol","(1alpha,3beta,5Z,7E)-9,10-Secocholesta-5,7,10(19)-triene-1,3,25-triol|1,25(OH)2-D3|1,25-DHCC|1,25-Dihydroxycholecalciferol|1,25-Dihydroxycholecaliferol|CALCITRIOL|Calcijex|Calcitriol|Rocaltrol|calcitriol","A synthetic physiologically-active analog of vitamin D, specifically the vitamin D3 form.  Calcitriol regulates calcium in vivo by promoting absorption in the intestine, reabsorption in the kidneys, and, along with parathyroid hormone, regulation of bone growth.  A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Calcitriol also induces cell cycle arrest at G0/G1 phase of the cell cycle, cell differentiation, and apoptosis, resulting in inhibition of proliferation of some tumor cell types.  This agent may be chemopreventive for colon and prostate cancers. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1355","Calcium Citrate","2-Hydroxy-1,2,3-propanetricarboxylic Acid, Calcium Salt (2:3)|Acicontral|CALCIUM CITRATE|Calcium Citrate|Citracal|Tricalcium Citrate","The citrate salt of calcium. An element necessary for normal nerve, muscle, and cardiac function, calcium as the citrate salt helps to maintain calcium balance and prevent bone loss when taken orally. This agent may also be chemopreventive for colon and other cancers. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C336","Calcium Gluconate","CALCIUM GLUCONATE|Calcium D-gluconate|Calcium Gluconate|Calglucon|calcium gluconate","The gluconate salt of calcium. An element or mineral necessary for normal nerve, muscle, and cardiac function, calcium as the gluconate salt helps to maintain calcium balance and prevent bone loss when taken orally. This agent may also be chemopreventive for colon and other cancers. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C335","Calcium Saccharate","2,3,4,5-tetrahydroxy-1,6- dioxido-hexane-1,6-dione, Calcium|Antacidin|CALCIUM SACCHARATE|CGT|Calcium D-Glucarate|Calcium D-Saccharate|Calcium Glucarate|Calcium Saccharate|D-Glucaric Acid, Calcium Salt (1:1)|Saccharated Lime","The calcium salt form of glucaric acid, a natural substance found in many fruits and vegetables, with potential anti-cancer property. One of the key processes in which the human body eliminates toxic chemicals as well as hormones (such as estrogen) is by attaching glucuronic acid to them in the liver and then excreting the complex in the bile. When beta-glucuronidase breaks the bond, it prolongs the stay of the hormone or toxic chemical in the body. Elevated beta-glucuronidase activity has been implicated to be associated with an increased risk for hormone-dependent cancers like breast, prostate, and colon cancers. Therefore, supplementing calcium glucarate may suppress the developments of hormone-dependent cancers.","Organic Chemical|Pharmacologic Substance"]
["C121642","Calculus bovis/Moschus/Olibanum/Myrrha Capsule","Calculus bovis/Moschus/Olibanum/Myrrha Capsule|Wangbang Pharmaceutical Xihuang Capsule|XHP|Xihuang Capsule","An orally available traditional Chinese medicine (TCM)-based capsule formulation containing Calculus bovis, the dried gallstones of cattle, Moschus, also referred to as deer musk, the resin Olibanum and the resin Myrrha, with potential antineoplastic and chemopreventive activities. Although the exact mechanisms of action through which the active ingredients in the Calculus bovis/Moschus/Olibanum/Myrrha capsule elicit their effects have yet to be fully elucidated, they may, upon intake, exert their antineoplastic activity through modulation of the immune system, inhibition of tumor cell proliferation and induction of apoptosis.","Pharmacologic Substance"]
["C1035","Calicheamicin Gamma 1I","Calicheamicin Gamma 1I","An oligosaccharide enediyne antitumor antibiotic isolated from Micromonospora echinospora ssp. Calichensis.  Calicheamicin Gamma 1I binds to the minor groove of DNA, resulting in site-specific double-strand breaks and apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C338","Camptothecin","(+)-Camptothecin|(S)-4-ethyl-4-hydroxy-1H-pyrano-[3',4':6,7]indolozino[1,2-b]quinoline-3,14(4H,12H)-dione|1H-Pyrano[3',3'.6,7]indolizino[1,2-b]quinoline-3,14(4H,12H)-dione, 4-ethyl-4hydroxy-(S)-(9CI)|20(S)-Camptothecine|20-(S)-camptothecine|21, 22-Secocamptothecin-21-oic acid lactone|21, 22-secocamptothecin-21-oic acid lactone|CAMPTOTHECIN|Camptothecin|camptothecin|camptothecine","An alkaloid isolated from the Chinese tree Camptotheca acuminata, with antineoplastic activity.  During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C80047","Camptothecin Analogue TLC388","Camptothecin Analogue TLC388|Lipotecan|TLC388","A synthetic analogue of camptothecin with potential antineoplastic and radio-sensitizing activities. Camptothecin analogue TLC388 selectively stabilizes topoisomerase I-DNA covalent complexes during S-phase, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. Topoisomerase I relaxes negative super-coiled DNA during replication and transcription. This agent has been chemically modified to enhance the potency and stability of camptothecin.","Organic Chemical|Pharmacologic Substance"]
["C2344","Camptothecin Sodium","Camptothecin Sodium Salt|Camptothecin Sodium|Camptothecin sodium|Camptothecin, sodium salt|Sodium camptothecin","The sodium salt of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, with antineoplastic activity.  During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. The sodium salt of camptothecin is more water-soluble than the parent molecule. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C84857","Camptothecin-20(S)-O-Propionate Hydrate","CZ48|Camptothecin-20(S)-O-Propionate Hydrate","The hydrated, crystalline propionate ester (attached in position C-20) prodrug of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, with potential antineoplastic activity. Upon entry into cells, camptothecin-20(S)-O-propionate is hydrolyzed by esterases into the active form camptothecin. Camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery, thus inhibiting DNA replication and triggering apoptotic cell death. Camptothecin readily undergoes hydrolysis at physiological pH, changing its conformation from the active, S-configured lactone structure to an inactive carboxylate form. The ester chain in the vicinity of the S-configured lactone moiety, a key determinant for the chemotherapeutic efficacy of the camptothecins, inhibits protein binding, rendering this agent resistant to hydrolysis and prolonging its half-life.","Pharmacologic Substance"]
["C2442","Canarypox-hIL-12 Melanoma Vaccine","ALVAC-hIL-12 melanoma vaccine|ALVAC-hIL-12|Canarypox-hIL-12 Melanoma Vaccine","A vaccine consisting of a replication-defective recombinant canarypox virus (ALVAC) that encodes the gene for human interleukin-12 (hIL-12).  Produced mainly by B-cells, IL-12 is an endogenous cytokine that activates natural killer (NK) cells, promotes cytotoxic T lymphocyte (CTL) responses, induces the release of interferon-gamma (IFN-gamma), and may exhibit antitumor and anti-angiogenic effects.  Vaccination with canarypox-hIL-12 melanoma vaccine may stimulate the host immune system to mount an immune response against tumor cells, thereby inhibiting tumor growth and/or metastasis. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C1775","Cancell","126-F|Cancell|Cantron|Entelev|JS-101|JS-114|Jim's Juice|Protocel|Sheridan's Formula","Cancell (Entelev or Cantron), is a liquid that has been produced in various forms, principally by two manufacturers, since the late 1930s.  The exact composition of Cancell/Entelev is unknown, but the U.S. Food and Drug Administration (FDA) has listed the components as inositol, nitric acid, sodium sulfite, potassium hydroxide, sulfuric acid, and catechol.  NCI studies determined that the mixture lacked substantial antitumor activity. (from CancerNet)","Organic Chemical|Pharmacologic Substance"]
["C121776","Cancer Peptide Vaccine S-588410","Cancer Peptide Vaccine S-588410|S-588410","A cancer peptide vaccine containing five human leukocyte antigen (HLA)-A*2402-restricted epitope peptides derived from as of yet not disclosed oncoantigens, with potential immunostimulating and antineoplastic activities. Upon administration of the cancer peptide vaccine S-588410, the peptides may stimulate a cytotoxic T-lymphocyte (CTL) response against cancer cells expressing the antigens. This decreases proliferation of susceptible tumor cells.","Pharmacologic Substance"]
["C104745","Cancer Stemness Kinase Inhibitor BBI503","BBI503|Cancer Stemness Kinase Inhibitor BBI503","An orally available cancer cell stemness kinase inhibitor with potential antineoplastic activity. Even though the exact target has not been fully elucidated, BBI503 targets and inhibits one or more pathways involved in cancer stem cell survival. As a result, cancer stem cell (CSC) growth as well as heterogeneous cancer cell growth is inhibited. CSCs, self-replicating cells able to differentiate into heterogeneous cancer cells, appear to be responsible for both tumor relapse and metastasis.","Organic Chemical|Pharmacologic Substance"]
["C1880","Canertinib Dihydrochloride","CANERTINIB DIHYDROCHLORIDE|CI-1033|Canertinib Dihydrochloride|N-[-4-[(3-Chloro-4-fluorophenyl)amino]-7-[3-(4-morpholinyl)propoxy]-6-quinazolinyl]-2-propenamide Dihydrochloride|PD-0183805-002B|PD183805|canertinib dihydrochloride|canertinib","The hydrochloride salt of an orally bio-available quinazoline with potential antineoplastic and radiosensitizing activities. Canertinib binds to the intracellular domains of epidermal growth factor receptor tyrosine kinases (ErbB family), irreversibly inhibiting their signal transduction functions and resulting in tumor cell apoptosis and suppression of tumor cell proliferation. This agent also acts as a radiosensitizing agent and displays synergistic activity with other chemotherapeutic agents.","Organic Chemical|Pharmacologic Substance"]
["C83581","Canfosfamide","(2R)-L-gamma-Glutamyl-3-((2-((bis(bis(2-chloroethyl)amino)phosphinyl)oxy)ethyl)sulfonyl)-L-alanyl-2-phenylglycine|CANFOSFAMIDE|Canfosfamide|Ter 286","A modified glutathione analogue and nitrogen mustard prodrug, with potential antineoplastic activity. Canfosfamide is selectively activated by glutathione S-transferase P1-1 into an alkylating metabolite that forms covalent linkages with nucleophilic centers in tumor cell DNA, which may induce a cellular stress response and cytotoxicity, and decrease tumor cell proliferation. Glutathione S-transferase P1-1 is an enzyme that is overexpressed in many human malignancies.","Pharmacologic Substance"]
["C2641","Canfosfamide Hydrochloride","CANFOSFAMIDE HYDROCHLORIDE|Canfosfamide Hydrochloride|TLK286|Telcyta|canfosfamide hydrochloride","The hydrochloride salt of a modified glutathione analogue with potential antineoplastic activity. Canfosfamide is selectively activated by glutathione S-transferase P1-1 into an alkylating metabolite that forms covalent linkages with nucleophilic centers in tumor cell DNA, which may induce a cellular stress response and cytotoxicity, and decrease tumor proliferation. S-transferase P1-1 is an enzyme that is overexpressed in many human malignancies.","Organic Chemical|Pharmacologic Substance"]
["C118452","Cannabidiol","1,3-Benzenediol, 2-(3-methyl-6-(1-methylethenyl)-2-cyclohexen-1-yl)-5-pentyl-, (1R-trans)-|CANNABIDIOL|CBD|Cannabidiol|GWP42003-P","A phytocannabinoid derived from Cannabis species, which is devoid of psychoactive activity, with analgesic, anti-inflammatory, antineoplastic and chemopreventive activities. Upon administration, cannabidiol (CBD) exerts its anti-proliferative, anti-angiogenic and pro-apoptotic activity through various mechanisms, which likely do not involve signaling by cannabinoid receptor 1 (CB1), CB2, or vanilloid receptor 1. CBD stimulates endoplasmic reticulum (ER) stress and inhibits AKT/mTOR signaling, thereby activating autophagy and promoting apoptosis. In addition, CBD enhances the generation of reactive oxygen species (ROS), which further enhances apoptosis. This agent also upregulates the expression of intercellular adhesion molecule 1 (ICAM-1) and tissue inhibitor of matrix metalloproteinases-1 (TIMP1) and decreases the expression of inhibitor of DNA binding 1 (ID-1). This inhibits cancer cell invasiveness and metastasis. CBD may also activate the transient receptor potential vanilloid type 2 (TRPV2), which may increase the uptake of various cytotoxic agents in cancer cells. The analgesic effect of CBD is mediated through the binding of this agent to and activation of CB1.","Organic Chemical|Pharmacologic Substance"]
["C61576","Cantuzumab Ravtansine","CANTUZUMAB RAVTANSINE|Cantuzumab Ravtansine|HuC242-DM4|IMGN242|Maytansinoid DM4-Conjugated Humanized Monoclonal Antibody huC242|huC242-DM4|maytansinoid DM4-conjugated humanized monoclonal antibody huC242","An immunotoxin of a humanized monoclonal antibody C242 (MoAb HuC242) conjugated to a derivative of the cytotoxic agent maytansine, DM4, with potential antitumor activity. Cantuzumab ravtansine is generated from MoAb C242, which is raised against a cell surface superantigen, CA242, found in a variety of human tumor cells. Upon binding and entry, the immunoconjugate releases the maytansinoid agent DM4, which binds to tubulin, thereby affecting microtubule assembly/disassembly dynamics. As a result, this agent prevents cell division and reduces cell growth of cancer cells that express CA242.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1794","Capecitabine","5'-Deoxy-5-fluoro-N-[(pentyloxy)carbonyl]-cytidine|CAPECITABINE|Capecitabine|Ro 09-1978/000|Xeloda|capecitabine","A fluoropyrimidine carbamate belonging to the class of antineoplastic agents called antimetabolites.  As a prodrug, capecitabine is selectively activated by tumor cells to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells.  FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C99629","Capecitabine Rapidly Disintegrating Tablet","Capecitabine RDT|Capecitabine Rapidly Disintegrating Tablet","A rapidly disintegrating film-coated tablet composed of the fluoropyrimidine carbamate antimetabolite capecitabine with antineoplastic activity. As a prodrug, capecitabine is converted to 5'-deoxy-5-fluorocytidine (5'-DFCR) by hepatic carboxylesterase and then to 5'-deoxy-5-fluorouridine (5'-DFUR) by cytidine deaminase and is eventually activated by thymidine phosphorylase to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine triphosphate production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand. Capecitabine rapidly disintegrating tablet (RDT) contains the water insoluble, disintegrating agent crospovidone which very rapidly disperses and swells in water making this RDT easier to swallow than the traditional capecitabine tablet.","Pharmacologic Substance"]
["C90564","Capmatinib","2-Fluoro-N-methyl-4-(7-(quinolin-6-ylmethyl)imidazo[1,2-b][1,2,4]triazin-2-yl)benzamide|Capmatinib|INC280|INCB028060","An orally bioavailable inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. Capmatinib selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C340","Captopril","(S)-1-(3-Mercapto-2-methyl-1-oxopropyl)-L-proline|CAPTOPRIL|Capoten|Captopril|captopril","A sulfhydryl-containing analog of proline with antihypertensive activity and potential antineoplastic activity. Captopril competitively inhibits angiotensin converting enzyme (ACE), thereby decreasing levels of angiotensin II, increasing plasma renin activity, and decreasing aldosterone secretion.  This agent may also inhibit tumor angiogenesis by inhibiting endothelial cell matrix metalloproteinases (MMPs) and endothelial cell migration. Captopril may also exhibit antineoplastic activity independent of effects on tumor angiogenesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1037","Caracemide","Acetamide, N-[(Methylamino)carbonyl]-N-[[(methylamino)carbonyl]oxy]-(9CI)|Acetamide, N-[(methylamino)carbonyl]-N-[[(methylamino)carbonyl]oxy]- (9CI)|CARACEMIDE|Caracemide|N-Acetyl-N-(methylcarbamoyloxy)-N'-methylurea","An agent derived from acetohydroxamic acid with potential antineoplastic activity.  Caracemide inhibits ribonuclease reductase, resulting in decreased DNA synthesis and tumor growth; it also inhibits acetylcholinesterase.  In vivo, caracemide contributes to the formation of the neurotoxin methyl isocyanate; this effect, along with the agent's acetylcholinesterase activity, may be responsible for the severe central nervous system toxicity observed in clinical trials. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1154","Carbendazim","1H-Benzimidazol-2-yl-carbamic Acid, Methyl Ester|1H-benzimidazol-2-ylcarbamic Acid Methyl Ester|2-(Methoxycarbonylamino)benzimidazole|2-Benzimidazolecarcamic Acid Methyl Ester|2-Methyl benzimidazolecarbamate|BAS 3460|BAS-3460|BAS-67054|BCM|BMC|Bavistin|CARBENDAZIM|CTR 6669|CTR-6669|Carbendazim|Carbendazole|Derosal|FB642|HOE 17411|HOE-17411|MBC|Methyl 2-Benzimidazolecarbamate|Methyl 2-benzimidazolecarbamate|Methyl Benzimidazol-2-ylcarbamate|Methyl-1H-benzimidazol-2-yl Carbamate|Methyl-2-benzimidazole Carbamate|Methyl-2-benzimidazolecarbamate|Methyl-alpha-benzimidazole Carbamate|carbendazim","A broad-spectrum benzimidazole antifungal with potential antimitotic and antineoplastic activities. Although the exact mechanism of action is unclear, carbendazim appears to binds to an unspecified site on tubulin and suppresses microtubule assembly dynamic. This results in cell cycle arrest at the G2/M phase and an induction of apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C1356","Carbetimer","Carbetimer|N-137|NED-137|carbethimer|carboxyaminidate","Carbetimer (carboxyimamidate) is a low molecular weight derivatized copolymer of ethylene and maleic anhydride.  It has demonstrated antitumor activity against several animal models.  It has calcium chelation activity but seems to inhibit growth of sensitive cells by disrupting nucleoside uptake and metabolism.","Organic Chemical|Pharmacologic Substance"]
["C1038","Carbogen","Carbogen|carbogen","An inhalant consisting of hyperoxic gas (95%-98% oxygen and 2%-5% carbon dioxide) with radiosensitizing properties.  Inhaled carbogen reduces diffusion-limited tumor hypoxia, increasing tumor radiosensitivity due to the increased availability of molecular oxygen for cytotoxic radiation-induced oxygen free radical production. (NCI04)","Inorganic Chemical|Pharmacologic Substance"]
["C103819","Carbon C 11 Erlotinib Hydrochloride","C11-Erlotinib Hydrochloride|Carbon C 11 Erlotinib Hydrochloride","The hydrochloride salt form of the quinazoline derivative erlotinib labeled with the positron-emitting isotope carbon C 11, with potential use in imaging.  Competing with adenosine triphosphate, erlotinib reversibly binds to the intracellular catalytic tyrosine kinase domain of the epidermal growth factor receptor (EGFR). Following exposure to this agent, EGFR expression status can be determined and EGFR overexpressing tumor cells can be visualized using positron emission tomography (PET) imaging. This may be useful in determining the tumor cell response to a particular EGFR kinase inhibitor in individual patients. EGFR, a receptor tyrosine kinase, is overexpressed in numerous cancer cell types, and plays a significant role in tumor cell progression.","Indicator, Reagent, or Diagnostic Aid|Pharmacologic Substance"]
["C118360","Carbon C 11 Methylaminoisobutyrate","11C-MeAIB|Carbon C 11 Methylaminoisobutyrate|N-methyl-11C-methylaminoisobutyric Acid","A synthetic neutral amino acid analog radiolabeled with carbon C 11 with potential use for metabolic tumor imaging during positron emission tomography (PET). Upon administration, carbon C 11 methylaminoisobutyrate ([(11)C]MeAIB) is taken up by and accumulates in cancer cells through the A-type (alanine-preferring) amino acid transport system. Upon imaging of the radioisotope, the distribution patterns of MeAIB and its uptake by cancer cells can be further elucidated. This may establish its usefulness as a tumor tracer in the diagnosis of certain cancers. Amino acid transport system A is highly upregulated in malignant cells and facilitates the uptake of amino acids needed for tumor cell proliferation.","Indicator, Reagent, or Diagnostic Aid|Pharmacologic Substance"]
["C95725","Carbon C 11 N-desmethyl-Loperamide","(11C)N-Desmethyl-Loperamide|(11C)dLop|Carbon C 11 N-desmethyl-Loperamide","A radiopharmaceutical containing N-desmethyl loperamide (dLop) labeled with carbon 11 (11C), used to measure the activity of efflux transporter P-glycoprotein (P-gp) in positron emission tomography (PET). Upon administration, carbon C 11 N-desmethyl-loperamide acts as a substrate for the efflux transporter P-gp. Upon uptake by P-gp at the blood-brain barrier (BBB) and subsequent PET imaging, this radioligand may allow for prediction of P-gp function and expression in brain tumor patients. As P-gp activity may influence response to therapy, measuring P-gp activity may be beneficial when choosing chemotherapy. P-gp, encoded by the MDR-1 gene and a member of the ATP-binding cassette (ABC) superfamily of transmembrane transporters, is overexpressed by some MDR tumors and may contribute to multidrug resistance to chemotherapy.","Indicator, Reagent, or Diagnostic Aid"]
["C121962","Carbon C 11 PBR-28","(11C)PBR-28|Acetamide, N-((2-(methoxy-11C)-phenyl)methyl)-N-(6-phenoxy-3-pyridinyl)-|Carbon C 11 PBR-28|PBR-28 C-11|[11C] PBR28","A radioconjugate composed of a ligand for the 18 kDa translocator protein (TSPO) conjugated to the radioisotope carbon C 11, that can be used as a diagnostic imaging agent to detect TSPO-expressing cells using positron emission tomography (PET). Upon administration of carbon C 11 PBR-28, the PBR-28 moiety targets and binds to TSPO-expressing cells. Upon PET, carbon C 11 can be detected and TSPO-expressing cells can be visualized. This can facilitate detection of inflammatory sites and cancer cells. TSPO, also called the peripheral benzodiazepine receptor (PBR), is found on the outer mitochondrial membrane and is overexpressed on a variety of cancer cells and during inflammation.","Pharmacologic Substance"]
["C122684","Carbon C 11 Sarcosine","11C-labeled Sarcosine|11C-sarcosine|Carbon C 11 Sarcosine","A radiotracer consisting of sarcosine, the N-methyl derivative of the amino acid glycine, labeled with the positron-emitting isotope carbon C 11, that can be used for tumor imaging upon positron emission tomography/computed tomography (PET/CT). Upon administration, C-11 sarcosine is taken up by and accumulates in tumor cells, thereby allowing tumor imaging with PET/CT. Sarcosine, a non-proteinogenic amino acid and oncometabolite, is elevated in certain tumor cell types. Its expression seems to correlate with increased tumor invasiveness.","Pharmacologic Substance"]
["C116790","Carbon C 11 Sepantronium Bromide","11C-YM155|Carbon C 11 Sepantronium Bromide","A radiotracer composed of the bromide salt form of sepantronium, a small-molecule survivin antagonist and proapoptotic agent, labeled with the radionuclide carbon C 11, with potential positron emission tomography (PET) imaging activity. Upon administration, sepantronium is selectively taken up by tumor cells, binds to the survivin promoter and inhibits the transcription of survivin, which results in decreased survivin expression. Upon PET imaging, the tissue distribution of sepantronium and its tumor uptake can be assessed. Survivin, a member of the inhibitor of apoptosis (IAP) gene family, is overexpressed in a variety of human cancers; its expression in tumors is associated with a more aggressive phenotype, increased cancer cell proliferation, shorter survival times, and a decreased response to chemotherapy.","Pharmacologic Substance"]
["C85472","Carbon C 14 Eribulin Acetate","14C-Eribulin Acetate|Carbon C 14 Eribulin Acetate","A radioconjugate containing the acetate salt of eribulin, labeled with the beta particle-emitting radioisotope carbon C 14, with radioisotopic and potential antineoplastic activities. Upon administration, eribulin binds to the vinca domain of tubulin and inhibits the polymerization of tubulin and the assembly of microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest at G2/M phase, and, potentially, tumor regression. The radioisotope moiety of this agent acts as a radioactive tracer.","Pharmacologic Substance"]
["C90556","Carbon C 14 Ombrabulin","Carbon C 14 Ombrabulin|[14C]-AVE8062","A synthetic water-soluble analogue of combretastatin A4, derived from the South African willow bush (Combretum caffrum), labeled with carbon C 14 with potential antineoplastic activity. The ombrabulin moiety of carbon C 14 ombrabulin binds to the colchicine binding site of endothelial cell tubulin, thereby inhibiting tubulin polymerization and inducing mitotic arrest and apoptosis in endothelial cells. As apoptotic endothelial cells detach from their substrata, tumor blood vessels collapse; the acute disruption of tumor blood flow may result in tumor necrosis. The radioisotope moiety of this agent acts as a radioactive tracer.","Pharmacologic Substance"]
["C113806","Carbon C11 Temozolomide","Carbon C11 Temozolomide|[11C] Temozolomide","A radioconjugate composed of temozolomide, a imidazotetrazine analog of dacarbazine, labeled with the radioisotope carbon C11, with potential positron emission tomography (PET) imaging activity. As a cytotoxic alkylating agent, temozolomide is hydrolyzed at physiologic pH to the pharmacologically active compound, 5-(3-methyl-(triazen-1-yl)-imidazole)-4-carboxamide (MTIC). MTIC is further hydrolyzed to 5-aminoimidazole-4-carboxamide (AIC) and a methyldiazonium cation. The cation is able to methylate DNA, particularly at the O6 and N7 positions of guanine residues, resulting in cell cycle arrest, inhibition of DNA replication and the induction of apoptosis. Temozolomide is metabolized to MITC at all sites, crosses the blood-brain-barrier and penetrates well into the central nervous system. Upon PET, the biodistribution, uptake in cancer cells and the efficacy of temozolomide can be assessed.","Pharmacologic Substance"]
["C88339","Carbon C-14 Dacomitinib","Carbon C 14 PF-00299804|Carbon C-14 Dacomitinib|[14C]PF-00299804","A radioconjugate consisting of an orally bioavailable small-molecule inhibitor of the epidermal growth factor receptor (erbB or HER) family of tyrosine kinases radiolabeled with carbon-14 with potential antineoplastic and beta-emitting radioisotope activity. PF-00299804 specifically and irreversibly binds to and inhibits human Her-1, Her-2, and Her-4, resulting in the proliferation inhibition and apoptosis of tumor cells that overexpress these receptors. The HER receptor family of tyrosine kinases, often overexpressed by a variety of tumor cell types, may contribute to tumor cell proliferation, differentiation, migration, and survival. PF-00299804 radiolabeled with carbon C-14 may be used as a radiotracer in pharmacological studies of PF-00299804 metabolism.","Pharmacologic Substance"]
["C38712","Carbon-11 Acetate","C-11 Acetate|C11 Acetate|Carbon-11 Acetate|carbon-11 acetate","The acetate salt of the radioisotope carbon-11. Although the mechanism is unclear, carbon-11 acetate preferentially accumulates in tumor tissue, serving as a tracer for imaging tumors with positron emission tomography (PET). (NCI04)","Indicator, Reagent, or Diagnostic Aid"]
["C1282","Carboplatin","(SP-4-2)-diammine[1,1-cyclobutanedicarboxylato(2--)-O,O']platinum|1,1-cyclobutanedicarboxylic acid platinum complex|Blastocarb|CARBOPLATIN|CBDCA|Carboplat|Carboplatin Hexal|Carboplatin|Carboplatino|Carbosin|Carbosol|Carbotec|Cis-Diammine(cyclobutane-1,1-dicarboxylato)platinum|Displata|Ercar|JM-8|Nealorin|Novoplatinum|Paraplat|Paraplatin AQ|Paraplatin|Paraplatine|Platinwas|Ribocarbo|carboplatin|cis-diammine(1,1-cyclobutanedicarboxylato) platinum(II)|cis-diammine(cyclobutanedicarboxylato)platinum II|platinum, diammine(1,1-cyclobutanedicarboxylato(2-))-, (SP-4-2)","A second-generation platinum compound with a broad spectrum of antineoplastic properties.  Carboplatin contains a platinum atom complexed with two ammonia groups and a cyclobutane-dicarboxyl residue.  This agent is activated intracellularly to form reactive platinum complexes that bind to nucleophilic groups such as GC-rich sites in DNA, thereby inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links.  These carboplatin-induced DNA and protein effects result in apoptosis and cell growth inhibition.  This agent possesses tumoricidal activity similar to that of its parent compound, cisplatin, but is more stable and less toxic. (NCI04)","Inorganic Chemical|Pharmacologic Substance"]
["C342","Carboquone","CARBOQUONE|Carboquone","An aziridinylbenzoquinone-based alkylating agent with potential antineoplastic activity. The alkylating group in carboquone becomes activated upon reduction of quinone to the hydroquinone form. This eventually results in the alkylation and crosslinking of DNA, thereby inhibiting DNA replication followed by an induction of apoptosis. In addition, reactive oxygen species may form during redox cycling which may contribute to this agent's cytotoxic activity.","Organic Chemical|Pharmacologic Substance"]
["C1141","Carboxyamidotriazole","1H-1,2,3-Triazole-4-carboxamide, 5-amino-1-((3,5-dichloro-4(4-chlorobenzoyl)phenyl)methyl)|5-Amino-1-((3,5-dichloro-4-(4-chlorobenzoyl)phenyl)methyl)-1H-1,2,3-triazole-4-carboxamide|CAI|Carboxyamido-triazole|Carboxyamidotriazole|Carboxyaminoimidazole|L651582|carboxyamidotriazole","An orally-active agent with potential antineoplastic activity.  Carboxyamidotriazole binds to and inhibits non-voltage-operated Ca2+ channels, blocking both Ca2+ influx into cells and Ca2+ release from intracellular stores and resulting in the disruption of calcium channel-mediated signal transduction and inhibition of vascular endothelial growth factor (VEGF) signaling, endothelial proliferation, and angiogenesis.  This agent may also inhibit tumor cell growth, invasion and metastasis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C91090","Carboxyamidotriazole Orotate","1,2,3-Carboxyamido-triazole Orotate|CTO|Carboxyamidotriazole Orotate","The orotate salt form of carboxyamidotriazole (CAI), an orally bioavailable small molecule with potential antiangiogenic and antiproliferative activities. Carboxyamidotriazole binds to and inhibits non-voltage-operated calcium channels, blocking both Ca2+ influx into cells and Ca2+ release from intracellular stores, resulting in the disruption of calcium channel-mediated signal transduction. CAI inhibits PI3 activity and vascular endothelial growth factor (VEGF) signaling. This may inhibit endothelial proliferation, tumor cell growth, invasion and metastasis.","Organic Chemical|Pharmacologic Substance"]
["C1169","Carboxyphenyl Retinamide","4-carboxyphenyl retinamide|Carboxyphenyl Retinamide|N-(4-Carboxyphenyl)retinamide|N-(4-carboxyphenyl)retinamide","A synthetic phenylretinamide analogue of retinol (vitamin A) with potential antineoplastic and chemopreventive activities.  Carboxyphenyl retinamide induces cell differentiation and inhibits tumor cell growth and carcinogenesis.  This agent may also induce cell cycle arrest in the G1 phase in some cancer cell types. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2414","Carcinoembryonic Antigen Peptide 1","CAP-1|CEA Peptide 1|CEA Peptide 9-mer|CEA peptide-1|Carcinoembryonic Antigen Peptide 1|Carcinoembryonic Antigen Peptide-1|Carcinoembryonic Peptide-1|carcinoembryonic antigen peptide-1","A nine amino acid peptide fragment of carcinoembryonic antigen (CEA), a protein that is overexpressed in several cancer cell types, including gastrointestinal, breast, and non-small cell lung. Autologous vaccination with activated autologous dendritic cells (DC) or peripheral blood mononuclear cells (PBMC) which have been exposed to CEA peptide 1 in vitro may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing CEA, thereby inhibiting tumor growth. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C2622","Carcinoembryonic Antigen Peptide 1-6D","CAP-1-6D Peptide|CEA:571-579 (576D)|Carcinoembryonic Antigen Peptide 1-6D|Modified CEA Peptide|mCEA Peptide","A 9-residue human leukocyte antigen (HLA)-restricted fragment of carcinoembryonic antigen (CEA). Vaccination with carcinoembryonic antigen peptide 1-6D, which has the amino acid sequence YLSGANLNL, may elicit a cytotoxic T lymphocyte (CTL) immune response against tumors expressing CEA.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C70644","Carcinoembryonic Antigen Peptide 1-6D Virus-Like Replicon Particles Vaccine","AVX701|CEA(6D) VRP|Carcinoembryonic Antigen Peptide 1-6D Virus-Like Replicon Particles Vaccine","A cancer vaccine, consisting of alphavirus vector-derived virus-like replicon particles expressing the 9-amino-acid carcinoembryonic antigen peptide (CAP) 1-6D, with potential antineoplastic activity. Vaccination with this agent may elicit a cytotoxic T lymphocyte (CTL) immune response against CEA-expressing tumor cells.","Pharmacologic Substance"]
["C2439","Carcinoembryonic Antigen RNA-pulsed DC Cancer Vaccine","CEA RNA-pulsed DC cancer vaccine|CEA RNA-pulsed dendritic cell cancer vaccine|Carcinoembryonic Antigen RNA-pulsed DC Cancer Vaccine|carcinoembryonic antigen RNA-pulsed dendritic cell cancer vaccine","A vaccine comprised of autologous dendritic cells pulsed with mRNA-encoded Carcinoembryonic Antigen (CEA) targeting tumor cells expressing CEA. (NCI)","Immunologic Factor|Pharmacologic Substance"]
["C64775","Carcinoembryonic Antigen-Expressing Measles Virus","Carcinoembryonic Antigen-Expressing Measles Virus|MV-CEA","An attenuated oncolytic Edmonston (Ed) strain of measles virus (MV) encoding the soluble extracellular N-terminal domain of human carcinoembryonic antigen (CEA) (MV-CEA) with potential antineoplastic activity. The cellular receptor of MV is human CD46 antigen, a type 1 integral membrane glycoprotein found on nearly all human tissues and overexpressed on many cancer cell types. Mediated through CD46, both haemagglutinin and fusion glycoproteins of MV are required for the attachment to and fusion of host cell membranes, thereby leading to syncytia and cell lysis. The expressed CEA, a tumor associated antigen, can be detected in serum and used as a sensitive marker to monitor viral gene expression in order to easily optimize individual therapy. Compared to wild-type MV, the Ed strain of MV has a lower affinity for the MV receptor signaling lymphocyte-activation molecule (CD150), mainly expressed in B- and T-lymphocytes, but a higher affinity for CD46.","Pharmacologic Substance|Virus"]
["C52196","Carfilzomib","(2S)-N-((1S)-1-Benzyl-2-(((1S)-3-methyl-1-(((2R)-2-methyloxiran-2-yl)carbonyl)butyl)amino)-2-oxoethyl)-4-methyl-2-(((2S)-2-((morpholin-4-ylacetyl)amino)-4-phenylbutanoyl)amino)pentanamide|CARFILZOMIB|Carfilzomib|Kyprolis|PR-171","An epoxomicin derivate with potential antineoplastic activity. Carfilzomib irreversibly binds to and inhibits the chymotrypsin-like activity of the 20S catalytic core subunit of the proteasome, a protease complex responsible for degrading a large variety of cellular proteins. Inhibition of proteasome-mediated proteolysis results in an accumulation of polyubiquinated proteins, which may lead to cell cycle arrest, induction of apoptosis, and inhibition of tumor growth.","Pharmacologic Substance"]
["C80048","Caricotamide/Tretazicar","Caricotamide/Tretazicar|EP-0152R/CB1954|Prolarix","A combination therapy consisting of the prodrug tretazicar and the enzyme co-substrate caricotamide with potential antineoplastic activity. In the presence of separately and simultaneously administered caricotamide, tretazicar is converted to the short-lived cytotoxic DNA cross-linking agent dinitrobenzamide by NAD(P)H quinine oxidoreductase 2 (NQO2), resulting in the inhibition of DNA replication and the induction of apoptosis. NQO2 has been found to be elevated in certain cancers such as hepatocellular carcinoma (HCC).","Pharmacologic Substance"]
["C71010","Carlumab","Anti-human Small-inducible Cytokine A2 Monoclonal Antibody CNTO 888|CARLUMAB|CNTO 888|Carlumab|Immunoglobulin G1, anti-(human monocyte chemoattractant protein-1) (human monoclonal CNTO888 gamma 1-chain), disulfide with human monoclonal CNTO888 kappa-chain, dimer","A human IgG1 kappa monoclonal antibody directed against human CC chemokine ligand 2 (CCL2) with potential antineoplastic activity. Carlumab binds to and inhibits CLL2, which may result in inhibition of angiogenesis and, so, tumor cell proliferation. Endothelium-derived CLL2 (monocyte chemoattractant protein; MCP1) is a member of the beta-chemokine family, can stimulate monocyte/macrophage migration and smooth muscle cell (SMC) proliferation, and plays a role in angiogenesis and tumor cell migration; CCL2 induction of angiogenesis may involve the upregulation of hypoxia-inducible factor 1 alpha (HIF-1 alpha) gene expression which, in turn, induces vascular endothelial growth factor-A (VEGF-A) gene expression.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C955","Carmofur","1(2H)-Pyrimidinecarboxamide, 5-fluoro-N-hexyl-3,4-dihydro-2,4-dioxo-|1-Hexylcarbamoyl-5-Fluorouracil|CARMOFUR|Carmofur|HCFU","An antimetabolite (pyrimidine analogue) antineoplastic derivative of 5-fluorouracil. (NCI)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C349","Carmustine","1,3-Bis(2-chloroethyl)-1-nitrosourea|1,3-Bis(beta-chloroethyl)-1-nitrosourea|BCNU|Becenum|Becenun|BiCNU|Bis(chloroethyl) Nitrosourea|Bis-Chloronitrosourea|CARMUSTINE|Carmubris|Carmustin|Carmustine|Carmustinum|FDA 0345|Gliadel|N,N'-Bis(2-chloroethyl)-N-nitrosourea|N,N'-bis(2-chloroethyl)-N-nitrosourea|Nitrourean|Nitrumon|SK 27702|SRI 1720|WR-139021|carmustine","An antineoplastic nitrosourea. Carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis.  This agent also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect.  Carmustine is highly lipophilic and crosses the blood-brain barrier readily. (NCI04)","Hazardous or Poisonous Substance|Pharmacologic Substance"]
["C2602","Carmustine in Ethanol","Carmustine in Ethanol|DTI-015","A formulation containing carmustine dissolved in ethanol for intra-tumoral administration that allows carmustine to enter both aqueous and lipid compartments of the target tissue. As an antineoplastic nitrosourea, carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. Carmustine also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect. Carmustine is highly lipophilic and crosses the blood-brain barrier readily.","Organic Chemical|Pharmacologic Substance"]
["C102847","Carmustine Sustained-Release Implant Wafer","CASANT Wafer|Carmustine Sustained-Release Implant Wafer","A sustained release (SR) implant wafer containing the lipophilic nitrosourea carmustine (BCNU) with antineoplastic activity. Upon intracranial administration of the implant wafer and subsequent release of BCNU from the wafer, this agent alkylates and cross-links DNA during all phases of the cell cycle, resulting in the disruption of DNA function, cell cycle arrest, and apoptosis. This wafer contains the biodegradable copolymer PLGA (poly(lactide-co-glycolide) as the major drug delivery vehicle which is slowly degraded into water and carbon dioxide thereby continously releasing BCNU over approximately 3-4 weeks. Compared to systemic administration of BCNU alone, this local SR formulation is able to maintain higher drug concentrations locally over a longer period of time while minimizing exposure to other tissues.","Pharmacologic Substance"]
["C115961","Carrageenan-containing Gel","Carrageenan-containing Gel|Divine 9 with Carragel","A water-based, vaginal moisturizing gel containing a mixture of lambda- and kappa- carrageenans, sulfated polysaccharides derived from red seaweed (Chondrus crispus), with potential microbicidal activity against various viruses, including human papillomavirus (HPV), human immunodeficiencyvirus (HIV) and human herpes simplex virus (HSV). Upon vaginal insertion via an applicator, carrageenan specifically binds to the viral capsids, which prevents the binding of virions to heparan sulfate proteoglycan (HSPG) receptors or other, as of yet not fully identified, cellular proteins. In addition, the viral binding of carrageenan may also interfere with conformational changes within the virions after cellular attachment. This inhibits viral infection. Certain HPV types cause cervical cancer; therefore, the prevention of HPV infection by this gel may subsequently prevent the development of cervical cancer.","Pharmacologic Substance"]
["C352","Carubicin","(2S,3S)-3-acetyl-1,2,3,4,6,11-hexahydro-3,5,10,12-tetrahydroxy-6,11-dioxo-1-naphthacenyl 3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranoside|(8S-cis)-acetyl-10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-1,6,8,11-tetrahydroxy-5,12-naphthacenedione|4-O-demethyldaunorubicin|5,12-Naphthacenedione, 8-acetyl-10-[(3-amino-2,3, 6-trideoxy-.alpha.-L-lyxo-hexopyranosyl)oxy]-7,8,9, 10-tetrahydro-1,6,8,11-tetra-hydroxy- (8S-cis)- (8CI 9CI)|5,12-naphthacenedione, 8-acetyl-10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-1,6,8,11-tetra-hydroxy-(8S-cis)-(8CI 9CI)|5,12-naphthacenedione, 8-acetyl-10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-1,6,8,11-tetra-hydroxy-,(8S-cis)-(8CI)-(9CI)|CARMINOMYCIN|CARUBICIN|CMM|Carminomycin I|Carminomycin|Carubicin|Demethyldaunomycin|Karminomitsin|Karminomycin","An anthracycline antineoplastic antibiotic isolated from the bacterium Actinomadura carminata. Carubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.","Antibiotic|Organic Chemical"]
["C1582","Carubicin Hydrochloride","CARUBICIN HYDROCHLORIDE|Carubicin Hydrochloride|Carubicin hydrochloride","The hydrochloride salt of the anthracycline antineoplastic antibiotic carubicin.  Carubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis.","Antibiotic|Organic Chemical"]
["C1441","Carzelesin","2-Benzofurancarboxamide, N-(2-((1-(chloromethyl)-1,6-dihydro-8-methyl-5-(((phenylamino)carbonyl)oxy)benzo(1,2-b:4,3-b')dipyrrol-3(2H)-yl)carbonyl)-1H-indol-5-yl)-6-(diethylamino)-, (S)-|CARZELESIN|Carzelesin|U-80244|carzelesin","A cyclopropylpyrroloindole prodrug analogue and DNA minor groove binding agent, with antineoplastic activity.  After hydrolysis, the cyclopropyl group of carzelesin alkylates N3-adenine in a sequence-selective fashion. This results in tumor growth inhibition.","Organic Chemical|Pharmacologic Substance"]
["C1040","Carzinophilin","CARZINOPHILIN|CZP|Cardinophillin|Cardinophyllin|Carzinophilin|Carzinophyllin","An ethylenimine antineoplastic antibiotic isolated from the bacterium Streptomyces sahachiroi.  Carzinophilin forms interstrand DNA cross-links, thereby inhibiting DNA synthesis. (NCI04)","Antibiotic|Organic Chemical"]
["C118292","Cathelicidin LL-37","Antimicrobial Peptide, Human LLGDFFRKSKEKIGKEFKRIVQRIKDFLRNLVPRTES|Cathelicidin LL-37|LL-37","A synthetic form of a human antimicrobial peptide (37 amino acids), belonging to the cathelicidin family, with antimicrobial, anti-inflammatory, immunostimulating and potential antineoplastic activities. Upon intratumoral injection of the cathelicidin LL-37, this peptide increases p53 expression, and induces phosphatidylserine externalization, DNA fragmentation, cell cycle arrest and caspase-independent apoptosis-inducing factor (AIF)/ endonuclease G (EndoG)-mediated apoptotic cell death in susceptible cancer cells. This suppresses tumor cell proliferation.  LL-37, a protein secreted by bone marrow cells, circulating leukocytes, and various epithelial tissues, plays a crucial role in the innate host immune defense via the regulation of leukocyte chemotaxis and cytokine production; it also promotes wound healing.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C69130","Cationic Liposome-Encapsulated Paclitaxel","Cationic Liposome-Encapsulated Paclitaxel|EndoTAG-1|LipoPac|MBT-0206","A cationic liposome preparation of paclitaxel with antineoplastic activity. Paclitaxel, the active ingredient in cationic liposome-encapsulated paclitaxel, binds to tubulin and inhibits the disassembly of microtubules, resulting in the inhibition of mitosis and cellular proliferation, and apoptosis. Cationic liposome encapsulation of paclitaxel allows the delivery of high doses of paclitaxel to target tissues while minimizing systemic toxicity. Tumor endothelial cells may preferentially bind and internalize cationic liposomes.","Pharmacologic Substance"]
["C62445","Catumaxomab","Catumaxomab|Removab","A trifunctional bispecific monoclonal antibody with potential antineoplastic activity. Catumaxomab has two antigen-recognition sites: one for human CD3, a T cell surface antigen; and one for human epithelial cell adhesion molecule (EpCAM), a cell surface antigen expressed by a variety of epithelial tumor cells. In addition, the modified Fc portion of this antibody binds Fc receptors on antigen presenting cells (APCs) such as macrophages and dendritic cells (DCs). Catumaxomab brings T cells, EpCAM-expressing epithelial tumor cells and APCs together into tricellular complexes, which may result in a potent cytotoxic T-lymphocyte (CTL) response against EpCAM-expressing epithelial tumor cells. Fc-mediated binding of APCs in the tricellular complex potentiates EpCAM antigen presentation to T cells and the activation of anti-tumor cytotoxic T cell functions.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2367","CB10-277","1-p-carboxy-3,3-dimethylphenyltriazine|CB10-277","A synthetic derivative of dimethylphenyl-triazene related to dacarbazine, with antineoplastic properties.  Related to the agent dacarbazine, CB10-277 is converted in vivo to a monomethyl triazene form that alkylates DNA, resulting in inhibition of DNA replication and repair; in addition, this agent may act as a purine analogue, resulting in inhibition of DNA synthesis, and may interact with protein sulfhydryl groups. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C95894","CBP/beta-catenin Antagonist PRI-724","CBP/beta-catenin Antagonist PRI-724|PRI-724","A potent, specific inhibitor of the canonical Wnt signaling pathway in cancer stem cells with potential antineoplastic activity. Wnt signaling pathway inhibitor PRI-724 specifically inhibits the recruiting of beta-catenin with its coactivator CBP (the binding protein of the cAMP response element-binding protein CREB); together with other transcription factors beta-catenin/CBP binds to WRE (Wnt-responsive element) and activates transcription of a wide range of target genes of Wnt/beta-catenin signaling. Blocking the interaction of CBP and beta-catenin by this agent prevents gene expression of many proteins necessary for growth, thereby potentially suppressing cancer cell growth. The Wnt/beta-catenin signaling pathway regulates cell morphology, motility, and proliferation; aberrant regulation of this pathway leads to neoplastic proliferation.","Pharmacologic Substance"]
["C2210","CC-1088","CC-1088","An analog of thalidomide with potential antineoplastic activity that belongs to the functional class of agents called selective cytokine inhibitory drugs (SelCIDs).  SelCIDs inhibit phosphodiesterase-4 (PDE 4), an enzyme involved in tumor necrosis factor alpha (TNF alpha) production.  CC-1088 inhibits production of the cytokines vascular endothelial growth factor (VEGF) (a pro-angiogenic factor) and interleukin-6 (IL-6). (NCI04)","Pharmacologic Substance"]
["C49095","CC-401","CC-401","A second generation ATP-competitive anthrapyrazolone c-Jun N terminal kinase (JNK) inhibitor with potential antineoplastic activity. Based on the chemistry of SP600125, another anthrapyrazolone inhibitor of JNK, CC-401 competitively binds the ATP binding site of JNK, resulting in inhibition of the phosphorylation of the N-terminal activation domain of transcription factor c-Jun; decreased transcription activity of c-Jun; and a variety of cellular effects including decreased cellular proliferation.","Pharmacologic Substance"]
["C28880","CC-49/218 sFv","CC-49/218 sFv","An immunoglobulin derived from the single-chain antigen-binding domain (sFv) of the monoclonal antibody CC-49 with potential antineoplastic activity.  The parent monoclonal antibody CC-49 binds to the tumor-associated glycoprotein TAG-72 with high affinity, recognizing many tumor cell types that express TAG-72. Because of its single-chain structure, CC-49/218 sFv may exhibit a longer half-life than the parent monoclonal antibody CC-49; 218 represents the linker sequence that helps reduce aggregation and proteolysis of this agent.  (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C38711","CC-8490","CC-8490|SPC8490","A benzopyran with potential antineoplastic activity.  CC-8490 acts as a selective estrogen receptor modulator (SERM), inhibiting the proliferation of estrogen-sensitive breast cancer cells.  This agent also inhibits growth and induces apoptosis of glioblastoma cells via a mechanism independent of estrogen receptor-related mechanisms. (NCI04)","Pharmacologic Substance"]
["C98281","CCL21-expressing H1944 Cell Vaccine","CCL21-expressing H1944 Cell Vaccine|Recombinant Human 6C Cytokine-expressing H1944 Cell Vaccine","A cancer cell vaccine comprised of the allogeneic human lung adenocarcinoma cell line H1944 that has been transduced ex vivo with adenoviral vector encoding human cytokine chemokine C-C motif ligand 21 (CCL21), with potential immunomodulating and antineoplastic activities. Upon administration, CCL21-expressing H1944 cell vaccine expresses the chemokine CCL21, which may induce an antitumoral cytotoxic T-lymphocyte immune response in the tumor microenvironment. CCL21 has been shown to attract antigen presenting cells (APCs), like leukocytes and DCs, and natural killer (NK) cells and their T-cell effectors to induce a cytotoxic immune response. H1944 cells contain tumor-associated antigens (TAAs) overexpressed in non-small cell lung cancer (NSCLC).","Pharmacologic Substance"]
["C120302","CCR2 Antagonist CCX872-B","CCR2 Antagonist CCX872-B|CCX872-B","An orally available human C-C chemokine receptor type 2 (CCR2) antagonist, with potential immunomodulating and antineoplastic activities. Upon oral administration, CCR2 antagonist CCX872-B specifically binds to CCR2 and prevents the binding its cognate endothelium-derived chemokine ligand CCL2 (monocyte chemoattractant protein-1 or MCP1). This may result in the inhibition of both CCR2 activation and CCR2-mediated signal transduction, which may inhibit inflammatory processes, angiogenesis, tumor cell migration, and tumor cell proliferation. The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, and stimulates their migration and infiltration; it plays a key role in inflammation. CCR2 is overexpressed in certain cancer cell types, where it is involved in angiogenesis, tumor cell migration and proliferation.","Pharmacologic Substance"]
["C97507","CCR2 Antagonist PF-04136309","CCR2 Antagonist PF-04136309|PF-04136309","An orally available human chemokine receptor 2 (CCR2) antagonist with potential immunomodulating and antineoplastic activities. Upon oral administration, CCR2 antagonist PF-04136309 specifically binds to CCR2 and prevents binding of the endothelium-derived chemokine ligand CLL2 (monocyte chemoattractant protein-1 or MCP1) to its receptor CCR2, which may result in inhibition of CCR2 activation and signal transduction. This may inhibit inflammatory processes as well as angiogenesis, tumor cell migration, and tumor cell proliferation. The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, stimulates the migration and infiltration of these cell types, and plays an important role in inflammation, angiogenesis, and tumor cell migration and proliferation.","Pharmacologic Substance"]
["C116321","CD105/Yb-1/SOX2/CDH3/MDM2-polyepitope Plasmid DNA Vaccine","CD105/Yb-1/SOX2/CDH3/MDM2 Plasmid Vaccine|CD105/Yb-1/SOX2/CDH3/MDM2-polyepitope Plasmid DNA Vaccine|STEMVAC Th1 Polyepitope Plasmid-based Vaccine|STEMVAC","A plasmid DNA vaccine containing the mammalian expression vector pUMVC3 (pNGVL3) encoding epitopes of CD105 (Endoglin), Y-box binding protein 1 (Yb-1), SRY-box 2 (SOX2), cadherin 3 (CDH3), and murine double minute 2 (MDM2) proteins, with potential immunomodulating and antineoplastic activities. Upon intradermal administration of pUMVC3-CD105/Yb-1/SOX2/CDH3/MDM2-epitopes plasmid DNA vaccine, the plasmid transfects cells and the peptides are expressed. This generates a specific memory Th1 (T-helper) cell immune response, stimulates secretion of cytokines by the T cells and leads to a cytotoxic T-lymphocyte (CTL) response against CD105/Yb-1/SOX2/CDH3/MDM2-expressing tumor cells. CD105/Yb-1/SOX2/CDH3/MDM2 proteins are highly immunogenic tumor associated antigens that are overexpressed in breast cancer. Additionally, these antigens are associated with breast cancer stem cells and with epithelial to mesenchymal transformation (EMT).","Pharmacologic Substance"]
["C113794","CD133 Antigen Peptide-pulsed Autologous Dendritic Cell Vaccine","CD-133 Dendritic Cell Vaccine|CD133 Antigen Peptide-pulsed Autologous Dendritic Cell Vaccine|CD133 DC Vaccine","A cell-based cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with human leukocyte antigen (HLA)-A2-restricted peptides derived from the CD133 antigen, with potential antineoplastic activity. Upon intradermal administration, the CD133 antigen peptide-pulsed autologous DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against CD133-expressing tumor cells, resulting in tumor cell lysis. CD133, a cancer stem cell marker, is expressed on hematopoietic stem and progenitor cells and overexpressed on many types of cancer cells; it is associated with resistance to chemotherapy and increased cancer survival. HLA-A2 is an MHC class I molecule that presents antigenic peptides to CD8+ T-cells. Epitope design that is restricted to those epitopes that bind most efficiently to HLA-A2 may improve antigenic peptide immunogenicity.","Immunologic Factor|Pharmacologic Substance"]
["C107505","CD138CAR-CD137/TCRzeta-expressing T Lymphocytes","CART-138 TCR zeta:CD137|CD138CAR-CD137/TCRzeta-expressing T Lymphocytes","T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) specific for syndecan-1 (CD138) (CART-138 T cells) coupled to the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCRzeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD138CAR- CD137/TCRzeta -expressing T lymphocytes directs the T-lymphocytes to syndecan-1-expressing tumor cells and induces selective toxicity in those tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of syndecan-1. Syndecan-1, a type 1 transmembrane proteoglycan and tumor associated antigen, is overexpressed in a variety of cancer cells. It plays a key role in the regulation of cell growth, differentiation, and adhesion, and its expression is correlated with poor prognosis.","Cell|Pharmacologic Substance"]
["C122406","CD19/CD3 Dual-affinity Retargeting Protein JNJ-64052781","CD19 x CD3 DART Protein JNJ-64052781|CD19/CD3 Dual-affinity Retargeting Protein JNJ-64052781|JNJ-64052781","An anti-CD19/anti-CD3 bispecific, humanized antibody-like protein, with potential immunostimulatory and antineoplastic activities. Anti-CD19/anti-CD3 dual-affinity retargeting (DART) protein JNJ-64052781 possesses two antigen-recognition and binding sites, one for the CD3 complex, a group of T-cell surface glycoproteins that complex with the T-cell receptor (TCR), and one for CD19, a tumor-associated antigen (TAA) overexpressed on the surface of B-cells. Upon administration, JNJ-64052781 binds to CD3-expressing T-cells and CD19-expressing cancer cells, thereby crosslinking CD19-expressing tumor B-cells and cytotoxic T-lymphocytes (CTLs). This may result in a potent CTL-mediated cell lysis of CD19-expressing B-lymphocytes. CD19, a B-cell specific membrane antigen, is expressed during normal B-cell development and on B-cell malignancies.","Immunologic Factor|Pharmacologic Substance"]
["C107242","CD19CAR-CD28zeta-4-1BB-expressing Allogeneic T Lymphocytes","Allogeneic CD19.CAR/28137zeta T-lymphocytes|CD19CAR-CD28zeta-4-1BB-expressing Allogeneic T Lymphocytes","Allogeneic T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to the costimulatory signaling domain CD28, the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD28 zeta-4-1BB-expressing allogeneic T lymphocytes directs the T-lymphocytes to and induces selective toxicity in CD19-expressing tumor cells. CD28, a T-cell surface-associated co-stimulatory molecule, is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. Furthermore, inclusion of the 4-1BB signaling domain may increase the antitumor activity compared to the inclusion of the CD28 costimulatory domain and TCR zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies.","Cell|Pharmacologic Substance"]
["C116069","CD19CAR-CD3zeta-4-1BB-CD28-expressing Autologous T-Lymphocytes","CD19CAR-CD3zeta-4-1BB-CD28-expressing Autologous T-Lymphocytes","Autologous T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to three co-stimulatory signaling domains derived from CD28, 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, the CD19CAR-CD3zeta-4-1BB-CD28-expressing autologous T-lymphocytes direct the T-lymphocytes to CD19-expressing tumor cells and induce their selective toxicity. CD28, a T-cell surface-associated co-stimulatory molecule, is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. CD3-zeta is a transmembrane signaling adaptor polypeptide that regulates the assembly of TCR complexes, modulates the expression of the complex on the cell surface and plays a key role in antigen recognition. CD19 antigen, a B-cell specific cell surface antigen, is expressed in all B-cell lineage malignancies.","Cell|Pharmacologic Substance"]
["C101258","CD19CAR-CD3zeta-4-1BB-expressing Allogeneic T-lymphocyte Cells","CART-19 Cells|CD19CAR-CD3zeta-4-1BB-expressing Allogeneic T-lymphocyte Cells","Allogeneic T-lymphocytes transduced with a modified lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), coupled to the signaling domain of 4-1BB (CD137), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD3zeta-4-1BB-expressing allogeneic T-lymphocyte cells direct the T-lymphocytes to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19 and the inclusion of this signaling domain may increase the antitumor activity compared to the inclusion of the CD3-zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies.","Cell|Pharmacologic Substance"]
["C102758","CD19CAR-CD3zeta-4-1BB-expressing Autologous T-lymphocytes","CART-19|CART19|CD19CAR-CD3zeta-4-1BB-expressing Autologous T-lymphocytes|CTL019 T-cells|CTL019","Autologous T-lymphocytes transduced with a modified lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), coupled to the signaling domain of 4-1BB (CD137), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD3zeta-4-1BB-expressing autologous T-lymphocytes direct the T-lymphocytes to CD19-expressing tumor cells, thereby inducing a selective toxicity in CD19-expressing tumor cells. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19 and the inclusion of this signaling domain may increase the antitumor activity compared to the inclusion of the CD3-zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD3-zeta (or CD247) is a transmembrane signaling adaptor polypeptide that regulates the assembly of complete TCR complexes and their expression on the cell surface.","Cell|Pharmacologic Substance"]
["C88266","CD19CAR-CD3zeta-expressing Autologous T lymphocytes","Autologous CART-19:TCR Cells|CD19CAR-CD3zeta-expressing Autologous T lymphocytes","Autologous T-lymphocytes transduced with a modified lentiviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD19CAR-CD3zeta-expressing autologous T-lymphocytes are directed to CD19-expressing tumor cells, thereby inducing a selective toxicity only in these tumor cells. The CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. CD3-zeta (or CD247) is a transmembrane signaling adaptor polypeptide that regulates the assembly of complete T-cell receptor complexes and their expression on the cell surface.","Cell|Pharmacologic Substance"]
["C125903","CD24 Extracellular Domain-IgG1 Fc Domain Recombinant Fusion Protein CD24Fc","CD24 Extracellular Domain-IgG1 Fc Domain Recombinant Fusion Protein CD24Fc|CD24Fc CD24IgG|CD24Fc","A recombinant fusion protein composed of the extracellular domain of the mature human glycoprotein CD24 linked to a human immunoglobulin G1 (IgG1) Fc domain, with potential immune checkpoint inhibitory, anti-inflammatory and antineoplastic activities. Upon administration, the CD24 extracellular domain-IgG1 Fc domain recombinant fusion protein CD24Fc binds to injured cell components, also called DAMPs (Danger-Associated Molecular Patterns), thereby preventing the interaction of DAMPs with toll-like receptors (TLRs) and inhibiting both nuclear factor-kappa B (NFkB) activation and secretion of inflammatory cytokines. In addition, CD24Fc binds to and activates Siglec G/10, a sialic acid-binding immunoglobulin-type lectin, and stimulates SHP-1-mediated inhibitory signaling, while also preventing NFkB activation and secretion of inflammatory mediators, which further prevents inflammatory responses. DAMPs activate the innate immune system. CD24 binds to both DAMPs and Siglec G/10 to regulate immune responses.CD24/Siglec G/10 interaction plays a key role in a number of immune-mediated diseases including graft-versus-host disease (GvHD), multiple sclerosis and rheumatoid arthritis.","Pharmacologic Substance"]
["C117232","CD28CAR/CD137CAR-expressing T-Lymphocytes","CD28CAR/CD137CAR-expressing T-Lymphocytes","Third generation, chimeric antigen receptor (CAR) cells composed of T-lymphocytes transduced with a lentiviral vector expressing a CAR consisting of an a single chain variable fragment specific for a particular antigen, coupled to the two co-stimulatory signaling domains Cluster of Differentiation 28 (CD28) and Cluster of Differentiation 137 (CD137; 4-1BB), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD28CAR/CD137CAR-expressing T-lymphocytes are directed to, and induce selective toxicity in tumor cells expressing the particular antigen. CD28, a T-cell surface-associated co-stimulatory molecule, is required for T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of the antigen. Furthermore, inclusion of the 4-1BB signaling domain may increase the antitumor activity when compared to the inclusion of the CD28 co-stimulatory domain and CD3-zeta alone.","Cell|Pharmacologic Substance"]
["C74017","CD3/CD28 Costimulated Autologous T-Cells","CD3/CD28 Costimulated Autologous T-Cells","A population of T cells that have been sensitized to vaccine tumor antigen(s) in vivo; collected from the patient; co-stimulated with antibodies to the T-cell cell surface proteins CD3 and CD28 and expanded ex vivo; and then infused into the same patient. CD3, part of the T cell receptor complex, and CD28, a T-cell surface-associated co-stimulatory molecule, are both required for full T-cell activation. Adoptive transfer of CD3/CD28 costimulated vaccine-primed autologous T-cells may induce the production of interferon-gamma (IFN-gamma) and granulocyte-macrophage colony-stimulating factor (GM-CSF) and associated antitumor effects and a graft-versus-tumor (GVT) response.","Cell"]
["C116738","CD30 CAR-expressing Autologous T Lymphocytes","CAR.CD30-expressing Autologous T Lymphocytes|CD30 CAR-expressing Autologous T Lymphocytes","A preparation of autologous T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the CD30 antigen, with potential immunostimulating and antineoplastic activities. Upon administration, the CD30 CAR-expressing autologous T-lymphocytes specifically recognize and bind to CD30-expressing tumor cells, resulting in tumor cell lysis. CD30, a cell surface receptor and a member of the tumor necrosis factor (TNF) receptor superfamily, is transiently expressed on activated lymphocytes and is constitutively expressed in hematologic malignancies.","Cell|Pharmacologic Substance"]
["C107190","CD33CAR-CD3zeta-4-1BB-expressing Autologous T-Lymphocytes","Anti-CD33 TCR zeta:CD137 CAR T Cells|CART-33 TCR zeta:CD137 Cells|CART33 TCR zeta:CD137 Cells|CD33CAR-CD3zeta-4-1BB-expressing Autologous T-Lymphocytes","Autologous T-lymphocytes transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD33 scFv (single chain variable fragment) coupled to the signaling domain of 4-1BB (CD137) and the zeta chain of the T-cell receptor (TCRzeta), with potential immunomodulating and antineoplastic activities. Upon transfusion, CD33-specific CAR retroviral vector-transduced autologous T lymphocytes target CD33-expressing tumor cells and induce selective toxicity in CD33-expressing tumor cells. Following binding to CD33, the 4-1BB co-stimulatory molecule signaling domain enhances both activation and signaling. Inclusion of the 4-1BB signaling domain may also increase the antitumor activity when compared to the inclusion of the CD3-zeta chain alone. CD33 is expressed on normal non-pluripotent hematopoietic stem cells as well as on myeloid leukemia cells.","Cell|Pharmacologic Substance"]
["C74008","CD40 Agonist Monoclonal Antibody CP-870,893","CD40 Agonist Monoclonal Antibody CP-870,893|CP-870,893","A fully human monoclonal antibody (mAb) agonist of the cell surface receptor CD40 with potential immunostimulatory and antineoplastic activities. Similar to the CD40 ligand (CD40L or CD154), CD40 agonist monoclonal antibody CP-870,893 binds to CD40 on a variety of immune cell types, triggering the cellular proliferation and activation of antigen-presenting cells (APCs), activating B cells and T cells, and enhancing the immune response; in addition, this agent may activate CD40 present on the surfaces of some solid tumor cells, resulting in apoptosis and decreased tumor growth. CD40, a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells, many B-cell malignancies, and some solid tumors, mediating both indirect tumor cell killing through the activation of the immune system and direct tumor cell apoptosis.","Pharmacologic Substance"]
["C119740","CD40 Agonist Monoclonal Antibody RO7009789","CD40 Agonist Monoclonal Antibody RO7009789|RO7009789","A monoclonal antibody agonist of the cell surface receptor CD40, with potential immunostimulatory and antineoplastic activities. Similar to the endogenous CD40 ligand (CD40L or CD154), CD40 agonist monoclonal antibody RO7009789 binds to CD40 on a variety of immune cell types. This triggers the cellular proliferation and activation of antigen-presenting cells (APCs), and activates B-cells and T-cells, resulting in an enhanced immune response. RO7009789 also binds to and activates CD40 present on the surfaces of some solid tumor cells, leading to apoptosis and decreased tumor growth. CD40, a cell surface receptor and member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells and certain cancer cells; it mediates both indirect tumor cell killing through the activation of the immune system and direct tumor cell apoptosis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C123734","CD40 Agonistic Monoclonal Antibody APX005M","APX 005|APX 005M|APX-005M|APX005M|CD40 Agonistic Monoclonal Antibody APX005M|EPI-0050","A humanized monoclonal antibody agonist of the cell surface receptor CD40, with potential immunostimulatory and antineoplastic activities. Similar to the endogenous CD40 ligand (CD40L or CD154), CD40 agonistic monoclonal antibody APX005M binds to CD40 on a variety of immune cell types. This triggers the cellular proliferation and activation of antigen-presenting cells (APCs), and activates B-cells, and effector and memory T-cells. This results in an enhanced immune response against tumor cells. APX005M also binds to and activates CD40 present on the surfaces of some solid tumor cells, leading to apoptosis and decreased tumor growth. CD40, a cell surface receptor and member of the tumor necrosis factor (TNF) receptor superfamily, is expressed on various immune cells and certain cancer cells; it mediates both indirect tumor cell killing through the activation of the immune system and direct tumor cell apoptosis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C129596","CD4-specific Telomerase Peptide Vaccine UCPVax","CD4-specific Telomerase Peptide Vaccine UCPVax|UCP2/UCP4 CD4-specific Telomerase Peptide Vaccine UCPVax|UCPVax","A therapeutic peptide vaccine containing the human telomerase reverse transcriptase catalytic subunit (hTERT)-derived universal cancer peptides 2 (UCP2) and 4 (UCP4), and combined with the immunoadjuvant Montanide ISA 51 VG, with potential immunostimulating and antineoplastic activities. Vaccination with the CD4-specific telomerase peptide vaccine UCPVax activates the immune system to mount a T-helper 1 (TH1) CD4-positive T-lymphocyte immune response against and ultimately killing telomerase-expressing cells. Telomerase, a reverse transcriptase normally repressed in healthy cells, is overexpressed in most cancer cells and plays a key role in cellular proliferation.","Immunologic Factor|Pharmacologic Substance"]
["C2464","CD80 Breast Cancer Vaccine","CD80 Breast Cancer Vaccine","A vaccine comprised of CD80-transfected allogenic breast cancer cells to induce T-cell response.","Immunologic Factor|Pharmacologic Substance"]
["C90562","CD95 ECD/IgG-Fc Fusion Protein APG101","APG101|CD95 ECD/IgG-Fc Fusion Protein APG101","A human, soluble fusion protein consisting of the extracellular domain of the CD95 receptor fused to the Fc-domain of the human IgG antibody, with potential antineoplastic activity. CD95 ECD/IgG-Fc fusion protein APG101 binds to the CD95 ligand (CD95L) and blocks the binding of CD95L to the CD95 receptor. In tumor cells, blockage of CD95L-mediated signaling pathways may prevent cell migration and invasive cell growth; in healthy cells, blockage of CD95L-mediated signaling pathways may prevent apoptosis and may protect cell damage. Activation of the CD95 receptor plays an important role in the initiation of apoptosis in healthy cells or the invasive growth of cancer cells.","Pharmacologic Substance"]
["C115102","CDA Inhibitor E7727/Decitabine Combination Agent ASTX727","ASTX727|CDA Inhibitor E7727/Decitabine Combination Agent ASTX727","An orally available combination agent containing the cytidine deaminase (CDA) inhibitor E7727 and the cytidine antimetabolite decitabine, with potential antineoplastic activity. Upon oral administration of ASTX727, the CDA inhibitor E7727 binds to and inhibits CDA, an enzyme primarily found in the gastrointestinal (GI) tract and liver that catalyzes the deamination of cytidine and cytidine analogs. This prevents the breakdown of decitabine, increases its bioavailability and efficacy while decreasing GI toxicity due to the administration of lower doses of decitabine. Decitabine exerts its antineoplastic activity through the incorporation of its triphosphate form into DNA, which inhibits DNA methyltransferase and results in hypomethylation of DNA. This interferes with DNA replication and decreases tumor cell growth.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C126641","CDC7 Inhibitor TAK-931","CDC7 Inhibitor TAK-931|Cell Division Cycle 7 Inhibitor TAK-931|TAK-931","An orally bioavailable inhibitor of cell division cycle 7 (cell division cycle 7-related protein kinase; CDC7), with potential antineoplastic activity. Upon administration, TAK-931 binds to and inhibits CDC7; this prevents the initiation of DNA replication during mitosis, which causes cell cycle arrest and induces apoptosis. This inhibits cell growth in CDC7-overexpressing tumor cells. CDC7, a serine/threonine kinase and cell division cycle protein, is overexpressed in a variety of cancers and plays a key role in the activation of DNA replication and the regulation of cell cycle progression.","Pharmacologic Substance"]
["C82418","CDC7 Kinase Inhibitor BMS-863233","BMS-863233|CDC7 Kinase Inhibitor BMS-863233|Cell Division Cycle 7 Homolog Kinase Inhibitor BMS-863233","An orally bioavailable cell division cycle 7 homolog (CDC7) kinase inhibitor with potential antineoplastic activity. CDC7 kinase inhibitor BMS-863233 binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. CDC7, a serine-threonine kinase overexpressed in a variety of tumor cell types, plays an essential role in the initiation of DNA replication by activating origins of replication.","Pharmacologic Substance"]
["C88316","CDC7 Kinase Inhibitor NMS-1116354","CDC7 Kinase Inhibitor NMS-1116354|NMS-1116354","An orally bioavailable cell division cycle 7 homolog (CDC7) kinase inhibitor with potential antineoplastic activity. CDC7 kinase inhibitor NMS-1116354 binds to and inhibits the activity of CDC7, which may result in the inhibition of DNA replication and mitosis, the induction of tumor cell apoptosis, and the inhibition of tumor cell proliferation in CDC7-overexpressing tumor cells. The serine-threonine kinase CDC7 initiates DNA replication by phosphorylating MCM2 (minichromosome maintenance complex component 2) at Ser40 and Ser53.","Pharmacologic Substance"]
["C64762","CDK Inhibitor P276-00","CDK Inhibitor P276-00|Cyclin Dependent Kinase Inhibitor P276|P276-00|P276","A flavone and cyclin dependent kinase (CDK) inhibitor with potential antineoplastic activity. P276-00 selectively binds to and inhibits Cdk4/cyclin D1, Cdk1/cyclin B and Cdk9/cyclin T1, serine/threonine kinases that play key roles in the regulation of the cell cycle and cellular proliferation. Inhibition of these kinases leads to cell cycle arrest during the G1/S transition, thereby leading to an induction of apoptosis, and inhibition of tumor cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C62523","CDK Inhibitor SNS-032","BMS-387032|CDK Inhibitor SNS-032|SNS-032","A small aminothiazole molecule and cyclin dependent kinase (CDK) inhibitor with potential antineoplastic activity. SNS-032 binds to and prevents the phosphorylation of cyclin-dependent kinases, especially CDK2, 7, and 9 that regulate cell cycle progression. Inhibition of CDKs leads to cell cycle arrest and induces apoptosis. As a result, this agent causes cytotoxicity and prevents further tumor cell growth.","Pharmacologic Substance"]
["C105851","CDK/JAK2/FLT3 Inhibitor TG02 Citrate","CDK/JAK2/FLT3 Inhibitor TG02 Citrate|SB1317 Citrate|TG02 Citrate","An orally bioavailable citrate salt form of TG02, a multi-kinase inhibitor for cyclin dependent kinase (CDK) subtypes 1, 2, 7 and 9, Janus-associated kinase 2 (JAK2), FMS-related tyrosine kinase 3 (FLT3, FLK2, STK1), with potential antineoplastic activity. Upon oral administration, CDK/JAK2/FLT3 Inhibitor TG02 binds to and inhibits the CDK subtypes, JAK2, and FLT3. TG02 also inhibits, to a lesser extent, TYK2, TYRO3, STAT5 and P38delta. This may result in both an induction of apoptosis and an inhibition of tumor cell proliferation in cancer cells that overexpress these kinases. JAK2, often upregulated or mutated in a variety of cancer cells, mediates STAT3 activation and plays a key role in tumor cell proliferation and survival. CDKs are serine/threonine kinases that play key roles in the regulation of the cell cycle and cellular proliferation. FLT3, a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias.","Pharmacologic Substance"]
["C123902","CDK2/5/9 Inhibitor CYC065","CDK2/5/9 Inhibitor CYC065|CYC065|Cyclin Dependent Kinase Inhibitor 2/5/9 CYC065","An orally bioavailable inhibitor of cyclin dependent kinases 2, 5 and 9 (CDK2/5/9), with potential antineoplastic and chemoprotective activities. Upon oral administration, CYC065 selectively binds to and inhibits the activity of CDK2, 5 and 9, which leads to inhibition of CDK2, 5 and 9-dependent cellular pathways, downregulation of genes involved in the pro-survival pathway, prevention of the activation of DNA double-strand break repair pathways, and induction of both cell cycle arrest and apoptosis. This inhibits the proliferation of CDK2/5/9-overexpressing tumor cells. In addition, CYC065 protects hematopoietic stem and progenitor cells (HSPCs), prevents myelosuppression, and preserves the function of the bone marrow. CDKs are serine/threonine kinases involved in the regulation of the cell cycle and may be overexpressed in certain cancer cell types; they play key roles in tumor cell proliferation, the regulation of transcription, and DNA damage repair.","Organic Chemical|Pharmacologic Substance"]
["C88312","CDK2/TRKA Inhibitor PHA-848125 AC","CDK2/TRKA Inhibitor PHA-848125 AC|N,1,4,4-Tetramethyl-8-[[4-(4-methylpiperazin-1-yl)phenyl]amino]-4,5-dihydro-1H-pyrazolo[4,3-h]quinazoline-3-carboxamide|PHA-848125 AC","An orally bioavailable inhibitor of cyclin-dependent kinases (CDKs) and thropomyosin receptor kinase A (TRKA), with potential antineoplastic activity. CDK2/TRKA inhibitor PHA-848125 AC potently inhibits cyclin-dependent kinase 2 (CDK2) and exhibits activity against other CDKs including CDK1 and CDK4, in addition to TRKA. Inhibition of these kinases may result in cell cycle arrest and apoptosis of tumor cells that express these kinases. CDKs are serine/threonine kinases involved in regulation of the cell cycle and may be overexpressed in some cancer cell types. The neurotrophin receptor TRKA is mutated in a variety of cancer cell types.","Pharmacologic Substance"]
["C80049","CDK4 Inhibitor P1446A-05","CDK4 Inhibitor P1446A-05|P1446A-05","A protein kinase inhibitor specific for the cyclin-dependent kinase 4 (CDK4) with potential antineoplastic activity. CDK4 inhibitor P1446A-05 specifically inhibits CDK4-mediated G1-S phase transition, arresting cell cycling and inhibiting cancer cell growth. The serine/threonine kinase CDK4 is found in a complex with D-type G1 cyclins and is the first kinase to become activated upon mitogenic stimulation, releasing cells from a quiescent stage into the G1/S growth cycling stage; CDK-cyclin complexes have been shown to phosphorylate the retinoblastoma (Rb) transcription factor in early G1, displacing histone deacetylase (HDAC) and blocking transcriptional repression.","Pharmacologic Substance"]
["C123281","CDK4/6 Inhibitor G1T28","CDK4/6 Inhibitor G1T28|G1T28","A small molecule, competitive inhibitor of cyclin dependent kinases 4 and 6 (CDK4/6), with potential antineoplastic and chemoprotective activities. Upon intravenous administration, G1T28 binds to and inhibits the activity of CDK4/6, thereby blocking the phosphorylation of the retinoblastoma protein (Rb) in early G1. This prevents G1/S phase transition, causes cell cycle arrest in the G1 phase, induces apoptosis, and inhibits the proliferation of CDK4/6-overexpressing tumor cells. In patients with CDK4/6-independent tumor cells, G1T28 may protect against multi-lineage chemotherapy-induced myelosuppression (CIM) by transiently and reversibly inducing G1 cell cycle arrest in hematopoietic stem and progenitor cells (HSPCs) and preventing transition to the S phase. This protects all hematopoietic lineages, including red blood cells, platelets, neutrophils and lymphocytes, from the DNA-damaging effects of certain chemotherapeutics and preserves the function of the bone marrow and the immune system. CDKs are serine/threonine kinases involved in the regulation of the cell cycle and may be overexpressed in certain cancer cell types. HSPCs are dependent upon CDK4/6 for proliferation.","Pharmacologic Substance"]
["C125899","CDK4/6 Inhibitor SHR6390","CDK4/6 Inhibitor SHR6390|SHR6390","A cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. Upon administration, CDK4/6 inhibitor SHR6390 selectively inhibits cyclin-dependent kinase 4 (CDK4) and 6 (CDK6). This inhibits retinoblastoma (Rb) protein phosphorylation early in the G1 phase, which prevents CDK-mediated G1-S phase transition and leads to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of cell cycle progression.","Pharmacologic Substance"]
["C64761","CDKI AT7519","AT7519|AT7519M|CDK inhibitor AT7519M|CDKI AT7519|Cyclin-Dependent Kinase Inhibitor AT7519M","An orally bioavailable small molecule with potential antineoplastic activity. AT7519M selectively binds to and inhibits cyclin dependent kinases (CDKs), which may result in cell cycle arrest, induction of apoptosis, and inhibition of tumor cell proliferation. CDKs are serine/threonine kinases involved in regulation of the cell cycle and may be overexpressed in some types of cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C64544","CDKI R547","CDKI R547|Cyclin Dependent Kinase Inhibitor R547|Cyclin-Dependent Kinase Inhibitor R547|R547","An orally bioavailable diaminopyrimidine compound and a cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. CDKs are ATP-dependent serine/threonine kinases that are important regulators of cell cycle progression and are frequently overexpressed in cancerous cells. R547 selectively binds to and inhibits CDKs, especially CDK1/cyclin B, CDK2/cyclin E, and CDK4/cyclin D1. The inhibition of CDKs results in cell cycle arrest, inhibition of tumor cell proliferation, and induction of apoptosis. By inhibiting CDK activity, R547 also reduces phosphorylation of the retinoblastoma (Rb) protein, thereby preventing activation of transcription factor E2F and leading to further suppression of tumor cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C90555","CEA/Tetanus Toxoid T Helper Epitope Fusion Protein-Expressing DNA Plasmid Vaccine","CEA/Tetanus Toxoid T Helper Epitope Fusion Protein-Expressing DNA Plasmid Vaccine|tetwtCEA DNA","A plasmid vaccine encoding wild type human carcinoembryonic antigen (CEA) fused to a tetanus toxoid T helper epitope, with potential antineoplastic activity. Upon vaccination and subsequent intradermal electroporation, CEA/tetanus toxoid T helper epitope fusion protein-expressing DNA plasmid vaccine may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells. CEA, a tumor associated antigen, is overexpressed in a variety of cancer cell types. The tetanus toxoid helper peptide epitope, obtained from the bacterial Clostridium tetani toxoid, binds to class II MHC molecules and increases the helper T-cell response thereby inducing an increased and long-term immune response.","Immunologic Factor|Pharmacologic Substance"]
["C131129","CEA-MUC-1-TRICOM Vaccine CV301","CEA-MUC-1-TRICOM Vaccine CV301|CV-301|CV301-V/F|CV301|CVAC-301|MVA-BN/Fowlpox-CEA-MUC-1-TRICOM Vaccine CV301|PANVAC",": A cancer prime/boost vaccine-based immunotherapeutic consisting of a prime, which is comprised of a proprietary version of the recombinant vaccinia viral vector, modified vaccinia Ankara-Bavarian Nordic (MVA-BN) and a recombinant fowlpox viral vector, used for the boosts, encoding both the two tumor-associated antigens (TAA), carcinoembryonic antigen (CEA) and mucin-1 (MUC-1), and TRICOM, which is comprised of three immune-enhancing co-stimulatory molecules, B7-1, ICAM-1 and LFA-3, with potential immunostimulatory and antineoplastic activities. The administration of the vaccinia priming dose is followed by multiple boosting doses of the fowlpox vector. CEA-MUC-1-TRICOM Vaccine CV301 may enhance presentation of CEA and MUC-1 to antigen-presenting cells (APCs) and may activate a cytotoxic T-lymphocyte (CTL) response against CEA- and MUC-1-expressing tumor cells. In addition, CV301 upregulates the expression of PD-L1 due to CTL-mediated tumor attack; additionally, when combined with a PD-1 immune checkpoint inhibitor, the antitumor effect may be increased. CEA and MUC-1 are overexpressed in certain cancers.","Pharmacologic Substance"]
["C126800","CEBPA-targeting saRNA MTL-CEBPA Liposome","CEBPA-targeting saRNA MTL-CEBPA Liposome|MTL-501|MTL-CEBPA","A lipid-based nanoparticle formulation composed of liposomes encapsulating a small oligonucleotide encoding a small activating RNA (saRNA) targeting the CCAAT enhancer binding protein alpha (CEBPA; C/EBP-a) gene, with potential antineoplastic activity. Although the exact mechanism of action through which saRNAs exert their effect(s) is still largely being investigated, it appears that, upon administration, the CEBPA-targeting saRNA MTL-CEBPA liposome targets and binds to a specific DNA regulatory target region, most likely the promoter region, for the CEBPA gene. This restores CEBPA gene transcription, and increases both CEBPA mRNA levels and protein expression. This in turn activates the expression of tumor suppressor genes and may halt proliferation of susceptible tumor cells. Specifically, upregulation of CEBPA in liver cells abrogates liver cancer cell proliferation, thereby prevents liver failure and normalizes liver function. CEBPA, a transcription factor that plays a key role in the regulation of the expression of genes with many functions, including those involved in cellular proliferation, metastasis and normal hepatocyte function, is found in many tissues, including liver cells, adipose tissue and myeloid cells. CEBPA is downregulated in certain types of cancer cells, such as liver cancer cells. saRNA is a short, double-stranded RNA that is structurally related to siRNAs; saRNA is most likely to bind to a target site on the promoter of the CEBPA gene and upregulates its gene expression.","Pharmacologic Substance"]
["C78081","Cedefingol","CEDEFINGOL|Cedefingol","A derivative of sphingosine, with potential antineoplastic activity. As a sphingosine derivative, cedefingol appears to inhibit protein kinase C (PKC), a kinase that plays an important role in tumorigenesis.","Pharmacologic Substance"]
["C48379","Cediranib Maleate","AZD2171 Maleate|AZD2171|CEDIRANIB MALEATE|Cediranib Maleate|Quinazoline, 4-((4-fluoro-2-methyl-1H-indol-5-yl)oxy)-6-methoxy-7-(3-(1-pyrrolidinyl)propoxy)-|Recentin|cediranib maleate","The maleate salt of an indole ether quinazoline derivative with antineoplastic activities. Competing with adenosine triphosphate, cediranib binds to and inhibits all three vascular endothelial growth factor receptor (VEGFR-1,-2,-3) tyrosine kinases, thereby blocking VEGF-signaling, angiogenesis, and tumor cell growth.","Pharmacologic Substance"]
["C1728","Celecoxib","4-(5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide|Benzenesulfonamide, 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-|CELECOXIB|Celebrex|Celecoxib|SC-58635|YM 177|celecoxib","A nonsteroidal anti-inflammatory drug (NSAID) with a diaryl-substituted pyrazole structure. Celecoxib selectively inhibits cyclo-oxygenase-2 activity (COX-2); COX-2 inhibition may result in apoptosis and a reduction in tumor angiogenesis and metastasis.","Organic Chemical|Pharmacologic Substance"]
["C67075","Cell Cycle Checkpoint/DNA Repair Antagonist IC83","Cell Cycle Checkpoint/DNA Repair Antagonist IC83|IC83","A proprietary agent with potential antineoplastic activity. IC83 appears to target cell cycle checkpoint/DNA repair enzymes, which are involved in the recognition and repair of damaged DNA and are overexpressed in many types of cancer cells. Inhibition of cell cycle checkpoint/DNA repair enzymes may enhance the cytotoxicity of DNA damaging agents and dissipate tumor cell resistance to chemotherapy and radiation therapy.","Pharmacologic Substance"]
["C75875","Cemadotin","CEMADOTIN|Cemadotin|LU-103793|LU103793","A synthetic dolastatin 15 analogue with potential antineoplastic activity.  Cemadotin suppresses spindle microtubule dynamics by binding to tubulin, thereby blocking mitosis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1634","Cemadotin Hydrochloride","Cemadotin Hydrochloride|LU-103793|LU103793","The hydrochloride salt form of cemadotin, a synthetic dolastatin 15 analogue with potential antineoplastic activity.  Cemadotin suppresses spindle microtubule dynamics by binding to tubulin, thereby blocking mitosis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C37454","Cenersen","Aezea|Cenersen|EL625|OL(1)p53","A phosphorothioate oligonucleotide harboring nucleotide sequences complementary to tumor suppressor p53 mRNA. Cenersen hybridizes with p53 mRNA molecules, and induces Rnase H dependent hydrolysis of p53 transcripts in the double stranded section of the hybrids, thereby resulting in loss of p53 production. Loss of p53 activity leads to sensitization of cancer cells to other therapeutics.","Pharmacologic Substance"]
["C64540","Cenisertib","AS703569|Aurora Kinase Inhibitor AS703569|CENISERTIB|Cenisertib|R763","A water-soluble, synthetic small molecule with potential antineoplastic activity. Cenisertib selectively binds to and inhibits aurora kinases (AKs), a family of serine-threonine kinases which are important regulators of cell division and proliferation, and which are overexpressed in certain types of cancer. Inhibition of aurora kinases inhibits cell division and proliferation and induces apoptosis in tumor cells overexpressing AKs.","Pharmacologic Substance"]
["C91080","CENP-E Inhibitor GSK-923295","CENP-E Inhibitor GSK-923295|Centromere-Associated Protein E Inhibitor GSK-923295|GSK-923295","A small-molecule inhibitor of the mitotic kinesin centromere-associated protein E (CENP-E), with potential antineoplastic activity. Upon administration, GSK-923295 binds to and inhibits CENP-E, thereby preventing cell division, inducing cell cycle arrest, and ultimately leading to an inhibition of cell proliferation. CENP-E, a kinetochore-associated mitotic kinesin, plays an essential role in chromosome movement during mitosis and regulates cell-cycle transition from metaphase to anaphase.","Pharmacologic Substance"]
["C131177","Cereblon Modulator CC-90009","CC 90009|CC-90009|Cereblon Modulator CC-90009","A modulator of cereblon (CRBN), which is part of the cullin 4-RING E3 ubiquitin ligase complex (CRL4-CRBN E3 ubiquitin ligase; CUL4-CRBN E3 ubiquitin ligase), with potential immunomodulating and pro-apoptotic activities. Upon administration, CC-90009 specifically binds to CRBN, thereby affecting the activity of the ubiquitin E3 ligase complex. This leads to the ubiquitination of certain substrate proteins and induces the proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3), which are transcriptional repressors in T-cells. This reduces the levels of these transcription factors, and modulates the activity of the immune system, which may include the activation of T-lymphocytes. In addition, this downregulates the expression of other proteins, including interferon regulatory factor 4 (IRF4) and c-myc, which plays a key role in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.","Pharmacologic Substance"]
["C115112","Ceritinib","2,4-Pyrimidinediamine, 5-chloro-N4-(2-((1-methylethyl)sulfonyl)phenyl)-N2-(5-methyl-2-(1-methylethoxy)-4-(4-piperidinyl)phenyl)-|Ceritinib|LDK 378|LDK378|Zykadia","An orally available inhibitor of the receptor tyrosine kinase activity of anaplastic lymphoma kinase (ALK) with antineoplastic activity. Upon administration, ceritinib binds to and inhibits wild-type ALK kinase, ALK fusion proteins and ALK point mutation variants. Inhibition of ALK leads to both the disruption of ALK-mediated signaling and the inhibition of cell growth in ALK-overexpressing tumor cells. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a variety of tumor cell types.","Pharmacologic Substance"]
["C28882","Cesalin","Cesalin","An antineoplastic protein isolated from the seeds of the plant Caesalpinia gilliesii with antineoplastic activity.  Cesalin intercalates into and crosslinks DNA and inhibits the incorporation of the nucleotides uridine and thymidine into DNA, thereby inhibiting DNA and protein synthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1723","Cetuximab","CETUXIMAB|Cetuximab|Chimeric Anti-EGFR Monoclonal Antibody|Chimeric MoAb C225|Chimeric Monoclonal Antibody C225|Erbitux|IMC-C225|cetuximab","A recombinant, chimeric monoclonal antibody directed against the epidermal growth factor (EGFR) with antineoplastic activity. Cetuximab binds to the extracellular domain of the EGFR, thereby preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization may result in an inhibition in signal transduction and anti-proliferative effects. This agent may inhibit EGFR-dependent primary tumor growth and metastasis. EGFR is overexpressed on the cell surfaces of various solid tumors.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C121850","Cetuximab-IR700 Conjugate RM-1929","Cet-IR700|Cetuximab-IR700 Conjugate RM-1929|RM-1929","A chemical conjugate composed of the dye IR700 linked to cetuximab, a monoclonal antibody directed against the epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon injection, the cetuximab moiety targets and binds to EGFR-expressing tumor cells, resulting in the internalization of the conjugate. Upon localized application of near-infrared (NIR) light, the IR700 dye becomes activated, disrupts the cell membrane and selectively kills the EGFR-expressing tumor cells. EGFR, a tyrosine kinase receptor, is overexpressed in a variety of cancers.","Pharmacologic Substance"]
["C77064","Cevipabulin","CEVIPABULIN|Cevipabulin|Cevipabulinum","A synthetic, water soluble tubulin-binding agent with potential antineoplastic activity. Cevipabulin appears to bind at the vinca-binding site on tubulin, but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. The disruption in microtubule dynamics may eventually inhibit cell division and reduce cellular growth.","Pharmacologic Substance"]
["C73815","Cevipabulin Fumarate","CEVIPABULIN FUMARATE|Cevipabulin Fumarate|TTI-237|[1,2,4]Triazolo[1,5-a]pyrimidin-7-amine, 5-chloro-6-[2,6-difluoro-4-[3-(methylamino)propoxy]phenyl]-N-[(1S)-2,2,2-trifluoro-1-methylethyl]-, (2E)-2-butenedioate (1:1), dihydrate","The fumarate salt of cevipabulin, a synthetic, water soluble tubulin-binding agent with potential antineoplastic activity. Cevipabulin appears to bind at the vinca-binding site on tubulin, but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. The disruption in microtubule dynamics may eventually inhibit cell division and reduce cellular growth., a small, water soluble, synthetic tubulin-binding agent with potential antineoplastic activity.  Cevipabulin appears to bind at the vinca-binding site on tubulin, but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. The disruption in microtubule dynamics may eventually inhibit cell division and may reduce cellular growth.","Pharmacologic Substance"]
["C96746","Cevipabulin Succinate","5-chloro-6-(2,6-difluoro-4-(3-(methylamino)propoxy)phenyl)-N-((1S)-2,2,2-trifluoro-1-methylethyl)(1,2,4)triazolo(1,5-a)pyrimidin-7-amine succinate dihydrate|CEVIPABULIN SUCCINATE|Cevipabulin Succinate|TTI-237 Succinate Dihydrate","The succinate salt form of cevipabulin, a synthetic, water soluble tubulin-binding agent with potential antineoplastic activity. Cevipabulin binds at the vinca-binding site on tubulin, but seems to act more similar to taxane-site binding agents in that it enhances tubulin polymerization and does not induce tubulin depolymerization. This stabilizes tubulin and prevents microtubule disassembly. The disruption in microtubule dynamics may eventually inhibit cell division and reduce cellular growth.","Pharmacologic Substance"]
["C96227","cFMS Tyrosine Kinase Inhibitor ARRY-382","ARRY-382|cFMS Tyrosine Kinase Inhibitor ARRY-382","A small molecule and orally available inhibitor of colony-stimulating factor-1 receptor (CSF1R; cFMS) with potential antineoplastic activity. cFMS tyrosine kinase inhibitor ARRY-382 binds to and inhibits the activity of cFMS. By preventing colony-stimulating factor-1 (CSF-1)-cFMS signaling, this agent may inhibit tumor cell proliferation in cFMS-overexpressing tumor cells. cFMS, a tyrosine kinase receptor, is overexpressed in certain tumor cell types and plays an essential role in macrophage differentiation and regulation of cell proliferation.","Pharmacologic Substance"]
["C1767","Chaparrin","Chaparrin","A quassinoid phytochemical isolated from Simaba cedron and other plant species with potential antineoplastic activity.  Chaparrin is a mixture of compounds that includes flavonoids, antioxidants, and nordihydroguaiaretic acid (NDGA).  NDGA is an antioxidant and lipoxygenase inhibitor that promotes cell differentiation, induces G1 phase cell-cycle arrest, and causes apoptosis in certain cancer cell lines. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1046","Chaparrinone","Chaparrinone|Picras-3-ene-2,16-dione, 11,20-epoxy-1,11,12-trihydroxy-, (1beta,11beta,12alpha)-","A quassinoid phytochemical isolated from Ailanthus integrifolia sp. calycina and other plant species with potential antineoplastic activity.  Chaparrinone inhibits protein synthesis, has antimalarial properties, and is cytotoxic to some tumor cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C66961","Checkpoint Kinase Inhibitor AZD7762","AZD7762|Checkpoint Kinase Inhibitor AZD7762","A synthetic small molecule inhibitor of checkpoint kinases (Chks) with potential chemosensitizing activity. AZD7762 binds to and inhibits Chks, which may prevent cell cycle arrest and subsequent nucleotide excision repair in DNA-damaged tumor cells, resulting in tumor cell apoptosis. This agent may enhance the cytotoxicity of DNA-damaging agents. Chks are protein kinases that regulate either G1/S or G2/M transitions in the cell cycle. In the presence of DNA damage or incomplete DNA replication, Chks become activated and initiate cell cycle arrest to allow DNA repair or the completion of DNA replication.","Organic Chemical|Pharmacologic Substance"]
["C61102","Checkpoint Kinase Inhibitor XL844","Checkpoint Kinase Inhibitor XL844|Chk Inhibitor XL844|XL844","A synthetic small-molecule inhibitor of checkpoint kinases 1 and 2 (Chk1 and Chk2) with potential antineoplastic activity. XL844 binds to and inhibits Chks 1 and 2, resulting in inhibition of cell cycle arrest, progressive DNA damage, inhibition of DNA repair, and, ultimately, tumor cell apoptosis. This agent also inhibits vascular endothelial growth factor receptor 1 (VEGFR1) and vascular endothelial growth factor receptor 3 (VEGFR3), important mediators of tumor angiogenesis and lymphogenesis, respectively. In the presence of extensive damage or absence of timely repair, these checkpoint-signaling pathways may also trigger a pathway that effects apoptosis. Normal functions of Chks involve the initiation of cell-cycle arrest and the up-regulation of transcription genes involved with DNA excision repair and dNTP synthesis.","Organic Chemical|Pharmacologic Substance"]
["C115970","Chiauranib","CS2164|Chiauranib","An orally available, small molecule inhibitor of select serine-threonine kinases, including aurora kinase B (aurora B), vascular endothelial growth factor receptors (VEGFRs), stem cell factor receptor (c-KIT), and platelet-derived growth factor receptors (PDGFRs), with potential antineoplastic activity. Upon oral administration, chiauranib binds to and inhibits the activity of aurora B, VEGFRs, c-kit and PDGFRs, which may result in a decrease in the proliferation of tumor cells that overexpress these kinases. These kinases are overexpressed by a variety of cancer cell types.","Pharmacologic Substance"]
["C97263","Chidamide","CS055|Chidamide|HBI-8000|N-(2-amino-5-fluorine benzyl)-4-[N-(pyridine-3-acrylyl) ammonia methyl] Benzamide|N-(2-amino-5-fluorophenyl)-4-[[[1-oxo-3-(3-pyridinyl)-2-propen-1-yl]amino]methyl]-benzamide","An orally bioavailable benzamide-type inhibitor of histone deacetylase (HDAC) isoenzymes 1, 2, 3 and 10, with potential antineoplastic activity. Chidamide binds to and inhibits HDACs, leading to an increase of acetylation levels of histone proteins. This agent also inhibits the expression of kinases in the PI3K/Akt and MAPK/Ras signaling pathways and may result in cell cycle arrest and the induction of tumor cell apoptosis. This may inhibit tumor cell proliferation in susceptible tumor cells. HDACs, a class of enzymes that deacetylate chromatin histone proteins, are upregulated in many tumor types and play key roles in gene expression. Compared to some other benzamide-type HDAC inhibitors, chidamide is more stable, more resistant to degradation and has a longer half-life.","Pharmacologic Substance"]
["C122397","Chimeric Humanized Anti-CD47 Antibody","Chimeric Humanized Anti-CD47 Antibody|Humanized High-chimeric Antibody CD47","A humanized, high-chimeric antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, chimeric humanized anti-CD47 antibody selectively binds to CD47 expressed on tumor cells and blocks the interaction of CD47 with signal regulatory protein alpha (SIRPa), a protein expressed on phagocytic cells. This prevents CD47/SIRPa-mediated signaling and abrogates the CD47/SIRPa-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1), expressed on macrophages. This results in macrophage activation and the specific phagocytosis of tumor cells. In addition, blocking CD47 signaling activates both an anti-tumor T-lymphocyte immune response and T cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSC) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPa, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate.","Pharmacologic Substance"]
["C119741","ChiNing Decoction","ChiNing Decoction","A decoction of Liang Ge San, a traditional Chinese herbal medicine, with potential anti-inflammatory and anti-stomatitis activities. Although the complete mechanism of action through which the ChiNing decoction works has yet to be fully elucidated, upon oral administration, the active ingredients may inhibit the inflammatory response, possibly by reducing the levels of pro-inflammatory cytokines, such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNFa), in the saliva. This may protect the oral mucosa against these inflammatory mediators, and may reduce and relieve radiation-induced stomatitis and the associated pain.","Pharmacologic Substance"]
["C129580","Chk1 Inhibitor CCT245737","(R)-5-((4-((Morpholin-2-ylmethyl)amino)-5-(trifluoromethyl)pyridin-2-yl)amino)pyrazine-2-carbonitrile|CCT245737|Checkpoint Kinase 1 Inhibitor CCT245737|Chk1 Inhibitor CCT245737","An orally bioavailable inhibitor of checkpoint kinase 1 (chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, chk1 inhibitor CCT245737 selectively binds to chk1, thereby preventing chk1 activity and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. CCT245737 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, an adenosine triphosphate (ATP)-dependent serine/threonine kinase overexpressed in a variety of cancer cell types, mediates cell cycle checkpoint control and is essential for DNA repair; it plays a key role in resistance to chemotherapeutic agents by repairing DNA damage.","Pharmacologic Substance"]
["C116756","Chk1 Inhibitor GDC-0425","Chk1 Inhibitor GDC-0425|GDC-0425|RG7602","An orally bioavailable inhibitor of checkpoint kinase 1 (chk1), with potential antineoplastic and chemosensitization activities. Upon oral administration, chk1 inhibitor GDC-0425 selectively binds to chk1, thereby preventing activity of chk1 and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA, inhibition of cell cycle arrest, and induction of apoptosis. GDC-0425 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, an ATP-dependent serine/threonine kinase, mediates cell cycle checkpoint control, is essential for DNA repair, and plays a key role in resistance to chemotherapeutic agents.","Pharmacologic Substance"]
["C116845","Chk1 Inhibitor GDC-0575","Checkpoint Kinase 1 Inhibitor GDC-0575|Chk1 Inhibitor GDC-0575|GDC-0575","A small molecule inhibitor of cell cycle checkpoint kinase 1 (Chk1), with potential chemosensitization activity. Chk1 inhibitor GDC-0575 specifically binds to and inhibits Chk1; this may result in tumor cells bypassing Chk1-dependent cell cycle arrest in the S and G2/M phases, which permits the cells to undergo DNA repair prior to entry into mitosis. Therefore, Chk1 inhibition may sensitize tumor cells to the DNA-damaging effects of certain chemotherapeutic agents. Chk1 is an ATP-dependent serine-threonine kinase that phosphorylates cdc25 phosphatases in response to DNA damage. This results in both inhibitory tyrosine phosphorylation of cyclin-dependent kinase (CDK)-cyclin complexes and cell cycle arrest, which facilitates DNA damage repair.","Pharmacologic Substance"]
["C79867","CHK1 Inhibitor MK-8776","(R)-6-Bromo-3-(1-methyl-1H-pyrazol-4-yl)-5-(piperidin-3-yl)pyrazolo[1,5-a]pyrimidin-7-amine|CHK1 Inhibitor MK-8776|MK-8776|MK8776|SCH 900776|SCH-900776","An agent targeting cell cycle checkpoint kinase 1 (Chk1) with potential radiosensitization and chemosensitization activities. Chk1 inhibitor MK-8776 specifically binds to and inhibits Chk1, which may result in tumor cells bypassing Chk1-dependent cell cycle arrest in the S and G2/M phases to undergo DNA repair prior to entry into mitosis; tumor cells may thus be sensitized to the DNA-damaging effects of ionizing radiation and alkylating chemotherapeutic agents. Chk1 is an ATP-dependent serine-threonine kinase that in response to DNA damage phosphorylates cdc25 phosphatases, resulting in inhibitory tyrosine phosphorylation of CDK-cyclin complexes and cell cycle arrest.","Pharmacologic Substance"]
["C68820","CHK1 Inhibitor PF-477736","CHK1 Inhibitor PF-477736|PF-00477736|PF-477736","A proprietary compound targeting cell cycle checkpoint kinase 1 (chk1) with potential chemopotentiation activity. Chk1 inhibitor PF-477736 inhibits chk1, an ATP-dependent serine-threonine kinase that is a key component in the DNA replication-monitoring S/G2 checkpoint system. By overriding the last checkpoint defense against DNA damaging agent-induced lethal damage, chk1 inhibitor PF-477736 may potentiate the antitumor efficacy of various chemotherapeutic agents against tumor cells with intrinsic checkpoint defects.","Pharmacologic Substance"]
["C362","Chlorambucil",".gamma.-(p-bis(2-chloroethyl)aminophenyl)butyric acid|.gamma.-[p-Di(2-chloroethyl)aminophenyl]butyric acid|.gamma.-[p-bis(2-chloroethyl)aminophenyl]butyric acid|4-[Bis(2-chloroethyl)amino]benzenebutanoic acid|4-[bis(2-chloroethyl)amino]benzenebutanoic acid|4-[p-[Bis(2-chloroethyl)amino]phenyl]butyric acid|4-[p-[bis(2-chloroethyl)amino]phenyl]butyric acid|Alti-chlorambucil|Ambochlorin|Amboclorin|Aminochlorambucil|Benzenebutanoic acid, 4-[bis(2-chloroethyl)amino]- (9CI)|Butyric acid, 4-(p-[bis(2-chloroethyl)amino]phenyl)-|Butyric acid, 4-(p-bis(2-chloroethyl)aminophenyl)-|CB 1348|CB-1348|CHL|CHLORAMBUCIL|Chlorambucil|Chlorambucilum|Chloraminophen|Chloraminophene|Chlorbutin|Chlorbutine|Chloroambucil|Chlorobutin|Chlorobutine|Ecloril|Elcoril|Leukeran|Leukersan|Leukoran|Linfolizin|Linfolysin|Lympholysin|N,N-Di-2-chloroethyl-.gamma.-p-aminophenylbutyric acid|N,N-di-2-chloroethyl-gamma-p-aminophenylbutyric acid|Phenylbutyric acid nitrogen mustard|WR-139013|aminochlorambucil|benzenebutanoic acid, 4-[bis(2-chloroethyl)amino]- (9CI)|butyric acid, 4-(p-bis(2-chloroethyl)aminophenyl)|chlorambucil|chlorbutinum|chloroambucil|gamma-(p-bis(2-chloroethyl)aminophenyl)butyric acid|gamma-[p-di(2-chloroethyl)aminophenyl]butyric acid|p-(N, N-Di-2-chloroethyl)aminophenyl butyric acid|p-(N, N-di-2-chloroethyl)aminophenyl butyric acid|p-N, N-Di-(.beta.-chloroethyl)aminophenyl butyric acid|p-N, N-di-(beta-chloroethyl)aminophenyl butyric acid|phenylbutyric acid nitrogen mustard","An orally-active antineoplastic aromatic nitrogen mustard. Chlorambucil alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis.  (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2085","Chlorodihydropyrimidine","5-Chlorodihydropyrimidine|Chlorodihydropyrimidine","A pyrimidine derivative with antitumor activity. Chlorodihydropyrimidine competitively and reversibly inhibits dihydropyrimidine dehydrogenase, a rate-limiting enzyme in the catabolism of fluoropyrimidines thereby blocking the degradation of the fluoropyrimidines.","Organic Chemical|Pharmacologic Substance"]
["C61671","Chloroquine","CHLOROQUINE|Chloroquine","A 4-aminoquinoline with antimalarial, anti-inflammatory, and potential chemosensitization and radiosensitization activities. Although the mechanism is not well understood, chloroquine is shown to inhibit the parasitic enzyme heme polymerase that converts the toxic heme into non-toxic hemazoin, thereby resulting in the accumulation of toxic heme within the parasite. This agent may also interfere with the biosynthesis of nucleic acids. Chloroquine's potential chemosensitizing and radiosensitizing activities in cancer may be related to its inhibition of autophagy, a cellular mechanism involving lysosomal degradation that minimizes the production of reactive oxygen species (ROS) related to tumor reoxygenation and tumor exposure to chemotherapeutic agents and radiation.","Pharmacologic Substance"]
["C982","Chloroquinoxaline Sulfonamide","Benzenesulfonamide, 4-amino-N-(5-chloro-2-quinoxalinyl)-|Benzenesulfonamide, 4-amino-N-[5-chloro-2-quinoxalinyl]-|CQS|Chloroquinoxaline Sulfonamide|Chloroquinoxaline sulfonamide|Chlorsulfaquinoxaline|chloroquinoxaline sulfonamide|chlorosulfaquinoxaline","A chlorinated heterocyclic sulfanilamide with potential antineoplastic activity and potential immunosuppressive activity.  Chloroquinoxaline sulfonamide poisons topoisomerase II alpha and topoisomerase II beta, thereby causing double-stranded breaks in DNA, accumulation of unrepaired DNA, and apoptosis.  This agent also exhibits lymphotoxicity by inhibiting lymphocyte activation in a cell cycle-specific manner. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C94723","Chlorotoxin","CHLOROTOXIN|CTX|Chlorotoxin|TM-601|chlorotoxin","A neurotoxin with potential anticancer property. Chlorotoxin (CTX) is a 36-amino acid peptide found in the venom of the deathstalker scorpion, and a chloride channel blocker. This toxin binds preferentially to glioma cells via the transmembrane endopeptidase matrix metalloproteinase-2 (MMP-2), and thereby prevents the spread of tumor cells. MMP-2 is specifically up-regulated in gliomas and related cancers, but is not normally expressed in brain.","Amino Acid, Peptide, or Protein|Biologically Active Substance"]
["C1049","Chlorozotocin","1-(2-chloroethyl)-1-nitroso-3-(D-glucos-2-yl)urea|2-[3-(2-chloroethyl)-3-nitrosoureido]-2-deoxy-D-glucopyranose|2-[[[(2-chloroethyl)nitrosamino]carbonyl]amino]-2-deoxy-D-glucose|CHLOROZOTOCIN|CHLZ|CZT|Chlorozotocin|Chlorozotocyna|D-Glucopyranose, 2-[[[(2-chloroethyl)nitrosoamino]carbonyl]amino]-2-deoxy-|D-Glucopyranose|D-Glucose, 2-[[[(2-chloroethyl)nitrosoamino]carbonyl]amino]-2-deoxy- (9CI)|D-glucopyranose, 2-[[[(2-chloroethyl)nitrosoamino]carbonyl]amino]-2-deoxy|D-glucose, 2-[[[(2-chloroethyl)nitrosoamino]carbonyl]amino]-2-deoxy- (9CI)|DCNU","A glucose-linked chloroethylnitrosourea with potential antineoplastic activity.  Chlorozotocin alkylates DNA and proteins, induces the formation of interstrand DNA and DNA-protein crosslinks, and causes DNA strand breakage, thereby damaging DNA and resulting in cell death.  This agent has been shown to exhibit antitumor and immunomodulatory effects in cell lines and animal models.  Chlorozotocin is a mutagen and is less myelotoxic than other nitrosoureas. (NCI04)","Antibiotic|Organic Chemical"]
["C94213","Choline Kinase Alpha Inhibitor TCD-717","CHKA Inhibitor TCD-717|Choline Kinase Alpha Inhibitor TCD-717|TCD-717","A small-molecule inhibitor of choline kinase alpha (CHKA), with potential antineoplastic activity. TCD-717 targets and binds to CHKA, an enzyme that plays a key role in the synthesis of phosphatidylcholine, the major phospholipid in eukaryotic cell membranes. Blockade of this enzyme induces cells to activate a different route for phospholipid production which causes a toxic effect and eventually leads to cell destruction. CHKA, overexpressed in human cancer cells while only minimally expressed in normal cells, appears to play a significant role in cellular proliferation, evasion of apoptosis, increased cell motility and metastasis.","Pharmacologic Substance"]
["C62597","CHP-HER-2 Peptide Vaccine","CHP-HER-2 Peptide Vaccine|Cholesterol-Bearing Hydrophobized Pullulan HER2 Protein 146","A peptide vaccine, containing nanoparticles of cholesteryl hydrophobized pullulan (CHP) complexed with the tumor-associated antigen HER-2/neu (ErbB-2), with potential antineoplastic activity. Her-2/neu, a member of the epidermal growth factor receptor (EGFR) family of tyrosine kinases, is overexpressed in various tumors, including breast, ovarian, and gastric cancers. Vaccination with CHP-HER-2 peptide vaccine may stimulate the host immune system to mount a humoral as well as a cytotoxic T-cell response against tumor cells expressing the HER-2/neu antigen. This results in an inhibition of tumor cell proliferation and tumor cell death. The self-aggregating CHP, composed of a pullulan backbone and cholesterol branches, forms stable colloidal nanoparticles in water.","Immunologic Factor|Pharmacologic Substance"]
["C62598","CHP-NY-ESO-1 Peptide Vaccine IMF-001","CHP-NY-ESO-1 Peptide Vaccine IMF-001|Cholesteryl Pullulan-NY-ESO-1 Vaccine IMF-001|IMF-001","A peptide cancer vaccine containing nanoparticles of cholesteryl hydrophobized pullulan (CHP) complexed with the cancer-testis antigen NY-ESO-1 protein, with potential immunostimulating and antineoplastic activities.  Upon administration, CHP-NY-ESO-1 peptide vaccine IMF-001 may stimulate the host immune system to mount a humoral and cytotoxic T-cell response against tumor cells expressing NY-ESO-1 antigen, resulting in tumor cell lysis. The self-aggregating CHP, composed of a pullulan backbone and cholesterol branches, forms stable colloidal nanoparticles in water. NY-ESO-1, an antigen found in normal testis, is upregulated in various cancers, including bladder, breast, hepatocellular, melanoma, and prostate cancers.","Immunologic Factor|Pharmacologic Substance"]
["C895","Chromomycin A3","3B-O-(4-O-Acetyl-2,6-dideoxy-3-C-methyl-alpha-L-arabino-hexopyranosyl)-7-methylolivomycin D|Aburamycin B|Antibiotic 69895 A|Antibiotic B 599|Antibiotic from Streptomyces griseus|CHROMOMYCIN A3|Chromomycin A3|Olivomycin D, 3B-O-(4-O-Acetyl-2, 6-dideoxy-3-C-methyl-alpha-L-arabino-hexopyranosyl)-7-methyl- (9CI)|Olivomycin D, 3B-O-(4-O-acetyl-2, 6-dideoxy-3-C-methyl-.alpha.-L-arabino-hexopyranosyl)-7-methyl- (9CI)|TOYOMYCIN|Toyomycin","A glycosidic antineoplastic antibiotic isolated from the bacterium Streptomyces griseus.  Chromomycin A3 reversibly binds to guanine-cytosine (G-C) base pairs in the minor groove of DNA, thereby inhibiting RNA synthesis.  This agent is used as a fluorescent chromosome dye. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C118451","Cidan Herbal Capsule","Cidan Herbal Capsule|Zedoary rhizome/Pseudobulbus cremastrae seu pleiones/Yatantzu/Strychni pulveratum/Beehive/Artificial Bezoar/Bombyx mori/Danshen Root/Radix astragali/Angelica/Camphol Alcohol Capsule","A capsule-based formulation containing artificial bezoar, Strychni pulveratum (strychnos powder), camphol alcohol (borneol or borneo camphor) and extracts from Zedoary rhizome (Rhizoma curcumae), Pseudobulbus cremastrae seu pleiones (dried pseudobulb of Cremastra appendiculata), Yatantzu (seed of Brucca javanica), beehive, Bombyx mori (Bombyx batryticatus or silkworm), Danshen (dried root of Salvia miltiorrhiza or red sage root), Radix astragali, and Angelica, with potential antineoplastic activity. Upon oral administration of the cidan herbal capsule, the active ingredients in the plant extracts may induce tumor cell apoptosis and reduce tumor cell proliferation.","Pharmacologic Substance"]
["C1834","Cilengitide","CILENGITIDE|Cilengitide|EMD 121974|EMD-121974|cilengitide|cyclo(L-arginylglycyl-L-a-aspartyl-D-phenylalanyl-N-methyl-L-valyl)","A cyclic Arg-Gly-Asp peptide with potential antineoplastic activity.  Cilengitide binds to and inhibits the activities of the alpha(v)beta(3) and alpha(v)beta(5) integrins, thereby inhibiting endothelial cell-cell interactions, endothelial cell-matrix interactions, and angiogenesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C374","Cimetidine","CIMETIDINE|Cimetidine|Guanidine, N''-Cyano-N-Methyl-N'-(2-(((5-Methyl-1H-Imidazol-4-yl)Methyl)Thio)Ethyl)-|N-Cyano-N'-methyl-N''-[2-[[(5-methyl-1H-imidazol-4-yl)methyl]thio]ethyl]guanidine|Tagamet|cimetidine","A histamine H(2)-receptor antagonist.  Enhancing anti-tumor cell-mediated responses, cimetidine blocks histamine's ability to stimulate suppressor T lymphocyte activity and to inhibit natural killer (NK) cell activity and interleukin-2 production.  Cimetidine also may inhibit tumor growth by suppressing histamine's growth-factor activity and blocking histamine-induced stimulation of vascular endothelial growth factor (VEGF), a pro-angiogenic growth factor. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C47450","Cinacalcet Hydrochloride","1-Naphthalenemethanamine, a-methyl-N-(3-(3-(trifluoromethyl)phenyl)propyl)-,(aR)-, Hydrochloride|CINACALCET HYDROCHLORIDE|Cinacalcet Hydrochloride|Mimpara|Sensipar","The orally bioavailable hydrochloride salt of the calcimimetic cinacalcet. Cinacalcet increases the sensitivity of calcium-sensing receptors on chief cells in the parathyroid gland to extracellular calcium, thereby reducing parathyroid hormone (PTH) secretion. A reduction in PTH levels inhibits osteoclast activity, which may result in a decrease in cortical bone turnover and bone fibrosis, and normalization of serum calcium and phosphorus levels. In addition, by reducing PTH levels, cinacalcet may reduce PSA levels; PTH appears to raise PSA levels and may increase prostate cancer cell growth.","Pharmacologic Substance"]
["C95021","Cinobufagin","Cinobufacini|Cinobufagin","A bufadienolide compound extracted from the dried venom secreted by the parotid glands of toads and one of the glycosides in the traditional Chinese medicine ChanSu, with potential antineoplastic activity. Although the mechanism of action of cinobufagin is still under investigation, it has been found to suppress cancer cell proliferation and cause apoptosis in cancer cells via a sequence of apoptotic modulators that include mitochondrial Bax and cytosolic chromosome c, and caspases 3, 8, and 9. Possible upstream mediators of cinobufagin-induced apoptosis include Fas and p53.","Organic Chemical|Pharmacologic Substance"]
["C2599","Cintredekin Besudotox","CINTREDEKIN BESUDOTOX|Cintredekin Besudotox|IL 13-PE38QQR|IL-13 Toxin|Interleukin-13 PE38QQR Immunotoxin|interleukin-13 PE38QQR immunotoxin","A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R).The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis.","Organic Chemical|Pharmacologic Substance"]
["C118284","Cirmtuzumab","Cirmtuzumab|UC-961","A humanized monoclonal antibody against the extracellular domain of the human receptor tyrosine kinase-like orphan receptor 1 (ROR1), with potential antineoplastic activity. Upon administration, cirmtuzumab binds to ROR1 and blocks ROR1-mediated signaling. This prevents tumor cell proliferation in cancer cells overexpressing ROR1. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1 (NTRKR1), is normally expressed during embryogenesis.  It is overexpressed in certain leukemias and solid tumors, but minimally expressed in healthy cells.","Pharmacologic Substance"]
["C376","Cisplatin","(SP-4-2)-Diamminedichloroplatinum|Abiplatin|Blastolem|Briplatin|CDDP|CISPLATIN|Cis-diammine-dichloroplatinum|Cis-diamminedichloridoplatinum|Cis-diamminedichloro Platinum (II)|Cis-diamminedichloroplatinum|Cis-dichloroammine Platinum (II)|Cis-platinous Diamine Dichloride|Cis-platinum II Diamine Dichloride|Cis-platinum II|Cis-platinum|Cismaplat|Cisplatin|Cisplatina|Cisplatinum|Cisplatyl|Citoplatino|Citosin|Cysplatyna|DDP|Lederplatin|Metaplatin|Neoplatin|Peyrone's Chloride|Peyrone's Salt|Placis|Plastistil|Platamine|Platiblastin-S|Platiblastin|Platinex|Platinol- AQ|Platinol-AQ VHA Plus|Platinol-AQ|Platinol|Platinoxan|Platinum Diamminodichloride|Platinum, Diaminedichloro-, cis- (8CI)|Platinum|Platiran|Platistin|Platosin|cisplatin","An alkylating-like inorganic platinum agent (cis-diamminedichloroplatinum) with antineoplastic activity. Cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition.","Inorganic Chemical|Pharmacologic Substance"]
["C2502","Cisplatin Liposomal","Cisplatin Liposomal|Cisplatin, Liposomal|Liposomal Cisplatin|SPI-077|SPI-77|STEALTH Cisplatin|STEALTH Liposomal Cisplatin|STEALTH Liposomal Encapsulated Cisplatin|STEALTH Liposome Cisplatin","A synthetic formulation in which the antineoplastic agent cisplatin is encapsulated in lipids.  Cisplatin liposomal consists of small aggregates of cisplatin covered by a single lipid bilayer. Encasement in liposomes improves cisplatin's tumor bioavailability and toxicity profile. Liposomal encapsulation does not affect the pharmacological properties of cisplatin directly.  Cisplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups such as GC-rich sites in DNA, inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in apoptosis and cell growth inhibition. (NCI04)","Inorganic Chemical|Pharmacologic Substance"]
["C17879","Cisplatin-E Therapeutic Implant","CDDP-e therapeutic implant|CDDP/epi gel|CDDP/epi|CEG|Cisplatin-E Therapeutic Implant|Cisplatin-Epinephrine|Cisplatin/Epinephrine Gel|Intradose MPI-5010|Intradose|MP 5010 TI|MP 5010 Therapeutic Implant|MPI 5010","An injectable gel comprised of a collagen matrix containing the inorganic platinum (Pt) agent cisplatin and the sympathomimetic agent epinephrine with potential antineoplastic activity. After intratumoral injection, cisplatin forms highly reactive, positively charged, platinum complexes, which covalently bind to nucleophilic groups in DNA, preferably at the N7 position of guanine bases. This induces both intra- and inter-strand DNA cross-links. In addition, cisplatin forms DNA-Pt-protein cross-links. Cross-link formation results in both the induction of apoptosis and cell growth inhibition. Epinephrine, a potent vasoconstrictor, is added to the gel to both enhance the penetration of cisplatin into tumor tissue and reduce its dispersion into the surrounding tissues. Intratumoral injection of cisplatin-E therapeutic implant may increase local chemotherapeutic efficacy, as compared to the systemic administration of cisplatin, while reducing its systemic toxicity.","Pharmacologic Substance"]
["C99125","cis-Urocanic Acid","cis-UCA|cis-Urocanic Acid","A derivative of the amino acid histidine, formed in the mammalian skin from trans-urocanic acid upon ultraviolet radiation, and protodynamic agent, with potential anti-inflammatory and antiproliferative activity. Upon intravesical instillation of cis-urocanic acid (cis-UCA), this agent is protonated at the imidazolyl moiety in the mildly acidic extracellular tumor environment and penetrates into the cancer cell. Once inside the cell and due to the slightly alkaline pH inside the tumor cell, cis-UCA is deprotonated, i.e. the imidazolyl proton is released into the cytosol which eventually raises the intracellular acidity. This acidification impairs many cellular processes, such as metabolic activity, and may lead to cell cycle arrest, an induction of cellular apoptosis and necrotic cell death. In addition, cis-UCA enhances ERK and JNK signaling pathways by inhibiting the activity of serine/threonine and tyrosine phosphatases.","Organic Chemical|Pharmacologic Substance"]
["C71694","Citatuzumab Bogatox","Anti-EpCAM Antibody Fragment-Bouganin Fusion Protein|CITATUZUMAB BOGATOX|Citatuzumab Bogatox|VB6-845","A fusion protein immunotoxin consisting of a humanized, single-chain monoclonal antibody Fab fragment specific for the epithelial cell adhesion molecule (EpCAM) conjugated with a modified bouganin cytotoxin with potential antineoplastic activity. Citatuzumab bogatox binds to EpCAM, delivering modified bouganin cytotoxin directly to EpCam-positive tumor cells, which may result in the inhibition of tumor cell protein synthesis and tumor cell death. EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers. Bouganin is a plant-derived ribosome-inactivating protein (RIP), a toxic plant N-glycosidase that depurinates the universally conserved alpha-sarcin loop of ribosomal rRNA, inactivating the ribosome and preventing protein synthesis. Compared to unmodified bouganins, modified bouganins may have a reduced propensity to activate human T cells.","Pharmacologic Substance"]
["C79828","Cixutumumab","Anti-IGF-1R Recombinant Monoclonal Antibody IMC-A12|CIXUTUMUMAB|Cixutumumab|IMC-A12|cixutumumab","A fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor (IGF-1R) with potential antineoplastic activity. Cixutumumab selectively binds to membrane-bound IGF-1R, thereby preventing the binding of the natural ligand IGF-1 and the subsequent activation of PI3K/AKT signaling pathway. Downregulation of the PI3K/AKT survival pathway may result in the induction of cancer cell apoptosis and may decrease cancer cellular proliferation. IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily overexpressed by many cancer cell types, stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF-1R signaling has been implicated in tumorigenesis and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C102849","CK2-targeting Synthetic Peptide CIGB-300","CIGB-300|CK2-targeting Synthetic Peptide CIGB-300|P15-tat","A synthetic peptide targeting the substrates of casein kinase 2 (CK2), with potential antineoplastic activity. Upon administration and nucleolar localization, CK2-targeting synthetic peptide CIGB-300 binds to phosphoacceptor sites on the CK2 substrates, in particular the oncoprotein nucleophosmin (B23 or NPM1). This blocks the activation of B23 and induces apoptosis, thereby inhibiting tumor cell growth in susceptible tumor cells. CK2, a protein kinase often overexpressed in a variety of cancer cell types, appears to be correlated with malignant transformation, tumor growth and survival. Overexpression of B23 has been correlated with increased cellular growth and proliferation as well as inhibition of differentiation and apoptosis.","Pharmacologic Substance"]
["C121647","c-Kit Inhibitor PLX9486","PLX9486|c-Kit Inhibitor PLX9486","An orally bioavailable protein tyrosine kinase inhibitor of mutated forms of the tumor-associated antigen mast/stem cell factor receptor c-Kit (SCFR), with potential antineoplastic activity. Upon oral administration, c-Kit inhibitor PLX9486 binds to and inhibits specific c-Kit mutants. This may result in an inhibition of tumor cell proliferation in cancer cell types that overexpress these c-Kit mutations. c-Kit, a transmembrane protein and receptor tyrosine kinase, is overexpressed in solid tumors and hematological malignancies; it plays a key role in the regulation of cell differentiation and proliferation.","Pharmacologic Substance"]
["C1052","CL 246738","3,6-bis-(2-piperidinoethoxyl)acridine trihydrochloride|CL 246,738|CL 246738","An immunomodulator, 3,6-bis(2-piperidinoethoxy) acridine trihydrochloride, used in a phase I study for possible immunostimulatory effects in colorectal cancer. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C1336","Cladribine","2-CdA|2-Chloro-2-Deoxyadenosine|2-Chlorodeoxyadenosine|2CDA|CLADRIBINE|CdA|Cladribina|Cladribine|Leustat|Leustatin|Leustatine|RWJ-26251|cladribine","A purine nucleoside antimetabolite analogue. Cladribine triphosphate, a phosphorylated metabolite of cladribine, incorporates into DNA, resulting in single-strand breaks in DNA, depletion of nicotinamide adenine dinucleotide (NAD) and adenosine triphosphate (ATP), and apoptosis.  Because this agent is resistant to adenosine deaminase, an enzyme that inactivates some antineoplastic agents, it is selectively toxic to lymphocytes and monocytes which exhibit little deoxynucleotide deaminase activity. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C78082","Clanfenur","CLANFENUR|Clanfenur","A substituted benzoylphenylurea and an analogue of the pesticide diflubenzuron with potential antineoplastic activity. Unlike most of the anti-cancer drugs causing bone marrow suppression, clanfenur stimulates hematopoiesis both in vivo and in vitro.","Pharmacologic Substance"]
["C1054","Clarithromycin","6-O-Methylerythromycin|Abbott-56268|Biaxin|CLARITHROMYCIN|Clarithromycin|clarithromycin","A semisynthetic 14-membered ring macrolide antibiotic.  Clarithromycin binds to the 50S ribosomal subunit and inhibits RNA-dependent protein synthesis in susceptible organisms.  Clarithromycin has been shown to eradicate gastric MALT (mucosa-associated lymphoid tissue) lymphomas, presumably due to the eradication of tumorigenic Helicobacter pylori infection. This agent also acts as a biological response modulator, possibly inhibiting angiogenesis and tumor growth through alterations in growth factor expression. (NCI04)","Antibiotic|Organic Chemical"]
["C85475","Claudiximab","Claudiximab|iMAB362","A chimeric monoclonal antibody directed against the antigen GC182 with potential immunostimulatory and antineoplastic activities. Upon administration, claudiximab specifically binds to GC128, which may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against GC182-expressing tumor cells, resulting in decreased tumor cell proliferation. The CD20-like antigen GC182, a gastric differentiation protein, is often overexpressed on the cell surfaces of a variety of tumor cells, including gastric, pancreatic, esophageal cancer and non-small cell lung cancer (NSCLC) cells.","Pharmacologic Substance"]
["C65337","Clioquinol","5-Chloro-7-iodo-8-hydroxyquinoline|5-Chloro-7-iodo-quinolin-8-ol|AI3-16451|CLIOQUINOL|Clioquinol|Iodochlorohydroxyquinoline|Mycoquin","An orally bioavailable, lipophilic, copper-binding, halogenated 8-hydroxyquinoline with antifungal, antiparasitic and potential antitumor activities. Clioquinol forms a stable chelate with copper (copper (II) ions), which inhibits the chymotrypsin-like activity of the proteasome; consequently, ubiquitinated proteins may accumulate in tumor cells, followed by tumor cell apoptosis and the inhibition of tumor angiogenesis. In addition, the clioquinol-copper complex appears to decrease the expression of androgen receptors (AR) in human copper-enriched prostate cancer cells. Serum levels of copper are often elevated in patients with cancer; copper chelation may inhibit copper-dependent endothelial cell proliferation and tumor secretion of angiogenic factors.","Pharmacologic Substance"]
["C88638","Clivatuzumab","CLIVATUZUMAB|Clivatuzumab","A humanized monoclonal antibody directed against the pancreatic cancer antigen MUC1, with potential antineoplastic activity. Clivatuzumab binds to tumor cells expressing the MUC1 antigen and prevents MUC1-mediated signaling. MUC1, a mucin antigen, is overexpressed in pancreatic cancer but not in normal, healthy pancreatic cells.","Immunologic Factor|Pharmacologic Substance"]
["C26638","Clofarabine","2-Chloro-9-(2-deoxy-2-fluoro-beta-D-arabinofuranosyl)-9H-purin-6-amine|2-Chloro-9-(2-deoxy-2-fluoroarabinofuranosyl)adenine|CLOFARABINE|Clofarabine|Clofarex|Clolar|clofarabine","A second generation purine nucleoside analog with antineoplastic activity. Clofarabine is phosphorylated intracellularly to the cytotoxic active 5'-triphosphate metabolite, which inhibits the enzymatic activities of ribonucleotide reductase and DNA polymerase, resulting in inhibition of DNA repair and synthesis of DNA and RNA. This nucleoside analog also disrupts mitochondrial function and membrane integrity, resulting in the release of pre-apoptotic factors, including cytochrome C and apoptotic-inducing factors, which activate apoptosis.","Pharmacologic Substance"]
["C28888","Clomesone","2-Chloroethyl (methylsulfonyl)methanesulfonate|CLOMESONE|Chlorethyl SOSO|Clomesone|SRI 6155","The 2-chloroethyl ester of (methylsulfonyl) methanesulfonic acid with potential antineoplastic effects.  Acting as a chloroethylating agent, clomesone induces the formation of DNA interstrand crosslinks in some cell lines, and exhibits antitumor activity in some animal models.  Alkylating agents exert cytotoxic and, in some cases, chemotherapeutic effects by transferring alkyl groups to DNA, thereby damaging DNA and interfering with DNA synthesis and cell division. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C61607","Clomiphene","2-[p-(2-Chloro-1,2-diphenylvinyl)phenoxy]triethylamine|CLOMIPHENE|Clomiphene","A triphenylethylene nonsteroidal ovulatory stimulant evaluated for antineoplastic activity against breast cancer.  Clomiphene has both estrogenic and anti-estrogenic activities that compete with estrogen for binding at estrogen receptor sites in target tissues.  This agent causes the release of the pituitary gonadotropins follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to ovulation. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C379","Clomiphene Citrate","2-[p-(2-Chloro-1,2-diphenylvinyl)phenoxy]triethylamine Citrate (1:1)|2-[p-(2-Chloro-1,2-diphenylvinyl)phenoxy]triethylamine Citrate|CLOMIPHENE CITRATE|Clomid|Clomiphene Citrate|Serophene","The citrate salt form of clomiphene, a triphenylethylene nonsteroidal ovulatory stimulant evaluated for antineoplastic activity against breast cancer. Clomiphene has both estrogenic and anti-estrogenic activities that compete with estrogen for binding at estrogen receptor sites in target tissues.  This agent causes the release of the pituitary gonadotropins follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to ovulation. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C97329","Clonidine-containing Mucoadhesive Buccal Tablet","Clonidine Lauriad|Clonidine-containing Mucoadhesive Buccal Tablet","An extended release, proprietary mucoadhesive buccal tablet formulation containing the hydrochloride salt form of clonidine, the imidazoline derivative and adrenergic alpha 2 receptor agonist, with anti-inflammatory activity. Upon contact of the tablet with the buccal mucosa, clonidine binds to the adrenergic receptors on macrophages and lymphocytes and may reduce the release of pro-inflammatory mediators such as tumor necrosis factor alpha (TNFalpha). As a result, this agent may prevent chemoradiation therapy-induced mucositis.","Pharmacologic Substance"]
["C62762","Clostridium Novyi-NT Spores","C. novyi-NT Spores|Clostridium Novyi-NT Spores","Spores of the bacterial strain Clostridium novyi-NT, the attenuated obligate anaerobic C. novyi, with potential immunostimulating, bacteriolytic, and antineoplastic activities. Upon intravenous administration, Clostridium novyi-NT spores germinate exclusively in hypoxic tissue, such as avascular regions of tumors. Germination results in lysis and destruction of surrounding viable tumor cells. Due to their anaerobic nature, C. novyi-NT spores do not proliferate in oxygenated tumor regions. However, this agent may stimulate the immune system to exert a cellular immune response, resulting in additional killing of tumor cells not lysed by the bacteria, including those in the well-oxygenated tumor area.","Bacterium|Pharmacologic Substance"]
["C106230","cMet CAR-mRNA Electroporated Autologous T Lymphocytes","cMet CAR-mRNA Electroporated Autologous T Lymphocytes|cMet RNA CAR T Cells","A preparation of autologous T-lymphocytes that have been electroporated with an mRNA encoding a chimeric antigen receptor (CAR) consisting of an anti-human hepatocyte growth factor receptor (HGFR or cMet) scFv (single chain variable fragment) and the zeta chain of the TCR/CD3 complex (CD3-zeta) coupled to the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activities. Upon intratumoral administration, cMet CAR-mRNA electroporated autologous T lymphocytes direct T-cells to cMet-expressing tumor cells, which induces a selective toxicity in cMet-expressing tumor cells and causes tumor cell lysis. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of cMet. The inclusion of the 4-1BB signaling domain may increase the antitumor activity as compared to the inclusion of the CD3-zeta chain alone. The mRNA CAR is expressed for a limited amount of time, which can prevent serious, unforeseen side effects. cMet, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.","Cell|Pharmacologic Substance"]
["C129314","c-Met Inhibitor AL2846","AL 2846|AL-2846|AL2846|c-Met Inhibitor AL2846","An orally bioavailable small molecule inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration AL2846 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C82677","c-Met Inhibitor AMG 208","AMG 208|c-Met Inhibitor AMG 208","A selective small-molecule inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor AMG 208 inhibits the ligand-dependent and ligand-independent activation of c-Met, inhibiting its tyrosine kinase activity, which may result in cell growth inhibition in tumors that overexpress c-Met. C-Met encodes the hepatocyte growth factor receptor tyrosine kinase, plays an important role in epithelial cell proliferation and has been shown to be overexpressed in a variety of cancers.","Pharmacologic Substance"]
["C95203","c-Met Inhibitor AMG 337","AMG 337|AMG337|c-Met Inhibitor AMG 337","An orally bioavailable inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor AMG 337 selectively binds to c-Met, thereby disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein, the product of the proto-oncogene c-Met, is a receptor tyrosine kinase also known as hepatocyte growth factor receptor (HGFR); this protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C128895","c-Met Inhibitor HS-10241","HS-10241|c-Met Inhibitor HS-10241","An orally bioavailable small molecule inhibitor of the oncoprotein c-Met (hepatocyte growth factor receptor; HGFR), with potential antineoplastic activity. Upon oral administration, HS-10241 targets and binds to the c-Met protein, prevents c-Met phosphorylation and disrupts c-Met-dependent signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C77893","c-Met Inhibitor JNJ-38877605","JNJ-38877605|c-Met Inhibitor JNJ-38877605","An orally bioavailable, small-molecule receptor tyrosine kinase inhibitor with potential antineoplastic activity. c-Met inhibitor JNJ-38877605 selectively inhibits c-Met, a receptor tyrosine kinase (RTK) involved in cancer cell survival and invasiveness, and tumor angiogenesis. c-Met is also known as hepatocyte growth factor receptor (HGFR).","Organic Chemical|Pharmacologic Substance"]
["C90591","c-Met Inhibitor MK2461","MK2461|c-Met Inhibitor MK2461","A selective small-molecule inhibitor of the proto-oncogene c-Met with potential antineoplastic activity. c-Met inhibitor MK2461 preferentially inhibits activated c-Met in an ATP-competitive manner, thereby inhibiting its tyrosine kinase activity, which may inhibit c-Met signaling and result in cell growth inhibition in tumors that overexpress c-Met. c-Met, encoding the hepatocyte growth factor receptor (HGFR) tyrosine kinase, plays an important role in tumor cell proliferation and has been shown to be overexpressed or mutated in a variety of cancers.","Pharmacologic Substance"]
["C116866","c-Met Inhibitor MK8033","1-(3-(1-Methyl-1H-pyrazol-4-yl)-5-oxo-5H-benzo[4,5]cyclohepta[1,2-b]pyridin-7-yl)-N-(pyridin-2-ylmethyl)methanesulfonamide|MK-8033|MK8033|c-Met Inhibitor MK8033","An orally bioavailable inhibitor of c-Met, with potential antineoplastic activity. Upon administration, c-Met inhibitor MK8033 binds to and inhibits the autophosphorylation of the c-Met protein, which disrupts c-Met signal transduction pathways and may induce cell death in tumor cells overexpressing or expressing constitutively activated c-Met protein. In addition, MK8033 inhibits Ron (receptor originated from nantes, MST1R). c-Met protein, which is encoded by the proto-oncogene MET, is a receptor tyrosine kinase also known as hepatocyte growth factor receptor (HGFR); this protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis. Ron, a member of the Met family of cell surface receptor tyrosine kinases, is also overexpressed on certain tumor cell types.","Pharmacologic Substance"]
["C106370","c-Met Inhibitor MSC2156119J","MSC2156119J|c-Met Inhibitor MSC2156119J","An orally bioavailable inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. c-Met inhibitor MSC2156119J selectively binds to c-Met, which inhibits c-Met phosphorylation and disrupts c-Met-mediated signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C129717","c-Met Inhibitor PLB1001","PLB-1001|PLB1001|c-Met Inhibitor PLB1001","An orally bioavailable inhibitor of the proto-oncogene c-Met (hepatocyte growth factor receptor; HGFR) with potential antineoplastic activity. Upon administration, PLB1001 selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing or expressing constitutively activated c-Met protein. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C116740","CMV pp65 Peptide-pulsed Autologous Dendritic Cell Vaccine","CMV pp65 Peptide-pulsed Autologous DC Vaccine|CMV pp65 Peptide-pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with the human cytomegalovirus (CMV) phosphoprotein pp65, with potential immunostimulatory and antineoplastic activities. Upon administration, the CMV pp65 peptide-pulsed autologous DC vaccine exposes the immune system to the CMV pp65 peptide, which may result in a cytotoxic T-lymphocyte (CTL) response against CMV pp65-expressing tumor cells leading to cell lysis. The CMV pp65 protein, also called the 65 kDa lower matrix phosphoprotein, is the primary component of the enveloped subviral particle of CMV and is expressed in certain tumor types, such as glioblastoma.","Pharmacologic Substance"]
["C78467","CMVpp65-A*0201 Peptide Vaccine","CMVpp65-A*0201 Peptide Vaccine","A peptide-based cancer vaccine containing a mutated form of the HLA-A*0201-restricted cytomegaloviral epitope CMVpp65(495-503) with potential immunostimulatory and antitumor activities. Upon subcutaneous administration, CMVpp65-A*0201 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against CMV-positive cells, resulting in cell lysis. HLA-A*0201 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*0201 may improve antigenic peptide immunogenicity. CMVpp65, a tegument protein of the herpes virus CMV, is the main viral antigen found in peripheral blood mononuclear cells (PBMCs) after viral infection and may activate cell-mediated immunity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1541","C-myb Antisense Oligonucleotide G4460","C-myb Antisense Oligonucleotide G4460|G4460|INX-3001|LR-3001|OL(1)p53|c-MYB Antisense Oligodeoxynucleotide|c-MYB Antisense|c-Myb Antisense OND|c-Myb LR-3001","A 24-base phosphorothiolate antisense oligodeoxynucleotide (ODN) for the proto-oncogene c-myb with potential antineoplastic activity. C-myb antisense oligonucleotide G4460 binds to codon sequences 2 to 9 of c-myb mRNA, inhibiting translation of the transcript. Suppression of c-myb expression with this agent may result in the restoration of normal differentiation pathways, increased antiproliferative effects, and the induction of apoptosis in early progenitor hematopoietic cells and in tumor cells that overexpress c-myb. Tumor-cell overexpression of c-myb blocks differentiation, promotes proliferation, and inhibits apoptosis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C99898","CNDO-109-activated Allogeneic Natural Killer Cells","CNDO-109-AANK Cells|CNDO-109-activated Allogeneic Natural Killer Cells","A preparation of non-interleukin-2 primed, tumor activated allogeneic natural killer (NK) cells with potential immunostimulating activity. The allogeneic NK cells obtained from a first or second degree relative of the patient are co-incubated with a lysate from the CTV-1 cell line, a minimally differentiated myeloid line derived from an acute myelogenous leukemia patient. Infusion of CNDO-109-activated allogeneic NK cells may be able to lyse and destroy NK-resistant tumor cells and a broad spectrum of tumor cells.","Cell|Pharmacologic Substance"]
["C48383","CNGRC Peptide-TNF Alpha Conjugate","CNGRC Peptide-TNF Alpha Conjugate|NGR-TNF|NGR-hTNF|tumor vasculature-targeted tumor necrosis factor alpha","A cytokine-peptide conjugate composed of the cytokine tumor necrosis factor alpha (TNF-alpha) chemically linked to the peptide CNGRC. The peptide moiety CNGRC, a ligand for the membrane-bound metalloprotease CD13, binds to endothelial cells of the angiogenic vasculature that express CD13 (also known as aminopeptidase N); subsequently, the TNF-alpha moiety induces apoptosis in endothelial cells expressing CD13, thereby inhibiting tumor-associated angiogenesis. (NCI05)","Pharmacologic Substance"]
["C68923","Cobimetinib","COBIMETINIB|Cobimetinib|Cotellic|GDC-0973|MEK Inhibitor GDC-0973|XL518","An orally bioavailable small-molecule inhibitor of mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Preclinical studies have demonstrated that this agent is effective in inhibiting the growth of tumor cells bearing a B-RAF mutation, which has been found to be associated with many tumor types. A threonine-tyrosine kinase and a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors, MEK1 is required for the transmission of growth-promoting signals from numerous receptor tyrosine kinases.","Pharmacologic Substance"]
["C916","Coenzyme Q10","2-(3,7,11,15,19,23,27,31,35,39-Decamethyl-2,6,10,14,18,22,26,30,34,38-tetracontadecanyl)-5,6-dimethoxy-3-methyl-2,5-cyclohexadiene-1,4-dione|Co-Q10|CoQ10|Coenzyme Q10|Q10|UBIDECARENONE|Ubidecarenone|Ubiquinone 10|coenzyme Q10|ubiquinone|vitamin Q10","A naturally occurring benzoquinone important in electron transport in mitochondrial membranes. Coenzyme Q10 functions as an endogenous antioxidant; deficiencies of this enzyme have been observed in patients with many different types of cancer and limited studies have suggested that coenzyme Q10 may induce tumor regression in patients with breast cancer. This agent may have immunostimulatory effects. (NCI04)","Biologically Active Substance|Organic Chemical|Pharmacologic Substance"]
["C82344","Cold Contaminant-free Iobenguane I-131","Azedra|Cold Contaminant-free I 131-MIBG|Cold Contaminant-free Iobenguane I 131|Cold Contaminant-free Iobenguane I-131|Ultratrace Iodine I 131 Metaiodobenzylguanidine|Ultratrace MIBG","An I 131 radioiodinated synthetic analogue of the neurotransmitter norepinephrine, manufactured with a proprietary process, with radioisotopic and potential antineoplastic activities. Cold contaminant-free iobenguane I 131 (MIBG) localizes to adrenergic tissue and may be used to image or eradicate tumor cells that accumulate and metabolize norepinephrine. This agent is manufactured using a technology that avoids the production of unwanted \"cold contaminants\" (i.e., carrier molecules), which may cause undesirable side effects and compete with MIBG for binding on target receptor sites.","Indicator, Reagent, or Diagnostic Aid|Pharmacologic Substance"]
["C62538","Colloidal Gold-Bound Tumor Necrosis Factor","Aurimmune|CYT-6091|Colloidal Gold-Bound Recombinant Human Tumor Necrosis Factor|Colloidal Gold-Bound Tumor Necrosis Factor|TNF-bound colloidal gold|colloidal gold-bound TNF|colloidal gold-bound rhTNF|colloidal gold-bound tumor necrosis factor","A nanoparticle delivery system for recombinant human tumor necrosis factor (TNF) consisting of recombinant TNF bound to pegylated colloidal gold nanoparticles with potential antineoplastic activity. Upon intravenous administration, colloidal gold-bound recombinant human TNF travels through the bloodstream, avoiding immune detection and uptake by the reticuloendothelial system because of nanoparticle pegylation. Due to their size, the colloidal gold nanoparticles exit the circulatory system only at hyperpermeable tumor neovasculature sites; TNF then binds to and activates tumor cell TNF receptors, which may result in an increase in tumor cell apoptosis and a reduction in tumor cell proliferation. Compared to the administration of unbound TNF, colloidal gold-bound TNF may improve the efficacy and safety of TNF administration by delivering TNF specifically to tumor tissue.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C79806","Colorectal Tumor-Associated Peptides Vaccine IMA910","Colorectal Tumor-Associated Peptides Vaccine IMA910|IMA910","A synthetic tumor-associated peptide (TUMAP)-based cancer vaccine directed against colorectal cancer with potential immunostimulatory and antineoplastic activities. Synthetic colorectal tumor-associated peptides vaccine IMA910 contains 13 different synthetic TUMAPs, each of which represents a tumor associated antigen (TAA) specific for colorectal cancer. Upon administration, this agent may elicit a cytotoxic T-lymphocyte (CTL) response against colorectal tumors expressing these TAAs, which may result in a reduction in colorectal tumor cell proliferation.","Pharmacologic Substance"]
["C80014","Combretastatin","3-Hydroxy-4-methoxy-alpha-(3,4,5-trimethoxyphenyl)benzeneethanol|COMBRETASTATIN|Combretastatin, (+-)|Combretastatin","A stilbenoid phenol, originally isolated from the bark of the African bush willow tree Combretum caffrum, with vascular disrupting and antineoplastic activities. Combretastatin targets and binds to the colchicine-binding site of tubulin, thereby impairs the polymerization of tubulin dimers and prevents the formation of microtubules in the endothelial cells of tumor. As a result, this may eventually lead to a destruction of the tumor vasculature, disruption of tumor blood flow and tumor cell necrosis.","Organic Chemical|Pharmacologic Substance"]
["C84867","Combretastatin A1 Diphosphate","1,2-Benzenediol, 3-methoxy-6-((1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl)-, 1,2-bis(dihydrogen Phosphate)|CA1P|Combretastatin A-1 bis(phosphate)|Combretastatin A1 Diphosphate|OXI 4503|OXI-4503|OXi4503","The diphosphate prodrug of the stilbenoid combretastatin A1, originally isolated from the plant Combretum caffrum, with vascular-disrupting and antineoplastic activities. Upon administration, combretastatin A1 diphosphate (CA1P) is dephosphorylated to the active metabolite combretastatin A1 (CA1), which promotes rapid microtubule depolymerization; endothelial cell mitotic arrest and apoptosis, destruction of the tumor vasculature, disruption of tumor blood flow and tumor cell necrosis may ensue. In addition, orthoquinone intermediates, metabolized from combretastatin A1 by oxidative enzymes found to be elevated in some tumor types, may bind to tumor cell thiol-specific antioxidant proteins and DNA, and stimulate oxidative stress by enhancing superoxide/hydrogen peroxide production. CA1 binds to tubulin at the same site as colchicine but with higher affinity.","Pharmacologic Substance"]
["C120314","Compound Kushen Injection","CKI|Compound Kushen Injection|Yanshu Injection","A traditional Chinese medicine (TCM) formulation composed of compound Kushen injection (CKI) containing aqueous extracts from the roots of Kushen (Radix Sophorae Flavescentis) and Baituling (Rhizoma smilacis Glabrae), with potential antineoplastic and immunomodulating activities. CKI contains numerous chemicals including alkaloids, such as matrine and oxymatrine, flavonoids, alkylxanthones, quinones, triterpene glycosides, fatty acids, and essential oils. Although the exact mechanism(s) of action through which CKI exerts its effects has yet to be fully elucidated, CKI is able to interfere with the activation of various signal transduction pathways, such as the Wnt/beta-catenin signaling pathway, inhibit nuclear factor-kappa B (NF-KB) activation, and block the activity of multiple receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR). CKI induces apoptosis in and inhibits proliferation, migration, invasion and adhesion of tumor cells. CKI also modulates the production of inflammatory mediators.","Pharmacologic Substance"]
["C71015","Conatumumab","AMG 655|Anti-TRAIL Receptor 2 Monoclonal Antibody AMG 655|CONATUMUMAB|Conatumumab|Immunoglobulin G1, Anti-(Human Tumor Necrosis Factor Receptor Superfamily Member 10b (Death Receptor 5, Trail-R2, CD262 Antigen))|Monoclonal XG1-048 (Arg(Sup 219),Glu(Sup 361),Met(Sup 363))Gamma-1 Heavy Chain (225-215')-Disulphide With Kappa Light Chain (231-231'':234-234'')-Bisdisulphide Dimer","A fully human monoclonal agonist antibody directed against the extracellular domain of human TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) receptor 2 (TR-2) with potential antineoplastic activity. Conatumumab mimics the activity of native TRAIL, binding to and activating TR-2, thereby activating caspase cascades and inducing tumor cell apoptosis. TR-2 is expressed by a variety of solid tumors and cancers of hematopoietic origin.","Amino Acid, Peptide, or Protein"]
["C99762","Conditionally Replicative Adenovirus 5/3-delta24","Ad5/3-delta24|CRAd 3/5-delta|CRAd 5/3-delta24|Conditionally Replicative Adenovirus 3/5-delta|Conditionally Replicative Adenovirus 5/3-delta24","A replication competent, oncolytic adenovirus serotype 5 (Ad5) with its knob domain of fiber protein substituted by that of the serotype 3 (Ad5/3-delta24), with potential oncolytic activity. Upon administration, oncolytic adenovirus Ad5/3-delta24 binds to specific Ad3 receptors that are highly expressed on certain tumor cells. This results in the replication of oncolytic adenovirus Ad5/3-delta24 in tumor cells and induces tumor cell lysis which may potentially result in the activation of a systemic immune response against tumor-associated antigens. The Ad5/3-delta24 has a 24 base pair deletion in constant region 2 of the E1A gene which allows for selective replication in cells that are defective in the retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (CDKN2A or p16INK4a). As most tumor cells are defective in the Rb/p16 pathway, this virus selectively replicates in these cells. The replacement of the Ad5 fiber knob, which mediates viral-cell receptor binding, allows for a Coxsackie-adenovirus receptor (CAR)-independent infection of tumor cells; CAR expression is often deficient on cancer cells.","Pharmacologic Substance|Virus"]
["C96796","Copanlisib","BAY 80-6946|Copanlisib|PI3K Inhibitor BAY 80-6946","A phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. Copanlisib inhibits the activation of the PI3K signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C79824","Copper Cu 64-ATSM","(64)Cu-ATSM|Copper Cu 64-ATSM|Copper-64-diacetyl-bis(N4-methylthiosemicarbazone)|copper Cu 64-ATSM","A radioconjugate consisting of a lipophilic copper(II)bis(thiosemicarbazone) labeled with the positron- and beta-emitting isotope (64)Cu with hypoxia-selective and antineoplastic activities. With a high membrane permeability and redox potential, copper Cu 64-ATSM is preferentially taken up by hypoxic cells compared to normoxic cells; the extent of retention in tissue is inversely related to the state of tissue oxygenation allowing the quantitation of tissue hypoxia by positron emission tomography (PET). In addition, the radioactive copper moiety of this agent may deliver a selective cytotoxic dose of beta radiation to hypoxic tumor cells.","Pharmacologic Substance"]
["C80050","Copper Gluconate","COPPER GLUCONATE|Copper Gluconate|Cupric Gluconate","The orally bioavailable copper salt of D-gluconic acid. In addition to its roles as an enzyme cofactor for cytochrome C oxidase and superoxide dismutase, copper forms complexes with the thiocarbamate disulfiram (DSF) forming DSF-copper complexes, which enhances the DSF-mediated inhibition of the 26S proteasome; proteasome inhibition may result in inhibition of cellular protein degradation, cessation of cell cycle progression, inhibition of cellular proliferation, and the induction of apoptosis in susceptible tumor cell populations.","Pharmacologic Substance"]
["C1057","Cordycepin","3'-Deoxyadenosine|3'-dA-CE Phosphoramidite|3-dAdenosine|9-Cordyceposidoadenine|COR|CORDYCEPIN|Cordycepin|Cordycepine|Kordicepin|cordycepin","A purine nucleoside antimetabolite and antibiotic isolated from the fungus Cordyceps militaris with potential antineoplastic activity. Cordycepin is an adenosine analogue, which is readily phosphorylated to its mono-, di-, and triphosphate intracellularly. Triphosphate cordycepin can be incorporated into RNA, and inhibits transcription elongation and RNA synthesis due to the absence of a hydroxyl moiety at the 3' position.  Because it can be converted to an inactive metabolite by adenosine deaminase, this agent must be administered with an adenosine deaminase inhibitor in order to be effective. Cordycepin has displayed cytotoxicity against some leukemic cell lines in vitro.","Nucleic Acid, Nucleoside, or Nucleotide"]
["C967","Cordycepin Triphosphate","3'-Deoxyadenosine-5'-(tetrahydrogen triphosphate)|CORDYCEPIN TRIPHOSPHATE|Cordycepin Triphosphate|Cordycepin-5'-triphosphate","The triphosphate salt of Cordycepin, a purine nucleoside antimetabolite analogue and antibiotic isolated from the fungus Cordyceps militaris with potential antineoplastic activity. Cordycepin incorporates into RNA, and, inhibits RNA chain elongation and synthesis due to the absence of a hydroxyl moiety at the 3' position.  Because it is converted to an inactive metabolite by adenosine deaminase, this agent must be administered with an adenosine deaminase inhibitor in order to be effective.  Cordycepin has displayed cytotoxicity against some leukemic cell lines in vitro. (NCI04)","Antibiotic|Nucleic Acid, Nucleoside, or Nucleotide"]
["C78184","Coriolus Versicolor Extract","Coriolus Versicolor Extract|Coriolus versicolor extract|Yunzhi Extract","An extract derived from the mushroom Coriolus versicolor, containing polysaccharide K (PSK) and polysaccharide-peptide (PSP), with potential immunomodulating and antineoplastic activities. Coriolus versicolor extract has been shown to stimulate the production of lymphocytes and cytokines, such as interferons and interleukins, and may exhibit antioxidant activities. However, the precise mechanism of action(s) of this agent is unknown.","Pharmacologic Substance"]
["C76112","Corticorelin Acetate","CORTICORELIN ACETATE|Corticorelin Acetate|Human Corticotropin-Releasing Factor|Xerecept|hCRF|human corticotropin-releasing factor","The acetate salt form of coticorelin, a synthetic peptide of neurohormone corticotropin-releasing factor (CRF), with potential antitumor and antiangiogenesis activities. Upon administration, corticorelin stimulates adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary gland. In turn, ACTH stimulates cortisol production from the adrenal cortex and is regulated by a negative feedback mechanism. Corticorelin appears to inhibit swelling around brain tumors through reduction in vascular leakage and maintenance of endothelial cell integrity. This agent potentially suppresses vascularization and tumor cell growth through reduction of vascular endothelial growth factor (VEGF) that appears to be via activation of corticotrophin-releasing factor receptor 2 (CRFR2), a G protein-coupled receptor.","Pharmacologic Substance"]
["C1877","Cositecan","(4S)-4-Ethyl-4-hydroxy-11-(2-(trimethylsilyl)ethyl)-1,12-dihydro-14H-pyrano(3',4':6,7)indolizino(1,2-b)quinoline-3,14(4H)-dione|BNP1350|COSITECAN|Cositecan|DB 172|Karenitecin|karenitecin","A synthetic silicon-containing agent related to camptothecin with antineoplastic properties.  Cositecan stabilizes the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks and consequently triggering apoptosis.  Because it is lipophilic, cositecan exhibits enhanced tissue penetration and bio-availability compared to water-soluble camptothecins.","Organic Chemical|Pharmacologic Substance"]
["C61493","Coxsackievirus A21","CVA21|Coxsackievirus A21","A naturally occurring enterovirus with potential antitumor activity. Upon intratumoral administration, coxsackievirus A21 targets and binds to intracellular adhesion molecule 1 (ICAM-1) and decay acceleration factor (DAF), both cell surface molecules that are both overexpressed on certain malignant cells. After entering the cells, coxsackievirus A21 replicates in these cancer cells, thereby causing cancer cell lysis. This results in a reduction of tumor cell growth.","Pharmacologic Substance|Virus"]
["C26648","CP-724,714","CP-724,714","An orally bioavailable quinazoline with potential antineoplastic activity.  CP-724,714 selectively binds to the intracellular domain of HER2, reversibly inhibiting its tyrosine kinase activity and resulting in suppression of tumor cell growth.  HER2, a member of the epidermal growth factor receptor (EGFR) family, is overexpressed in many adenocarcinomas, particularly breast cancers. (NCI04)","Pharmacologic Substance"]
["C88342","CpG Oligodeoxynucleotide GNKG168","CpG ODN GNKG168|CpG Oligodeoxynucleotide GNKG168|GNKG168","A synthetic, 21-mer, unmethylated CpG motif-based oligodeoxynucleotide (ODN), with immunostimulatory activity. CpG oligodeoxynucleotide GNKG168 binds to and activates Toll-like receptor 9 (TLR9) and is taken up into cells by endocytosis; once internalized, it may activate numerous signaling transduction pathways resulting in the release of multiple cytokines, such as immunoglobulins (Igs), interferons (IFNs), interleukins (ILs) and tumor necrosis factor (TNF). Through activation of TLR9, this ODN can directly stimulate B-lymphocytes, dendritic and natural killer (NK) cells, resulting in an increase in innate immunity and antibody-dependent cellular cytotoxicity (ADCC). In addition, through the release of IL-12 and IFN, this agent may induce a preferential shift to the T-helper 1(Th1) phenotype resulting in enhanced CD8+ T cell-mediated antitumor cytotoxicity.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C28945","Creatine Monohydrate","CREATINE MONOHYDRATE|Creatine Monohydrate|Creatine Supplement|N-(Aminoiminomethyl)-N-methylglycine Monohydrate","The monohydrate form of creatine similar or identical to endogenous creatine produced in the liver, kidneys, and pancreas. Creatine, in phosphate form, helps supply energy to muscle cells for contraction. After intense effort, when ATP deposits are depleted, creatine phosphate donates phosphate groups toward the fast synthesis of ATP. Dietary supplementation with creatine may improve muscle wasting associated with cancer and other chronic diseases.","Pharmacologic Substance"]
["C64639","Crenolanib","4-Piperidinamine, 1-[2-[5-[(3-methyl-3-oxetanyl)methoxy]-1Hbenzimidazol-1-yl]-8-quinolinyl]-|ARO-002|CP-868,596|CP-868596|CRENOLANIB|Crenolanib|PDGFR Inhibitor CP-868596|[1-[2-[5-(3-Methyloxetan-3-ylmethoxy)benzimidazol-1-yl]quinolin-8-yl]piperidin-4-yl]amine","An orally bioavailable benzimidazole targeting the platelet-derived growth factor receptor (PDGFR) subtypes alpha and beta and FMS-related tyrosine kinase 3 (Flt3), with potential antineoplastic activity. Upon oral administration, crenolanib binds to and inhibits both wild-type and mutated forms of PDGFR and Flt3, which may result in the inhibition of PDGFR- and Flt3-related signal transduction pathways. This results in inhibition of tumor angiogenesis and tumor cell proliferation in PDGFR and/or Flt3 overexpressing tumor cells. PDGFR and Flt3, class III receptor tyrosine kinases, are upregulated or mutated in many tumor cell types.","Organic Chemical|Pharmacologic Substance"]
["C106204","Crenolanib Besylate","4-Piperidinamine, 1-[2-[5-[(3-methyl-3-oxetanyl)methoxy]-1Hbenzimidazol-1-yl]-8-quinolinyl]-, Benzenesulfonate (1:1)|ARO-002-26|CP-868,596-26|CP-86859626|Crenolanib Besylate|[1-[2-[5-(3-Methyloxetan-3-ylmethoxy)benzimidazol-1-yl]quinolin-8-yl]piperidin-4-yl]amine Monobenzenesulfonate","The besylate salt form of crenolanib, an orally bioavailable benzimidazole targeting the platelet-derived growth factor receptor (PDGFR) subtypes alpha and beta and FMS-related tyrosine kinase 3 (Flt3), with potential antineoplastic activity. Upon oral administration, crenolanib binds to and inhibits both wild-type and mutated forms of PDGFR and Flt3, which may result in the inhibition of PDGFR- and Flt3-related signal transduction pathways. This results in inhibition of tumor angiogenesis and tumor cell proliferation in PDGFR and/or Flt3 overexpressing tumor cells. PDGFR and Flt3, class III receptor tyrosine kinases, are upregulated or mutated in many tumor cell types.","Organic Chemical|Pharmacologic Substance"]
["C74061","Crizotinib","(R)-3-(1-(2,6-Dichloro-3-Fluorophenyl)Ethoxy)-5-(1-(Piperidin-4-Yl)-1h-Pyrazol-4-Yl)Pyridin-2-Amine|2-Pyridinamine, 3-((1R)-1-(2,6-Dichloro-3-Fluorophenyl)Ethoxy)-5-(1-(4-Piperidinyl)-1H-Pyrazol-4-yl)-|CRIZOTINIB|Crizotinib|MET Tyrosine Kinase Inhibitor PF-02341066|MET tyrosine kinase inhibitor PF-02341066|PF-02341066|PF-2341066|Xalkori","An orally available aminopyridine-based inhibitor of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) and the c-Met/hepatocyte growth factor receptor (HGFR) with antineoplastic activity. Crizotinib, in an ATP-competitive manner, binds to and inhibits ALK kinase and ALK fusion proteins. In addition, crizotinib inhibits c-Met kinase, and disrupts the c-Met signaling pathway. Altogether, this agent inhibits tumor cell growth. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development. ALK dysregulation and gene rearrangements are associated with a series of tumors.","Pharmacologic Substance"]
["C129048","CRL4(CRBN) E3 Ubiquitin Ligase Modulator CC-220","(S)-3-(4-((4-(Morpholinomethyl)benzyl)oxy)-1-oxoisoindolin-2-yl)piperidine-2,6-dione|CC 220|CC-220|CRL4(CRBN) E3 Ubiquitin Ligase Modulator CC-220","A modulator of the E3 ubiquitin ligase complex containing cereblon (CRL4-CRBN E3 ubiquitin ligase), with immunomodulating and pro-apoptotic activities. Upon administration CC-220 specifically binds to the cereblon (CRBN) part of the ligase complex, thereby affecting the ubiquitin E3 ligase activity, and targeting certain substrate proteins for ubiquitination. This induces the proteasome-mediated degradation of certain transcription factors, including Ikaros (IKZF1) and Aiolos (IKZF3) which are transcriptional repressors in T-cells. This leads to a reduction of their protein levels, and the modulation of the immune system, including activation of T-lymphocytes. In addition, this leads to a downregulation of other proteins, including interferon regulatory factor 4 (IRF4), which plays a key role in the proliferation of certain cancer cell types. CRBN, the substrate recognition component of the E3 ubiquitin ligase complex, plays a key role in the ubiquitination of certain proteins.","Pharmacologic Substance"]
["C66938","Crolibulin","CROLIBULIN|Crolibulin|EPC2407|Microtubule Inhibitor EPC2407","A small molecule tubulin polymerization inhibitor with potential antineoplastic activity. Microtubulin inhibitor EPC2407 binds to the colchicine-binding site on beta-tubulin and inhibits the polymerization of tubulin into microtubules, which may result in cell cycle arrest, the induction of apoptosis, and the inhibition of tumor cell proliferation. As a vascular disruption agent (VDA), this agent also disrupts tumor neovascularization, which may result in a reduction in tumor blood flow and tumor hypoxia and ischemic necrosis.","Organic Chemical|Pharmacologic Substance"]
["C1546","Cryptophycin","10-((3-Chloro-4-methoxyphenyl)methyl)-6-methyl-3-(2-methylpropyl)-16-(1-(3-phenyloxiranyl)ethyl)-1,4-dioxa-8,11-diazacyclohexadec-13-ene-2,5,9,12-tetrone|Cryptophycin 1|Cryptophycin","The cryptophycins are a family of 16-membered macrolide antimitotic agents isolated from the cyanobacteria Nostoc sp. The mechanism of anticancer activity of the cryptophycins has been associated with their destabilization of microtubules and induction of bcl-2 phosphorylation leading to apoptosis. Cryptophycins demonstrated activity against the wide spectrum of solid tumors including those that overexpress the multidrug resistance efflux pump P-glycoprotein. (NCI)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C1826","Cryptophycin 52","C-52|Cryptophycin 52|Cyclo[2,2-dimethyl-.beta.-alanyl-(2S)-2-hydroxy-4-methylpentanoyl-(2E,5S,6S)-5-hydroxy-6-[(2R,3R)-3-phenyloxiranyl]-2-heptenoyl-3-chloro-O-methyl-D-tyrosyl]|Cyclo[2,2-dimethyl-beta-alanyl-(2S)-2-hydroxy-4-methylpentanoyl-(2E,5S,6S)-5-hydroxy-6-[(2R,3R)-3-phenyloxiranyl]-2-heptenoyl-3-chloro-O-methyl-D-tyrosyl]|LY 355703","A member of the cryptophycin family of antitumor agents that binds to microtubules, inducing growth arrest and apoptosis in solid tumors. (NCI)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C95769","Crystalline Genistein Formulation AXP107-11","AXP107-11|Crystalline Genistein Formulation AXP107-11","An orally available crystalline formulation of genistein, a soy-derived isoflavone and phytoestrogen with potential antineoplastic, chemosensitizing, and antioxidant activities. Similar to genistein, crystalline genistein formulation AXP107-11 increases expression of phosphatase and tensin homolog (PTEN), which deactivates protein kinase Akt and mitogen-activated protein kinases (MAPK1 and 3; ERK2 and 1), thereby disrupting PI3K/Akt signal transduction and inducing apoptosis. This agent also induces antioxidant enzymes through AMP-activated protein kinase (AMPK) activation, inhibits NF-kB activation and decreases inflammation response, thereby sensitizing tumors to chemotherapy. Compared to genistein itself, this crystalline formulation shows improved solubility and bioavailability.","Organic Chemical"]
["C129653","CSF-1R Inhibitor BLZ945","4-((2-(((1R,2R)-2-hydroxycyclohexyl)amino)benzo[d]thiazol-6-yl)oxy)-N-methylpicolinamide|4-[2((1R,2R)-2-Hydroxycyclohexylamino)-benzothiazol-6-yloxyl]-pyridine- 2-carboxylic Acid Methylamide|BLZ 945|BLZ-945|BLZ945|CSF-1R Inhibitor BLZ945","An orally bioavailable inhibitor of colony stimulating factor 1 receptor (CSF-1R; CSF1R), with potential antineoplastic activity. CSF1R inhibitor BLZ945 selectively binds to CSF1R expressed on tumor-associated macrophages (TAMs), blocks the activity of CSF1R, and inhibits CSF1R-mediated signal transduction pathways. This inhibits the activity and proliferation of TAMs, and reprograms the immunosuppressive nature of existing TAMs. Altogether, this reduces TAM-mediated immune suppression in the tumor microenvironment, re-activates the immune system, and improves anti-tumor cell responses mediated by T-cells.  CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor for its ligand, colony stimulating factor 1 (CSF1); this receptor is overexpressed by TAMs in the tumor microenvironment, and plays a major role in both immune suppression and the induction of tumor cell proliferation.","Pharmacologic Substance"]
["C129688","CSF1R Inhibitor PLX73086","AC-708|AC708|CSF1R Inhibitor PLX73086|PLX7 3086|PLX73086","An inhibitor of colony stimulating factor 1 receptor (CSF1R; CSF-1R), with potential antineoplastic activity. Upon administration, CSF1R inhibitor PLX73086 targets and binds to CSF1R, thereby blocking CSF1R activation and CSF1R-mediated signaling. This inhibits the activity of tumor-associated macrophages (TAMs) in the tumor tissue and prevents TAM-related tumor cell growth. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor for its ligand colony stimulating factor 1 (CSF1) and plays major roles in tumor cell proliferation and metastasis.","Pharmacologic Substance"]
["C1729","CT2584 HMS","1-(11-(dodecylamino)-10-hydroxyundecyl)-3,7-dihydro-3,7-dimethyl-1H-purine-2,6-dione|1-(11-Dodecylamino-10-Hydroxyundecyl)-3,7-Dimethylxanthine|Apra|CT-2584 HMS|CT-2584|CT2584 HMS","A lipid metabolism modulator which may inhibit angiogenesis, thereby possibly having antitumor activity. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C401","Curcumin","(E,E)-1,7-Bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione|C.I. 75300|C.I. Natural Yellow 3|CURCUMIN|Curcumin|Diferuloylmethane|Turmeric Yellow|curcumin","A phytopolylphenol pigment isolated from the plant Curcuma longa, commonly known as turmeric, with a variety of pharmacologic properties.  Curcumin blocks the formation of reactive-oxygen species, possesses anti-inflammatory properties as a result of inhibition of cyclooxygenases (COX) and other enzymes involved in inflammation; and disrupts cell signal transduction by various mechanisms including inhibition of protein kinase C.  These effects may play a role in the agent's observed antineoplastic properties, which include inhibition of tumor cell proliferation and suppression of chemically induced carcinogenesis and tumor growth in animal models of cancer. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1055","Custirsen Sodium","(3'-5')d(P-thio)([2'-O-(2-methoxyethyl)]m5rC-[2'-O-(2-methoxyethyl)]rA-[2'-O-(2- methoxyethyl)]rG-[2'-O-(2-methoxyethyl)]m5rC-A-G-C-A-G-A-G-T-C-T-T-C-A-[2'-O-(2- methoxyethyl)]m5rU-[2'-O-(2-methoxyethyl)]m5rC-[2'-O-(2-methoxyethyl)]rA-[2'-O-(2- methoxyethyl)]m5rU), Eicosasodium Salt|Antisense TRPM-2|Antisense Testosterone-Repressed Prostate Message 2|CUSTIRSEN SODIUM|Clusterin Antisense Oligonucleotide|Custirsen Sodium|ISIS 112989|OGX-011|TRPM-2 Antisense|custirsen sodium","The eicosasodium salt of a mixed-backbone antisense oligodeoxynucleotide with chemosensitizing properties. Custirsen inhibits testosterone-repressed prostate message-2 (TRPM-2). Administration of custirsen abrogates the anti-apoptotic effect of TRPM-2, thereby sensitizing cells to chemotherapy and resulting in tumor cell death. TRPM-2 is an anti-apoptotic clusterin that is overexpressed by prostate cancer cells and is associated with chemoresistance.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C88264","C-VISA BikDD:Liposome","C-VISA BikDD Plasmid: DOTAP:Cholesterol Liposome-Based Nanoparticle|C-VISA BikDD:Liposome","A formulation composed of DOTAP:cholesterol liposome nanoparticles complexed with the plasmid C-VISA BiKDD, with potential antineoplastic activity. C-VISA BikDD: liposome consists of a pancreatic-cancer-specific expression vector VISA (VP16-GAL4-WPRE integrated systemic amplifier) and a pancreatic-cancer-specific promoter CCKAR (cholecystokinin type A receptor) (CCKAR-VISA or C-VISA) which drives expression of the gene BikDD, a mutant form of the potent proapoptotic gene Bik (Bcl-2 interacting killer). Upon administration and transduction into pancreatic tumor cells, expression of BikDD by C-VISA BikDD:liposome may induce pancreatic tumor cell apoptosis and suppress pancreatic tumor cell proliferation. BikDD binds with greater affinity to anti-apoptotic proteins bcl-2, bcl-xl, bcl-w and Mcl-1 and is more potent than wild-type Bik. DOTAP:cholesterol liposome is composed of cationic lipid dioleoyl-trimethylammonium propane (DOTAP) and cholesterol at molar ratio of 1:1.","Pharmacologic Substance"]
["C123383","CXC Chemokine Receptor 2 Antagonist AZD5069","AZD5069|CXC Chemokine Receptor 2 Antagonist AZD5069|CXCR2 Antagonist AZD5069","An orally bioavailable, selective and reversible antagonist of CXC chemokine receptor 2 (CXCR2), with potential anti-inflammatory and antineoplastic activities. Upon administration, CXC chemokine receptor 2 antagonist AZD5069 directly binds to CXCR2 and inhibits its activation. This inhibits CXCR2-mediated signaling and may inhibit tumor cell proliferation in CXCR2-overexpressing tumor cells. In addition, AZD5069 reduces both neutrophil recruitment and migration from the systemic circulation into sites of inflammation, including the lung mucosa; it may also prevent neutrophil migration from the bone marrow. This results in the reduction of inflammation, mucus production, and neutrophil proteinase-mediated tissue destruction in the lung. CXCR2, a G protein-coupled receptor protein also known as IL-8 receptor B (IL-8RB), is upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation and progression; it is known to be elevated in several inflammatory diseases, such as chronic obstructive pulmonary disease (COPD), asthma and fibrotic pulmonary disorders.","Pharmacologic Substance"]
["C88309","CXCR4 Antagonist BL-8040","BKT140|BL-8040|CXCR4 Antagonist BL-8040","An orally bioavailable inhibitor of CXC Chemokine Receptor 4 (CXCR4) with potential antineoplastic activity. CXCR4 antagonist BL-8040 selectively binds to the chemokine receptor CXCR4, preventing the binding of stromal derived factor 1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation, which may result in decreased tumor cell proliferation and migration. In addition, inhibition of CXCR4 may induce mobilization of hematopoietic cells from the bone marrow into blood. The G protein-coupled receptor CXCR4 plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; SDF-1/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.","Pharmacologic Substance"]
["C74022","CXCR4 Inhibitor MSX-122","CXCR4 Inhibitor MSX-122|MSX-122","An orally bioavailable inhibitor of CXCR4 with potential antineoplastic and antiviral activities. CXCR4 inhibitor MSX-122 binds to the chemokine receptor CXCR4, preventing the binding of stromal derived factor-1 (SDF-1) to the CXCR4 receptor and receptor activation, which may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the GPCR (G protein-coupled receptor) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; it is also a co-receptor for HIV entry into T cells.","Pharmacologic Substance"]
["C91094","CXCR4 Inhibitor POL6326","CXCR4 Inhibitor POL6326|POL6326","An orally bioavailable inhibitor of CXC chemokine receptor 4 (CXCR4) with receptor binding and hematopoietic stem cell-mobilization activities. CXCR4 inhibitor POL6326 binds to the chemokine receptor CXCR4, thereby preventing the binding of stromal derived factor-1 (SDF-1 or CXCL12) to the CXCR4 receptor and subsequent receptor activation. This may induce the mobilization of hematopoietic stem and progenitor cells from the bone marrow into blood. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types; CXCL12/CXCR4 interaction induces retention of hematopoietic cells in the bone marrow.","Pharmacologic Substance"]
["C126660","CXCR4 Inhibitor X4P-001","(S)-N1-((1H-benzo[d]imidazol-2-yl)methyl)-N1-(5,6,7,8-tetrahydroquinolin-8-yl)butane-1,4-diamine|AMD-070|AMD-11070|AMD11070|CXCR4 Inhibitor X4P-001|X4P-001","An orally bioavailable inhibitor of C-X-C chemokine receptor type 4 (CXCR4), with potential antineoplastic and immune checkpoint inhibitory activities. Upon administration, the CXCR4 inhibitor X4P-001 selectively binds to CXCR4 and prevents the binding of CXCR4 to its ligand, stromal cell-derived factor 1 (SDF-1 or CXCL12). This inhibits receptor activation and results in decreased proliferation and migration of CXCR4-overexpressing tumor cells. In addition, inhibition of CXCR4 prevents the recruitment of regulatory T-cells and myeloid-derived suppressor cells (MDSCs) to the tumor microenvironment, thereby abrogating CXCR4-mediated immunosuppression and enabling the activation of a cytotoxic T-lymphocyte-mediated immune response against cancer cells. The G protein-coupled receptor CXCR4, which is upregulated in several tumor cell types, induces the recruitment of immunosuppressive cells in the tumor microenvironment, suppresses immune surveillance, and promotes tumor angiogenesis and tumor cell proliferation. It is also a co-receptor for HIV entry into T-cells.","Pharmacologic Substance"]
["C106253","CXCR4 Peptide Antagonist LY2510924","CXCR4 Peptide Antagonist LY2510924|LY2510924","An inhibitor of CXC chemokine receptor 4 (CXCR4), with potential antineoplastic activity. Upon subcutaneous administration, CXCR4 inhibitor LY2510924 binds to the chemokine receptor CXCR4, thereby preventing CXCR4 binding to its ligand, stromal derived factor-1 (SDF-1), and subsequent receptor activation. This may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types.","Pharmacologic Substance"]
["C97665","Cyclin B1 Peptide-pulsed Autologous Dendritic Cell Vaccine","CCNB1 Peptide-pulsed Autologous Dendritic Cell Vaccine|Cyclin B1 Peptide-pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine comprised of autologous dendritic cells (DCs) pulsed with cyclin B1 peptide, with potential immunostimulatory and antineoplastic activities. Upon administration, cyclin B1 peptide-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and anti-cyclin B1 antibody responses against cyclin B1-expressing cancer cells, resulting in tumor cell lysis. Cyclin B1, a key regulator of the cell cycle and cell division, is overexpressed in a variety of cancer cells.","Pharmacologic Substance"]
["C62600","Cyclodextrin-Based Polymer-Camptothecin CRLX101","CRLX101|Camptothecin-Polymer Conjugate IT-101|Cyclodextrin-Based Polymer-Camptothecin CRLX101|IT-101","A formulation of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, conjugated with to a hydrophilic, cyclodextrin-based linear polymer with potential antineoplastic activity. Upon intravenous administration, camptothecin is slowly released from the formulation at the tumor site and taken up by tumor cells. During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. Compared to camptothecin alone, the cyclodextrin-based polymer formulation has a prolonged half life and greatly improves the biodistribution of camptothecin resulting in an accumulation of camptothecin at the tumor site, which enhances tumor exposure while greatly reducing toxic side effects. In addition, cyclodextrin-based polymer-camptothecin may be able to overcome certain kinds of multidrug resistance.","Organic Chemical|Pharmacologic Substance"]
["C28899","Cyclodisone","Cyclodisone","A cyclic sulfonate ester with potential antineoplastic activity.  As an alkylating agent, clyclodisone induces the formation of DNA interstrand crosslinks, DNA strand breaks, and alkali-labile lesions in the DNA of some tumor cell lines.  Alkylating agents exert cytotoxic and chemotherapeutic effects by transferring alkyl groups to DNA, thereby damaging DNA and interfering with DNA synthesis and cell division. (NCI04)","Pharmacologic Substance"]
["C404","Cycloleucine","1-Aminocyclopentane|1-Aminocyclopentanecarboxylic acid|1-aminocyclopentanecarboxylic acid|ACP|ACPC|CB 1639|CB-1639|CYCLOLEUCINE|Cycloleucine","A non-metabolizable synthetic amino acid, formed through the cyclization of the amino acid leucine, with immunosuppressive, antineoplastic, and cytostatic activities. Cycloleucine competitively inhibits the enzyme methionine adenosyltransferase, resulting in the inhibition of S-adenosylmethionine (SAM) synthesis from methionine and ATP, and subsequent nucleic acid methylation and polyamine production; RNA, and perhaps to a lesser extent, DNA biosyntheses and cell cycle progression are finally disrupted. This agent is also a competitive inhibitor at the glycine modulatory site of the N-methyl-D-aspartate (NMDA) receptor.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1359","Cyclopentenyl Cytosine","2(1H)-Pyrimidinone, 4-amino-1-[4, 5-dihydroxy- 3-(hydroxymethyl)-2-cyclopenten-1-yl]-|CPE-C|Cyclopentenyl Cytosine|Cyclopentenylcytosine Triphosphate|Cyclopentenylcytosine","A pro-drug carbocyclic analogue of cytidine with antineoplastic and antiviral activities. Cyclopentenyl cytosine (CPEC) is converted to the active metabolite cyclopentenyl cytosine 5'-triphosphate (CPEC-TP); CPEC-TP competitively inhibits cytidine triphosphate (CTP) synthase, thereby depleting intracellular cytidine pools and inhibiting DNA and RNA synthesis. This agent may also induce differentiation of some tumor cell types. The antiviral activity of this agent is broad-spectrum.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C405","Cyclophosphamide","(-)-Cyclophosphamide|1-bis(2-chloroethyl)-amino-1-oxo-2-aza-5-oxaphosphoridin monohydrate|2-[bis(2-chloroethyl)amino]tetrahydro-2H-1,3,2-oxazaphosphorine 2-oxide monohydrate|2-[bis(b-chloroethyl)amino]-1-oxa-3-aza-2-phosphacyclohexane-2-oxide monohydrate|2-[di(chloroethyl)amino]-1-oxa-3-aza-2-phosphacyclohexane 2-oxide monohydrate|2H-1,3,2-Oxazaphosphorine, 2-[bis(2-chloroethyl)amino]tetrahydro-, 2-oxide, monohydrate|Bis(2-chloroethyl)phosphoramide cyclic propanolamide ester monohydrate|CP monohydrate|CTX|CYCLO-cell|CYCLOPHOSPHAMIDE|Carloxan|Ciclofosfamida|Ciclofosfamide|Cicloxal|Clafen|Claphene|Cycloblastin|Cycloblastine|Cyclophospham|Cyclophosphamid monohydrate|Cyclophosphamide|Cyclophosphamidum|Cyclophosphan|Cyclophosphane|Cyclophosphanum|Cyclostin|Cyclostine|Cytophosphan|Cytophosphane|Cytoxan|Fosfaseron|Genoxal|Genuxal|Ledoxina|Mitoxan|N,N-bis(2-chloroethyl)-N',O-propylenephosphoric acid ester diamide monohydrate|N,N-bis(2-chloroethyl)-N'-(3-hydroxypropyl)phosphorodiamidic acid intramolecular ester monohydrate|N,N-bis(2-chloroethyl)tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide monohydrate|N,N-bis(b-chloroethyl)-N',O-trimethylenephosphoric acid ester diamide monohydrate|N,N-bis(beta-chloroethyl)-N',O-propylenephosphoric acid ester diamide monohydrate|N,N-bis(beta-chloroethyl)-N',O-trimethylenephosphoric acid ester diamide monohydrate|Neosar|Revimmune|Syklofosfamid|WR- 138719|bis(2-chloroethyl)phosphamide cyclic propanolamide ester monohydrate|cyclophosphamide","A synthetic alkylating agent chemically related to the nitrogen mustards with antineoplastic and immunosuppressive activities. In the liver, cyclophosphamide is converted to the active metabolites aldophosphamide and phosphoramide mustard, which bind to DNA, thereby inhibiting DNA replication and initiating cell death.","Organic Chemical|Pharmacologic Substance"]
["C61694","Cyclophosphamide Anhydrous","2H-1,3,2-oxazaphosphorin-2-amine, N,N-is(2-chloroethyl)tetrahydro-,2-oxide|CYCLOPHOSPHAMIDE ANHYDROUS|Cyclophosphamide Anhydrous|N,N-Bis(2-chloroethyl)tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-Oxide","The anhydrous form of cyclophosphamide, a synthetic nitrogen mustard alkylating agent, with antineoplastic and immunosuppressive activities. In the liver, cyclophosphamide is converted to active metabolites including phosphoramide mustard, which binds to and crosslinks DNA and RNA, thereby inhibiting DNA replication and protein synthesis. This agent, at low doses, is also a potent immunosuppressant primarily by depleting T-regulatory cells.","Pharmacologic Substance"]
["C95716","CYL-02 Plasmid DNA","CYL-02 Plasmid DNA|CYL-02","A gene transfer preparation of a plasmid DNA encoding mouse somatostatin receptor subtype 2 (sst2) and a fusion protein of human deoxycytidine kinase (DCK) and uridine monophosphate kinase (UMK), complexed to a synthetic polycationic carrier, polyethylenimine, with antineoplastic adjuvant application. Upon administration, CYL-02 plasmid DNA expresses DCK::UMK fusion protein that converts gemcitabine into its toxic phosphorylated metabolite. Expression of sst2 protein by this agent could induce both antioncogenic and local antitumor bystander effects. A loss of sst2 gene expression often is found in pancreatic and colorectal cancers, and is the receptor for somatostatin which negatively regulates a number of processes such as epithelial cell proliferation. Combination effects of these gene products allows for less chemotherapy to cause tumor cell lysis in not only the original tumor, but in distant tumors as well.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C102855","CYP17 Inhibitor CFG920","CFG920|CYP17 Inhibitor CFG920","An orally available inhibitor of the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17), with potential antiandrogen and antineoplastic activities. Upon oral administration, CYP17 inhibitor CFG920 inhibits the enzymatic activity of CYP17A1 in both the testes and adrenal glands, thereby inhibiting androgen production. This may decrease androgen-dependent growth signaling and may inhibit cell proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1, localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities, and plays a key role in the steroidogenic pathway that produces steroidal hormones.","Pharmacologic Substance"]
["C113652","CYP17 Inhibitor VT-464","CYP17 Inhibitor VT-464|VT-464","An orally available non-steroidal, lyase-selective inhibitor of the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17), with potential anti-androgenic and antineoplastic activities. Upon oral administration, CYP17 inhibitor VT-464 selectively inhibits the enzymatic activity of the cytochrome P450 C17,20 lyase in both the testes and adrenal glands, thereby inhibiting androgen production. This may decrease androgen-dependent growth signaling and may inhibit cell proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1, localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities; it plays a key role in the steroidogenic pathway. The lyase-selective activity of VT-464 prevents the increased synthesis of mineralocorticoids that is normally seen with non-selective CYP17 inhibitors, which also inhibit the 17-alpha-hydroxylase activity of CYP17A1.","Pharmacologic Substance"]
["C120310","CYP17 Lyase Inhibitor ASN001","ASN001|CYP17 Lyase Inhibitor ASN001","An orally available non-steroidal, lyase-selective inhibitor of the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17), with potential anti-androgenic and antineoplastic activities. Upon oral administration, CYP17 lyase inhibitor ASN001 selectively binds to and inhibits the lyase activity of CYP17A1 in both the testes and adrenal glands, resulting in a significant reduction in androgen production to castrate-range levels. This may both decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1, which is localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities; it plays a key role in the steroidogenic pathway. The selective inhibition of CYP17A1 lyase activity by ASN001 prevents the increased synthesis of mineralocorticoids that is normally seen with non-selective CYP17 inhibitors, which also inhibit the 17-alpha-hydroxylase activity of CYP17A1.","Pharmacologic Substance"]
["C120304","CYP17/Androgen Receptor Inhibitor ODM 204","CYP17/Androgen Receptor Inhibitor ODM 204|ODM 204|ODM-204","An orally available inhibitor of both the steroid 17-alpha-hydroxylase/C17,20 lyase (CYP17A1 or CYP17) and androgen receptor (AR), with potential anti-androgen and antineoplastic activities. Upon oral administration, CYP17/AR inhibitor ODM 204 selectively inhibits the enzymatic activity of CYP17A1 in both the testes and adrenal glands, thereby inhibiting androgen production. This may both decrease androgen-dependent growth signaling and inhibit the proliferation of androgen-dependent tumor cells. In addition, ODM 204 binds to ARs in target tissues and inhibits androgen-induced receptor activation and AR nuclear translocation, which prevents the binding to and transcription of AR-responsive genes. This leads to an inhibition of growth in AR-expressing prostate cancer cells. The cytochrome P450 enzyme CYP17A1, which is localized to the endoplasmic reticulum, exhibits both 17alpha-hydroxylase and 17,20-lyase activities.","Pharmacologic Substance"]
["C407","Cyproterone","CYPROTERONE|Cyproterone|Med Cyproterone|SH-881","A synthetic steroidal anti-androgen with antineoplastic activity. Cyproterone, in its acetate form, binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation and inhibiting the growth of testosterone-sensitive tumor cells.  This agent also exerts progesterogenic activity, resulting in a reduction in testicular androgen secretion and total androgen blockade. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1059","Cyproterone Acetate","3'H-Cyclopropa(1,2)pregna-1,4,6-triene-3,20-dione, 17-(Acetyloxy)-6-chloro-1,2-dihydro-, (1beta,2beta)-|6-Chloro-1b,2b-dihydro-17a-hydroxy-3'H-cyclopropa[1,2]pregna-1,4,6-triene-3,20-dione Acetate|Andro-Diane|Androcur|CYPROTERONE ACETATE|Chloro-6-hydroxy-17 Alpha Methylene-1 Alpha, 2 Alpha Pregnadiene-4,6 Dione-3, 20 Acetate|CyPat|Cyprone|Cyprostat|Cyproteronazetat|Cyproterone Acetate|Cyproteroni Acetas|Diane|Dianette|SH 714|SH-714|cyproterone acetate","The acetate salt of a synthetic steroidal antiandrogen with weak progestational and antineoplastic activities. Cyproterone binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation in target tissues and inhibiting the growth of testosterone-sensitive tumor cells. This agent also exerts progestational agonist properties at the level of the pituitary that reduce luteinizing hormone (LH), resulting in reductions in testicular androgen secretion and serum testosterone levels. Treatment with cyproterone alone results in incomplete suppression of serum testosterone levels.","Organic Chemical|Pharmacologic Substance"]
["C408","Cytarabine",".beta.-Cytosine arabinoside|1-.beta.-D-Arabinofuranosyl-4-amino-2(1H)pyrimidinone|1-.beta.-D-Arabinofuranosylcytosine|1-Beta-D-arabinofuranosyl-4-amino-2(1H)pyrimidinone|1-Beta-D-arabinofuranosylcytosine|1.beta.-D-Arabinofuranosylcytosine|2(1H)-Pyrimidinone, 4-Amino-1-beta-D-arabinofuranosyl-|2(1H)-Pyrimidinone, 4-amino-1.beta.-D-arabinofuranosyl-|4-Amino-1-beta-D-arabinofuranosyl-2(1H)-pyrimidinone|ARA-cell|Alexan|Ara-C|Arabine|Arabinofuranosylcytosine|Arabinosylcytosine|Aracytidine|Aracytin|Aracytine|Beta-Cytosine Arabinoside|Beta-cytosine Arabinoside|CHX-3311|CYTARABINE|Cytarabine|Cytarabinum|Cytarbel|Cytosar-U|Cytosar|Cytosine Arabinoside|Cytosine-.beta.-arabinoside|Cytosine-beta-arabinoside|Erpalfa|Starasid|Tarabine PFS|U 19920|U-19920|Udicil|WR-28453|cytarabine","An antimetabolite analogue of cytidine with a modified sugar moiety (arabinose instead of ribose). Cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA.  Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle.  This agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C128888","Cytarabine Monophosphate Prodrug MB07133","(2R,4S)-4-amino-1-[5-O-[2-oxo-4-(4-pyridyl)-1,3,2-dioxaphosphorinan-2-yl]-beta-d-arabinofuranosyl]-2(1H)-pyrimidinone|Cytarabine Monophosphate Prodrug MB07133|Cytarabine Prodrug MB07133|MB07133","A prodrug of the monophosphate (MP) form of the antimetabolite cytarabine (araCMP), an analogue of cytidine with a modified sugar moiety (arabinose instead of ribose), with potential antineoplastic activity. Upon administration of the cytarabine MP prodrug MB07133, the targeting moiety of this agent specifically delivers the cytarabine moiety to the liver. In turn, araCMP is selectively converted to araC triphosphate (araCTP) by a liver kinase, where it binds to and competes with cytidine for incorporation into DNA, thereby inhibiting DNA polymerase, and DNA synthesis. This leads to the inhibition of tumor cell proliferation and destruction of liver cancer cells. The liver is not able to convert araC into araCMP; araCMP is not converted into araCTP in tissues other than the liver. This enhances efficacy and minimizes systemic toxicity.","Pharmacologic Substance"]
["C113444","Cytidine Analog RX-3117","4-Amino-1-((1S,4R,5S)-2-fluoro-4,5-dihydroxy-3-(hydroxymethyl)cyclopent-2-en-1-yl)pyrimidin-2(1H)-one|Cytidine Analog RX-3117|Fluorocyclopentenylcytosine|RX-3117|TV-1360","An orally available small molecule and nucleoside antimetabolite with potential antineoplastic activity. Upon administration, the cytidine analog RX-3117 is taken up by cells through a carrier-mediated transporter, phosphorylated by uridine cytidine kinase (UCK) and then further phosphorylated to its diphosphate (RX-DP) and triphosphate forms (RX-TP). The triphosphate form is incorporated into RNA and inhibits RNA synthesis. The diphosphate RX-DP is reduced by ribonucleotide reductase (RR) to dRX-DP; its triphosphate form (dRX-TP) is incorporated into DNA. In addition, RX-3117 also inhibits DNA methyltransferase 1 (DNMT1). This eventually leads to cell cycle arrest and the induction of apoptosis. UCK is the rate-limiting enzyme in the pyrimidine-nucleotide salvage pathway.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C28950","Cytochlor","CYTOCHLOR|Cytochlor|cytochlor","A radio-sensitizing pyrimidine nucleoside with potential antineoplastic activity.  Cytochlor is metabolized first to a phosphate derivative, CldCMP, by the enzyme deoxycytidine kinase and then to the active uracyl derivative, CldUMP, by the enzyme dCMP deaminase; deoxycytidine kinase and dCMP deaminase have been found in abnormally high concentrations in most cancers. CldUMP, the active metabolite, incorporates into DNA and, upon exposure to radiation, induces the formation of uracil radicals and double-strand DNA breaks. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C71757","Cytokine-Induced Killer Cells","CIK|Cytokine-Induced Killer Cells","A preparation of autologous lymphocytes with potential immunopotentiating and antineoplastic activities. Cytokine-induced killer (CIK) cells are CD3- and CD56-positive, non-major histocompatibility complex (MHC)-restricted, natural killer (NK)-like T lymphocytes, generated ex-vivo by incubation of peripheral blood lymphocytes (PBLs) with anti-CD3 monoclonal antibody, interleukin (IL)-2, IL-1, and interferon gamma (IFN-gamma) and then expanded. When reintroduced back to patients after autologous stem cell transplantation, CIK cells may recognize and kill tumor cells associated with minimal residual disease (MRD). CIK cells may have enhanced cytotoxic activity compared to lymphokine-activated killer (LAK) cells.","Cell|Pharmacologic Substance"]
["C2748","D1/3-Mage-3-His Fusion Protein","D1/3 MAGE3 HIS|D1/3-MAGE-3 Fusion Protein|D1/3-Mage-3-His Fusion Protein (SB MAGE-3)|D1/3-Mage-3-His Fusion Protein","A recombinant, chimeric protein derived from a melanoma antigenic epitope (MAGE-3) and recognized by specific cytotoxic T lymphocytes.  MAGE-3, a human peptide epitope present in the cytosol of melanoma cells, may be expressed as the fusion protein D1/3-Mage-3; this fusion protein may boost antitumoral immune responses when used in a vaccine formulation. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2383","DAB389 Epidermal Growth Factor","DAB389 EGF|DAB389 Epidermal Growth Factor","A recombinant fusion protein composed of the diphtheria toxin with the receptor-binding domain replaced by human epidermal growth factor (EGF).  When administered, EGF binds to the endothelial cell growth factor receptor, EGFR, which is upregulated in many solid tumors.  After binding to the EGF receptor, the agent is internalized by the cell, where the diphtheria toxin moiety exerts its cytotoxic effect, inhibiting protein synthesis through ADP-ribosylation of elongation factor 2. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82386","Dabrafenib","BRAF Inhibitor GSK2118436|Benzenesulfonamide, N-(3-(5-(2-amino-4-pyrimidinyl)-2-(1,1-dimethylethyl)-4-thiazolyl)-2-fluorophenyl)-2,6-difluoro-|DABRAFENIB|Dabrafenib|GSK-2118436A|GSK2118436","An orally bioavailable inhibitor of B-raf (BRAF) protein with potential antineoplastic activity. Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. B-raf belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway, which may be constitutively activated due to BRAF gene mutations.","Pharmacologic Substance"]
["C128059","Dabrafenib Mesylate","DABRAFENIB MESYLATE|Dabrafenib Mesylate|Dabrafenib Methanesulfonate|GSK2118436 Methane Sulfonate Salt|GSK2118436B|Tafinlar","The mesylate salt form of dabrafenib, an orally bioavailable inhibitor of B-raf (BRAF) protein with potential antineoplastic activity. Dabrafenib selectively binds to and inhibits the activity of B-raf, which may inhibit the proliferation of tumor cells which contain a mutated BRAF gene. B-raf belongs to the raf/mil family of serine/threonine protein kinases and plays a role in regulating the MAP kinase/ERKs signaling pathway, which may be constitutively activated due to BRAF gene mutations.","Pharmacologic Substance"]
["C411","Dacarbazine","1H-imidazole-4-carboxamide, 5-(3,3-dimethyl-1-triazenyl)-|4-(Dimethyltriazeno)imidazole-5-carboxamide|5(or 4)-(dimethyltriazeno)imidazole-4(or 5)-carboxamide|5-(3-3-dimethyl-1-triazenyl)-1H-imidazole-4-carboxamide|5-(Dimethyltriazeno)imidazole-4-carboxamide|5-(dimethyltriazeno)imidazole-4-carboxamide|Asercit|Biocarbazine|DACARBAZINE|DIC|DTIC-Dome|DTIC|Dacarbazina Almirall|Dacarbazina|Dacarbazine - DTIC|Dacarbazine|Dacatic|Dakarbazin|Deticene|Detimedac|Dimethyl (triazeno) imidazolecarboxamide|Dimethyl Triazeno Imidazol Carboxamide|Dimethyl Triazeno Imidazole Carboxamide|Dimethyl-triazeno-imidazole-carboximide|Fauldetic|Imidazole Carboxamide Dimethyltriazeno|Imidazole Carboxamide|Imidazole carboxamide|WR-139007|dacarbazine|dimethyl-triazeno-imidazole carboxamide","A triazene derivative with antineoplastic activity. Dacarbazine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C62179","Dacetuzumab","Anti-huCD40 mAb|DACETUZUMAB|Dacetuzumab|Monoclonal Antibody SGN-40|SGN-40|huS2C6","A humanized monoclonal antibody directed against the CD40 receptor with potential antineoplastic activity. Dacetuzumab specifically binds to and inhibits the CD40 receptor, thereby inducing apoptosis and inhibiting cellular proliferation via antibody-dependent cellular cytotoxicity (ADCC) in cells that overexpress this receptor. The CD40 receptor, a member of the tumor necrosis factor (TNF) receptor super-family, is highly expressed on most B lineage hematologic malignancies including multiple myeloma, non-Hodgkin's lymphoma, chronic lymphocytic leukemia, Hodgkin's disease and acute lymphoblastic leukemia.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C64784","DACH Polymer Platinate AP5346","AP5346|DACH Polymer Platinate AP5346","A low molecular weight polymer-conjugated platinum complex with potential antineoplastic activity. This polymer drug delivery system consists of cytotoxic diaminocyclohexane (DACH)-platinum (Pt) coupled to a water-soluble biocompatible hydroxypropylmethacrylamide (HPMA) copolymer via a pH sensitive linker. Due to decreased pH at the tumor site, the linker is cleaved and the chelated active moiety DACH-Pt is released in tumor cells. DACH-Pt alkylates macromolecules and causes both inter- and intra-strand platinum-DNA crosslinks, which impede DNA replication and transcription, thereby resulting in cell-cycle independent cytotoxicity. The HPMA-based drug delivery system enhances the concentration of DACH-Pt at the tumor site and prolongs the half life of the agent, thereby increasing exposure and efficacy at the target tumor sites while minimizing side effects in normal tissues.","Organic Chemical|Pharmacologic Substance"]
["C113175","DACH-Platin Micelle NC-4016","DACH-Platin Micelle NC-4016|DACH-Pt/m NC-4016|Dach-Platin Micelle NC-4016|Diaminocyclohexane Platinum Micelle NC-4016|NC-4016","Polymeric micellar nanoparticles containing diaminocyclohexane platinum (DACH-platin or DACH-Pt) with potential antineoplastic activity. DACH-platin micelle NC-4016 is prepared through the formation of a polymer-metal complex between DACH-platin and the polyethylene glycol-poly (glutamic acid) block copolymer, PEG-P(Glu). DACH-platin, an active metabolite of the platinum-based antineoplastic agent oxaliplatin, is highly hydrophobic and toxic when administered systemically. The use of polymeric micelles incorporating DACH-platin may both increase cell permeability and enhance the retention of the agent. This allows an extended half-life in the blood circulation and a selective and high accumulation of DACH-platin at tumor sites. This results in increased anticancer efficacy while reducing side effects due to DACH-platin toxicity. Upon intravenous administration and internalization by tumor cells, DACH-platin binds to and causes both inter- and intra-strand cross-links in DNA, forming platinum adducts and triggering tumor cell apoptosis.","Pharmacologic Substance"]
["C53398","Dacomitinib","(2E)-N-(4-((3-Chloro-4-Fluorophenyl)Amino)-7-Methoxyquinazolin-6-yl)-4-Piperidin-1-ylbut-2-Enamide|DACOMITINIB|Dacomitinib|EGFR Inhibitor PF-00299804|PF-00299804-03|PF-00299804|PF-299804","A highly selective, orally bioavailable small-molecule inhibitor of the HER family of tyrosine kinases with potential antineoplastic activity. Dacomitinib specifically and irreversibly binds to and inhibits human Her-1, Her-2, and Her-4, resulting in the proliferation inhibition and apoptosis of tumor cells that overexpress these receptors.","Pharmacologic Substance"]
["C28955","Dacplatinum","(4-carboxyphthalato)(1,2-diaminocyclohexane)-platinum(II)|DACCP|Dacplatinum","A second-generation platinum analog with potential antineoplastic activity.  Dacplatinum alkylates DNA at the N-7 position of guanine, thereby producing DNA interstrand crosslinks and DNA strand breaks, and inhibiting DNA replication. (NCI04)","Inorganic Chemical|Pharmacologic Substance"]
["C412","Dactinomycin","2-bis[Cyclo(N-methyl-L-valyl-sarcosyl-L-prolyl-D-valyl-L-threonyl)]-1,9 dimethyl-4,6 3H-phenoxazinone-3|ACTINOMYCIN D|Actinomycin A IV|Actinomycin C1|Actinomycin D|Actinomycin I1|Actinomycin IV|Actinomycin X 1|Actinomycin-[thr-val-pro-sar-meval]|Cosmegen|DACT|DACTINOMYCIN|Dactinomycin|Dactinomycine|Lyovac Cosmegen|Lyovac cosmegen|Meractinomycin|dactinomycin","A chromopeptide antineoplastic antibiotic isolated from the bacterium Streptomyces parvulus.  Dactinomycin intercalates between adjacent guanine-cytosine base pairs, blocking the transcription of DNA by RNA polymerase; it also causes single-strand DNA breaks, possibly via a free-radical intermediate or an interaction with topoisomerase II. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C88296","Dalantercept","ACE-041|ALK1-Fc Fusion Protein ACE-041|Activin Receptor-like Kinase 1 Inhibitor ACE-041|DALANTERCEPT|Dalantercept","A soluble fusion protein containing the extracellular domain of activin receptor-like kinase-1 (ALK1) fused to a human Fc domain (ALK1-Fc fusion protein), with potential antiangiogenic and antineoplastic activities. Upon administration, dalantercept binds to various ALK1 ligands, preventing activation of tumor cell ALK1 receptors and so inhibiting the ALK1 signaling pathway; growth factor-induced angiogenesis is thus inhibited, which may result in the inhibition of tumor cell proliferation and tumor cell death. ALK1 is a type I cell surface receptor with serine/threonine kinase activity that mediates signaling by members of the transforming growth factor-beta (TGFbeta) superfamily and plays a key role in angiogenesis; ligands for this receptor include TGFbeta1 and TGFbeta2. The Fc moiety of this fusion protein mediates clearance of ligand-fusion protein complexes by the reticuloendothelial system (RES).","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C74011","Dalotuzumab","Anti-IGF-1R Recombinant Monoclonal Antibody MK-0646|DALOTUZUMAB|Dalotuzumab|MK-0646|anti-IGF1R recombinant monoclonal antibody MK-0646","A recombinant humanized monoclonal antibody directed against the insulin-like growth factor 1 receptor (IGF1R) with potential antineoplastic activity. Dalotuzumab binds to membrane-bound IGF1R, preventing binding of the ligand IGF1 and the subsequent triggering of the PI3K/Akt signaling pathway; inhibition of this survival signaling pathway may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. The activation of IGF1R, a tyrosine kinase and a member of the insulin receptor family, stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF1R signaling has been highly implicated in tumorigenesis and metastasis.","Pharmacologic Substance"]
["C66984","Daniquidone","8-Aminoisoindolo(1,2-b)quinazolin-12(10H)-one|Batracylin|Bay H 2049|DANIQUIDONE|Daniquidone|batracylin","A water-insoluble heterocyclic amide with potential antineoplastic activity. Daniquidone inhibits topoisomerases I and II, thereby inhibiting DNA replication and repair, and RNA and protein synthesis. The acetylated form of daniquidone is highly toxic and is capable of inducing unscheduled DNA synthesis; rapid acetylators are more likely to experience toxicity with this agent.","Organic Chemical|Pharmacologic Substance"]
["C61587","Danusertib","Benzamide, 4-(4-methyl-1-piperazinyl)-N-(1,4,5,6-tetrahydro-5-((2R)- methoxyphenylacetyl)pyrrolo(3,4-c)pyrazol-3-yl)-|DANUSERTIB|Danusertib|PHA-739358","A small-molecule 3-aminopyrazole derivative with potential antineoplastic activity. Danusertib binds to and inhibits the Aurora kinases, which may result in cell growth arrest and apoptosis in tumor cells in which Aurora kinases are overexpressed. This agent may preferentially bind to and inhibit Aurora B kinase. Aurora kinases, a family of serine-threonine kinases, are important regulators of cellular proliferation and division.","Pharmacologic Substance"]
["C67043","Daporinad","(2E)-N-(4-(1-Benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)prop-2-enamide|APO866|DAPORINAD|Daporinad|FK-866|K 22.175|NMPRTase Inhibitor APO866","A small molecule with potential antineoplastic and antiangiogenic activities. Daporinad binds to and inhibits nicotinamide phosphoribosyltransferase (NMPRTase), inhibiting the biosynthesis of nicotinamide adenine dinucleotide (NAD+) from niacinamide (vitamin B3), which may deplete energy reserves in metabolically active tumor cells and induce tumor cell apoptosis. In addition, this agent may inhibit tumor cell production of vascular endothelial growth factor (VEGF), resulting in the inhibition of tumor angiogenesis. The coenzyme NAD+ plays an essential role in cellular redox reactions, including the redox reaction linking the citric acid cycle and oxidative phosphorylation.","Pharmacologic Substance"]
["C74007","Daratumumab","Anti-CD38 Monoclonal Antibody|DARATUMUMAB|Daratumumab|Darzalex|HuMax-CD38|JNJ-54767414","A fully human monoclonal antibody directed against the cell surface glycoprotein CD-38 with potential antineoplastic activity. The binding of anti-CD38 monoclonal antibody to natural killer (NK) cells mimics the normal CD38-CD31 interaction on the NK cell surface. CD38 is also present on multiple myeloma (MM) cells and plasma leukemia cells; this agent may preferentially bind these cells, triggering antitumoral antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). CD38, a cell surface glycoprotein, is present on various immune cells and has been shown to regulate the cytotoxic response of activated NK cells.","Pharmacologic Substance"]
["C61490","Darinaparsin","DARINAPARSIN|DMAIII(SG)|Darinaparsin|S-Dimethylarsino-Glutathione|ZIO-101","A small-molecule organic arsenical with potential antineoplastic activity. Although the exact mechanism of action is unclear, darinaparsin, a highly toxic metabolic intermediate of inorganic arsenicals (iAs) that occurs in vivo, appears to generate volatile cytotoxic arsenic compounds when glutathione (GSH) concentrations are low. The arsenic compounds generated from darinaparsin disrupt mitochondrial bioenergetics, producing reactive oxygen species (ROS) and inducing ROS-mediated tumor cell apoptosis; in addition, this agent or its byproducts may initiate cell death by interrupting the G2/M phase of the cell cycle and may exhibit antiangiogenic effects. Compared to inorganic arsenic compounds such as arsenic trioxide (As2O3), darinaparsin appears to exhibit a wide therapeutic window.","Pharmacologic Substance"]
["C38713","Dasatinib","BMS-354825|DASATINIB|Dasatinib|Sprycel|dasatinib","An orally bioavailable synthetic small molecule-inhibitor of SRC-family protein-tyrosine kinases.  Dasatinib binds to and inhibits the growth-promoting activities of these kinases. Apparently because of its less stringent binding affinity for the BCR-ABL kinase, dasatinib has been shown to overcome the resistance to imatinib of chronic myeloid leukemia (CML) cells harboring BCR-ABL kinase domain point mutations. SRC-family protein-tyrosine kinases interact with a variety of cell-surface receptors and participate in intracellular signal transduction pathways; tumorigenic forms can occur through altered regulation or expression of the endogenous protein and by way of virally-encoded kinase genes.","Pharmacologic Substance"]
["C62091","Daunorubicin","(8S-cis)-8-Acetyl-10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-5,12-naphthacenedione|5,12-Naphthacenedione, 8-acetyl-10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-, (8S-cis)-|DAUNOMYCIN|DAUNORUBICIN|DNR|Daunomycin|Daunorrubicina|Daunorubicin|L-lyxo-Hexopyranoside, 3beta-acetyl-1,2,3,4,6,11-hexahydro-3,5,12-trihydroxy-10-metldioxo-1a-naphthacenyl 3-amino-2,3,6-trideoxy-,alpha-|Leukaemomycin C|RUBOMYCIN C|Rubidomycin|Rubomycin C|daunomycin|daunorubicin","An anthracycline antineoplastic antibiotic with therapeutic effects similar to those of doxorubicin.  Daunorubicin exhibits cytotoxic activity through topoisomerase-mediated interaction with DNA, thereby inhibiting DNA replication and repair and RNA and protein synthesis.","Pharmacologic Substance"]
["C47471","Daunorubicin Citrate","5,12-Naphthacenedione, 8-acetyl-10-((3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy)-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-, (8S,10S)-, 2-hydroxy-1,2,3-propanetricarboxylate (1:1)|DAUNORUBICIN CITRATE|Daunorubicin Citrate","A semi-synthetic anthracycline glycoside antibiotic obtained from Streptomyces with antineoplastic activity. Daunorubicin citrate intercalates DNA, which leads to inhibition of DNA and RNA synthesis, and consequently blocks cell division and results in apoptosis. This anti-tumor antibiotic is most active in the S phase of cell division. Daunorubicin is indicated in the treatment of a wide variety of cancers including acute non-lymphocytic leukemia, non-Hodgkin's lymphomas, Ewing's sarcoma, Wilms' tumor, and chronic myelocytic leukemia. (NCI05)","Pharmacologic Substance"]
["C1583","Daunorubicin Hydrochloride","5,12-Naphthacenedione, 8-acetyl-10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-, (8S-cis)-, hydrochloride|5,12-Naphthacenedione, 8-acetyl-10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-, hydrochloride, (8S-cis)-(9CI)|CERUBIDINE|Cerubidin|Cerubidine|Cloridrato de Daunorubicina|DAUNORUBICIN HYDROCHLORIDE|Daunoblastin|Daunoblastina|Daunoblastine|Daunomycin Hydrochloride|Daunomycin hydrochloride|Daunomycin, hydrochloride|Daunorubicin Hydrochloride|Daunorubicin hydrochloride|Daunorubicin.HCl|Daunorubicini Hydrochloridum|FI-6339|L-lyxo-Hexopyranoside, 3beta-acetyl-1,2,3,4,6,11-hexahydro-3,5,12-trihydroxy-10-metldioxo-1a-naphthacenyl 3-amino-2,3,6-trideoxy-,alpha-,hydrochloride|Ondena|RP-13057|Rubidomycin Hydrochloride|Rubilem|daunomycin hydrochloride|daunorubicin hydrochloride","The hydrochloride salt of an anthracycline antineoplastic antibiotic with therapeutic effects similar to those of doxorubicin.  Daunorubicin exhibits cytotoxic activity through topoisomerase-mediated interaction with DNA, thereby inhibiting DNA replication and repair and RNA and protein synthesis.","Pharmacologic Substance"]
["C73986","DC-OVA Vaccine","DC-OVA Vaccine","An autologous, multivalent dendritic cell vaccine targeting ovarian cancer with potential immunostimulating and antineoplastic activities. DC-OVA vaccine is produced in vitro by pulsing autologous dendritic cells with killed autologous primary ovarian tumors as a source of tumor-associated antigens (TAAs); the pulsed DCs are then matured using various cytokines. Upon administration, DC-OVA vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against ovarian cancer TAA-expressing ovarian cancer cells.","Cell|Immunologic Factor"]
["C90543","DCR Ligand-Bearing Liposome-Encapsulated Melanoma Antigens Vaccine","DCR Ligand-Bearing Liposome-Encapsulated Melanoma Antigens Vaccine|Dendritic Cell Receptor Ligand-Bearing Liposome-Encapsulated Melanoma Antigens Vaccine|Lipovaxin-MM","A cancer cell-based vaccine containing liposome encapsulated melanoma antigens and an immunomodulatory factor, attached, via a metal chelator, to a dendritic cell receptor (DCR) ligand-containing a metal-affinity tag, with potential immunomodulating and antineoplastic activity. Upon intravenous administration of DCR ligand-bearing liposome-encapsulated melanoma antigens vaccine, the DCR ligand moiety of this vaccine targets receptors on dendritic cells (DCs), thereby presenting the antigens to DCs which may, in turn, stimulate the DCs and may activate the immune system to mount a cytotoxic T lymphocyte (CTL) response against melanoma cancer cell associated antigens.","Immunologic Factor|Pharmacologic Substance"]
["C84859","DEC-205/NY-ESO-1 Fusion Protein CDX-1401","CDX-1401|DEC-205/NY-ESO-1 Fusion Protein CDX-1401","A fusion protein consisting of a fully human monoclonal antibody directed against the endocytic dendritic cell (DC) receptor, DEC-205, linked to the tumor-associated antigen (TAA) NY-ESO-1 with potential immunostimulating and antineoplastic activities. The monoclonal antibody moiety of DEC-205/NY-ESO-1 fusion protein CDX-1401 binds to the endocytic DC receptor, which may result in DC endocytic internalization of this agent, specifically delivering the NY-ESO-1 moiety. DC processing of NY-ESO-1 may boost the immune system to mount a cytotoxic T-lymphocyte response (CTL) against cancer cells expressing NY-ESO-1. NY-ESO-1, a cell surface protein expressed in normal fetal and adult testes, is upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C981","Decitabine","2'-Deoxy-5-azacytidine|4-Amino-1-(2-deoxy-beta-D-erythro-pentofuranosyl)-1,3,5-triazin-2(1H)-one|5-Aza-2'-deoxycytidine|5-Aza-2'deoxycytidine|5-Aza-2-deoxycytidine|5-Azadeoxycytidine|DECITABINE|Dacogen|Decitabine for Injection|Decitabine|Deoxyazacytidine|Dezocitidine|decitabine","A cytidine antimetabolite analogue with potential antineoplastic activity. Decitabine incorporates into DNA and inhibits DNA methyltransferase, resulting in hypomethylation of DNA and intra-S-phase arrest of DNA replication. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C79809","Defactinib","Benzamide, N-methyl-4-((4-(((3-(methyl(methylsulfonyl)amino)-2-pyrazinyl)methyl)amino)-5-(trifluoromethyl)-2-pyrimidinyl)amino)-|DEFACTINIB|Defactinib","An orally bioavailable, small-molecule focal adhesion kinase (FAK) inhibitor with potential antiangiogenic and antineoplastic activities. Defactinib inhibits FAK, which may prevent the integrin-mediated activation of several downstream signal transduction pathways, including those involving RAS/MEK/ERK and PI3K/Akt, thus inhibiting tumor cell migration, proliferation, survival, and tumor angiogenesis. The tyrosine kinase FAK, a signal transducer for integrins, is normally activated by binding to integrins in the extracellular matrix (ECM) but may be upregulated and constitutively activated in various tumor cell types.","Organic Chemical|Pharmacologic Substance"]
["C128039","Defactinib Hydrochloride","Benzamide, N-methyl-4-((4-(((3-(methyl(methylsulfonyl)amino)-2-pyrazinyl)methyl)amino)-5-(trifluoromethyl)-2-pyrimidinyl)amino)-, Hydrochloride (1:1)|DEFACTINIB HYDROCHLORIDE|Defactinib Hydrochloride|PF-04554878|VS-6063","The hydrochloride salt form of defactinib, an orally bioavailable, small-molecule focal adhesion kinase (FAK) inhibitor with potential antiangiogenic and antineoplastic activities. Defactinib inhibits FAK, which may prevent the integrin-mediated activation of several downstream signal transduction pathways, including those involving RAS/MEK/ERK and PI3K/Akt, thus inhibiting tumor cell migration, proliferation, survival, and tumor angiogenesis. The tyrosine kinase FAK, a signal transducer for integrins, is normally activated by binding to integrins in the extracellular matrix (ECM) but may be upregulated and constitutively activated in various tumor cell types.","Organic Chemical|Pharmacologic Substance"]
["C48385","Degarelix","DEGARELIX|Degarelix|FE200486|Firmagon|N-acetyl-3-(naphtalen-2-yl)-D-alanyl-4-chloro-D-phenylalanyl-3-(pyridin-3-yl)-D-alanyl-L-seryl-4-((((4S)-2,6-dioxohexahydropyrimidin-4-yl)carbonyl)amino)-L-phenylalanyl-4-(carbamoylamino)-D-phenylalanyl-L-leucyl-N6-(1-methylethyl)-L-lysyl-L-prolyl-D-alaninamide|degarelix","A long-acting, synthetic peptide with gonadotrophin-releasing hormone (GnRH) antagonistic properties. Degarelix targets and blocks GnRH receptors located on the surfaces of gonadotroph cells in the anterior pituitary, thereby reducing secretion of luteinizing hormone (LH) by pituitary gonadotroph cells and so decreasing testosterone production by interstitial (Leydig) cells in the testes.","Pharmacologic Substance"]
["C80443","Degarelix Acetate","D-Alaninamide, N-acetyl-3-(2-naphthalenyl)-D-alanyl-4-chloro-D-phenylalanyl-3-(3- pyridinyl)-D-alanyl-L- seryl-4-[[[(4S)-hexahydro-2,6-dioxo-4-pyrimidinyl]carbonyl]amino]- L-phenylalanyl-4-[(aminocarbonyl)amino]-D-phenylalanyl-L-leucyl-N6-(1-methylethyl)-L- lysyl-L-prolyl, Acetate, Hydrate|DEGARELIX ACETATE|Degarelix Acetate|FE200486 Acetate Hydrate","The acetate form of a long-acting, synthetic peptide with gonadotrophin-releasing hormone (GnRH) antagonistic properties. Degarelix targets and blocks GnRH receptors located on the surfaces of gonadotroph cells in the anterior pituitary, thereby reducing secretion of luteinizing hormone (LH) by pituitary gonadotroph cells and so decreasing testosterone production by interstitial (Leydig) cells in the testes.","Pharmacologic Substance"]
["C67061","Deglycosylated Ricin A Chain-Conjugated Anti-CD19/Anti-CD22 Immunotoxins","Combotox|Deglycosylated Ricin A Chain-Conjugated Anti-CD19/Anti-CD22 Immunotoxins","A combination preparation of 1:1 mixture of two immunotoxins, HD37-dgA and RFB4-dgA, with potential antineoplastic activity. Both anti-CD19 IgG monoclonal antibody HD37 and anti-CD22 IgG monoclonal antibody RFB4 are attached to a single deglycosylated ricin A chain (dgA) via N-succinimidyl-oxycarbonyl-alpha-methyl-alpha-(2-pyridyldithio) toluene (SMPT) linker. CD19 and CD22 molecules are cell suface antigens present on the majority of B acute lymphoblastic leukemia cells. This combination agent is able to specifically recognize and bind to CD19 and CD22 expressing tumor cells, thereby targeting the delivery of the cytotoxic ricin A chain to leukemia cells expressing these antigens. Ricin A chain is toxic to ribosomal activity and protein synthesis, and inhibits cell growth.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C74075","Delanzomib","((1R)-1-((2S,3R)-3-hydroxy-2-(6-phenylpyridine-2-carboxamido)butanamido)-3-methylbutyl)boronic Acid|CEP 18770|CEP-18770|CT-47098|DELANZOMIB|Delanzomib|NPH-007098|NPH007098|Proteasome Inhibitor CEP 18770","An orally bioavailable synthetic P2 threonine boronic acid inhibitor of the chymotrypsin-like activity of the proteasome, with potential antineoplastic activity. Delanzomib represses the proteasomal degradation of a variety of proteins, including inhibitory kappaBalpha (IkappaBalpha), resulting in the cytoplasmic sequestration of the transcription factor NF-kappaB; inhibition of NF-kappaB nuclear translocation and transcriptional up-regulation of a variety of cell growth-promoting factors; and apoptotic cell death in susceptible tumor cell populations. In vitro studies indicate that this agent exhibits a favorable cytotoxicity profile toward normal human epithelial cells, bone marrow progenitors, and bone marrow-derived stromal cells relative to the proteasome inhibitor bortezomib. The intracellular protein IkappaBalpha functions as a primary inhibitor of the proinflammatory transcription factor NF-kappaB.","Pharmacologic Substance"]
["C80041","Demcizumab","Anti-DLL4 Monoclonal Antibody OMP-21M18|Anti-Delta-like 4 Monoclonal Antibody OMP-21M18|Demcizumab|OMP-21M18","A humanized monoclonal antibody directed against the N-terminal epitope of Notch ligand DLL4 (delta-like 4) with potential antineoplastic activity. Demcizumab binds to the membrane-binding portion of DLL4 and prevents its interaction with Notch-1 and Notch-4 receptors, thereby inhibiting Notch-mediated signaling and gene transcription, which may impede tumor angiogenesis. Activation of Notch receptors by DLL4 stimulates proteolytic cleavage of the Notch intracellular domain (NICD); after cleavage, NICD is translocated into the nucleus and mediates the transcriptional regulation of a variety of genes involved in vascular development. The expression of DLL4 is highly restricted to the vascular endothelium.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C419","Demecolcine","(-)-Colchamine|DEMECOLCINE|Demecolcine|Methylcolchicine|N-Methyl-N-desacetylcolchicine|Santavy's Substance F|X 153","A colchicine analog with potential antimitotic and antineoplastic activities. Demecolcine acid binds to the colchicine-binding site of tubulin, inhibiting its polymerization into microtubules, causing cell cycle arrest at metaphase and preventing cell division.","Organic Chemical|Pharmacologic Substance"]
["C1988","Dendritic Cell Tumor Cell Lysate Vaccine","DC tumor cell lysate vaccine|Dendritic Cell Tumor Cell Lysate Vaccine|dendritic cell-pulsed tumor cell lysate vaccine","A vaccine composed of dendritic cells pulsed with tumor cells lysates that stimulate a potent and specific cell mediated anti-tumor immune response. (NCI)","Immunologic Factor|Pharmacologic Substance"]
["C26446","Dendritic Cell-Autologous Lung Tumor Vaccine","DCVax-Lung|Dendritic Cell-Autologous Lung Tumor Vaccine","A cancer vaccine consisting of lymphocytes harvested from a patient with lung cancer and induced to become antigen-presenting cells (APCs) known as dendritic cells.  The dendritic cells are transduced with the gene encoding an antigen specific to the patient's cancer and then returned to the patient.  In the host, the altered cells stimulate the immune system to mount a primary T cell response against lung tumor cells expressing the target antigen.  Dendritic cell-autologous lung tumor vaccines have been investigated for use in cancer immunotherapy. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C2473","Dendritic Cell-CEA Peptide Vaccine","CEA peptide-pulsed DC vaccine|CEA peptide-pulsed dendritic cell vaccine|Dendritic Cell CEA Peptide Vaccine|Dendritic Cell-CEA Peptide Vaccine|Dendritic cell-carcinoembryonic antigen peptide vaccine|Vaccine, dendritic cell-CEA peptide|peptide vaccine, dendritic cell-CEA","A cancer vaccine consisting of dendritic cells harvested from a patient with cancer and pulsed or transduced with a peptide fragment of carcinoembryonic antigen (CEA), a tumor-associated antigen expressed by a wide range of cancers.  When the altered dendritic cells are returned to the patient, they may stimulate the host immune system to mount a cytotoxic T-lymphocyte immune response against tumor cells expressing CEA.","Immunologic Factor|Pharmacologic Substance"]
["C2214","Dendritic Cell-gp100-MART-1 Antigen Vaccine","Dendritic Cell-gp100-MART-1 Antigen Vaccine|gp100/Mart-1-transduced dendritic cell vaccine","An autologous dendritic cells vaccine with antineoplastic property. Dendritic cells harvested from cancer patients are pulsed with human gp100 melanoma antigen and MART-1 (melanoma antigen recognized by T-cells) antigen; both antigens are up-regulated in melanomas. Vaccination with this vaccine may elicit the host immune response against MART-1 or gp100 expressing cells.","Immunologic Factor|Pharmacologic Substance"]
["C71760","Dendritic Cell-Idiotype-Keyhole Limpet Hemocyanin Vaccine","DC-Id-KLH Vaccine|Dendritic Cell-Idiotype-Keyhole Limpet Hemocyanin Vaccine","A cell-based vaccine composed of allogeneic dendritic cells (DC), pulsed with patient-specific non-Hodgkin's lymphoma idiotype (Id) determinants conjugated to keyhole limpet hemocyanin (KLH), with potential antitumor activity. Upon administration, this vaccine may stimulate the host immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against Id-expressing lymphoma cells, resulting in tumor cell lysis.","Pharmacologic Substance"]
["C2426","Dendritic Cell-MART-1 Peptide Vaccine","Dendritic Cell-MART-1 Peptide Vaccine|MART-1 peptide-pulsed DC vaccine|MART-1 peptide-pulsed dendritic cell vaccine|Vaccine, dendritic cell-MART-1 peptide|dendritic cell MART-1 peptide vaccine","A cancer vaccine consisting of dendritic cells harvested from a patient with cancer and pulsed or transduced with a peptide fragment of MART-1 (melanoma antigen recognized by T-cells), an antigen expressed by melanoma cells.  When the altered dendritic cells are returned to the patient, they stimulate the host immune system to mount a cytotoxic T-lymphocyte immune response against tumor cells expressing MART-1. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C125634","Dendritic Cell-Precision Multiple Antigen T-Lymphocytes","DC-PMAT|Dendritic Cell-Precision Multiple Antigen T-Cells|Dendritic Cell-Precision Multiple Antigen T-Lymphocytes","A preparation of dendritic cell-precision multiple antigen T-cells (DC-PMAT) that have been induced to specifically target multiple undisclosed tumor-associated antigens (TAAs), with potential antitumor activity. Although the exact mechanism(s) of action through which DC-PMAT cells exert their effects has yet to be elucidated, upon infusion, these cells may stimulate the host immune system to mount a highly-specific cytotoxic T-lymphocyte (CTL) response against tumors expressing common TAAs, which leads to tumor cell lysis.","Cell|Pharmacologic Substance"]
["C115976","Dendritic Cell-targeting Lentiviral Vector ID-LV305","DCvex-NY-ESO-1|Dendritic Cell-targeting Lentiviral Vector ID-LV305|ID-LV305","An engineered lentiviral vector targeting dendritic cells (DCs) and containing nucleic acids encoding for the human tumor-associated cancer-testis antigen NY-ESO-1, with potential immunostimulatory and antineoplastic activities. Upon intradermal administration, the DC-targeting lentiviral vector ID-LV305 targets and binds to dermal DCs via the DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) receptor. Upon internalization of the vector, the NY-ESO-1 protein is expressed, stimulates DC maturation and activates the immune system to mount a cytotoxic T-lymphocyte (CTL) response against NY-ESO-1-expressing cells, which may result in tumor cell lysis. NY-ESO-1 is expressed in normal testes and on the surfaces of various tumor cells, and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C62492","Denenicokin","DENENICOKIN|Denenicokin|IL-21|L-methionyl(Human Interleukin-21)|Recombinant Human Interleukin-21|rIL-21|rhIL-21","A recombinant peptide similar to or identical to endogenous human cytokine interleukin-21 (IL-21) with potential antineoplastic activity. Denenicokin binds to and activates IL-21 receptors, expressed on T-cells, B-cells, dendritic cells (DC), and natural killer (NK) cells, modulating the proliferation and/or differentiation of T and B cells, promoting T cell survival, and increasing the cytolytic activity of cytotoxic T lymphocytes (CTLs) and NK cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77065","Denibulin","DENIBULIN|Denibulin","A small molecular vascular disrupting agent (VDA), with potential antimitotic and antineoplastic activities. Denibulin selectively targets and reversibly binds to the colchicine-binding site on tubulin and inhibits microtubule assembly. This results in the disruption of the cytoskeleton of tumor endothelial cells, ultimately leading to cell cycle arrest, blockage of cell division and apoptosis. This causes inadequate blood flow to the tumor and eventually leads to a decrease in tumor cell proliferation.","Pharmacologic Substance"]
["C72736","Denibulin Hydrochloride","DENIBULIN HYDROCHLORIDE|Denibulin Hydrochloride|MN-029","The hydrochloride salt of denibulin, a small molecular vascular disrupting agent, with potential antimitotic and antineoplastic activities. Denibulin selectively targets and reversibly binds to the colchicine-binding site on tubulin and inhibits microtubule assembly. This results in the disruption of the cytoskeleton of tumor endothelial cells, ultimately leading to cell cycle arrest, blockage of cell division and apoptosis. This causes inadequate blood flow to the tumor and eventually leads to a decrease in tumor cell proliferation., a small molecule vascular disrupting agent (VDA), with potential antimitotic and antineoplastic activity. Denibulin selectively targets and reversibly binds to the colchicine-binding site on tubulin and inhibits microtubule assembly. This results in the disruption of the cytoskeleton of tumor endothelial cells (EC), ultimately leading to cell cycle arrest, blockage of cell division and apoptosis. This causes inadequate blood flow to the tumor and eventually leads to a decrease in tumor cell proliferation.","Pharmacologic Substance"]
["C1476","Denileukin Diftitox","DAB(389)-Interleukin-2|DAB(389)IL-2|DAB389 Interleukin-2 Immunotoxin|DAB389 Interleukin-2|DAB389IL-2|DAB389IL2|DENILEUKIN DIFTITOX|Denileukin Diftitox|Interleukin-2 Fusion Protein|Interleukin-2 Fusion Toxin|LY335348|Ontak|denileukin diftitox","A cytotoxic recombinant protein consisting of interleukin-2 (IL-2) protein sequences fused to diphtheria toxin. The IL-2 protein sequence moiety of denileukin difitox directs the cytocidal action of diphtheria toxin to cells that express IL-2 receptors. After the toxin moiety is internalized into target IL-2 receptor-expressing cells, its catalytic domain catalyzes the transfer of the ADP-ribose moiety of NAD to a posttranslationally modified histidine residue of elongation factor 2 (EF-2), called diphthamine. This covalent modification inactivates EF-2 and disrupts polypeptide chain elongation, resulting in cell death. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C105150","Denintuzumab Mafodotin","ADC SGN-19A|DENITUZUMAB MAFODOTIN|Denintuzumab Mafodotin|Immunoglobulin G1-kappa Auristatin F Conjugate, Anti-(homosapiens CD19 (B Lymphocyte Surface Antigen B4, leu-12)), Humanized Monoclonal Antibody|SGN-19A|SGN-CD19A","An immunoconjugate consisting of an anti-CD19 monoclonal antibody conjugated to the auristatin derivative monomethyl auristatin F (MMAF), with potential antineoplastic activity. Upon administration of denintuzumab mafodotin, the antibody moiety targets the cell surface antigen CD19, found on a number of B-cell-derived cancers. Upon antibody/antigen binding and internalization, the immunoconjugate releases MMAF, which binds to tubulin and inhibits its polymerization. Inhibition of tubulin polymerization may result in G2/M phase arrest and tumor cell apoptosis. This causes inhibition of cell growth of CD19-expressing tumor cells. CD19, a B-cell antigen, is overexpressed by a variety of different cancer cell types.","Pharmacologic Substance"]
["C61313","Denosumab","AMG 162|AMG-162|DENOSUMAB|Denosumab|Prolia|Xgeva|denosumab","A fully human monoclonal antibody directed against the receptor activator of nuclear factor kappa beta ligand (RANKL) with antiosteoclast activity. Denosumab specifically binds to RANKL and blocks the interaction of RANKL with RANK, a receptor located on osteoclast cell surfaces, resulting in inhibition of osteoclast activity, a decrease in bone resorption, and a potential increase in bone mineral density. RANKL, a protein expressed by osteoblastic cells, plays an important role in osteoclastic differentiation and activation.","Pharmacologic Substance"]
["C82697","Deoxycytidine Analogue TAS-109","Deoxycytidine Analogue TAS-109|TAS-109","An analogue of the nucleoside deoxycytidine with potential antineoplastic activity. Nucleoside analogue TAS-109 is incorporated into DNA and directly inhibits the activity of DNA polymerase, which may result in inhibition of DNA replication and cell cycle arrest in the S and G2/M phases, DNA fragmentation, and tumor cell apoptosis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C95206","Depatuxizumab","ABT-806|DEPATUXIZUMAB|Depatuxizumab|Immunoglobulin G1, Anti-(Human Epidermal Growth Factor Receptor) (Human-mus musculus Monoclonal ABT-806 Heavy Chain), Disulfide with Human-mus musculus Monoclonal ABT-806 Light Chain, Dimer|anti-EGFR MoAb ABT-806|anti-EGFR mAb ABT-806|mAb-806","A humanized monoclonal antibody (MoAb) against human epidermal growth factor receptor (EGFR) with antineoplastic activity. Depatuxizumab targets the EGFR deletion variant, de2-7 EGFR as well as wild-type EGFR expressed in cells overexpressing the receptor, thereby preventing the activation and subsequent dimerization of the receptor; the decrease in receptor activation and dimerization result in an inhibition in signal transduction and anti-proliferative effects. This MoAb targets cells expressing aberrant EGFR, hence making it an ideal candidate for generation of radioisotope or toxin conjugates.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C74023","DEPDC1/MPHOSH1 Peptide Vaccine","DEPDC1/MPHOSH1 Peptide Vaccine","A cancer vaccine containing HLA-A*2402-restricted epitopes derived from DEP domain containing 1 (DEPDC1) and M phase phosphoprotein 1 (MPHOSPH1) with potential immunostimulatory and antineoplastic activities. Upon administration, DEPDC1/MPHOSH1 peptide vaccine may elicit a specific cytotoxic T lymphocyte (CTL) response against tumor cells expressing DEPDC1 and MPHOSPH1, tumor antigens that are overexpressed in bladder cancer cells.","Pharmacologic Substance"]
["C38709","Deslorelin","6-D-Tryptophan-9-(N-ethyl-L-prolinamide)-1-9-luteinizing Hormone-releasing Factor (Swine)|DESLORELIN|Deslorelin|Ovuplant|deslorelin","A synthetic nonapeptide analogue of the natural gonadotrophin releasing hormone (GnRH) with potential antineoplastic activity. Deslorelin binds to and activates pituitary gonadotropin releasing hormone (GnRH) receptors. Continuous, prolonged administration of goserelin in males results in pituitary GnRH receptor desensitization and inhibition of pituitary secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to a significant decline in testosterone production; in females, prolonged administration results in a decrease in estradiol production. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C82600","Deslorelin Acetate","5-Oxo-L-Prolyl-L-Histidyl-L-Tryptophyl-L-Seryl-L-Tyrosyl-D-Tryptophyl-L-Leucyl-L-Arginyl-N-Ethyl-L-Prolinamide Acetate|6-D-Tryptophan-9-(N-Ethyl-L-Prolinamide)-1-9-Luteinizing Hormone-Releasing Factor (Swine) Acetate|DESLORELIN ACETATE|Deslorelin Acetate","A synthetic nonapeptide analogue of the natural gonadotrophin releasing hormone (GnRH) with potential antineoplastic activity. Deslorelin binds to and activates pituitary gonadotropin releasing hormone (GnRH) receptors. Continuous, prolonged administration of goserelin in males results in pituitary GnRH receptor desensitization and inhibition of pituitary secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to a significant decline in testosterone production; in females, prolonged administration results in a decrease in estradiol production. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1066","Detorubicin","14-Diethoxyacetoxydaunorubicin|DETORUBICIN|Detorubicin|Diethoxy-,2-(4-((3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy)-1,2,3,4,6,11-hexahydro-2,5,12-trihydroxy-7-methoxy-6,11-dioxo-2-naphthacenyl)-2-oxoethyl ester,(2S-cis) Acetic Acid","A semi-synthetic derivative of the anthracycline antineoplastic antibiotic daunorubicin. Detorubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. This agent also produces toxic free-radical intermediates and interacts with cell membrane lipids causing lipid peroxidation. Detorubicin is less toxic than daunorubicin.","Antibiotic|Organic Chemical"]
["C422","Dexamethasone","(11Beta,16alpha)-9-fluoro-11,17,21-trihydroxy-16-methylpregna-1,4-diene-3,20-dione|1-Dehydro-16alpha-methyl-9alpha-fluorohydrocortisone|16Alpha-methyl-9alpha-fluoro-1,4-pregnadiene-11beta,17alpha,21-triol-3,20-dione|16Alpha-methyl-9alpha-fluoro-delta1-hydrocortisone|16Alpha-methyl-9alpha-fluoroprednisolone|9Alpha-fluoro-11beta,17alpha,21-trihydroxy-16alpha-methylpregna-1,4-diene-3,20-dione|9Alpha-fluoro-16alpha-methylprednisolone|9alpha-Fluoro-16alpha- methylprednisolone|Aacidexam|Adexone|Aknichthol Dexa|Alba-Dex|Alin Depot|Alin Oftalmico|Alin|Amplidermis|Anemul mono|Auricularum|Auxiloson|Baycuten N|Baycuten|Cortidexason|Cortisumman|DEXAMETHASONE|Decacort|Decadrol|Decadron|Decalix|Decameth|Decasone R.p.|Dectancyl|Dekacort|Deltafluorene|Deronil|Desamethasone|Desameton|Dexa-Mamallet|Dexa-Rhinosan|Dexa-Scheroson|Dexa-sine|Dexacortal|Dexacortin|Dexafarma|Dexafluorene|Dexalocal|Dexamecortin|Dexameth|Dexamethasone|Dexamethasonum|Dexamonozon|Dexapos|Dexinoral|Dexone|Dinormon|Fluoro-9alpha Methyl-16alpha Prednisolone|Fluorodelta|Fortecortin|Gammacorten|Hexadecadrol|Hexadrol|Lokalison-F|Loverine|Methylfluorprednisolone|Millicorten|Mymethasone|Orgadrone|Spersadex|Visumetazone|dexamethasone","A synthetic adrenal corticosteroid with potent anti-inflammatory properties. In addition to binding to specific nuclear steroid receptors, dexamethasone also interferes with NF-kB activation and apoptotic pathways. This agent lacks the salt-retaining properties of other related adrenal hormones. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C99381","Dexanabinol","1,1-Dimethylheptyl-11-hydroxytetrahydrocannabinol|7-Hydroxy-delta-6-tetrahydrocannabinoldimethylheptyl|DEXANABINOL|Dexanabinol|HU-211","A synthetic, terpene-based cannabinoid derivative devoid of cannabinoid receptors 1 and 2 agonist activity and with potential neuroprotective, antiinflammatory and antineoplastic activities. Functioning as an N-Methyl-D-aspartate (NMDA) receptor antagonist, dexanabinol protects neuronal cells against NMDA and glutamate neurotoxicity. This agent also scavenges peroxy radicals and protects neurons from the damages of reactive oxygen species. Furthermore, dexanabinol inhibits the activity of nuclear factor kappa B (NF-kB), thereby preventing the expression of NF-kB target genes, such as tumor necrosis factor alpha, cytokines and inducible nitric oxide synthase. As a result, this agent may restore apoptotic processes in cancerous cells. NF-kB is activated in a variety of cancer cells and plays a key role in the regulation of apoptosis and cellular proliferation.","Pharmacologic Substance"]
["C1333","Dexrazoxane","(+)-(S)-4,4'-(1-Methyl-1,2-ethanediyl)di(2,6-piperazinedione)|2, 6-Piperazinedione, 4,4'-propylenedi-, (P)- (8CI)|2,6-Piperazinedione, 4, 4'-(1-methyl-1,2-ethanediyl)bis-, (S)- (9CI)|2,6-Piperazinedione, 4,4'-(1-methyl-1,2-ethanediyl)bis-,(S)-(9CI)|2,6-Piperazinedione, 4,4'propylenedi-,(P)-(8CI)|ADR-529|DEXRAZOXANE|Dexrazoxane|ICRF-187|Razoxane (+)-form|Soluble ICRF (L-isomer)|dexrazoxane","A bisdioxopiperazine with iron-chelating, chemoprotective, cardioprotective, and antineoplastic activities. After hydrolysis to an active form that is similar to ethylenediaminetetraacetic acid (EDTA), dexrazoxane chelates iron, limiting the formation of free radical-generating anthracycline-iron complexes, which may minimize anthracycline-iron complex-mediated oxidative damage to cardiac and soft tissues. This agent also inhibits the catalytic activity of topoisomerase II, which may result in tumor cell growth inhibition.","Organic Chemical|Pharmacologic Substance"]
["C66945","Dexrazoxane Hydrochloride","Cardioxane|DEXRAZOXANE HYDROCHLORIDE|Dexrazoxane Hydrochloride|Totect|Zinecard|dexrazoxane hydrochloride","The hydrochloride salt of a bisdioxopiperazine with iron-chelating, chemoprotective, cardioprotective, and antineoplastic activities. After hydrolysis to an active form that is similar to ethylenediaminetetraacetic acid (EDTA), dexrazoxane chelates iron, limiting the formation of free radical-generating anthracycline-iron complexes, which may minimize anthracycline-iron complex-mediated oxidative damage to cardiac and soft tissues.  This agent also inhibits the catalytic activity of topoisomerase II, which may result in tumor cell growth inhibition.","Pharmacologic Substance"]
["C968","Dezaguanine","3-Deazaguanine|CI-908|DEZAGUANINE|Deazaguanine|Dezaguanine","A purine nucleoside analogue with antineoplastic and antiviral activities.  By replacing guanine, dezaguanine incorporates into DNA and inhibits de novo purine synthesis, thereby inducing cell death. (NCI)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C80635","Dezaguanine Mesylate","3-Deazaguanine Mesylate|DEZAGUANINE MESYLATE|Dezaguanine Mesylate","The mesylate salt form of dezaguanine, a purine nucleoside analogue with antineoplastic and antiviral activities.  By competing with guanine, dezaguanine gets incorporated into DNA and inhibits DNA synthesis, thereby inducing cell death.","Pharmacologic Substance"]
["C2649","DHA-Paclitaxel","DHA-Paclitaxel|DHA-paclitaxel|Docosahexaenoic Acid-Paclitaxel conjugate|TXP|Taxoprexin","A prodrug comprised of the naturally occurring omega-3 fatty acid docosahexaenoic acid (DHA) covalently conjugated to the anti-microtubule agent paclitaxel.  Because tumor cells take up DHA, DHA-paclitaxel is delivered directly to tumor tissue, where the paclitaxel moiety binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. Paclitaxel also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2).  DHA-paclitaxel exhibits improved pharmacokinetic and toxicity profiles when compared to conventional paclitaxel and has demonstrated antineoplastic activity in animal models of cancer. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2707","DHEA Mustard","DHEA Mustard|Dehydroepiandrosterone mustard|dehydroepiandrosterone mustard","A steroidal alkylating agent with potential antineoplastic activity.  Alkylating agents exert cytotoxic and, in some cases, chemotherapeutic effects by transferring alkyl groups to DNA, thereby damaging DNA and interfering with DNA replication and cell division. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C425","Dianhydrogalactitol","1,2,5,6 dianhydrogalactitol|1,2:5, 6-Dianhydrogalactitol|1,2:5, 6-diepoxydulcitol|1,2:5,6 dianhydrogalactitol|1,2:5,6-Dianhydrodulcitol|1,2:5,6-Diepoxydulcitol|1,2:5,6-dianhydrodulcitol|DAG|Dianhydrodulcitol|Dianhydrogalactitol|Dulcitol diepoxide|Galactitol, 1,2:5,6-dianhydro- (8CI 9CI)|Galactitol|dianhydrodulcitol|diepoxydulcitol|diepoxygalactitol|dulcitol diepoxide|galactitol, 1,2:5,6-dianhydro- (8CI 9CI)","A bifunctional hexitol derivative with potential antineoplastic activity. Dianhydrogalactitol alkylates and cross-links DNA via an epoxide group during all phases of the cell cycle, resulting in disruption of DNA function and cell cycle arrest. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2186","Diarylsulfonylurea Compound","Diarylsulfonylurea Compound|Diarylsulfonylureas","A sulfonylurea compound containing aryl groups with potential antineoplastic activity. Originally developed as herbicides, diarylsulfonylureas have shown a broad spectrum of antitumor activity in vivo. The precise mechanism of antitumor action has not yet been elucidated, however, certain diarylsulfonylurea compounds have been shown in preliminary studies to exert antimitotic effects through their inhibition of tubulin polymerization, and others have been shown to be effective antitumor agents in animal models by the mechanism of uncoupling mitochondrial oxidative phosphorylation.","Chemical Viewed Structurally"]
["C62508","Diazepinomicin","11h-dibenzo(B,E)(1,4)diazepin-11-one, 5,10-dihydro-4,6,8-trihydroxy-10-((2E,6E)-3,7,11-trimethyl-2,6,10-dodecatrien-1-yl)-|BU-4664L|DIAZEPINOMICIN|Diazepinomicin|ECO-4601|TLN-4601","A potent inhibitor of the RAS/RAF/MAPK signaling pathway with potential antineoplastic activity. Diazepinomicin binds to and inhibits Ras kinase, thereby preventing the phosphorylation and activation of proteins downstream of the Ras signal transduction pathway, including serine/threonine kinase RAF (BRAF) and extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK-2), that play a crucial role in regulating cell growth and survival. Diazepinomicin also selectively binds to the peripheral benzodiazepine receptor (BZRP), a receptor highly expressed in certain cancer cells, thus inducing cell cycle arrest and apoptosis in BZRP-expressing cells. In addition, diazepinomicin is able to cross the blood-brain barrier, thereby reaching therapeutic concentrations in the brain.","Pharmacologic Substance"]
["C1363","Diaziquone","1,4-Cyclohexadiene-1,4-dicarbamic acid, 2, 5-bis(1-aziridinyl)-3,6-dioxo-, diethyl ester|1,4-cyclohexadiene-1,4-dicarbamic acid, 2, 5-bis(1-aziridinyl)-3,6-dioxo-, diethyl ester|1,4-cyclohexadiene-1,4-dicarbamic acid,2,5-bis(1-aziridinyl)-3,6-dioxo,-diethyl ester|2,5-bis(1-aciridinyl)-3,6-bis(ethoxycarbonylamino)-1,4-benzoquinone|2,5-bis(1-aziridinyl)-3,6-bis(ethoxycarbonylamino)-1,4-benzoquinone|2,5-bis(1-aziridinyl)-3,6-dioxo-1,4-cyclohexadiene-1,4-dicarbamic acid diethyl ester|2,5-diaziridinyl-3,6-bis(ethoxycarbonyl-amino)-1,4-benzoquinone|AZQ|Aziridinyl Benzoquinone|Aziridinylbenzoquinone carbamic acid|Aziridinylbenzoquinone|CI-904|Carbamic acid, [2,5-bis(1-aziridinyl)-3,6-dioxo-1, 4-cyclohexadiene-1,4-diyl]bis-, diethyl ester (9CI)|DIAZIQUONE|Diaziquone|[2,5-bis(1-aziridinyl)-3,6-dioxo-1,4-cyclohexadiene-1,4-diyl]biscarbamic acid diethyl ester|carbamic acid, [2,5-bis(1-aziridinyl)-3,6-dioxo-1, 4-cyclohexadiene-1,4-diyl]bis-, diethyl ester (9CI)|diaziquone","A water-soluble, synthetic aziridinylbenzoquinone with potential antineoplastic activity. Bioactivation of aziridinylbenzoquinone RH1 occurs through the two-electron reduction of the quinone to the hydroquinone by the two-electron quinone reductase DT-diaphorase (DTD). The resultant hydroquinone selectively alkylates and cross-links DNA at the 5'-GNC-3' sequence, inihibiting DNA replication, inducing apoptosis, and inhibiting tumor cell proliferation. DTD is over-expressed in many tumors relative to normal tissue, including lung, colon, breast and liver tumors.","Chemical Viewed Structurally|Organic Chemical|Pharmacologic Substance"]
["C427","Diazooxonorleucine","6-DIAZO-5-OXO-L-NORLEUCINE|6-diazo-5-oxo-L-norleucine|6-diazo-5-oxo-norleucine|DON|Diazooxonorleucine","An L-glutamine diazo analogue amino acid antibiotic isolated from a species of the bacterial genus Streptomyces with potential antineoplastic activity. Diazooxonorleucine inhibits several glutamine-dependent biosynthetic pathways involved in the syntheses of D-glucosamine phosphate, purines and pyrimidines. This agent inhibits phosphate-activated glutaminase, a key enzyme for the synthesis of releasable glutamine, depleting cells of this essential amino acid and reducing their capacity to proliferate.","Amino Acid, Peptide, or Protein|Antibiotic"]
["C81362","Dibrospidium Chloride","DIBROSPIDIUM CHLORIDE|Dibrospidium Chloride","A dispirotripiperazine derivative and alkylating agent with potential antineoplastic and anti-inflammatory activities. Dibrospidium chloride has been examined for the treatment of bone cancer.","Pharmacologic Substance"]
["C28959","Dichloroallyl Lawsone","Dichloroallyl Lawsone","A triazine derivative with antineoplastic activity.  Dichloroallyl lawsone inhibits mitochondrial dihydroorotate dehydrogenase (DHOD), an enzyme that catalyzes the only redox step in de novo pyrimidine biosynthesis, and nucleotide (RNA and DNA) biosynthesis. (NCI04)","Pharmacologic Substance"]
["C107676","Dicycloplatin","DCP|Dicycloplatin","A third-generation, supramolecular platinum-based compound composed of carboplatin linked, by a strong hydrogen bond, to 1,1-cyclobutane dicarboxylate (CBDCA), with potential antineoplastic activity. Although the exact mechanism of action has yet to be fully elucidated, dicycloplatin appears to have a mechanism of action similar to that of other platinum-based compounds, which involves both DNA binding and the formation of DNA crosslinks. This mechanism results in the induction of apoptosis and cell growth inhibition. Compared to carboplatin alone, dicycloplatin shows enhanced solubility and stability in aqueous solution and appears to have a more favorable toxicity profile.","Organic Chemical|Pharmacologic Substance"]
["C87238","Dienogest","17-Hydroxy-3-Oxo-19-Nor-17Alpha-Pregna-4,9-Diene-21-Nitrile|19-Norpregna-4,9-Diene-21-Nitrile, 17-Hydroxy-3-Oxo-, (17Alpha)-|DIENOGEST|Dienogest|M 18575|MJR-35|STS 557|ZK 37659","An orally-active, semisynthetic, fourth generation, nonethinylated progestogen with antiproliferative, antiandrogenic, anti-inflammatory and antiangiogenic activities that is used in hormone therapy and as a female contraceptive. Upon oral administration, dienogest binds intracellular progesterone receptors which then translocate to the nucleus where the drug-receptor complex interacts with progesterone response elements, thus altering the expression of target genes. Dienogest reduces the production of estradiol, prevents ovulation and alters the cervical mucus and endometrium. In addition, dienogest appears to suppress the expression of cell cycle regulator cyclin D1. Altogether, this may prevent the growth of endometrial epithelial cells and may reduce symptoms associated with leiomyoma.","Pharmacologic Substance"]
["C1168","Diethylnorspermine","CI-1006|DENSPM|Diethylnorspermine|N(1),N(11)-diethylnorspermine|N1,N11-bis(ethyl)norspermine","A synthetic bis-ethyl analogue of spermine with potential antineoplastic activity. N(1),N(11)-bis(ethyl)norspermine (DENSPM), a N-terminally alkylated tetraamine and polyamine mimetics, disrupts polyamine pool homeostasis by modulating the activities of the biosynthetic enzymes, ornithine decarboxylase (ODC), and S-adenosylmethionine decarboxylase (AdoMetDC). This agent also reduces polyamine concentrations through the induction of the catabolic enzyme spermidine/spermine N1-acetyltransferase 1 (SSAT). Polyamines, an integral part of the DNA helix structure, play a critical role in cell division, differentiation and membrane function. Disruption of normal polyamine concentrations by DENSPM may lead to cell growth inhibition.","Organic Chemical|Pharmacologic Substance"]
["C2634","Digitoxin","(3beta,5beta)-3-[(O-2,6-Dideoxy-beta-D-ribo-hexopyranosyl-(1-4)-O-2,6-dideoxy-beta-D-ribo-hexopyranosyl-(1-4)-2,6-dideoxy-beta-D-ribo-hexopyranosyl)oxy]-14-hydroxycard-20(22)-enolide|CP4071|Cardidigin|Crystalline Digitalin|Crystodigin|DIGITOXIN|Digitoxin","A lipid soluble cardiac glycoside that inhibits the plasma membrane sodium potassium ATPase, leading to increased intracellular sodium and calcium levels and decreased intracellular potassium levels.  In studies increased intracellular calcium precedes cell death and decreased intracellular potassium increase caspase activation and DNA fragmentation, causing apoptosis and inhibition of cancer cell growth. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C28990","Digoxin","12beta-Hydroxydigitoxin|3beta,12beta,14-Trihydroxy-5beta,14beta-card-20(22)-enolid-3-tridigitoxosid|Cardiogoxin|DIGOXIN|Digoxigenin-tridigitoxosid|Digoxin|Lanoxin|digoxin","A cardiac glycoside. Digoxin inhibits the sodium potassium adenosine triphosphatase (ATPase) pump, thereby increasing intracellular calcium and enhancing cardiac contractility.  This agent also acts directly on the atrioventricular node to suppress conduction, thereby slowing conduction velocity.  Apparently due to its effects on intracellular calcium concentrations, digoxin induces apoptosis of tumor cells via a pathway involving mitochondrial cytochrome c and caspases 8 and 3. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C980","Dihydro-5-Azacytidine","1,3,5-triazin-2(1H)-one, 4-amino-3, 6-dihydro-1-beta-D-ribofuranosyl monohydrochloride|5,6-DIHYDRO-5-AZACYTIDINE|5,6-Dihydro-5-azacytidine hydrochloride|5,6-dihydro-5-azacytidine HCl|5,6-dihydro-5-azacytidine hydrochloride|DHAC|Dihydro-5-Azacytidine","A synthetic nucleoside analogue of deoxycytidine. Dihydro-5-azacytidine inhibits DNA methyltransferase, thereby interfering with abnormal DNA methylation patterns that are associated with genetic instability in some tumor cells. Inhibition of this enzyme may restore expression of tumor-suppressor genes and result in antitumor activity. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1463","Dihydrolenperone","1-Butanone, 1-(4-fluorophenyl)-4-[4-[(4-fluorophenyl)hydroxymethyl]-1-piperidi nyl]-|1-Butanone, 1-(4-fluorophenyl)-4-[4-[(4-fluorophenyl)hydroxymethyl]-1-piperidinyl]-|DIHYDROLENPERONE|Dihydro-lenperone|Dihydrolenperone|RMI 11974","A butyrophenone that has been investigated for antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C53434","Diindolylmethane","3,3'-Diindolymethane|3,3'-Methylenebis-1H-indole|CCRIS 5806|DIM-Plus|DIM|DIMPRO|Di-Indoly Methane|Diindolylmethane|diindolylmethane","A phytonutrient and plant indole found in cruciferous vegetables including broccoli, Brussels sprouts, cabbage, cauliflower and kale, with potential anti-androgenic and antineoplastic activities. As a dimer of indole-3-carbinol, diindolylmethane (DIM) promotes beneficial estrogen metabolism in both sexes by reducing the levels of 16-hydroxy estrogen metabolites and increasing the formation of 2-hydroxy estrogen metabolites, resulting in increased antioxidant activity. Although this agent induces apoptosis in tumor cells in vitro, the exact mechanism by which DIM exhibits its antineoplastic activity in vivo is unknown.","Organic Chemical|Pharmacologic Substance"]
["C78451","DI-Leu16-IL2 Immunocytokine","DI-Leu16-IL-2|DI-Leu16-IL2 Immunocytokine|De-Immunized Anti-CD20-IL-2 Immunocytokine DI-Leu16-IL-2","A recombinant fusion protein consisting of de-immunized and humanized anti-CD20 monoclonal antibody Leu16 fused to human cytokine interleukin-2 (IL2) with potential antineoplastic activity. The antibody moiety of DI-Leu16-IL2 immunocytokine binds to tumor cells expressing the CD20 antigen, which may result in an antibody-dependent cell-mediated cytotoxicity (ADCC) towards CD20-expressing tumor cells; the localized IL2 moiety of this fusion protein may stimulate natural killer (NK) and T-lymphocyte mediated immune responses, enhancing the ADCC response. De-immunization involves the modification of potential helper T cell epitopes that bind to MHC class II molecules; humanization involves combining recombinant murine variable (V) regions with human immunoglobulin light and heavy chain constant regions. CD20 antigen, a hydrophobic transmembrane protein located on normal pre-B and mature B lymphocytes, is overexpressed by various cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1073","Dimethylmyleran","2,5-Dimethanesulfonoxyhexane|DMB|DMM|Dimethyl-Myleran|Dimethylbusulfan|Dimethylmyleran","An aliphatic analogue of busulfan with potential antineoplastic activity.  As an alkylating agent, dimethylbusulfan induces neutropenia and has been shown to exhibit antitumor effects in some animal models.  Alkylating agents exert cytotoxic and chemotherapeutic effects by transferring alkyl groups to DNA, thereby damaging DNA and interfering with DNA synthesis and cell division. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C78854","Dinaciclib","2-Piperidineethanol, 1-[3-ethyl-7-[[(1-oxido-3-pyridinyl)methyl]amino]pyrazolo[1,5- a]pyrimidin-5-yl]-, (2S)-|CDK Inhibitor SCH 727965|CDK inhibitor SCH 727965|DINACICLIB|Dinaciclib|MK-7965|SCH 727965|dinaciclib","A pyrazolo[1,5-a]pyrimidine with potential antineoplastic activity. Dinaciclib selectively inhibits cyclin dependent kinases CDK1, CDK2, CDK5, and CDK9; inhibition of CDK1 and CDK2 may result in cell cycle repression and tumor cell apoptosis.","Pharmacologic Substance"]
["C85456","Dinitrophenyl-Modified Autologous Renal Cell Carcinoma Tumor cell Vaccine","DNP-Modified Autologous Renal Cell Carcinoma Tumor Cell Vaccine|Dinitrophenyl-Modified Autologous Renal Cell Carcinoma Tumor cell Vaccine","A cancer vaccine consisting of autologous renal cell carcinoma (RCC) tumor cells modified with the hapten 2,4-dinitrophenol (DNP) with potential immunostimulating and antineoplastic activities. Administration of DNP-modified autologous renal cell carcinoma tumor cell vaccine may induce a cytotoxic T-lymphocyte (CTL) response against renal cell carcinoma tumor cells. DNP conjugation may enhance the immunogenicity of weakly immunogenic antigens.","Cell|Pharmacologic Substance"]
["C1570","Dinutuximab","Ch 14.18UTC|Ch14.18|DINUTUXIMAB|Dinutuximab|MOAB Ch14.18|Unituxin|monoclonal antibody Ch14.18","A chimeric mouse/human monoclonal antibody with potential antineoplastic activity. Dinutuximab binds to the ganglioside GD2 and induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity against GD2-expressing tumor cells.  GD2 is overexpressed in malignant melanoma, neuroblastoma, osteosarcoma, and small cell carcinoma of the lung.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C115103","Dioscorea nipponica Makino Extract DNE3","DNE3|Dioscorea nipponica Extract with Ethyl Acetate|Dioscorea nipponica Makino Extract DNE3","An extract of the plant Dioscorea nipponica Makino and inhibitor of both the serine/threonine protein kinase Akt (protein kinase B) and members of the phosphatidylinositol 3-kinase (PI3K) family of lipid kinases, with potential antineoplastic and anti-metastatic activities. Dioscorea nipponica Makino extracted with ethyl acetate (DNE3) binds to and inhibits PI3K and Akt. This inhibits PI3K/Akt-mediated signaling and prevents both growth and survival of PI3K/Akt-overexpressing tumor cells. In addition, DNE3 increases the expression of tissue inhibitor of metalloproteinase-2 (TIMP-2), inhibits the secretion of matrix metalloproteinases (MMPs), primarily MMP-2 and MMP-9, and inhibits the serine protease urokinase (urokinase-type plasminogen activator; u-PA). This inhibits tumor cell invasion, migration, motility, and adhesion. This agent also inhibits the activation of both cAMP response element-binding (CREB) and activating protein-1 (AP-1), and increases the expression of IkappaB (IkB), which inhibits the activation of nuclear factor-kappa B (NF-kB). These processes further contribute to this agent's anti-tumor potential in susceptible tumor cells.","Pharmacologic Substance"]
["C126273","Diphtheria Toxin Fragment-Interleukin-2 Fusion Protein E7777","Diphtheria Toxin Fragment-Interleukin-2 Fusion Protein E7777|E7777","A cytotoxic recombinant fusion protein consisting of the human cytokine interleukin-2 (IL-2) fused to diphtheria toxin fragments A and B, containing both the catalytic and translocation domains, with potential antineoplastic activity. Upon administration, the IL-2 moiety of diphtheria toxin fragment-IL-2 fusion protein E7777 binds to IL-2 receptors. After internalization by IL-2 receptor-expressing cells via endocytosis, the agent is proteolytically cleaved. This releases the catalytic domain of the toxin moiety, which catalyzes the transfer of the ADP-ribose moiety of NAD to a diphthamide residue of elongation factor 2 (EF-2). This covalent modification inactivates EF-2 and disrupts polypeptide chain elongation, resulting in an inhibition of translation and cell death. E7777 has the same amino acid sequence as denileukin diftitox (DD), but has an increased purity profile and an increased percentage of monomeric, active protein, which improves its efficacy.","Pharmacologic Substance"]
["C82681","Distilled Water","Distilled Water","An ultra-pure form of water with potential antineoplastic activity. Derived by boiling impure water and condensing the resultant steam in a sterile container, distilled water has been shown to kill bladder cancer cells in vitro through osmotic lysis (cytolysis)","Inorganic Chemical"]
["C432","Ditiocarb","DDTC|DIECA|DITIOCARB|DTC|Diethylcarbamodithioic Acid|Diethyldione|Diethyldithiocarbamate|Diethyldithiocarbamic Acid|Diethyldithiocarbaminic Acid|Diethyldithione|Ditiocarb","A sulfhydryl-containing carbamate that is the primary in vivo metabolite of disulfiram. Diethyldithiocarbamate chelates zinc, thereby inhibiting metalloproteinases, thereby preventing the degradation of the extracellular matrix and inhibiting an initial step in cancer metastasis and angiogenesis. A known inhibitor of superoxide dismutase, this agent can either potentiate or protect against cell oxidative damage caused by ionizing radiation, depending on the time of administration. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C113331","DKK1-Neutralizing Monoclonal Antibody DKN-01","DKK1-Neutralizing Monoclonal Antibody DKN-01|DKN-01","A humanized monoclonal antibody directed against Wnt antagonist Dickkopf-1 (DKK1) with potential anti-osteolytic activity. DKK1-neutralizing monoclonal antibody DKN-01 binds to and inhibits DKK1, which restores Wnt pathway signaling. Reactivation of the Wnt signaling pathway may result in the differentiation and activation of osteoblasts within the bone matrix and the reversal of tumor-induced osteolytic disease. Elevated levels of circulating DKK1, a potent Wnt signaling pathway antagonist, is associated with a number of neoplastic diseases.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C113807","DLK1/EPHA2/HBB/NRP1/RGS5/TEM1 Peptide-pulsed Alpha-type-1 Polarized Dendritic Cell Vaccine","DLK1/EPHA2/HBB/NRP1/RGS5/TEM1 Peptide-pulsed Alpha-type-1 Polarized Dendritic Cell Vaccine|Tumor Blood Vessel Antigen Peptide-pulsed Alpha-type-1 Polarized Dendritic Cell Vaccine|alphaDC1-TBVA Vaccine","A cell based cancer vaccine composed of mature polarized dendritic cells (alphaDC1) pulsed with six human leukocyte antigen (HLA)-A2-presented tumor blood vessel antigen (TBVA)-derived peptides, with potential immunostimulatory and antineoplastic activities. Dendritic cells (DCs) were treated with a \"type-1 polarizing cytokine cocktail\", including interleukin-1beta, tumor necrosis factor alpha (TNF-a), interferon-alpha (IFN-a), IFN-gamma and polyinosinic:polycytidylic acid (pI:C) to produce mature alpha type-1 polarized DCs (alphaDC1) that are capable of producing high levels of interleukin-12p70 (IL-12p70). The alphaDC1 are subsequently pulsed with TBVA-derived peptides, including delta-like homologue 1 (DLK1) 310-318, EPH receptor A2 (EPHA2) 883-891, beta-globin (HBB) 31-39, neuropilin-1 (NRP1) 433-441, regulator of G-protein signaling 5 (RGS5) 5-13 and tumor endothelial marker 1 (TEM1) 691-700. Upon administration, these DCs are able to induce a potent cytotoxic T-lymphocyte (CTL) response against the TBVAs expressed on tumor-associated stromal cells, which results in stromal cell lysis and inhibition of angiogenesis. Disrupting the surrounding tumor vasculature inhibits tumor cell growth and survival. alphaDC1 are able to induce a potent tumor antigen-specific CTL response due to their high co-stimulatory activity and the secretion of anti-cancer cytokines, such as IL-12p70.","Immunologic Factor|Pharmacologic Substance"]
["C77864","DM4-Conjugated Anti-Cripto Monoclonal Antibody BIIB015","BIIB015|DM4-Conjugated Anti-Cripto Monoclonal Antibody BIIB015","A humanized IgG1 monoclonal antibody directed against the cell surface-associated protein Cripto and conjugated to the maytansinoid DM4 with potential antineoplastic activity. The monoclonal antibody moiety of DM4-conjugated anti-Cripto monoclonal antibody BIIB015 binds to the tumor associated antigen (TAA) Cripto; upon internalization, the DM4 moiety binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of Cripto-expressing tumor cells. Constitutively expressed during embryogenesis, Cripto belongs to the EGF-CFC family of growth factor-like molecules and plays a key role in signaling pathways of certain transforming growth factor-beta superfamily members; as a TAA, Cripto is overexpressed in carcinomas such as those of the breast, ovary, stomach, lung, and pancreas while its expression is absent in normal tissues.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C90539","DM-CHOC-PEN","4-Demethylcholesteryloxycarbonylpenclomedine|DM-CHOC-PEN","A cholesterol carbonate derivative of 4-demethylpenclomedine (DM-PEN) with potential antineoplastic alkylating activity. Upon intravenous administration of 4-demethylcholesteryloxycarbonylpenclomedine, the carbonium moiety binds to and alkylates DNA at the N7 guanine position, thereby causing DNA crosslinks. This prevents DNA replication, inhibits cellular proliferation and triggers apoptosis. In addition, due to its lipophilic cholesteryl moiety this agent is able to cross the blood brain barrier (BBB) and therefore can be given intravenously compared to other alkylating agents that need to be given intra-cranially.","Pharmacologic Substance"]
["C69140","D-methionine Formulation MRX-1024","D-methionine Formulation MRX-1024|MRX-1024","A proprietary oral formulation of D-methionine with antioxidant and antimucositis activities. D-methionine formulation MRX-1024 may selectively protect the oral mucosa from the toxic effects of chemotherapy and radiation therapy without compromising antitumor activity. D-methionine may be converted into the L- isomer in vivo, particularly in instances of L-methionine deprivation; both isomers have antioxidant activity which may be due, in part, to their sulfur moieties and chelating properties. L-methionine, an essential amino acid, also may help to maintain the ratio of reduced glutathione to oxidized glutathione in cells undergoing oxidative stress and may provide a source of L-cysteine for glutathione synthesis.","Pharmacologic Substance"]
["C92588","DNA Interference Oligonucleotide PNT2258","DNA Interference Oligonucleotide PNT2258|DNAi Drug PNT2258|PNT2258","A liposomal formulation of the 24-mer oligonucleotide PNT100, with potential antineoplastic activity. PNT2258 targets and complements to untranscribed DNA sequence upstream of BCL2 promoters, thereby interfering with DNA replication and transcription of the BCL2 gene. This may promote and restore the apoptotic pathway in BCL2-overexpressing tumor cells. BCL2, an anti-apoptotic protein, is overexpressed in a wide variety of tumors.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C95888","DNA Minor Groove Binding Agent PM060184","DNA Minor Groove Binding Agent PM060184|PM060184","A marine-derived, synthetically produced compound with potential antineoplastic activity. DNA minor groove-binding agent PM060184 covalently binds to residues lying in the minor groove of DNA, which may result in delayed progression through S phase, cell cycle arrest in the G2/M phase and cell death.","Pharmacologic Substance"]
["C29435","DNA Minor Groove Binding Agent SG2000","(11aS,11a'S)-8,8'-(propane-1,3-diylbis(oxy))bis(7-methoxy-2-methylene-2,3-dihydro-1H-benzo[e]pyrrolo[1,2-a][1,4]diazepin-5(11aH)-one)|BN2629|DNA Minor Groove Binding Agent SG2000|NSC 694501|Pyrrolobenzodiazepine Dimer|SG2000|SJG-136|SJG136","A sequence-selective pyrrolobenzodiazepine (PBD) dimer with potential antineoplastic activity. Following intravenous administration, DNA minor groove binding agent SG2000 preferentially and covalently binds to purine-GATC-pyrimidine sequences, with the imine/carbinolamine moieties of SG2000 binding to the N2 positions of guanines on opposite strands of DNA. This induces interstrand cross-links and inhibits both DNA replication and gene transcription, which lead to the inhibition of cell growth. With a preference for binding to purine-GATC-pyrimidine sequences, SG2000 adducts do not appear to be susceptible to p53-mediated DNA excision repair.","Organic Chemical|Pharmacologic Substance"]
["C116709","DNA Plasmid Encoding Interleukin-12 INO-9012","DNA Plasmid Encoding Interleukin-12 INO-9012|INO-9012","A plasmid DNA vaccine encoding the human pro-inflammatory cytokine interleukin-12 (IL-12) with potential immunoactivating activity. Upon intramuscular delivery by electroporation of DNA plasmid encoding interleukin-12 INO-9012, IL-12 is translated in cells and activates the immune system by promoting the activation of natural killer cells (NK cells), inducing secretion of interferon-gamma and promoting cytotoxic T-cell responses against tumor cells. This may result in both immune-mediated tumor cell death and the inhibition of tumor cell proliferation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C123919","DNA Plasmid-encoding Interleukin-12/HPV DNA Plasmids Therapeutic Vaccine INO-3112","DNA Plasmid-encoding Interleukin-12/HPV DNA Plasmids Therapeutic Vaccine INO-3112|INO-3112 Vaccine|INO-3112|VGX-3100 Plus INO-9012","A DNA-based combination immunotherapeutic, INO-3112, composed of VGX-3100, a preparation of DNA plasmids encoding the E6 and E7 genes of human papillomavirus (HPV) subtypes 16 and 18, combined with INO-9012, a DNA plasmid encoding the immune activator and pro-inflammatory cytokine human interleukin-12 (IL-12) with potential immunoactivating and antineoplastic activities. Upon intramuscular delivery by electroporation of VGX-3100, the HPV E6 and E7 proteins are translated in cells and elicit a cytotoxic T-lymphocyte (CTL) response against cancer cells expressing the E6 and E7 antigens, resulting in tumor cell lysis. HPV type 16 and HPV type 18 are associated with the development of certain types of cancer. Upon intramuscular delivery by electroporation of INO-9012, IL-12 is expressed and activates the immune system by promoting the activation of natural killer cells (NK cells), inducing secretion of interferon-gamma (IFN-g) and promoting CTL responses against tumor cells. This boosts the immune response and results in increased CTL-mediated tumor cell death as compared with the administration of VGX-3100 alone.","Immunologic Factor|Pharmacologic Substance"]
["C123923","DNA Vaccine VB10.16","DNA Vaccine VB10.16|VB10.16 Vaccine|VB10.16","A therapeutic DNA vaccine composed of three parts, one encodes the E6/E7 fusion protein of human papillomavirus (HPV) type 16 (HPV16), the second is a dimerization entity and the third part encodes a protein that specifically binds to antigen presenting cells (APCs), with potential immunostimulating and antineoplastic activities. Upon intramuscular administration, the DNA vaccine VB10.16 expresses HPV16 E6/7 and a protein that targets receptors on APCs. Upon binding to APCs and subsequent internalization, the APCs mature and the HPV16 E6/7 antigenic protein is presented by the APCs. This attracts and stimulates B-lymphocytes, CD4-positive T-lymphocytes and elicits a cytotoxic T-lymphocyte (CTL) response against cancer cells expressing HPV16-associated E6 and E7 oncoproteins, which result in tumor cell lysis. HPV16 E6/7, a viral antigen, plays a key role in the development of certain types of cancer.","Pharmacologic Substance"]
["C67089","DNA Vector pPRA-PSM Vaccine","DNA Plasmid Vector pPRA-PSM Vaccine|DNA Vector pPRA-PSM Vaccine|PRA-PSM-Expressing Plasmid","A cancer vaccine consisting of a DNA plasmid encoding epitopes of the human preferential antigen of melanoma (PRAME) and the prostate specific membrane antigen (PSMA) with potential immunostimulating activity. Upon direct administration of this vaccine into lymph nodes, peptides expressed by DNA plasmid vector pPRA-PSM may activate the immune system, resulting in a cytotoxic T-lymphocyte (CTL) response against PRAME- and PSMA-expressing cells. PRAME and PSMA are tumor associated antigens upregulated in a number of cancer cell types. As part of the MKC1106-PP regimen exploiting the 'prime-boost strategy', this plasmid is responsible for priming the immune response and is used in conjunction with a peptide vaccine consisting of PRAME and PSMA that boosts the immune system against PRAME- and PSMA-expressing tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C129061","DNA-dependent Protein Kinase Inhibitor VX-984","DNA-PK Inhibitor VX-984|DNA-dependent Protein Kinase Inhibitor VX-984|VX-984|VX984","An ATP-competitive inhibitor of the catalytic subunit of DNA-dependent protein kinase (DNA-PK), with potential sensitizing and enhancing activities for both chemo- and radiotherapies. Upon administration, DNA-PK inhibitor VX-984 binds to and inhibits the catalytic subunit of DNA-PK, thereby interfering with the non-homologous end joining (NHEJ) process and preventing repair of DNA double strand breaks (DSBs) caused by ionizing radiation or chemotherapeutic treatment. This increases chemo- and radiotherapy cytotoxicity and leads to enhanced tumor cell death. The enhanced ability of tumor cells to repair DSBs plays a major role in the resistance of tumor cells to chemo- and radiotherapy; DNA-PK plays a key role in the NHEJ pathway and DSB repair.","Organic Chemical|Pharmacologic Substance"]
["C120036","DNA-PK Inhibitor MSC2490484A","DNA-PK Inhibitor MSC2490484A|MSC2490484A","An orally available inhibitor of DNA-dependent protein kinase (DNA-PK), with potential antineoplastic and chemo/radiosensitizing activities. Upon oral administration, the DNA-PK inhibitor MSC2490484A binds to and inhibits the activity of DNA-PK. This inhibits the ability of tumor cells to repair damaged DNA, which may lead to a reduction in cellular proliferation of cancer cells expressing DNA-PK. DNA-PK, a serine/threonine kinase and a member of the PI3K-related kinase subfamily of protein kinases, is activated upon DNA damage and plays a key role in repairing DNA double-strand breaks (DSBs) via the DNA nonhomologous end joining (NHEJ) pathway. The enhanced ability of tumor cells to repair DSBs plays a major role in the resistance of tumor cells to chemo- and radiotherapy.","Organic Chemical|Pharmacologic Substance"]
["C97040","DNA-PK/TOR Kinase Inhibitor CC-115","CC-115|DNA-PK/TOR Kinase Inhibitor CC-115","A dual inhibitor of DNA-dependent protein kinase (DNA-PK) and mammalian target of rapamycin (mTOR), with potential antineoplastic activity. CC-115 binds to and inhibits the activity of DNA-PK and both raptor-mTOR (TOR complex 1 or TORC1) and rictor-mTOR (TOR complex 2 or TORC2), which may lead to a reduction in cellular proliferation of cancer cells expressing DNA-PK and TOR. DNA-PK, a serine/threonine kinase and a member of the PI3K-related kinase subfamily of protein kinases, is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks via the DNA nonhomologous end joining (NHEJ) pathway; mTOR, a serine/threonine kinase that is upregulated in a variety of tumors, plays an important role downstream in the PI3K/Akt/mTOR signaling pathway.","Pharmacologic Substance"]
["C114378","DNR-expressing Nasopharyngeal Carcinoma-specific Cytotoxic T-Lymphocytes","DNR NPC-specific CTLs|DNR-expressing Nasopharyngeal Carcinoma-specific Cytotoxic T-Lymphocytes","A preparation of autologous, dominant-negative receptor (DNR)-expressing nasopharyngeal carcinoma (NPC)-specific cytotoxic T-lymphocytes (CTLs), with potential antineoplastic activity. The DNR-expressing NPC-specific CTLs specifically target Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1), latent membrane proteins (LMP) and BamHIA rightward frame 1 (BARF1), and are transduced with a retroviral vector expressing DNR, a dominant-negative form of the transforming growth factor beta (TGFb) receptor, which blocks TGF-beta-mediated signaling. Upon administration, the CTLs recognize and target NPC cells, which may result in both CTL-mediated cell lysis and the inhibition of tumor cell proliferation. Tumor-expressed TGF-beta inhibits T-lymphocyte activation and expansion; resistance to TGF-beta allows for optimal CTL activity. EBV infection plays a key role in NPC tumorigenesis.","Cell|Pharmacologic Substance"]
["C1526","Docetaxel","DOCETAXEL|Docecad|Docetaxel|N-Debenzoyl-N-(tert-butoxycarbonyl)-10-deacetyltaxol|RP56976|Taxotere Injection Concentrate|Taxotere|[2aR-[2a alphaa,4beta,4a beta,6beta,9alpha,(alphaR*,betaS*),-11alpha,12alpha,12a alpha,12b alpha]]-beta-[[(1,1-dimethylethoxy)carbonyl]-amino]-alpha-hydroxybenzemepropanoic Acid 12b-(Acetyloxy)-12(benzyloxy)-2a,3,4,4a,5,6,8,10,11,12,12a,12b-dodecahydeo-4,-6,11-trihydroxy-4a,8,13,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca[3,4]benz[1,2-b]oxet-9-yl Ester|docetaxel","A semi-synthetic, second-generation taxane derived from a compound found in the European yew tree, Taxus baccata.  Docetaxel displays potent and broad antineoplastic properties; it binds to and stabilizes tubulin, thereby inhibiting microtubule disassembly which results in cell- cycle arrest at the G2/M phase and cell death.  This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and displays immunomodulatory and pro-inflammatory properties by inducing various mediators of the inflammatory response.  Docetaxel has been studied for use as a radiation-sensitizing agent. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C61734","Docetaxel Anhydrous","DOCETAXEL ANHYDROUS|Docetaxel Anhydrous","The anhydrous form of docetaxel, a semisynthetic side-chain analogue of paclitaxel with antineoplastic property. Docetaxel binds specifically to the beta-tubulin subunit of microtubules and thereby antagonizes the disassembly of the microtubule proteins. This results in the persistence of aberrant microtubule structures and results in cell-cycle arrest and subsequent cell death.","Pharmacologic Substance"]
["C78196","Docetaxel Emulsion ANX-514","ANX-514|Docetaxel Emulsion ANX-514","An injectable emulsion formulation containing the taxane docetaxel, a semisynthetic analogue of paclitaxel, with antineoplastic activity. Docetaxel binds specifically to the beta-tubulin subunit of the microtubule, stabilizing tubulin and inhibiting microtubule disassembly, which results in cell-cycle arrest at the G2/M phase and cell death. This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and induces various mediators of the inflammatory response. Docetaxel emulsion ANX-514 is formulated without polysorbate 80 or other detergents in order to reduce the incidence and severity of hypersensitivity reactions. In addition, the exclusion of polysorbate 80 in this formulation precludes foaming during the preparation process, thus facilitating preparation and administration.","Pharmacologic Substance"]
["C88322","Docetaxel Formulation CKD-810","CKD-810|Docetaxel Formulation CKD-810","An injectable formulation containing the taxane docetaxel, a semisynthetic analogue of paclitaxel, with antineoplastic activity. Docetaxel binds specifically to the beta-tubulin subunit of the microtubule, stabilizing tubulin and inhibiting microtubule disassembly, which results in cell-cycle arrest at the G2/M phase and cell death. This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and induces various mediators of the inflammatory response.","Pharmacologic Substance"]
["C102568","Docetaxel Lipid Microspheres","DLE|DT-LM|Docetaxel Lipid Emulsion|Docetaxel Lipid Microspheres","A lipid microsphere (LM)-based formulation containing the poorly water soluble taxane docetaxel, a semi-synthetic analogue of paclitaxel, with antineoplastic activity. Docetaxel binds specifically to the beta-tubulin subunit of the microtubule, stabilizing tubulin and inhibiting microtubule disassembly, which causes cell cycle arrest at the G2/M phase and leads to cell death. This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and induces various mediators of the inflammatory response. Compared to docetaxel alone, the LM formulation may enhance stability, improve efficacy and may reduce toxicity; this formulation does not contain toxic detergents needed to solubilize docetaxel which further improves its side effect profile.","Pharmacologic Substance"]
["C121539","Docetaxel-loaded Nanopharmaceutical CRLX301","CRLX301|Docetaxel-loaded Nanopharmaceutical CRLX301","A nanoparticle-based formulation containing the poorly water-soluble, second-generation taxane analog docetaxel, with antineoplastic activity. Upon intravenous administration of the docetaxel-loaded nanopharmaceutical CRLX301, the nanoparticles are able to accumulate at the tumor site due to the unique characteristics of the tumor's vasculature, while avoiding normal, healthy tissue. In turn, CRLX301 is taken up by the tumor cell via macropinocytosis. Subsequently, docetaxel is slowly released into the cytoplasm where it binds to and stabilizes the beta-subunit of tubulin, thereby stabilizing microtubules and inhibiting microtubule disassembly. This prevents mitosis and results in cell death. Compared to the administration of docetaxel alone, this formulation is able to increase docetaxel's efficacy while avoiding systemic exposure, which minimizes its toxicity.","Pharmacologic Substance"]
["C91087","Docetaxel-PNP","Docetaxel-PNP","A polymeric nanoparticle (PNP) formulation containing the taxane docetaxel, a semi-synthetic analogue of paclitaxel, with antineoplastic activity. Docetaxel binds specifically to the beta-tubulin subunit of the microtubule, stabilizing tubulin and inhibiting microtubule disassembly, which results in cell-cycle arrest at the G2/M phase, preventing cell proliferation. This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and induces various mediators of the inflammatory response. Compared to docetaxel alone, the PNP formulation may enhance stability and improve delivery.","Organic Chemical|Pharmacologic Substance"]
["C1300","Dolastatin 10","B720389K560|Dolastatin 10|Dolastatin-10|L-Valinamide, N,N-dimethyl-L-valyl-N-[2-methoxy-4-[2-[1- methoxy-2-methyl-3-oxo-3-[[2-phenyl-1-(2-thiazolyl)ethyl]amino]propyl]-1-pyrrolidinyl]-1-(1-methylpropyl)-4-oxobutyl]-N-methyl-, [2S-[1[1R*(R*),2S*],2R*[1S*,2S*,3(R*)]]]|dolastatin 10","A pentapeptide originally isolated from the marine mollusk Dolabella auricularia with potential antineoplastic activity.  Binding to tubulin, Dolastatin 10 inhibits microtubule assembly, resulting in the formation of tubulin aggregates and inhibition of mitosis.  This agent also induces tumor cell apoptosis through a mechanism involving bcl-2, an oncoprotein that is overexpressed in some cancers. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1439","Dolastatin 15","Dolastatin 15|L-Proline, 1-(1-(N-(N-(N,N-dimethyl-L-valyl)-L-valyl)-N-methyl-L-valyl)-L-prolyl)-, 1-((2,5-dihydro-3-methoxy-5-oxo-2-(phenylmethyl)-1H-pyrrol-1-yl)carbonyl)-2-methylpropyl ester, (S-(R*,R*))-","A depsipeptide originally isolated from the marine mollusk Dolabella auricularia with potential antineoplastic activity.  Less potent than the structurally-related compound dolastatin 10, dolastatin 15 binds weakly to tubulin and blocks microtubule assembly, thereby inhibiting mitosis.  Dolastatin 15 also induces tumor cell apoptosis through a mechanism involving bcl-2, an oncoprotein that is overexpressed in some cancers. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C118294","Donafenib","Donafenib","An orally available multikinase inhibitor that targets Raf kinase and various receptor tyrosine kinases (RTKs), with potential antineoplastic activity. Upon oral administration, donafenib binds to and blocks the activity of Raf kinase, and inhibits Raf-mediated signal transduction pathways. This inhibits cell proliferation in Raf-expressing tumor cells. In addition, this agent may inhibit unidentified RTKs, and thus may further block tumor cell proliferation in susceptible tumor cells. Raf, a serine/threonine protein kinase, plays a key role in the Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway. Deregulation of this pathway often results in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C91712","Donor Lymphocytes","Donor Lymphocytes","A population of lymphocytes from the blood of a donor and administered to a patient who has already received a stem cell transplant from the same donor (Allogeneic Hematopoietic Stem Cell Transplantation). The donor lymphocytes may be able to boost the patient's immune system and kill remaining cancer cells.","Cell|Pharmacologic Substance"]
["C123817","Donor-derived WT1/PRAME/NY-ESO-1/Survivin-specific T-lymphocytes","Donor-derived WT1/PRAME/NY-ESO-1/Survivin-specific T-lymphocytes|Multi-TAA Specific T Cells","Allogeneic T-lymphocytes specifically reactive to the tumor-associated antigens (TAAs) human Wilms tumor protein-1 (WT1), Preferentially Expressed Antigen in Melanoma (PRAME), the cancer-testis antigen NY-ESO-1, and survivin, with potential antineoplastic activity. Donor derived T-cells are mixed, ex vivo, with protein fragments derived from the TAAs WT1, PRAME, NY-ESO-1, and survivin. Upon intravenous administration, the donor-derived WT1/PRAME/NY-ESO-1/Survivin-specific T-lymphocytes recognize and kill cancer cells expressing these TAAs. WT1, NY-ESO-1, PRAME, and survivin, are expressed on certain tumor cell types and play key role in tumor cell proliferation and survival.","Cell|Pharmacologic Substance"]
["C88345","Dopamine-Somatostatin Chimeric Molecule BIM-23A760","BIM-23A760|Dopamine-Somatostatin Chimeric Molecule BIM-23A760","A chimeric molecule directed against dopamine and somatostatin receptors with potential antineoplastic activity. Combining two pharmacological moieties, a somatostatin analogue and a dopamine agonist, dopamine-somatostatin chimeric molecule BIM-23A760 binds with high affinity to dopamine D2 receptor (D2R) and somatostatin receptor subtype 2 (SSTR2), and to a lesser extent to somatostatin receptor subtype 5 (SSTR5). This agent appears to exert its effect mainly by binding to D2R to activate the ERK1/2 and p38 MAPK pathways, thus inducing apoptosis and inhibiting cellular proliferation in non-functioning pituitary adenoma (NFPA) and neuroendocrine tumors. By binding to SSTR2, this agent may inhibit the secretion of growth hormone (GH) by the pituitary gland.","Pharmacologic Substance"]
["C103179","DOT1L Inhibitor EPZ-5676","DOT1L Inhibitor EPZ-5676|EPZ-5676","A small molecule inhibitor of histone methyltransferase with potential antineoplastic activity. Upon intravenous administration, EPZ-5676 specifically blocks the activity of the histone lysine-methyltransferase DOT1L, thereby inhibiting the methylation of nucleosomal histone H3 on lysine 79 (H3K79) that is bound to the mixed lineage leukemia (MLL) fusion protein which targets genes and blocks the expression of leukemogenic genes. This eventually leads to an induction of apoptosis in the leukemic cells bearing the MLL gene translocations. DOT1L, a non-SET domain-containing histone methyltransferase, specifically methylates H3K79 and plays a key role in normal cell differentiation and in the development of leukemia with MLL gene rearrangement on chromosome 11 and promotes the expression of leukemia-causing genes.","Pharmacologic Substance"]
["C91708","DOTAP:Cholesterol-Fus1 Liposome Complex","DOTAP:Cholesterol-Fus1 Liposome Complex|INGN 401","A formulation composed of DOTAP:cholesterol liposomal nanoparticles complexed with a plasmid expression cassette encoding human FUS1 protein, with potential antineoplastic activity. Upon administration, DOTAP:chol-Fus1 liposome complex accumulates mainly in the lungs and particularly in cancer cells. Upon transfer of the Fus1 gene into tumor cells, the expression of Fus1 may induce tumor cell apoptosis and suppress tumor cell proliferation. Fus1, a potent tumor-suppressor protein, is present in normal, healthy cells but often absent in certain cancer cells. DOTAP:cholesterol liposome is composed of cationic lipid dioleoyl-trimethylammonium propane (DOTAP) and cholesterol at a molar ratio of 1:1.","Pharmacologic Substance"]
["C76199","Dovitinib","DOVITINIB|Dovitinib","A benzimidazole-quinolinone compound and receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Dovitinib binds to and inhibits the phosphorylation of type III-V RTKs, such as vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) that promote tumor cell proliferation and survival in certain cancer cells. In addition, this agent also inhibits other members of the RTK superfamily, including fibroblast growth factor receptor 1 and 3, FMS-like tyrosine kinase 3, stem cell factor receptor (c-KIT), and colony stimulating factor receptor 1. This may further lead to a reduction of cellular proliferation and angiogenesis, and an induction of tumor cell apoptosis.","Pharmacologic Substance"]
["C62435","Dovitinib Lactate","4-Amino-5-fluoro-3-(6-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one mono 2-hydroxypropanoate Hydrate|CHIR-258|DOVITINIB LACTATE|Dovitinib Lactate|RTK Inhibitor TKI258|TKI258","The orally bioavailable lactate salt of a benzimidazole-quinolinone compound with potential antineoplastic activity. Dovitinib strongly binds to fibroblast growth factor receptor 3 (FGFR3) and inhibits its phosphorylation, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell death. In addition, this agent may inhibit other members of the RTK superfamily, including the vascular endothelial growth factor receptor; fibroblast growth factor receptor 1; platelet-derived growth factor receptor type 3; FMS-like tyrosine kinase 3; stem cell factor receptor (c-KIT); and colony-stimulating factor receptor 1; this may result in an additional reduction in cellular proliferation and angiogenesis, and the induction of tumor cell apoptosis. The activation of FGFR3 is associated with cell proliferation and survival in certain cancer cell types.","Pharmacologic Substance"]
["C61737","Doxazosin","DOXAZOSIN|Doxazosin","A quinazoline with antihypertensive and antineoplastic properties. Doxazosin is an alpha-adrenergic antagonist that selectively inhibits alpha-1 adrenergic receptors. Blockages of the alpha-1 adrenergic action on the vascular smooth muscles lead to a decrease in vascular resistance and antihypertensive activity. This agent also shows high affinity to alpha-1c adrenoceptor, the predominant functional type in the prostate, which may partially attribute to its effect in treatment of benign prostatic hyperplasia. Furthermore, doxazosin induces apoptosis in prostate cancer cells mediated through inhibition of protein kinase B (PKB)/Akt-signaling death receptor regulatory pathway.","Pharmacologic Substance"]
["C2645","Doxercalciferol","(1alpha,3beta,5Z,7E,22E)-9,10-Secoergosta-5,7,10(19),22-tetraene-1,3-diol|1-Alpha-Hydroxyvitamin D2|DOXERCALCIFEROL|Doxercalciferol|Hectorol|doxercalciferol","A synthetic analog of vitamin D with potential antineoplastic activity. In the liver, doxercalciferol is converted to its biologically active vitamin D metabolites, which control the intestinal absorption of dietary calcium, the tubular reabsorption of calcium by the kidney and, in conjunction with parathyroid hormone (PTH), the mobilization of calcium from the skeleton. Through interaction with specific receptor proteins in target tissues, these vitamin D metabolites act directly on osteoblasts to stimulate skeletal growth, and on the parathyroid glands to suppress PTH synthesis and secretion. This agent has also been shown to inhibit the growth of retinoblastomas, and may exhibit some antiproliferative activity against prostate cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C978","Doxifluridine","5'-Deoxy-5-fluorouridine|5-DFUR|DOXIFLURIDINE|Doxifluridine","A fluoropyrimidine derivative and oral prodrug of the antineoplastic agent 5-fluorouracil (5-FU) with antitumor activity. Doxifluridine, designed to circumvent the rapid degradation of 5-FU by dihydropyrimidine dehydrogenase in the gut wall, is converted into 5-FU in the presence of pyrimidine nucleoside phosphorylase. 5-FU interferes with DNA synthesis and subsequent cell division by reducing normal thymidine production and interferes with RNA transcription by competing with uridine triphosphate for incorporation into the RNA strand.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C456","Doxorubicin","(8S-cis)-10-[(3-Amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroacetyl)-1-methoxy-5,12-naphthacenedione|(8S-cis)-10-[(3-Amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-5,12-naphthacenedione|14-Hydroxydaunomycin|Adriablastin|DOXORUBICIN|Doxorubicin|Hydroxyl Daunorubicin|Hydroxyldaunorubicin|doxorubicin","An anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.","Pharmacologic Substance"]
["C1326","Doxorubicin Hydrochloride","14-Hydroxydaunorubicin Hydrochloride|3-Hydroxyacetyldaunorubicin Hydrochloride|5,12-Naphthacenedione, 10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8, 9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-, hydrochloride, (8S-cis)- (9CI)|5,12-Naphthacenedione, 10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-,hydrochloride, (8S-cis)-(9CI)|ADM|ADRIAMYCIN, HYDROCHLORIDE|Adriacin|Adriamycin Hydrochloride|Adriamycin PFS|Adriamycin RDF|Adriamycin hydrochloride|Adriamycin|Adriamycine|Adriblastina|Adriblastine|Adrimedac|Chloridrato de Doxorrubicina|DOX|DOXO-CELL|DOXORUBICIN HYDROCHLORIDE|Doxolem|Doxorubicin Hydrochloride|Doxorubicin hydrochloride|Doxorubicin.HCl|Doxorubin|FI 106|FI-106|Farmiblastina|L-Lyxo-hexopyranoside, 3b-glycol-1,2,3,4,6,11-hexahydro-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1a-naphthacenyl 3-amino-2,3,6-trideoxy-alpha-, hydrochloride|Rubex|doxorubicin hydrochloride|hydroxydaunorubicin","The hydrochloride salt of doxorubicin, an anthracycline antibiotic with antineoplastic activity. Doxorubicin, isolated from the bacterium Streptomyces peucetius var. caesius, is the hydroxylated congener of daunorubicin. Doxorubicin intercalates between base pairs in the DNA helix, thereby preventing DNA replication and ultimately inhibiting protein synthesis. Additionally, doxorubicin inhibits topoisomerase II which results in an increased and stabilized cleavable enzyme-DNA linked complex during DNA replication and subsequently prevents the ligation of the nucleotide strand after double-strand breakage. Doxorubicin also forms oxygen free radicals resulting in cytotoxicity secondary to lipid peroxidation of cell membrane lipids; the formation of oxygen free radicals also contributes to the toxicity of the anthracycline antibiotics, namely the cardiac and cutaneous vascular effects.","Pharmacologic Substance"]
["C82419","Doxorubicin-Eluting Beads","Doxorubicin-Eluting Beads","A drug-device combination product consisting of small polymeric beads impregnated with the anthracycline antibiotic doxorubicin with potential antineoplastic activity. The beads consist of polyvinyl alcohol (PVA) microspheres modified with sulfonic acid groups and loaded with doxorubicin. During transarterial chemoembolization (TACE), doxorubicin-eluting beads embolize to the tumor vasculature and release cytotoxic doxorubicin, which may result in both ischemic necrosis of tumor tissue due to mechanical blockage of the tumor vasculature and doxorubicin-mediated inhibition of tumor cell proliferation.","Pharmacologic Substance"]
["C1366","Doxorubicin-HPMA Conjugate","Doxorubicin-HPMA Conjugate|Doxorubicin-HPMA Copolymer Conjugate|Doxorubicin-HPMA|HPMA-Doxorubicin|P(GFLG)-ADR|PK1","A copolymer conjugate of the antineoplastic anthracycline doxorubicin and the water-soluble polymer N-(2-hydroxypropyl) methacrylamide (HPMA). Doxorubicin, an intercalator and a topoisomerase II inhibitor, prevents DNA replication and ultimately inhibits protein synthesis. This agent also generates oxygen free radicals, resulting in cytotoxic lipid peroxidation of cell membrane lipid. HPMA conjugation enhances the permeability and retention of this agent within the tumor vasculature. Poorly cleared by the lymphatic system, this formulation undergoes increased cleavage by tumor cell lysosomal proteinases, resulting in increased, sustained intracellular concentrations of free doxorubicin. Compared to other doxorubicin-containing formulations, this formulation may exhibit an improved toxicity profile due to the lower concentrations of free doxorubicin to which non-malignant tissues are exposed.","Pharmacologic Substance"]
["C128897","Doxorubicin-loaded EGFR-targeting Nanocells","Doxorubicin-loaded EGFR-targeting Nanocell|Doxorubicin-loaded EGFR-targeting Nanocells|EGFR (Vectibix Sequence)-Targeted EnGeneIC Dream Vectors Containing Doxorubicin|EGFR(V)-EDV-Dox|EGFR-targeted EnGeneIC Dream Vectors Containing Doxorubicin","A nanocell formulation targeting the epidermal growth factor receptor (EGFR) using bispecific antibodies (bsAb) against EGFR and containing the antineoplastic anthracycline antibiotic doxorubicin, with potential antineoplastic activity. Upon administration of doxorubicin-loaded EGFR-targeting nanocells, the nanocells are stable in the bloodstream and the anti-EGFR bsAb moiety targets and binds to EGFR-expressing tumor cells. Upon binding, the nanocell allows for specific delivery of doxorubicin to tumor cells overexpressing EGFR. Upon endocytosis by the tumor cells, the nanocell is broken down and releases doxorubicin, which intercalates into DNA and interferes with topoisomerase II activity, thereby inhibiting DNA replication and RNA synthesis. Compared to doxorubicin alone or liposomal doxorubicin, targeted delivery of doxorubicin improves efficacy while lowering the toxicity profile. EGFR, a tyrosine kinase receptor, is overexpressed in many cancer cell types. The nanocell is a bacterially derived nanosphere; the bacterial components are unlikely to induce an immune response in the immunosuppressed tumor microenvironment.","Pharmacologic Substance"]
["C2644","Doxorubicin-Magnetic Targeted Carrier Complex","DOX-MTC|Doxorubicin-Magnetic Targeted Carrier Complex|MTC-DOX","A formulation of the anthracycline antibiotic doxorubicin in which doxorubicin is bound to microscopic beads of activated carbon and iron as a magnetic-targeted carrier (MTC). Doxorubicin, an intercalator and a topoisomerase II inhibitor, prevents DNA replication and ultimately inhibits protein synthesis. This agent also generates oxygen free radicals, resulting in cytotoxic lipid peroxidation of cell membrane lipids. Guided by the placement of a magnet on the body surface overlying a tumor site, the doxorubicin-MTC complex delivers doxorubicin directly to the tumor site, thereby targeting and prolonging the duration of doxorubicin-mediated cytotoxicity to the tumor bed while minimizing systemic toxicity.","Pharmacologic Substance"]
["C120213","DPT/BCG/Measles/Serratia/Pneumococcus Vaccine","DPT/BCG/Measles/Serratia/Pneumococcus Vaccine|G250 Peptide Vaccine","A proprietary lipid emulsion containing five vaccines: diphtheria, pertussis, tetanus (DPT), Bacille Calmette-Guerin (BCG), measles, Serratia marcescens and pneumococcal, with potential immunostimulating activity. Subcutaneous administration of the DPT/BCG/measles/Serratia/pneumococcus vaccine activates the immune system and may both abrogate tumor-induced immune tolerance and induce an antitumor immune response, which may eradicate the tumor.","Pharmacologic Substance"]
["C120214","DPT/Typhoid/Staphylococcus aureus/Paratyphoid A/Paratyphoid B Vaccine","DPT/Typhoid/Staphylococcus aureus/Paratyphoid A/Paratyphoid B Vaccine","A proprietary lipid emulsion containing five vaccines: diphtheria, pertussis, tetanus (DPT), typhoid, Staphylococcus aureus, paratyphoid A and paratyphoid B, with potential immunostimulating activity. Subcutaneous administration of the DPT/typhoid/Staphylococcus aureus/paratyphoid A/paratyphoid B vaccine activates the immune system and may both abrogate tumor-induced immune tolerance and induce an antitumor immune response, which may eradicate the tumor.","Pharmacologic Substance"]
["C116886","DR5-targeting Tetrameric Nanobody Agonist TAS266","DR5-targeting Tetrameric Nanobody Agonist TAS266|TAS266|Tetrameric Nanobody Agonist-targeting death receptor 5 TAS266","An agonistic tetravalent nanobody, in which the four single, high affinity heavy chain variable domain (VHH) antibodies are separated by a peptide linker, targeting death receptor type 5 (DR5), with potential antineoplastic activity. Upon administration, DR5-targeting tetrameric nanobody agonist TAS266, with its four DR5-specific single-chain antibodies, specifically binds to and activates DR5 receptors. This results in the activation of caspase cascades and induction of apoptosis in DR5-expressing tumor cells. DR5, a cell surface receptor and member of the tumor necrosis factor (TNF)-receptor superfamily, triggers apoptosis. Compared to certain anti-DR5 antibody agonists, TAS266 shows increased receptor activation.","Pharmacologic Substance"]
["C1077","Dromostanolone Propionate","2 Alpha-Methyldihydrotestosterone Propionate|2-Alpha-Methyldihydrotestosterone Propionate|2.alpha.-Methyldihydrotestosterone propionate|Compound 32379|DROMOSTANOLONE PROPIONATE|Drolban|Dromostanolone Propionate|Drostanolone Propionate|Drostanolone propionate|Emdisterone|Masterid|Masteril|Masteron|Masterone|Permastril","The propionate salt form of dromostanolone, a synthetic anabolic steroid related to dihydrotestosterone that has antiestrogenic effects.  Dromostanolone inhibits the growth of estrogen receptor-presenting breast cancers; its virilizing effects limit its clinical usefulness. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C64769","DT(388)IL3 Fusion Protein SL-401","DT(388)-IL3 Fusion Protein|DT(388)IL3 Fusion Protein SL-401|DT388IL3 fusion protein|Diphtheria Toxin(388)-Interleukin-3 Fusion Protein|IL3R-targeting Fusion Protein SL-401|SL-401","A recombinant protein consisting of human interleukin 3 (IL3) fused to the first 388 amino acids of diphtheria toxin [DT(388)] (DT388IL3) with potential antineoplastic activity. Upon intravenous administration, the IL3 moiety of the DT(388)IL3 fusion protein SL-401 binds to IL3 receptors on cells expressing the receptor. Subsequently, the DT(388) toxin moiety, which contains both translocation and catalytic domains, is transported across the cell membrane via endocytosis. Within the cytosol, the catalytic domain of the toxin both catalyzes the ADP-ribosylation of, and inactivates, translation elongation factor 2 (EF-2), which results in the inhibition of translation during protein synthesis. IL3 may be overexpressed by a variety of cancers, including blastic plasmacytoid dendritic cell neoplasm and acute myeloid leukemia (AML).","Organic Chemical|Pharmacologic Substance"]
["C64845","DTA-H19 Plasmid","DTA-H19 Plasmid|DTA-H19|Diphtheria Toxin A-H19 Plasmid","A plasmid DNA encoding the A chain of the diphtheria toxin (DT-A) driven by the transcriptional regulatory sequences of human H19, with potential antineoplastic activity. Because the expression of DT-A is under the control of H19 promotor elements, DT-A is selectively expressed in tumor cells capable of turning on H-19. DT-A catalyzes ADP-ribosylation of translation elongation factor 2 (EF-2), resulting in the inhibition of protein synthesis and apoptosis. In addition, DT-A protein released from lysed cells cannot enter and kill neighboring cells because of the absence of the DT-B chain, further enhancing the selective cytotoxicity of this agent. Human H19 is a paternally-imprinted, oncofetal gene encoding an RNA product; it acts as a riboregulator in gene expression and is found at substantial levels in different human tumor cell types while its expression in normal adult tissue is limited.","Gene or Genome|Organic Chemical|Pharmacologic Substance"]
["C74043","Dual IGF-1R/InsR Inhibitor BMS-754807","BMS-754807|Dual IGF-1R/InsR Inhibitor BMS-754807","An oral small molecule inhibitor of insulin-like growth factor 1 receptor (IGF-1R) and insulin receptor (InsR) tyrosine kinases with potential antineoplastic activity. Dual IGF-IR/InsR inhibitor BMS-754807 binds reversibly to and inhibits the activities of IGF-1R and InsR, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. IGF-1R and InsR tyrosine kinases, overexpressed in a variety of human cancers, play significant roles in mitogenesis, angiogenesis, and tumor cell survival.","Pharmacologic Substance"]
["C91731","Dual PI3 Kinase/mTOR Inhibitor GDC-0980","Dual PI3 Kinase/mTOR Inhibitor GDC-0980|GDC-0980","An orally available agent targeting phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinase in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor GDC-0980 inhibits both PI3K kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition of cancer cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion.","Pharmacologic Substance"]
["C116750","Dual Variable Domain Immunoglobulin ABT-165","ABT-165|DVD-Ig ABT-165|Dual Variable Domain Immunoglobulin ABT-165","A dual-specific, tetravalent immunoglobulin (Ig) G-like molecule targeting two as of yet not publicly known targets, with potential antineoplastic activity. The target-binding variable domains of two monoclonal antibodies, which are not publicly known, are combined, via linkers, to create the tetravalent, dual-targeting single agent ABT-165. Upon administration of dual variable domain immunoglobulin (DVD-Ig) ABT-165, the target-binding variable domains specifically recognize and simultaneously bind to their two antigens expressed on tumor cells. This may both prevent antigen-mediated signaling and lead to an inhibition of cellular proliferation in susceptible tumor cells. The antigen targets are overexpressed on certain tumor cell types. The DVD-Ig may have enhanced physicochemical and pharmacokinetic properties as compared to their antibody counterparts.","Pharmacologic Substance"]
["C1062","Duborimycin","13-Hydroxydaunomycin|5,12-Naphthacenedione, 10-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8, 9,10-tetrahydro-6,8,11-trihydroxy-8-(1-hydroxyethyl)-1-methoxy-, (8S-cis)-, hydrochloride|Daunomycinol HCl|Daunomycinol|Daunorubicineal|Daunorubicinol|Duborimycin Hydrochloride|Duborimycin|Duborimycine, Hydrochloride|Duborimycine","An anthracycline antineoplastic antibiotic with therapeutic effects similar to those of doxorubicin.  Duborimycin exhibits cytotoxic activity through topoisomerase-mediated interaction with DNA, thereby inhibiting DNA replication and repair and RNA and protein synthesis. (NCI04)","Antibiotic|Organic Chemical"]
["C1685","Dulanermin","114-281-protein TRAIL|AMG 951|APO2L/TRAIL|DULANERMIN|Dulanermin|RG3639|rTRAIL","A recombinant human soluble protein corresponding to amino acids 114-281 of the Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (RhApo2L/TRAIL) with potential antineoplastic activity. Dulanermin binds to and activates TRAIL receptors 1 and 2 (TRAIL-R1/R2), which may activate caspases and induce p53-independent apoptosis in TRAIL-R1/R2-expressing tumor cells. The pro-apoptotic cell surface receptors TRAIL-R1 and -R2, also known as DR4 (death receptor 4) and DR5 (death receptor 5), are members of the TNF receptor family and are overexpressed by a variety of cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116628","Duligotuzumab","DULIGOTUMAB|Duligotuzumab|MEHD 7945A|MEHD-7945A|MEHD7945A|RG 7597","An immunoglobulin (Ig) G1 monoclonal antibody directed against both human epidermal growth factor receptor 3 (HER3 or ERBB3) and human epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Duligotuzumab binds to both EGFR and HER3 and inhibits their activation. This may prevent EGFR/HER3-mediated signaling and inhibit EGFR/HER3-dependent tumor cell proliferation. In addition, MEHD7945A induces antibody-dependent cell-mediated cytotoxicity (ADCC) against EGR/HER3-expressing tumor cells. EGFR and HER3, members of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, are frequently overexpressed in tumors; their expression is associated with both poor prognosis and drug resistance.","Pharmacologic Substance"]
["C103194","Durvalumab","DURVALUMAB|Durvalumab|Immunoglobulin G1, Anti-(Human Protein B7-H1) (Human Monoclonal MEDI4736 Heavy Chain), Disulfide with Human Monoclonal MEDI4736 Kappa-chain, Dimer|MEDI-4736|MEDI4736","A monoclonal antibody directed against B7H1 (B7 homolog 1; programmed cell death ligand 1) with potential immunostimulating activity. Upon intravenous administration, durvalumab binds to the cell surface antigen B7H1, thereby blocking B7H1 signaling. This may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against B7H1-expressing tumor cells. B7H1, a member of the B7 protein superfamily and a negative regulator of cytokine synthesis, is overexpressed on certain tumor cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116885","dUTPase/DPD Inhibitor TAS-114","TAS-114|dUTPase/DPD Inhibitor TAS-114","An orally bioavailable inhibitor of both deoxyuridine triphosphatase (dUTPase) and dihydropyrimidine dehydrogenase (DPD), with potential antineoplastic adjuvant activity. Upon oral administration in combination with a prodrug of the pyrimidine antagonist 5-fluorouracil (5-FU), TAS-114 inhibits (DPD), the liver enzyme responsible for rapid catabolism of 5-FU into inactive metabolites. This prevents first-pass metabolism of 5-FU, allowing oral administration of the 5-FU prodrug and increasing the efficacy of 5-FU. In addition, as a dUTPase inhibitor, TAS-114 enhances the antitumor activity of 5-FU by preventing the hydrolysis and breakdown of 5-fluoro-deoxyuridine triphosphate (FdUTP) and deoxyuridine triphosphate (dUTP), which are active metabolites of 5-FU. This promotes DNA polymerase-dependent incorporation of these antimetabolites into DNA and leads to DNA damage and tumor cell death. Co-administration with TAS-114 allows lower dosing of 5-FU prodrugs, which decreases 5-FU-related toxicity, while maintaining therapeutic levels of 5-FU at the tumor site.","Pharmacologic Substance"]
["C1928","Dynemicin","Dynemicin","An antitumor antibiotic of the enediyne class. It has demonstrated high DNA cleavage activity in the presence of NADPH, antimicrobial and tumor growth-inhibiting properties. Dynemicin recognizes and cleaves conformationally flexible regions of DNA. It attacks bases at 3'-side of purine residues such as 5'-AG, 5'-AT, and 5'-GC sequences. (NCI)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C1079","Dynemicin A","Dynemicin A","An enediyne antineoplastic antibiotic hybrid containing an anthraquinone moiety isolated from the bacterium Micromonospora chersina.  The anthraquinone moiety intercalates into DNA and the benzene diradical intermediate of the enediyne core binds to the minor groove of DNA, resulting in double-strand breaks in DNA, inhibition of DNA replication and apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C2420","E1A Lipid Complex","E1A Lipid Complex|E1A-Lipid Complex|Lipid Complex, E1A","E1A gene combined with lipids that serve as a means to deliver the E1A gene into the cancer cells. The combination of lipids and the E1A gene is called the E1A Lipid Complex.","Pharmacologic Substance"]
["C64767","E2F1 Pathway Activator ARQ 171","ARQ 171|E2F1 Pathway Activator ARQ 171","A second-generation E2F1 pathway activator with potential antineoplastic activity. ARQ 171 induces the expression of E2F transcription factor 1, thereby activating the E2F1-mediated checkpoint process. E2F1, down-regulated in cancer cells, regulates expression of genes involved in the cell cycle progression from G1 into S phase. The G1/S checkpoint process selectively induces cell cycle arrest in cancer cells with irreparable DNA damages and triggers subsequent apoptosis, while allowing cell division to proceed in cells without or with minor reparable DNA damage. As a result, this agent exerts anti-tumor activity through checkpoint activation independent of p53 mediated tumor suppression.","Organic Chemical|Pharmacologic Substance"]
["C61501","E7820","E7820","A small molecule and aromatic sulfonamide derivative with potential antiangiogenic and antitumor activities. E7820 inhibits angiogenesis by suppressing integrin alpha 2, a cell adhesion molecule expressed on endothelial cells. Inhibition of integrin alpha 2 leads to an inhibition of cell-cell interactions, endothelial cell-matrix interactions, vascular endothelial cell proliferation and angiogenesis.","Pharmacologic Substance"]
["C462","Echinomycin","BRN 0078671|Bis-Quinoline Analogue|Echinomycin A|Echinomycin|Levomycin|N,N'-(2,4,12,15,17,25-hexamethyl-11,24-bis(1-methylethyl)-27-(methylthio)-3,6,10,13,16,19,23,26-octaoxo-9,22-dioxa-28-thia-2,5,12,15,18,25-hexaazabicyclo(12.12.3)nonacosane-7,20-diyl)bis(2-quinoxalinecarboxamide)|Quinomycin A|SK 302B","A polypeptide quinoxaline antineoplastic antibiotic isolated from the bacterium Streptomyces echinatus.  Echinomycin intercalates into DNA at two locations simultaneously in a sequence-specific fashion, thereby inhibiting DNA replication and RNA synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C61095","Ecromeximab","Chimeric Monoclonal Antibody KW-2871|ECROMEXIMAB|Ecromeximab|Immunoglobulin G1, Anti-(Gd3 Ganglioside) (Human-Mouse Monoclonal Km871 Gamma-1-Chain), Disulfide with Human-Mouse Monoclonal KM871 Kappa-Chain, Dimer|KM871|KW-2871|Monoclonal Antibody KW-2871","A low-fucose, human-mouse chimeric IgG1 monoclonal antibody with potential antineoplastic activity targeting at the ganglioside GD3, a surface antigen expressed on many malignant melanoma cells. Monoclonal antibody KW-2871 binds to GD3-positive cells, thereby initiating antibody-dependent cytotoxicity against GD3-positive cells. This agent is prepared by fusing murine immunoglobulin (Ig) light and heavy variable regions derived from the murine IgG3 antibody KM-641 to a human constant (Fc) region. The low fucose content of the oligosaccharide side chains of this antibody may enhance binding of the antibody Fc region to lymphocyte Fc receptors.","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C958","Edatrexate","10-EDAM|10-EdAM|10-Ethyl-10-deaza-aminopterin|CGP-30694|EDAM|EDATREXATE|Edatrexate|N-[4-[1-[(2, 4-Diamino-6-pteridinyl)-methyl]propyl]benzoyl]-L-glutamic acid|N-[4-[1-[(2,4-Diamino-6-pteridinyl)-methyl]propyl]benzoyl]-L-glutamic Acid|edatrexate","A polyglutamatable folate antagonist analogue of methotrexate with antineoplastic activity. Edatrexate inhibits dihydrofolate reductase, thereby increasing cellular levels of polyglutamates, inhibiting thymidylate synthase and glycinamide ribonucleotide formyl transferase, impairing synthesis of purine nucleotides and amino acids, and resulting in tumor cell death. Edatrexate may overcome tumor resistance to methotrexate, which loses its activity after it is polyglutamated. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C956","Edelfosine","1-O-Octadecyl-2-O-methyl-rac-glycero-3-phosphocholine|1-Octadecyl-2-methoxy-rac-glycero-3-phosphocholine|EDELFOSINE|ET-18-OCH3|Edelfosine|Edelfosinum|Et-18-OCH3","A synthetic analog of lysophosphatidylcholine, an ether lipid, possessing anti-leishmanial and antineoplastic activity.  The mechanism of action for edelfosine has not been fully elucidated.  Targeting cellular membranes, edelfosine modulates membrane permeability, membrane lipid composition, and phospholipid metabolism.  Edelfosine also inhibits the phosphatidylinositol 3 kinase (PI3K)-AKT/PKB survival pathway, possibly activating the pro-apoptotic stress-activated protein kinase (SAPK/JNK) pathways, thereby inducing apoptosis.  In addition, this agent inhibits protein kinase C, intracellular activation of the Fas/CD95 receptor, and intracellular acidification.  Anti-leishmanial activity may be due to inhibition of a glycosomal alkyl-specific-acylCoA acyltransferase. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C2665","Edotecarin","6-N-(1-hydroxymethyla-2-hydroxy)ethylamino-12,13-dihydro-13-(beta-D-gluco pyranosyl)-5H-indolo[2,3-a]-pyrrolol[3,4-c]-carbazole-5,7(6H)-dione|EDOTECARIN|Edotecarin|J-107088|edotecarin","A synthetic indolocarbazole with antineoplastic activity. Edotecarin inhibits the enzyme topoisomerase I through stabilization of the DNA-enzyme complex and enhanced single-strand DNA cleavage, resulting in inhibition of DNA replication and decreased tumor cell proliferation. (NCI04)","Pharmacologic Substance"]
["C1554","Edrecolomab","EDRECOLOMAB|Edrecolomab|Immunoglobulin G2A (Mouse Monoclonal 17-1A Gamma-Chain Anti-Human Colon Cancer Tumor-Associated Antigen), Disulfide With Mouse Monoclonal 17-1A Light Chain, Dimer|MOAB 17-1A|Monoclonal Antibody 17-1A|Panorex|edrecolomab","A murine monoclonal IgG2a antibody to tumor-associated epithelial cell adhesion molecule (EpCAM, or 17-1A) antigen. Edrecolomab attaches to EpCAM, a human cell surface glycoprotein that is found on normal epithelial cells and some tumor cells, such as those of colon and breast carcinomas. Upon binding, this agent recruits the body's immune effector cells, which may exhibit antitumor cytotoxicity. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C83819","Efatutazone","2,4-Thiazolidinedione, 5-((4-((6-(4-Amino-3,5-Dimethylphenoxy)-1-Methyl-1H-Benzimidazol-2-yl)Methoxy)Phenyl)Methyl)-|EFATUTAZONE|Efatutazone|Inolitazone|Rac-5-((4-((6-(4-Amino-3,5-Dimethylphenoxy)-1-Methyl-1H-Benzimidazol-2-yl)Methoxy)Phenyl)Methyl)-1,3-Thiazolidine-2,4-Dione","An orally bioavailable thiazolidinedione and an agonist of peroxisome proliferator-activated receptor gamma (PPAR-gamma) with potential antineoplastic activity. Efatutazone binds to and activates PPAR-gamma thus inducing cell differentiation and apoptosis, leading to a reduction in cellular proliferation. PPAR-gamma is a nuclear hormone receptor and a ligand-activated transcription factor that controls the expression of genes involved in macromolecule metabolism and cell differentiation, specifically adipocyte differentiation.","Pharmacologic Substance"]
["C64764","Efatutazone Dihydrochloride","2,4-thiazolidinedione, 5-((4-((6-(4-amino-3,5-dimethylphenoxy)-1-methyl-1h-benzimidazol-2-yl)methoxy)phenyl)methyl)-, Hydrochloride (1:2)|CS-7017|EFATUTAZONE DIHYDROCHLORIDE|Efatutazone Dihydrochloride|Inolitazone Dihydrochloride","The dihydrochloride salt of efatutazone, an orally bioavailable agonist of peroxisome proliferator-activated receptor gamma (PPAR-gamma) with potential antineoplastic activity. Efatutazone binds to and activates PPAR-gamma, a nuclear hormone receptor and a ligand-activated transcription factor controling gene expression involved in macromolecule metabolism and cell differentiation, specifically adipocyte differentiation. Mediated through activation of PPAR-gamma, this agent is capable of inducing cell differentiation and apoptosis, thereby leading to a reduction in cellular proliferation.","Organic Chemical|Pharmacologic Substance"]
["C226","Eflornithine","2-(Difluoromethyl)-DL-ornithine|2-Difluoromethylornithine|Alpha-Difluoromethylornithine|D,L-alpha-Difluoromethylornithine|DFMO|Difluoromethylornithine|Difluromethylornithine|EFLORNITHINE|Eflornithine|difluoromethylornithine|eflornithine","A difluoromethylated ornithine compound with antineoplastic activity.  Eflornithine irreversibly inhibits ornithine decarboxylase, an enzyme required for polyamine biosynthesis, thereby inhibiting the formation and proliferation of tumor cells. Polyamines are involved in nucleosome oligomerization and DNA conformation, creating a chromatin environment that stimulates neoplastic transformation of cells. This agent has been shown to induce apoptosis in leiomyoma cells. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1579","Eflornithine Hydrochloride","2-(Difluoromethyl)-dl-ornithine Hydrochloride, Monohydrate|2-Difluoromethyl-dl-ornithine, Monohydrochloride, Monohydrate|EFLORNITHINE HYDROCHLORIDE|Eflornithine Hydrochloride|Eflornithine hydrochloride|Eflornithine.HCl|MDL 71782|Ornidyl|RMI-71782|Vaniqa|alpha-Difluoromethylornithine hydrochloride","The hydrochloride form of eflornithine, a difluoromethylated ornithine compound with antineoplastic activity.  Eflornithine irreversibly inhibits ornithine decarboxylase, an enzyme required for polyamine biosynthesis, thereby inhibiting the formation and proliferation of tumor cells. Polyamines are involved in nucleosome oligomerization and DNA conformation, creating a chromatin environment that stimulates neoplastic transformation of cells. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C90557","Eg5 Kinesin-Related Motor Protein Inhibitor 4SC-205","Eg5 Kinesin Inhibitor 4SC-205|Eg5 Kinesin-Related Motor Protein Inhibitor 4SC-205|SC-205","A small-molecule inhibitor of the human kinesin-related motor protein Eg5 with potential antineoplastic activity. Eg5 kinesin-related motor protein inhibitor 4SC-205 selectively inhibits the activity of Eg5, which may result in mitotic disruption, apoptosis and cell death. The ATP-dependent Eg5 kinesin-related motor protein (also known as KIF11 or kinesin spindle protein-5) is a plus-end directed kinesin motor protein essential for the regulation of spindle dynamics, including assembly and maintenance, during mitosis.","Pharmacologic Substance"]
["C82694","Eg5 Kinesin-Related Motor Protein Inhibitor ARQ 621","ARQ 621|Eg5 Kinesin-Related Motor Protein Inhibitor ARQ 621|Eg5 inhibitor ARQ 621","A small-molecule inhibitor of the kinesin-related motor protein Eg5 with potential antineoplastic activity. Eg5 kinesin-related motor protein inhibitor ARQ 621 selectively inhibits the activity of Eg5, which may result in mitotic disruption, apoptosis and cell death. The ATP-dependent Eg5 kinesin-related motor protein (also known as KIF11 or kinesin spindle protein-5) is a plus-end directed kinesin motor protein involved in the regulation of spindle dynamics, including assembly and maintenance, during mitosis.","Pharmacologic Substance"]
["C26646","EGb761","EGb761","A standardized ginkgo biloba extract with antioxidant and neuroprotective activities.  EGb761 has been shown to inhibit the proliferation of certain tumor cells in vitro. (NCI04)","Pharmacologic Substance"]
["C123722","EGFR Antagonist Hemay022","EGFR Antagonist Hemay022|EGFR Inhibitor Hemay022|Hemay022","An orally available, irreversible inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, Hemay022 covalently binds to and inhibits the activity of EGFR, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.","Pharmacologic Substance"]
["C2617","EGFR Antisense DNA","EGFR Antisense DNA","A synthetic sequence of DNA constructed in the antisense orientation to a sequence of DNA in epidermal growth factor receptor (EGFR), a member of the erbB gene family. EGFR antisense DNA suppresses the expression of EGFR by tumor cells, thereby inhibiting tumor cell proliferation and decreasing tumor growth. This agent also appears to reduce the invasiveness of certain breast cancer cells. Members of the erbB gene family are overexpressed in many cancers and play roles in carcinogenesis and the regulation of cell proliferation. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C107191","EGFR CAR-CD3zeta-4-1BB-expressing Autologous T-Lymphocytes","CART-EGFR TCR zeta:CD137 Cells|EGFR CAR-CD3zeta-4-1BB-expressing Autologous T-Lymphocytes","Autologous human T-lymphocytes transduced with a retroviral vector encoding an anti-epidermal growth factor receptor (EGFR) chimeric T cell receptor (chimeric antigen receptor or CAR) gene coupled to the signaling domains from both CD3 zeta and CD137 (4-1BB), with potential immunostimulatory and antineoplastic activities. Upon administration, the chimeric EGFR antigen receptor-modified autologous T lymphocytes bind to the EGFR antigen on tumor cell surfaces; subsequently, EGFR-expressing tumor cells may be lysed. Following binding to EGFR, the 4-1BB co-stimulatory molecule signaling domain enhances both activation and signaling. Inclusion of the 4-1BB signaling domain may also increase the antitumor activity when compared to the inclusion of the CD3-zeta chain alone. EGFR, a receptor tyrosine kinase (RTK) overexpressed by a variety of cancer cell types, plays key roles in tumor cell proliferation and tumor angiogenesis.","Cell|Pharmacologic Substance"]
["C105612","EGFR Inhibitor ABT-414","ABT-414|EGFR Inhibitor ABT-414","An epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon intravenous infusion, ABT-414 inhibits the activity of EGFR, thereby preventing EGFR-mediated signaling. This may inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase overexpressed in certain tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.","Pharmacologic Substance"]
["C115110","EGFR Inhibitor ASP8273","ASP8273|EGFR Inhibitor ASP8273","An orally available, irreversible, third-generation, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, ASP8273 covalently binds to and inhibits the activity of mutant forms of EGFR, including the T790M EGFR mutant, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. ASP8273 preferentially inhibits mutated forms of EGFR including T790M, a secondarily acquired resistance mutation, and may have therapeutic benefits in tumors with T790M-mediated resistance when compared to other EGFR tyrosine kinase inhibitors. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced as compared to non-selective EGFR inhibitors which also inhibit wild-type EGFR.","Pharmacologic Substance"]
["C118289","EGFR Inhibitor AZD3759","AZD3759|EGFR Inhibitor AZD3759","An orally available inhibitor of the epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Upon oral administration, AZD3759 binds to and inhibits the activity of EGFR as well as certain mutant forms of EGFR. This prevents EGFR-mediated signaling, and may lead to both induction of cell death and inhibition of tumor growth in EGFR-overexpressing cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.","Pharmacologic Substance"]
["C99905","EGFR Inhibitor CO-1686","CO-1686|EGFR Inhibitor CO-1686|Rociletinib","An orally available small molecule, irreversible inhibitor of epidermal growth factor receptor (EGFR) with potential antineoplastic activity. EGFR inhibitor CO-1686 binds to and inhibits mutant forms of EGFR, including T790M, thereby leading to cell death of resistant tumor cells. Compared to other EGFR inhibitors, CO-1686 inhibits T790M, a secondary acquired resistance mutation, as well as other mutant EGFRs and may have therapeutic benefits in tumors with T790M-mediated resistance to other EGFR tyrosine kinase inhibitors. This agent shows minimal activity against wild-type EGFR, hence does not cause certain dose-limiting toxicities.","Pharmacologic Substance"]
["C115109","EGFR Inhibitor EGF816","EGF816|EGFR Inhibitor EGF816","An orally available, irreversible, third-generation, mutant-selective epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, EGF816 covalently binds to and inhibits the activity of mutant forms of EGFR, including the T790M EGFR mutant, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. EGF816 preferentially inhibits mutated forms of EGFR including T790M, a secondarily acquired resistance mutation, and may have therapeutic benefits in tumors with T790M-mediated resistance when compared to other EGFR tyrosine kinase inhibitors. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced as compared to non-selective EGFR inhibitors which also inhibit wild-type EGFR.","Pharmacologic Substance"]
["C101791","EGFR Inhibitor HM61713","EGFR Inhibitor HM61713|HM61713","An orally available small molecule, mutant-selective inhibitor of epidermal growth factor receptor (EGFR) with potential antineoplastic activity. EGFR inhibitor HM61713 binds to and inhibits mutant forms of EGFR, thereby leading to cell death of EGFR-expressing tumor cells. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced as compared to non-selective EGFR inhibitors which also inhibit the EGFR wild type form.","Pharmacologic Substance"]
["C122392","EGFR Mutant-selective Inhibitor AC0010MA","AC0010MA|EGFR Mutant-selective Inhibitor AC0010MA","An orally available, third generation, selective inhibitor of mutant forms of the epidermal growth factor receptor (EGFR), including the second-site resistance mutation T790M, with potential antineoplastic activity. EGFR mutant-selective inhibitor AC0010MA specifically and irreversibly binds to and inhibits the activity of mutant forms of EGFR, which prevents EGFR mutant-mediated signaling and leads to cell death in EGFR mutant-expressing tumor cells. Compared to some other EGFR inhibitors, AC0010MA may have therapeutic benefits in tumors with T790M-mediated drug resistance. This agent does not inhibit wild-type EGFR (EGFRwt), and does not cause dose-limiting toxicities that occur during the use of non-selective EGFR inhibitors, which also inhibit EGFRwt. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.","Pharmacologic Substance"]
["C120307","EGFR T790M Inhibitor PF-06747775","EGFR T790M Inhibitor PF-06747775|PF-06747775","An orally available inhibitor of the epidermal growth factor receptor (EGFR) mutant form T790M, with potential antineoplastic activity. EGFR T790M inhibitor PF-06747775 specifically binds to and inhibits EGFR T790M, a secondary acquired resistance mutation, which prevents EGFR-mediated signaling and leads to cell death in EGFR/T790M-expressing tumor cells. Compared to some other EGFR inhibitors, PF-06747775 may have therapeutic benefits in tumors with T790M-mediated drug resistance. This agent shows minimal activity against wild-type EGFR (WT EGFR), and does not cause dose-limiting toxicities that occur during the use of non-selective EGFR inhibitors, which can inhibit WT EGFR. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.","Pharmacologic Substance"]
["C126752","EGFR/HER2 Inhibitor AP32788","AP32788|EGFR/HER2 Inhibitor AP32788","An orally available inhibitor of specific mutant forms of both human epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2; ERBB2), with potential antineoplastic activity. Upon oral administration, EGFR/HER2 inhibitor AP32788 specifically and irreversibly binds to and inhibits certain mutant forms of EGFR and HER2. This prevents EGFR- and HER2-mediated signaling and leads to cell death in EGFR mutant- and HER2 mutant-expressing tumor cells. EGFR and HER2, receptor tyrosine kinases mutated in many tumor cell types, play key roles in tumor cell proliferation and tumor vascularization.","Pharmacologic Substance"]
["C64627","EGFR/HER2 Inhibitor AV-412","AV-412|EGFR/HER2 Inhibitor AV-412|MP-412","A second-generation, orally bioavailable dual kinase inhibitor with potential antineoplastic activity. EGFR/HER2 inhibitor AV-412 binds to and inhibits the epidermal growth factor receptor (EGFR) and the human epidermal growth factor receptor 2 (HER2), which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. This agent may be active against EGFR/HER2-expressing tumor cells that are resistant to first-generation kinase inhibitors. EGFR and HER2 are receptor tyrosine kinases that play major roles in tumor cell proliferation and tumor vascularization.","Organic Chemical|Pharmacologic Substance"]
["C90589","EGFR/HER2 Kinase Inhibitor TAK-285","EGFR/HER2 Kinase Inhibitor TAK-285|TAK-285","An orally bioavailable, small molecule and dual kinase inhibitor of human epidermal growth factor receptors 1 (EGFR/ErbB1) and 2 (HER2/ErbB2), with potential antineoplastic activity. EGFR/HER2 kinase inhibitor TAK-285 binds to and inhibits EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumors. This agent may be active against EGFR/HER2-expressing tumor cells that are resistant to trastuzumab. EGFR and HER2, receptor tyrosine kinases overexpressed in a variety of tumor cell types, play major roles in tumor cell proliferation and tumor vascularization. In addition, TAK-285 appears to pass the blood brain barrier (BBB) and does not appear to be a substrate for efflux pumps.","Pharmacologic Substance"]
["C71536","EGFRBi-Armed Autologous T Cells","EGFRBi-Armed Autologous T Cells","Autologous activated T cells, loaded with a bispecific antibody produced by heteroconjugation of anti-CD3 and anti-epidermal growth factor receptor (EGFR) monoclonal antibodies, with potential antineoplastic activity. Binding of EGFRBi-armed autologous activated T cells to EGFR-positive tumor cells may result in increased T cell-mediated cytotoxicity towards tumor cells expressing EGFR.  Arming activated T cells with this bispecific antibody may significantly increase T cell secretion of anti-tumor associated cytokines such as IL2, RANTES, IFN-gamma, and TNF-alpha.","Cell|Pharmacologic Substance"]
["C117727","EGFRvIII-specific CAR-transduced Autologous T Lymphocytes","CART-EGFRvIII Autologous T Cells|EGFRvIII-specific CAR-transduced Autologous T Lymphocytes","Autologous human T-lymphocytes transduced with a retroviral vector encoding an anti-epidermal growth factor receptor variant III (EGFRvIII) mutant chimeric T-cell receptor (chimeric antigen receptor or CAR) gene, with potential immunostimulatory and antineoplastic activities. Upon administration, the EGFRvIII-specific CAR-transduced autologous T-lymphocytes bind to the EGFRvIII antigen on tumor cell surfaces; subsequently, EGFRvIII-expressing tumor cells may be lysed. EGFRvIII, an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety of cancer cell types but absent in normal, healthy cells. It plays a key role in tumor cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy.","Cell|Pharmacologic Substance"]
["C67080","Eicosapentaenoic Acid","All cis-5,8,11,14,17-Eicosapentaenoic Acid|EPA|Eicosapentaenoic Acid|Fatty Acid 20:5|IPA|Icosapentaenoic Acid|Timnodonic Acid","An essential, polyunsaturated, 20-carbon omega-3 fatty acid with anti-inflammatory and potential antineoplastic and chemopreventive activities. Eicosapentaenoic acid (EPA) may activate caspase 3, resulting in apoptosis in susceptible tumor cell populations. In addition, this agent may inhibit cyclooxygenase-2 (COX-2), resulting in inhibition of prostaglandin synthesis and prostaglandin-mediated inflammatory processes.","Organic Chemical"]
["C120042","Eicosapentaenoic Acid-enriched Nutritional Supplement","EPA-enriched Nutritional Supplement|Eicosapentaenoic Acid-enriched Nutritional Supplement","A nutritional supplement enriched with eicosapentaenoic acid (EPA), which is an essential, polyunsaturated, 20-carbon omega-3 fatty acid found in fish oil, with potential anti-inflammatory and anti-cachectic activities. Upon oral intake of the EPA-enriched nutritional supplement, EPA is incorporated in cell membrane phospholipids and replaces arachidonic acid. This affects the production of pro-inflammatory mediators, such as tumor necrosis factor-alpha (TNF-a), interleukin-1 (IL-1) and IL-6, through the inhibition of nuclear factor kappa B (NF-kB) activity. This inhibits inflammation and may abrogate the cachexia-mediated decrease of lean body mass (LBM), which may lead to increased body weight. Pro-inflammatory mediators, such as TNF-a, interferon-gamma, and certain interleukins, such as IL-6 and IL-1b, play a key role in cachexia.","Pharmacologic Substance"]
["C95740","eIF4E Antisense Oligonucleotide ISIS 183750","ISIS 183750|LY2275796|eIF4E Antisense Oligonucleotide ISIS 183750|eIF4E Inhibitor ISIS 183750|eIF4E Modulator ISIS 183750","A second-generation antisense oligonucleotide targeting the eukaryotic translation initiation factor 4E (eIF4E) with potential antitumor activity. Antisense oligonucleotide ISIS EIF4ERx suppresses the expression of eIF4E in fast dividing tumor cells. Blocking the expression of eIF4E results in inhibition of the synthesis of tumor angiogenic factors, thereby leading to the inhibition of cellular proliferation and apoptosis in tumor cells. eIF4E is overexpressed in a variety of cancers, is involved in the mRNA-ribosome binding step of eukaryotic protein synthesis and is the rate-limiting component of the eukaryotic translation apparatus.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C53401","Elacytarabine","4-amino-1-[5-O-[(9E)-octadec-9-enoyl]-beta-D-arabinofuranosyl]pyrimidin-2(1H)-one|CP-4055|ELACYTARABINE|Elacyt|Elacytarabine","The lipophilic 5'-elaidic acid ester of the deoxycytidine analog cytosine arabinoside (cytarabine; Ara-C) with potential antineoplastic activity. As a prodrug, elacytarabine is converted intracellularly into cytarabine triphosphate by deoxycytidine kinase and subsequently competes with cytidine for incorporation into DNA, thereby inhibiting DNA synthesis. Compared to cytarabine, elacytarabine shows increased cellular uptake and retention, resulting in increased activation by deoxycytidine kinase to cytarabine triphosphate, decreased deamination and deactivation by deoxycytidine deaminase, and increased inhibition of DNA synthesis. This agent also inhibits RNA synthesis, an effect not seen with cytarabine.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C75291","Elesclomol","1-N'-benzenecarbothioyl-3-(2-benzenecarbothioyl-2-methylhydrazinyl)-N'-methyl- oxopropanehydrazidide|ELESCLOMOL|Elesclomol|Propanedioic Acid, Bis[2-methyl-2-(phenylthioxomethyl)hydrazide]","A small-molecule bis(thio-hydrazide amide) with oxidative stress induction, pro-apoptotic, and potential antineoplastic activities. Elesclomol induces oxidative stress, creating high levels of reactive oxygen species (ROS), such as hydrogen peroxide, in both cancer cells and normal cells. Because tumor cells have elevated levels of ROS compared to normal cells, the increase in oxidative stress beyond baseline levels elevates ROS beyond sustainable levels, exhausting tumor cell antioxidant capacity, which may result in the induction of the mitochondrial apoptosis pathway. Normal cells are spared because the increase in the level of oxidative stress induced by this agent is below the threshold at which apoptosis is induced.","Pharmacologic Substance"]
["C79840","Elesclomol Sodium","1-N'-benzenecarbothioyl-3-(2-benzenecarbothioyl-2-methylhydrazinyl)-N'-methyl- oxopropanehydrazidide Sodium|ELESCLOMOL SODIUM|Elesclomol Sodium|Propanedioic Acid, Bis[2-methyl-2-(phenylthioxomethyl)hydrazide], Sodium Salt|STA-4783|elesclomol sodium","The water soluble sodium salt of a small-molecule bis(thio-hydrazide amide) with oxidative stress induction, pro-apoptotic, and potential antineoplastic activities. Elesclomol induces oxidative stress, creating high levels of reactive oxygen species (ROS), such as hydrogen peroxide, in both cancer cells and normal cells. Because tumor cells have elevated levels of ROS compared to normal cells, the increase in oxidative stress beyond baseline levels elevates ROS beyond sustainable levels, exhausting tumor cell antioxidant capacity, which may result in the induction of the mitochondrial apoptosis pathway. Normal cells are spared because the increase in the level of oxidative stress induced by this agent is below the threshold at which apoptosis is induced.","Pharmacologic Substance"]
["C1615","Elinafide","ELINAFIDE|Elinafide|LU 79553|LU-79553|N,N'-(Trimethylenebis(iminoethylene))dinaphthalimide","A symmetrical dimeric bis-naphthalimide compound and a topoisomerase II inhibitor with antineoplastic activity. Elinafide contains two neutral chromophores joined by a cationic linker and is capable of bis-intercalation at the TpG and CpA steps of the DNA hexanucleotide. Intercalation inhibits topoisomerase II activity and causing DNA stand breakage, thereby leads to inhibition of DNA, RNA, and protein synthesis.","Organic Chemical|Pharmacologic Substance"]
["C66949","Elisidepsin","Depsipeptide PM02734|ELISIDEPSIN|Elisidepsin|L-Valine, N-((4S)-4-methyl-1-oxohexyl)-D-valyl-L-threonyl-L-valyl-D-valyl-D-prolyl-L-ornithyl-D-alloisoleucyl-D-allothreonyl-D-alloisoleucyl-D-valyl-L-phenylalanyl-(2Z)-2-amino-2-butenoyl-, (13-8)-lactone, 2,2,2-trifluoroacetate (1:1)|PM02734","A synthetic cyclic depsipeptide of the kahalalides family with potential antineoplastic activity. PM02734 is a derivative of a natural marine compound extracted from the sacoglossan sea slug, Elysia rufescens. Although the exact mechanism of action has yet to be elucidated, elisidepsin exhibits anti-proliferative activity in a wide variety of cancer types, such as breast, colon, pancreas, lung, and prostate.","Organic Chemical|Pharmacologic Substance"]
["C118627","Ellagic Acid/Annona muricata Supplement","Ellagic Acid/Annona muricata Supplement","A nutritional supplement containing the phytochemical polyphenol, ellagic acid, and an extract of Annona muricata, with potential chemopreventive activity. Although the exact mechanism of action for ellagic acid has yet to be fully elucidated, this agent acts as an anti-oxidant and reduces oxidative stress. This agent also appears to protect the body against certain carcinogens, either through preventing DNA binding or by increasing the rate of their metabolism and deactivation. Certain extracts of Annona muricata, a member of the custard apple plants and belonging to the Annonaceae family, may have antiviral activity, potential targets include human papilloma virus (HPV), and may be cytotoxic against various types of cancer cells.","Pharmacologic Substance"]
["C90495","Elliptinium","9-Hydroxy-2,5,11-trimethyl-6H-pyrido[4,3-b]carbazolium|9-Hydroxy-2-methylellipticinium|ELLIPTINIUM|Elliptinium|N-2-Methyl-9-hydroxyellipticinium|NMHE","A derivative of the alkaloid ellipticine isolated from species of the plant family Apocynaceae, including Bleekeria vitensis, a plant with anti-cancer properties.  As a topoisomerase II inhibitor and intercalating agent, elliptinium stabilizes the cleavable complex of topoisomerase II and induces DNA breakages, thereby inhibiting DNA replication and RNA and protein synthesis.","Organic Chemical|Pharmacologic Substance"]
["C1367","Elliptinium Acetate","6H-Pyrido[4, 3-b]carbazolium, 9-hydroxy-2,5,11-trimethyl-acetate (salt)|9-Hydroxy-2,5,11-trimethyl-6H-pyrido[4,3-b]carbazolium Acetate (Salt)|9-Hydroxy-2-methylellipticinium Acetate|9-Hydroxy-2-methylellipticinium acetate|Celiptium|ELLIPTINIUM ACETATE|Elliptinium Acetate|N-2-Methyl-9-hydroxyellipticinium Acetate","Acetate salt of elliptinium, a derivative of the alkaloid ellipticine isolated from species of the plant family Apocynaceae, including Bleekeria vitensis, a plant with anti-cancer properties.  As a topoisomerase II inhibitor and intercalating agent, elliptinium stabilizes the cleavable complex of topoisomerase II and induces DNA breakages, thereby inhibiting DNA replication and RNA and protein synthesis.","Organic Chemical|Pharmacologic Substance"]
["C73262","Elmustine","1-(2-Chloroethyl)-3-(2-hydroxyethyl)-1-nitrosourea|1-Nitroso-1-chloroethyl-3-hydroxyethylurea|ELMUSTINE|Elmustine|HeCNU|Hydroxyethyl CNU","A (2-chloroethy1)nitrosourea derivative related to carmustine, with antineoplastic activity.","Pharmacologic Substance"]
["C66982","Elotuzumab","BMS-901608|ELOTUZUMAB|Elotuzumab|Empliciti|HuLuc-63|HuLuc63|PDL-063|PDL063","A humanized monoclonal antibody directed against the human CS1 (CD2 subset 1, CRACC, SLAMF7) antigen with potential antineoplastic activity. Elotuzumab binds to the CS1 antigen, which may trigger antibody-dependent cellular cytotoxicity (ADCC) in cells expressing CS1. CS1 is a cell surface glycoprotein belonging to the CD2 subset of the immunoglobulin superfamily (IgSF) and is highly expressed by multiple myeloma cells, but minimally expressed by normal cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1080","Elsamitrucin","10-O-Elsaminosylelsarosylchartarin|BBM 2478A|BMY-28090|BRN 5214813|Benzo(h)(1)benzopyrano(5,4,3-cde)(1)ebnzopyran-5,12-dione,10((2-O-(2-amino-2,6-dideoxy-3-O-methyl-alpha-D-galactopyranosyl)-6-deoxy-3-C-methyl-beta-D-galactopyranosyl)oxy)-6-hydroxy-1-methyl|ELSAMITRUCIN|Elsamicin A|Elsamitrucin|Elsamitrucina|Elsamitrucine|Elsamitrucinum","An heterocyclic antineoplastic antibiotic isolated from the bacterium Actinomycete strain J907-21.  Elsamitrucin intercalates into DNA at guanine-cytosine (G-C)-rich sequences and inhibits topoisomerase I and II, resulting in single-strand breaks and inhibition of DNA replication. (NCI04)","Antibiotic|Organic Chemical"]
["C2714","EMD 55900","EMD 55 900|EMD 55900|Mab 425|Monoclonal Antibody 425","A murine monoclonal antibody targeting the epidermal growth factor receptor (EGFR) exhibiting anti-tumor activity. EMD 55900 antibody binds to the extracellular domain of EGFR close to the EGF binding domain and does not induce any tyrosine kinase activity on its own. As a result, EMD 55900 binding inhibits receptor activation by natural ligands thereby interrupting activation of downstream signaling cascade, required for tumor cell growth and proliferation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2195","Emepepimut-S","BLP25 Liposome Vaccine|BLP25|BP1-7-KLH|EMD 531444|Emepepimut-S|Glycine, L-seryl-L-threonyl-L-alanyl-L-prolyl-L-prolyl-L-alanyl-L-histidylglycyl-L-valyl-L-threonyl-L-seryl-L-alanyl-L-prolyl-L-alpha-aspartyl-L-threonyl-L-arginyl-L-prolyl-L-alanyl-L-prolylglycyl-L-seryl-L-threonyl-L-alanyl-L-prolyl-L-prolyl-N6-(1-oxohexadecyl)-L-lysyl-|L-BLP25|Stimuvax|Tecemotide","A liposome-encapsulated peptide vaccine consisting of a synthetic peptide derived from the mucin 1 (MUC-1) antigen with potential antineoplastic activity. Upon vaccination, MUC-1 peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against MUC-1-expressing tumor cells, resulting in growth inhibition. MUC-1 antigen is a high-molecular-weight transmembrane glycoprotein that is overexpressed on the cell surfaces of many epithelial tumor cells as well as on the cell surfaces of some B-cell lymphoma cells and multiple myeloma cells.","Immunologic Factor|Pharmacologic Substance"]
["C1022","Emitefur","(2) m-[[3-(Ethoxymethyl)-5-fluoro-3,6-dihydro-2,6-dioxo-1(2H)-pyrimidinyl]carbonyl]benzoic Acid, 2-Ester with 2,6-Dihydroxynicotinonitrile Benzoate (Ester)|3-((3-(Ethoxymethyl)-5-fluoro-3,6-dihydro-2,6-dioxo-1(2H)-pyrimidinyl)carbonyl)benzoic acid, 6-(benzoyloxy)-3-cyano-2-pyridinyl ester|3-[3-(6-Benzoyloxy-3-cyrano-2-pyridyloxycarbonyl)benzoyl]-1-(ethoxymethyl)-5-fluorouracil|BOF-A2|EMITEFUR|Emitefur|Last-F|[[Ethoxymethyl-5-fluoro-3,6-dihydro-2,6-dioxo-1(2H)-pyrimidinyl]carbonyl]benzoic Acid, 6-(Benzoyloxy)-3-cyano-2-pyridinyl Ester|emitefur","An orally available antimetabolite composed of the 1-ethoxymethyl derivative of 5-fluorouracil (5-FU) and the dihydropyrimidine dehydrogenase (DPYD) inhibitor 3-cyano-2,6-dihydroxypyridine (CNDP) in a 1:1 molar ratio, with antineoplastic activity.  Upon administration, the prodrug emitefur is converted into 5-FU, while CNDP prevents the degradation of 5-FU by inhibiting DPYD and thereby prolonging the half-life of 5-FU. This increases 5-FU's concentration and thus its antitumor activity through inhibition of DNA and RNA synthesis, as well as inhibition of thymidylate synthase activity. In addition, by inhibiting the formation of 5-FU metabolites, some toxic effects associated with these metabolites may be reduced. DPYD is the rate-limiting enzyme in the catabolism of 5-FU.","Organic Chemical|Pharmacologic Substance"]
["C29019","Emofolin Sodium","Emofolin Sodium|MeTHHF Disodium|Methyltetrahydrohomofolate","The sodium salt of a synthetic antimetabolite analogue of folate with antineoplastic activity.  Emfolin sodium competes for the folate binding site of the enzyme dihydrofolate reductase, resulting in inhibition of tetrahydrofolate synthesis, depletion of nucleotide pools, and inhibition of DNA, RNA and protein synthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C113786","Enadenotucirev","Chimeric Oncolytic Adenovirus Ad3/Ad11p Containing Two Deletions in the Viral Genome in the E3 Region (2444 bp) and in the E4 Region (24 bp) and 197 Non-homologous Nucleotides in the E2B Region|ColoAd-1|ColoAd1 Oncolytic Virus|ColoAd1|ENADENOTUCIREV|EnAd|Enadenotucirev","A complex, replication-selective, E1B and partial E3 gene deleted, adenovirus type 11p (Ad11p)/Ad3 chimeric oncolytic virus with potential antineoplastic activity. Upon intralesional injection of enadenotucirev, the adenovirus selectively and rapidly replicates in cancer cells; however, it is unable to replicate in normal, healthy cells. This induces a selective adenovirus-mediated cytotoxicity in cancer cells, which leads to cancer cell lysis. Following the lysis of infected cells, the replicated virus is released and can infect adjacent cells, which both induces further tumor cell oncolysis and may activate the immune system to kill the infected tumor cells. The E1B protein causes p53 inactivation in host cells, which promotes viral replication. Deletion of E1B prevents replication in normal, healthy cells that express wild-type p53. The mutation and subsequent inactivation of p53 in cancer cells enables the E1B-deleted adenovirus to selectively replicate in cancer cells. Partial deletion of the E3 gene, which encodes the adenovirus death protein, enhances the safety profile of the administered adenovirus.","Pharmacologic Substance"]
["C80045","Enavatuzumab","Anti-tumor Necrosis Factor-like Weak Inducer of Apoptosis Monoclonal Antibody PDL192|ENAVATUZUMAB|Enavatuzumab|PDL 192","A humanized monoclonal antibody directed against the tumor necrosis factor-like weak inducer of apoptosis receptor (TWEAKR) with potential antineoplastic, immunomodulating and antiangiogenic activities. Enavatuzumab binds to TWEAKR and inhibits TWEAK ligand binding and activation of NF-kappaB-mediated cytokine release, which may result in tumor cell apoptosis. TWEAKR is a cell-surface receptor with homology to tumor necrosis factor receptors. Upon binding with its ligand, TWEAKR has been shown to stimulate cytokine release and cell proliferation, migration, and survival; it may also promote apoptosis under some conditions. This receptor may be overexpressed in a variety of tumors including those of the pancreas, colon, lung, kidney, and breast.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C28211","Enclomiphene","ENCLOMIPHENE|Enclomifene|Enclomiphene|ICI 46476|RMI 16,289|trans Clomiphene|trans-2-(4-(2-Chloro-1,2-diphenylethenyl)phenoxy)-N,N-diethylethanamine","The trans-isomer of clomiphene citrate (CC).  Enclomiphene has a higher rate of clearance and is less active than the cis-isomer, cis-clomiphene.  Clomiphene citrate has been evaluated for antineoplastic activity against breast cancer. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C61745","Enclomiphene Citrate","ENCLOMIPHENE CITRATE|Enclomiphene Citrate","The orally bioavailable citrate salt of enclomiphene, the trans-isomer of the nonsteroidal triphenylethylene compound clomiphene, with tissue-selective estrogenic and antiestrogenic activities. As a selective estrogen receptor modulator (SERM), enclomiphene binds to hypothalamic estrogen receptors, blocking the negative feedback of endogenous estrogens and stimulating the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus; released GnRH subsequently stimulates the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, resulting in ovulation. In addition, this agent may bind to estrogen receptors on breast cancer cells, resulting in the inhibition of estrogen-stimulated proliferation in susceptible cell populations.","Pharmacologic Substance"]
["C98283","Encorafenib","ENCORAFENIB|Encorafenib|LGX 818|LGX-818|LGX818","An orally available Raf kinase inhibitor with potential antineoplastic activity. Encorafenib specifically inhibits Raf kinase, a serine/threonine enzyme in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway. By inhibiting the activation of the RAF/MEK/ERK signaling pathway, the administration of LGX818 may result in a decrease in proliferation of tumor cells. The Raf mutation BRAF V600E is frequently upregulated in a variety of human tumors and results in the constitutive activation of the RAF/MEK/ERK signaling pathway that regulates cellular proliferation and survival.","Organic Chemical|Pharmacologic Substance"]
["C11252","Eniluracil / 5-FU Combination Tablet","776C85/5-FU|Eniluracil / 5-FU Combination Tablet|Ethynyluracil/Fluorouracil|GW776/5-FU|GW776/5-Fluorouracil","A combination tablet of ethynyluracil and fluorouracil. Fluorouracil is an antimetabolite fluoropyrimidine analog of the nucleoside pyrimidine with antineoplastic activity. Ethynyluracil is an orally-active fluoropyrimidine analog that inhibits dihydropyrimidine dehydrogenase, the rate-limiting enzyme that catabolizes and inactivates 5-fluorouracil in the liver. This may lead to an increase in the bioavailability and, effectiveness of fluorouracil.","Organic Chemical|Pharmacologic Substance"]
["C95323","Enloplatin","CL 287,110|CL-287110|Cis-(1,1-Cyclobutanedicarboxylato)(Tetrahydro-4H-Pyran-4,4-Bis(Methylamine))Platinum|ENLOPLATIN|Enloplatin|Platinum, (1,1-Cyclobutanedicarboxylato(2-))(Tetrahydro-4h-Pyran-4,4-Dimethanamine-N,N')-, (Sp-4-2)-","A platinum-based alkylating agent with antineoplastic activity. Although its pharmacokinetic properties are similar to that of carboplatin, enloplatin appears to be non-cross resistant with other platinum-based agents, such as cisplatin and carboplatin.","Inorganic Chemical|Pharmacologic Substance"]
["C69161","Enobosarm","ENOBOSARM|Enobosarm|Gtx-024|Ostarine|Propanamide, 3-(4-cyanophenoxy)-N-(4-cyano-3-(trifluoromethyl)phenyl)-2-hydroxy-2-methyl-, (2S)-","A non-steroidal agent with anabolic activity. Selective androgen receptor modulator (SARM) GTx-024 is designed to work like testosterone, thus promoting and/or maintaining libido, fertility, prostate growth, and muscle growth and strength. Mimicking testosterone's action, this agent may increase lean body mass, thereby ameliorating muscle wasting in the hypermetabolic state of cancer cachexia.","Pharmacologic Substance"]
["C83689","Enpromate","1,1-Diphenyl-2-propynyl-N-cyclohexylcarbamate|Acetylenic Carbamate|ENPROMATE|Enpromate|Lilly 59156","A synthetic acetylenic carbamate, an alkylating agent, with antineoplastic activity.","Pharmacologic Substance"]
["C90532","Ensituximab","Anti-CPAA Monoclonal Antibody NPC-1C|Anti-Colorectal and Pancreatic Carcinoma-Associated Antigen Monoclonal Antibody NPC-1C|ENSITUXIMAB|Ensituximab|NPC-1C","A chimeric monoclonal antibody against human colorectal and pancreatic carcinoma-associated antigens (CPAAs) with potential immunomodulating and anti-tumor activities. Anti-CPAA monoclonal antibody NPC-1C binds to CPAAs, which may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response and an antibody-dependent cellular cytotoxicity (ADCC) response against CPAA-expressing tumor cells. CPAAs, cell surface proteins, are upregulated on colon and pancreatic tumor cells. NPC-1C contains the variable region of the heavy and light chain of murine NPC-1 and linked in-frame to constant regions of a human IgG1 isotype.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82660","Enteric-Coated TRPM8 Agonist D-3263 Hydrochloride","EC D-3263 HCl|Enteric-Coated TRPM8 Agonist D-3263 Hydrochloride","An enteric-coated orally bioavailable formulation of the hydrochloride salt of a small-molecule agonist for transient receptor potential melastatin member 8 (TRPM8 or Trp-p8) with potential antineoplastic activity. The active ingredient in enteric-coated TRPM8 agonist D-3263 hydrochloride binds to and activates TRPM8, which may result in an increase in calcium and sodium entry; the disruption of calcium and sodium homeostasis; and the induction of cell death in TRPM8-expressing tumor cells. This agent may decrease dihydrotestosterone (DHT) levels, which may contribute to its inhibitory effects on prostate cancer and BPH. TRPM8 is a transmembrane calcium channel protein that is normally expressed in prostate cells and appears to be overexpressed in benign prostatic hyperplasia (BPH) and in prostate cancer.","Pharmacologic Substance"]
["C1863","Entinostat","Carbamic Acid, N-[[4-[[(2-aminophenyl)amino]carbonyl]phenyl]methyl]-, 3- pyridinylmethyl Ester|Carbamic acid, [[4-[[(2-aminophenyl)amino]carbonyl]phenyl] methyl]-, 3-pyridinylmethyl ester (9CI)|ENTINOSTAT|Entinostat|HDAC inhibitor SNDX-275|MS 27-275|MS-275|N-(2-Aminophenyl)-4-[N-(pyridin-3-yl-methoxycarbonyl)aminomethyl]b enzamide|SNDX-275|entinostat","A synthetic benzamide derivative with potential antineoplastic activity. Entinostat binds to and inhibits histone deacetylase, an enzyme that regulates chromatin structure and gene transcription. This agent appears to exert dose-dependent effects in human leukemia cells including cyclin-dependent kinase inhibitor 1A (p21/CIP1/WAF1)-dependent growth arrest and differentiation at low drug concentrations; a marked induction of reactive oxygen species (ROS); mitochondrial damage; caspase activation; and, at higher concentrations, apoptosis. In normal cells, cyclin-dependent kinase inhibitor 1A expression has been associated with cell-cycle exit and differentiation.","Pharmacologic Substance"]
["C99166","Entolimod","CBLB502|Entolimod|TLR5 Agonist CBLB502","A polypeptide derived from the Salmonella filament protein flagellin with potential radioprotective and anticancer activities. As a toll-like receptor 5 (TLR5) agonist, entolimod binds to and activates TLR5 thereby stimulating tumor necrosis factor production and activating nuclear factor kappa B (NF-kB). This induces NF-kB-mediated signaling pathways and inhibits the induction of apoptosis. This may prevent apoptosis in normal, healthy cells during radiotherapy of cancerous cells and may allow for increased doses of ionizing radiation. In addition, entolimod may inhibit radiation-independent proliferation in TLR5-expressing tumor cells.","Pharmacologic Substance"]
["C105402","Entospletinib","6-(1H-Indazol-6-yl)-N-(4-(morpholin-4-yl)phenyl)imidazo(1,2-a)pyrazin-8-amine|ENTO|ENTOSPLETINIB|Entospletinib|GS 9973|GS-9973|Imidazo(1,2-a)pyrazin-8-amine, 6-(1H-indazol-6-yl)-N-(4-(4-morpholinyl)phenyl)-","An orally available inhibitor of spleen tyrosine kinase (Syk), with potential antineoplastic activity. Upon oral administration of entospletinib, this agent may inhibit the activity of Syk, which inhibits B-cell receptor (BCR) signaling and leads to an inhibition of tumor cell activation, migration, adhesion and proliferation. Syk, a non-receptor cytoplasmic, BCR-associated tyrosine kinase, is expressed in hematopoietic tissues and is often overexpressed in hematopoeitic malignancies.","Pharmacologic Substance"]
["C114984","Entrectinib","ENTRECTINIB|Entrectinib|N-(5-(3,5-Difluorobenzyl)-1H-indazol-3-yl)-4-(4-methylpiperazin-1yl)-2-(tetrahydro-2H-pyran-4-ylamino)benzamide|RXDX-101","An orally bioavailable inhibitor of the tyrosine kinases tropomyosin receptor kinases (Trk) A, B and C, C-ros oncogene 1 (ROS1) and anaplastic lymphoma kinase (ALK), with potential antineoplastic activity. Upon administration, entrectinib binds to and inhibits TrkA, TrkB, TrkC, ROS1 and ALK. Inhibition of these kinases may result in a disruption of TrkA-, TrkB-, TrkC-, ROS1-, and ALK-mediated signaling. This leads to an induction of apoptosis and an inhibition of tumor cell proliferation in tumor cells that express these kinases. TrkA, TrkB, TrkC, ROS1 and ALK are overexpressed in a variety of cancer cell types.","Pharmacologic Substance"]
["C71744","Enzalutamide","ASP9785|Benzamide, 4-(3-(4-cyano-3-(trifluoromethyl)phenyl)-5,5-dimethyl-4-oxo-2-thioxo-1-imidazolidinyl)-2-fluoro-N-methyl-|ENZALUTAMIDE|Enzalutamide|MDV3100|Xtandi","An orally bioavailable, organic, non-steroidal small molecule targeting the androgen receptor (AR) with potential antineoplastic activity. Through a mechanism that is reported to be different from other approved AR antagonists, enzalutamide inhibits the activity of prostate cancer cell ARs, which may result in a reduction in prostate cancer cell proliferation and, correspondingly, a reduction in the serum prostate specific antigen (PSA) level. AR over-expression in prostate cancer represents a key mechanism associated with prostate cancer hormone resistance.","Pharmacologic Substance"]
["C26658","Enzastaurin Hydrochloride","3-(1-Methyl-1H-indol-3-yl)-4-[1-[1-(2-pyridinylmethyl)-4-piperidinyl]-1H-indol-3-yl]-1H-pyrrole-2,5-dione Dihydrochloride|ENZASTAURIN HYDROCHLORIDE|Enzastaurin Hydrochloride|LY317615|enzastaurin hydrochloride","The hydrochloride salt of enzastaurin, a synthetic macrocyclic bisindolemaleimide with potential antineoplastic activity.  Binding to the ATP-binding site, enzastaurin selectively inhibits protein kinase C beta, an enzyme involved in the induction of vascular endothelial growth factor (VEGF)-stimulated neo-angiogenesis. This agent may decrease tumor blood supply and so tumor burden.","Pharmacologic Substance"]
["C121644","Enzymatically-hydrolyzed Whey Protein-based Nutritional Supplement","Enzymatically-hydrolyzed Whey Protein-based Nutritional Supplement|Peptamen","An orally available, gluten-free, enzymatically hydrolyzed cysteine-rich whey-protein based nutritional supplement containing essential vitamins, minerals, and trace elements, as well as fat and carbohydrates. Upon oral intake of the nutritional supplement, the whey protein may improve gastric functioning and gastrointestinal health, thereby reducing vomiting and diarrhea. The whey-based hydrolyzed protein helps to alleviate the digestive burden for the pancreas and may be beneficial for patients with a pancreas-associated disease, such as pancreatitis or pancreatic cancer. Due to the high levels of cysteine in the whey protein, this supplement increases levels of the antioxidant glutathione (GSH). The polyunsaturated fatty acids in this supplement are incorporated in cell membranes and affect the production of pro-inflammatory mediators, eliciting an anti-inflammatory effect. Medium chain triglycerides (MCT) in this supplement enhance fat absorption and may aid in the prevention of fat malabsorption. Altogether, this supplement may prevent both malnutrition and weight loss.","Pharmacologic Substance"]
["C124131","EP4 Receptor Antagonist AAT-007","AAT-007|CJ-023,423|EP4 Receptor Antagonist AAT-007|N-[[2,4-(2-ethyl-4,6-dimethyl-1H-imidazo[4,5-c]pyridin-1-yl)phenylethylamino]carbonyl]-4-methyl-benzenesulfonamide|RQ-00000007|RQ-07","An orally bioavailable antagonist of the prostaglandin E receptor subtype 4 (EP4), with potential analgesic, immunomodulating and antineoplastic activities. Upon administration of the EP4 receptor antagonist AAT-007, this agent selectively binds to and inhibits the binding of prostaglandin E2 (PGE2) and prevents the activation of the EP4 receptor. This inhibits PGE2-EP4 receptor-mediated signaling and prevents proliferation in tumor cells in which the PGE2-EP4 signaling pathway is over-activated. In addition, EP4 receptor inhibition modulates the immune system by preventing both interleukin-23 (IL-23) production and the IL-23-mediated expansion of Th17 cells. As EP4 is expressed by peripheral sensory neurons, blockade of EP4-mediated signaling may induce an analgesic effect. EP4, a prostanoid receptor subtype, is a G protein-coupled receptor that is expressed in certain types of cancers; it promotes tumor cell proliferation and invasion.","Pharmacologic Substance"]
["C92582","Epacadostat","1,2,5-Oxadiazole-3-carboximidamide, 4-((2-((Aminosulfonyl)amino)ethyl)amino)-N-(3-bromo-4-fluorophenyl)-N'-hydroxy-, (C(Z))-|EPACADOSTAT|Epacadostat|INCB 024360|INCB024360","An orally available hydroxyamidine and inhibitor of indoleamine 2,3-dioxygenase (IDO1), with potential immunomodulating and antineoplastic activities. Epacadostat targets and binds to IDO1, an enzyme responsible for the oxidation of tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, INCB024360 increases and restores the proliferation and activation of various immune cells, including dendritic cells (DCs), NK cells, and T-lymphocytes, as well as interferon (IFN) production, and a reduction in tumor-associated regulatory T cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may inhibit the growth of IDO1-expressing tumor cells. IDO1 is overexpressed by a variety of tumor cell types and DCs.","Pharmacologic Substance"]
["C126801","EpCAM-specific CAR-expressing Autologous T-lymphocytes","EpCAM-specific CAR Autologous T-cells|EpCAM-specific CAR-expressing Autologous T-lymphocytes","A preparation of autologous T-lymphocytes that have been genetically modified to express a chimeric antigen receptor (CAR) specific for the antigen epithelial cell adhesion molecule (EpCAM), with potential immunostimulating and antineoplastic activities. Upon administration, the EpCAM-specific CAR-expressing autologous T-lymphocytes specifically recognize and bind to EpCAM-expressing tumor cells, resulting in tumor cell lysis. EpCAM, a cell surface protein, is expressed by a variety of tumor cells.","Pharmacologic Substance"]
["C101889","EphA2-targeting DOPC-encapsulated siRNA","EphA2-targeting DOPC-encapsulated siRNA|siRNA-EphA2-DOPC","A liposomal formulation consisting of short-interfering RNAs (siRNAs) directed against ephrin type-A receptor 2 (EphA2) and encapsulated into 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine (DOPC) neutral liposomes, with potential antineoplastic activity. Upon internalization, EphA2-targeting DOPC-encapsulated siRNA can hybridize to EphA2 DNA and mRNA, thereby interfering with both the transcription and translation of EphA2, and thus inhibiting tumor cell growth. The cell-surface receptor EphA2, a member of the ephrin family of receptor tyrosine kinases (RTKs) involved in mammalian development, is overexpressed by a variety of different cancer cell types and plays an important role in tumor growth.","Pharmacologic Substance"]
["C78083","Epipropidine","EPIPROPIDINE|Epipropidine","An epoxide and alkylating agent with antineoplastic activity. Epipropidone is not used clinically due to its unstable nature.","Pharmacologic Substance"]
["C62028","Epirubicin","(8S-cis)-10-((3-Amino-2,3,6-trideoxy-beta-L-arabino-hexopyranosyl)oxy)-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-5,12-naphthacenedione|3-Glycoloyl-1,2,3,4,6,11-hexahydro-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1-naphthacenyl-3-amino-2,3,6-trideoxy-alpha-L-arabino-hexopyranoside|4'-Epiadriamycin|4'-Epidoxorubicin|4'-epi DX|EPIRUBICIN|Epi DX|Epidoxorubicin|Epirubicin|Pidorubicin|epirubicin","A 4'-epi-isomer of the anthracycline antineoplastic antibiotic doxorubicin.  Epirubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis.  This agent also produces toxic free-radical intermediates and interacts with cell membrane lipids causing lipid peroxidation.","Antibiotic|Organic Chemical"]
["C474","Epirubicin Hydrochloride","(8S-cis)-10-((3-Amino-2,3,6-trideoxy-beta-L-arabino-hexopyranosyl)oxy)-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-5,12-naphthacenedione Hydrochloride|3-Glycoloyl-1,2,3,4,6,11-hexahydro-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1-naphthacenyl-3-amino-2,3,6-trideoxy-alpha-L-arabino-hexopyranoside Hydrochloride|EPIRUBICIN HYDROCHLORIDE|Ellence|Epirubicin Hydrochloride|IMI-28|Pharmorubicin PFS|epirubicin hydrochloride","The hydrochloride salt of the 4'-epi-isomer of the anthracycline antineoplastic antibiotic doxorubicin. Epirubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. This agent also produces toxic free-radical intermediates and interacts with cell membrane lipids causing lipid peroxidation.","Antibiotic|Organic Chemical"]
["C1089","Epitiostanol","10275-S|EPITIOSTANOL|Epitiostanol","An androgenic anabolic steroid having potent anti-estrogenic effect, which inhibits the progression of estrogen-stimulated cancers such as breast cancer. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C118450","Epothilone Analog UTD1","Epothilone Analog UTD1|UTD1","A genetically engineered epothilone analog with potential antineoplastic activity. Upon administration, epothilone analog UTD1 binds to tubulin, induces microtubule polymerization and stabilizes microtubules against depolymerization, which may result in the inhibition of cell division, the induction of G2/M arrest, and apoptosis. Compared to first-generation epothilones, this agent exhibits greater safety and enhanced activity against certain multidrug-resistant (MDR) tumors.","Organic Chemical|Pharmacologic Substance"]
["C77892","Epothilone KOS-1584","9,10-Didehydroepothilone D|Epothilone KOS-1584|KOS-1584","A second-generation epothilone with potential antineoplastic activity. Epothilone KOS-1584 binds to tubulin and induces microtubule polymerization and stabilizes microtubules against depolymerization, which may result in the inhibition of cell division, the induction of G2/M arrest, and apoptosis. Compared to first-generation epothilones, this agent exhibits greater safety and efficacy with an enhanced pharmaceutical profile, including enhanced water solubility and tumor penetration, and reduced CNS exposure. In addition, epothilone KOS-1584 is a poor substrate for the P-glycoprotein (P-gp) drug efflux pump.","Organic Chemical|Pharmacologic Substance"]
["C1887","Epratuzumab","EPRATUZUMAB|Epratuzumab|Humanized Anti-CD22 Monoclonal Antibody IgG1|LymphoCide|epratuzumab|hLL2","A recombinant, humanized monoclonal antibody directed against CD22, a cell surface glycoprotein present on mature B-cells and on many types of malignant B-cells.  After binding to CD22, epratuzumab's predominant antitumor activity appears to be mediated through antibody-dependent cellular cytotoxicity (ADCC).","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C95720","ERa36 Modulator Icaritin","4H-1-Benzopyran-4-one, 3,5,7-trihydroxy-2-(4-methoxyphenyl)-8-(3-methyl-2-butenyl)-|ERa36 Modulator Icaritin","A metabolite of icariin, a principal flavonoid glycoside in Herba Epimedii (a traditional Chinese medicine herb used in treating osteoporosis) with potential antineoplastic activity. ERa36 modulator icaritin selectively binds to a novel variant of estrogen receptor alpha, a36, and mediates a membrane-initiated \"nongenomic\" signaling pathway, which is linked to activate signaling pathways like the MAPK/ERK and the PI3K/Akt pathways. This agent induces cell cycle arrest at G1, or G2/M arrest depending upon the dose. Consistently with G1 arrest, icaritin increases protein expressions of pRb, p27(Kip1) and p16(Ink4a), while decreasing phosphorylated pRb, Cyclin D1 and CDK4. 40% of ER-negative breast cancer tumors express high levels of ERa36, and this subset of patients is less likely to benefit from tamoxifen treatment compared with those with ERa66-positive/ERa36-negative tumors.","Pharmacologic Substance"]
["C70625","Erastin Analogue PRLX 93936","Erastin Analogue PRLX 93936|PRLX 93936","A structural analogue of erastin with potential antineoplastic activity. Erastin analogue PRLX 93936 appears to inhibit mitochondrial outer membrane protein VDACs (voltage-dependent anion channels) 2 and 3, resulting in an oxidative, non-apoptotic cell death. Erastin analogue PRLX 93936 exhibits greater lethality in cell lines harboring mutations in the GTPase protein oncogenes HRAS and KRAS or the serine-threonine protein kinase oncogene BRAF than in non-tumorigenic cell lines. VDACs 2 and 3 are up-regulated in a wide variety of tumor cell lines.","Pharmacologic Substance"]
["C77896","ErbB-2 Inhibitor ARRY-380","ARRY-380|ErbB-2 Inhibitor ARRY-380|ONT-380","An orally bioavailable inhibitor of the human epidermal growth factor receptor tyrosine kinase ErbB-2 (also called HER2) with potential antineoplastic activity. ErbB-2 inhibitor ARRY-380 selectively binds to and inhibits the phosphorylation of ErbB-2, which may prevent the activation of ErbB-2 signal transduction pathways, resulting in growth inhibition and death of ErbB-2-expressing tumor cells. ErbB-2 is overexpressed in a variety of cancers and plays an important role in cellular proliferation and differentiation.","Organic Chemical|Pharmacologic Substance"]
["C73258","Erbulozole","Carbamic acid, (4-(((2-(1H-imidazol-1-ylmethyl)-2-(4-methoxyphenyl)-1,3-dioxolan-4-yl)methyl)thio)phenyl)-,ethyl ester, cis-(+-)-|ERBULOZOLE|Erbulozole|R55104","A water soluble congener of tubulozole and a tubulin binding agent with potential antimitotic and antineoplastic activities. Erbulozole targets and binds to tubulin, thereby preventing the polymerization of tubulin. This may lead to an inhibition of cell division and induction of apoptosis.","Pharmacologic Substance"]
["C96748","Eribulin","2-(3-Amino-2-hydroxypropyl)hexacosahydro-3-methoxy-26-methyl-20,27-bis(methylene)11,15-18,21-24,28-triepoxy-7,9-ethano-12,15-methano-9H,15H-furo(3,2-i)furo(2',3'-5,6)pyrano(4,3-b)(1,4)dioxacyclopentacosin-5-(4H)-one|ER-086526|ERIBULIN|Eribulin","An analogue of halichondrin B, a substance derived from a marine sponge (Lissodendoryx sp.) with antineoplastic activity. Eribulin binds to the vinca domain of tubulin and inhibits the polymerization of tubulin and the assembly of microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest at G2/M phase, and, potentially, tumor regression.","Organic Chemical|Pharmacologic Substance"]
["C26644","Eribulin Mesylate","2-(3-Amino-2-hydroxypropyl)hexacosahydro-3-methoxy-26-methyl-20,27-bis(methylene)11,15-18,21-24,28-triepoxy-7,9-ethano-12,15-methano-9H,15H-furo(3,2-i)furo(2',3'-5,6)pyrano(4,3-b)(1,4)dioxacyclopentacosin-5-(4H)-one|B1939 Mesylate|E7389|ER-086526|ERIBULIN MESYLATE|Eribulin Mesylate|Halaven|Halichondrin B Analog|eribulin mesylate","The mesylate salt of a synthetic analogue of halichondrin B, a substance derived from a marine sponge (Lissodendoryx sp.) with antineoplastic activity. Eribulin binds to the vinca domain of tubulin and inhibits the polymerization of tubulin and the assembly of microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest at G2/M phase, and, potentially, tumor regression.","Organic Chemical|Pharmacologic Substance"]
["C119747","ERK Inhibitor CC-90003","CC-90003|ERK Inhibitor CC-90003","An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, CC-90003 inhibits ERK activity, and prevents the activation of ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.","Pharmacologic Substance"]
["C107241","ERK Inhibitor GDC-0994","ERK Inhibitor GDC-0994|GDC-0994","An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, GDC-0994 inhibits both ERK phosphorylation and activation of ERK-mediated signal transduction pathways. This prevents ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.","Pharmacologic Substance"]
["C126687","ERK Inhibitor LTT462","ERK Inhibitor LTT462|LTT 462|LTT462","An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, LTT462 binds to and inhibits ERK, thereby preventing the activation of ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is upregulated in numerous tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.","Pharmacologic Substance"]
["C104045","ERK Inhibitor MK-8353","ERK Inhibitor MK-8353|MK-8353-001|MK-8353|SCH 900353","An orally available inhibitor of extracellular signal-regulated kinase (ERK), with potential antineoplastic activity. Upon oral administration, MK-8353 inhibits both ERK phosphorylation and activation of ERK-mediated signal transduction pathways; thereby, preventing ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is often upregulated in a variety of tumor cell types and plays a role in tumor cell proliferation, differentiation and survival.","Pharmacologic Substance"]
["C65530","Erlotinib","ERLOTINIB|Erlotinib|erlotinib","A quinazoline derivative with antineoplastic properties.  Competing with adenosine triphosphate, erlotinib reversibly binds to the intracellular catalytic domain of epidermal growth factor receptor (EGFR) tyrosine kinase, thereby reversibly inhibiting EGFR phosphorylation and blocking the signal transduction events and tumorigenic effects associated with EGFR activation.","Pharmacologic Substance"]
["C2693","Erlotinib Hydrochloride","CP-358,774|Cp-358,774|ERLOTINIB HYDROCHLORIDE|Erlotinib Hydrochloride|N-(3-Ethynylphenyl)-6,7-bis(2-methoxyethoxy)-4-quinazolinamine Monohydrochloride|OSI-774|Tarceva|erlotinib hydrochloride","The hydrochloride salt of a quinazoline derivative with antineoplastic properties.  Competing with adenosine triphosphate, erlotinib reversibly binds to the intracellular catalytic domain of epidermal growth factor receptor (EGFR) tyrosine kinase, thereby reversibly inhibiting EGFR phosphorylation and blocking the signal transduction events and tumorigenic effects associated with EGFR activation.","Organic Chemical|Pharmacologic Substance"]
["C2658","Ertumaxomab","Anti-CD3 x anti-HER-2-neu Bispecific Monoclonal Antibody|Ertumaxomab","A murine monoclonal antibody with two antigen-recognition sites: one for CD3, an antigen expressed on mature T cells, and one for HER-2-neu, a tumor-associated antigen that promotes tumor growth.  Ertumaxomab attaches to CD3-expressing T cells and HER-2-neu-expressing tumor cells, selectively cross-linking tumor and immunologic cells which results in the recruitment of cytotoxic T cells to the T cell/tumor cell aggregate.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C99767","Erythrocyte-encapsulated L-asparaginase Suspension","Erythrocyte-encapsulated L-asparaginase Suspension|GRASPA","A suspension of erythrocytes encapsulating L-asparaginase with potential antineoplastic activity. Upon administration of erythrocyte-encapsulated L-asparaginase suspension, L-asparagine is hydrolyzed to L-aspartic acid and ammonia in plasma, thereby depleting tumor cells of asparagine. Due to low asparagine synthetase activity in tumor cells, de novo synthesis of asparagine is suppressed within tumor cells. Shortage of asparagine prevents synthesis of important proteins necessary for tumor cell growth. Encapsulation of asparaginase in erythrocytes decreases the immunogenicity of exogenous protein, enhances its circulation time and may limit toxicity.","Enzyme|Pharmacologic Substance"]
["C119743","E-selectin Antagonist GMI-1271","E-selectin Antagonist GMI-1271|GMI-1271","A synthetic, glycomimetic molecule and E-selectin (CD62E) antagonist, with potential anti-thrombotic, antineoplastic and chemopotentiating activities. Upon administration, GMI-1271 binds to E-selectin expressed on endothelial cells and prevents their interaction with selectin-E ligand-expressing cancer cells. This may prevent tumor cell activation, migration and metastasis. GMI-1271 also interferes with the binding of selectin E-expressing vascular endothelial cells to selectin-E ligand-expressing monocytes and neutrophils, thereby disrupting their activation. Consequently, this inhibits both the activation of the coagulation cascade and thrombus formation. This agent also prevents both leukocyte activation and inflammation. E-selectin is a cell adhesion molecule involved in cell rolling, signaling and chemotaxis; it also plays a crucial role in inflammatory processes and cancer.","Pharmacologic Substance"]
["C972","Esorubicin","4'-Deoxyadriamycin|4'-Deoxydoxorubicin|Deoxyadriamycin|Deoxydoxorubicin|ESORUBICIN|Esorubicin|IMI-58","A synthetic derivative of the anthracycline antineoplastic antibiotic doxorubicin with potential antineoplastic activity. Esorubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. This agent exhibits less cardiotoxicity than the parent antibiotic doxorubicin, but may cause more severe myelosupression compared to other compounds within the anthracycline class.","Antibiotic|Organic Chemical"]
["C74943","Esorubicin Hydrochloride","(2S-(2alpha(8R*,10R*),4beta,6beta))-10-((4-Aminotetrahydro-6-methyl-2H-pyran-2-yl)oxy)-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxynaphthacene-5,12-dione Hydrochloride|4'-Deoxyadriamycin HCl|4'-Deoxydoxorubicin HCl|ESORUBICIN HYDROCHLORIDE|Esorubicin Hydrochloride","A hydrochloride salt of esorubicin, a derivative of the anthracycline antineoplastic antibiotic doxorubicin, with potential antineoplastic activity. Esorubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis. This agent exhibits less cardiotoxicity than the parent antibiotic doxorubicin, but may cause more severe myelosupression compared to other compounds within the anthracycline class.","Antibiotic|Pharmacologic Substance"]
["C1301","Esperamicin A1","Esperamicin A1","An enediyne antineoplastic antibiotic hybrid containing an anthranilate moiety.  Esperamicin A1 is isolated from the bacterium Actinomadura verrucosospora.  The anthranilate component of esperamicin A1 intercalates DNA and the benzene diradical intermediate of the enediyne core binds to the minor groove of DNA, resulting in single- and double-stranded breaks in DNA and apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C26649","Essiac","Esiak|Essiac","An herbal formula containing burdock root (Arctium lappa), Turkey rhubarb root (Rheum palmatum), sheep sorrel (Rumex acetosella), and slippery elm bark (Ulmus fulva) with potential immunostimulating, anti-inflammatory and anti-tumor activities. The extract's chemical profile, their respective concentrations and the mechanism of action of Essiac are largely unknown due to the proprietary nature of the formula and product inconsistency. Several chemical classes in Essiac are consistently represented and may attribute to its therapeutic effect, including anthraquinone derivatives such as rhein and emodin, high molecular polysaccharides, and lignans such as arctigenin. However, all these chemicals are unlikely to occur in high concentrations in Essiac, and its potential therapeutic effect may be attributed to a potential synergistic effect of these various compounds.","Pharmacologic Substance"]
["C479","Estramustine","17beta-(estra-1,3,5(10)-triene-3,17-diol 3-(bis(2-chloroethyl)carbamate))|ESTRAMUSTINE|Estradiol 3-[bis(2-chloroethyl)carbamate]|Estramustine|Leo 275|RO 21-8837|estra-1,3,5(10)triene-317beta-diol 3-[N,N-bis-(2-chloroethyl)carbamate]|estradiol 3-bis(2-chloroethyl)carbamate|estramustine","A synthetic molecule combining estradiol and nornitrogen mustard through a carbamate link. Estramustine and its major metabolite estramustine bind to microtubule-associated proteins (MAPs) and tubulin, thereby inhibiting microtubule dynamics and leading to anaphase arrest in a dose-dependent fashion. This agent also exhibits anti-androgenic effects. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C96432","Estrogen Receptor Agonist GTx-758","Capesaris|Estrogen Receptor Agonist GTx-758|GTx-758","An orally available, nonsteroidal selective estrogen receptor (ER) alpha agonist with potential antineoplastic activity. Upon administration of GTx-758, this agent suppresses the secretion of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) by the pituitary gland through feedback inhibition. In males, the inhibition of LH secretion prevents the synthesis of androgens, including testosterone, by the testes. This may result in suppressed total serum testosterone to the levels observed in castration.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1626","Etalocib","2-[2-Propyl-3-[3-[2-ethyl-4-(4-fluorophenyl)-5-hydroxyphenoxy]propoxy]phenoxy]benzoic Acid|2-[3-[3-[(5-Ethyl-4'-fluoro-2-hydroxy[1,1'-biphenyl]-4-yl)oxy]propoxy]-2-propylphenoxy]benzoic Acid|ETALOCIB|Etalocib|LY293111","A second-generation selective leukotriene B4 receptor (LTB4R) antagonist with potential antineoplastic activity. Although the exact underlying mechanism through which LY293111 exerts its effects has not been fully elucidated, this agent selectively binds to and blocks LTB4Rs, thereby inhibiting the downstream signalling pathway. LY29311 has been shown to induce apoptosis and inhibits cellular proliferation in LTB4R expressing cells, such as pancreatic cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C2381","Etanercept","ETANERCEPT|Enbrel|Etanercept|TNFR:Fc|Tumor Necrosis Factor Receptor IgG Chimera|etanercept","A recombinant soluble dimeric fusion protein consisting of the extracellular ligand-binding region of recombinant human tumor necrosis factor (rhTNF) receptor attached to the constant (Fc) region of human immunoglobulin G (FcIgG). The receptor moiety of etanercept binds to circulating TNF (2 molecules of TNF per receptor) and inhibits its attachment to endogenous TNF cell surface receptors, thereby rendering TNF inactive and inhibiting TNF-mediated mechanisms of inflammation. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1092","Etanidazole","1H-Imidazole-1-acetamide, N-(2-hydroxyethyl)-2-nitro-|2-Nitroimidazole-1-acetamide, N-(2-hydroxyethyl)-|ETANIDAZOLE|Etanidazole|SR-2508|etanidazole","A 2-nitroimidazole with radiosensitizing properties. Etanidazole depletes glutathione and inhibits glutathione transferase, thereby enhancing the cytotoxicity of ionizing radiation. This agent may also be useful as an imaging agent for identifying hypoxic, drug-resistant regions of primary tumors or metastases.  (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1800","Etaracizumab","Abegrin|ETARACIZUMAB|Etaracizumab|Humanized Monoclonal Antibody LM609|MEDI-522|Monoclonal Antibody Anti-Avb3 Integrin Medi-522|Monoclonal Antibody Anti-alpha V Beta 3 Integrin MEDI-522|Vitaxin|etaracizumab|humanized monoclonal antibody MEDI-522","A humanized monoclonal IgG1 antibody directed against the vitronectin receptor alpha v beta 3 integrin. Etaracizumab blocks the binding of ligands, such as vitronectin, to alpha v beta 3 integrin, resulting in inhibition of angiogenesis and metastasis. Alpha v beta 3 integrin is a cell adhesion and signaling receptor that is expressed on the surface of tumor vessel endothelial cells, some tumor cells, and a number of other cell types.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C96705","Etarotene","6-((E)-p-(Ethylsulfonyl)-alpha-methylstyryl)-1,2,3,4-tetrahydronaphthalene|Arotinoid Ethyl Sulfone|Arotinoid Ethyl Sulphone|ETAROTENE|Etarotene|Naphthalene, 6-(2-(4-(ethylsulfonyl)phenyl)-1-methylethenyl)-1,2,3,4-tetrahydro-1,1,4,4-tetramethyl-, (E)-|Ro 15-1570/000","An ethylsulfonyl derivative of arotinoic acid with differentiation inducing and potential antineoplastic activities. Like other retinoic acid agents, etarotene binds to and activates retinoic acid receptors (RARs), thereby inducing changes in the expression of certain genes leading to cell differentiation and decreased cell proliferation in susceptible cells.","Pharmacologic Substance"]
["C116713","Ethaselen","1, 2-[Bis (1, 2-Benzisoselenazolone-3 (2H) -Ketone)] Ethane|BBSKE|Ethaselen","An orally bioavailable organoselenium inhibitor of thioredoxin reductase 1 (TrxR1), with potential antineoplastic activity. Upon oral administration, ethaselen specifically binds to the selenocysteine-cysteine redox pair in the C-terminal active site of TrxR1 and inhibits its activity, which may result in growth inhibition and the induction of apoptosis in TrxR1 overexpressing tumor cells. TrxR1, upregulated in many cancer cell types, plays a key role in various redox-dependent cellular pathways, regulates transcription factor activity, inhibits apoptosis, and promotes cell growth and survival.","Pharmacologic Substance"]
["C486","Ethinyl Estradiol","(17alpha)-19-Norpregna-1,3,5(10)-trien-20-yne-3,17-diol|Diogyn E|Diogyn-E|ETHINYL ESTRADIOL|Estinyl|Ethinoral|Ethinyl Estradiol|Ethinylestradiol|Eticylol|Feminone|Inestra|Lynoral|Orestralyn","A semisynthetic estrogen. Ethinyl estradiol binds to the estrogen receptor complex and enters the nucleus, activating DNA transcription of genes involved in estrogenic cellular responses. This agent also inhibits 5-alpha reductase in epididymal tissue, which lowers testosterone levels and may delay progression of prostatic cancer. In addition to its antineoplastic effects, ethinyl estradiol protects against osteoporosis. In animal models, short-term therapy with this agent has been shown to provide long-term protection against breast cancer, mimicking the antitumor effects of pregnancy. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2371","Ethylchlorformate","Ethylchlorformate","A substance used to treat tumor cells for synthesis of a tumor-specific immunotherapeutic agent, ethyl chloroformate polymerized tumor protein, for use in Immunotherapy.","Organic Chemical|Pharmacologic Substance"]
["C28579","Ethylchlorformate Vaccine","Ethylchlorformate Vaccine","A tumor vaccine comprised of ethylchlorformate polymerized tumor protein, obtained by treating tumor cells with ethylchloroformate to produce a tumor-specific immunotherapeutic agent. (NCI)","Immunologic Factor|Pharmacologic Substance"]
["C1009","Ethyleneimine","Aminoethylene|Azacyclopropane|Azirane|Aziridine|Dimethyleneimine|Dimethylenimine|ETHYLENEIMINE|Ethyleneimine|Ethylenimine|Ethylimine","A monofunctional alkylating agent with potential antineoplastic activity.  Reacting with DNA mainly at guanine and adenine residues, ethylenimine alkylates DNA, thereby producing DNA interstrand crosslinks and DNA breaks, and interfering with DNA replication and cell division. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C26563","Ethylnitrosourea","1-Ethyl-1-nitrosourea|ENU|Ethylnitrosourea|N-ETHYL-N-NITROSOUREA|N-Ethyl-N-nitrosourea|N-Nitroso-N-Ethylurea|Nitrosoethylurea","A nitrosourea with potential antineoplastic activity.  Used experimentally as a mutagen and carcinogen, ethylnitrosourea alkylates DNA and proteins, thereby damaging DNA and inducing point mutations. (NCI04)","Hazardous or Poisonous Substance|Organic Chemical"]
["C125901","Etidronate-Cytarabine Conjugate MBC-11","Etidronate-Cytarabine Conjugate MBC-11|Etidronate-ara-C Conjugate MBC-11|MBC-11","A synthetic conjugate composed of the bisphosphonate etidronate linked to the cytostatic agent and antimetabolite cytarabine, with potential antineoplastic and antiresorptive activities. Upon intravenous administration of the etidronate-cytarabine conjugate MBC-11, the etidronate moiety targets bone and the two moieties are released upon hydrolysis. Etidronate binds to hydroxyapatite crystals in bone tissues and prevents its resorption. This prevents bone destruction and induces bone cell mineralization. In addition, the bone-targeting nature of this agent allows for the accumulation of cytarabine in bone tissue, where it is able to exert its antitumor effect locally by competing with cytidine for incorporation into DNA, thereby inhibiting DNA synthesis, while reducing systemic exposure. This leads to a destruction of bone-associated tumor cells, an inhibition of tumor cell proliferation and bone metastasis, and prevents tumor-mediated bone destruction.","Pharmacologic Substance"]
["C489","Etoglucid","1,2-Bis[2-(2, 3-epoxypropoxy)ethoxy]ethane|1,2-bis[2-(2,3-epoxypropoxy)ethoxy]ethane|1,2:15,16-Diepoxy-4,7,10, 13-tetraoxahexadecane|1,2:15,16-diepoxy-4,7,10,13-tetraoxahexadecane|2,2'-(2,5,8,11-tetraoxadodecane-1,12-diyl)bisoxirane|ETOGLUCID|Epodyl|Ethane, 1, 2-bis[2-(2,3-epoxypropoxy)ethoxy]-|Ethoglucid|Etoglucid|ICI 32865|ICI-32865|Triethylene Glycol Diglycidyl Ether|Triethylene glycol diglycidyl ether","An epoxide compound with potential antineoplastic alkylating activity. Etoglucid is able to crosslink DNA via its epoxide group, resulting in disruption of DNA function and cell cycle arrest.","Organic Chemical|Pharmacologic Substance"]
["C491","Etoposide","4'-Demethylepipodophyllotoxin 9-[4,6-O-ethylidene-beta-D-glucopyranoside]|9-[(4,6-O-Ethylidene-beta-D-glucopyranosyl]oxy)-5,8,8a,9-tetrahydro-5-(4-hydroxy-3,5-dimethoxyphenyl)furo[3',4':6,7]naphtho[2,3-d]-1,3-dioxol-6(5aH)-one|Demethyl Epipodophyllotoxin Ethylidine Glucoside|EPEG|ETOPOSIDE|Etoposide|Lastet|Toposar|VP 16-213|VP-16-213|VP-16|Vepesid|etoposide","A semisynthetic derivative of podophyllotoxin, a substance extracted from the mandrake root Podophyllum peltatum.  Possessing potent antineoplastic properties, etoposide binds to and inhibits topoisomerase II and its function in ligating cleaved DNA molecules, resulting in the accumulation of single- or double-strand DNA breaks, the inhibition of DNA replication and transcription, and apoptotic cell death.  Etoposide acts primarily in the G2 and S phases of the cell cycle. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1093","Etoposide Phosphate","ETOPOSIDE PHOSPHATE|Etopophos|Etoposide Phosphate|etoposide phosphate","A phosphate salt of a semisynthetic derivative of podophyllotoxin. Etoposide binds to the enzyme topoisomerase II, inducing double-strand DNA breaks, inhibiting DNA repair, and resulting in decreased DNA synthesis and tumor cell proliferation. Cells in the S and G2 phases of the cell cycle are most sensitive to this agent. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C114977","Etoposide Prodrug CAP7.1","CAP7.1|Etoposide Prodrug CAP7.1","A prodrug of etoposide, a semisynthetic derivative of podophyllotoxin extracted from the mandrake root Podophyllum peltatum, with potential antineoplastic activity. Upon intravenous administration of the etoposide prodrug CAP7.1, etoposide is released after enzymatic cleavage of CAP7.1 by specific carboxylesterases (CE) 1 and 2, which are upregulated in certain tumor cell types. Etoposide acts primarily in the G2 and S phases of the cell cycle. This drug binds to and inhibits topoisomerase II, an enzyme elevated in tumor cells. This results in the accumulation of double-strand DNA breaks, the inhibition of DNA replication and transcription and the induction of apoptotic cell death. The tumor-specific activation of etoposide increases its efficacy while lowering its systemic toxicity.","Pharmacologic Substance"]
["C73236","Etoprine","2,4-Diamino-5-(3,4-dichlorophenyl)-6-ethylpyrimidine|AI3-25008|DDEP|ETOPRINE|Ethodichlorophen|Etoprine","A lipophilic, diaminopyrimidine folate antagonist with potential antineoplastic activity. Etoprine inhibits dihydrofolate reductase, resulting in decreased cellular folate metabolism. This may eventually result in a reduction of cellular growth and the induction of apoptosis. In addition, this agent inhibits histamine-N-methyltransferase, resulting in decreased histamine catabolism. Lipid-soluble etoprine is capable of crossing the blood-brain barrier.","Pharmacologic Substance"]
["C52188","Etoricoxib","5-Chloro-2-(6-methylpyridin-3-yl)-3-(4-methylsulfonylphenyl) Pyridine|Arcoxia|ETORICOXIB|Etoricoxib|L-791456|MK-0663","A synthetic, nonsteroidal anti-inflammatory drug (NSAID) with antipyretic, analgesic, and potential antineoplastic properties. Etoricoxib specifically binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in inhibition of the conversion of arachidonic acid into prostaglandins. Inhibition of COX-2 may induce apoptosis and inhibit tumor cell proliferation and angiogenesis.","Pharmacologic Substance"]
["C125657","Ets-family Transcription Factor Inhibitor TK216","Ets-family Transcription Factor Inhibitor TK216|TK-216|TK216","A proprietary biologic that inhibits the transcriptional-promoting activity of E26 transformation-specific (Ets, E-twenty-six) family transcription factors, with potential antineoplastic activity. Although the exact mechanism(s) of action through which this agent exerts its effect has yet to be fully elucidated, upon administration, Ets-family transcription factor inhibitor TK216 inhibits transcriptional activation mediated by Ets family proteins, including the oncogenic Ewing sarcoma breakpoint region 1/Friend leukemia virus integration 1 (EWSR1/FLI1; EWS/FLI1) fusion protein. This agent may both inhibit the malignant downstream effects mediated by genomic rearrangements that result in the overexpression of Ets family transcription factors and decrease tumor cell growth and proliferation. A chromosomal translocation t(11;22)(q24;q12) fuses the EWSR1 gene and the FLI1 gene and encodes the EWSR1/FLI1 fusion protein, which is an oncoprotein expressed by peripheral primitive neuroectodermal (pPNET) tumors.","Pharmacologic Substance"]
["C48387","Everolimus","(1R,9S,12S,15R,16E,18R,19R,21R,23S,24E,26E,28E,30S,32S,35R)-1,18-Dihydroxy-12-((1R)-2-((1S,3R,4R)-4-(2-hydroxyethoxy)-3-methoxycyclohexyl)-1-methylethyl)-19,30-dimethoxy-15,17,21,23,29,35-hexamethyl-11,36-dioxa-4-azatricyclo(30.3.1.04,9)hexatriaconta-16,24,26,28-tetraene-2,3,10,14,20-pentaone|42-O-(2-Hydroxy)ethyl Rapamycin|Afinitor|Certican|EVEROLIMUS|Everolimus|RAD 001|RAD001|Votubia|Zortress|everolimus","A derivative of the natural macrocyclic lactone sirolimus with immunosuppressant and anti-angiogenic properties. In cells, everolimus binds to the immunophilin FK Binding Protein-12 (FKBP-12) to generate an immunosuppressive complex that binds to and inhibits the activation of the mammalian Target of Rapamycin (mTOR), a key regulatory kinase. Inhibition of mTOR activation results in the inhibition of T lymphocyte activation and proliferation associated with antigen and cytokine (IL-2, IL-4, and IL-15) stimulation and the inhibition of antibody production. (NCI05)","Pharmacologic Substance"]
["C102880","Everolimus Tablets for Oral Suspension","Afinitor Disperz|Everolimus Tablets for Oral Suspension","Tablets for oral suspension containing everolimus, a derivative of the natural macrocyclic lactone sirolimus, with immunosuppressive and antineoplastic activities. After suspension of the everolimus tablets in water and oral administration, this agent inhibits the activation of the serine/threonine kinase mammalian target of rapamycin (mTOR) by binding to mTOR's cytosolic receptor immunophilin FK Binding Protein-12 (FKBP-12). Inhibition of the mTOR complex may result in the inhibition of the phosphatidylinositol 3 kinase/Akt/mTOR pathway and an inhibition in the expression of vascular endothelial cell growth factor (VEGF) and hypoxia-inducible factor. Ultimately, this may result in decreased tumor cell proliferation and tumor angiogenesis. This pediatric formulation can dissolve easily in a small volume of water making it easier to swallow and is available in smaller dose increments thereby allowing for greater dosing flexibility.","Pharmacologic Substance"]
["C114985","Ex Vivo-activated Autologous Lymph Node Lymphocytes","Ex Vivo-activated Autologous Lymph Node Lymphocytes|X-ACT Autologous Lymph Node Lymphocytes|X-ACT","Autologous human lymph node T-lymphocytes, with potential immunostimulatory and antineoplastic activity. Upon collection of immune cells from the tumor-draining lymph node, the human lymph node lymphocytes are activated with anti-CD3/anti-CD28 microbeads, cultured with recombinant, human interleukin-2 (IL-2), expanded and isolated ex vivo. Upon reintroduction into the patient, the ex vivo-activated autologous lymph node lymphocytes recognize and lyse the tumor cells.","Pharmacologic Substance"]
["C52192","Ex Vivo-Expanded HER2-Specific T Cells","Ex Vivo-Expanded HER2-Specific T Cells|HER2 Specific T-Cells","T cells specific for the human epidermal growth factor receptor 2 (HER2) with potential immunopotentiating activity. T cells directed against HER2, overexpressed on many tumor cells, are collected from HER2-expressing tumor tissue, expanded ex vivo and, then re-introduced in the patient. Re-introduction of ex vivo-expanded HER2-specific T cells may enhance the cytotoxic T cell response against tumor cells overexpressing HER2, resulting in inhibition of tumor growth.","Pharmacologic Substance"]
["C1679","Exatecan Mesylate","DX-8951f|EXATECAN MESYLATE|Exatecan Mesylate Hydrate|Exatecan Mesylate|exatecan mesylate","A semisynthetic, water-soluble derivative of camptothecin with antineoplastic activity. Exatecan mesylate inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA and inhibiting religation of DNA breaks, thereby inhibiting DNA replication and triggering apoptotic cell death. This agent does not require enzymatic activation and exhibits greater potency than camptothecin and other camptothecin analogues. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1097","Exemestane","6-Methyleneandrosta-1,4-diene-3,17-dione|Aromasin|EXEMESTANE|Exemestane|FCE-24304|exemestane","A synthetic androgen analogue.  Exemestane binds irreversibly to and inhibits the enzyme aromatase, thereby blocking the conversion of cholesterol to pregnenolone and the peripheral aromatization of androgenic precursors into estrogens. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C112498","Extended Release Flucytosine","Extended Release 5-FC|Extended Release 5-Fluorocytosine|Extended Release Flucytosine|Extended-Release 5-FC|Extended-Release 5-Fluorocytosine|Extended-Release Flucytosine|Toca FC","An extended release (ER) oral tablet that contains flucytosine (5-FC), a fluorinated cytosine analog, with antifungal activity and potential anti-cancer activity. Following oral administration of ER 5-FC, the 5-FC is deaminated to its active metabolite 5-fluorouracil (5-FU). 5-FU replaces uracil during RNA synthesis, which consequently inhibits downstream protein synthesis. In addition, 5-FU is metabolized further to 5-fluorodeoxyuridylic acid monophosphate, which inhibits thymidylate synthetase. Inhibition of this enzyme interrupts nucleotide synthesis, DNA replication and cell proliferation. Negative regulation of protein synthesis, DNA replication and cell proliferation can lead to cell death. Following ingestion of ER 5-FC, intravenous injection of a retroviral vector encoding cytosine deaminase (TC 511) at a tumor site may result in higher local concentrations of 5-FU and its metabolites, and increased tumor cell death than other 5-FU treatment regimens.","Pharmacologic Substance"]
["C113797","Extended-release Onapristone","ER Onapristone|Extended-release Onapristone","An extended-release (ER) formulation of onapristone, an orally bioavailable progesterone receptor (PR) antagonist, with antineoplastic activity. Onapristone binds to the PR and inhibits both PR activation and the associated expression of PR-responsive genes. This may inhibit PR-mediated proliferative effects in cancer cells overexpressing PR. PR is expressed on certain cancer cell types and plays a key role in proliferation and survival.","Organic Chemical|Pharmacologic Substance"]
["C127114","EZH1/2 Inhibitor DS-3201","DS 3201b|DS-3201|DS-3201b|EZH1/2 Inhibitor DS-3201","An orally available selective inhibitor of the histone lysine methyltransferases enhancer of zeste homolog 1 (EZH1) and 2 (EZH2), with potential antineoplastic activity. Upon oral administration, DS-3201 selectively inhibits the activity of both wild-type and mutated forms of EZH1 and EZH2. Inhibition of EZH1/2 specifically prevents the methylation of lysine 27 on histone H3 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways, enhances transcription of certain target genes, and results in decreased proliferation of EZH1/2-expressing cancer cells. EZH1/2, histone lysine methyltransferase (HMT) class enzymes and catalytic subunits of the polycomb repressive complex 2 (PRC2), are overexpressed or mutated in a variety of cancer cells and play key roles in tumor cell proliferation, progression, stem cell self-renewal and migration.","Organic Chemical|Pharmacologic Substance"]
["C121639","EZH2 Inhibitor CPI-1205","CPI-1205|EZH2 Inhibitor CPI-1205","An orally available selective inhibitor of the histone lysine methyltransferase EZH2, with potential antineoplastic activity. Upon oral administration, CPI-1205 selectively inhibits the activity of both wild-type and mutated forms of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 on lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased proliferation of EZH2-expressing cancer cells. EZH2, a histone lysine methyltransferase (HMT) class enzyme and the catalytic subunit of the polycomb repressive complex 2 (PRC2), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation; its expression is correlated with tumor initiation, progression, stem cell self-renewal, migration and angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C91395","F16-IL2 Fusion Protein","F16-IL2 Fusion Protein|Teleukin","An immunocytokine of the human monoclonal antibody fragment F16 (scFv) against the extra-domain A1 of tenascin-C fused, via a short 5-amino acid linker, to a recombinant form of the human cytokine interleukin-2 (IL-2) with potential immunostimulating and antineoplastic activities. The monoclonal antibody portion of the F16-IL2 fusion protein binds to tumor cells expressing the tumor associated antigen (TAA) tenascin-C. In turn, the IL-2 moiety of the fusion protein stimulates natural killer (NK) cells, macrophages and neutrophils and induces T-cell antitumor cellular immune responses thereby selectively killing tenascin-C-expressing tumor cells. In addition, F16-IL2 may potentiate the cytotoxicity of other chemotherapeutic agents. Tenascin-C, a glycoprotein of the extracellular matrix, is expressed in many cancer cell types.","Pharmacologic Substance"]
["C107239","FACT Complex-targeting Curaxin CBL0137","CBL0137|FACT Complex-targeting Curaxin CBL0137","An orally available curaxin-based agent targeting the Facilitates Chromatin Transcription (FACT) complex, with potential antineoplastic activity. Upon administration, CBL0137 binds to FACT and sequesters the FACT complex on chromatin, which inhibits its activity. This prevents transcription of certain genes involved in cancer-associated signaling pathways; it specifically inhibits the transcription of both NF-kappa B and heat shock transcription factor 1 (HSF1) and simultaneously activates p53. This causes an increase in tumor cell apoptosis and a decrease in tumor cell proliferation, in FACT-positive cancers. In addition, this agent is able to sensitize FACT-positive tumor cells to the cytotoxic effects of other chemotherapeutic agents. FACT, a transcription and replication factor composed of the Structure Specific Recognition Protein (SSRP1) and suppressor of Ty 16 (Spt16) proteins, is expressed in a variety of tumor cells while almost absent in normal cells; its expression is associated with increased tumor aggressiveness and poor prognosis.","Pharmacologic Substance"]
["C88324","Factor VIIa Inhibitor PCI-27483","Factor VIIa Inhibitor PCI-27483|PCI-27483","A reversible small-molecule inhibitor of activated factor VII (factor VIIa) with potential antineoplastic and antithrombotic activities.  FVII, a serine protease, becomes activated (FVIIa) upon binding with TF forming the FVIIa/TF complex, which induces intracellular signaling pathways by activating protease activated receptor 2 (PAR-2). Upon subcutaneous administration, factor VIIa inhibitor PCI-27483 selectively inhibits factor FVIIa in the VIIa/TF complex, which may prevent PAR-2 activation and PAR2-mediated signal transduction pathways, thereby inhibiting tumor cell proliferation, angiogenesis, and metastasis of TF-overexpressing tumor cells. In addition, this agent inhibits both the extrinsic and intrinsic coagulation cascades, preventing blood clot formation. TF, a blood protein overexpressed on the cell surface of a variety of tumor cell types, may correlate with poor prognosis; PAR-2 (also known as thrombin receptor-like 1) is a G protein-coupled receptor (GPCR) and a protease-activated receptor.","Pharmacologic Substance"]
["C129313","Factor VII-targeting Immunoconjugate Protein ICON-1","FVII Modified Conjugate ICON-1|FVII-targeting Immunoconjugate Protein ICON-1|Factor VII-targeting Immunoconjugate Protein ICON-1|Human Immuno-conjugate 1|ICON-1|VII-Fc Fusion Protein ICON-1","A human immunoconjugate (ICON) fusion protein composed of a modified version of human factor VII (FVII) which targets tissue factor (TF) that is fused to the Fc domain of the human immunoglobulin G1, with potential anti-thrombotic and antineoplastic activities. Acting in a similar manner as plasma FVII, the natural ligand of TF, ICON-1 targets and binds to TF expressed on neovascular endothelia, thereby preventing TF-mediated signaling pathways, and leading to the initiation of an immune response and the destruction of neovascular tissue. This prevents angiogenesis, inflammation and blood coagulation. Upon intravitreal administration, ICON-1 may block TF-induced angiogenesis and treat wet age-related macular degeneration (AMD) and ocular melanoma. TF, a naturally occurring glycoprotein in humans, regulates blood clotting, angiogenesis, and inflammation.","Pharmacologic Substance"]
["C1044","Fadrozole Hydrochloride","4-(5,6,7,8-Tetrahydroimidazo(1,5-a)pyridin-5-yl)benzonitrile Hydrochloride|4-(5,6,7,8-Tetrahydroimidazo[1,5-a]pyridin-5-yl)benzonitrile Monohydrochloride|Afema|Arensin|CGS-16949A|FADROZOLE HYDROCHLORIDE|Fadrozole Hydrochloride","The hydrochloride salt of the nonsteroidal aromatase inhibitor fadrozole with potential antineoplastic activity. Fadrozole specifically inhibits aromatase, blocking the aromatization of androstenedione and testosterone into estrone and estradiol, respectively, the final step in estrogen biosynthesis; the reduction in estrogen levels may inhibit growth in estrogen-dependent cancers. Aromatase, a member of the cytochrome P-450 superfamily, is found in many tissues; overexpression has been linked to the development of preneoplastic and neoplastic changes in breast tissue.","Organic Chemical|Pharmacologic Substance"]
["C88346","FAK Inhibitor GSK2256098","FAK Inhibitor GSK2256098|Focal Adhesion Kinase Inhibitor GSK2256098|GSK2256098","A focal adhesion kinase-1 (FAK) inhibitor with potential antiangiogenic and antineoplastic activities. FAK inhibitor GSK2256098 inhibits FAK, which may prevent the integrin-mediated activation of several downstream signal transduction pathways, including ERK, JNK/MAPK and PI3K/Akt, thereby inhibiting tumor cell migration, proliferation and survival, and tumor angiogenesis. The tyrosine kinase FAK is normally activated by binding to integrins in the extracellular matrix (ECM) but may be upregulated and constitutively activated in various tumor cell types.","Pharmacologic Substance"]
["C78199","FAK Inhibitor PF-00562271","FAK Inhibitor PF-00562271|Focal Adhesion Kinase Inhibitor PF-00562271|PF-00562271","An orally bioavailable small molecule and ATP-competitive focal adhesion kinase (FAK) inhibitor with potential antineoplastic and antiangiogenic activities. FAK inhibitor PF-00562271 inhibits the tyrosine kinase FAK, and to a lesser extent, proline-rich tyrosine kinase (PYK2), which may inhibit tumor cell migration, proliferation, and survival. As FAK is a signal transducer for integrins, inhibition of FAK by this agent may prevent integrin-mediated activation of several downstream signals including ERK, JNK/MAPK and PI3K/Akt. FAK and PYK2, upregulated in many tumor cell types, are involved in tumor cell invasion, migration and proliferation.","Organic Chemical|Pharmacologic Substance"]
["C107238","FAK Inhibitor VS-4718","FAK Inhibitor VS-4718|VS-4718","An orally bioavailable focal adhesion kinase (FAK) inhibitor with potential antineoplastic activity. Upon administration, VS-4718 inhibits FAK, blocks fibronectin-stimulated FAK autophosphorylation of Tyr397, and may prevent the integrin-mediated activation of several downstream signal transduction pathways, including ERK, JNK/MAPK and PI3K/Akt. This results in the reduction of the number of cancer stem cells (CSCs) and inhibits tumor cell migration, proliferation and survival. The cytoplasmic tyrosine kinase FAK is a signal transducer for integrins and is constitutively activated in various tumor cell types; it is involved in tumor cell invasion, migration and proliferation and plays a key role in the development, function and survival of CSCs.","Organic Chemical|Pharmacologic Substance"]
["C29316","Falimarev","Falimarev|Fowlpox-CEA(D609)-MUC1(L93)-TRICOM Vaccine|Fowlpox-CEA-MUC-1-TRICOM|PANVAC-F|fCEA-MUC-1-TRI|falimarev|rFowlpox-CEA(D609)/MUC1(L93)/TRICOM Vaccine|recombinant fowlpox-CEA-MUC-1-TRICOM vaccine","A cancer vaccine comprised of a recombinant fowlpox viral vector encoding the carcinoembryonic antigen (CEA), MUC-1, a transmembrane glycoprotein secreted by glandular epithelial tissues, and TRICOM, comprised of three co-stimulatory molecule transgenes (B7-1, ICAM-1 and LFA-3). This agent may enhance CEA and MUC-1 presentation to antigen-presenting cells (APC) and may activate a cytotoxic T-cell response against CEA- and MUC-1-expressing tumor cells.","Pharmacologic Substance|Virus"]
["C97512","Famitinib","Famitinib","An orally bioavailable receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Famitinib binds to and inhibits several RTKs, dysregulated in a variety of tumors, including stem cell factor receptor (c-Kit; SCFR), vascular endothelial growth factor receptor (VEGFR) 2 and 3, platelet-derived growth factor receptor (PDGFR) and FMS-like tyrosine kinases Flt1 and Flt3. Inhibition of these RTKs may result in an inhibition of tumor growth and angiogenesis, and eventually tumor regression in tumor cells overexpressing these RTKs.","Organic Chemical|Pharmacologic Substance"]
["C103829","FAP-specific CD8-positive T Cells","FAP-specific CD8-positive T Cells","A preparation of CD8-positive T cells specific for human fibroblast activating protein (FAP) with potential immunopotentiating activity. T cells have been genetically modified to express a chimeric antigen receptor specific for FAP. Upon infusion, the FAP-specific CD8-positive T cells bind to FAP-expressing tumor cells and exhibit a selective toxicity to tumor cells. This may result in both tumor cell lysis and inhibition of tumor cell growth. FAP, a cell surface glycoprotein, is overexpressed on tumor-associated fibroblasts but minimally expressed on normal, healthy cells.","Cell|Pharmacologic Substance"]
["C61503","Farletuzumab","FARLETUZUMAB|Farletuzumab|MORAb-003","A humanized, immunoglobulin G1 monoclonal antibody with potential antitumor activity. Farletuzumab specifically targets at glycoprotein 3 (GP-3), a cell surface antigen that is overexpressed on many epithelial-derived cancer cells. Upon binding to the GP-3 antigen, farletuzumab triggers a host immune response against GP-3 expressing cells resulting in cell lysis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C67041","Fas Receptor Agonist APO010","APO010|Fas Receptor Agonist APO010|Mega-FasLigand","A recombinant, soluble, hexameric fusion protein consisting of three human Fas ligand (FasL) extracellular domains fused to the dimer-forming collagen domain of human adiponectin with potential pro-apoptotic and antineoplastic activities. Assembled into a soluble hexameric structure mimicking the ligand clustering of endogenous active FasL, Fas receptor agonist APO010 activates the Fas receptor, resulting in caspase-dependent apoptosis in susceptible tumor cell populations. FasL is a transmembrane protein of the tumor necrosis factor (TNF) superfamily and a pro-apoptotic ligand for the death receptor Fas.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C118285","FASN Inhibitor TVB-2640","FASN Inhibitor TVB-2640|TVB-2640","An orally bioavailable fatty acid synthase (FASN) inhibitor, with potential antineoplastic activity. Upon administration, TVB-2640 binds to and blocks FASN, which prevents the synthesis of palmitate needed for tumor cell growth and survival. This leads to a reduction in cell signaling, an induction of tumor cell apoptosis and the inhibition of cell proliferation in susceptible tumor cells. FASN, an enzyme responsible for the de novo synthesis of palmitic acid, is overexpressed in tumor cells and plays a key role in tumor metabolism, lipid signaling, tumor cell survival and drug resistance; tumor cells are dependent on increased fatty acid production for their enhanced metabolic needs and rapid growth.","Pharmacologic Substance"]
["C1096","Fazarabine","1,3, 5-Triazin-2(1H)-one, 4-Amino-1-beta-D- arabinofuranosyl- (9CI)|1,3, 5-Triazin-2(1H)-one, 4-amino-1-.beta.-D- arabinofuranosyl- (9CI)|1-.beta.-D-Arabinofuranosyl-5-azacytosine|1-Beta-D-arabinofuranosyl-5-azacytosine|Ara AC|FAZARABINE|Fazarabine|Kymarabine|ara-AC|fazarabine","An orally-active pyrimidine analogue of an aza-substituted cytidine in which the ribose moiety is replaced by an arabinose sugar. Similar in action to cytarabine, fazarabine is phosphorylated by deoxycytidine kinase to a triphosphate form which competes with thymidine for incorporation into DNA; its incorporation into DNA inhibits DNA synthesis, resulting in tumor cell death and tumor necrosis. The presence of deoxycytidine kinase in a tumor is a determinant of tumor sensitivity to this drug. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C65629","Febuxostat","2-(3-Cyano-4-(2-methylpropoxy)phenyl)-4-methylthiazole-5-carboxylic Acid|Adenuric|FEBUXOSTAT|Febuxostat|TMX 67|Uloric","An orally available, non-purine inhibitor of xanthine oxidase with uric acid lowering activity. Upon oral administration, febuxostat selectively and noncompetitively inhibits the activity of xanthine oxidase, an enzyme that converts oxypurines, including hypoxanthine and xanthine, into uric acid. By inhibiting xanthine oxidase, uric acid production is reduced and serum uric acid levels are lowered. Febuxostat may provide protection against acute renal failure caused by the excessive release of uric acid that occurs upon massive tumor cell lysis resulting from the treatment of some malignancies.","Pharmacologic Substance"]
["C1098","Fenretinide","4-(all-trans-retino-yl)aminophenol|4-HPR|4-Hydroxyphenylretinamide|All-trans-4'-Hydroxyretinanilide|FENRETINIDE|Fenretinide|Fenretinimide|HPR-4|McN-R-1967|N-(4-hydroxyphenyl)retinamide|all-trans-4'-hydroxyretinanilide|all-trans-N-(4-Hydroxyphenyl)retinamide|all-trans-N-4'-hydroxyretinanilide|fenretinide","An orally-active synthetic phenylretinamide analogue of retinol (vitamin A) with potential antineoplastic and chemopreventive activities.  Fenretinide binds to and activates retinoic acid receptors (RARs), thereby inducing cell differentiation and apoptosis in some tumor cell types.  This agent also inhibits tumor growth by modulating angiogenesis-associated growth factors and their receptors and exhibits retinoid receptor-independent apoptotic properties. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C63482","Fenretinide Lipid Matrix","Fenretinide LXS|Fenretinide Lipid Matrix|Fenretinide Lym-X-Sorb|fenretinide LXS|fenretinide Lym-X-Sorb","An orally bioavailable powder formulation of a synthetic phenylretinamide analogue of retinol with potential chemopreventive and antineoplastic activities. Fenretinide binds to and activates retinoic acid receptors (RARs), thereby inducing cell differentiation and apoptosis in some tumor cell types, including those of the colon, breast, prostate, and neuroblastoma. Independent of RAR activation, this agent also modulates gene expression that leads to ceramide-induced, caspase-independent programmed cell death (PCD) via effectors such as ganglioside GD3 and reactive oxygen species (ROS). Compared to the capsule form, the powder contains a mixture of wheat flour, fats, and sugar that may contribute to the enhanced bioavailability of fenretinide.","Organic Chemical|Pharmacologic Substance"]
["C71541","Fermented Soybean Protein Beverage","Fermented Soybean Protein Beverage|Haelan 951","A fermented soybean-derived phytochemical beverage with potential antineoplastic activity. Fermented soybean protein beverage is reported to exhibit immunostimulatory, anti-viral, pro-apoptotic, anti-angiogenic, anti-proliferative, and anti-inflammatory activities and to enhance the cytotoxic effects of natural killer (NK) cells. The fermentation process is reported to hydrolyze many soybean proteins into amino acids and nitrogen-rich compounds and to protect and enhance the activities of isoflavones such as genistein, protease inhibitors, saponins, phytosterols, inositol hexaphosphate, and other beneficial dietary nutrients and micronutrients found in soybeans.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C64763","Fermented Wheat Germ Extract","Avemar|FWGE|Fermented Wheat Germ Extract","An extract of fermented wheat germ containing a concentrated, standardized amount of methoxy-substituted benzoquinones with immunomodulatory and potential antineoplastic activities. Fermented wheat germ extract (FWGE) inhibits the activities of several enzymes involved in de novo nucleic acid synthesis and in supplying the dNTP pool required for DNA replication. This agent also induces caspase-3- mediated inactivation of poly(ADP)ribose polymerase (PARP), a key enzyme in DNA repair that is overexpressed in many cancers; cleavage of PARP prevents DNA repair and induces apoptosis. The benzoquinones may contribute to the immunomodulatory effects of FWGE, down-regulating major histocompatibility complex class I (MHC-1) protein on the surface of cancer cells, allowing natural killer (NK) cell surveillance; and up-regulating the expression of intracellular adhesion molecule 1 (ICAM-1) on tumor endothelial cells.","Organic Chemical|Pharmacologic Substance"]
["C77970","FGF Receptor Antagonist HGS1036","FGF Receptor Antagonist HGS1036|FP-1039|GSK3052230|HGS1036","A soluble fusion protein consisting of the extracellular domain of human fibroblast growth factor receptor 1 (FGFR1) fused to the Fc portion of human immunoglobulin G1 (IgG1) with potential antineoplastic and anti-angiogenic activities. FGFR1 receptor antagonist FP-1039 prevents FGFR ligands, such as FGF1, FGF2, FGF4, from binding to their cognate receptors, thereby inhibiting the activation of the related FGFR tyrosine kinases. Inhibition of FGFR1 by this agent may retard tumor cell proliferation and induce tumor cell death. FP-1039 may also inhibit vascular endothelial growth factor (VEGF)-induced angiogenesis. FGFR1 is a receptor tyrosine kinase upregulated in certain tumor cells and involved in tumor cellular proliferation, differentiation, angiogenesis, and survival; most ligands that bind to FGFR1 also bind to the related receptors FGFR3 and FGFR4.","Pharmacologic Substance"]
["C118672","FGF/FGFR Pathway Inhibitor E7090","E7090|FGF/FGFR Pathway Inhibitor E7090","An inhibitor of the fibroblast growth factor (FGF)/fibroblast growth factor receptor (FGFR) pathway, with potential antineoplastic activity. Upon administration, the FGF/FGFR pathway inhibitor E7090 selectively interferes with the binding of FGF to FGFR through an as of yet not fully elucidated mechanism. This inhibits FGFR-mediated signaling and leads to both cell proliferation inhibition and cell death in FGFR-overexpressing tumor cells. FGFR is a receptor tyrosine kinase essential to tumor cell proliferation, differentiation, and survival; its expression is upregulated in many tumor cell types.","Pharmacologic Substance"]
["C122719","FGFR Inhibitor ASP5878","ASP5878|FGFR Inhibitor ASP5878","An orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR), with potential antineoplastic activity. Upon oral administration, FGFR inhibitor ASP5878 binds to and inhibits FGFR, which results in the inhibition of FGFR-mediated signal transduction pathways. This inhibits proliferation in FGFR-overexpressing tumor cells. FGFR, a family of receptor tyrosine kinases upregulated in many tumor cell types, plays a key role in cellular proliferation and survival.","Pharmacologic Substance"]
["C88272","FGFR Inhibitor AZD4547","AZD4547|FGFR Inhibitor AZD4547","An orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) with potential antineoplastic activity. FGFR inhibitor AZD4547 binds to and inhibits FGFR, which may result in the inhibition of FGFR-related signal transduction pathways, and, so, the inhibition of tumor cell proliferation and tumor cell death. FGFR, up-regulated in many tumor cell types, is a receptor tyrosine kinase essential to tumor cellular proliferation, differentiation and survival.","Pharmacologic Substance"]
["C111988","FGFR Inhibitor Debio 1347","CH5183284|Debiopharm 1347|FF284|FGFR Inhibitor Debio 1347|debio 1347-101|debio 1347","An orally bioavailable inhibitor of the fibroblast growth factor receptor subtypes 1 (FGFR-1), 2 (FGFR-2) and 3 (FGFR-3), with potential antineoplastic activity. FGFR inhibitor debio 1347 binds to and inhibits FGFR-1, -2, and -3, which result in the inhibition of FGFR-mediated signal transduction pathways. This leads to the inhibition of both tumor cell proliferation and angiogenesis, and causes cell death in FGFR-overexpressing tumor cells. FGFR, a family of receptor tyrosine kinases upregulated in many tumor cell types, is essential for tumor cellular proliferation, differentiation and survival.","Pharmacologic Substance"]
["C121553","FGFR Inhibitor INCB054828","FGFR Inhibitor INCB054828|INCB054828","An orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) types 1, 2, and 3 (FGFR1/2/3), with potential antineoplastic activity. FGFR inhibitor INCB054828 binds to and inhibits FGFR1/2/3, which may result in the inhibition of FGFR1/2/3-related signal transduction pathways. This inhibits proliferation in FGFR1/2/3-overexpressing tumor cells. FGFR, a family of receptor tyrosine kinases upregulated in many tumor cell types, plays a key role in cellular proliferation, migration, and survival.","Pharmacologic Substance"]
["C114283","FGFR Inhibitor TAS-120","FGFR Inhibitor TAS-120|TAS-120","An orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) with potential antineoplastic activity. FGFR inhibitor TAS-120 selectively and irreversibly binds to and inhibits FGFR, which may result in the inhibition of both the FGFR-mediated signal transduction pathway and tumor cell proliferation, and increased cell death in FGFR-overexpressing tumor cells. FGFR is a receptor tyrosine kinase essential to tumor cell proliferation, differentiation and survival and its expression is upregulated in many tumor cell types.","Pharmacologic Substance"]
["C116894","FGFR/VEGFR/PDGFR/FLT3/SRC Inhibitor XL999","FGFR/VEGFR/PDGFR/FLT3/SRC Inhibitor XL999|SSKI XL999|Spectrum Selective Kinase Inhibitor XL999|XL-999|XL999","A small molecule inhibitor of numerous tyrosine kinases (TKs) including fibroblast growth factor receptor (FGFR), vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), FMS-related tyrosine kinase 3 (FLT3), and SRC, with potential antineoplastic activity. Upon administration, XL999 binds to and inhibits the activity of these TKs, thereby preventing both the activation of downstream signaling pathways and the proliferation of tumor cells overexpressing these TKs. FGFR, VEGFR, PDGFR, FLT-3, and SRC are upregulated in a variety of cancer cell types and play key roles in tumor cell proliferation, angiogenesis, and metastasis.","Pharmacologic Substance"]
["C123826","FGFR4 Inhibitor BLU-554","BLU-554|FGFR4 Inhibitor BLU-554|Fibroblast Growth Factor Receptor 4 Inhibitor BLU-554","An orally bioavailable inhibitor of human fibroblast growth factor receptor 4 (FGFR4), with potential antineoplastic activity. Upon oral administration, BLU-554 specifically binds to and blocks the binding of the ligand FGF19 to FGFR4. This prevents the activation of FGFR4, inhibits FGFR4-mediated signaling and leads to an inhibition of tumor cell proliferation in FGFR4-overexpressing cells. FGFR4 is a receptor tyrosine kinase and is involved in tumor cell proliferation, differentiation, angiogenesis, and survival. FGF19 is overexpressed by certain tumor cell types.","Pharmacologic Substance"]
["C120102","FGFR4 Inhibitor FGF401","FGF401|FGFR4 Inhibitor FGF401","An inhibitor of human fibroblast growth factor receptor 4 (FGFR4), with potential antineoplastic activity. Upon administration, FGF401 binds to and inhibits the activity of FGFR4, which leads to an inhibition of tumor cell proliferation in FGFR4-overexpressing cells. FGFR4 is a receptor tyrosine kinase upregulated in certain tumor cells and involved in tumor cell proliferation, differentiation, angiogenesis, and survival.","Pharmacologic Substance"]
["C128862","FGFR4 Inhibitor H3B-6527","FGFR4 Inhibitor H3B-6527|Fibroblast Growth Factor Receptor 4 Inhibitor H3B-6527|H3B 6527|H3B-6527|H3B6527","An orally bioavailable inhibitor of human fibroblast growth factor receptor 4 (FGFR4), with potential antineoplastic activity. Upon administration, H3B-6527 specifically binds to and blocks FGFR4. This prevents the activation of FGFR4, inhibits FGFR4-mediated signaling and leads to an inhibition of cell proliferation in FGFR4-overexpressing tumor cells. FGFR4, a receptor tyrosine kinase overexpressed by certain tumor cell types, is involved in tumor cell proliferation, differentiation, angiogenesis, and survival; FGFR4 expression is associated with poor prognosis.","Pharmacologic Substance"]
["C78844","Ficlatuzumab","AV-299|Anti-HGF Monoclonal Antibody SCH900105|Ficlatuzumab|SCH 900105","A humanized monoclonal antibody directed against human hepatocyte growth factor (HGF) with potential antineoplastic activity. Ficlatuzumab binds to the soluble ligand HGF, preventing the binding of HGF to its receptor c-Met and activation of the HGF/c-Met signaling pathway, which may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C52187","Figitumumab","CP-751,871|CP-751871|FIGITUMUMAB|Figitumumab","A human monoclonal antibody directed against the insulin-like growth factor type I receptor (IGF1R) with potential antineoplastic activity. Figitumumab selectively binds to IGF1R, preventing insulin-like growth factor type 1 (IGF1) from binding to the receptor and subsequent receptor autophosphorylation. Inhibition of IGF1R autophosphorylation may result in a reduction in receptor expression on tumor cells that express IGF1R, a reduction in the anti-apoptotic effect of IGF, and inhibition of tumor growth. IGF1R is a receptor tyrosine kinase expressed on most tumor cells and is involved in mitogenesis, angiogenesis, and tumor cell survival.","Pharmacologic Substance"]
["C70651","Firtecan Pegol","EZN-2208|FIRTECAN PEGOL|Firtecan Pegol|PEG-SN38|Poly(oxy-1,2-ethanediyl), alpha,alpha',alpha'',alpha'''-(oxydi-3,1,2-propanetriyl)tetrakis(omega-(2-((2-(((4S)- 4,11-diethyl-9-hydroxy-3,4,12,14-tetrahydro-3,14-dioxo-1H-pyrano(3',4':6,7) indolizino(1,2-b)quinolin-4-yl)oxy)-2-oxoethyl)amino)-2-oxoethoxy)-","A polyethylene glycol (PEG) conjugate of 7-ethyl-10-hydroxycamptothecin with potential antineoplastic activity. After hydrolysis in vivo, 7-ethyl-10-hydroxycamptothecin (SN38), an active metabolite of irinotecan, is released from firtecan pegol; 7-ethyl-10-hydroxycamptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, resulting in single-stranded and double-stranded DNA breaks, the inhibition of DNA replication, and the induction of apoptosis. This agent is designed to deliver the active metabolite to tumor cells without the need for conversion as is the case with irinotecan. Compared to unPEGylated 7-ethyl-10-hydroxycamptothecin, PEGylation improves solubility and allows for parental delivery, and may result in a longer half-life and higher exposure for tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C104273","Fish Oil/Glycerol/Egg Lecithin-based Emulsion","Fish Oil/Glycerol/Egg Lecithin-based Emulsion|Omegaven","An injectable, nutritional lipid emulsion composed of 10% fish oil and high amounts of the fish oil-derived polyunsaturated omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Additionally, the fish oil/glycerol/egg lecithin-based emulsion contains, myristic acid, palmitic acid, palmitoleic acid, stearic acid, oleic acid, linoleic acid, linolenic acid, octadecatetraenoic acid, eicosaenoic acid, arachidonic acid, docosaenoic acid, and docosapentaenoic acid. This agent supplies essential fatty acids that can be incorporated into cell membranes. The fatty acids may decrease the production of certain pro-inflammatory cytokines, including interleukin 1 (IL-1), IL-6 and tumor necrosis factor (TNF). In addition to fish oil, this lipid emulsion contains egg phospholipids to maintain membrane integrity; glycerol to provide energy through glycolysis; and the antioxidant alpha-tocopherol (vitamin E).","Pharmacologic Substance"]
["C2715","FJ5002","FJ5002","A derivative of rhodacyanine with potential antineoplastic activity.  FJ5002 inhibits telomerase by interfering with holoenzyme assembly and telomere interaction, thus leading to replication-dependent shortening of telomeres with a concurrent increase in aneuploid metaphases and apoptotic cells.  Telomerase is active in most tumors cells, but is quiescent in adjacent normal cells. (NCI04)","Pharmacologic Substance"]
["C91384","Flanvotumab","Anti-gp75 Monoclonal Antibody IMC-20D7S|FLANVOTUMAB|Flanvotumab|IMC-20D7S|IMC20D7S","A monoclonal antibody directed against the melanosomal membrane protein gp75 (or Tyrosinase-Related Protein 1 (TRP1)) with potential immunostimulatory and antineoplastic activities. Anti-gp75 monoclonal antibody IMC-20D7S targets and binds to gp75. This may lead to the induction of cytotoxic T cell immune and antibody-mediated immune responses against melanoma cells expressing gp75. gp75, a pigmentation-associated antigen, is expressed in melanosomes of human melanocytes and melanomas.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C26650","Flaxseed","FLAX SEED|Flaxseed|Flour, Flaxseed|Linseed|flaxseed|linseed","Seed isolated from one of several species of the plant genus Linum. Flaxseed-derived foods, lignans, and essential fatty acids such as alpha-linolenic acid, possess anti-inflammatory, lipid-lowering, antioxidant, and antineoplastic properties.","Food"]
["C504","Floxuridine","1-(2-Deoxy-beta-D-ribofuranosyl)-5-fluorouracil|2'-Deoxy-5-fluorouridine|2-Deoxy-5-fluorouridine|5-FUDR|5-FUdR|5-Fluoro-2'-deoxy-beta-uridine|5-Fluoro-2'-deoxyuridine|5-Fluorodeoxyuridine|5-Fluorouracil Deoxyriboside|5-Fluorouracil deoxyriboside|5-Fluorouridine Deoxyribose|FDUR|FLOXURIDINE|FUDR|FUdR|Floxuridin|Floxuridine|Fluorodeoxyuridine|Fluorouridine Deoxyribose|Fluoruridine Deoxyribose|Fluoruridine deoxyribose|WR-138720|floxuridine","A fluorinated pyrimidine monophosphate analogue of 5-fluoro-2'-deoxyuridine-5'-phosphate (FUDR-MP) with antineoplastic activity. As an antimetabolite, floxuridine inhibits thymidylate synthase, resulting in disruption of DNA synthesis and cytotoxicity. This agent is also metabolized to fluorouracil and other metabolites that can be incorporated into RNA and inhibit the utilization of preformed uracil in RNA synthesis. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C116858","FLT3/ABL/Aurora Kinase Inhibitor KW-2449","FLT3/ABL/Aurora Kinase Inhibitor KW-2449|KW-2449","An orally available inhibitor of FMS-related tyrosine kinase 3 (FLT3, STK1, or FLK2), the tyrosine kinase ABL, and aurora kinases, with potential antineoplastic activity. Upon administration, FLT3/ABL/Aurora kinase inhibitor KW-2449 specifically binds to and inhibits both wild-type and mutated forms of FLT3, ABL and aurora kinases, which both interferes with the activation of signal transduction pathways mediated by these kinases and reduces the proliferation of susceptible cancer cells. FLT3 and ABL kinases are upregulated in certain tumor cells and play important roles in tumor cell proliferation and metastasis. Aurora kinases, serine-threonine kinases overexpressed by a wide variety of cancer cell types, play essential roles in mitotic checkpoint control.","Pharmacologic Substance"]
["C120209","FLT3/CDK4/6 Inhibitor FLX925","FLT3/CDK4/6 Inhibitor FLX925|FLX925","An orally available inhibitor of FMS-related tyrosine kinase 3 (FLT3, STK1, or FLK2) and the cyclin-dependent kinases 4 (CDK4) and 6 (CDK6), with potential antineoplastic activity. Upon administration, FLT3/CDK4/6 inhibitor FLX925 specifically binds to and inhibits FLT3, which interferes with the activation of FLT3-mediated signal transduction pathways and reduces cell proliferation in cancer cells that overexpress FLT3. In addition FLX925 inhibits CDK4 and 6 and prevents the phosphorylation of retinoblastoma (Rb) protein in early G1. Inhibition of Rb phosphorylation prevents CDK-mediated G1-S phase transition, which causes G1 phase cell cycle arrest, suppresses DNA synthesis and inhibits cancer cell growth. FLT3, a class III tyrosine kinase receptor, is overexpressed in a variety of cancers. Overexpression of CDK4/6, which is seen in certain types of cancer, causes cell cycle deregulation.","Pharmacologic Substance"]
["C101520","FLT3/KIT Kinase Inhibitor AKN-028","AKN-028|BVT-II|FLT3/KIT Kinase Inhibitor AKN-028","An orally bioavailable protein tyrosine kinase inhibitor for FMS-related tyrosine kinase 3 (FLT3; STK1) and stem cell factor receptor (SCFR; KIT), with potential antineoplastic activity. FLT3/KIT kinase inhibitor AKN-028 binds to and inhibits both the wild-type and mutated forms of FLT3 and SCFR. This may result in an inhibition of tumor cell proliferation in cancer cell types that overexpress these receptor tyrosine kinases.","Pharmacologic Substance"]
["C39677","Flu Matrix Peptide p58-66","Flu Matrix Peptide p58-66|Flu Matrix Peptide","A short chain synthetic antigenic peptide (GILGFVFTL) derived from the influenza virus A matrix protein and presented by HLA-A2 major histocompatibility complex (MHC) class I molecules. Flu matrix peptide p58-66 stimulates the lytic functions of cytotoxic T lymphocytes (CTLs), which may result in the eradication of virus-infected or malignant tumor cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1094","Fludarabine","2-Fluoro-9-beta-arabinofuranosyladenine|2-Fluorovidarabine|9-Beta-D-arabinofuranosyl-2-fluoro-9H-purin-6-amine|9-Beta-D-arabinofuranosyl-2-fluoroadenine|FLUDARABINE|Fludarabine|Fluradosa|fludarabine","A fluorinated nucleotide antimetabolite analog of the antiviral agent vidarabine (ara-A) with antineoplastic activity. Administered parenterally as a phosphate salt, fludarabine phosphate is rapidly dephosphorylated to 2-fluoro-ara-A and then phosphorylated intracellularly by deoxycytidine kinase to the active triphosphate, 2-fluoro-ara-ATP. This metabolite may inhibit DNA polymerase alpha, ribonucleotide reductase and DNA primase, thereby interrupting DNA synthesis and inhibiting tumor cell growth.  (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1102","Fludarabine Phosphate","2-F-ara-AMP|9H-Purin-6-amine, 2-fluoro-9-(5-O-phosphono-.beta.-D-arabinofuranosyl)-|9H-purin-6-amine, 2-fluoro-9-(5-O-phosphono-beta-D-arabinofuranosyl)|Beneflur|FLUDARABINE PHOSPHATE|Fludara|Fludarabine Phosphate|Fludarabine-5'-Monophosphate|Oforta|SH T 586|fludarabine phosphate","The phosphate salt of a fluorinated nucleotide antimetabolite analog of the antiviral agent vidarabine (ara-A) with antineoplastic activity. Fludarabine phosphate is rapidly dephosphorylated to 2-fluoro-ara-A and then phosphorylated intracellularly by deoxycytidine kinase to the active triphosphate, 2-fluoro-ara-ATP. This metabolite may inhibit DNA polymerase alpha, ribonucleotide reductase and DNA primase, thereby interrupting DNA synthesis and inhibiting tumor cell growth.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C117723","Flumatinib Mesylate","4-(4-Methyl-piperazin-1-ylmethyl)-N-[6-methyl-5-(4-pyridin-3-yl-pyrimidin-2-ylamino)-pyridin-3-yl]-3-trifluoromethyl-benzamide Mesylate|Flumatinib Mesylate|HH-GV-678|HH-GV678","The orally bioavailable, mesylate salt form of the tyrosine kinase inhibitor flumatinib, with potential antineoplastic activity. Upon administration, flumatinib inhibits the wild-type forms of Bcr-Abl, platelet-derived growth factor receptor (PDGFR) and mast/stem cell growth factor receptor (SCFR; c-Kit) and forms of these proteins with certain point mutations. This results in the inhibition of both Bcr-Abl-, PDGFR- and c-Kit-mediated signal transduction pathways, and the proliferation of tumor cells in which these kinases are overexpressed. Bcr-Abl fusion protein is an abnormal, constitutively active enzyme expressed in Philadelphia chromosome positive chronic myeloid leukemia (CML), acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML). PDGFR, upregulated in many tumor cell types, is a receptor tyrosine kinase essential to cell migration and the development of the microvasculature. c-kit, a receptor tyrosine kinase mutated and constitutively activated in certain tumors, plays a key role in tumor cell survival, proliferation, and differentiation.","Pharmacologic Substance"]
["C120100","Fluorine F 18 Ara-G","18F-F-Ara-G|2'-Deoxy-2'-[18F]Fluoro-9-beta-D-arabinofuranosylguanine|Fluorine F 18 Ara-G|[18F]F-ara-G","A radioconjugate composed of the guanosine analog arabinosyl guanine (Ara-G), a high-affinity substrate for both cytoplasmic deoxycytidine kinase (DCK) and mitochondrial deoxyguanosine kinase (dGK), labeled with fluorine F 18, that can potentially be used as a tracer for imaging of activated T-lymphocytes during positron emission tomography (PET). Upon administration, fluorine F 18 ara-G is taken up by and accumulates in activated T-lymphocytes with high levels of DCK and dGK. After phosphorylation by DCK and dGK, the 18F moiety can be visualized by PET imaging. Fluorine F 18 ara-G can potentially be used as an imaging agent to detect anti-tumor immune responses and to predict the therapeutic efficacy of immunotherapies. DCK and dGK, both nucleoside salvage pathway enzymes, are overexpressed in activated T-cells.","Indicator, Reagent, or Diagnostic Aid|Pharmacologic Substance"]
["C29042","Fluorodopan","Fluorodopan","An alkylating agent with potential antineoplastic activity.  Fluorodopan alkylates DNA at the N7 position of guanine.  Alkylating agents exert cytotoxic and, in some cases, chemotherapeutic effects by transferring alkyl groups to DNA, thereby damaging DNA and interfering with DNA replication and cell division. (NCI04)","Pharmacologic Substance"]
["C94728","Fluoropyrimidine","Fluoropyrimidine|fluoropyrimidine","Any fluoropyrimidine-based agent with potential antineoplastic activity. As an antimetabolite, a fluoropyrimidine interferes with pyrimidine utilization and incorporation into DNA and RNA.","Chemical Viewed Functionally"]
["C505","Fluorouracil","2,4-Dioxo-5-fluoropyrimidine|5-FU|5-Fluoro-2,4(1H, 3H)-pyrimidinedione|5-Fluoro-2,4(1H,3H)-pyrimidinedione|5-Fluorouracil|5-Fluracil|5-Fu|5-fluorouracil|AccuSite|Adrucil|Carac|FLUOROURACIL|Fluoro Uracil|Fluorouracil|Fluouracil|Flurablastin|Fluracedyl|Fluracil|Fluril|Fluroblastin|Ribofluor|Ro 2-9757|Ro-2-9757|fluorouracil","An antimetabolite fluoropyrimidine analog of the nucleoside pyrimidine with antineoplastic activity. Fluorouracil and its metabolites possess a number of different mechanisms of action. In vivo, fluoruracil is converted to the active metabolite 5-fluoroxyuridine monophosphate (F-UMP); replacing uracil, F-UMP incorporates into RNA and inhibits RNA processing, thereby inhibiting cell growth. Another active metabolite, 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate (F-dUMP), inhibits thymidylate synthase, resulting in the depletion of thymidine triphosphate (TTP), one of the four nucleotide triphosphates used in the in vivo synthesis of DNA. Other fluorouracil metabolites incorporate into both RNA and DNA; incorporation into RNA results in major effects on both RNA processing and functions.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C90544","Fluorouracil Implant","Fluorouracil Implant|Sinofuan","An implant containing a sustained release particle of fluorouracil, an antimetabolite fluoropyrimidine analog of the nucleoside pyrimidine, with antineoplastic activity. Upon implantation and subsequent release, fluorouracil is converted into the active metabolite 5-fluoroxyuridine monophosphate that competes with the pyrimidine uracil during RNA synthesis while another active metabolite, 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate, inhibits thymidylate synthase and thus DNA synthesis.","Pharmacologic Substance"]
["C17877","Fluorouracil-E Therapeutic Implant","5-FU-e TI|5-FU/epi gel|5-Fluorouracil/epi|Fluorouracil-E Therapeutic Implant|Fluorouracil-epinephrine therapeutic implant|Fluorouracil/epi","An injectable collagen matrix gel containing the antimetabolite fluorouracil and the sympathicomimetic agent epinephrine with potential antineoplastic activity. After intratumoral injection, fluorouracil is converted into the active metabolite 5-fluoroxyuridine monophosphate that competes with uracil during RNA synthesis while another active metabolite, 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate, inhibits thymidylate synthase and, so, DNA synthesis. Epinephrine, a potent vasoconstrictor, is added to the gel to enhance penetration of fluorouracil into tumor tissue and reduce dispersion to surrounding tissues, thus enhancing the local concentration of fluorouracil. Compared to systemic administration, the intratumoral injection of fluorouracil combined with epinephrine may increase fluorouracil's chemotherapeutic efficacy while minimizing systemic toxicity.","Pharmacologic Substance"]
["C507","Fluoxymesterone","(11Beta,17beta)-9-fluoro-11,17-dihydroxy-17-methylandrost-4-en-3-one|11Beta,17beta-dihydroxy-9alpha-fluoro-17alpha-methyl-4-androsten-3-one|9Alpha-fluoro-11beta-hydroxy-17alpha-methyltestosterone|Androfluorene|Android-F|Androsterolo|FLUOXYMESTERONE|FXM|Fluoxymesterone|Halodrin|Halotestin|Ora Testryl|Ora-Testryl|Ora-testryl|Oratestin|Stenox|Testoral|Ultandren","A halogenated derivative of 17-alpha-methyltestosterone.  Similar to testosterone, fluoxymesterone binds to and activates specific nuclear receptors, resulting in an increase in protein anabolism, a decrease in amino acid catabolism, and retention of nitrogen, potassium, and phosphorus.  This agent also may competitively inhibit prolactin receptors and estrogen receptors, thereby inhibiting the growth of hormone-dependent tumor lines. Fluoxymesterone is approximately five times more potent than methyltestosterone. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C509","Flutamide","2-Methyl-N-[4-nitro-3-(trifluoromethyl)phenyl]propanamide|4'-Nitro-3'-trifluoromethylisobutyranilide|Alpha,alpha,alpha-trifluoro-2-methy-4'-nitro-m-propionotoluidide|Apimid|Cebatrol|Chimax|Cytomid|Drogenil|Euflex|Eulexin|Eulexine|FLUT|FLUTAMIDE|Flucinom|Flucinome|Flugerel|Fluken|Flulem|Fluta-Gry|Flutabene|Flutacan|Flutamex|Flutamide|Flutamin|Flutan|Flutaplex|Fugerel|Grisetin|Niftolide|Oncosal|Profamid|Propanamide, 2-Methyl-N-(4-nitro-3-(trifluoromethyl)phenyl)-|Prostacur|Prostadirex|Prostica|Prostogenat|SCH 13521|Sch 13521|Tafenil|Tecnoflut|Testotard|flutamide","A toluidine derivative and a nonsteroidal antiandrogen that is structurally related to bicalutamide and nilutamide. Flutamide and its more potent active metabolite 2-hydroxyflutamide competitively block dihydrotestosterone binding at androgen receptors, forming inactive complexes which cannot translocate into the cell nucleus. Formation of inactive receptors inhibits androgen-dependent DNA and protein synthesis, resulting in tumor cell growth arrest or transient tumor regression. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C61768","Fluvastatin","FLUVASTATIN|Fluvastatin","A synthetic lipid-lowering agent with antilipidemic and potential antineoplastic properties. Fluvastatin competitively inhibits hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses through the suppression of MHC II (major histocompatibility complex II) on interferon gamma-stimulated antigen-presenting cells such as human vascular endothelial cells. Due to its anti-inflammatory effects mediated by alterations of lipid metabolism, fluvastatin may possess chemopreventive and therapeutic antineoplastic properties.","Pharmacologic Substance"]
["C29062","Fluvastatin Sodium","(3R,5S,6E)-(+/-)-7-(3-(4-Fluorophenyl)-1-(1-methylethyl)-1H-indol-2-yl)-3,5-dihydroxy-6-heptenoic Acid|FLUVASTATIN SODIUM|Fluvastatin Sodium|Lescol","The sodium salt of a synthetic lipid-lowering agent with potential antineoplastic activity. Fluvastatin competitively inhibits hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses through the suppression of MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. Through the inhibition of mevalonate synthesis, statins, like fluvastatin, have been shown to inhibit the production of dolichol, geranylpyrophosphate (GPP) and farnesylpyrophosphate (FPP) and the isoprenylation of the intracellular G-proteins Ras and Rho, which may result in antiangiogenic, apoptotic, and antimetastatic effects in susceptible tumor cell populations.","Pharmacologic Substance"]
["C126274","Fluzoparib","Fluzoparib","An orally available inhibitor of poly (ADP-ribose) polymerase (PARP) types 1 and 2, with potential antineoplastic activity. Upon oral administration, fluzoparib inhibits PARP 1 and 2 activity, which inhibits PARP-mediated repair of damaged DNA via the base excision repair (BER) pathway, enhances the accumulation of DNA strand breaks, promotes genomic instability, and leads to an induction of apoptosis. The PARP family of proteins catalyze post-translational ADP-ribosylation of nuclear proteins, which then transduce signals to recruit other proteins to repair damaged DNA. PARP inhibition may enhance the cytotoxicity of DNA-damaging agents and may reverse tumor cell chemoresistance and radioresistance.","Pharmacologic Substance"]
["C101519","FMS Inhibitor JNJ-40346527","FMS Inhibitor JNJ-40346527|JNJ-40346527","A small molecule and orally available inhibitor of colony-stimulating factor-1 receptor (CSF1R; FMS) with potential antineoplastic activity. FMS tyrosine kinase inhibitor JNJ-40346527 blocks the receptor-ligand interaction between FMS and its ligand CSF1, thereby preventing autophosphorylation of FMS. As a result, unphosphorylated FMS can not activate FMS-mediated signaling pathways, thus potentially inhibiting cell proliferation in FMS-overexpressed tumor cells. FMS, a tyrosine kinase receptor, is overexpressed in certain tumor cell types and plays an essential role in macrophage differentiation, recruitment, and activation as well as the regulation of cell proliferation.","Pharmacologic Substance"]
["C105804","Fms/Trk Tyrosine Kinase Inhibitor PLX7486 Tosylate","Fms/Trk Tyrosine Kinase Inhibitor PLX7486 Tosylate|PLX7486-TsOH","The tosylate salt form of PLX7486, a selective inhibitor of the receptor tyrosine kinases colony-stimulating factor-1 receptor (CSF1R; fms) and neurotrophic tyrosine kinase receptor types 1, 2 and 3 (TrkA, TrkB, and TrkC, respectively) with potential antineoplastic activity. Upon administration, PLX7486 binds to and inhibits the activity of these tyrosine kinases. This inhibits Fms and Trk-mediated signaling transduction pathways that are upregulated in certain cancer cell types. This may eventually halt tumor cell proliferation in Fms and TrkA, TrkB, and/or TrkC-overexpressing tumor cells. Fms and TrkA, TrkB, and TrkC are receptor tyrosine kinases that are upregulated or mutated in a variety of tumors and promote tumor cell proliferation and survival.","Pharmacologic Substance"]
["C101530","Folate Binding Protein E39 Peptide Vaccine","E39 Peptide Vaccine|FBP E39 Peptide Vaccine|Folate Binding Protein E39 Peptide Vaccine","A cancer vaccine comprised of human leukocyte antigen (HLA) A2 restricted folate binding protein (FBP) epitope E39 (amino acids 191 to 199), with potential immunostimulatory and antineoplastic activity. Upon intradermal injection, FBP E39 peptide vaccine may induce a specific cytotoxic T-lymphocyte (CTL) response against FBP-expressing tumor cell types. FBP is a membrane-bound, tumor-associated antigen highly overexpressed in various tumor cell types, such as in breast, ovarian and endometrial cancers; E 39 is a strong immunogenic peptide.","Immunologic Factor|Pharmacologic Substance"]
["C113660","Folate Binding Protein J65 Peptide Vaccine","FBP J65 Peptide Vaccine|Folate Binding Protein J65 Peptide Vaccine|J65 Peptide Vaccine","A cancer vaccine comprised of human leukocyte antigen (HLA)-A2-restricted folate binding protein (FBP) epitope J65 (9 amino acids; EIWTFSTKV), with potential immunostimulatory and antineoplastic activities. Upon intradermal injection, FBP J65 peptide vaccine may induce a specific cytotoxic T-lymphocyte (CTL) response against J65 FBP-expressing tumor cell types. FBP is a membrane-bound, tumor-associated antigen overexpressed in various tumor types, including breast, ovarian and endometrial cancers. J65 is a strongly immunogenic peptide.","Immunologic Factor|Pharmacologic Substance"]
["C71524","Folate Receptor Targeted Epothilone BMS753493","Folate Receptor Targeted Epothilone BMS753493","A folate receptor-targeting antimitotic agent with potential antineoplastic activity. Folate receptor-targeted epothilone BMS753493 contains an epothilone moiety linked to a single folate molecule. Mediated through the folate moiety, this agent delivers the antimitotic epothilone component into cells expressing folic acid receptors, frequently upregulated in many types of tumor cells. After ligand-receptor internalization, the epothilone moiety induces microtubule polymerization and stabilizes microtubules against depolymerization, resulting in the inhibition of mitosis and cellular proliferation.","Chemical Viewed Structurally"]
["C113176","Folate Receptor-Targeted Tubulysin Conjugate EC1456","EC1456|Folate Receptor-Targeted Tubulysin Conjugate EC1456|Folate Receptor-Targeting Folate-Tubulysin Conjugate EC1456","An injectable targeted small molecule drug conjugate (SMDC) consisting of folate (vitamin B9) covalently linked to the potent mitotic poison and cytotoxic agent, tubulysin B hydrazide (Tub-B-H) with potential antineoplastic activity. Upon administration, the folate moiety of folate receptor-targeted tubulysin conjugate EC1456 preferentially binds to tumor cells expressing folate receptors (FR). After binding to FR, the agent is internalized by tumor cells and the Tub-B-H moiety inhibits the polymerization of tubulin into microtubules. This may lead to both cell cycle arrest and tumor cell apoptosis. FR, the membrane-bound, high-affinity receptor for folate, is overexpressed on a wide range of primary and metastatic human cancers.","Pharmacologic Substance"]
["C81935","Folate Receptor-Targeted Vinca Alkaloid EC0489","EC0489|Folate Receptor-Targeted Vinca Alkaloid EC0489","A folate receptor-targeting cytotoxic drug conjugate consisting of a folate vitamin analogue linked to a vinca alkaloid microtubule destabilizing agent with potential antineoplastic activity. Mediated through its folate moiety, folate receptor-targeted vinca alkaloid EC0489 delivers the cytotoxic vinca alkaloid moiety directly to cells expressing folic acid receptors, frequently upregulated in many types of tumor cells. After ligand-receptor internalization, the vinca alkaloid moiety binds to tubulin and disrupts microtubule assembly-disassembly dynamics, resulting in cell cycle arrest and apoptosis. The relative tumor cell specificity of this agent reduces the toxicity profile of its vinca alkaloid moiety.","Organic Chemical|Pharmacologic Substance"]
["C66987","Folate Receptor-Targeted Vinca Alkaloid/Mitomycin C EC0225","EC0225|Folate Linked Vinca Alkaloid/Mitomycin C EC0225|Folate Receptor-Targeted Vinca Alkaloid/Mitomycin C EC0225","A folate receptor-targeting cytotoxic agent with potential antineoplastic activity. Folate receptor-targeted vinca alkaloid/mitomycin C EC0225 contains two potent cytotoxic agents, a vinca alkaloid and mitomycin C, linked to a single folate molecule. Mediated through the folate moiety, this agent delivers the cytotoxic agents directly into cells expressing folic acid receptors, frequently upregulated in many types of tumor cells. After ligand-receptor internalization, the vinca alkaloid moiety binds to tubulin and disrupts microtubule assembly-disassembly dynamics, resulting in cell cycle arrest and apoptosis. Mitomycin C alkylates DNA, producing DNA cross-links and inhibiting DNA replication. The relative tumor cell specificity of EC0225 reduces the toxicity profiles of its cytotoxic agent moieties.","Organic Chemical|Pharmacologic Substance"]
["C62479","Folate-FITC","EC-17|EC17|Folate Fluorescein Isothiocyanate Conjugate|Folate-FITC|L-glutamine, N2-(4-(((2-amino-3,4-dihydro-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-n-(2-((((3',6'-dihydroxy-3-oxospiro(isobenzofuran-1(3h),9'-(9h)xanthen)-5-yl)amino)thioxomethyl)amino)ethyl)-","A conjugate consisting of fluorescein isothiocyanate (FITC) conjugated with folate with potential antineoplastic activity. Folate-FITC binds to folate receptors, which are overexpressed on the surfaces of many cancer cells including kidney and ovarian cancer cells. Once bound to the cancer cell through the folate moiety of the conjugate, circulating anti-fluorescein antibodies may recognize and bind to the FITC moiety, resulting in antibody-dependent cellular cytotoxicity.","Pharmacologic Substance"]
["C61304","Folitixorin","5,10-Methylenetetrahydrofolate|5,10-methylene-5,6,7,8-tetrahydrofolic Acid|CoFactor|FOLITIXORIN|Folitixorin|N-(4-(3-Amino-1,2,5,6,6a,7-hexahydro-1-oxoimidazo(1,5-f)pteridin-8(9H)-yl)benzoyl)-L-glutamic Acid|Tetrahydromethylenefolate","A folate-based biomodulator with potential antineoplastic activity. 5,10-methylenetetrahydrofolate (MTHF) stabilizes the covalent binding of the fluorouracil metabolite 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate (FdUMP) to its target enzyme, thymidylate synthase, which results in inhibition of thymidylate synthase, depletion of thymidine triphosphate (TTP), a necessary constituent of DNA, and tumor cell death. Unlike leucovorin, MTHF, as the active form of folate, does not require metabolic activation and may increase the chemotherapeutic effects of fluorouracil with lower toxicity.","Pharmacologic Substance"]
["C80058","Foretinib","FORETINIB|Foretinib|GSK1363089|MET/VEGFR-2 inhibitor GSK1363089|Multitargeted Tyrosine Kinase Inhibitor GSK1363089|N-(3-Fluoro-4-((6-methoxy-7-(3-(morpholin-4-yl)propoxy)quinolin-4-yl)oxy)phenyl)-N'-(4-fluorophenyl)cyclopropane-1,1-dicarboxamide|XL880|foretinib","An orally bioavailable small molecule with potential antineoplastic activity. Foretinib binds to and selectively inhibits hepatocyte growth factor (HGF) receptor c-MET and vascular endothelial growth factor receptor 2 (VEGFR2), which may result in the inhibition of tumor angiogenesis, tumor cell proliferation and metastasis. The proto-oncogene c-MET has been found to be over-expressed in a variety of cancers. VEGFR2 is found on endothelial and hematopoietic cells and mediates the development of the vasculature and hematopoietic cells through VEGF signaling.","Pharmacologic Substance"]
["C974","Formestane","4-Hydroxyandrost-4-ene-3,17-dione|4-Hydroxyandrostenedione|4-OHA|4-OHAD|CGP-32349|FORMESTANE|Formestane|Lentaron","A synthetic steroidal substance with antineoplastic activity.  Formestane binds irreversibly to and inhibits the enzyme aromatase, thereby blocking the conversion of cholesterol to pregnenolone and the peripheral aromatization of androgenic precursors into estrogens. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C82378","Fosbretabulin","2-Methoxy-5-((1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl)phenyl Phosphate|Combretastatin A-4 Phosphate|FOSBRETABULIN|Fosbretabulin|Phenol, 2-methoxy-5-((1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl)-, Dihydrogen Phosphate","A water-soluble prodrug derived from the African bush willow (Combretum caffrum) with antineoplastic activity. Fosbretabulin is dephosphorylated to its active metabolite, combretastatin A4, which binds to tubulin and inhibits microtubule polymerization, resulting in mitotic arrest and apoptosis in endothelial cells. As apoptotic endothelial cells detach from their substrata, tumor blood vessels collapse; the acute disruption of tumor blood flow may result in tumor necrosis.","Organic Chemical|Pharmacologic Substance"]
["C2503","Fosbretabulin Disodium","2-methoxy-5-[(1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl]phenyl Disodium Phosphate|CA4DP|Combretastatin A4 Disodium Phosphate|FOSBRETABULIN DISODIUM|Fosbretabulin Disodium|Phenol, 2-methoxy-5-[(1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl]-, Dihydrogen Phosphate, Disodium Salt","The disodium salt of a water-soluble phosphate derivative of a natural stilbenoid phenol derived from the African bush willow (Combretum caffrum) with potential vascular disrupting and antineoplastic activities. Upon administration, the prodrug fosbretabulin is dephosphorylated to its active metabolite, the microtubule-depolymerizing agent combretastatin A4, which binds to tubulin dimers and prevents microtubule polymerization, resulting in mitotic arrest and apoptosis in endothelial cells. In addition, this agent disrupts the engagement of the endothelial cell-specific junctional molecule vascular endothelial-cadherin (VE-cadherin) and so the activity of the VE-cadherin/beta-catenin/Akt signaling pathway, which may result in the inhibition of endothelial cell migration and capillary tube formation. As a result of fosbretabulin's dual mechanism of action, the tumor vasculature collapses, resulting in reduced tumor blood flow and ischemic necrosis of tumor tissue.","Organic Chemical|Pharmacologic Substance"]
["C83721","Fosbretabulin Tromethamine","1,3-Dihydroxy-2-(Hydroxymethyl)Propan-2-Aminium 2-Methoxy-5-((1z)-2-(3,4,5-Trimethoxyphenyl)Ethenyl)Phenyl Hydrogen Phosphate|1,3-Propanediol, 2-Amino-2-(Hydroxymethyl)-, Compd. With 2-Methoxy-5-((1z)-2-(3,4,5-Trimethoxyphenyl)Ethenyl)Phenyl Dihydrogen Phosphate (1:1)|CA4P|FOSBRETABULIN TROMETHAMINE|Fosbretabulin Tromethamine|Zybrestat","The tromethamine salt form of prodrug fosbretabulin, a water-soluble phosphate derivative of a stilbenoid phenol derived from the African bush willow (Combretum caffrum) with antineoplastic activities. Upon administration, fosbretabulin is dephosphorylated to its active metabolite, combretastatin A4, which targets and binds to tubulin dimers and prevents microtubule polymerization, thereby resulting in mitotic arrest and apoptosis in endothelial cells. As apoptotic endothelial cells detach from their substrata, tumor blood vessels collapse; the acute disruption of tumor blood flow may result in tumor necrosis.","Pharmacologic Substance"]
["C1371","Fosquidone","FOSQUIDONE|Fosquidone|GR 63178A","A water-soluble pentacyclic pyrolloquinone analogue of mitoquidone with potential antineoplastic activity. Currently, the mechanism of action of fosquidone is unknown. In vitro studies indicate that this agent does not bind to DNA or inhibit topoisomerases.","Organic Chemical|Pharmacologic Substance"]
["C1372","Fostriecin","2H-pyran-2-one,5,6-dihydro-6-(3,6,13-trihydroxy-3-methyl-4-(phosphonooxy)-1,7,9,11,-tridecatetraenyl)-,trans|FOSTRIECIN|FST|Fostriecin|Phosphotrienin","An anti-tumor antibiotic isolated from the bacterium Streptomyces pulveraceus. Fostriecin inhibits topoisomerase II catalytic activity, resulting in impaired DNA and RNA synthesis in various malignant cell types.  This agent also inhibits serine/threonine protein phosphatase type 2A in some tumor cell types, thereby interfering with cellular proliferation and differentiation. (NCI04)","Antibiotic|Organic Chemical"]
["C1106","Fotemustine","1-[N-(2-chloroethyl)-N-nitrosoureido]ethylphosphonic acid diethyl ester|FOTEMUSTINE|Fotemustine|Muphoran|S 10036|[1-[[[(2-chloroethyl)nitrosamino]-carbonyl]amino]ethyl]phosphonic acid diethyl ester|diethyl[1-[3-(2-chloroethyl)-3-nitrosoureido]ethyl]phosphonate|fotemustine","A chloroethylating nitrosourea with antineoplastic activity. Fotemustine alkylates guanine by forming chloroethyl adducts at the 6 position of guanine, resulting in N1-guanine and N3-cytosine cross linkages, inhibition of DNA synthesis, cell cycle arrest, and finally apoptosis. This agent is lipophilic and crosses the blood-brain barrier.","Organic Chemical|Pharmacologic Substance"]
["C65767","Fotretamine","2,2,4,4,6-Pentaethylenimino-6-morpholino-cyclotriphosphazatrien|FOTRETAMINE|Fotretamine|Fotrin|Photrin|Photrine","A pentaethyleneimine derivative with antineoplastic alkylating activity. Fotretamine causes chromosomal breaks in lymphocytes which contributes to its immunosuppressive activity.","Pharmacologic Substance"]
["C48390","Fowlpox Virus Vaccine Vector","FOWLVAC|Fowlpox Virus Vaccine Vector","A recombinant fowlpox virus-based vaccine vector designed to express various tumor-associated peptide antigens. Strong CD8 cytotoxic T cell responses may be induced after prolonged immunization with fowlpox virus vaccines and have been associated with tumor regression. Fowlpox virus is an attractive vector because its genome is easy to manipulate and it does not multiply in human tissues. (NCI05)","Pharmacologic Substance"]
["C48465","Fowlpox-NY-ESO-1 Vaccine","Fowlpox-NY-ESO-1 Vaccine|rF-NY-ESO-1","A cancer vaccine consisting of a recombinant fowlpox virus vector encoding an immunogenic peptide derived from the cancer-testis antigen NY-ESO-1, an antigen found in normal testis and various tumors, including bladder, breast, hepatocellular, melanoma, and prostate cancers. Vaccination with NY-ESO-1 peptide vaccine may stimulate the host immune system to mount a humoral and cytotoxic T lymphocyte (CTL) response against tumor cells expressing NY-ESO-1 antigen, resulting in tumor cell lysis. (NCI05)","Immunologic Factor|Pharmacologic Substance"]
["C128889","French Maritime Pine Bark Extract","French Maritime Pine Bark Extract|PYC|Pycnogenol","A nutritional supplement containing an extract obtained from the French maritime pine bark Pinus pinaster, with potential immunomodulating and antioxidant activities. The French maritime pine bark extract contains high amounts of the phytochemicals proanthocyanidins. Proanthocyanidins are able to scavenge free radicals, and therefore may inhibit cellular damage. This extract may also ameliorate the symptoms of lymphedema and improve blood flow. It might also stimulate the immune system and have antioxidant effects.","Pharmacologic Substance"]
["C63546","Fresolimumab","Anti-TGF-Beta Monoclonal Antibody GC1008|Fresolimumab|GC1008|Human Anti-TGF-Beta Monoclonal Antibody GC1008|Immunoglobulin G4, anti-(transforming growth factor beta) (human monoclonal GC-1008 heavy chain), disulfide with human monoclonal GC-1008 light chain, Dimer|anti-TGF-beta monoclonal antibody GC1008","A pan-specific, recombinant, fully human monoclonal antibody directed against human transforming growth factor (TGF) -beta 1, 2 and 3 with potential antineoplastic activity. Fresolimumab binds to and inhibits the activity of all isoforms of TGF-beta, which may result in the inhibition of tumor cell growth, angiogenesis, and migration. TGF-beta, a cytokine often over-expressed in various malignancies, may play an important role in promoting the growth, progression, and migration of tumor cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C38707","Fruit and Vegetable Extract","Fruit and Vegetable Extract|Fruit and Vegetable Extracts|Juice Plus|Vegetables-Fruit Mixture","Extracts from plants, such as fruits and vegetables, that contain fiber, vitamins, minerals, and other natural substances with antioxidant, lipid-lowering, and antiproliferative properties. Used in chemoprevention therapy, these extracts may prevent the development or recurrence of cancer. (NCI04)","Pharmacologic Substance"]
["C102852","Fruquintinib","Fruquintinib|HMPL-013|VEGFR-1/2/3 Inhibitor HMPL-013","An orally available, small molecule inhibitor of vascular endothelial growth factor receptors (VEGFRs), with potential anti-angiogenic and antineoplastic activities. Upon oral administration, fruquintinib inhibits VEGF-induced phosphorylation of VEGFRs 1, 2, and 3 which may result in the inhibition of migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and tumor cell death. Expression of VEGFRs may be upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C1379","Fulvestrant","7a-[9-[(4,4,5,5,5,-Pentafluoropentyl)sulphinyl]nonyl]-estra-1,3,5(10)-triene-3,17b-diol|FULVESTRANT|Faslodex(ICI 182,780)|Faslodex|Fulvestrant|ICI 182,780|ICI 182780|ZD9238|fulvestrant","A synthetic estrogen receptor antagonist.  Unlike tamoxifen (which has partial agonist effects) and the aromatase inhibitors (which reduce the estrogen available to tumor cells), fulvestrant binds competitively to estrogen receptors in breast cancer cells, resulting in estrogen receptor deformation and decreased estrogen binding. In vitro studies indicate that fulvestrant reversibly inhibits the growth of tamoxifen-resistant, estrogen-sensitive, human breast cancer cell lines. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C88321","Fumagillin-Derived Polymer Conjugate XMT-1107","Fumagillin-Derived Polymer Conjugate XMT-1107|XMT-1107","A polymeric prodrug consisting of the fumagillol-derived small molecule XMT-1191 tethered to the hydrophilic, biodegradable70 kDa polymer poly[1-hydroxymethylethylene hydroxymethylformal] (PHF) with potential antiangiogenic and antineoplastic activities. Upon administration, fumagillin-derived polymer conjugate XMT-1107 releases XMT-1191, which may inhibit angiogenesis through the irreversible inhibition of the methionine aminopeptidase 2 (METAP2); although the exact mechanism of action has yet to be fully elucidated, this agent appears to induce cell cycle arrest in endothelial cells, inhibiting their proliferation and migration. Compared to an unconjugated fumagillin analog, XMT-1107 exhibits improved solubility and an extended half life due to its PHF backbone. METAP2, a member of the methionyl aminopeptidase family, binds two cobalt or manganese ions and protects the alpha subunit of eukaryotic initiation factor 2 (EIF2) from inhibitory phosphorylation by removing the amino-terminal methionine residue from nascent protein; this aminopeptidase may be overexpressed in a variety of tumor cell types.","Pharmacologic Substance"]
["C121852","Fursultiamine","Fursultiamine|TTFD|Thiamine Tetrahydrofurfuryl Disulfide","A nutritional supplement and vitamin B1 derivative, with potential antineoplastic activity. Upon oral administration, fursultiamine inhibits the expressions of octamer-binding transcription factor 4 (OCT-4), SRY (sex determining region Y)-box 2 (SOX-2), and Nanog homeobox (NANOG) in cancer stem cells (CSCs). This may inhibit the proliferation of CSCs thereby preventing tumor cell growth. In addition, fursultiamine inhibits the expression of ATP-binding cassette (ABC) transporters subfamily B member 1 (ABCB1) and subfamily G member 2 (ABCG2) in cancer CSCs, which may abrogate resistance to chemo- and radiotherapy in CSCs. CSCs promote tumor initiation, progression and metastasis; they play a key role in cancer recurrence and resistance to chemotherapy and radiation.","Pharmacologic Substance"]
["C2676","G207","G207","A neuroattenuated, replication-competent, recombinant herpes simplex virus-1 (HSV-1) with potential oncolytic activity. Upon intracerebral administration, oncolytic HSV-1 G207 preferentially replicates within glioma cells, which may elicit tumor-specific systemic immune and cytotoxic T lymphocyte (CTL) responses in addition to direct cytopathic effects. Derived from wild-type HSV-1 strain F, this agent has been neuroattenuated by deletions in both copies of the gamma34.5 gene, the major determinant of HSV neurovirulence. In addition, the HSV-1 gene UL39, encoding the viral ribonucleotide reductase large subunit infected cell protein 6 (ICP6), has been inactivated through the insertion of the Escherichia coli lacZ gene. By inactivating UL39, viral ribonucleotide reductase activity is disrupted, resulting in the inhibition of nucleotide metabolism and viral DNA synthesis in nondividing cells but not in dividing cells.","Pharmacologic Substance|Virus"]
["C53410","G250 Peptide Vaccine","G250 Peptide Vaccine","A cancer vaccine containing of a synthetic form of the renal cell carcinoma (RCC)-associated antigen G250 with potential antineoplastic activity. Vaccination with G250 peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for the G250 antigen, resulting in decreased tumor growth. Found in the majority of renal cell carcinomas, G250 is a cell surface tumor-associated antigen (TAA) that contains an HLA-A2.1-restricted epitope that is recognized by CTLs.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C128640","Gadolinium-based Contrast Agent P03277","GBCA P03277|Gadolinium-based Contrast Agent P03277|Gadolinium-based Magnetic Resonance Contrast Agent P03277|P 03277|P03277","A gadolinium-based paramagnetic contrast agent, with potential imaging enhancing activity upon magnetic resonance imaging (MRI). Upon administration of P03277 and placement in a magnetic field, this agent produces a large magnetic moment and creates a large local magnetic field, which can enhance the relaxation rate of nearby protons. This change in proton relaxation dynamics, increases the MRI signal intensity of tissues in which this agent has accumulated; therefore, contrast and visualization of those tissues is enhanced compared to unenhanced MRI.","Indicator, Reagent, or Diagnostic Aid|Organic Chemical"]
["C102982","Gag:267-274 Peptide Vaccine","Gag:267-274 Peptide Vaccine","A peptide vaccine containing the amino acids 267 through 274 of the human immunodeficiency virus type 1 (HIV-1) gag core protein (gag:267-274), with potential immunostimulating activity. Upon vaccination, the immune system may exert a potent cytotoxic T-lymphocyte (CTL) response against the xenoantigen gag:267-274 and produces pro-inflammatory cytokines. The concomitant administration of a cancer peptide vaccine may benefit from an already activated immune system and may augment an immune response against the administered tumor associated antigen(s). Gag:267-274 peptide is highly immunogenic and may potentially be used as a cancer immunoadjuvant.","Immunologic Factor|Pharmacologic Substance"]
["C76791","Galamustine","GALAMUSTINE|Galamustine","A galactose mustard compound, an alkylating agent, with antineoplastic activity.","Pharmacologic Substance"]
["C81422","Galarubicin","(8S,10S)-10-((2.6-Dideoxy-2-fluoro-alpha-L-talopyranosyl)oxy)-8-glycoloyl-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-5,12-naphthacenedione 8(sup 2)-ester with Beta-alanine|GALARUBICIN|Galarubicin","An anthracycline derivative with antineoplastic activity developed to circumvent doxorubicin resistance.","Pharmacologic Substance"]
["C115111","Galectin Inhibitor GR-MD-02","GR-MD-02|Galactoarabino-rhamnogalacturonate|Galectin Inhibitor GR-MD-02","A carbohydrate-based galectin inhibitor, with potential antineoplastic activity. Galectin inhibitor GR-MD-02 binds to the carbohydrate-binding domain of galectins, especially galectin-3, and may result in an induction of apoptosis mediated through activation of both mitochondria and caspases. This may reduce tumor growth in galectin-overexpressing tumor cells. Galectins, often overexpressed on tumor cells, play a key role in cancer cell proliferation, apoptosis, tumor angiogenesis and evasion of immune responses.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C103828","Galectin-1 Inhibitor OTX008","Gal-1 Inhibitor OTX008|Galectin-1 Inhibitor OTX008|OTX008","A calixarene-based compound and galectin-1 (Gal-1) inhibitor with potential anti-angiogenic and antineoplastic activities. Upon subcutaneous administration, galectin-1 inhibitor OTX008 binds Gal-1 which leads to Gal-1 oxidation and proteosomal degradation, through an as of yet not fully elucidated mechanism, and eventually downregulation of Gal-1. This decreases tumor cell growth and inhibits angiogenesis. Gal-1, a multifunctional carbohydrate-binding protein, is often overexpressed on tumor cells and plays a key role in cancer cell proliferation, apoptosis, tumor angiogenesis and evasion of immune responses.","Pharmacologic Substance"]
["C84866","Galeterone","Androsta-5,16-dien-3-ol, 17-(1h-benzimidazol-1-yl)-, (3beta)-|GALETERONE|Galeterone|Specific Androgen Receptor Modulator/CYP17 Lyase Inhibitor TOK-001|TOK-001|VN/124-1|VN/124","An orally bioavailable small-molecule androgen receptor modulator and CYP17 lyase inhibitor with potential antiandrogen activity. Galeterone exhibits three distinct mechanisms of action: 1) as an androgen receptor antagonist, 2) as a CYP17 lyase inhibitor and 3) by decreasing overall androgen receptor levels in prostate cancer tumors, all of which may result in a decrease in androgen-dependent growth signaling. Localized to the endoplasmic reticulum (ER), the cytochrome P450 enzyme CYP17 (P450C17 or CYP17A1) exhibits both 17alpha-hydroxylase and 17,20-lyase activities, and plays a key role in the steroidogenic pathway that produces progestins, mineralocorticoids, glucocorticoids, androgens, and estrogens.","Pharmacologic Substance"]
["C116710","Gallium Ga 68 OPS202","68Ga-OPS202|Gallium Ga 68 OPS202","A radioconjugate consisting of the somatostatin antagonistic peptide OPS202 that is labeled with the positron-emitting radionuclide gallium Ga 68, which may be used as a somatostatin receptor (SSTR) imaging agent in conjunction with positron emission tomography (PET) to image neuroendocrine tumors (NETs). Gallium Ga 68 OPS202 binds to SSTR subtype 2 present on the cell membranes of many types of NETs. This allows for visualization of SSTR-positive cells upon imaging. SSTR subtypes have been shown to be present in large numbers on NETs and their metastases, while most other normal tissues express low levels of SSTR subtypes.","Pharmacologic Substance"]
["C73254","Galocitabine","GALOCITABINE|Galocitabine|Ro 09-1390","An orally available 5-fluorouracil (5-FU) prodrug with potential antineoplastic activity. Upon administration, galocitabine is converted into 5'-deoxy-5-fluorocytidine, 5'-deoxy-fluorouridine, and 5-FU. 5-FU is further metabolized into other cytotoxic metabolites that interfere with RNA and DNA synthesis via inhibition of thymidylate synthase. As a result, this agent eventually inhibits tumor cell growth.","Pharmacologic Substance"]
["C116891","Galunisertib","4-(2-(6-Methylpyridin-2-yl)-5,6-dihydro-4H-pyrrolo[1,2-b]pyrazol-3-yl)quinoline-6-carboxamide|GALUNISERTIB|Galunisertib|LY-2157299|LY2157299","An orally available, small molecule antagonist of the tyrosine kinase transforming growth factor-beta (TGF-b) receptor type 1 (TGFBR1), with potential antineoplastic activity. Upon administration, galunisertib specifically targets and binds to the kinase domain of TGFBR1, thereby preventing the activation of TGF-b-mediated signaling pathways. This may inhibit the proliferation of TGF-b-overexpressing tumor cells. Dysregulation of the TGF-b signaling pathway is seen in a number of cancers and is associated with increased cancer cell proliferation, migration, invasion and tumor progression.","Pharmacologic Substance"]
["C118444","Gamboge Resin Extract TSB-9-W1","Gamboge Resin Extract TSB-9-W1|TSB-9-W1","An orally bioavailable extract from the yellow to brown gum-resin of the gamboge tree (genus Garcinia) belonging to the Clusiaceae (or Guttiferae) family, with potential anti-inflammatory and antineoplastic activities. Gamboge resin extract TSB-9-W1 contains various active ingredients, including gambogic acid, formoxanthone A, betulin, betulinic acid, morellic acid, isomorellic acid, isogambogic acid, isomorellinol and desoxymorellin. Upon oral administration, the various active components of the gamboge resin extract TSB-9-W1 may bind to and inhibit the activity of a variety of cancer-related proteins, may induce apoptosis, and may exert cytotoxic activity on tumor cells, thereby inhibiting tumor cell proliferation. TSB-9 is derived from TSB-14, which is the acetone-extract of gamboge resin, and pulverized into powder form; TSB-9 is 90% extract and 10% brown sugar. TSB-9-W1 is a milled form of TSB-9 with a particle size of 5 micrometers.","Pharmacologic Substance"]
["C82383","Gamma Secretase Inhibitor PF-03084014","Gamma Secretase Inhibitor PF-03084014|PF-03084014","A selective gamma secretase (GS) inhibitor with potential antitumor activity. Gamma secretase inhibitor PF-03084014 binds to GS, blocking proteolytic activation of Notch receptors; Notch signaling pathway inhibition may follow, which may result in the induction of apoptosis in tumor cells that overexpress Notch. The integral membrane protein GS is a multi-subunit protease complex that cleaves single-pass transmembrane proteins, such as Notch receptors, at residues within their transmembrane domains. Overexpression of the Notch signaling pathway has been correlated with increased tumor cell growth and survival.","Pharmacologic Substance"]
["C101517","Gamma-delta Tocotrienol","GDT|Gamma-delta Tocotrienol|gdT3","An orally available nutritional supplement containing the gamma and delta forms of the vitamin E family member tocotrienol, with hypocholesterolemic, antithrombotic, antioxidant, and potential antineoplastic activity. Upon oral administration, gamma-delta tocotrienol accumulates in cancer cells and may exert their anti-cancer activity in part through 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase downregulation and/or degradation, cell cycle arrest, and induction of caspase-mediated apoptosis. In addition, this agent may inhibit angiogenesis partially through the blockage of vascular endothelial growth factor receptor (VEGFR) and the inhibition of tumor cell-induced vessel formation. Altogether, this may result in the inhibition of tumor cell growth. Further, this agent prevents free radical formation and inhibits lipid peroxidation. Tocotrienols contain 3 double bonds, absent in tocopherols, on its farnesyl isoprenoid side chain that likely contribute to its anti-cancer activities.","Pharmacologic Substance"]
["C88333","Gamma-Secretase Inhibitor RO4929097","Gamma-Secretase Inhibitor RO4929097|RO4929097","An orally bioavailable, small-molecule gamma secretase (GS) inhibitorwith potential antitumor activity. Gamma secretase inhibitor RO4929097 binds to GS and blocks activation of Notch receptors, which may inhibit tumor cell proliferation. The integral membrane protein GS is a multi-subunit protease complex that cleaves single-pass transmembrane proteins, such as Notch receptors, at residues within their transmembrane domains. Overexpression of the Notch signaling pathway has been correlated with increased tumor cell growth.","Pharmacologic Substance"]
["C116857","Gandotinib","Gandotinib|LY 2784544|LY2784544","An orally bioavailable imidazopyridazine and inhibitor of Janus kinase 2 mutant V617F (JAK2V617F), with potential antineoplastic activity. Upon oral administration, gandotinib selectively and competitively inhibits the activation of JAK2V617F, which may result in the inhibition of the JAK-STAT signaling pathway and the induction of apoptosis in JAK2V617F-expressing tumor cells. JAK2V617F has a substitution of phenylalanine for valine at amino acid position 617 and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C77872","Ganetespib","3-(2,4-dihydroxy-5-isopropylphenyl)-4-(1-methylindol-5-yl)-5-hydroxy-4h-1,2,4-triazole 3h-1,2,4-triazol-3-one|5-(2,4-dihydroxy-5-(1-methylethyl)phenyl)-2,4-dihydro-4-(1-methyl-1h-indol-5-yl)-|GANETESPIB|Ganetespib|Hsp90 Inhibitor STA-9090|STA-9090","A synthetic small-molecule inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Ganetespib binds to and inhibits Hsp90, resulting in the proteasomal degradation of oncogenic client proteins, the inhibition of cell proliferation and the elevation of heat shock protein 72 (Hsp72); it may inhibit the activity of multiple kinases, such as c-Kit, EGFR, and Bcr-Abl, which as client proteins depend on functional HsP90 for maintenance. Hsp90, a 90 kDa molecular chaperone upregulated in a variety of tumor cells, plays a key role in the conformational maturation, stability and function of \"client\" proteins within the cell, many of which are involved in signal transduction, cell cycle regulation and apoptosis, including kinases, transcription factors and hormone receptors.  Hsp72 exhibits anti-apoptotic functions; its up-regulation may be used as a surrogate marker for Hsp90 inhibition.","Organic Chemical|Pharmacologic Substance"]
["C1110","Ganglioside GD2","GD2 ganglioside|GalNAc(beta 1->4)-[NeuAc(alpha 2->8)NeuAc(alpha 2->3)]Gal(beta 1->4)GlcCer|Ganglioside GD2","A cell surface antigen expressed on all tumors of neuroectodermal origin, including melanoma, neuroblastomas, sarcoma, astrocytomas, and small cell lung cancer. GD2, an O-acetylated disialoganglioside, belongs to the group of glycosphingolipids that are widely expressed in many tissues and organs in vertebrates and have been suggested to be involved in the regulation of development and differentiation as recognition molecules or signal modulators. Due to its high level of expression in neuroblastoma, GD2 has the potential to be used as a component of anti-neuroblastoma vaccines, in addition to being used in polyvalent anti-melanoma vaccines.","Immunologic Factor|Organic Chemical"]
["C516","Ganglioside GM2","GM2 ganglioside|Ganglioside GM2","A glycosphingolipid antigen expressed by a variety of human cancer cells. GM2 containing vaccines have been shown to elicit antibodies production in melanoma patients without deleterious effects associated with an immune response to GM2. Mutations in at least 1 of 3 recessive genes: HEXA, HEXB, and GM2A cause defects in GM2 catabolism, leading to lysosomal lipid storage disorders that manifest primarily as neurodegenerative diseases, including Tay-Sachs and Sandhoff Disease.","Immunologic Factor|Organic Chemical"]
["C71531","Ganitumab","AMG 479|Anti-IGF-1R Human Monoclonal Antibody AMG-479|GANITUMAB|Ganitumab","A recombinant, fully human monoclonal antibody directed against the insulin-like growth factor 1 receptor (IGF-1R) with potential antineoplastic activity. Ganitumab binds to membrane-bound IGF-1R, preventing binding of the ligand IGF-1 and the subsequent triggering of the PI3K/Akt signaling pathway; inhibition of this survival signaling pathway may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. IGF-1R is a tyrosine kinase and a member of the insulin receptor family. IGF-1R activation stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF-1R signaling has been highly implicated in tumorigenesis and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C118365","Ganoderma lucidum Spores Powder Capsule","Ganoderma l. Spores Powder Capsule|Ganoderma lucidum Spores Powder Capsule|Lingzhi Spores Powder Capsule","An orally available powder-based nutritional supplement containing the spores of the mushroom Ganoderma lucidum (Ganoderma l.), a traditional Chinese medicine, with potential protective, sedative, anti-oxidant, immunomodulating, and antineoplastic activities. The spores contain various bioactive components including polysaccharides, triterpenoids, peptidoglycans, amino acids, fatty acids, vitamins, and minerals. Upon oral administration of the Ganoderma lucidum spores powder capsule, the active ingredients may modulate the immune system, may activate dendritic cells, natural killer cells, and macrophages and may modulate the production of certain cytokines, such as tumor necrosis factor-alpha (TNFa), interleukin (IL) 1-beta (IL-1b), IL-2, IL-6 and IL-8. This supplement may improve cancer-related fatigue and may be used as a sleep aid; it may also have a beneficial effect on the heart, lung, liver, pancreas, kidney, and the central nervous system.","Pharmacologic Substance"]
["C38706","Garlic","Ajo|Allium Sativum|Allium sativum|GARLIC|Garlic|garlic","A bulbous herb isolated from the plant Allium sativum with potential antineoplastic activity. Garlic contains a number of different organosulfur compounds, some of which have displayed antineoplastic activity. (NCI04)","Pharmacologic Substance"]
["C29069","Garlic Extract","Allium sativum Extract|CCRIS 7640|EINECS 232-371-1|Garlic Extract","The alcoholic extract of the bulb or whole garlic plant Allium sativum (Liliaceae) with potential antineoplastic activity. The garlic plant has long been considered a beneficial plant for health and has been used as an antihelmintic, a rubefacient, an anti-infective, and an antihypertensive. Fresh or aged, garlic extracts contain compounds such as diallyl and allyl propyl disulfides with potent antioxidant, cholesterol-lowering properties; regular ingestion may be preventative for atherosclerosis and cardiovascular diseases. (NCI04)","Pharmacologic Substance"]
["C1692","Gastrin Immunotoxin","Anti-Gastrin Therapeutic Vaccine|Anti-gastrin 17|G17DT Immunogen|G17DT|Gastrimmune|Gastrin Immunotoxin|Neutralize Hormone G17|Neutralizing G17 Hormone","An immunotoxin containing an epitope of human gastrin conjugated to diphtheria toxin, with antineoplastic activity. The gastrin epitope in this vaccine is chemically identical or similar to the endogenous gastrin-17 (G-17), a 17-amino acid peptide hormone that stimulates secretion of gastric acid by the stomach. Diphtheria toxin inhibits protein synthesis via modifying translation elongation factor 2 (EF-2). Vaccination with this immunotoxin may elicit production of antibodies against gastrinoma cells overexpressing gastrin, in addition to the toxic effects on protein synthesis exerted by the diphtheria toxin moiety.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C66935","Gataparsen Sodium","Antisurvivin Antisense Oligonucleotide LY2181308|Gataparsen Sodium|LY2181308 Heptadecasodium Salt|LY2181308","A second-generation antisense oligonucleotide against survivin mRNA with potential antitumor activity. Oligonucleotide LY2181308 hybridizes to survivin mRNA, thereby blocking translation of survivin protein, a member of the inhibitor of apoptosis (IAP) family. Survivin, expressed during embryonal development, is upregulated in a variety of human cancers while absent in most normal adult cells; its expression in tumors is associated with a more aggressive phenotype, shorter survival times, and a decreased response to chemotherapy. Silencing expression of survivin potentially leads to restoration of the apoptotic process in cancer cells, thereby facilitating chemotherapeutic treatments.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C74035","GD2 Lactone/GD3 Lactone-KLH Conjugate Bivalent Vaccine","GD2 Lactone/GD3 Lactone-KLH Conjugate Bivalent Vaccine","A cancer vaccine, containing epitopes of the gangliosides GD2 and GD3 conjugated with the immunostimulant keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Vaccination with GD2 lactone/GD3 lactone-KLH conjugate bivalent vaccine may elicit antibodies against tumor cells expressing either epitope, resulting in complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC). Located primarily in the nervous system, gangliosides, such as GD2 and GD3, are cell membrane components involved in cellular recognition and cell-cell communication.","Pharmacologic Substance"]
["C123820","GD2-CAR-expressing Autologous T-lymphocytes","GD2-CAR-expressing Autologous T-lymphocytes|tvs-CTL Vaccine","Genetically modified, autologous T-lymphocytes transduced with a retroviral vector encoding a 14g2a.zeta chimeric antigen receptor (CAR) directed against the disialoganglioside GD2, with potential immunomodulating and antineoplastic activities. Upon intravenous administration, the activated T-lymphocytes target the GD2 antigen on tumor cells and selectively kill those cells. The tumor-associated antigen GD2 is overexpressed on the surface of almost all tumors of neuroectodermal origin.","Cell|Pharmacologic Substance"]
["C2400","GD2-KLH Vaccine","GD2-KLH Vaccine|Ganglioside GD2-KLH|KLH-conjugated GD2 Ganglioside Vaccine","A cancer vaccine containing an epitope of glycosphingolipid GD2 conjugated with the immunostimulant keyhole limpet hemocyanin (KLH), with potential antineoplastic activity.  The disialoganglioside GD2 is a tumor-associated antigen expressed on the surface of several cancers, including neuroblastoma medulloblastomas, astrocytomas, melanomas, small-cell lung cancer, osteosarcomas, and other soft tissue sarcomas. Vaccination with GD2-KLH vaccine may elicit antibody production against cells expressing GD2 ganglioside, thereby reducing tumor cell growth.","Immunologic Factor|Pharmacologic Substance"]
["C91732","Gedatolisib","1-(4-[[4-(dimethylamino)piperidin-1-yl]carbonyl]phenyl)-3-[4-(4,6-dimorpholin-4-yl-1,3,5-triazin-2-yl)phenyl]urea|GEDATOLISIB|Gedatolisib|PF 05212384|PF-05212384|PKI 587|PKI-587|Urea, N-(4-((4-(dimethylamino)-1-piperidinyl)carbonyl)phenyl)-N'-(4-(4,6-di-4-morpholinyl-1,3,5-triazin-2-yl)phenyl)-","An agent targeting the phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. Upon intravenous administration, gedatolisib inhibits both PI3K and mTOR kinases, which may result in apoptosis and growth inhibition of cancer cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.","Pharmacologic Substance"]
["C1855","Gefitinib","4-(3'-Chloro-4'-fluoroanilino)-7-methoxy-6-(3-morpholinopropoxy)quinazoline|GEFITINIB|Gefitinib|Iressa|N-(3-chloro-4-fluorophenyl)-7-methoxy-6-[3-(4-morpholin) propoxy]-4-quinazolinamine|ZD 1839|ZD1839|gefitinib","An anilinoquinazoline with antineoplastic activity. Gefitinib inhibits the catalytic activity of numerous tyrosine kinases including the epidermal growth factor receptor (EGFR), which may result in inhibition of tyrosine kinase-dependent tumor growth. Specifically, this agent competes with the binding of ATP to the tyrosine kinase domain of EGFR, thereby inhibiting receptor autophosphorylation and resulting in inhibition of signal transduction. Gefitinib may also induce cell cycle arrest and inhibit angiogenesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1112","Geldanamycin","Antibiotic (U-29,135)|Antibiotic U 29135|GELDANAMYCIN|Geldanamycin","A benzoquinone antineoplastic antibiotic isolated from the bacterium Streptomyces hygroscopicus.  Geldanamycin binds to and inhibits the cytosolic chaperone functions of heat shock protein 90 (HSP90).  HSP90 maintains the stability and functional shape of many oncogenic signaling proteins; the inhibition of HSP90 promotes the proteasomal degradation of oncogenic signaling proteins that may be over-expressed or overactive in tumor cells. (NCI04)","Antibiotic|Organic Chemical"]
["C2016","GEM 220","GEM 220|Gene Expression Modulator 220","A mixed-backbone antisense oligonucleotide that is complementary to a pro-angiogenic vascular endothelial growth factor (VEGF) mRNA sequence.  Because of its antiangiogenic properties, GEM 220 has been studied as a potential antineoplastic agent. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1810","GEM 231","GEM 231|GEM231|Gene Expression Modulator 231","A mixed backbone oligonucleotide exhibiting antitumor activity.  GEM-231 is complementary to the RI alpha subunit of Protein Kinase A (PKA), resulting in downregulation of PKA expression and ultimately tumor growth. (NCI)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C66876","Gemcitabine","1-(2-Oxo-4-amino-1,2-dihydropyrimidin-1-yl)-2-deoxy-2,2-difluororibose|2'Deoxy-2',2'-Difluorocytidine|Difluorodeoxycytidine|GEMCITABINE|Gemcitabine|dFdC|dFdCyd|gemcitabine","A broad-spectrum antimetabolite and deoxycytidine analogue with antineoplastic activity. Upon administration, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA.  This locks DNA polymerase thereby resulting in \"masked termination\" during DNA replication. On the other hand, dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis. The reduction in the intracellular concentration of dCTP potentiates the incorporation of dFdCTP into DNA.","Nucleic Acid, Nucleoside, or Nucleotide"]
["C79803","Gemcitabine Elaidate","CP-4126|GEMCITABINE ELAIDATE|Gemcitabine 5'-Elaidic Acid Ester|Gemcitabine Elaidate","A lipophilic, unsaturated fatty acid ester derivative of gemcitabine (dFdC), an antimetabolite deoxynucleoside analogue, with potential antineoplastic activity. Upon hydrolysis intracellularly by esterases, the prodrug gemcitabine is converted into the active metabolites difluorodeoxycytidine di- and tri-phosphate (dFdCDP and dFdCTP) by deoxycytidine kinase. dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis; dFdCTP is incorporated into DNA, resulting in DNA strand termination and apoptosis. Due to its lipophilicity, gemcitabine 5'-elaidic acid ester exhibits an increased cellular uptake and accumulation, resulting in an increased conversion to active metabolites, compared to gemcitabine. In addition, this formulation of gemcitabine may be less susceptible to deamination and deactivation by deoxycytidine deaminase.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C961","Gemcitabine Hydrochloride","1-(2-Oxo-4-amino-1,2-dihydropyrimidin-1-yl)-2-deoxy-2,2-difluororibose, hydrochloride|2'Deoxy-2',2'-Difluorocytidine, Hydrochloride|Difluorodeoxycytidine Hydrochloride|GEMCITABINE HYDROCHLORIDE|Gemcitabine Hydrochloride|Gemzar|LY-188011|LY188011|dFdCyd|gemcitabine hydrochloride","The hydrochloride salt of an analogue of the antimetabolite nucleoside deoxycytidine with antineoplastic activity. Gemcitabine is converted intracellularly to the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis; dFdCTP is incorporated into DNA, resulting in DNA strand termination and apoptosis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C105613","Gemcitabine Hydrochloride Emulsion","D07001-F4|Gemcitabine Hydrochloride Emulsion","An orally available nanoparticle-based formulation containing the hydrochloride salt form of gemcitabine, a broad-spectrum antimetabolite and deoxycytidine analogue, with antineoplastic activity. The formulation consists of an oil-in-water emulsion in which gemicitabine is solubilized in the excipient matrix containing a mixture of oil and (co)surfactants. Upon oral administration, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA, resulting in premature termination of DNA replication and the induction of apoptosis. Further, dFdCDP inhibits ribonucleotide reductase and reduces the deoxynucleotide pool available for DNA synthesis. Compared to gemcitabine alone, the emulsion allows for increased oral bioavailability and decreases its susceptibility to deamination and deactivation by cytidine deaminase.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C102856","Gemcitabine Prodrug LY2334737","Gemcitabine Prodrug LY2334737|LY2334737","An orally available valproic acid prodrug of gemcitabine, a broad-spectrum antimetabolite and deoxycytidine analogue with antineoplastic activity. Upon administration, gemcitabine prodrug LY2334737 is hydrolyzed by carboxylesterase 2 (CES2) and releases gemcitabine systemically over a period of time consistent with formation rate-limited kinetics. In turn, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate and triphosphate (dFdCDP and dFdCTP) by deoxycytidine kinase. dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA replication; dFdCTP is incorporated into DNA, resulting in premature termination of DNA replication and eventually the induction of apoptosis. Compared to gemcitabine, this prodrug is able to avoid hydrolysis in enterocytes and the portal circulation thus avoiding first pass metabolism and increasing systemic gemcitabine availability. In addition, the slow release of gemcitabine may enhance efficacy while lowering toxicity. CES2, a serine ester hydrolase, is expressed in certain tumors which may allow for increased conversion of gemcitabine at the tumor site thus increases cytotoxicity.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C102752","Gemcitabine-Phosphoramidate Hydrochloride NUC-1031","Acelarin|Gemcitabine-Phosphoramidate Hydrochloride NUC-1031|Gemictabine ProTide|NUC-1031","A pyrimidine analogue and a proprietary prodrug based on an aryloxy phosphoramidate derivative of gemcitabine with potential antineoplastic activity. Upon intravenous administration and cellular uptake, NUC-1031 is converted into the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA replication; dFdCTP is incorporated into DNA, resulting in premature termination of DNA replication and eventually induction of apoptosis. With the phosphoramidate moiety on the gemcitabine monophosphate group, NUC-1031 has improved properties over its parent molecule: 1) is more lipophilic and accumulates in cancer cells by passive diffusion and does not require a nucleoside transporter, 2) as the agent is delivered in the monophosphate form, the first phosphorylation step by deoxycytidine kinase is not required, 3) this agent is not susceptible to deactivation by cytidine deaminase cleavage of the monophosphorylated form. Altogether, this may help overcome resistance to gemcitabine.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1806","Gemtuzumab Ozogamicin","CDP-771|CMA-676|Calicheamicin-Conjugated Humanized Anti-CD33 Monoclonal Antibody|GEMTUZUMAB OZOGAMICIN|Gemtuzumab Ozogamicin|Mylotarg|WAY-CMA-676|gemtuzumab ozogamicin|gemtuzumab|hP67.6-Calicheamicin","A recombinant, humanized anti-CD33 monoclonal antibody attached to the cytotoxic antitumor antibiotic calicheamicin.  In this conjugate, the antibody binds to and is internalized by tumor cells expressing CD33 antigen (a sialic acid-dependent glycoprotein commonly found on the surface of leukemic blasts), thereby delivering the attached calicheamicin to CD33-expressing tumor cells. Calicheamicin binds to the minor groove of DNA, causing double strand DNA breaks and resulting in inhibition of DNA synthesis. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C116846","Genetically Engineered NY-ESO-1-specific T Lymphocytes","Genetically Engineered NY-ESO-1-specific T Lymphocytes","A preparation of human T-lymphocytes recognizing the tumor-associated antigen (TAA), cancer/testis antigen 1 (NY-ESO-1), with potential immunostimulating and antineoplastic activities. Genetically engineered NY-ESO-1-specific T-lymphocytes target tumor cells expressing the NY-ESO-1 antigen, resulting in tumor cell lysis. NY-ESO-1, an antigen found in normal testis, is overexpressed on the surface of various tumor cell types.","Cell|Pharmacologic Substance"]
["C118973","Genetically-modified MAGE-A3-expressing MG1 Maraba Virus Vaccine","Genetically-modified MAGE-A3-expressing MG1 Maraba Virus Vaccine|MG1 Maraba/MAGE-A3|MG1MA3","A vaccine consisting of the attenuated, genetically-modified, oncolytic form of the Maraba virus, MG1, which has been engineered to express a gene encoding the cancer testis antigen melanoma antigen family A3 (MAGE-A3), with potential antineoplastic activity. Upon administration of genetically-modified MAGE-A3-expressing MG1 Maraba virus vaccine, the attenuated Maraba virus selectively and rapidly replicates in cancer cells; however, it is unable to replicate in normal, healthy cells. This induces a selective Maraba virus-mediated cytotoxicity in those cancer cells, and leads to cancer cell lysis. In addition, the expression of MAGE-A3 further stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing MAGE-A3. The tumor-associated antigen MAGE-A3 is overexpressed by a variety of cancer cell types. The attenuated virus is a double mutant strain with single amino acid substitutions occurring in both G protein (Q242R) and M protein (L123W).","Pharmacologic Substance|Virus"]
["C1113","Genistein","4',5, 7-Trihydroxyisoflavone|4',5,7-Trihydroxyisoflavone|5,7-Dihydroxy-3-(4-hydroxyphenyl)-4H-1-benzopyran-4-one|GENISTEIN|Genestein|Genistein|Genisteol|Prunetol|genistein","A soy-derived isoflavone and phytoestrogen with antineoplastic activity. Genistein binds to and inhibits protein-tyrosine kinase, thereby disrupting signal transduction and inducing cell differentiation.  This agent also inhibits topoisomerase-II, leading to DNA fragmentation and apoptosis, and induces G2/M cell cycle arrest.  Genistein exhibits antioxidant, antiangiogenic, and immunosuppressive activities. (NCI04)","Organic Chemical"]
["C104414","Geranylgeranyltransferase I Inhibitor","GGTI-I|GGTase-I Inhibitor|Geranylgeranyltransferase I Inhibitor","A substance that inhibits protein geranylgeranyltransferase type 1 (GGTase-I), with potential antineoplastic activity. GGTase-I is involved in the posttranslational modification of a number of oncogenic GTPases, including K-Ras, N-Ras, RhoA, RhoC, Cdc42, RalA, RalB and Rac1. Inhibition of the prenylation of these oncogenic proteins inhibits both their oncogenic activity and membrane localization. This may result in cell cycle arrest and apoptosis. Protein geranylgeranylation, catayzed by GGTase-I, plays a critical role in malignant transformation and cancer cell proliferation, migration and invasion.","Pharmacologic Substance"]
["C61489","GI-4000 Vaccine","GI-4000 Vaccine","A vaccine containing a heat-killed recombinant Saccharomyces cerevisiae yeast transfected with mutated forms of Ras, an oncogene frequently found in solid tumors, with potential immunostimulant and antitumor activity. Upon administration, GI-4000 vaccine elicits an immune response by stimulating a specific cytotoxic T-cell response against the mutated forms of Ras. This may lead to a destruction of cancer cells expressing a Ras mutation.","Pharmacologic Substance"]
["C116722","Gilteritinib","6-Ethyl-3-((3-methoxy-4-(4-(4-methylpiperazin-1-yl)piperidin-1-yl)phenyl)amino)-5-((tetrahydro-2H-pyran-4-yl)amino)pyrazine-2-carboxamide|ASP-2215|ASP2215|GILTERITINIB|Gilteritinib","An orally bioavailable inhibitor of the receptor tyrosine kinases (RTKs) FMS-related tyrosine kinase 3 (FLT3, STK1, or FLK2), AXL (UFO or JTK11) and anaplastic lymphoma kinase (ALK or CD246), with potential antineoplastic activity. Gilteritinib binds to and inhibits both the wild-type and mutated forms of FLT3, AXL and ALK. This may result in an inhibition of FLT3, AXL, and ALK-mediated signal transduction pathways and reduces tumor cell proliferation in cancer cell types that overexpress these RTKs. FLT3, AXL and ALK, overexpressed or mutated in a variety of cancer cell types, play a key role in tumor cell growth and survival.","Organic Chemical|Pharmacologic Substance"]
["C65804","Gimatecan","7-t-Butoxyiminomethylcamptothecin|GIMATECAN|Gimatecan|LBQ707|ST1481|STI481|gimatecan","An orally bioavailable, semi-synthetic lipophilic analogue of camptothecin, a quinoline alkaloid extracted from the Asian tree Camptotheca acuminate, with potential antineoplastic and antiangiogenic activities. Gimatecan binds to and inhibits the activity of topoisomerase I, stabilizing the cleavable complex of topoisomerase I-DNA, which inhibits the religation of single-stranded DNA breaks generated by topoisomerase I; lethal double-stranded DNA breaks occur when the topoisomerase I-DNA complex is encountered by the DNA replication machinery, DNA replication is disrupted, and the tumor cell undergoes apoptosis. Although the mechanism of its antiangiogenic activity has yet to be full elucidated, this agent may inhibit endothelial cell migration, tumor neovascularization, and the expression of proangiogenic basic fibroblast growth factor (bFGF).","Pharmacologic Substance"]
["C2416","Gimeracil","5-Chloro-2,4-pyridinediol|CDHP|Chlorodihydroxypyridine|GIMERACIL|Gimeracil","A pyridine derivative with antitumor activity. Gimeracil enhances the antitumor activity of fluoropyrimidines by competitively and reversibly inhibiting the enzyme dihydropyrimidine dehydrogenase causing decreased degradation of the fluoropyrimidines.","Organic Chemical|Pharmacologic Substance"]
["C2691","Ginger Extract","Ginger Extract","An extract of the rhizome of the perennial plant Zingiber officinale with potential antineoplastic activity. Ginger extract contains a number of different phenolic compounds, some of which have displayed antineoplastic, anti-inflammatory, and antioxidant activities. This agent also exhibits antiemetic properties.","Pharmacologic Substance"]
["C125000","Ginseng Compound","Ginseng Compound","A compound containing the traditional Chinese medicine (TCM) ginseng, a herb belonging to the Araliaceae family, with potential antioxidant, chemopreventive, anti-inflammatory and antineoplastic activities. Upon administration of the ginseng compound, the active ingredients, mainly ginsenosides, inhibit various signal transduction pathways that play key roles in carcinogenesis and inflammation. This leads to the induction of apoptosis in and inhibits proliferation of tumor cells. In addition, ginsenosides enhance the activity of various antioxidant enzymes, induce nitric oxide (NO) formation, inhibit the formation of reactive oxygen species (ROS) and protect against free radical-induced DNA damage. Ginseng also modulates various components of the immune system, including the activation of dendritic cells (DCs).","Pharmacologic Substance"]
["C103300","Ginsenoside Rg3 Capsule","Ginsenoside Rg3 Capsule|Shen Yi Capsule","A capsule containing the steroidal saponin ginsenoside Rg3 isolated from the root of Panax ginseng, with potential cancer preventive and anti-angiogenic activities. Upon oral administration, ginsenoside Rg3 appears to inhibit endothelial cell proliferation, migration and tubular formation, and promotes cancer cell apoptosis. This agent also modulates the activities of certain growth factors, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and matrix metalloproteinases (MMPs), on tumor angiogenesis. In addition, ginsenoside Rg3 may be able to sensitize cancer cells to some chemotherapeutic agents.","Pharmacologic Substance"]
["C1960","Girentuximab","Chimeric Monoclonal Antibody cG250|GIRENTUXIMAB|Girentuximab|MoAb G250|Monoclonal Antibody G250|Rencarex|WX-G250|cG250","A chimeric monoclonal antibody directed against G250, a cell surface antigen found in the majority of renal cell carcinomas. Following binding, monoclonal antibody G250 (mAb G250) may be internalized by G250 antigen-expressing renal carcinoma cells; mAb G250 may be useful as a carrier for radioisotopes and other antineoplastic therapeutic agents. (NCI05)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1373","Girodazole","3-Amino-1-[4-(2 amino-1H-imidazolyl)]-propanol, 2HCl|Girodazole|Giroline|RP 49532A","A compound isolated from the marine sponge Pseudaxinyssa cantharella exhibiting anti-tumor activity.  Studies indicate girodazole acts during the elongation/termination steps of protein synthesis, resulting in protein synthesis inhibition. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C124651","GITR Agonist MEDI1873","GITR Agonist MEDI1873|GITR Stimulant MEDI1873|MEDI 1873|MEDI1873|TNFRSF18 Agonist MEDI1873|TNFRSF18 Protein Stimulant MEDI1873","An agonist of human glucocorticoid-induced tumor necrosis factor receptor (tumor necrosis factor superfamily, member 18; TNFRSF18; GITR), with potential immunomodulating and antineoplastic activities. Upon administration, GITR agonist MEDI1873 binds to GITR found on multiple types of T-cells, thereby inducing both the activation and proliferation of tumor antigen-specific T effector cells. This abrogates the suppression of T effector cells which is induced by inappropriately activated T regulatory cells (Tregs), and activates the immune system to help eradicate tumor cells. GITR, a member of the TNF receptor superfamily, is expressed on the surface of multiple types of immune cells, including regulatory T-cells, effector T-cells, B-cells, dendritic cells (DCs) and natural killer (NK) cells.","Pharmacologic Substance"]
["C94216","GITRL RNA-transfected Autologous Dendritic Cell Vaccine","GITRL RNA DC|GITRL RNA-transfected Autologous DC|GITRL RNA-transfected Autologous Dendritic Cell Vaccine","An autologous dendritic cell (DC) cancer vaccine with potential immunostimulatory activity. GITRL RNA-transfected autologous DC vaccine is prepared by transfecting DCs with RNAs encoding tumor necrosis factor (ligand) superfamily, member 18 (TNFSF18 or GlTRL); expression of GlTRL results in modulating T lymphocyte survival in peripheral tissues. Co-vaccination of this vaccine with melanoma antigen specific vaccine may eliminate the adverse effects associated with systemic administration of immune modulators, while also enhancing vaccine-induced immune responses.","Cell|Pharmacologic Substance"]
["C71716","Givinostat","GIVINOSTAT|Gavinostat|Givinostat|ITF2357","An orally bioavailable hydroxymate inhibitor of histone deacetylase (HDAC) with potential anti-inflammatory, anti-angiogenic, and antineoplastic activities. Givinostat inhibits class I and class II HDACs, resulting in an accumulation of highly acetylated histones, followed by the induction of chromatin remodeling and an altered pattern of gene expression. At low, nonapoptotic concentrations, this agent inhibits the production of pro-inflammatory cytokines such as tumor necrosis factor- (TNF-), interleukin-1 (IL-1), IL-6 and interferon-gamma. Givinostat has also been shown to activate the intrinsic apoptotic pathway, inducing apoptosis in hepatoma cells and leukemic cells. This agent may also exhibit anti-angiogenic activity, inhibiting the production of angiogenic factors such as IL-6 and vascular endothelial cell growth factor (VEGF) by bone marrow stromal cells.","Pharmacologic Substance"]
["C1866","GL331","GL331","An epipodophyllotoxin analogue possessing antineoplastic properties.  GL331 binds to and inhibits topoisomerase II, resulting in the accumulation of single- or double-strand DNA breaks, the inhibition of DNA replication and transcription, and apoptotic cell death. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C1114","Glaucarubolone","Glaucarubolone","A polycyclic lactone quassinoid phytochemical isolated from the seeds of Hannoa undulata and other plant species with potential antineoplastic activity.  This agent also has antiviral and antitumor properties. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C78449","Glembatumumab Vedotin","Antibody-Drug Conjugate CR011-vcMMAE|CDX-011|CR011-vcMMAE Immunotoxin|CR011-vcMMAE|Glembatumumab Vedotin","An antibody-drug conjugate, consisting of the fully human monoclonal antibody CR011 directed against glycoprotein NMB (GPNMB) and conjugated via a cathepsin B-sensitive valine-citrulline (vc) linkage to the cytotoxic agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. Upon administration, the monoclonal antibody CR011 moiety binds to glycoprotein nmb (GPNMB), expressed on the surfaces of a variety of cancer cell types; upon endocytosis, the synthetic dolastin analogue MMAE is released via enzymatic cleavage into the tumor cell cytosol, where it binds to tubulin and inhibits tubulin polymerization, which may result in G2/M phase arrest and apoptosis. The vc linkage system is highly stable in serum, rendering the cytotoxicity of glembatumumab vedotin specific for GPNMB-positive cells. GPNMB is a transmembrane protein overexpressed on the surfaces of various cancer cell types, including melanoma, breast, and prostate cancer cells.","Pharmacologic Substance"]
["C77876","Glesatinib","GLESATINIB|Glesatinib|MG90265|MG90265X|MGCD265|TKI MGCD265","An orally bioavailable, small-molecule, multitargeted tyrosine kinase inhibitor with potential antineoplastic activity. Glesatinib binds to and inhibits the phosphorylation of several receptor tyrosine kinases (RTKs), including the c-Met receptor (hepatocyte growth factor receptor); the Tek/Tie-2 receptor; vascular endothelial growth factor receptor (VEGFR) types 1, 2, and 3; and the macrophage-stimulating 1 receptor (MST1R or RON). Inhibition of these RTKs and their downstream signaling pathways may result in the inhibition of tumor angiogenesis and tumor cell proliferation in tumors overexpressing these RTKs.","Organic Chemical|Pharmacologic Substance"]
["C107502","Glioblastoma Cancer Vaccine ERC1671","ERC-1671|ERC1671|Glioblastoma Cancer Vaccine ERC1671|Gliovac","A cancer vaccine composed of a combination of autologous glioblastoma (GBM) tumor cells, allogeneic GBM tumor cells, generated from three different GBM donor cancer patients, and the lysates of all of these cells, with potential antineoplastic activity. Upon intradermal administration of GBM cancer vaccine ERC1671, the mixture of the autologous and allogeneic cells and lysates stimulates the immune system to mount a cytotoxic T-lymphocyte (CTL) response against GBM-associated antigens, which leads to the destruction of glioblastoma cells.","Cell|Pharmacologic Substance"]
["C94211","Glioblastoma Multiforme Multipeptide Vaccine IMA950","Glioblastoma Multiforme Multipeptide Vaccine IMA950|IMA950","A cancer vaccine comprised of 11 peptides associated with glioblastoma multiforme (GBM), with potential immunomodulating and antineoplastic activities. Vaccination with glioblastoma multiforme multi-antigen vaccine IMA950 stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response as well as a T-helper (Th) immune response against tumor cells expressing these peptides, potentially resulting in decreased tumor growth of GBM. Peptides in IMA950 consist of the following: brevican (BCAN); chondroitin sulfate proteoglycan 4 (CSPG4); fatty acid binding protein 7, brain (FABP7); insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3); neuroligin 4, X-linked (NLGN4X); neuronal cell adhesion molecule (NRCAM); protein tyrosine phosphatase, receptor-type, Z polypeptide 1 (PTPRZ1); tenascin C (TNC); Met proto-oncogene (MET); baculoviral IAP repeat-containing 5 (BIRC5); and hepatitis B virus core antigen.","Immunologic Factor|Pharmacologic Substance"]
["C74036","Glioma-Associated Antigen Peptide-Pulsed Autologous Dendritic Cell Vaccine","Glioma-Associated Antigen Peptide-Pulsed Autologous Dendritic Cell Vaccine","A cancer vaccine comprised of autologous dendritic cells pulsed with synthetic glioma-associated antigen (GAA) peptides with potential antineoplastic activity. Upon administration, this vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against GAA peptide-expressing glioma cells, resulting in tumor cell lysis.","Pharmacologic Substance"]
["C114496","Glioma-associated Peptide-loaded Dendritic Cell Vaccine SL-701","Glioma-associated Peptide-loaded Dendritic Cell Vaccine SL-701|SL-701","A cell-based cancer vaccine comprised of dendritic cells (DCs) pulsed with various, synthetic glioma-associated antigen (GAA) peptides, with potential antineoplastic activity. Upon subcutaneous administration, the glioma-associated peptide-loaded DC vaccine SL-701 exposes the immune system to various GAA peptides. This may stimulate both anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against the GAA-expressing glioma cells, which may result in tumor cell lysis.","Cell|Pharmacologic Substance"]
["C119745","Globo H-DT Vaccine OBI-833","Globo H-CRM197 Vaccine|Globo H-DT Vaccine OBI-833|OBI-833","A carbohydrate-based vaccine comprised of the Globo H hexasaccharide 1 (Globo H) antigen conjugated to DT-CRM197, a non-toxic, mutated form of diphtheria toxin (DT), with potential immunostimulating and antineoplastic activities. Upon administration of Globo H-DT vaccine OBI-833, the carbohydrate antigen Globo H may stimulate a cytotoxic T-lymphocyte (CTL) response against Globo H-expressing tumor cells, thereby decreasing tumor cell proliferation. The hexasaccharide Globo H is a tumor-associated antigen (TAA) commonly found on a variety of tumor cells. DT-CRM197, also called diphtheria toxin cross-reacting material 197, is used to increase the immunogenicity of the Globo H carbohydrate antigen.","Immunologic Factor|Pharmacologic Substance"]
["C28503","Globo H-GM2-Lewis-y-MUC1-32-mer-TF(c)-Tn(c)-KLH Conjugate Vaccine","Globo H-GM2-Lewis-y-MUC1-32-mer-TF(c)-Tn(c)-KLH Conjugate Vaccine","A multivalent vaccine comprised of the epitope antigens of Globo H hexasaccharide 1 (Globo H), GM2 ganglioside, Lewis-Y, MUC1-32-mer, TF(c), and Tn(c) conjugated with keyhole limpet hemocyanin, with potential antineoplastic activity. The antigens included in this vaccine are associated various cancer cells. Vaccination with this multivalent vaccine may induce production of IgG and IgM antibodies as well as an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumors expressing these antigens.","Immunologic Factor|Pharmacologic Substance"]
["C99766","Globo H-KLH Immunostimulant OPT-822","Globo H-KLH Immunostimulant OPT-822|OPT-822","A carbohydrate-based immunostimulant comprised of the Globo H hexasaccharide 1 (Globo H) epitope linked to the immunostimulant carrier protein keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Upon administration of Globo H-KLH immunostimulant OPT-822, the carbohydrate antigen Globo H may stimulate a cytotoxic T-lymphocyte (CTL) response against Globo H-expressing tumor cells, thereby decreasing tumor cell proliferation. Globo H is a tumor associated antigen (TAA) commonly found on a variety of tumor cells including breast cancer cells. KLH improves antigenic immune recognition and T-cell responses.","Pharmacologic Substance"]
["C28551","Globo-H-GM2-Lewis-y-MUC1-32(aa)-sTn(c)-TF(c)-Tn(c)-KLH Conjugate Vaccine","Globo-H-GM2-Lewis-y-MUC1-32(aa)-sTn(c)-TF(c)-Tn(c)-KLH Conjugate Vaccine","A heptavalent vaccine consisting of the tumor-associated carbohydrate antigens globohexaosylceramide (globo-H), GM2, Lewis-y, MUC1-32(aa), sTn(c), TF(c), and Tn(c) conjugated with keyhole limpet hemocyanin (KLH), an immunomodulator.  This vaccine may induce the production of IgG and IgM antibodies and an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumors expressing these antigens. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C113798","Globulin Component Macrophage-activating Factor","GC Protein-derived Macrophage-activating Factor|GC-MAF|GcMAF|Globulin Component Macrophage-activating Factor","A recombinant form of GC (group-specific component) protein-derived macrophage-activating factor (GC-MAF) with potential immunostimulating and antineoplastic activities. Upon administration, globulin component macrophage-activating factor is able to stimulate macrophages to kill cancer cells, inhibit angiogenesis and stimulate the immune system. This decreases tumor cell proliferation. GC, also known as vitamin D binding protein (VDBP), is converted to GC-MAF by enzymes located in the membrane of B- and T-lymphocytes. However, deglycosylated GC protein cannot be converted to GC-MAF. Endogenous GC-MAF is often not activated in patients with cancer due to an increased activity of nagalase (also called alpha-N-acetylgalactosaminidase), an enzyme secreted by cancer cells that mediates the deglycosylation of GC; thus preventing macrophage activation and immunosuppression.","Pharmacologic Substance"]
["C346","Glucarpidase","CPDG2|CPG2|Carboxypeptidase G2|GLUCARPIDASE|Glucarpidase|Voraxaze|carboxypeptidase-G2","A zinc-dependent enzyme isolated from a strain of the bacterium Pseudomonas. Because glucarpidase rapidly hydrolyzes methotrexate into inactive metabolites, it may be useful as a rescue agent for methotrexate-induced nephrotoxicity. In antibody-directed enzyme prodrug therapy (ADEPT), this agent is conjugated with an antibody that binds to a specific tumor cell type, allowing for glucarpidase-catalyzed activation of a co-administered prodrug at the site of the tumor.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C127838","Glucocorticoid Receptor Antagonist CORT125134","CORT-125134|CORT125134|Glucocorticoid Receptor Antagonist CORT125134","An orally available antagonist of the glucocorticoid receptor (GR), with potential antineoplastic activity. Upon administration, CORT125134 competitively binds to and blocks GRs. This inhibits the activity of GRs, and prevents both the translocation of the ligand-GR complexes to the nucleus and gene expression of GR-associated genes. This decreases the negative effects that result from excess levels of endogenous glucocorticoids, like those seen when tumors overproduce glucocorticoids. In addition, by binding to GRs and preventing their activity, inhibition with CORT125134 also inhibits the proliferation of GR-overexpressing cancer cells. GRs are overexpressed in certain tumor cell types and promote tumor cell proliferation.","Pharmacologic Substance"]
["C1612","Glufosfamide","Beta-D-Glucosyl-Ifosfamide Mustard|D-19575|GLUFOSFAMIDE|Glufosfamide|glc-IPM|glufosfamide","A compound consisting of the mustard agent ifosforamide conjugated to glucose, with potential alkylating activity. Glufosfamide is cleaved by glucosidases in tumor cells and forms ifosforamide. In turn, ifosforamide alkylates and forms DNA crosslinks, thereby inhibiting DNA replication and subsequent cell growth. The glucose moiety may enhance this agent's uptake by tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C114381","Glutaminase Inhibitor CB-839","CB-839|Glutaminase Inhibitor CB-839","An orally bioavailable inhibitor of glutaminase, with potential antineoplastic activity. Upon oral administration, CB-839 selectively and irreversibly inhibits glutaminase, a mitochondrial enzyme that is essential for the conversion of the amino acid glutamine into glutamate. By blocking glutamine utilization, proliferation in rapidly growing cells is impaired. Glutamine-dependent tumors rely on the conversion of exogenous glutamine into glutamate and glutamate metabolites to both provide energy and generate building blocks for the production of macromolecules, which are needed for cellular growth and survival.","Pharmacologic Substance"]
["C106121","Glutathione Pegylated Liposomal Doxorubicin Hydrochloride Formulation 2B3-101","2B3-101|Glutathione Pegylated Liposomal Doxorubicin Hydrochloride Formulation 2B3-101","A glutathione (GSH) pegylated, liposome-encapsulated preparation of the hydrochloride salt form of the anthracycline antineoplastic antibiotic doxorubicin, with potential anetineoplastic activity. Upon administration, the glutathione pegylated liposomal formulation 2B3-101 specifically delivers doxorubicin into the brain. Doxorubicin intercalates between DNA base pairs and interferes with topoisomerase II activity, which inhibits both DNA replication and RNA synthesis, resulting in cancer cell death and tumor regression. Doxorubicin also generates reactive oxygen species, which causes cell membrane lipid peroxidation leading to cytotoxicity. The pegylated liposomal delivery of doxorubicin improves drug penetration into tumors and prolongs circulation time, thereby increasing doxorubicin's efficacy and decreasing its toxicity. Conjugation of GSH to the PEG molecules directs the liposomes to the GSH transporters on the blood brain barrier (BBB) and improves the delivery of doxorubicin into the brain.","Pharmacologic Substance"]
["C97917","Glycooptimized Trastuzumab-GEX","Ant-HER2 Monoclonal Antibody GT-Mab 7.3-GEX|GT-Mab 7.3-GEX|Glycooptimized Trastuzumab-GEX|TrasGEX","A glycoengineered form of a monoclonal antibody directed against the human epidermal growth factor receptor-2 (HER2), with potential antineoplastic activity. Glycooptimized trastuzumab-GEX specifically binds to the extracellular domain of HER2, thereby inducing an antibody-dependent cell-mediated cytotoxicity (ADCC) against HER2-expressing tumor cells. This eventually results in apoptosis and growth inhibition of tumor cells. HER2, a member of the receptor tyrosine kinase EGFR superfamily, is overexpressed on the cell surfaces of various solid tumors. This agent has a specific glycosylation profile that may enhance its ADCC response against HER2-expressing tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48391","GM.CD40L Cell Vaccine","GM.CD40L Cell Vaccine|GM.CD40L","A cell-based vaccine composed of irradiated tumor cells transduced with granulocyte-macrophage colony-stimulating factor (GM-CSF) and CD40-ligand (CD40L) genes. Upon administration, this vaccine may stimulate an anti-tumoral dendritic cell-mediated host immune response. (NCI05)","Pharmacologic Substance"]
["C91377","GM2/GD2/GD3 Lactone-KLH Conjugate Trivalent Vaccine","GM2/GD2/GD3 Lactone-KLH Conjugate Trivalent Vaccine","A trivalent cancer vaccine containing the ganglioside lactones GM2, GD2 and GD3 conjugated with the immunostimulant keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Vaccination with GM2 lactone/GD2 lactone/GD3 lactone-KLH conjugate trivalent vaccine may elicit antibodies against tumor cells expressing any of these epitopes, resulting in an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells expressing these gangliosides. GM2, GD2 and GD3 are tumor associated antigens (TAAs) that are overexpressed in a variety of tumor cell membranes.","Immunologic Factor|Pharmacologic Substance"]
["C2376","GM2-KLH Vaccine","GM2-KLH Ganglioside|GM2-KLH Vaccine|GM2-KLH vaccine|GM2-KLH|KLH-conjugated GM2 Ganglioside Vaccine","A cancer vaccine consisting of GM2 ganglioside, a melanoma-specific antigen, conjugated with the immunostimulant keyhole limpet hemocyanin. Vaccination with GM2-KLH vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against GM2 ganglioside-expressing melanoma cells, resulting in tumor growth inhibition. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C11571","GM2-KLH Vaccine/QS21","GM2-KLH Vaccine/QS21|GM2-KLH/QS-21|GM2-KLH/QS21|GMK","A cancer vaccine based on the immunogenic ganglioside GM2, The GM2-KLH Vaccine/QS21 vaccine consists of GM2 conjugated with KLH keyhole limpet hemocyanin (KLH), a potent immunostimulant, and is admixed with the adjuvant QS21, a saponin fraction extracted from the bark of the South American tree Quillaja saponaria Molina. GM2 is a cell surface carbohydrate antigen expressed by most melanoma cells and various other tumor cell types. (NCI04)","Therapeutic or Preventive Procedure"]
["C29067","GM-CSF DNA","GM-CSF DNA","DNA that encodes granulocyte-macrophage colony stimulating factor (GM-CSF).  GM-CSF enhances the host immune response to poorly immunogenic tumors, possibly by activating T-cell and macrophage anti-tumor responses, and, so, decreasing tumor growth. (NCI04)","Pharmacologic Substance"]
["C98287","GM-CSF-encoding Oncolytic Adenovirus CGTG-102","CGTG-102|GM-CSF-encoding Oncolytic Adenovirus CGTG-102","A recombinant, oncolytic serotype 5/3 capsid-modified adenovirus encoding the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) with potential antineoplastic activity. Upon administration, the oncolytic adenovirus selectively infects and replicates in tumor cells, which may result in tumor cell lysis. Synergistically, GM-CSF (sargramostim) expressed by the oncolytic adenovirus enhances antigen presentation, promotes natural killer (NK) cell-mediated killing and causes a cytotoxic T cell (CTL) response against tumor cells harboring the oncolytic adenovirus, resulting in an immune-mediated tumor cell death. CGTG-102 is designed to replicate only in cells with defects in the p16/Rb/E2F pathway, attributed to a mutation common in many solid tumors. Replacement of the Ad5 capsid protein knob with a knob domain from serotype 3 causes higher transduction in cancer cells as compared to normal cells.","Pharmacologic Substance"]
["C52190","GM-K562 Cell Vaccine","GM-K562 Cell Vaccine","A cell-based vaccine comprised of K562 cells transfected with the granulocyte macrophage-colony stimulating factor (GM-CSF) gene with potential immunopotentiating properties. Vaccination with GM-K562 cells may stimulate the host immune system to produce an antitumoral T-lymphocyte response, thereby inhibiting tumor growth. K562 cells are derived from the human erythroleukemia cell line K562. GM-CSF (also known as sagramostim) expressed by vaccine cells binds to specific cell surface receptors, modulating the proliferation and differentiation of a variety of hematopoietic progenitor cells with some specificity towards stimulation of leukocyte production. GM-CSF also promotes antigen presentation, up-regulates antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function; it may also augment host antitumoral immunity.","Pharmacologic Substance"]
["C114498","GnRH Antagonist TAK-385","GnRH Antagonist TAK-385|Relugolix|TAK-385|Urea, N-(4-(1-((2,6-difluorophenyl)methyl)-5-((dimethylamino)methyl)-1,2,3,4-tetrahydro-3-(6-methoxy-3-pyridazinyl)-2,4-dioxothieno(2,3-d)pyrimidin-6-yl)phenyl)-N'-methoxy-","An orally available, non-peptide gonadotropin-releasing hormone (GnRH or luteinizing hormone-releasing hormone (LHRH)) antagonist, with potential antineoplastic activity. GnRH antagonist TAK-385 competitively binds to and blocks the GnRH receptor in the anterior pituitary gland, which both prevents GnRH binding to the GnRH receptor and inhibits the secretion and release of both luteinizing hormone (LH) and follicle stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone from Leydig cells in the testes. Since testosterone is required to sustain prostate growth, reducing testosterone levels may inhibit hormone-dependent prostate cancer cell proliferation.","Pharmacologic Substance"]
["C74037","Gold Sodium Thiomalate","Aurolate|Aurothiomalate Disodium|GOLD SODIUM THIOMALATE|Gold Sodium Thiomalate|Myochrysine","The sodium salt of gold thiomalic acid, an organogold compound with antirheumatic and potential antineoplastic activities. Gold sodium thiomalate (GST) appears to inhibit the activity of atypical protein kinase C iota (PKCiota) by forming a cysteinyl-aurothiomalate adduct with the cysteine residue Cys-69 within the PB1 binding domain of PKCiota. This prevents the binding of Par6 (Partitioning defective protein 6) to PKCiota, thereby inhibiting PKCiota-mediated oncogenic signaling, which may result in the inhibition of tumor cell proliferation, the promotion of tumor cell differentiation, and the induction of tumor cell apoptosis. Atypical PKCiota, a serine/threonine kinase overexpressed in numerous cancer cell types, plays an important role in cancer proliferation, invasion, and survival; Par6 is a scaffold protein that facilitates atypical PKC-mediated phosphorylation of cytoplasmic proteins involved in epithelial and neuronal cell polarization.","Pharmacologic Substance"]
["C26444","Golnerminogene Pradenovec","ADgv EGR.TNF.11D|Ad 5-TNF Alpha|Adenovirus 5-Tumor Necrosis Factor Alpha|Golnerminogene Pradenovec|TNFerade","A recombinant agent consisting of a genetically-modified adenovirus 5 vector encoding the protein cytokine tumor necrosis factor (TNF) alpha. TNF exhibits potent anti-tumor cytolytic properties; the adenovirus 5 vector efficiently infects tumor cells, delivering tumor-specific TNF.","Pharmacologic Substance"]
["C76497","Golotimod","(2R)-2-Amino-5-(((1S)-1-carboxy-2-(1H-indol-3-yl)ethyl)amino)-5-oxopentanoic Acid|GOLOTIMOD|Gamma-D-Glutamyl-L-Tryptophan|Golotimod|SCV 07|SCV-07|SCV07|gamma-D-Glu-L-trp","An orally bioavailable synthetic peptide containing the amino acids D-glutamine and L-tryptophan connected by a gamma-glutamyl linkage with potential immunostimulating, antimicrobial and antineoplastic activities. Although the exact mechanism of action is unknown, golotimod appears to inhibit the expression of STAT-3, reversing immunosuppression and stimulating an anti-tumor immune response. This agent may stimulate the production of T-lymphocytes, in particular the helper T (Th1) cells, activate macrophages, and increase levels of interleukin 2 and interferon gamma. STAT-3, a transcription factor upregulated in many cancer cell types, is involved in tumor cell growth and survival and immunosuppression.","Pharmacologic Substance"]
["C82363","Golvatinib","1,1-cyclopropanedicarboxamide, N-(2-fluoro-4-((2-(((4-(4-methyl-1-piperazinyl)-1-piperidinyl)carbonyl)amino)-4-pyridinyl)oxy)phenyl)-N'-(4-fluorophenyl)-|E7050|GOLVATINIB|Golvatinib|c-Met/VEGFR-2 Kinase Inhibitor E7050","An orally bioavailable dual kinase inhibitor of c-Met (hepatocyte growth factor receptor) and VEGFR-2 (vascular endothelial growth factor receptor-2) tyrosine kinases with potential antineoplastic activity. c-Met/VEGFR kinase inhibitor E7050 binds to and inhibits the activities of both c-Met and VEGFR-2, which may inhibit tumor cell growth and survival of tumor cells that overexpress these receptor tyrosine kinases. c-Met and VEGFR-2 are upregulated in a variety of tumor cell types and play important roles in tumor cell growth, migration and angiogenesis.","Pharmacologic Substance"]
["C1910","Gonadotropin-releasing Hormone Analog","GnRH Agonist|GnRH Analog|Gonadotropin-Releasing Hormone Agonist|Gonadotropin-Releasing Hormone Analogue|Gonadotropin-releasing Hormone Analog|LH-RH Analogs|LH-RH agonist|LHRH Agonist|Luteinizing Hormone-Releasing Hormone Analog|gonadotropin-releasing hormone agonist|luteinizing hormone-releasing hormone agonist","A synthetic analogue of the endogenous hormone gonadotropin-releasing hormone (GnRH), with potential antineoplastic activity. Upon administration, GnRH analogue mimics endogenous GnRH and strongly binds to and activates pituitary GnRH receptors, which stimulates the synthesis and secretion of the gonadotropic hormones, follicle stimulating hormone (FSH) and luteinizing hormone (LH). Continuous, prolonged activation by the GnRH analogue results in pituitary GnRH receptor desensitization and receptor downregulation. This causes inhibition of pituitary gonadotropin secretion of LH and FSH. In males, the inhibition of LH secretion prevents the production and release of testosterone from Leydig cells in the testes and causes a significant decline in testosterone production that is near the levels seen after castration. This may inhibit androgen receptor-positive tumor progression. In females, this results in a decrease in estradiol production. GnRH, also called luteinizing hormone-releasing hormone (LH-RH), is normally synthesized in and secreted by the hypothalamus. Synthetic analogues of GnRH have a stronger receptor binding affinity than the endogenous form.","Chemical Viewed Functionally"]
["C1374","Goserelin","6-[O-(1,1-Dimethylethyl)-D-serine]-10-deglycinamide Luteinizing Hormone-Releasing Factor (Pig) 2-(aminocarbonyl)hydrazide|GOSERELIN|Goserelin|ICI-118630|goserelin","A synthetic decapeptide analog of luteinizing hormone-releasing hormone (LHRH) with antineoplastic activity. Goserelin binds to and activates pituitary gonadotropin releasing hormone (GnRH) receptors. Prolonged administration of goserelin inhibits the secretion of pituitary gonadotropin, thereby decreasing levels of testosterone (in males) and estradiol (in females).  Administration of this agent in a depot formulation may result in the regression of sex hormone-sensitive tumors and a reduction in sex organ size and function. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C529","Gossypol","(+/-)-Gossypol|(2,2'-Binaphthalene)-8,8'-dicarboxaldehyde, 1,1',6,6'7, 7'-hexahydroxy-5,5'-diisopropyl-3,3'-dimethyl-|1,1',6,6',7,7'-Hexahydroxy-3,3'-dimethyl-5,5'-bis(1-methylethyl)[2,2'-binaphthalene]-8,8'-dicarboxaldehyde|1,1',6,6',7,7'-Hexahydroxy-5,5'-diisopropyl-3-3'-dimethyl[2,2'-binaphthalene]-8,8'-dicarboxaldehyde|2,2'-bis(1,6,7-trihydroxy-4-methyl-5-isopropyl-8-aldehydonaphthalene)|2,2'-bis[8-Formyl-1,6,7-trihydroxy-5-isopropyl-3-methylnaphthalene]|BL-193|Cottonseed Meal Toxin|GOSSYPOL|Gossypol|No Fertil|Pogosin|Tash 1|cottonseed meal toxin|gossypol","An orally-active polyphenolic aldehyde with potential antineoplastic activity. Derived primarily from unrefined cottonseed oil, gossypol induces cell cycle arrest at the G0/G1 phase, thereby inhibiting DNA replication and inducing apoptosis. This agent also inhibits cell-signaling enzymes, resulting in inhibition of cell growth, and may act as a male contraceptive.","Organic Chemical|Pharmacologic Substance"]
["C1118","Gossypol Acetic Acid","GOSSYPOL ACETIC ACID|Gossypol Acetate|Gossypol Acetic Acid|gossypol acetic acid","The naturally occurring acetic acid form of gossypol, and an orally available polyphenolic aldehyde derived mostly from cottonseed with potential antineoplastic activity.  The biologic activities of gossypol acetic acid are similar to those of gossypol and include suppression of DNA replication, inhibition of tumor cell proliferation, and male contraceptive effects. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2757","gp100 Adenovirus Vaccine","gp100 Adenovirus Vaccine","A vaccine consisting of a replication-defective recombinant adenovirus that encodes the melanoma antigen glycoprotein 100 (gp100) with potential antineoplastic activity. Vaccination with gp100 adenovirus vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for the gp100 antigen, resulting in decreased tumor growth. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C2386","gp100 Antigen","glycoprotein 100|gp 100|gp100 Antigen|gp100","A melanoma-associated antigen.  When administered in a vaccine formulation, gp100 antigen may stimulate a cytotoxic T cell HLA-A2.1-restricted immune response against tumors that express this antigen, which may result in a reduction in tumor size. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C16167","gp100 Human Melanoma Peptide Vaccine with Incomplete Freund's Adjuvant","gp100 Human Melanoma Peptide Vaccine with Incomplete Freund's Adjuvant|gp100 human melanoma peptide vaccine/incomplete Freund's adjuvant|gp100 human melanoma-associated antigen with incomplete Freund's adjuvant|gp100 human melanoma-associated antigen/incomplete Freund's adjuvant","A vaccine consisting of synthetic glycoprotein 100 (gp100) melanoma antigen and incomplete Freund's adjuvant (IFA), an emulsifying agent and immune system stimulant, with antineoplastic activity.  Vaccination with gp100 human melanoma peptide vaccine with IFA may stimulate the host immune system to direct cytotoxic T lymphocytes (CTL) against gp100 positive melanoma cells, resulting in decreased tumor growth. (NCI04)","Therapeutic or Preventive Procedure"]
["C2764","gp100:154-162 Peptide Vaccine","gp100:154-162 Peptide Vaccine|gp100:154-162 Peptide","A peptide consisting of amino acid residues 154 through 162 of the melanoma-melanocyte antigen gp100. Vaccination with gp100:154-162 peptide may enhance tumor-specific T-cell immunity. gp100 antigen is a self-antigen expressed by melanocytes, pigmented retinal cells, and most melanoma lesions and is recognized via class I and II HLA-restricted mechanisms.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C49022","gp100:209-217(210M) Peptide Vaccine","G9 209-2M|gp100:209-217(210M) Peptide Vaccine|gp100:209-217(210M)","A synthetic peptide cancer vaccine consisting of amino acid residues 209 through 217 of the glycoprotein 100 (gp100) melanoma antigen, with a methionine substitution at position 210 designed to improve immunogenicity. Vaccination with gp100:209-217(210M) peptide may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing gp100.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2767","gp100:280-288 Peptide Vaccine","gP100 Peptide Melanoma Vaccine YLEPGPVTA|gp100:280-288 Peptide Vaccine|gp100:280-288 Peptide","A vaccine consisting of the amino acids 280 through 288 of the melanoma antigen glycoprotein 100 (gp100) with potential antineoplastic activity.  Vaccination with gp100:280-288 peptide may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for the gp100 antigen, resulting in decreased tumor growth. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C49042","gp100:280-288(288V) Peptide Vaccine","gp100:280-288(288V) Peptide Vaccine","A peptide vaccine consisting of the amino acids 280 through 288 of the melanoma antigen glycoprotein 100 (gp100) with potential antineoplastic activity.  gp100:280-288(288V) peptide has a valine substitution at amino acid position 288 to improve immunogenicity. Vaccination with gp100:280-288(288V) peptide may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for the gp100 antigen, resulting in decreased tumor growth.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2761","gp100-Fowlpox Vaccine","gp100-Fowlpox Vaccine","A cancer vaccine comprised of a recombinant fowlpox virus vector encoding the melanoma antigen glycoprotein 100 (gp 100) with potential antineoplastic activity.  The expression of gp100 may generate a cellular immune response to melanoma cells; this effect is enhanced by the co-administration of interleukin 2 (IL-2). (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C91720","GP2 Peptide/GM-CSF Vaccine","GP2 Peptide/GM-CSF Vaccine","A vaccine containing a HER2/Neu-derived epitope (amino acids 654-662) (GP2), and combined with granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential antineoplastic and immunoadjuvant activity. Upon vaccination, GP2 may activate the immune system to mount a cytotoxic T-lymphocyte (CTL) immune response against HER2/Neu expressing cancer cells. GM-CSF may potentiate a tumor-specific cytotoxic T-lymphocyte (CTL) response against cancer cells expressing the HER2/Neu antigen. HER2/neu, a tumor associated antigen (TAA), is overexpressed in a variety of tumor cell types and is highly immunogenic.","Immunologic Factor|Pharmacologic Substance"]
["C2406","gp209-2M Antigen","antigen, gp209-2m|gp209-2M Antigen|gp209-2M","A modified peptide antigen derived from gp209, with potential immunomodulatory and antineoplastic activities. gp209-2M antigen (IMDQVPFSV) has a methionine substitution of threonine at position 2 of gp209 peptide (ITDQVPFSV), which is the immunogenic epitope of human melanoma tumor glycoprotein gp100. Vaccination with this peptide may evoke a cytotoxic T lymphocyte (CTL) response against tumor cells expression of the gp100 antigen.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C113653","gp96-secreting Allogeneic Bladder Cancer Cell Vaccine HS-410","HS-410|gp96-secreting Allogeneic Bladder Cancer Cell Vaccine HS-410","An allogeneic urothelial bladder cancer cell vaccine expressing a recombinant secretory form of the immunoadjuvant heat shock protein gp96 fused with an immunoglobulin Fc domain (gp96-Ig) protein, with potential antineoplastic activity. Upon administration of the gp96-Ig-secreting allogeneic bladder cancer cell vaccine HS-410, the live, irradiated tumor cells continuously secrete gp96-Ig along with its chaperoned tumor associated antigens (TAAs). This enhances antigen cross presentation to cytotoxic T-lymphocytes (CTLs) and, upon expansion, leads to the induction of a potent CTL response against the TAAs on the endogenous bladder cancer cells. This vaccine also induces a memory T cell response that could fight recurring cancer cells. gp96-Ig is constructed by replacing the KDEL endoplasmic reticulum (ER) retention sequence of gp96 with the Fc portion of the IgG1 protein. This allows for gp96, normally an ER-resident chaperone peptide, to be released from cells.","Pharmacologic Substance"]
["C2627","GPI-0100","GPI-0100","A semi-synthetic triterpene glycoside, derived from the naturally occurring saponins. GPI-0100 functions as an adjuvant when given as part of a vaccine preparation to improve the immunogenicity of antigens such as proteins, carbohydrates. GPI-0100 containing vaccines have been used with both viral and tumor antigens to elicit a Type 1 helper T cell response for those diseases in which a cytotoxic T lymphocyte (CTL) response is desired.","Immunologic Factor|Pharmacologic Substance"]
["C95893","G-Quadruplex Stabilizer BMVC","3,6-bis (1-methyl-4-vinylpyridinium) Carbazole Diiodide|3,6-bis[2-(1-methylpyridinium)vinyl]carbazole Diiodide|BMVC|G-Quadruplex Stabilizer BMVC","A carbazole derivative (3,6-bis[2-(1-methylpyridinium)vinyl]carbazole diiodide) that selectively targets to the G-quadruplex DNA structure, used as a fluorescent probe for cancer cytological diagnosis and with potential antitumor activity. G-quadruplex stabilizer BMVC, preferentially uptaken by cancer cells, binds to and stabilize the telomeric G-quadruplex structure at the end of DNA; when visualized with fluorescent imaging device, BMVC emits bright fluorescent light and can be used to differentiate tumor cells from normal cells. The BMVC/G-quadruplex complexes also interfere with the activity of telomerase, which is highly active in tumor cells and plays a key role in tumorigenesis while expressed at very low levels in most somatic cells.","Pharmacologic Substance"]
["C67048","Green Tea","Green Tea","Tea derived from the dried leaves of the plant Camellia sinensis with potential antioxidant, chemopreventive, and lipid-lowering activities. Green tea contains polyphenols that are believed to be responsible for its chemopreventive effect. The polyphenol fraction contains mainly Epigallocatechin-3-gallate (EGCG) and other catechins, such as epicatechin (EC), gallocatechin gallate (GCG), epigallocatechin (EGC), and epicatechin gallate (ECG). Green tea polyphenols act as antioxidants and free radical scavengers and may affect enzymes involved in cellular replication and tumor angiogenesis by modulating angiogenic factors, such as vascular endothelial growth factor (VEGF).","Plant"]
["C2694","Green Tea Extract","Green Tea Extract|Green Tea Polyphenols|Tea, Green Extract|Tea, Green, Polyphenols|green tea extract","A defined, decaffeinated green tea polyphenol mixture isolated from Camellia sinensis, a plant native to Asia, with antiviral and antioxidant activities and potential chemopreventive activity. Green tea extract contains antioxidant compounds, including flavonoids, vitamins and polyphenols such as epigallocatechin-3-gallate (EGCG), which may have antineoplastic properties. Consumption of green tea extract may confer chemopreventive protection against various cancers including those of the prostate, stomach, and esophagus.","Organic Chemical|Pharmacologic Substance"]
["C97514","Green Tea Extract-based Antioxidant Supplement","Green Tea Extract-based Antioxidant Supplement|Oncoxin","A dietary supplement containing a green tea extract including the catechin epigallocatechin gallate and other vitamins and antioxidants, with potential antineoplastic and chemopreventive activities. The polyphenols in green tea act as antioxidants and scavenge free radicals which may inhibit cellular oxidation and prevent free radical damage to cells. In addition, polyphenols may affect enzymes involved in cellular reproduction and tumor angiogenesis by modulating angiogenic factors. Other ingredients in green tea extract-based antioxidant supplement include dry cinnamon extract, germanium, zinc sulfate, manganese sulfate, arginine, cysteine, malic acid, ascorbic acid (vitamin c), glycyrrhizinic acid, glycine, glucosamine, pyridoxal (vitamin B6), calcium pantothenate (vitamin B5), folic acid, cyanocobalamin (vitamin B12).","Pharmacologic Substance"]
["C116872","GS/pan-Notch Inhibitor BMS-906024","BMS-906024|GS/pan-Notch Inhibitor BMS-906024","An orally bioavailable, small-molecule gamma secretase (GS) and pan-Notch inhibitor, with potential antineoplastic activity. Upon administration, GS/pan-Notch inhibitor BMS-906024 binds to GS and blocks activation of Notch receptors, which may inhibit the proliferation of tumor cells with an overly-active Notch pathway. The integral membrane protein GS is a multi-subunit protease complex that cleaves single-pass transmembrane proteins, such as Notch receptors, at residues within their transmembrane domains that lead to their activation. Overexpression of the Notch signaling pathway has been correlated with increased tumor cell growth.","Pharmacologic Substance"]
["C118573","GS/pan-Notch Inhibitor BMS-986115","BMS-986115|GS/pan-Notch Inhibitor BMS-986115","An orally bioavailable, gamma secretase (GS) and pan-Notch inhibitor, with potential antineoplastic activity. Upon administration, GS/pan-Notch inhibitor BMS 986115 binds to GS and blocks the proteolytic cleavage and release of the Notch intracellular domain (NICD), which would normally follow ligand binding to the extracellular domain of the Notch receptor. This prevents both the subsequent translocation of NICD to the nucleus to form a transcription factor complex and the expression of Notch-regulated genes. This results in the induction of apoptosis and the inhibition of growth of tumor cells that overexpress Notch. Overexpression of the Notch signaling pathway plays an important role in tumor cell proliferation and survival. The integral membrane protein GS is a multi-subunit protease complex that cleaves single-pass transmembrane proteins, such as Notch receptors, at residues within their transmembrane domains and leads to their activation.","Pharmacologic Substance"]
["C116849","GSK-3 Inhibitor LY2090314","3-(9-Fluoro-2-(piperidine-1-carbonyl)-1,2,3,4-tetrahydro-[1,4]diazepino[6,7,1-hi]indol-7-yl)-4-(imidazo[1,2-a]pyridin-3-yl)-1H-pyrrole-2,5-dione|GSK-3 Inhibitor LY2090314|LY 2090314|LY-2090314|LY2090314","An inhibitor of glycogen synthase kinase-3 (GSK-3), with potential antineoplastic activity. Upon administration, LY2090314 binds to and inhibits GSK-3 in an ATP-competitive manner. This prevents GSK-3-mediated phosphorylation of beta-catenin, which inhibits the subsequent ubiquitination and proteosomal degradation of beta-catenin. This leads to the activation of the Wnt/beta-catenin pathway and the induction of apoptosis in susceptible tumor cells. GSK-3, a serine/threonine kinase, plays a key role in numerous pathways involved in protein synthesis, cellular proliferation, differentiation, and apoptosis. The Wnt/beta-catenin signaling pathway plays key roles in both cellular proliferation and differentiation. The increased expression of beta-catenin, a transcriptional activator, correlates with decreased cellular proliferation and improved prognosis in select cancers.","Pharmacologic Substance"]
["C26652","GTI-2040","GTI-2040","A 20-mer antisense oligonucleotide complementary to a coding region in the mRNA of the R2 small subunit component of human ribonucleotide reductase.  GTI-2040 decreases mRNA and protein levels of R2 in vitro and may inhibit tumor cell proliferation in human tumors in vivo. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C95209","Guadecitabine","DNMT inhibitor SGI-110|Guadecitabine|S110|SGI-110","A dinucleotide antimetabolite of a decitabine linked via phosphodiester bond to a guanosine, with potential antineoplastic activity. Following metabolic activation by phosphorylation and incorporation into DNA, guadecitabine inhibits DNA methyltransferase, thereby causing genome-wide and non-specific hypomethylation, and inducing cell cycle arrest at S-phase. This agent is resistant to cytidine deaminase, hence may result in gradual release of decitabine both extra and intracellularly, leading to more prolonged exposures to decitabine.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C65826","Guanabenz Acetate","3-((2,6-Dichlorophenyl)methylene)carbazamidine Monoacetate|GUANABENZ ACETATE|Guanabenz Acetate|Wytensin","The orally bioavailable, acetate salt form of guanabenz, a centrally-acting alpha-2 adrenergic receptor agonist, with anti-hypertensive and potential antineoplastic, cytoprotective and bone resorption inhibitory activities. Upon oral administration, guanabenz suppresses endoplasmic reticulum (ER) stress by inhibiting the stress-induced dephosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2a), thereby enhancing the phosphorylation level of eIF2a. This causes elF2a-mediated downregulation of the Rac1 pathway, upregulates the expression of activating transcription factor 4 (ATF4), which plays a key role in osteoblastogenesis, and downregulates the expression of nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), which is a transcription factor that plays a key role in osteoclastogenesis. This enhances osteoblastogenesis and suppresses osteoclastogenesis. Altogether, this promotes new bone formation and prevents bone degradation. In addition, guanabenz blocks the proliferation, survival, motility and invasiveness of tumor cells through the eIF2a-mediated downregulation of Rac1 signaling. Rac1, a Ras-related small GTPase belonging to the Rho family, plays a key role in tumor cell proliferation, survival and motility.","Pharmacologic Substance"]
["C101130","Guarana Supplement","Guarana Supplement|Paullinia cupana Supplement","An herbal supplement containing an extract from guarana (Paullinia cupana), a climbing plant of the Sapindaceae family which is native to the Amazon basin, with stimulant, antioxidant and potential chemoprotective activities. Guarana supplement contains various phytochemicals, including caffeine, theobromine, theophylline, tannins, saponins, catechins, epicatechins, proanthocyanidols and other compounds in minor concentrations. Caffeine is a central nervous system stimulant and may reduce chemotherapy-related fatigue. Tannins and other polyphenols may have chemopreventive activity. Intake of the guarana supplement may prevent cancer-related anorexia. In addition, animal studies have demonstrated that the ingestion of guarana resulted in decreased proliferation and increased apoptosis of tumor cells.","Pharmacologic Substance"]
["C1598","Gusperimus Trihydrochloride","(+-)-15-Deoxyspergualin|1-Amino-19-guanidino-11-hydroxy-4,9,12-triazanonadecane-10,13-dione|15-Deoxyspergualin Hydrochloride|15-Deoxyspergualin|7-[(Aminoiminomethyl)amino]-N-[2-[[4-[(3-aminopropyl)amino]butyl]amnio]-1-hydroxy-2-oxoethyl]heptanamide|BMS-181173|BMY-42215-1|DSG|Deoxyspergualin Hydrochloride|Deoxyspergualin|GUSPERIMUS TRIHYDROCHLORIDE|Gusperimus Trihydrochloride|N-[[[4-[(3-Aminopropyl)amino]-butyl]carbamoyl]hydroxymethyl]-7-guanidinoheptanamide|NKT-01|Spanidin","A derivative of the antitumor antibiotic spergualin with immunosuppressant activity.  Gusperimus inhibits the interleukin-2-stimulated maturation of T cells to the S and G2/M phases and the polarization of the T cells into IFN-gamma-secreting Th1 effector T cells, resulting in the inhibition of growth of activated naive CD4 T cells; this agent may suppress growth of certain T-cell leukemia cell lines. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1532","Gutolactone","Gutolactone","A quassinoid phytochemical isolated from the plant Simaba guianensis with potential antineoplastic and antimalarial activities. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2100","GV-1301","GV-1301","Antineoplastic vaccine being developed against liver cancer. (NCI)","Pharmacologic Substance"]
["C1979","GVAX Lung Cancer Vaccine","CG8123|GVAX Autologous Lung Cancer Vaccine|GVAX Lung Cancer Vaccine","An autologous lung cancer vaccine consisting of patient-specific lung cancer cells genetically modified to secrete granulocyte-macrophage colony stimulating factor (GM-CSF), an immunostimulatory cytokine. GM-CSF modulates the proliferation and differentiation of a variety of hematopoietic progenitor cells with some specificity towards stimulation of leukocyte production and may reverse treatment-induced neutropenias. This agent also promotes antigen presentation, up-regulates antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function and may augment host antitumoral immunity.  For safety, cells are irradiated prior to vaccination. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C91707","GVAX Pancreatic Cancer Vaccine","GVAX Pancreatic Cancer Vaccine","An irradiated, autologous pancreatic cancer vaccine consisting of patient-specific pancreatic cancer cells genetically modified to secrete the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulating and antineoplastic activities. Upon vaccination, GVAX pancreatic cancer vaccine secretes GM-CSF. In turn, GM-CSF may stimulate the body's immune system against tumor cells by enhancing the activation of dendritic cells (DCs) and promoting antigen presentation to both B- and T-cells. In addition, GM-CSF promotes antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function.","Immunologic Factor|Pharmacologic Substance"]
["C2525","GVAX Prostate Cancer Vaccine","Allogeneic Prostate Cancer Vaccine, GM- CSF Gene Transduced|Allogenic Prostate GVAX|GM-CSF Gene Transduced Allogeneic Prostate Cancer Vaccine|GM-CSF prostate cancer vaccine|GVAX Allogeneic Prostate Cancer Vaccine|GVAX Allogenic Prostate Cancer Vaccine|GVAX Prostate Cancer Vaccine|GVAX Prostate|Prostate Cancer Vaccine, GM-CSF Gene Transduced|Prostate Cancer Vaccine, GVAX","A whole cell vaccine expressing human granulocyte macrophage-colony stimulating factor (GM-CSF) with potential antineoplastic activity. Tumor cells from prostate cancer patients are harvested and then genetically modified to secrete GM-CSF, an immune stimulatory growth factor that plays a key role in stimulating the body's immune responses against tumor cells. Because the vaccine is derived from allogenic cells, it has demonstrated a favorable side effect profile than other approaches of delivering long-lasting GM-CSF.","Immunologic Factor|Pharmacologic Substance"]
["C114284","H1299 Tumor Cell Lysate Vaccine","H1299 Lysate Vaccine|H1299 Tumor Cell Lysate Vaccine","A cell lysate derived from a lung cancer cell line, H1299, with potential immunostimulatory and antineoplastic activities. Upon intramuscular administration, the H1299 tumor cell lysate exposes the immune system to an undefined amount of tumor associated antigens (TAA), particularly cancer testis antigens (CTAs), which may result in the induction of both anti-tumoral cytotoxic T-lymphocytes (CTL) and antibody-dependent responses against TAA-expressing cells, leading to tumor cell lysis. CTAs, such as MAGE, are selectively expressed in a variety of cancers but are not expressed in normal, healthy cells outside the testis.","Pharmacologic Substance"]
["C98280","Hafnium Oxide-containing Nanoparticles NBTXR3","Hafnium Oxide-containing Nanoparticles NBTXR3|NBTXR3","A suspension of nanoparticles containing inert inorganic hafnium oxide (HfO2) crystals with potential antineoplastic activity. Upon injection of NBTXR3 in the tumor, the hafnium oxide-containing nanoparticles accumulate into the tumor cells. Subsequent application of radiation beams to the tumor tissue causes HfO2 particles to emit huge amounts of electrons. This results in the formation of free radicals within the tumor cells, which in turn causes targeted destruction of the cancer cells. Compared to standard radiotherapy, because of the inert nature of NBTXR3, this agent emits electrons only during its exposure to radiation which improves radiotherapy efficiency.","Pharmacologic Substance"]
["C1120","Halofuginone","HALOFUGINONE|Halofuginone|trans-(+/-)-7-Bromo-6-chloro-3-[3-(3-hydroxy-2-piperidinyl)-2-oxopropyl]-4(3H)-quinazolinone","An orally-active quinazolinone alkaloid with potential antineoplastic activity. Halofuginone interferes with the signaling pathway of transforming growth factor beta (TGF beta) and inhibits expression of matrix metalloproteinase 2, thereby inhibiting collagen type I synthesis and inducing extracellular matrix degradation, resulting in inhibition of angiogenesis, tumor growth, or metastasis.","Organic Chemical|Pharmacologic Substance"]
["C2656","Halofuginone Hydrobromide","HALOFUGINONE HYDROBROMIDE|Halofuginone Hydrobromide|Halofuginone IV (intravenous)|Halofuginone hydrobromide|RU 19110|Tempostatin|halofuginone hydrobromide","The hydrobromide salt of halofuginone, a semisynthetic quinazolinone alkaloid anticoccidial derived from the plant Dichroa febrifuga, with antifibrotic and potential antineoplastic activities. Halofuginone specifically inhibits collagen type I gene expression and matrix metalloproteinase 2 (MMP-2) gene expression, which may result in the suppression of angiogenesis, tumor stromal cell development, and tumor cell growth. These effects appear to be due to halofuginone-mediated inhibition of the collagen type I and MMP-2 promoters. Collagen type I and MMP-2 play important roles in fibro-proliferative diseases.","Organic Chemical|Pharmacologic Substance"]
["C121570","HCV DNA Vaccine INO-8000","HCV DNA Vaccine INO-8000|INO-8000","A multi-antigen DNA vaccine consisting of plasmids encoding the hepatitis C virus (HCV) nonstructural proteins 3 (NS3), 4A (NS4A), 4B (NS4B) and 5A (NS5A), with potential immunomodulating and cancer preventive activities. Administered via intramuscular injection followed by electroporation, cells transfected with the HCV DNA vaccine INO-8000 express the encoded HCV proteins, which may elicit a cytotoxic T-lymphocyte (CTL) response against HCV-infected liver cells expressing the NS3, NS4A, NS4B or NS5A proteins. This results in the eradication of HCV-infected cells. HCV, a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family, is associated with the development of hepatocellular carcinoma (HCC).","Pharmacologic Substance"]
["C96797","HDAC Inhibitor 4SC-202","4SC-202|HDAC Inhibitor 4SC-202","An orally bioavailable benzamide and inhibitor of human class I histone deacetylases (HDACs) isoenzymes 1, 2 and 3, with potential antineoplastic activity. HDAC inhibitor 4SC-202 selectively binds to and inhibits class I HDACs leading to an accumulation of highly acetylated histones. This may result in an induction of chromatin remodeling, the selective transcription of tumor suppressor genes, and the tumor suppressor protein-mediated inhibition of tumor cell division and eventually the induction of tumor cell apoptosis. This may inhibit tumor cell proliferation in susceptible tumor cells. HDACs, upregulated in many tumor types, are a class of enzymes that deacetylate chromatin histone proteins.","Pharmacologic Substance"]
["C121641","HDAC Inhibitor ACY-241","ACY-241|HDAC Inhibitor ACY-241|Histone Deacetylase Inhibitor ACY-241","An orally available histone deacetylase (HDAC) inhibitor, with potential antineoplastic activity. Upon oral administration, ACY-241 inhibits the activity of HDACs; this results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This leads to the inhibition of tumor oncogene transcription, and the selective transcription of tumor suppressor genes, which inhibit tumor cell division and induce tumor cell apoptosis. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins.","Pharmacologic Substance"]
["C116850","HDAC Inhibitor AR-42","(S)-N-hydroxy-4-(3-methyl-2-phenylbutanamido)benzamide|AR-42|HDAC Inhibitor AR-42|HDAC-42|OSU-HDAC42","An orally available phenylbutyrate-derived histone deacetylase (HDAC) inhibitor, with potential antineoplastic activity. Upon oral administration, AR-42 inhibits the catalytic activity of HDAC, which results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This leads to the inhibition of tumor oncogene transcription, and the selective transcription of tumor suppressor genes, which inhibits tumor cell division and induces tumor cell apoptosis. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins.","Pharmacologic Substance"]
["C94225","HDAC inhibitor CG200745","(E)-N(1)-(3-(dimethylamino)propyl)-N(8)-hydroxy-2-((naphthalene-1-loxy)methyl)oct-2-enediamide|CG200745|HDAC inhibitor CG200745","A histone deacetylase (HDAC) inhibitor with potential antineoplastic activity. CG200745 inhibits the catalytic activity of HDAC, resulting in an accumulation of highly acetylated chromatin histones, followed by the induction of chromatin remodeling and an altered pattern of gene expression. In particular, this agent enhances the histone acetylation of the tumor suppressor gene p53. This results in an accumulation of p53, p53-dependent transactivation and apoptosis in tumor cells. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins.","Pharmacologic Substance"]
["C82690","HDAC Inhibitor CHR-2845","CHR-2845|HDAC Inhibitor CHR-2845|Histone Deacetylase Inhibitor CHR-2845","A hydroxamic acid-derived histone deacetylase (HDAC) inhibitor with potential antineoplastic activity. CHR-2845 inhibits HDAC leading to an accumulation of highly acetylated histones, which may result in chromatin remodeling, inhibition of tumor oncogene transcription, inhibition of tumor cell division, and the induction of tumor cell apoptosis. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins; this agent may specifically target HDACs in cells of the monocyte-macrophage lineage.","Pharmacologic Substance"]
["C78475","HDAC Inhibitor CHR-3996","CHR-3996|HDAC Inhibitor CHR-3996|Histone Deacetylase Inhibitor CHR-3996","An orally bioavailable, second-generation hydroxamic acid-based inhibitor of histone deacetylase (HDAC) with potential antineoplastic activity. HDAC inhibitor CHR-3996 inhibits HDAC, resulting in an accumulation of highly acetylated histones, the induction of chromatin remodeling, and the selective transcription of tumor suppressor genes; these events may result in the inhibition of tumor cell division and the induction of tumor cell apoptosis. This agent may upregulate HSP70 and downregulate anti-apoptotic Bcl-2 proteins more substantially than some first-generation HDAC inhibitors. HDACs, upregulated in many tumor cell types, are a family of metalloenzymes responsible for the deacetylation of chromatin histone proteins.","Organic Chemical|Pharmacologic Substance"]
["C112177","HDAC Inhibitor CXD101","AZD 9468|AZD9468|CXD101|HDAC Inhibitor CXD101|Histone Deacetylase Inhibitor CXD101","A novel histone deacetylase (HDAC) inhibitor with potential antineoplastic activity. Although the exact therapeutic mechanism of action for CXD101 is not known, oral administration of this agent should inhibit the catalytic activity of HDAC, which results in an accumulation of highly acetylated histones, followed by the induction of chromatin remodeling and an altered pattern of gene expression. HDAC, a family of enzymes upregulated in many tumor types, deacetylates chromatin-associated histone proteins.","Pharmacologic Substance"]
["C120312","HDAC Inhibitor MPT0E028","(E)-N-hydroxy-3-(1-(phenylsulfonyl)indolin-5-yl)acrylamide|3-(1-Benzenesulfonyl-2,3-dihydro-1H-indol-5-yl)-N-hydroxy-acrylamide|HDAC Inhibitor MPT0E028|MPT 0E028|MPT-0E028|MPT0E028","An orally bioavailable N-hydroxyacrylamide-derived inhibitor of both human pan-histone deacetylase (HDAC) enzymes and the serine/threonine protein kinase Akt (protein kinase B), with potential antineoplastic activity. Upon administration, HDAC inhibitor MPT0E028 selectively binds to and inhibits HDACs, which inhibits deacetylation of histone proteins and leads to the accumulation of highly acetylated histones. This may result in both an induction of chromatin remodeling, and the selective transcription of tumor suppressor genes. This prevents cell division and induces both cell cycle arrest and apoptosis, which may inhibit the proliferation of susceptible tumor cells. In addition, MPT0E028 inhibits the phosphorylation and activation of Akt, which prevents the activation of downstream signaling pathways, independent of its HDAC inhibitory activity. HDACs, upregulated in many tumor cell types, are a family of enzymes that deacetylate histone proteins. Akt, overexpressed in many tumor cell types, plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C121665","HDAC Inhibitor OBP-801","HDAC Inhibitor OBP-801|Histone Deacetylase Inhibitor OBP-801|OBP-801|YM753","An inhibitor of histone deacetylase (HDAC) enzymes, with potential antineoplastic activity. Upon administration, OBP-801 inhibits the activity of HDACs; this results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This leads to selective transcription of tumor suppressor genes, tumor suppressor protein-mediated inhibition of tumor cell division and induction of tumor cell apoptosis. This may inhibit proliferation of susceptible tumor cells. HDAC, which is upregulated in many tumor cell types, deacetylates chromatin histone proteins.","Pharmacologic Substance"]
["C97513","HDAC Inhibitor SHP-141","HDAC Inhibitor SHP-141|SHP-141","A topical formulation containing the histone deacetylase (HDAC) inhibitor with potential antineoplastic activity. Upon cutaneous administration, SHP-141 selectively binds to and inhibits HDAC, resulting in an accumulation of highly acetylated histones in the skin (dermis and epidermis), the induction of chromatin remodeling, and the selective transcription of tumor suppressor genes. These events may result in the inhibition of tumor cell division and the induction of tumor cell apoptosis. HDACs, upregulated in many tumor cell types, are a family of metalloenzymes responsible for the deacetylation of chromatin histone proteins. Topical administration of SHP-141 allows for high concentrations of this agent locally while minimizing systemic toxicity.","Pharmacologic Substance"]
["C78850","HDAC/EGFR/HER2 Inhibitor CUDC-101","CUDC-101|HDAC/EGFR/HER2 Inhibitor CUDC-101","A multi-targeted, small-molecule inhibitor of histone deacetylase (HDAC), epidermal growth factor receptor tyrosine kinase (EGFR/ErbB1), and human epidermal growth factor receptor 2 tyrosine kinase (HER2/neu or ErbB2) with potential antineoplastic activity. HDAC/EGFR/HER2 inhibitor CUDC-101 inhibits the activity of these three enzymes but the exact mechanism of action is presently unknown. This agent may help overcome resistance to inhibition of EGFR and Her2 through a simultaneous, synergistic inhibition of EGFR, Her2, and HDAC.","Pharmacologic Substance"]
["C77904","HDM2 Antagonist JNJ-26854165","HDM2 Antagonist JNJ-26854165|HDM2 Inhibitor JNJ-26854165|JNJ-26854165","An orally bioavailable HDM2 antagonist with potential antineoplastic activity. Hdm2 inhibitor JNJ-26854165 inhibits the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited, which may result in the restoration of p53 signaling and thus the p53-mediated induction of tumor cell apoptosis. HDM2 (human homolog of double minute 2), a zinc finger protein, is a negative regulator of the p53 pathway; often overexpressed in cancer cells, it has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C116325","HDM2 Inhibitor HDM201","HDM2 Inhibitor HDM201|HDM201","An orally bioavailable human double minute 2 homolog (HDM2) inhibitor with potential antineoplastic activity. HDM2 inhibitor HDM201 inhibits the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited, which may result in the restoration of both p53 signaling and p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger protein and negative regulator of the p53 pathway, is often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C116867","HDM2 Inhibitor MK-8242","HDM2 Inhibitor MK-8242|MK-8242|SCH 900242","An orally bioavailable inhibitor of human homolog of double minute 2 (HDM2), with potential antineoplastic activity. Upon oral administration, HDM2 inhibitor MK-8242 inhibits the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the degradation of p53 is inhibited, which may result in the restoration of p53 signaling. This induces p53-mediated tumor cell apoptosis. HDM2 is a member of the RING finger-type family of E3 ubiquitin protein ligases and targets p53 for degradation; it is often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C84862","Hedgehog Inhibitor PF-04449913","Hedgehog Inhibitor PF-04449913","An orally bioavailable small-molecule inhibitor of the Hedgehog (Hh) signaling pathway with potential antineoplastic activity. Hedgehog inhibitor PF-04449913 appears to inhibit Hh pathway signaling. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair. Constitutive activation of Hh pathway signaling has been observed in various types of malignancies.","Pharmacologic Substance"]
["C1377","Hematoporphyrin Derivative","HPD|Hematoporphyrin Derivative|Hematoporphyrin derivative|Photofrin|hematoporphyrin derivative|photofrin","A complex mixture of monomeric and aggregated porphyrins with photosensitizing activity. Upon systemic administration, hematoporphyrin derivatives accumulate in tumor cells and, once activated by red laser light (630 nm), in the presence of oxygen, produce singlet oxygen and other reactive oxygen radicals, resulting in local radical-mediated tumor cell death.","Pharmacologic Substance"]
["C49083","Hemiasterlin Analog E7974","E7974|Hemiasterlin Analog E7974","An analog of the sponge-derived anti-microtubule tripeptide hemiasterlin with antimitotic and potential antineoplastic activities. Hemiasterlin analog E7974 binds to the Vinca domain on tubulin, resulting in inhibition of tubulin polymerization and microtubule assembly; depolymerization of existing microtubules; inhibition of mitosis; and inhibition of cellular proliferation. This agent may have more affinity for the beta-3 tubulin isotype.","Pharmacologic Substance"]
["C97949","Henatinib Maleate","(R,Z)-2-[(5-Fluoro-1,2-dihydro-2-oxo-3H-indol-3-ylidene) methyl]-5-(2-hydroxy-3-morpholinopropyl)-3-methyl-5,6,7,8-tetrahydro-1H-pyrrolo[3,2-c] azepin-4-ketone Maleate|Henatinib Maleate","The maleate salt form of henatinib, an orally bioavalable, multitargeted tyrosine kinase inhibitor with potential antitumor and antiangiogenic activities. Henatinib inhibits vascular endothelial growth factor receptor type 2 (VEGFR2), a tyrosine kinase receptor upregulated in many tumor cells that plays a key role in angiogenesis. This may result in an inhibition of angiogenesis and eventually tumor cell proliferation. Henatinib, structurally similar to sunitinib, also inhibits, though to a lesser extent, mast/stem cell growth factor receptor (c-Kit) and, platelet-derived growth factor receptor (PDGFR) alpha and beta.","Pharmacologic Substance"]
["C102749","Heparan Sulfate Glycosaminoglycan Mimetic M402","HSGAG Mimetic M402|Heparan Sulfate Glycosaminoglycan Mimetic M402|M402","A low molecular weight heparin derivative and heparan sulfate proteoglycan (HSPG) mimetic with no or minimal anticoagulant activity and potential antineoplastic activities. Upon administration, M402 mimics HSPGs by binding to and inhibiting various heparin-binding growth factors, chemokines, and cytokines such as VEGF, HGF, FGF2, SDF-1a, heparanase and P-selectin all of which are essential for tumor angiogenesis and metastasis to occur. This inhibits heparin binding growth factor-mediated signaling and disrupts tumor-stromal interactions eventually leading to an inhibition of angiogenesis and tumor cell progression. In addition, M402 may enhance the cytotoxic effect of other chemotherapeutic agents.","Pharmacologic Substance"]
["C104412","Heparin Derivative SST0001","100NA,RO-H|Heparin Derivative SST0001|SST0001","An N-acetylated, glycol-split form of heparin that is devoid of anticoagulant activity and is an inhibitor of heparanase with antineoplastic and antiangiogenic activities. Upon subcutaneous administration, heparin derivative SST0001 inhibits the activity of heparanase. This prevents the heparanase-mediated cleavage of heparan sulfate (HS) proteoglycans on cell surfaces and within the extracellular matrix. In addition, this agent prevents the heparanase-induced production of a number of angiogenic growth factors, including matrix metalloproteinase-9, hepatocyte growth factor and vascular endothelial growth factor. Altogether, this leads to an inhibition of both tumor cell growth and angiogenesis. Heparanase, an enzyme that is responsible for the proteolytic cleavage of proteoglycans, is upregulated in a variety of tumor cell types and promotes tumor cell growth; it plays a key role in tumor cell invasion, metastasis and angiogenesis.","Pharmacologic Substance"]
["C99903","HER2 ECD+TM Virus-like Replicon Particles Vaccine AVX901","AVX901|HER2 ECD+TM Virus-like Replicon Particles Vaccine AVX901|HER2 ECDTM VRP|VRP-HER2 ECDTM","A cancer vaccine based on virus-like replicon particles (VRP) packaged with an alphaviral vector encoding the extracellular domain (ECD) and transmembrane (TM) regions of the human epidermal growth factor receptor 2 (EGFR2, NEU or HER2), with potential antineoplastic activity. After immunization with HER2 ECD+TM virus-like replicon particles vaccine AVX901, the VRPs infect cells and express HER2 ECD+TM protein that may activate the immune system to elicit a cytotoxic T-lymphocyte (CTL) response against HER2-expressing tumor cells. The alphaviral replicon of this vaccine is an attenuated strain of the Venezuelan equine encephalitis virus (VEEV) in which 3 of the 7 viral genes were substituted with a truncated HER2 gene to create a self-amplifying replicon RNA. HER2, a tyrosine kinase involved in several cell growth signaling pathways, is dysregulated or overexpressed in a wide variety of cancer cell types.","Pharmacologic Substance"]
["C2593","HER-2/neu Intracellular Domain Protein","HER-2 ICD Peptide|HER-2/neu ICD Protein|HER-2/neu Intracellular Domain Protein|HER2 ICD|HER2 Intracellular Domain","The cytoplasmic domain or intracellular domain (ICD) of the HER2/neu protein that exhibits tyrosine kinase activity. Based on sensitization theory, co-administration of trastuzumab (anti-HER-2/neu monoclonal antibody) and HER-2/neu intracellular domain protein may result in the potentiation of a HER2/neu-specific cytotoxic T lymphocyte (CTL) response against tumor cells overexpressing the HER2/neu protein. HER-2/neu protein, a glycoprotein cell surface receptor that is composed of an extracellular domain (ECD), a transmembrane domain, and an ICD, is overexpressed by many adenocarcinomas including breast adenocarcinoma.","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C2537","HER-2/neu Peptide Vaccine","HER-2-Neu Peptide Vaccine|HER-2/neu Helper-Peptide Vaccine|HER-2/neu Peptide Vaccine","A cancer vaccine comprised of peptides derived from the extracellular domain of the tumor-associated antigen Her-2/neu with potential antineoplastic activity. HER-2/neu peptide vaccine may induce antibodies with anti-tumor activity and may also elicit a specific CD8 T-cell response against specific tumor cell types. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C88317","HER2Bi-Armed Activated T Cells","Anti-CD3 x Anti-Her2/neu Bispecific Antibody-Armed Activated T Cells|HER2Bi-Armed ATCs|HER2Bi-Armed Activated T Cells","Activated T cells (ATC) that have been coated with bispecific antibodies (BiAb), with potential antineoplastic and immunomodulating activities. In vitro, T cells are activated through exposure to the anti-CD3 murine monoclonal antibody OKT3 and interleukin 2 for 14 days and then armed with anti-CD3 x anti-Her2 bispecific antibody (Her2Bi). Upon administration, HER2Bi-armed activated T cells attach to CD3-expressing T cells and HER2/neu-expressing tumor cells, selectively cross-linking T cells and tumor cells; this may result in the recruitment and activation of cytotoxic T lymphocyte (CTLs), CTL perforin-mediated tumor cell cytolysis, and the secretion of antitumor cytokines and chemokines.","Cell|Pharmacologic Substance"]
["C128283","HER-2-positive B-cell Peptide Antigen P467-DT-CRM197/Montanide Vaccine IMU-131","HER-2-positive B-cell Peptide Antigen P467-DT-CRM197/Montanide Vaccine IMU-131|HER-Vaxx Peptide Vaccine|HER-Vaxx|IMU-131 HER2/Neu Peptide Vaccine|IMU-131 Vaccine|IMU-131|P467-CRM197/Montanide Vaccine IMU-131","A cancer vaccine consisting of a fusion peptide, composed of three peptides derived from the extracellular domain (ECD) of the HER2 peptide antigen found on B-cells (P4, P6 and P7; P467), conjugated to the carrier protein DT-CRM197, a non-toxic, mutated form of diphtheria toxin (DT), and combined with the immunoadjuvant montanide ISA 51, with potential immunostimulatory and antineoplastic activities. Upon administration, IMU-131 vaccine induces the production of polyclonal antibodies against the HER2 protein. In turn, the antibodies bind to three separate binding sites on HER2 expressed on tumor cells and inhibit HER2 dimerization and activity, which leads to the inhibition of HER2-mediated signal transduction pathways. This induces apoptosis in and reduces cellular proliferation of HER2-overexpressing tumor cells. In addition, IMU-131 induces a cytotoxic T-lymphocyte (CTL) response against the HER2-expressing tumor cells. The tumor-associated antigen (TAA) HER2, also called Neu or ErbB2, is a tyrosine kinase receptor for epidermal growth factor (EGF) and is often overexpressed by a variety of tumor cell types. Montanide ISA 51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil (w/o) emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens. DT-CRM197 is used to increase the immunogenicity of the HER2/neu peptide antigen. In P467, the three B-cell epitopes were combined in a specific order into a single 49 amino acid peptide antigen.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C114293","HER2-pulsed Autologous Type-1 Polarized Dendritic Cell Vaccine","HER-2 pulsed DC1 Vaccine|HER2-pulsed Autologous Type-1 Polarized Dendritic Cell Vaccine","A dendritic cell (DC)-based cancer vaccine composed of autologous, type-1 polarized dendritic cells (DCs) pulsed with human leukocyte antigen (HLA)-A2-restricted HER-2-derived peptides, with potential immunomodulatory and antineoplastic activities. Autologous DCs were treated with GM-CSF, interleukin-4, interferon-gamma and bacterial lipopolysaccharide (LPS), a toll-like receptor type 4 agonist, to produce highly polarized DCs (alphaDC1) that are capable of producing high levels of interleukin-12p70 (IL-12p70). Upon administration, HER2-pulsed autologous DC vaccine may stimulate a potent cytotoxic T-lymphocyte (CTL) response against HER-2-positive tumor cells, which may result in tumor cell death and decreased tumor growth. HER-2, a tyrosine kinase receptor for epidermal growth factor (EGF) (also known as neu and ErbB2), is overexpressed by a variety of cancers.","Immunologic Factor|Pharmacologic Substance"]
["C96038","HER2-targeted Liposomal Doxorubicin Hydrochloride MM-302","HER2-targeted Liposomal Doxorubicin Hydrochloride MM-302|MM-302","An antibody-targeted lipidic nano-carrier containing the antineoplastic anthracycline antibiotic doxorubicin encapsulated within liposomes, and conjugated to a monoclonal antibody against the human epidermal growth factor receptor 2 (HER2), with potential antitumor activity. Upon administration of HER2-targeted liposomal doxorubicin hydrochloride MM-302, the immunoliposome allows for specific delivery of doxorubicin to tumors overexpressing the HER2 receptor. Once inside the HER2-expressing tumor cells, doxorubicin intercalates into DNA and interferes with topoisomerase II activity, thereby inhibiting DNA replication and RNA synthesis. Compared to doxorubicin alone or liposomal doxorubicin, targeted liposomal delivery of doxorubicin improves efficacy while lowering the toxicity profile. HER2, a tyrosine kinase receptor, is overexpressed in many cancer cell types.","Pharmacologic Substance"]
["C118953","HER2-targeting Antibody Fc Fragment FS102","Anti-HER2 FCAB FS102|FS102|Fcab FS102|HER2-targeting Antibody Fc Fragment FS102","A proprietary, antibody fragment composed of a constant (Fc) region that is engineered to bind to the tumor-associated antigen human epidermal growth factor receptor-2 (HER2), with potential antineoplastic activity. HER2-targeted antibody Fc fragment FS102 specifically binds to its HER2 epitope, and causes downregulation of HER2-mediated signaling. This leads to tumor cell apoptosis. HER2, a member of the receptor tyrosine kinase (RTK) epidermal growth factor receptor (EGFR) superfamily, is overexpressed on the cell surface of various solid tumors.","Pharmacologic Substance"]
["C2661","Herba Scutellaria Barbata","Ban Zhi Lian|Barbed Skullcap Herb|HSB|Herba Scutellaria Barbata|Herba Scutellariae Barbatae|Scutellaria barbata (Aqueous Extract)|Scutellaria barbata|herba scutellaria barbatae","A Chinese herb isolated from the plant Scutellaria barbata D. Don (Lamiaceae) with potential antineoplastic activity. Containing the antioxidant flavone scutellarin, herba Scutellaria barbata has been shown to induce apoptosis of ovarian and breast tumor cells in vitro.","Pharmacologic Substance"]
["C1124","Herbimycin","17-Demethoxy-15-methoxy-11-O-methylgeldanamycin, (15R)-|Herbimycin A|Herbimycin","A benzoquinone antineoplastic antibiotic isolated from the bacterium Streptomyces hygroscopicus.  Herbimycin binds to and inhibits the cytosolic chaperone functions of heat shock protein 90 (HSP90).  HSP90 maintains the stability and functional shape of many oncogenic signaling proteins; the inhibition of HSP90 promotes the proteasomal degradation of oncogenic signaling proteins that may be over-expressed or overactive in tumor cells. (NCI04)","Antibiotic|Organic Chemical"]
["C122401","Heterodimeric Interleukin-15","Heterodimeric Interleukin-15|IL-15/sIL-15Ra|hetIL-15","A fusion protein complex composed of heterodimeric IL-15 (hetIL-15), which consists of a synthetic form of the endogenous cytokine interleukin-15 chain (IL-15) complexed to the soluble IL-15 binding protein IL-15 receptor alpha chain (IL-15Ra) (IL15:sIL-15Ra), with potential immunomodulatory, anti-infective and antineoplastic activities. Upon administration, hetIL-15 binds to the IL-2/IL-15 receptor beta-common gamma chain (IL-2Rbeta-gamma) receptor on natural killer (NK) and T-lymphocytes, which activates and increases the levels of NK cells and CD8+ and CD4+ T-cells. The T-cells enhance the secretion of the cytokine interferon-gamma (IFN-g), which further potentiates the immune response against tumor cells. Altogether, this enhances tumor cell killing and decreases tumor cell proliferation. By coupling IL-15 to IL15Ra, this agent has an improved pharmacokinetic profile, shows an increased ability to bind IL-2Rbeta-gamma, and shows increased immunostimulatory activity as compared to IL-15 alone.","Pharmacologic Substance"]
["C1125","Hexamethylene Bisacetamide","Acetamide, N,N'-1, 6-hexanediylbis-|Acetamide, N,N'-hexamethylenebis-|HMBA|Hexamethylene Bisacetamide|Hexamethylene bisacetamide|Hexamethylenebisacetamide|Hexamethylenediacetamide|N, N'-Diacetylhexamethylenediamine|N,N'-1,6-Hexanediylbisacetamide|N,N'-Hexamethylenebisacetamide","A hybrid polar-planar compound with potential antineoplastic activity that induces terminal differentiation, inhibits cell growth, and causes apoptosis in several tumor cell lines.  Its precise mechanism of action is unknown. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C26654","Hexaminolevulinate","HAL|HEXAMINOLEVULINATE|Hexaminolevulinate|HexvixR|Hexyl 5-Aminolevulinate|hexyl 5-aminolevulinate","The hexyl ester of 5-aminolevulinic acid (ALA) with photodynamic properties. As a precursor of photoactive porphorins, hexyl 5-aminolevulinate induces the endogenous production of the photosensitizer protoporphyrin IX (PPIX) which accumulates selectively in tumor tissue. When exposed to specific wavelengths of light, PPIX is activated and, depending on the wavelength and/or intensity of light, either fluoresces, thereby allowing tumor imaging, or induces tumor cell apoptosis.","Pharmacologic Substance"]
["C29092","Hexylresorcinol","4-Hexylresorcinol|HEXYLRESORCINOL|Hexylresorcinol","A substituted phenol with bactericidal, antihelminthic and potential antineoplastic activities. Hexylresorcinol is used as an antiseptic in mouthwashes and skin wound cleansers. Hexylresorcinol may also inhibit oxidative DNA damage by enhancing the activity of antioxidant enzymes, including glutathione peroxidase and glutathione reductase, which facilitate scavenging reactive oxygen molecules by glutathione (GSH).","Pharmacologic Substance"]
["C70953","HIF-1alpha Inhibitor PX-478","(S)-4-(2-Amino-2-carboxyethyl)-N,N-bis(2-chloroethyl)aniline Oxide Dihydrochloride|HIF-1alpha Inhibitor PX-478|Hypoxia Inducible Factor 1-Alpha PX-478|L-Phenylalanine, 4-[Bis(2-chloroethyl)oxidoamino]-, Dihydrochloride; L-Phenylalanine, 4-[Bis(2-chloroethyl)oxidoamino]-, Hydrochloride (1:2)|PX-478","An orally active small molecule with potential antineoplastic activity. Although its mechanism of action has yet to be fully elucidated, HIF1-alpha inhibitor PX-478 appears to inhibit hypoxia-inducible factor 1-alpha (HIF1A) expression, which may result in decreased expression of HIF1A downstream target genes important to tumor growth and survival, a reduction in tumor cell proliferation, and the induction of tumor cell apoptosis. The inhibitory effect of this agent is independent of the tumor suppressor genes VHL and p53 and may be related to derangements in glucose uptake and metabolism due to inhibition of glucose transporter-1 (Glut-1).","Pharmacologic Substance"]
["C119618","HIF-2alpha Inhibitor PT2385","HIF-2alpha Inhibitor PT2385|PT2385","An orally active, small molecule inhibitor of hypoxia inducible factor (HIF)-2alpha, with potential antineoplastic activity. Upon oral administration, HIF-2alpha inhibitor PT2385 allosterically binds to HIF-2alpha, thereby preventing HIF-2alpha heterodimerization and its subsequent binding to DNA. This results in decreased transcription and expression of HIF-2alpha downstream target genes, many of which regulate tumor cell growth and survival. Blocking HIF-2alpha reduces the proliferation of HIF-2alpha-expressing tumor cells. HIF-2alpha, a heterodimeric transcription factor overexpressed in many cancers, promotes tumorigenesis.","Pharmacologic Substance"]
["C71154","High-Selenium Brassica juncea","BJ-Se|High-Selenium Brassica juncea|high-selenium Brassica juncea","A formulation of the mustard plant Brassica juncea grown in a medium that has been enriched with the trace element selenium with potential chemopreventive and chemopotentiating activities. Brassica juncea hyperaccumulates trace elements in soil. Selenium amino acid species found in selenized Brassica juncea include methylselenomethionine (MeSeMet) and methylselenocysteine (MeSeCys); both may be incorporated into selenoproteins in vivo. Selenium functions as a cofactor for antioxidant enzymes such as glutathione peroxidases and thioredoxin reductase, which protect cells from the free radical damage. In addition, in vitro MeSeCys has been shown to potentiate the antitumor effects of the irinotecan metabolite SN-38, by inducing phosphorylation of checkpoint kinase 2 (chk2) at threonine 68, which results in poly(ADP-ribose) polymerase cleavage, caspase 3 activation, and DNA fragmentation.","Pharmacologic Substance"]
["C113334","Histone-Lysine N-Methyltransferase EZH2 Inhibitor GSK2816126","EZH2 Inhibitor GSK2816126|GSK2816126|Histone-Lysine N-Methyltransferase EZH2 Inhibitor GSK2816126","A small molecule selective and S-adenosyl methionine (SAM) competitive inhibitor of histone-lysine N-methyltransferase EZH2, with potential antineoplastic activity. Upon administration, histone-lysine N-methyltransferase EZH2 inhibitor GSK2816126 inhibits the activity of EZH2 and specifically prevents the methylation of histone H3 lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased tumor cell proliferation in cancer cells that overexpress this enzyme. EZH2, which belongs to the class of histone methyltransferases (HMTs), is overexpressed or mutated in a variety of cancers and plays a key role in tumor cell proliferation.","Pharmacologic Substance"]
["C77424","Histrelin Acetate","HISTRELIN ACETATE|Histrelin Acetate|Supprelin|Vantas","The acetate salt form of histrelin, a long-acting, synthetic nonapeptide analog of gonadotropin-releasing hormone (GnRH) with potential anti-tumor activity. Upon administration, histrelin binds to and activates GnRH receptors; prolonged administration results in pituitary GnRH receptor desensitization and inhibition of follicle stimulating hormone (FSH) and luteinizing hormone (LH) secretion, leading to a significant decline in testosterone production in males and may inhibit androgen receptor-positive tumor progression; in females, prolonged administration results in decreased estradiol production.","Pharmacologic Substance"]
["C111689","HLA-A*0201 Restricted TERT(572Y)/TERT(572) Peptides Vaccine Vx-001","HLA-A*0201 Restricted TERT(572Y)/TERT(572) Peptides Vaccine Vx-001|HLA-A*0201 Restricted Telomerase-specific Vaccine Vx-001|Vx-001|Vx001","A peptide-based cancer vaccine consisting of two human leukocyte antigen (HLA)-A*0201 restricted 9-mer epitopes derived from the human telomerase reverse transcriptase (hTERT), TERT 572Y (YLFFYRKSV; TYR-Vx001) and TERT 572 (RLFFYRKSV; ARG-Vx001), with potential immunostimulating and antineoplastic activities. Subcutaneous injection of TERT(572Y) peptide followed by subcutaneous administration of the TERT(572) peptide may elicit a specific and possibly optimal cytotoxic T cell (CTL) response against hTERT-expressing tumor cells. hTERT, the catalytic subunit of human telomerase, is an human leukocyte antigen-A*0201-restricted cryptic epitope of telomerase. TERT is expressed in the majority of human cancer cells, is not expressed or is expressed at very low levels in normal cells and plays a key role in tumorigenesis. TERT572Y is the optimized variant of the native cryptic peptide TERT572 in which tyrosine has been substituted for an arginine at position 1; TERT572Y shows increased HLA-A*0201 binding affinity compared to TERT572.","Immunologic Factor|Pharmacologic Substance"]
["C84844","HLA-A*0201-Restricted TRP2-gp100-EphA2-HER2 multipeptide Vaccine","HLA-A*0201-Restricted TRP2-gp100-EphA2-HER2 multipeptide Vaccine","A cancer vaccine containing four HLA-A*0201-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Vaccine peptide epitopes are derived from the tumor associated antigens (TAAs) tyrosinase-related protein 2 (TRP2), glycoprotein 100 (gp100), Ephrin receptor A2 (EphA2) and human epidermal growth factor receptor 2 (HER2). Upon administration, HLA-A*0201-restricted TRp2-gp100-EphA2-HER2 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against TRP2-gp100-EphA2-HER2-expressing tumor cells, resulting in tumor cell lysis and decreased tumor cell proliferation. HLA-A*0201 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*0201 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77900","HLA-A*0201-Restricted URLC10-VEGFR1-VEGFR2 Multipeptide Vaccine","HLA-A*0201-Restricted URLC10-VEGFR1-VEGFR2 Multipeptide Vaccine","A cancer vaccine containing three HLA-A*0201-restricted peptide epitopes with potential immunostimulatory, antiangiogenic, and antitumor activities. Vaccine peptide epitopes are derived from the tumor associated antigen (TAA) URLC (up-regulated in lung cancer 10) and vascular endothelial growth factor receptors (VEGFR) 1 and 2. Upon administration, HLA-A*0201-restricted URLC10-VEGFR1-VEGFR2 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against URLC10-expressing tumor cells and the tumor microvasculature expressing VEGFR 1 and 2 peptides; this may result in tumor cell lysis, the inhibition of tumor angiogenesis, and decreased tumor growth. HLA-A*0201 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*0201 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77878","HLA-A*0201-Restricted VEGFR1 Peptide Vaccine","HLA-A*0201-Restricted VEGFR1 Peptide Vaccine","A cancer vaccine containing an HLA-A*0201-restricted vascular endothelial growth factor receptor 1 (VEGFR1) peptide (sequence: TLFWLLLTL) with potential immunostimulatory and antitumor activities. Upon administration, HLA-A*0201-restricted VEGFR1-derived peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing VEGFR1, resulting in tumor cell lysis and decreased tumor growth. HLA-A*0201 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*0201 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77905","HLA-A*0201-Restricted VEGFR1-VEGFR2 Multipeptide Vaccine","HLA-A*0201-Restricted VEGFR1-VEGFR2 Multipeptide Vaccine","A cancer vaccine containing two HLA-A*0201-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from: vascular endothelial growth factor receptors (VEGFR) 1 and 2. Upon administration, HLA-A*0201-restricted VEGFR1-VEGFR2 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing VEGFR 1 and 2 peptides, resulting in tumor cell lysis and decreased tumor growth. HLA-A*0201 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*0201 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C94223","HLA-A*2402-Restricted CDCA1-A24-56 Peptide Vaccine","HLA-A*2402-Restricted CDCA1-A24-56 Peptide Vaccine|HLA-A*2402-Restricted Cell Division Cycle Associated 1-A24-56 Peptide Vaccine","A cancer vaccine containing the HLA-A*2402-restricted peptide epitope derived from cell division associated gene 1 (CDCA1), with potential immunostimulatory and antitumor activities. Upon administration, HLA-A*2402-restricted CDCA1-A24-56 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against CDCA1-expressing tumor cells, resulting in tumor cell lysis and decreased tumor cell proliferation. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Immunologic Factor|Pharmacologic Substance"]
["C90568","HLA-A*2402-Restricted CDCA1-KIF20A Multipeptide Vaccine","HLA-A*2402-Restricted CDCA1-KIF20A Multipeptide Vaccine","A cancer vaccine containing two HLA-A*2402-restricted peptide epitopes derived from cancer-testis antigens with potential immunostimulatory and antitumor activities. The peptide epitopes are derived from cell division associated 1 (CDCA1) and kinesin-like family member 20A (KIF20A). Upon administration, HLA-A*2402-restricted CDCA1-KIF20A multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against CDCA1- and KIF20A-expressing tumor cells, resulting in tumor cell lysis and decreased tumor cell proliferation. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Immunologic Factor|Pharmacologic Substance"]
["C95207","HLA-A*2402-Restricted CDCA1-URLC10-KIF20A-DEPDC1-MPHOSPH1 Multipeptide Vaccine","HLA-A*2402-Restricted CDCA1-URLC10-KIF20A-DEPDC1-MPHOSPH1 Multipeptide Vaccine","A cancer vaccine containing five HLA-A*2402-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from CDCA1 (cell division cycle-associated protein 1), URLC10 (up-regulated lung cancer 10), KIF20A (kinesin-like family member 20A), DEPDC1 (DEP domain containing 1), and MPHOSPH1 (M phase phosphoprotein 1). Upon administration, this peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against CDCA1-,URLC10-,KIF20A-,DEPDC1-, or MPHOSPH1-expressing tumor cells, resulting in tumor cell lysis and decreased tumor growth. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77868","HLA-A*2402-Restricted KOC1-TTK-CO16-DEPDC1-MPHOSPH1 Multipeptide Vaccine","HLA-A*2402-Restricted KOC1-TTK-CO16-DEPDC1-MPHOSPH1 Multipeptide Vaccine","A cancer vaccine containing five HLA-A*2402-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from IGF II mRNA binding protein 3 (KOC1); TTK protein kinase (TTK); URLC10 (up-regulated lung cancer 10); DEP domain containing 1 (DEPDC1); and M phase phosphoprotein 1 (MPHOSPH1). Upon administration, HLA-A*2404-restricted KOC1-TTK-CO16-DEPDC1-MPHOSPH1 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing KOC1, TTK, CO16, DEPDC1 and MPHOSPH1 peptides, resulting in tumor cell lysis and decreased tumor growth. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C101893","HLA-A*2402-Restricted Multipeptide Vaccine S-488410","HLA-A*2402-Restricted Multipeptide Vaccine S-488410|S-488410","A cancer vaccine composed of HLA-*2402-restricted epitopic peptides derived from three cancer/testis (CT) antigens, with potential antineoplastic activity. Upon subcutaneous administration, HLA-A*2402-restricted multipeptide vaccine S-488410 may elicit a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing these CT antigens. CT antigens, normally expressed only in germ cells of the testis, are overexpressed in a wide variety of human cancers.","Immunologic Factor|Pharmacologic Substance"]
["C82421","HLA-A*2402-Restricted URLC10 Peptides Vaccine","HLA-A*2402-Restricted URLC10 Peptides Vaccine","A cancer vaccine containing HLA-A*2402-restricted epitope peptides URLC10 (up-regulated lung cancer 10) with potential immunostimulatory and antineoplastic activities. Upon administration, HLA-A*2402-restricted URLC10 peptides vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against URLC10-expressing tumor cells. URLC10, a tumor associated antigen, is often overexpressed in lung, esophageal and gastric cancers. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C90566","HLA-A*2402-Restricted URLC10-CDCA1-KIF20A Multipeptide Vaccine","HLA-A*2402-Restricted URLC10-CDCA1-KIF20A Multipeptide Vaccine","A cancer vaccine containing three HLA-A*2402-restricted peptide epitopes derived from cancer-testis antigens with potential immunostimulatory and antitumor activities. The peptide epitopes are derived from up-regulated lung cancer 10 (URLC10); cell division cycle associated 1 (CDCA1); and kinesin-like family member 20A (KIF20A). Upon administration, HLA-A*2402-restricted URLC10-CDCA1-KIF20A multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against URL10-, CDCA1-, and KIF20A-expressing tumor cells, resulting in tumor cell lysis and decreased tumor cell proliferation. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Immunologic Factor|Pharmacologic Substance"]
["C85455","HLA-A*2402-Restricted URLC10-CDCA1-VEGFR1-VEGFR2 Multipeptide Vaccine","HLA-A*2402-Restricted URLC10-CDCA1-VEGFR1-VEGFR2 Multipeptide Vaccine","A cancer vaccine containing four HLA-A*2402-restricted peptide epitopes with potential immunostimulatory and antitumor activities. The peptide epitopes are derived from URLC10 (up-regulated lung cancer 10); CDCA1 (cell division associated 1); and vascular endothelial growth factor receptors (VEGFRs) 1 and 2. Upon administration, HLA-A*2402-restricted URLC10-CDCA1-VEGFR1-VEGFR2 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against URL10-, CDCA1-, VEGFR1- and VEGFR2-expressing tumor cells, resulting in tumor cell lysis and decreased tumor cell proliferation. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77875","HLA-A*2402-Restricted URLC10-KOC1-VEGFR1-VEGFR2 Multipeptide Vaccine","HLA-A*2402-Restricted URLC10-KOC1-VEGFR1-VEGFR2 Multipeptide Vaccine","A cancer vaccine containing four HLA-A*2402-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from URLC10 (up-regulated lung cancer 10 or CO16); KOC1 (IGF II mRNA Binding Protein 3); and vascular endothelial growth factor receptors (VEGFRs) 1 and 2. Upon administration, this multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against URL10-, KOC1-, VEGFR1- and VEGFR2-expressing tumor cells, resulting in tumor cell lysis and decreased tumor growth. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77897","HLA-A*2402-Restricted URLC10-TTK-KOC1 Multipeptide Vaccine","HLA-A*2402-Restricted URLC10-TTK-KOC1 Multipeptide Vaccine","A cancer vaccine containing three HLA-A*2402-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from URLC10 (up-regulated lung cancer 10); TTK (TTK protein kinase); and KOC1 (IGF II mRNA Binding Protein 3). Upon administration, URLC10-TTK-KOC1 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing URLC10, TTK and KOC1 peptides, resulting in tumor cell lysis and decreased tumor growth. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C74039","HLA-A*2402-Restricted URLC10-TTK-VEGFR1-VEGFR2 Multipeptide Vaccine","HLA-A*2402-Restricted URLC10-TTK-VEGFR1-VEGFR2 Multipeptide Vaccine","A cancer vacine containing four HLA-A*2402-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from: URLC10 (up-regulated lung cancer 10), TTK (TTK protein kinase), and VEGFRs (vascular endothelial growth factor receptors) 1 and 2. Upon administration, URLC10-TTK-KOC1-VEGFR1-VEGFR2 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing URLC10, TTK, VEGFR 1 and 2 peptides, resulting in cell lysis and decreased tumor growth. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Pharmacologic Substance"]
["C77869","HLA-A*2402-Restricted VEGFR1 Peptide Vaccine","HLA-A*2402-Restricted VEGFR1 Peptide Vaccine","A cancer vaccine containing the HLA-A*2402-restricted vascular endothelial growth factor receptor 1 (VEGFR1) peptide epitope with potential immunostimulatory and antitumor activities. Upon administration, HLA-A*2402-restricted VEGFR1 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing VEGFR 1 peptide, resulting in tumor cell lysis and decreased tumor growth. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C95211","HLA-A*2402-Restricted VEGFR1/2 Multipeptide Vaccine","HLA-A*2402-Restricted VEGFR1/2 Multipeptide Vaccine","A cancer vaccine containing two HLA-A*2402-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from vascular endothelial growth factor receptors (VEGFRs) 1 and 2. Upon administration, this peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against VEGFR1- and VEGFR2-expressing tumor cells, resulting in tumor cell lysis and decreased tumor growth. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77867","HLA-A*2404-Restricted RNF43-TOMM34-VEGFR1-VEGFR2 Multipeptide Vaccine","HLA-A*2404-Restricted RNF43-TOMM34-VEGFR1-VEGFR2 Multipeptide Vaccine","A cancer vaccine containing four HLA-A*2402-restricted peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from ring finger protein 43 (RNF43); translocase of outer mitochondrial membrane 34 (TOMM34); and vascular endothelial growth factor receptors (VEGFR) 1 and 2. Upon administration, HLA-A*2404-restricted RNF43-TOMM34-VEGFR1-VEGFR2 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing RNF43, TOMM34, and VEGFR 1 and 2 peptides, resulting in tumor cell lysis and decreased tumor growth. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48393","HLA-A1, A2, B35-Restricted Survivin Peptides/Montanide ISA-51 Vaccine","HLA-A1, A2, B35-Restricted Survivin Peptides/Montanide ISA-51 Vaccine|Survivin Peptide Vaccine","A peptide vaccine comprised of synthetic HLA-A1, -A2 and -B35 restricted survivin epitopes combined with the adjuvant Montanide ISA-51 with potential antineoplastic activity. Upon administration, HLA-A1, A2, B35-restricted survivin peptides/Montanide ISA-51 vaccine may stimulate a cytotoxic T cell response against tumor cells that overexpress survivin, resulting in tumor cell lysis. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.","Pharmacologic Substance"]
["C90570","HLA-A1-Binding MAGE-1/MAGE-3 Multipeptide-Pulsed Autologous Dendritic Cell Vaccine","HLA-A1-Binding MAGE-1/MAGE-3 Multipeptide-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with human leukocyte antigen (HLA)-A1-binding melanoma-associated antigen peptides MAGE-1 and MAGE-3 with potential immunomodulating and antineoplastic activity. Upon vaccination, HLA-A1-binding MAGE-1/MAGE-3 multipeptide-pulsed autologous dendritic cell vaccine may stimulate the host immune system to mount an anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against MAGE1- and MAGE-3-expressing cancer cells, resulting in tumor cell lysis. HLA-A1 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A1 may improve antigenic peptide immunogenicity.","Immunologic Factor|Pharmacologic Substance"]
["C48394","HLA-A2, A3-Restricted FGF-5 Peptides/Montanide ISA-51 Vaccine","HLA-A2, A3-Restricted FGF-5 Peptides/Montanide ISA-51 Vaccine|HLA-A2-FGF-5","A peptide vaccine comprised of synthetic HLA-A2- and HLA-A3-binding peptides, derived from amino acid sequences of fibroblast growth factor-5 (FGF-5), combined with the adjuvant Montanide ISA-51 with potential antineoplastic activity. HLA-A2, A3-restricted FGF-5 peptides contain motifs recognized by the MHC class I molecules HLA-A2 and HLA-A3 and may stimulate a cytotoxic T-cell response against tumor cells that overexpress FGF-5. Montanide ISA-51, a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant, non-specifically stimulates cell-mediated immune responses to antigens.","Pharmacologic Substance"]
["C90569","HLA-A2-Binding TYR/MART-1/gp100 Multipeptide-Pulsed Autologous Dendritic Cell Vaccine","HLA-A2-Binding TYR/MART-1/gp100 Multipeptide-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with human leukocyte antigen (HLA)-A2-restricted melanoma-associated antigen peptides tyrosinase (TYR), MART-1(melanoma antigen recognized by T-cells) and melanoma antigen glycoprotein 100 (gp100), with potential immunomodulating and antineoplastic activity. Upon vaccination, HLA-A2-binding TYR/MART-1/gp100 multipeptide-pulsed autologous dendritic cell vaccine may stimulate the host immune system to mount an anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against Tyr-, MART-1 and gp100-expressing cancer cells, resulting in tumor cell lysis. HLA-A2 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A2 may improve antigenic peptide immunogenicity.","Immunologic Factor|Pharmacologic Substance"]
["C82661","HLA-A2-Restricted Synthetic Glioma Antigen Peptides Vaccine","HLA-A2-Restricted Synthetic Glioma Antigen Peptides Vaccine","A synthetic peptide cancer vaccine consisting of HLA-A2-restricted peptides derived from glioma-associated antigens (GAA) with potential immunostimulating and antineoplastic activities. Upon administration, HLA-A2-restricted synthetic glioma antigen peptides vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing the corresponding GAAs, resulting in glioma tumor cell lysis. HLA-A2 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A2 may improve antigenic peptide immunogenicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48633","HLA-B44-Restricted MAGE-3 Peptide","HLA-B44-Restricted MAGE-3 Peptide","A peptide comprised of the synthetic human leukocyte antigen (HLA)-B44-binding peptides derived from amino acid sequences of MAGE-3 with potential antitumor activity. Vaccination with HLA-B44-restricted MAGE-3 peptide may elicit a cytotoxic T lymphocyte immune response against tumor cells expressing MAGE-3. MAGE-3 is an antigen found on many tumor cell types, including melanoma and lung, prostate, colon, thyroid, and breast cancers.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C48634","HLA-B44-Restricted Tyrosinase Peptide","HLA-B44-Restricted Tyrosinase Peptide","A synthetic peptide consisting of synthetic human leukocyte antigen (HLA)-B44-binding peptides derived from amino acid sequences of the melanoma-associated enzyme tyrosinase with potential antitumor activity. Vaccination with HLA-B44-restricted tyrosinase peptide may stimulate cytotoxic T lymphocyte response against tyrosinase-expressing tumor cells, resulting in decreased tumor growth and cell lysis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C115979","HLA-DP0401/0402-Restricted MAGE-A3-Reactive T Cell Receptor-transduced Autologous T Cells","Anti-MAGE-A3-DP4 TCR PBL|HLA-DP0401/0402-Restricted MAGE-A3-Reactive T Cell Receptor-transduced Autologous T Cells","Human autologous T-lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the human leukocyte antigen (HLA)-DP0401/0402-restricted, melanoma antigen A3 (MAGE-A3), with potential antineoplastic activity. CD4-positive cells are isolated from a patient, transduced with an anti-MAGE-A3-DP0401/0402 restricted TCR, expanded ex vivo, and reintroduced into the HLA-DP0401/0402 positive patient. Then, the HLA-DP0401/0402-restricted, MAGE-A3-reactive TCR-transduced autologous T cells bind to tumor cells expressing the MAGE-A3 antigen, which may result in both an inhibition of growth and increased cell death for MAGE-A3-expressing cancer cells. The tumor-associated antigen MAGE-A3 is overexpressed by a variety of cancer cell types.","Cell|Pharmacologic Substance"]
["C61592","Hodgkin's Antigens-GM-CSF-Expressing Cell Vaccine","Hodgkin's Antigens-GM-CSF-Expressing Cell Vaccine|KGEL Vaccine","An allogeneic vaccine consisting of Hodgkin lymphoma cells transfected with the granulocyte macrophage-colony-stimulating factor (GM-CSF) gene with potential antineoplastic activity. Upon vaccination, Hodgkin antigens-GM-CSF-expressing cell vaccine may stimulate a cytotoxic T-lymphocyte (CTL) immune response against Hodgkin lymphoma-associated antigens, which may result in the lysis of tumor cells expressing these antigens. In addition, transfected Hodgkin lymphoma cells secrete GM-CSF, which may potentiate the CTL response against Hodgkin lymphoma-associated antigens.","Pharmacologic Substance"]
["C88336","Holmium Ho 166 Poly(L-Lactic Acid) Microspheres","Holmium Ho 166 Poly(L-Lactic Acid) Microspheres|Holmium-166 PLA Microspheres","Holmium Ho166 containing poly l-lactic acid (PLA) microspheres with potential antineoplastic actvity. Upon intra-arterial hepatic administration of holmium 166 microspheres, this agent is able to emit both beta particles direct killing cells and gamma photons for nuclear imaging. In addition, since holmium 166 is paramagnetic, this agent can be used for magnetic resonance imaging (MRI).","Pharmacologic Substance"]
["C2636","HPPH","2-(1-Hexyloxyethyl)-2-Devinyl Pyropheophorbide-a|HPPH|Photochlor","A lipophilic, second-generation, chlorin-based photosensitizer. Upon intravenous administration, HPPH selectively accumulates in the cytoplasm of cancer or pre-cancerous cells. When laser light is applied, a photodynamic reaction between HPPH and oxygen occurs, resulting in the production of cytotoxic free radicals and singlet oxygen and free radical-mediated cell death. Compared to the first-generation photosensitizer porfimer sodium, HPPH shows improved pharmacokinetic properties and causes only mild skin photosensitivity which declines rapidly within a few days after administration.","Organic Chemical|Pharmacologic Substance"]
["C117240","HPV 16 E7 Antigen-expressing Lactobacillis casei Vaccine BLS-ILB-E710c","Attenuated Live Listeria Encoding HPV 16 E7 Vaccine|BLS-ILB-E710c|BLS-ILS-E710c|HPV 16 E7 Antigen-expressing Lactobacillis casei Vaccine BLS-ILB-E710c|L. casei-E7 BLS_ILB_E710c|L.casei-PgsA-E7|LacE7 Vaccine","An orally available Lactobacillis casei (L. casei)-based vaccine expressing the human papillomavirus (HPV) type 16 isoform E7 protein linked to the poly-gamma-glutamate synthetase complex gene pgsA, with potential immunostimulating activity. Upon oral administration, the expressed HPV 16 E7 may stimulate the immune system to mount a mucosal cytotoxic T-lymphocyte (CTL) response against HPV 16 E7-expressing tumor cells. The poly-glutamic acid synthetase PgsA from Bacillus subtilis acts as an anchoring motif that facilitates the expression of the HPV antigen protein on the surface of the bacteria. HPV 16 E7, a cell surface glycoprotein and tumor associated antigen, is overexpressed in various viral-related cancers.","Pharmacologic Substance"]
["C2419","HPV 16 E7:12-20 Peptide Vaccine","HPV 16 E7:12-20 Peptide Vaccine|HPV-16 E7(12-20) peptide|HPV-16E7(12-20) peptide vaccine|HPV16 E7(12-20) peptide vaccine|HPV16 E7(12-20) peptide|HPV16E7(12-20)","A peptide based vaccine consisting of amino acids 12 through 20 of the E7 gene of the Human Papilloma Virus type 16.  HPV-16 E7 12-20 peptide vaccine may elicit a specific CD8 T-cell response to the E7 oncogene protein, thereby inhibiting the abrogation of p53 and pRb function and thus prevent tumorigenesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C38761","HPV 16 E7:86-93 Peptide Vaccine","E7(86-93) Lipopeptide|HPV 16 E7:86-93 Peptide Vaccine|HPV 16E7 86-93 Lipopeptide Vaccine|HPV-16E7 (86-93)","A synthetic peptide vaccine consisting of amino acids 86 through 93 (TLGIVCPI) of the viral oncoprotein human papillomavirus (HPV) 16 E7. Vaccination with HPV-16 E7:86-93 peptide, which binds to HLA-A* 0201 molecule, may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells positive for HPV-16 E7.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77909","HPV DNA Plasmids Therapeutic Vaccine VGX-3100","HPV DNA Plasmids Therapeutic Vaccine VGX-3100|VGX-3100","A DNA vaccine consisting of plasmids encoding the E6 and E7 genes of human papilloma virus (HPV) subtypes 16 and 18, respectively, with potential immunostimulating and antineoplastic activities. Administered via intramuscular electroporation, HPV DNA plasmids therapeutic vaccine VGX-3100 expresses E6 and E7 proteins, which may elicit a cytotoxic T-lymphocyte (CTL) response against cervical cancer cells expressing E6 and E7 proteins, resulting in tumor cell lysis. HPV type 16 and HPV type 18 are the most common HPV types involved in cervical carcinogenesis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C102787","HPV E6/E7 DNA Vaccine GX-188E","GX-188E|HPV E6/E7 DNA Vaccine GX-188E","A therapeutic DNA vaccine encoding the E6/E7 fusion protein of human papillomavirus (HPV) subtypes 16 and 18, plus the immune-enhancer, Fms-like tyrosine kinase-3 ligand (FLT3L), with potential immunostimulating and antineoplastic activities. DNA vaccine GX-188E is administered using a proprietary delivery system that electroporates the vaccine into cervical cells. Expression of the E6/E7 fusion product may elicit a cytotoxic T-lymphocyte (CTL) response against cervical cancer cells expressing E6 and E7 oncoproteins, resulting in tumor cell lysis. FLT3L is a ligand for the FLT3 tyrosine kinase receptor, which upon activation stimulates the proliferation of hematopoietic progenitor cells. HPV type 16 and 18 are the most common HPV types involved in cervical carcinogenesis.","Pharmacologic Substance"]
["C102874","HPV-16 E6 Peptides Vaccine/Candida albicans Extract","HPV-16 E6 Peptides Vaccine/Candida albicans Extract|HPV-16 E6 Peptides Vaccine/Candin","A human papillomavirus (HPV) type 16 vaccine containing four E6 peptides in combination with the extract of Candida albicans, with potential immunomodulating activity. Upon administration of HPV-16 E6 peptides vaccine/Candida albicans extract, the four HPV-16 E6 peptides and the candida albicans may activate the immune system to mount a cytotoxic T lymphocyte (CTL) response against cells expressing the E6 oncoprotein, resulting in tumor cell lysis. The HPV 16 transforming protein E6 is expressed in precancerous and malignant cervical lesions. Candida albicans allergenic extract may be used as a recall antigen to stimulate the immune system against HPV.","Pharmacologic Substance"]
["C128485","HPV-16 E7 TCR Expressing T-cells","HPV-16 E7 TCR Expressing T-cells|HPV-16 E7 TCR Expressing T-lymphocytes|HPV-16 E7 TCR-expressing T Lymphocytes|Human Papillomavirus Type 16 E7 TCR Expressing T-cells","A preparation of allogeneic, genetically engineered T-lymphocytes transduced with a retroviral vector MSGV1 that encodes a T-cell receptor (TCR) targeting a specific epitope of the human papillomavirus (HPV) type 16 oncoprotein E7 (HPV-16 E7 TCR), with potential antineoplastic activity. The TCR especially recognizes and binds with high affinity to the HPV 16 E7 11-19 epitope. Upon administration, HPV-16 E7 expressing T-cells target and bind to tumor cells expressing the HPV-16 E7 antigen leading to selective cytotoxicity in HLA-A2-positive, HPV-16 E7-expressing tumor cells. HPV16 E7, a tumor-associated antigen (TAA), overexpressed in a variety of tumor cell types while not expressed in normal, healthy cells, plays a key role in tumor cell proliferation. E7 11-19 is a naturally processed epitope of HPV-16 E7 that binds specifically to human leukocyte antigen (HLA)-A*02:01 and that has been isolated from the surface of HPV-16 positive, HLA-A*02:01-positive tumor cells.","Cell|Pharmacologic Substance"]
["C121648","HPV16 L2/E6/E7 Fusion Protein Vaccine TA-CIN","HPV16 L2/E6/E7 Fusion Protein Vaccine TA-CIN|TA-CIN|Tissue Antigen-Cervical Intraepithelial Neoplasia Vaccine","A recombinant human papillomavirus (HPV), genetically engineered fusion protein vaccine in which the three HPV16 viral proteins L2, E6 and E7 are fused together in a single tandem fusion protein (TA-CIN; HPV16 L2\\E6\\E7), with potential immunoprotective and antineoplastic properties. Upon administration, HPV16 L2\\E6\\E7 fusion protein vaccine TA-CIN may stimulate the immune system to generate HPV16 E6\\E7-specific CD4+ and CD8+ T-cell responses as well as the induction of L2-specific antibodies. In addition, this vaccine may prevent infection and the development of other HPV16-associated diseases. L2, a minor viral capsid protein, is able to induce a strong antibody response against certain HPV types.","Pharmacologic Substance"]
["C123378","HPV-6-targeting Immunotherapeutic Vaccine INO-3106","HPV-6 E6/E7 DNA Vaccine INO-3106|HPV-6-targeting Immunotherapeutic INO-3106|HPV-6-targeting Immunotherapeutic Vaccine INO-3106|INO-3106","A DNA vaccine consisting of plasmids encoding the E6 and E7 genes of human papilloma virus subtype 6 (HPV-6), with potential immunostimulating and antineoplastic activities. Administered via intramuscular electroporation, HPV-6-targeting immunotherapeutic vaccine INO-3106 expresses the HPV-6 E6 and E7 proteins, which may elicit a cytotoxic T-lymphocyte (CTL) response against tumor cells that are expressing those proteins, resulting in tumor cell lysis. HPV-6 infections are associated with aerodigestive malignancies.","Pharmacologic Substance"]
["C115969","Hsp70-peptide TKD/IL-2-activated Autologous Natural Killer Cells","Hsp70-peptide TKD/IL-2-activated Autologous NK Cells|Hsp70-peptide TKD/IL-2-activated Autologous Natural Killer Cells","A preparation of autologous natural killer (NK) cells that are stimulated ex vivo by a 14-mer heat shock protein 70 (Hsp70) TKD peptide and interleukin-2 (IL-2), with potential tumor-selective cytolytic activity. Upon re-infusion into the patient, the treated NK cells recognize and bind to Hsp70-expressing tumor cells, which induces NK-mediated tumor cell lysis. Hsp70, a membrane-bound, stress-inducible protein, is overexpressed on almost all tumor cells; however, it is absent or minimally present on normal, healthy cells. TKD is the C-terminal substrate-binding domain of Hsp70 and is the structure recognized by the activated NK cells.","Cell|Pharmacologic Substance"]
["C69139","Hsp90 Antagonist KW-2478","Hsp90 Antagonist KW-2478|KW-2478","An agent that targets the human heat-shock protein 90 (Hsp90) with potential antineoplastic activity. Although the mechanism of action remains to be fully elucidated, Hsp90 antagonist KW-2478 appears to inhibit Hsp90, resulting in impaired signal transduction, inhibition of cell proliferation, and the induction of apoptosis in tumor cells. HSP90 is a molecular chaperone that plays a key role in the conformational maturation of oncogenic signaling proteins, such as HER2/ERBB2, AKT, RAF1, BCR-ABL, and mutated p53, as well as many other molecules that are important in cell cycle regulation or immune responses.","Pharmacologic Substance"]
["C82691","Hsp90 Inhibitor AB-010","AB-010|Heat Shock Protein 90 Inhibitor AB-010|Hsp90 Inhibitor AB-010","An orally bioavailable nanoparticle albumin-bound inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Hsp90 inhibitor AB-010 selectively binds to Hsp90, inhibiting its chaperone function and promoting the degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival. This agent may inhibit the growth of a wide variety of cancer cell types; the incorporation of albumin into its formulation may facilitate its endothelial transcytosis through the gp60-regulated albumin transport pathway. Hsp90, a chaperone protein upregulated in a variety of tumor cells, regulates the folding and degradation of many oncogenic signaling proteins.","Pharmacologic Substance"]
["C71467","Hsp90 Inhibitor AUY922","AUY922|Hsp90 Inhibitor AUY922","A derivative of 4,5-diarylisoxazole and a third-generation heat shock protein 90 (Hsp90) inhibitor with potential antineoplastic activity. Hsp90 inhibitor AUY922 has been shown to bind with high affinity to and inhibit Hsp90, resulting in the proteasomal degradation of oncogenic client proteins; the inhibition of cell proliferation; and the elevation of heat shock protein 72 (Hsp72) in a wide range of human tumor cell lines. Hsp90, a 90 kDa molecular chaperone, plays a key role in the conformational maturation, stability and function of other substrate or \"client\" proteins within the cell, many of which are involved in signal transduction, cell cycle regulation and apoptosis, including kinases, transcription factors and hormone receptors.  Hsp72 exhibits anti-apoptotic functions; its up-regulation may be used as a surrogate marker for Hsp90 inhibition.","Pharmacologic Substance"]
["C62517","Hsp90 Inhibitor BIIB021","BIIB-021|BIIB021|CNF2024|Hsp90 Antagonist CNF2024|Hsp90 Inhibitor BIIB021","An orally active inhibitor of heat shock protein 90 (HSP90) with potential antineoplastic activity. HSP90, a chaperon protein upregulated in a variety of tumor cells, regulates the folding and degradation of many oncogenic signaling proteins. HSP90 inhibitor BIIB021 specifically blocks active HSP90, thereby inhibiting its chaperon function and promoting the degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival. As a result, CNF2024 has the potential to inhibit the growth of a wide range of cancer cells in both solid tumors and blood-based cancers.","Pharmacologic Substance"]
["C78846","Hsp90 Inhibitor BIIB028","BIIB028|Hsp90 Inhibitor BIIB028","A small-molecule inhibitor of heat shock protein (Hsp) 90 with potential antineoplastic activity. Hsp90 inhibitor BIIB028 blocks the binding of oncogenic client proteins to Hsp90, which may result in the proteasomal degradation of these proteins and so the inhibition of tumor cell proliferation. Hsp90 is a molecular chaperone that plays a key role in the conformational maturation of oncogenic signaling proteins, such as Her2/Erbb2, Akt, Raf1, Bcr-Abl, and mutated p53, in addition to other molecules involved in cell cycle regulation and immune responses.","Pharmacologic Substance"]
["C92572","Hsp90 Inhibitor Debio 0932","Debio 0932|Hsp90 Inhibitor Debio 0932","An orally active and small molecule inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Hsp90 inhibitor Debio 0932 specifically blocks Hsp90, thereby inhibiting its chaperone function and promoting the degradation of its client proteins, many of which are oncogenic signaling proteins involved in tumor cell proliferation and survival. This may lead to an inhibition of tumor cell proliferation. Hsp90, a chaperone protein upregulated in a variety of tumor cells, regulates the folding, stabilization and degradation of many oncogenic signaling proteins.","Pharmacologic Substance"]
["C116851","Hsp90 Inhibitor DS-2248","DS-2248|Heat Shock Protein 90 Inhibitor DS-2248|Hsp90 Inhibitor DS-2248","An orally active and small molecule inhibitor of heat shock protein 90 (Hsp90), with potential antineoplastic activity. Upon oral administration, Hsp90 inhibitor DS-2248 specifically blocks Hsp90, which inhibits its chaperone function and promotes the proteasomal degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival. This may lead to an inhibition of tumor cell proliferation. Hsp90, a chaperone complex protein upregulated in a variety of tumor cell types, regulates the folding and degradation of many oncogenic signaling proteins.","Pharmacologic Substance"]
["C82387","Hsp90 Inhibitor HSP990","HSP990|Hsp90 Inhibitor HSP990","An orally bioavailable inhibitor of human heat-shock protein 90 (Hsp90) with potential antineoplastic activity. Hsp90 inhibitor Hsp990 binds to and inhibits the activity of Hsp90, which may result in the proteasomal degradation of oncogenic client proteins, including HER2/ERBB2, and the inhibition of tumor cell proliferation. Hsp90, upregulated in a variety of tumor cells, is a molecular chaperone that plays a key role in the conformational maturation, stability and function of oncogenic signaling proteins, such as HER2/ERBB2, AKT, RAF1, BCR-ABL, and mutated p53, as well as many other molecules that are important in cell cycle regulation and/or immune responses.","Pharmacologic Substance"]
["C84836","Hsp90 Inhibitor MPC-3100","Hsp90 Inhibitor MPC-3100|MPC-3100","An orally bioavailable, synthetic, second-generation small-molecule inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Hsp90 inhibitor MPC-3100 selectively binds to Hsp90, thereby inhibiting its chaperone function and promoting the degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival; this agent may inhibit the growth and survival of a wide variety of cancer cell types. Hsp90, a chaperone protein upregulated in a variety of tumor cells, regulates the folding, stability, and degradation of many oncogenic signaling proteins.","Pharmacologic Substance"]
["C101227","Hsp90 Inhibitor PU-H71","9H-Purine-9-propanamine, 6-amino-8-((6-iodo-1,3-benzodioxol-5-yl)thio)-N-(1-methylethyl)-|Hsp90 Inhibitor PU-H71|PU-H-71|PU-H71|PUH71","A purine-based heat shock protein 90 (Hsp90) inhibitor with potential antineoplastic activity. Hsp90 inhibitor PU-H71 specifically inhibits active Hsp90, thereby inhibiting its chaperone function and promoting the proteasomal degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival. This may result in the inhibition of cellular proliferation in susceptible tumor cell populations. Hsp90, a molecular chaperone protein, is upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C91068","Hsp90 Inhibitor SNX-5422 Mesylate","Hsp90 Inhibitor SNX-5422 Mesylate|SNX-5422 Mesylate|SNX-5422 mesylate|SNX-5422","The orally bioavailable mesylate salt of a synthetic prodrug targeting the human heat-shock protein 90 (Hsp90) with potential antineoplastic activity. Although the mechanism of action remains to be fully elucidated, Hsp90 inhibitor SNX-5422 is rapidly converted to SNX-2112, which accumulates more readily in tumors relative to normal tissues. SNX-2112 inhibits Hsp90, which may result in the proteasomal degradation of oncogenic client proteins, including HER2/ERBB2, and the inhibition of tumor cell proliferation. Hsp90 is a molecular chaperone that plays a key role in the conformational maturation of oncogenic signaling proteins, such as HER2/ERBB2, AKT, RAF1, BCR-ABL, and mutated p53, as well as many other molecules that are important in cell cycle regulation or immune responses.","Pharmacologic Substance"]
["C74040","Hsp90 Inhibitor SNX-5542 Mesylate","Hsp90 Inhibitor SNX-5542 Mesylate|SNX-5542 Mesylate","The orally bioavailable mesylate salt of a synthetic prodrug targeting the human heat-shock protein 90 (Hsp90) with potential antineoplastic activity. Although the mechanism of action remains to be fully elucidated, Hsp90 inhibitor SNX-5542 is rapidly converted to SNX-2112, which accumulates in tumors relative to normal tissues. SNX-2112 inhibits Hsp90, which may result in the proteasomal degradation of oncogenic client proteins, including HER2/ERBB2, and the inhibition of tumor cell proliferation. Hsp90 is a molecular chaperone that plays a key role in the conformational maturation of oncogenic signaling proteins, such as HER2/ERBB2, AKT, RAF1, BCR-ABL, and mutated p53, as well as many other molecules that are important in cell cycle regulation or immune responses.","Pharmacologic Substance"]
["C79835","Hsp90 Inhibitor XL888","Heat Shock Protein 90 Inhibitor XL888|Hsp90 Inhibitor XL888|XL888","An orally bioavailable, ATP-competitive, small-molecule inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Hsp90 inhibitor XL888 specifically binds to Hsp90, inhibiting its chaperone function and promoting the proteasomal degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival; inhibition of tumor cell proliferation may result. Hsp90, a chaperone complex protein upregulated in a variety of tumor cell types, regulates the folding and degradation of many oncogenic signaling proteins, including Her-2 and Met.","Pharmacologic Substance"]
["C88318","HSV-1 HF10","HF10|HSV-1 HF10|HSV1 HF10|Herpes Simplex Virus Type 1 HF10","A non-engineered, naturally oncolytic, replication-competent spontaneous herpes simplex virus (HSV) type I mutant variant. Upon intratumoral injection, HSV1 HF10 transfects, replicates in, and lyses rapidly dividing cells such as tumor cells. In addition, this agent may increase host immune responses that may kill non-infected tumor cells.","Pharmacologic Substance"]
["C67047","HSV-TK-Transduced Donor Lymphocytes","HSV-TK Engineered Donor Lymphocytes|HSV-TK-Transduced Donor Lymphocytes|HSVTK Retrovirally-transduced Donor T Lymphocytes","A preparation of donor lymphocytes transduced with the suicide gene herpes simplex virus thymidine kinase (HSV-TK) with potential immunomodulating activity. Administration of HSV-TK-transduced lymphocytes after T cell-depleted allogeneic stem cell transplantation allows an early controllable immune reconstitution, which takes advantage of the antitumor effect of donor lymphocytes and helps to mitigate the risk of post-transplant opportunistic infection. To control graft-versus-host disease (GvHD) due to donor lymphocyte infusion, HSV-TK-transduced donor lymphocytes are selectively eliminated by administration of the antiviral agent ganciclovir. Ganciclovir, a prodrug, is readily phosphorylated by the suicide gene HSV-TK within HSV-TK-transduced lymphocytes to its monophosphate form and, subsequently, converted into its active triphosphate form, which specifically kills HSV-TK- transduced donor lymphocytes.","Cell"]
["C71761","hTERT I540/R572Y/D988Y Multipeptide Vaccine","hTERT I540/R572Y/D988Y Multipeptide Vaccine","A peptide vaccine consisting of multiple epitopes derived from the human telomerase reverse transcriptase (hTERT), the catalytic subunit of human telomerase, with potential immunostimulating and antineoplastic activities. hTERT I540/R572Y/D988Y multipeptide vaccine contains strongly antigenic peptide epitopes I540 (9-mer), R572Y (9-mer) and D988Y (10-mer). Vaccination with this agent may elicit a cytotoxic T cell (CTL) response against telomerase-expressing tumor cells. Directly linked to tumorigenesis, telomerase is expressed in the majority of human cancer cells but is infrequently expressed in normal cells.","Immunologic Factor|Pharmacologic Substance"]
["C99116","hTERT mRNA/Survivin Peptide-double-loaded Autologous Dendritic Cell Vaccine","Procure|hTERT mRNA/Survivin Peptide-double-loaded Autologous Dendritic Cell Vaccine","A cancer vaccine containing autologous dendritic cells (DCs) that are pulsed with mRNA encoding human telomerase reverse transcriptase (hTERT) and survivin peptide, with potential immunostimulatory and antineoplastic activities. Upon administration, hTERT mRNA/survivin peptide-double-loaded autologous dendritic cell vaccine may elicit an immune response against cancer cells expressing hTERT and survivin by activating cytotoxic T-cells (CTLs), natural killer cells (NKs), and B-lymphocytes. The tumor associated antigens (TAAs) hTERT, the catalytic subunit of human telomerase, and survivin, a member of the inhibitor of apoptosis (IAP) family of proteins, may be upregulated in certain tumor cell types and play key roles in tumor cell growth and survival.","Pharmacologic Substance"]
["C119616","hTERT Multipeptide/Montanide ISA-51 VG/Imiquimod Vaccine GX 301","GX 301|GX301|hTERT Multipeptide/Montanide ISA-51 VG/Imiquimod Vaccine GX 301","A therapeutic cancer vaccine consisting of four epitopes derived from the human telomerase reverse transcriptase (hTERT), the catalytic subunit of human telomerase, including hTERT (540-548) acetate, hTERT (611-626) acetate, hTERT (672-686) acetate and hTERT (766-780) acetate, emulsified individually in the adjuvant montanide ISA-51 VG and administered with the immune response modifier (IRM) imiquimod, with potential immunostimulating and antineoplastic activities. Each hTERT peptide emulsion is administered individually by intradermal injection. Subsequently, imiquimod is applied topically to the injection site(s). Vaccination with GX 301 may elicit a cytotoxic T-cell (CTL) response against telomerase-expressing tumor cells. Telomerase is expressed in the majority of human cancer cells, infrequently expressed in normal cells, and is directly linked to tumorigenesis. Imiquimod stimulates cytokine production through the activation of toll-like receptor 7 (TLR-7), and also exhibits antiproliferative effects. Montanide ISA-51, also known as incomplete Freund's adjuvant (IFA), is a stabilized water-in-oil emulsion containing mineral oil with mannide oleate, which contains vegetable-grade (VG) oleic acid derived from olive oil. ISA-51 non-specifically stimulates cell-mediated immune responses to antigens.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C80055","hTERT Vaccine V934/V935","V934/V935|hTERT Vaccine V934/V935","A cancer vaccine directed against human telomerase reverse transcriptase (hTERT), the catalytic subunit of human telomerase, with potential immunostimulating and antineoplastic activities. Upon administration, hTERT vaccine V934/V935 may elicit a cytotoxic T cell (CTL) response against telomerase-expressing tumor cells, which may result in tumor cell death. Telomerase is involved in the restoration and maintenance of telomere length and so the functional lifespan of cells. Abnormally reactivated in tumorigenesis, telomerase is expressed in the majority of human cancer cells but is not expressed or is expressed at very low levels in normal cells.","Immunologic Factor|Pharmacologic Substance"]
["C102879","hTERT/Survivin/CMV Multipeptide Vaccine","hTERT/Survivin/CMV Multipeptide Vaccine","A vaccine containing multiple peptides derived from the human telomerase reverse transcriptase (hTERT), survivin and cytomegalovirus (CMV), with potential immunostimulating and antineoplastic activities. Upon administration, hTERT/survivin/CMV multipeptide vaccine may elicit a cytotoxic T cell (CTL) response against tumor cells espressing hTERT, survivin and CMV. hTERT, the catalytic subunit of telomerase, and the inhibitor of apoptosis (IAP) family member survivin, both often upregulated in tumor cells, play key roles in tumor cell growth and survival. Further, CMV expression is correlated with certain types of cancer.","Pharmacologic Substance"]
["C84755","hTERT/Survivin/Melanoma Tumor Cell-Derived mRNA-Transfected Dendritic Cell Vaccine","hTERT/Survivin/Melanoma Tumor Cell-Derived mRNA-Transfected Dendritic Cell Vaccine","A cancer vaccine containing dendritic cells (DCs) that are transfected with messenger RNA (mRNA) encoding human telomerase reverse transcriptase (hTERT) and survivin in addition to patient-specific melanoma-derived mRNA with potential immunostimulatory and antineoplastic activities. Upon administration, hTERT/survivin/melanoma tumor cell-derived mRNA-transfected dendritic cell vaccine may elicit a highly specific cytotoxic T-cell (CTL) response against melanoma cells expressing hTERT, survivin, and patient-specific melanoma-associated antigens. hTERT, the catalytic subunit of human telomerase, and survivin, a member of the inhibitor of apoptosis (IAP) family of proteins, may be upregulated in certain tumor cell types, playing key roles in tumor cell growth and survival.","Pharmacologic Substance"]
["C119737","hTERT-encoding DNA Vaccine INVAC-1","INVAC-1|hTERT-encoding DNA Vaccine INVAC-1","A DNA vaccine consisting of a plasmid encoding a modified, inactive form of the human telomerase reverse transcriptase (hTERT), the catalytic subunit of human telomerase which synthesizes telomeric DNA at the chromosome ends, fused to ubiquitin, with potential immunostimulating and antineoplastic activities. Upon intradermal vaccination of the hTERT encoding DNA vaccine INVAC-1 in combination with electroporation, hTERT protein is expressed and activates the immune system to mount a cytotoxic T-cell (CTL) response against telomerase-expressing tumor cells, which may result in tumor cell death. Telomerase prolongs the functional lifespan of cells via the restoration and maintenance of telomere length. Abnormally activated in tumorigenesis, telomerase is expressed in the majority of human cancer cells, but its expression is low or non-existent in normal cells. hTERT conjugation to ubiquitin, a 76 amino-acid peptide involved in the regulation of normal protein intracellular turnover in the cytoplasm, enhances proteasome-dependent degradation of the hTERT protein, increases hTERT presentation by major histocompatibility complex (MHC) class I molecules and results in an increased immune response against hTERT.","Gene or Genome|Pharmacologic Substance"]
["C2509","Hu14.18-IL2 Fusion Protein","EMD 273063|Hu 14.18/IL - 2 Fusion Protein|Hu14.18-IL2 Fusion Protein|Hu14.18-IL2|hu14.18-interleukin-2 fusion protein","A recombinant protein consisting of the hu14.18 monoclonal antibody fused to the cytokine interleukin-2 (IL2) with potential antineoplastic activity. The monoclonal antibody portion of the hu14.18-IL2 fusion protein binds to tumor cells expressing the GD2 antigen (melanoma, neuroblastoma and certain other tumors); the Fc component of the fusion protein antibody moiety and natural killer (NK) cells mediate antibody-dependent cell-mediated cytotoxicity (ADCC) and complement-dependent cellular cytotoxicity (CDCC) towards GD2-expressing tumor cells. The localized IL2 moiety of the fusion protein stimulates NK and T-cell antitumor cellular immune responses.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82415","HuaChanSu","HuaChanSu","A traditional Chinese medicine (TCM) containing a water soluble Bufo toad skin extract that includes the cardiac glycosides bufalin, cinobufagin and resibufogenin with potential antineoplastic and antiangiogenic activities. Although the exact mechanism of action of this TCM has yet to be fully elucidated, huachansu, which may be administered in an injectable form, may induce cell cycle arrest and apoptosis by suppressing the expression of anti-apoptotic proteins, such as Bcl-2, while inducing the expression of pro-apoptotic proteins, such as BAX.","Pharmacologic Substance"]
["C125001","Huaier Extract Granule","Huaier Extract Granule|Huaier Granule|Trametes robiniophila murr Extract Granule","An orally bioavailable traditional Chinese medicine (TCM) composed of a granule containing an aqueous extract of Trametes robiniophila murr (Huaier), a mushroom found on hardwood tree trunks, with potential antineoplastic and anti-angiogenic activities. Although the exact mechanism of action through which Huaier exerts its effects is largely unknown, upon administration, this agent induces cell cycle arrest and apoptosis, and inhibits proliferation and migration of susceptible cancer cells through the modulation of various signal transduction pathways involved in carcinogenesis and angiogenesis.","Pharmacologic Substance"]
["C2626","Huang Lian","Huang Lian|Rhizoma Coptidis","A Chinese herb of a desiccated root from the plant Coptis chinensis. Although the mechanism of action remains to be fully elucidated, Huang Lian has antibacterial, antifungal, and antiprotozoal activities. In addition, this herb exhibits antioxidant property that influences positively on lipid metabolism, cause dilation of blood vessels, and may slow the growth of tumor cells. This herb contains rich amount of phytogens, such as berberine, palmatine, jatrorrhizine, columbamine, geniposide, and anti-HIV compound baicalin, which might explain the broad effects of this herb. Huang Lian is commonly used to treat diarrhea or dysentery in Chinese medicine.","Pharmacologic Substance"]
["C74041","huBC1-huIL12 Fusion Protein AS1409","AS1409|huBC1-huIL12 Fusion Protein AS1409","An immunoconjugate consisting of the anti-tumor cytokine interleukin-12 (IL-12) fused to the tumor-targeting antibody BC1 with potential immunostimulatory and antineoplastic activities. The antibody moiety of huBC1-huIL12 fusion protein AS1409 binds to the human fibronectin splice variant ED-B, delivering IL-12 directly to the tumor vasculature; tumor vasculature-targeted IL-12 initiates localized immune cascade responses and exhibits cytotoxic and anti-angiogenic activity while minimizing the systemic side effects of IL-12. The human fibronectin splice variant ED-B is over-expressed in the extracellular matrix and blood vessels of tumor tissues.","Pharmacologic Substance"]
["C29095","HuCC49deltaCH2-PA-DOTA","HuCC49DCH2-PA-DOTA|HuCC49deltaCH2-PA-DOTA","An immunoconjugate comprised of a humanized monoclonal antibody with antitumor activity. The monoclonal antibody CC49 is developed from the murine monoclonal antibody B72.3 and is humanized by grafting the hypervariable regions onto the variable light (VL) and variable heavy (VH) frameworks of the monoclonal antibodies LEN and 21/28' CL. In addition the CH2 domain in the constant region is deleted to increase plasma clearance. The resultant antibody binds to the pancarcinoma tumor-associated glycoprotein (TAG)-72 with high affinity. Furthermore, the antibody is conjugated to PA-DOTA, a bifunctional chelating agent and commonly radiolabeled, resulting in an effective agent for radioimmunotherapy.","Pharmacologic Substance"]
["C116788","Human Combinatorial Antibody Library-based Monoclonal Antibody VAY736","HuCAL-based Antibody VAY736|Human Combinatorial Antibody Library-based Monoclonal Antibody VAY736|VAY736","A fully human combinatorial antibody library (HuCAL)-derived monoclonal antibody targeting the B-cell-activating factor receptor (BAFF-R), with potential anti-inflammatory and antineoplastic activities. Upon administration of HuCAL-based antibody VAY736, the antibody targets and binds to BAFF-R, which inhibits both BAFF/BAFF-R interaction and BAFF-R-mediated signaling. This may decrease cell growth in tumor cells expressing BAFF-R. BAFF-R, also known as tumor necrosis factor receptor superfamily member 13C, is overexpressed in certain tumor cell types and autoimmune diseases. In cancer cells, BAFF-R plays a key role in B-cell proliferation and survival. VAY736 was developed using HuCAL technology.","Immunologic Factor|Pharmacologic Substance"]
["C2759","Human gp100 Plasmid DNA Vaccine","GP100 DNA/VR4951 (Vical)|Human gp100 Plasmid DNA Vaccine|gp100 Plasmid DNA","A vaccine consisting of a plasmid DNA encoding the human melanoma-associated antigen gp100.  Upon administration, expressed gp100 antigen may stimulate a cytotoxic T cell HLA-A2.1-restricted immune response against tumor cells that express this antigen, resulting in tumor cell lysis. (NCI05)","Gene or Genome|Pharmacologic Substance"]
["C66980","Human MHC Non-Restricted Cytotoxic T-Cell Line TALL-104","Human MHC Non-Restricted Cytotoxic T-Cell Line TALL-104|TALL-104","An allogeneic human cytotoxic T-lymphocyte cell line (TALL-104) with potential antineoplastic activity. TALL-104 is an IL-2-dependent human leukemic T cell line, expressing CD8 and T-cell receptor CD3, but not CD16. Because these cells are endowed with MHC-non-restricted killer activity, TALL-104 has destructive potential against a broad range of tumors, while sparing normal cells. Upon administration, TALL-104 targets and interacts with tumor cells and activates apoptotic and necrotic pathways, eventually leading to lysis of tumor cells. In addition, TALL-104 may induce secretion of various cytokines, such as interferon-gamma, thereby potentially enhancing the cytotoxic activity.","Cell|Pharmacologic Substance"]
["C29089","Human MOAB LICO 28a32","Human MOAB LICO 28a32","A human monoclonal immunoglobulin M (IgM) antibody with potential antineoplastic activity.  Human MOAB LICO 28a32 binds to the colon tumor-associated antigen 28A32 (CTAA 28A32) found on the cell surface and in the cytoplasm of colon carcinoma cells. (NCI04)","Pharmacologic Substance"]
["C62532","Human Monoclonal Antibody 216","Human Monoclonal Antibody 216|MoAb 216","A naturally-occurring human IgM monoclonal antibody with potential antineoplastic activity. Human monoclonal antibody 216, derived from the gene VH4-34, binds to the glycosylated epitope CDIM on the surface of both malignant and normal B cells. Upon binding to B cells, this antibody may crosslink two or more CDIM molecules, resulting in the formation of cell membrane pores, the disruption of cell membrane integrity, and B cell lysis; this mechanism of antibody-mediated cell death is direct and does not involve mechanisms of complement-mediated cytotoxicity or antibody-dependent cell-mediated cytotoxicity (ADCC). CDIM is the glyco-moiety of a 75kD B-cell cell surface glycoprotein.","Amino Acid, Peptide, or Protein"]
["C77858","Human Monoclonal Antibody B11-hCG Beta Fusion Protein CDX-1307","CDX-1307|Human Monoclonal Antibody B11-hCG Beta Fusion Protein CDX-1307","A human monoclonal antibody (B11) directed against the mannose receptor and linked to the beta-subunit of human chorionic gonadotropin (hCG beta) with potential immunostimulating and antineoplastic activities. The monoclonal antibody moiety of human monoclonal antibody B11-hCG beta fusion protein CDX-1307 binds to mannose receptors on antigen presenting cells (APCs), including human dendritic cells (DCs) and macrophages. Upon internalization and processing, APCs present the processed hCG beta antigen on their cell surfaces, which may initiate an antibody-dependent cell-mediated cytotoxicity (ADCC) response against hCG beta-expressing tumor cells. The tumor-associated antigen (TAA) hCG beta is selectively overexpressed by a number of tumors including breast, colorectal, pancreatic, bladder and ovarian tumors; its expression may correlate with the stage of disease.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C25758","Human Papillomavirus 16 E7 Peptide","HPV-16 E7 Peptide|Human Papillomavirus 16 E7 Peptide","A peptide vaccine consisting of amino acids 12 through 20 of the viral oncoprotein human papillomavirus (HPV) 16 E7. Vaccination with HPV-16 E7 peptide may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for HPV-16 E7, resulting in decreased tumor growth. HPV-16 infection is tumorigenic and highly associated with cervical cancer. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C2569","Human Papillomavirus 16 E7 Peptide/Padre 965.10","HPV16 E7/PADRE 965.10|Human Papillomavirus 16 E7 Peptide/Padre 965.10|Lipidated HPV-16 E7/Padre-965.10","A synthetic agent derived from human papillomavirus (HPV) E7 nuclear protein which is used to produce vaccines against HPV infection and HPV-related neoplasms.  HPV E7 oncogenic protein binds the retinoblastoma tumor suppressor protein, pRB, as well as a number of other cellular proteins, and serves as a transcriptional activator.  This protein is important in the induction and maintenance of cellular transformation and is co-expressed in the majority of HPV-containing carcinomas.  PADRE(R) is a proprietary family of molecules that enhances the immune systems response against an administered immunogen such as the HPV E7 nuclear protein. (NCI04)","Pharmacologic Substance"]
["C48395","Human Papillomavirus 16/18 L1 Virus-Like Particle/AS04 Vaccine","Cervarix|GSK-580299|HPV 16/18 L1 VLP/AS04 VAC|Human Papillomavirus 16/18 L1 Virus-Like Particle/AS04 Vaccine|human papillomavirus 16/18 L1 virus-like particle/AS04 vaccine","A recombinant, bivalent, human papillomavirus (HPV) vaccine, containing virus-like particles for HPV types 16 and 18 linked to the adjuvant ASO4, with potential immunoprotective and antineoplastic properties. Upon administration, HPV 16/18 L1 virus-like particle/ASO4 vaccine may generate humoral and cellular immunity against HPV types-16 and -18 antigens, thereby preventing cervical infection upon exposure to HPV types 16 and 18. In addition, this agent may stimulate an antitumoral cellular immune response against cervical cancer associated with HPV infection.","Pharmacologic Substance"]
["C2403","Human Papillomavirus Tumor Antigen Vaccine","Human Papillomavirus TA Vaccine|Human Papillomavirus TA|Human Papillomavirus Tumor Antigen Vaccine|TA-HPV|TA-Human Papillomavirus vaccine","A vaccinia viral based vaccine, encoding epitopes of E6 and E7 proteins from human papillomavirus (HPV) types 16 and 18, with immunostimulatory and antineoplastic activities. HPV types 16 and 18 account for approximately 70% of cervical cancers. Vaccination with this HPV-TA (tumor antigen) vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for E6 and E7 from either type 16 or 18 HPV, resulting in decreased tumor growth.","Immunologic Factor|Pharmacologic Substance"]
["C48396","Human Prostate-Specific Membrane Antigen Plasmid DNA Vaccine","Human PSMA DNA Vaccine|Human Prostate-Specific Membrane Antigen Plasmid DNA Vaccine","A vaccine consisting of a plasmid DNA encoding the human prostate-specific membrane antigen (PSMA). Upon administration, expressed PSMA may stimulate a cytotoxic T cell response against tumor cells that express this antigen, resulting in tumor cell lysis. (NCI05)","Pharmacologic Substance"]
["C118364","hVEGF26-104/RFASE Peptide Vaccine","hVEGF26-104/RFASE Peptide Vaccine|hVEGF26-104/RFASE","A therapeutic cancer vaccine containing a truncated, synthetic peptide mimic of the human angiogenic activator vascular endothelial growth factor (VEGF), consisting of 79 amino acids (amino acids 26-104 of VEGF), and emulsified in the immunoadjuvant RFASE, with potential immunostimulatory and antitumor activities. Upon intramuscular vaccination, the hVEGF26-104 moiety of hVEGF26-104/RFASE acts as an antigen and induces an immune response against VEGF, which results in anti-VEGF antibody binding to and neutralization of endogenous VEGF. This prevents the binding of endogenous VEGF to the VEGF receptor (VEGFR) and blocks VEGFR-mediated endothelial cell signaling, resulting in an inhibition of both angiogenesis and tumor cell proliferation. VEGF plays a key role in angiogenesis, tumor cell proliferation and invasion. RFASE, which belongs to the group of sulpholipopolysaccharides (SLPs), is a synthetic polysaccharide covalently coupled to lipid groups and sulphate groups, and is able to induce a strong humoral immune response upon antigen administration.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C49182","HYB2055","Amplivax|HYB2055|IMO-2055|Imoxine","A second generation synthetic oligonucleotide with immunomodulatory and potential antineoplastic activities. HYB2055 consists of unmethylated CpG dinucleotide motifs that are present abundantly in bacterial and parasitic DNA, and a novel DNA structure, called an immunomer that contributes to metabolic stability of the agent. Upon infections, CpG-containing DNA released from pathogenic organisms triggers host immune responses, which are mediated by the action of intracellular toll-like receptor 9 (TLR9), a pattern recognition receptor. This agent mimics bacterial DNA and selectively activates TLR9, thereby initiating immune signaling pathways, and leading to activation of B-cells and dendritic cells and induction of Th1-type cytokine production.","Organic Chemical|Pharmacologic Substance"]
["C550","Hycanthone","Etrenol|HYC|HYCANTHONE|Hycanthone Mesylate|Hycanthone mesylate|Hycanthone","A thioxanthene derivative of lucanthone with anti-schistosomal activity and potential antineoplastic activity. Hycanthone interferes with parasite nerve function, resulting in parasite paralysis and death.  This agent also intercalates into DNA and inhibits RNA synthesis in vitro. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C551","Hydralazine Hydrochloride","Apresoline|Apressin|HYDRALAZINE HYDROCHLORIDE|Hydralazine Hydrochloride","The hydrochloride salt of hydralazine, a phthalazine derivative with antihypertensive and potential antineoplastic activities. Hydralazine alters intracellular calcium release and interferes with smooth muscle cell calcium influx, resulting in arterial vasodilatation. This agent also inhibits the phosphorylation of myosin protein and chelation of trace metals required for smooth muscle contraction, resulting in an increase in heart rate, stroke volume and cardiac output. In addition to its cardiovascular effects, hydralazine inhibits DNA methyltransferase, which may result in inhibition of DNA methylation in tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C557","Hydroxychloroquine","HYDROXYCHLOROQUINE|Hydroxychloroquine|hydroxychloroquine","A 4-aminoquinoline with immunosuppressive, antiautophagy, and antimalarial activities. Although the precise mechanism of action is unknown, hydroxychloroquine may suppress immune function by interfering with the processing and presentation of antigens and the production of cytokines. As a lysosomotropic agent, hydroxychloroquine raises intralysosomal pH, impairing autophagic protein degradation; hydroxychloroquine-mediated accumulation of ineffective autophagosomes may result in cell death in tumor cells reliant on autophagy for survival.  In addition, this agent is highly active against the erythrocytic forms of P. vivax and malariae and most strains of P. falciparum but not the gametocytes of P. falciparum.","Organic Chemical|Pharmacologic Substance"]
["C960","Hydroxyprogesterone Caproate","17-[(1-Oxohexyl)oxy]pregn-4-ene-3,20-dione|17alpha-Hydroxyprogesterone Caproate|Delalutin|HYDROXYPROGESTERONE CAPROATE|Hydroxyprogesterone Caproate|Hydroxyprogesterone caproate|Makena","A synthetic progestational agent similar to the endogenous progesterone used in hormone therapy or as a female contraceptive. Mimicking the action of progesterone, hydroxyprogesterone caporate binds to and activates nuclear progesterone receptors in the reproductive system and causes the ligand-receptor complex to be translocated to the nucleus where it binds to and promotes expression of target genes. Due to the negative feedback mechanism seen with progesterone, this agent also blocks luteinizing hormone (LH) release from the pituitary gland, thereby leading to an inhibition of ovulation and an alteration in the cervical mucus and endometrium. Furthermore, without stimulation of LH, estrogen release from the ovaries is stopped, hence impeding the growth of estrogen-sensitive tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C63690","Hydroxytyrosol","2-(3,4-Dihydroxyphenyl)ethanol|3,4-DHPEA|3,4-Dihydroxyphenylethanol|4-(2-Hydroxyethyl)-1,2-benzenediol|HYDROXYTYROSOL|Hydroxytyrosol","A phenolic phytochemical naturally occurring in extra virgin olive oil, with potential antioxidant, anti-inflammatory and cancer preventive activities. Although the mechanisms of action through which hydroxytyrosol exerts its effects have yet to be fully determined, this agent affects the expression of various components of the inflammatory response, possibly through the modulation of the nuclear factor-kappa B (NF-kB) pathway. The effects include the modulation of pro-inflammatory cytokines, such as the inhibition of interleukin-1alpha (IL-1a), IL-1beta, IL-6, IL-12, and tumor necrosis factor-alpha (TNF-a); increased secretion of the anti-inflammatory cytokine IL-10; inhibition of the production of certain chemokines, such as C-X-C motif chemokine ligand 10 (CXCL10/IP-10), C-C motif chemokine ligand 2 (CCL2/MCP-1), and macrophage inflammatory protein-1beta (CCL4/MIP-1b); and inhibition of the expression of the enzymes inducible nitric oxide synthase (iNOS/NOS2) and prostaglandin E2 synthase (PGES), which prevent the production of nitric oxide (NO) and prostaglandin E (PGE2), respectively. In addition, hydroxytyrosol is able to regulate the expression of other genes involved in the regulation of tumor cell proliferation, such as extracellular signal-regulated and cyclin-dependent kinases. Also, hydroxytyrosol scavenges free radicals and prevents oxidative DNA damage. This induces apoptosis and inhibits proliferation in susceptible cancer cells.","Pharmacologic Substance"]
["C560","Hydroxyurea","Droxia|HYDROXYUREA|Hydrea|Hydroxycarbamide|Hydroxyurea|Litalir|Onco-Carbide|Onco-carbide|Oncocarbide|Oxeron|SQ 1089|SQ-1089|Syrea|WR 83799|hydroxyurea","A monohydroxyl-substituted urea (hydroxycarbamate) antimetabolite. Hydroxyurea selectively inhibits ribonucleoside diphosphate reductase, an enzyme required to convert ribonucleoside diphosphates into deoxyribonucleoside diphosphates, thereby preventing cells from leaving the G1/S phase of the cell cycle.  This agent also exhibits radiosensitizing activity by maintaining cells in the radiation-sensitive G1 phase and interfering with DNA repair. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C37456","Hypericin","4,5,7,4',5',7'-Hexahydroxy-2,2'-dimethyl-mesonapthtodianthron|HYPERICIN|Hypericin","An anthraquinone derivative that is naturally found in the yellow flower of Hypericum perforatum (St. John's wort) with antidepressant, potential antiviral, antineoplastic and immunostimulating activities. Hypericin appears to inhibit the neuronal uptake of serotonin, norepinephrine, dopamine, gamma-amino butyric acid (GABA) and L-glutamate, which may contribute to its antidepressant effect. Hypericin may also prevent the replication of encapsulated viruses probably due to inhibition of the assembly and shedding of virus particles in infected cells. This agent also exerts potent phototoxic effects by triggering apoptotic signaling that results in formation of reactive oxygen species.","Pharmacologic Substance"]
["C71722","Hypoxia-Activated Prodrug TH-302","HAP TH-302|Hypoxia-Activated Prodrug TH-302|TH-302","A hypoxia-activated prodrug consisting of a 2-nitroimidazole phosphoramidate conjugate with potential antineoplastic activity. The 2-nitroimidazole moiety of hypoxia-activated prodrug TH-302 acts as a hypoxic trigger, releasing the DNA-alkylating dibromo isophosphoramide mustard moiety within hypoxic regions of tumors. Normoxic tissues may be spared due to the hypoxia-specific activity of this agent, potentially reducing systemic toxicity.","Pharmacologic Substance"]
["C101523","Hypoxia-activated Prodrug TH-4000","Hypoxia-activated Prodrug TH-4000|Hypoxin|PR610|TH-4000","A proprietary, hypoxia-activated prodrug with potential antineoplastic activity. Upon administration, the hypoxia-activated prodrug TH-4000 is activated in the hypoxic cells within tumors into an irreversible pan-HER inhibitor via a mechanism of action not yet fully elucidated. As a result, this agent inhibits cellular proliferation and differentiation of tumor cells overexpressing HER kinases, which belong to the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases. Healthy, normal tissues may be spared due to the hypoxia-specific activity of this agent, potentially reducing systemic toxicity.","Pharmacologic Substance"]
["C2357","I 131 Antiferritin Immunoglobulin","I 131 Antiferritin Immunoglobulin|I 131-AFI|I 131-antiferritin IgG|Iodine I 131 Antiferritin Immunoglobulin|immunoglobulin, iodine I 131 antiferritin","A radioimmunoconjugate of a rabbit antihuman ferritin IgG labeled with iodine 131 (I-131). Using anti-ferritin IgG as a carrier for I-131 may result in the targeted imaging and/or destruction of cells expressing ferritin. Observed in 35% to 100% of patients with hepatocellular carcinoma, high serum ferritin levels may be due to ferritin production by the tumor cells, or related to the associated iron overload and/or cirrhosis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2477","I 131 Monoclonal Antibody A33","I 131 Monoclonal Antibody A33|Iodine I 131 Monoclonal Antibody A33","A radioimmunoconjugate of a humanized monoclonal antibody (MoAb) A33 labelled with Iodine 131 (I-131). MoAb A33 recognizes A33 antigen, a 43 KDa transmembrane glycoprotein of the immunoglobulin superfamily, highly and homogenously expressed in 95% of colorectal cancers, with only restricted expression in normal colonic mucosa. Using MoAb A33 as a carrier for I-131 results in the targeted imaging and/or destruction of cells expressed A33 antigen.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C26442","I 131 Monoclonal Antibody CC49","I 131 Monoclonal Antibody CC49|Iodine I 131 Monoclonal Antibody CC49","A radioimmunoconjugate of the humanized monoclonal antibody CC49 labeled with iodine I 131. Iodine I 131 monoclonal antibody CC49 delivers beta and gamma radiation-emitting I 131 radionuclide specifically to tumor cells that express tumor-associated glycoprotein (TAG)-72, allowing localization of TAG-72-expressing tumor cells with radioimaging devices in diagnostic applications or resulting in specific TAG-72-expressing tumor cell radiocytotoxicity in therapeutic applications. Monoclonal antibody CC49 binds to TAG-72, a pancarcinoma antigen, with high affinity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2515","I 131 Monoclonal Antibody F19","131I-mAbF19|I 131 Monoclonal Antibody F19|Iodine I 131 Monoclonal Antibody F19","A radioimmunoconjugate of a murine monoclonal antibody (MoAb) F19 labelled with Iodine 131 (I-131). MoAb F19 was raised against fibroblast activation protein (FAP), which is highly expressed by tumor stromal cells. Using MoAb F19 as a carrier for I-131 results in the targeted imaging and/or destruction of cells overexpressed FAP.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2103","I 131 Monoclonal Antibody Lym-1","I 131 Monoclonal Antibody Lym-1|Iodine I 131 Monoclonal Antibody Lym-1|Oncolym","A radioimmunoconjugate of a murine monoclonal antibody, MoAb Lym-1, labeled with iodine 131 (I-131). MoAb Lym-1 recognizes an epitope of the histocompatibility antigen HLA-DR, which is over-expressed on most B-cell lymphomas. I-131 MoAb Lym-1 delivers beta and gamma radiation emitting I-131 nuclide directly to tumor cells that express HLA-DR, thereby allowing imaging and/or treatment of cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C90574","IAP Inhibitor AT-406","AT-406|IAP Inhibitor AT-406|Pyrrolo(1,2-a)(1,5)diazocine-8-carboxamide, n-((1,1'-biphenyl)-2-ylmethyl)decahydro-5-(((2s)-2-(methylamino)-1-oxopropyl)amino)-3-(3-methyl-1-oxobutyl)-6-oxo-, (5s,8s,10ar)|SM-406","An orally bioavailable inhibitor of IAP (Inhibitor of Apoptosis Protein) family of proteins with potential apoptotic inducing and antineoplastic activity. IAP inhibitor AT-406 selectively inhibits the biological activity of IAP proteins, including X chromosome-linked IAP (XIAP), the cellular IAPs 1 (c-IAP1) and 2 (c-IAP2) and melanoma inhibitor of apoptosis protein (ML-IAP). This may restore and promote the induction of apoptosis through apoptotic signaling pathways. AT-406 may work synergistically with cytotoxic drugs to overcome tumor cell resistance to apoptosis. IAPs are overexpressed by many cancer cell types, suppressing apoptosis by binding and inhibiting active caspases-3, -7 and -9 via their BIR (baculoviral lAP repeat) domains.","Pharmacologic Substance"]
["C78484","IAP Inhibitor HGS1029","AEG40826-2HCl|HGS1029|IAP Inhibitor HGS1029","The hydrochloride salt of a small-molecule inhibitor of IAP (Inhibitor of Apoptosis Protein) family proteins with potential antineoplastic activity. IAP inhibitor HGS1029 selectively inhibits the biological activity of IAP proteins, which may restore apoptotic signaling pathways; this agent may work synergistically with cytotoxic drugs to overcome tumor cell resistance to apoptosis. IAPs are overexpressed by many cancer cell types, suppressing apoptosis by binding and inhibiting active caspases-3, -7 and -9 via their BIR (baculoviral lAP repeat) domains.","Organic Chemical|Pharmacologic Substance"]
["C123922","iAPA-based Dendritic Cells/Cytotoxic T Lymphocytes","Inhibition of Antigen Presentation Attenuators-based Dendritic Cells/Cytotoxic T Lymphocytes|iAPA-DC/CTL|iAPA-based Dendritic Cells/Cytotoxic T Lymphocytes","A cell-based product composed of dendritic cells (DCs) pulsed with tumor-associated antigens (TAAs) and devoid of the inhibitory effect of antigen presentation attenuators (iAPA) combined with cytotoxic T-lymphocytes (CTLs) (iAPA-DC/CTL), with potential immunostimulating and antineoplastic activities.  DCs are transduced with a viral vector containing small interfering RNAs (siRNAs) against APAs, which prevents the expression of APA genes and inhibits attenuation of antigen presentation. Upon administration of iAPA-DC/CTL, the DCs are able to efficiently present antigens to the immune system, stimulate the immune system against tumor-associated antigens (TAAs) and hyperactivate TAA-specific CTLs and T-helper cells. Also, the iAPA-based DCs inhibit the activity of the T-regulatory cells (Tregs), thereby abrogating their negative effect on CTL activation and preventing their immunosuppressive activity against TAAs. Altogether, this inhibits tumor cell proliferation. Additionally, the administered CTLs induce direct cancer cell lysis. APAs negatively regulate antigen presentation, activate Tregs and their immunosuppressive activity, affect inflammatory cytokine production by DCs, and negatively regulate the immunostimulatory activity of DCs; they have an overall inhibitory effect on the stimulation of the immune system.","Pharmacologic Substance"]
["C81934","Ibrutinib","2-Propen-1-one, 1-((3R)-3-(4-amino-3-(4-phenoxyphenyl)-1h-pyrazolo(3,4-d)pyrimidin-1-yl)-1-piperidinyl)-|BTK Inhibitor PCI-32765|CRA-032765|IBRUTINIB|Ibrutinib|Imbruvica|PCI-32765","An orally bioavailable, small-molecule inhibitor of Bruton's tyrosine kinase (BTK) with potential antineoplastic activity. Upon oral administration, ibrutinib binds to and irreversibly inhibits BTK activity, thereby preventing both B-cell activation and B-cell-mediated signaling. This leads to an inhibition of the growth of malignant B cells that overexpress BTK. BTK, a member of the src-related BTK/Tec family of cytoplasmic tyrosine kinases, is required for B cell receptor signaling, plays a key role in B-cell maturation, and is overexpressed in a number of B-cell malignancies. The expression of BTK in tumor cells is also associated with increased proliferation and survival.","Pharmacologic Substance"]
["C106123","iC9-GD2-CD28-OX40-expressing T Lymphocytes","iC9-GD2 T Lymphocytes|iC9-GD2-CD28-OX40-expressing T Lymphocytes","Modified T-lymphocytes expressing a 3rd generation chimeric antigen receptor (CAR) specific for the disialoganglioside GD2, which contains the CD3zeta chain, the signaling domains of the co-stimulatory molecules CD28 and CD134 (OX-40) and the suicide gene inducible caspase 9 (iCasp9), with potential immunomodulating and antineoplastic activities. Upon administration, iC9-GD2-CD28-OX40-expressing T lymphocytes target the GD2 antigen on tumor cells, thereby providing selective toxicity towards GD2-expressing tumor cells. iCasp9 consists of a human FK506 drug-binding domain with an F36V mutation (FKBP12-F36V) linked to human caspase 9. If the administered T cells lead to unacceptable side effects, the chemical homodimerizer AP1903 can be administered, which binds to the drug binding FKBP12-F36V domain and activates caspase 9, resulting in the apoptosis of the administered T-cells. The tumor associated antigen GD2 is overexpressed on the surface of almost all tumors of neuroectodermal origin. OX40 and CD28, both T-cell surface-associated co-stimulatory molecules, are required for full T-cell activation.","Cell|Pharmacologic Substance"]
["C99160","Icotinib Hydrochloride","BPI-2009H|Conmana|Icotinib Hydrochloride","An orally available quinazoline-based inhibitor of epidermal growth factor receptor (EGFR), with potential antineoplastic activity. Icotinib selectively inhibits the wild-type and several mutated forms of EGFR tyrosine kinase. This may lead to an inhibition of EGFR-mediated signal transduction and may inhibit cancer cell proliferation. EGFR, a receptor tyrosine kinase, has been upregulated in a variety of cancer cell types.","Organic Chemical|Pharmacologic Substance"]
["C79808","Icrucumab","Anti-VEGFR-1 Monoclonal Antibody IMC-18F1|Anti-Vascular Endothelial Growth Factor Receptor-1 Monoclonal Antibody IMC-18F1|ICRUCUMAB|IMC-18F1|IMC18F1|Icrucumab","A fully human IgG1 monoclonal antibody directed against human vascular endothelial growth factor receptor 1 (VEGFR-1/FLT-1) with potential antiangiogenesis and antineoplastic activities. Icrucumab specifically binds to and inhibits the activity of VEGFR-1, which may prevent the activation of downstream signaling pathways and so inhibit tumor angiogenesis; the subsequent reduction in tumor nutrient supply may inhibit tumor cell proliferation. Tumor cell overexpression of VEGFR-1 may be associated with tumor angiogenesis and tumor cell proliferation and invasion; VEGFR-1 may modulate VEGFR-2 signaling.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C562","Idarubicin","(1S,3S)-3-Acetyl-1,2,3,4,6,11-hexahydro-3,5,12-trihydroxy-6,11-dioxo-1-naphthacenyl-3-amino-2,3,6-trideoxy-alpha-L-hexopyranoside|(7S-cis)-9-Acetyl-7-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,9,11-trihydroxy-5,12-naphthacenedione|4-DMDR|4-Demethoxydaunomycin|4-Demethoxydaunorubicin|4-demethoxydaunorubicin|IDARUBICIN|Idarubicin|idarubicin","A semisynthetic 4-demethoxy analogue of the antineoplastic anthracycline antibiotic daunorubicin. Idarubicin intercalates into DNA and interferes with the activity of topoisomerase II, thereby inhibiting DNA replication, RNA transcription and protein synthesis. Due to its high lipophilicity, idarubicin penetrates cell membranes more efficiently than other anthracycline antibiotic compounds.","Antibiotic|Organic Chemical"]
["C1587","Idarubicin Hydrochloride","IDARUBICIN HYDROCHLORIDE|IMI-30|Idamycin|Idarubicin HCl|Idarubicin Hydrochloride|Idarubicin hydrochloride|SC-33428|Zavedos","The hydrochloride salt of the anthracycline antineoplastic antibiotic idarubicin.  Idarubicin intercalates into DNA and inhibits topoisomerase II, thereby inhibiting DNA replication and ultimately, interfering with RNA and protein synthesis.  Due to its high lipophilicity, idarubicin penetrates cell membranes more efficiently than other anthracycline antibiotic compounds","Organic Chemical|Pharmacologic Substance"]
["C90593","Idarubicin-Eluting Beads","Idarubicin-Eluting Beads","A sustained-release drug delivery embolization system containing small polymeric beads impregnated with the anthracycline antibiotic idarubicin with potential antineoplastic activity. The beads consist of polyvinyl alcohol (PVA) microspheres modified with sulfonic acid groups and loaded with idarubicin. During transarterial chemoembolization (TACE) in the hepatic artery, idarubicin-eluting beads embolize to the tumor vasculature, occlude tumor blood vessels and induce ischemic necrosis of tumor tissue due to mechanical blockage of the tumor vasculature. Simultaneously, idarubicin-eluting beads release cytotoxic idarubicin locally and in a sustained manner. This may result in idarubicin-mediated inhibition of tumor cell proliferation.","Pharmacologic Substance"]
["C99131","Idasanutlin","IDASANUTLIN|Idasanutlin|RG-7388|RG7388|RO-5503781|RO5503781","An orally available, small molecule, antagonist of MDM2 (mouse double minute 2; Mdm2 p53 binding protein homolog), with potential antineoplastic activity. Idasanutlin binds to MDM2 blocking the interaction between the MDM2 protein and the transcriptional activation domain of the tumor suppressor protein p53. By preventing the MDM2-p53 interaction, p53 is not enzymatically degraded and the transcriptional activity of p53 is restored. This may lead to p53-mediated induction of tumor cell apoptosis. MDM2, a zinc finger nuclear phosphoprotein and negative regulator of the p53 pathway, is often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C78825","Idelalisib","5-Fluoro-3-phenyl-2-((S)-1-(9H-purin-6-ylamino)-propyl)-3H- quinazolin-4-one|CAL-101|GS-1101|Idelalisib|Phosphoinositide-3 Kinase Delta Inhibitor CAL-101|Zydelig","An orally bioavailable, small molecule inhibitor of the delta isoform of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinase (PI3K) with potential immunomodulating and antineoplastic activities.  Idelalisib inhibits the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3), preventing the activation of the PI3K signaling pathway and inhibiting tumor cell proliferation, motility, and survival. Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in hematopoietic lineages. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells.","Pharmacologic Substance"]
["C114383","IDH1 Inhibitor AG-120","AG-120|IDH1 Inhibitor AG-120","An orally available inhibitor of isocitrate dehydrogenase type 1 (IDH1), with potential antineoplastic activity. Upon administration, AG-120 specifically inhibits a mutated form of IDH1 in the cytoplasm, which inhibits the formation of the oncometabolite, 2-hydroxyglutarate (2HG). This may lead to both an induction of cellular differentiation and an inhibition of cellular proliferation in IDH1-expressing tumor cells. IDH1, an enzyme in the citric acid cycle, is mutated in a variety of cancers; it initiates and drives cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.","Pharmacologic Substance"]
["C129687","IDH-1 Inhibitor FT-2102","FT 2102|FT-2102|IDH-1 Inhibitor FT-2102|IDH1-R132 Inhibitor FT-2102","An orally available inhibitor of isocitrate dehydrogenase type 1 (IDH1; IDH-1; IDH1 [NADP+] soluble) with a mutation at arginine (R) 132, IDH1(R132), with potential antineoplastic activity. Upon administration, IDH-1 inhibitor FT-2102 specifically inhibits IDH1(R132), thereby inhibiting the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing IDH(R132). IDH1(R132) mutations are highly expressed in certain malignancies, including gliomas; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.","Pharmacologic Substance"]
["C121457","IDH1(R132) Inhibitor IDH305","IDH1(R132) Inhibitor IDH305|IDH305","An inhibitor of the citric acid cycle enzyme isocitrate dehydrogenase [NADP] cytoplasmic (isocitrate dehydrogenase 1; IDH1) with mutations at residue R132 (IDH1(R132)), with potential antineoplastic activity. Upon administration, IDH305 specifically inhibits IDH1(R132) mutant forms in the cytoplasm, which inhibits the formation of the oncometabolite 2-hydroxyglutarate (2HG). This may lead to both an induction of cellular differentiation and an inhibition of cellular proliferation in IDH1(R132)-expressing tumor cells. IDH1(R132) mutations are highly expressed in certain malignancies, including gliomas; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.","Pharmacologic Substance"]
["C122678","IDH1R132H Mutation-targeting IDH1 Peptide Vaccine","IDH1R132H Mutation-targeting IDH1 Peptide Vaccine|IDH1R132H-specific Peptide Vaccine","A peptide vaccine consisting of a 20-mer peptide derived from isocitrate dehydrogenase type 1 (IDH1) containing the point mutation R132H (IDH1R132H), with potential antineoplastic activity. Upon subcutaneous vaccination with the IDH1R132H mutation-targeting IDH1 peptide vaccine, the vaccine stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells that express the IDH1R132H protein. R132H is a point mutation, which contains an amino acid substitution where arginine is replaced by histidine at position 132 of IDH1, and is highly expressed in gliomas as well as other tumor types; this mutation is associated with increased production of the oncometabolite R-2-hydroxyglutarate (2HG).","Immunologic Factor|Pharmacologic Substance"]
["C117235","IDH1R132H-Specific Peptide Vaccine PEPIDH1M","IDH1R132H-Specific Peptide Vaccine PEPIDH1M|PEPIDH1M Vaccine|PEPIDH1M","A peptide vaccine consisting of a peptide derived from isocitrate dehydrogenase 1 (IDH1) containing the point mutation R132H (IDH1R132H), with potential antineoplastic activity. Intradermal vaccination with the IDH1R132H-specific peptide vaccine PEPIDH1M may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells that express the IDH1R132H protein. The IDH1 point mutation of amino acid residue 132 is highly expressed in gliomas and is associated with increased production of the oncometabolite R-2-hydroxyglutarate (2HG).","Immunologic Factor|Pharmacologic Substance"]
["C111573","IDH2 Inhibitor AG-221","AG-221|CC-90007|IDH2 Inhibitor AG-221","An orally available inhibitor of isocitrate dehydrogenase type 2 (IDH2), with potential antineoplastic activity. Upon administration, AG-221 specifically inhibits IDH2 in the mitochondria, which inhibits the formation of 2-hydroxyglutarate (2HG). This may lead to both an induction of cellular differentiation and an inhibition of cellular proliferation in IDH2-expressing tumor cells. IDH2, an enzyme in the citric acid cycle, is mutated in a variety of cancers; It initiates and drives cancer growth by blocking differentiation and the production of the oncometabolite 2HG.","Pharmacologic Substance"]
["C74042","Idiotype-Pulsed Autologous Dendritic Cell Vaccine APC8020","APC8020|Idiotype-Pulsed Autologous Dendritic Cell Vaccine APC8020|Mylovenge","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with tumor-derived clonal immunoglobulin (Ig) with potential immunostimulatory and antineoplastic activities. Upon administration, idiotype-pulsed autologous dendritic cell vaccine APC8020, containing idiotype (Id) protein structures that can be recognized by antibodies and by CD41 T lymphocytes and CD81 T lymphocytes, may stimulate antitumoral cytotoxic T lymphocyte (CTL) and antibody responses against Id-expressing tumor cells. The Id represents the unique antigenic determinants in the variable regions of the clonal Ig.","Pharmacologic Substance"]
["C113793","IDO Inhibitor NLG919","GDC-0919|IDO Inhibitor NLG919|NLG-919|NLG919|RG6078","An orally available inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1), with potential immunomodulating and antineoplastic activities. Upon administration, NLG919 targets and binds to IDO1, a cytosolic enzyme responsible for the oxidation of the essential amino acid tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, this agent increases tryptophan levels, restores the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes, and causes a reduction in tumor-associated regulatory T-cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may induce a cytotoxic T-lymphocyte (CTL) response against the IDO1-expressing tumor cells. IDO1 is overexpressed by a variety of tumor cell types and plays an important role in immunosuppression. Tryptophan depletion is associated with immunosuppression caused by T-cell suppression.","Pharmacologic Substance"]
["C129790","IDO1 Inhibitor KHK2455","IDO-1 Inhibitor KHK2455|IDO1 Inhibitor KHK2455|KHK 2455|KHK2455","An orally available inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1 inhibitor KHK2455 targets and binds to IDO1, an enzyme responsible for the oxidation of tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, KHK2455 increases and restores the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes. KHK2455 also induces increased interferon (IFN) production, and causes a reduction in tumor-associated regulatory T-cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may inhibit the growth of IDO1-expressing tumor cells. IDO1, a cytosolic enzyme responsible for tryptophan catabolism and the conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs); it plays an important role in immunosuppression. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system.","Pharmacologic Substance"]
["C129375","IDO1 Inhibitor PF-06840003","IDO-1 Inhibitor PF-06840003|IDO1 Inhibitor PF-06840003|Indoleamine 2,3-Dioxygenase Inhibitor PF-06840003|PF 06840003|PF-06840003","An orally available hydroxyamidine and inhibitor of indoleamine 2,3-dioxygenase 1 (IDO1), with potential immunomodulating and antineoplastic activities. Upon administration, IDO1 inhibitor PF-06840003 targets and binds to IDO1, an enzyme responsible for the oxidation of tryptophan into kynurenine. By inhibiting IDO1 and decreasing kynurenine in tumor cells, PF-06840003 increases and restores the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes; PF-06840003 also induces increased interferon (IFN) production, and causes a reduction in tumor-associated regulatory T cells (Tregs). Activation of the immune system, which is suppressed in many cancers, may inhibit the growth of IDO1-expressing tumor cells. IDO1, a cytosolic enzyme responsible for tryptophan catabolism and the conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs); it plays an important role in immunosuppression. Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and subsequently suppresses the immune system.","Pharmacologic Substance"]
["C2642","Idronoxil","3-(4-Hydroxyphenyl)-2H-1-benzopyran-7-ol|IDRONOXIL|Idronoxil|NV-06|Phenoxodiol|phenoxodiol","A synthetic flavonoid derivative. Idronoxil activates the mitochondrial caspase system, inhibits X-linked inhibitor of apoptosis (XIAP), and disrupts FLICE inhibitory protein (FLIP) expression, resulting in tumor cell apoptosis. This agent also inhibits DNA topoisomerase II by stabilizing the cleavable complex, thereby preventing DNA replication and resulting in tumor cell death.","Organic Chemical|Pharmacologic Substance"]
["C564","Ifosfamide","2-oxo-N,3-bis-(2-chloroethyl) tetrahydro-2H-1,3,2-oxazaphosphorin- 2-amine|3-(2-chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-2H-1,3,2-oxazaphosphorin-2-oxide|Asta Z 4942|Asta Z-4942|Cyfos|Holoxan|Holoxane|IFO-Cell|IFO|IFOSFAMIDE|IFX|Ifex|Ifolem|Ifomida|Ifomide|Ifosfamide|Ifosfamidum|Ifoxan|Iphosphamid|Iphosphamide|Iso-Endoxan|Isoendoxan|Isophosphamide|MJF 9325|MJF-9325|Mitoxana|N,3-bis(2-chloroethyl)tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide|Naxamide|Seromida|Tronoxal|Z 4942|Z-4942|ifosfamide","A synthetic analogue of the nitrogen mustard cyclophosphamide with antineoplastic activity. Ifosfamide alkylates and forms DNA crosslinks, thereby preventing DNA strand separation and DNA replication.  This agent is a prodrug that must be activated through hydroxylation by hepatic microsomal enzymes. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C106118","IGF Ligand Neutralizing Antibody BI 836845","BI 836845|IGF Ligand Neutralizing Antibody BI 836845","A humanized IgG1 insulin-like growth factor (IGF) monoclonal antibody targeting the IGF ligands 1 (IGF-1) and 2 (IGF-2), with potential antineoplastic activity. Upon administration, IGF ligand neutralizing antibody BI 836845 binds to both IGF-1 and IGF-2 and inhibits the binding of these ligands to their receptor, IGF-1R. This blocks the insulin growth factor (IGF) signaling pathway, which is upregulated in a number of cancer cell types and plays a key role in cancer cell proliferation and chemoresistance. In addition, BI 836845 prevents the binding of IGF-2 to insulin receptor variant A (IR-A), preventing its activation.","Immunologic Factor|Pharmacologic Substance"]
["C101257","IGF-1R Antisense Oligodeoxynucleotide-treated Autologous Glioma Cells","IGF-1R Antisense Oligodeoxynucleotide-treated Autologous Glioma Cells|IGF-1R/AS ODN-treated Autologous Glioma Cells","Autologous glioma cells treated ex vivo with an 18-mer antisense oligodeoxynucleotide of insulin-like growth factor receptor 1 (IGF-1R/AS ODN), with potential antineoplastic activity. IGF-1R/AS ODN pre-treated glioma cells encapsulated in small Lucite diffusion chambers are implanted into a subcutaneous pocket in the patient's abdominal rectus sheath. Within the diffusion chambers, IGF-1R/AS ODN binds to IGF-1R mRNA, and shuts down the translation of IGF-1R in the glioma cells. Downregulation of IGF-1R induces apoptosis and causes the release of exosomes, which contain tumor-associated antigens (TAAs). The diffusion of exosomes and IGF-1R/AS ODN from the Lucite chambers may active the patient's immune system and mount a cytotoxic T-lymphocyte (CTL) response against cells expressing these TAAs. IGF-1R, a receptor tyrosine kinase, is overexpressed in a variety of tumor cell types and is essential for tumor cell growth, transformation and survival.","Cell|Pharmacologic Substance"]
["C104746","IGF-1R Inhibitor PL225B","IGF-1R Inhibitor PL225B|PL225B","An orally bioavailable inhibitor of the insulin-like growth factor 1 receptor (IGF-1R) with potential antineoplastic activity. IGF-1R inhibitor PL225B selectively binds to and inhibits the activities of IGF-1R, which may result in both the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis in IGF-1R-overexpressing tumor cells. IGF-1R, a receptor tyrosine kinase overexpressed in a variety of human cancers, plays a significant role in the stimulation of cellular proliferation, oncogenic transformation, and suppression of apoptosis.","Pharmacologic Substance"]
["C84871","IGF-1R/IR Inhibitor KW-2450","IGF-1R/IR Inhibitor KW-2450|KW-2450","An orally bioavailable inhibitor of insulin-like growth factor 1 receptor (IGF-1R) and insulin receptor (IR) tyrosine kinases with potential antineoplastic activity. IGF-1R/IR inhibitor KW-2450 selectively binds to and inhibits the activities of IGF-1R and IR, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. IGF-R1 and IR tyrosine kinases, overexpressed in a variety of human cancers, play significant roles in the stimulation of cellular proliferation, oncogenic transformation, and suppression of apoptosis.","Pharmacologic Substance"]
["C113789","IGF-methotrexate Conjugate","765IGF-MTX|IGF-methotrexate Conjugate","A conjugate containing the antimetabolite and antifolate agent methotrexate conjugated to insulin-like growth factor (IGF), with potential antineoplastic activity. After intravenous administration, the IGF moiety of the IGF-methotrexate conjugate binds to and is internalized by IGF receptors (IGFR) on the surface of tumor cells. Following cell entry, the methotrexate then binds to and inhibits the enzyme dihydrofolate reductase, which catalyzes the conversion of dihydrofolate to tetrahydrofolate. This results in both the inhibition of DNA and RNA synthesis and the induction of death in rapidly dividing cells. Binding to IGFR can localize the cytotoxic effect of methotrexate in tumor cells. This may increase its efficacy while decreasing its toxicity to normal, healthy cells. IGFR is overexpressed on many types of cancer cells and has been implicated in metastasis and resistance to apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C126840","IL-10 Immunomodulator MK-1966","IL-10 Immunomodulator MK-1966|MK 1966|MK-1966","An agent that downregulates the activity of the anti-inflammatory cytokine human interleukin-10 (IL-10), with potential immunomodulating and antineoplastic activities. Upon administration, IL-10 immunomodulator MK-1966 blocks the activity of IL-10 and may abrogate the IL-10-induced immunosuppressive tumor microenvironment. This activates cell-mediated immunity against cancer cells, increases cytokine production, including interferon-gamma (IFN-g), decreases T regulatory cell (Treg) activity, and induces a tumor-specific cytotoxic CD8+ T-cell-mediated immune response, which enhances tumor cell death.","Pharmacologic Substance"]
["C114294","IL-12-expressing HSV-1","IL-12-expressing HSV-1|M032|NSC 733972","A genetically engineered, replication selective, infected cell protein (ICP) 34.5 gene-deleted, oncolytic human simplex virus type 1 (HSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12), with potential antineoplastic activity. Upon intratumoral administration of HSV-1 expressing IL-12, the IL-12-expressing HSV-1 preferentially infects and replicates in tumor cells of neuronal origin causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. In addition, the IL-12-expressing HSV-1 promotes the secretion of IL-12 by the tumor cells. IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against the tumor cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. Deletion of the gene encoding for ICP34.5 imparts tumor selectivity by preventing replication in healthy cells.","Pharmacologic Substance|Virus"]
["C114385","IL-12-expressing Mesenchymal Stem Cell Vaccine GX-051","GX-051|IL-12-expressing Mesenchymal Stem Cell Vaccine GX-051|MSCs/IL-12M","Human mesenchymal stem cells (MSCs) transduced with a retroviral vector encoding a modified form of the cytokine interleukin-12 (IL-12), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration, IL-12-expressing MSC vaccine GX-051 secretes IL-12. IL-12 activates the immune system by both promoting the secretion of interferon-gamma, which activates natural killer cells (NKs), and inducing cytotoxic T-cell responses, which may result in both decreased cell proliferation and increased cell death in tumor cells.","Cell"]
["C117233","IL13Ralpha2-specific Hinge-optimized 41BB-co-stimulatory CAR Truncated CD19-expressing Autologous T-Lymphocytes","Autologous IL13(EQ)BBzeta/CD19t+ TCM-enriched T Cells|IL13Ralpha2-specific Hinge-optimized 41BB-co-stimulatory CAR Truncated CD19-expressing Autologous T-Lymphocytes","A preparation of ex vivo expanded, genetically modified autologous central memory-enriched T-cells (Tcm) transduced with a replication incompetent, self-inactivating (SIN) lentiviral vector expressing a hinge-optimized, chimeric antigen receptor (CAR) specific for interleukin-13 receptor alpha 2 (IL13Ra2), and containing the cluster of differentiation 137 (CD137; 4-1BB) co-stimulatory signaling domain fused to the signaling domain of the T cell antigen receptor complex zeta chain (CD3-zeta), and a truncated form of human cluster of differentiation 19 (CD19t), with potential immunostimulating and antineoplastic activities. Upon intratumoral or intracavitary administration, IL13Ra2-specific, hinge-optimized, 41BB-co-stimulatory CAR/truncated CD19 expressing T-lymphocytes are directed to, and induce selective toxicity and cytolysis in IL13Ra2-expressing tumor cells. IL13Ra2, overexpressed by a variety of tumor cell types, is associated with increased tumor cell proliferation, migration and invasiveness. The costimulatory signaling domain enhances both proliferation of T-cells and antitumor activity. Hinge optimization prevents the recognition and clearance of the CAR by endogenous Fc receptors (FcRs). CD19t is used as a surface marker to both quantify and track the gene modified T-cells in vivo.","Cell|Pharmacologic Substance"]
["C71743","IL-2 Recombinant Fusion Protein ALT-801","ALT-801|IL-2 Recombinant Fusion Protein ALT-801","A recombinant protein consisting of the cytokine interleukin-2 (IL-2) fused to a humanized soluble T-cell receptor (TCR) directed against a tumor suppressor p53-derived antigen with potential immunopotentiating and antineoplastic activities. The TCR moiety of IL-2 recombinant fusion protein ALT-801 binds to tumor cells displaying p53 epitope/MHC complexes; subsequently, the tumor cell-localized IL-2 moiety may stimulate natural killer (NK) cell and T cell cytotoxic immune responses against p53-expressing tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C78487","IL-2/Lptn Gene-Modified Allogeneic Neuroblastoma Tumor Cell Vaccine","IL-2/Lptn Gene-Modified Allogeneic Neuroblastoma Tumor Cell Vaccine|IL-2/Lptn Loaded Allogeneic Neuroblastoma Cell Vaccine|Interleukin-2/Lymphotactin Gene-Modified Allogeneic Neuroblastoma Tumor Cell Vaccine|SJNB-JF-IL2 and SJNB-JF-Lptn Cells and SKNLP Unmodified Neuroblastoma Cell Lines","A cancer vaccine consisting of allogeneic neuroblastoma tumor cells have been genetically modified to secrete the human cytokine interleukin-2 (IL-2) and the human chemokine lymphotactin (Lptn) with potential immunostimulating and antineoplastic activities. Upon administration, IL-2 and Lptn are secreted by the IL-2/Lptn gene-modified allogeneic neuroblastoma tumor cell vaccine, potentially enhancing the cytotoxic T lymphocyte (CTL) response elicited by vaccine neuroblastoma tumor-associated antigens (TAAs) against host neuroblastoma tumor cells.  Produced by activated progenitor T cells, Lptn belongs to the C chemokine subfamily and is a potent chemotactic factor for lymphocytes; IL-2 stimulates natural killer (NK) cells and may enhance a vaccine-elicited CTL immune response against tumor cells.","Cell|Pharmacologic Substance"]
["C79843","IL4-Pseudomonas Exotoxin Fusion Protein PRX321","IL4-PE|IL4-Pseudomonas Exotoxin Fusion Protein PRX321|INxin|PRX321","A fusion protein consisting of the cytokine interleukin-4 (IL-4) linked to a truncated form of Pseudomonas exotoxin with potential antineoplastic activity. Upon specific, high-affinity binding to IL-4 receptors located on the tumor cell surface., IL4-Pseudomonas exotoxin fusion protein PRX321 is internalized; the exotoxin moiety then binds to translation elongation factor 2 (EF-2), which may result in ADP ribosylation, deactivation of EF-2, inhibition of protein synthesis, and tumor cell apoptosis. The Pseudomonas exotoxin moiety of this agent has been engineered to reduce non-specific binding to cells expressing its receptor, the multiligand cell surface receptor alpha 2-macroglobulin receptor/low-density lipoprotein receptor-related protein (alpha 2MR/LRP). IL-4R is a type I transmembrane protein that binds IL-4 and IL-13 and may be overexpressed by cancers such as renal cell carcinoma and glioma.","Pharmacologic Substance"]
["C48397","Iloprost","(E)-(3aS,4R,5R,6aS)-Hexahydro-5-hydroxy-4-((E)-(3S,4RS)-3-hydroxy-4-methyl-1-octen-6-ynyl)-delta(sup 2(1H),delta)-pentalenevaleric Acid|Ciloprost|ILOPROST|Iloprost Clathrate|Iloprost|Pentanoic Acid, 5-(hexahydro-5-hydroxy-4-(3-hydroxy-4-methyl-1-octen-6-ynyl)-2(1H)-pentalenylidene)-|Ventavis|ZK 36374|iloprost","A prostacyclin analogue with potential chemopreventive activity. Iloprost binds to the prostacyclin receptor in various target cells, thereby causing vasodilation, inhibition of platelet aggregation, and decreased tumor cell adhesion to endothelium among other effects. Prostacyclin is a naturally occurring eicosanoid with anti-inflammatory, antineoplastic, and anti-metastatic properties. (NCI05)","Pharmacologic Substance"]
["C116729","Ilorasertib","1-(4-(4-Amino-7-(1-(2-hydroxyethyl)-1H-pyrazol-4-yl)thieno[3,2-c]pyridin-3-yl)phenyl)-3-(3-fluorophenyl)urea|A-968660.0|ABT-348|Ilorasertib","An orally bioavailable, adenosine triphospate mimetic, and inhibitor of Aurora kinases, vascular endothelial growth factor receptors (VEGFRs) and platelet-derived growth factor receptor (PDGFRs), with potential antineoplastic activity. Upon administration, ilorasertib selectively binds to and inhibits Aurora kinases A, B and C, which may disrupt both the assembly of the mitotic spindle apparatus and chromosome segregation, and inhibit both cellular division and proliferation in Aurora kinase-overexpressing tumor cells. In addition, ilorasertib selectively binds to and inhibits VEGFRs and PDGFRs, which may result in the inhibition of both angiogenesis and tumor cell proliferation in VEGFR/PDGFR-overexpressing tumor cells. This agent also inhibits the Src family of cytoplasmic tyrosine kinases. Aurora kinases A, B and C, are serine/threonine kinases that play essential roles in mitotic checkpoint control and are overexpressed by a wide variety of tumor cell types. Both VEGFRs and PDGFRs are receptor tyrosine kinase families whose members may be upregulated in various tumor cell types.","Pharmacologic Substance"]
["C1883","ILX23-7553","1,25-dihydroxy-16-ene-23-yne-cholecalciferol|ILX23-7553|Ro23-7553","A vitamin D3 analogue with potential antineoplastic activity.  ILX23-7553 binds to and activates the vitamin D receptor, a cytoplasmic polypeptide expressed in normal vitamin D responsive tissues, but also overexpressed in certain cancers including hepatocellular carcinoma and pancreatic cancer. Mediated through vitamin D receptor, this agent induces cancer cell differentiation, inhibits cancer cell growth and induces apoptosis. In addition, ILX23-7553 may also induce growth arrest and apoptosis independent of vitamin D receptor activation through mechanisms that are not fully elucidated.","Pharmacologic Substance"]
["C1632","ILX-295501","ILX 295501|ILX-295501|ILX295501|LY 295501|LY-295501|LY295501|N-(((3,4-Dichlorophenyl)amino)carbonyl)-2,3-dihydro-5-benzofuransulfonamide|N-(5-(2,3-Dihydrobenzofuryl)sulfonyl)-N'-(3,4-dichlorophenyl)urea","ILX-295501 is a novel sulfonylurea compound that has demonstrated in-vivo antitumor activity against a broad spectrum of solid tumors.","Organic Chemical|Pharmacologic Substance"]
["C104260","Imalumab","BAX-69|BAX069|BAX69|IMALUMAB|Imalumab|Immunoglobulin G1-kappa, Anti-(Homo sapiens MIF (Macrophage Migration Inhibitory Factor, Glycosylation-inhibiting Factor, GlIF, GIF)), Homo sapiens Monoclonal Antibody","A human, recombinant monoclonal antibody (MoAb) against macrophage migration inhibitory factor (MIF), with potential immunomodulating, anti-inflammatory and antineoplastic activities. Upon intravenous administration, imalumab binds to MIF, blocking its activity and preventing the MIF-mediated secretion of certain cytokines, including interleukin-1 beta and tumor necrosis factor-alpha. This may lead to an inhibition of cancer cell proliferation in MIF-overexpressing tumor cells. MIF, a pro-inflammatory cytokine overexpressed in some cancers, plays a key role in inflammation, immune responses and cancer cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C62035","Imatinib","4-[(4-Methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]benzamide|IMATINIB|Imatinib","An antineoplastic agent that inhibits the Bcr-Abl fusion protein tyrosine kinase, an abnormal enzyme produced by chronic myeloid leukemia cells that contain the Philadelphia chromosome.  Imatinib also inhibits the receptor tyrosine kinases for platelet-derived growth factor (PDGF) and stem cell factor (SCF)/c-kit; the SCF/c-kit receptor tyrosine kinase is activated in gastrointestinal stromal tumor (GIST).  This agent inhibits proliferation and induces apoptosis in cells that overexpress these oncoproteins.","Organic Chemical|Pharmacologic Substance"]
["C1687","Imatinib Mesylate","4-[(4-Methyl-1-piperazinyl)methyl]-N-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]benzamide Monomethanesulfonate|CGP 57148|CGP57148B|Gleevec|Glivec|IMATINIB MESYLATE|Imatinib Mesylate|STI 571|STI-571|STI571|imatinib mesylate","The mesylate salt of imatinib, a tyrosine kinase inhibitor with antineoplastic activity. Imatinib binds to an intracellular pocket located within tyrosine kinases (TK), thereby inhibiting ATP binding and preventing phosphorylation and the subsequent activation of growth receptors and their downstream signal transduction pathways. This agent inhibits TK encoded by the bcr-abl oncogene as well as receptor TKs encoded by the c-kit and platelet-derived growth factor receptor (PDGFR) oncogenes. Inhibition of the bcr-abl TK results in decreased proliferation and enhanced apoptosis in malignant cells of Philadelphia-positive (Ph+) hematological malignancies such as CML and ALL; effects on c-kit TK activity inhibit mast-cell and cellular proliferation in those diseases overexpressing c-kit, such as mastocytosis and gastrointestinal stromal tumor (GIST).","Organic Chemical|Pharmacologic Substance"]
["C49084","Imetelstat","DNA, d(3'-amino-3'-deoxy-P-thio)(T-A-G-G-G-T-T-A-G-A-C-A-A), 5'-[O-[2-hydroxy-3- [(1-oxohexadecyl)amino]propyl] hydrogen phosphorothioate]|IMETELSTAT|Imetelstat","A synthetic lipid-conjugated, 13-mer oligonucleotide N3'-P5'-thio-phosphoramidate with potential antineoplastic activity. Complementary to the template region of telomerase (hTR) RNA, imetelstat acts as a competitive enzyme inhibitor that binds and blocks the active site of the enzyme (a telomerase template antagonist), a mechanism of action which differs from that for the antisense oligonucleotide-mediated inhibition of telomerase activity through telomerase mRNA binding. Inhibition of telomerase activity in tumor cells by imetelstat results in telomere shortening, which leads to cell cycle arrest or apoptosis.","Pharmacologic Substance"]
["C84511","Imetelstat Sodium","DNA, d(3'-amino-3'-deoxy-P-thio)(T-A-G-G-G-T-T-A-G-A-C-A-A), 5'-[O-[2-hydroxy-3- [(1-oxohexadecyl)amino]propyl] hydrogen phosphorothioate], Sodium Salt (1:13)|GRN163L, Sodium Salt|GRN163L|IMETELSTAT SODIUM|Imetelstat Sodium","The sodium salt of imetelstat, a synthetic lipid-conjugated, 13-mer oligonucleotide N3' P5'-thio-phosphoramidate with potential antineoplastic activity. Complementary to the template region of telomerase RNA (hTR), imetelstat acts as a competitive enzyme inhibitor that binds and blocks the active site of the enzyme (a \"telomerase template antagonist\"), a mechanism of action which differs from that for the antisense oligonucleotide-mediated inhibition of telomerase activity through telomerase mRNA binding. Inhibition of telomerase activity in tumor cells by imetelstat results in telomere shortening, which leads to cell cycle arrest or apoptosis.","Pharmacologic Substance"]
["C29115","Imexon","4-imino-1,3-diazabicyclo[3,1,0]-hexan-2-one|Amplimexon|IMEXON|Imexon|imexon","A 2-cyanoaziridine derivative with antitumor activity in multiple myeloma.  Although its mechanism of action is not clearly known, imexon may induce apoptosis via a pathway involving cleaved caspase-3, caspase-9, and/or caspase-8.  Other cytotoxic mechanisms of action of this agent may involve thiol depletion, generation of reactive oxygen species (ROS), and decreases in the mitochondrial membrane potential. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2216","Imidazole Mustard","5-[3, 3-Bis(2-chloroethyl)-1-triazeno]-imidazole-4-carboxamide|5-[3, 3-Bis(2-chloroethyl)-1-triazeno]imidazole-4-carboxamide|5-[3,3-Bis(2-Chloroethyl)-1-Triazeno]Imidazole-4-Carboxamide|BIC|Imidazole Mustard|Imidazole mustard|TIC Mustard|TIC mustard","A synthetic derivative of imidazole with potent antineoplastic properties.  Imidazole mustard alkylates DNA, preferentially at guanine residues, resulting in DNA interstrand crosslinks and inhibition of DNA replication and RNA and protein synthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C29344","Imidazole-Pyrazole","2,3-Dihydro-1H-imidazo(1,2-b)pyrazole|BRN 0742753|IMPY|Imidazole-Pyrazole|Imidazolepyrazole","A synthetic agent, also known as IMPY, with antineoplastic properties.  IMPY inhibits ribonucleotide reductase, an enzyme that converts ribonucleotides to deoxyribonucleotides during DNA synthesis; this agent specifically binds the smaller, nonheme-iron subunit of the enzyme. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1431","Imiquimod","1H-Imidazo(4,5-c)quinolin-4-amine, 1-(2-methylpropyl)-|4-Amino-1-isobutyl-1H-imidazo(4,5-c)quinoline|Aldara|IMIQUIMOD|Imiquimod|R 837|S 26308|Zyclara|imiquimod","A synthetic agent with immune response modifying activity. As an immune response modifier (IRM), imiquimod stimulates cytokine production, especially interferon production, and exhibits antitumor activity, particularly against cutaneous cancers. Imiquimod's proapoptotic activity appears to be related to Bcl-2 overexpression in susceptible tumor cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C113795","Immediate-release Onapristone","IR Onapristone|Immediate-release Onapristone","An immediate-release (IR) formulation of onapristone, an orally bioavailable progesterone receptor (PR) antagonist, with antineoplastic activity. Onapristone binds to the PR and inhibits both PR activation and the associated expression of PR-responsive genes. This may inhibit PR-mediated proliferative effects in cancer cells overexpressing PR. PR is expressed on certain cancer cell types and plays a key role in proliferation and survival.","Organic Chemical|Pharmacologic Substance"]
["C113658","Immediate-release Tablet Afuresertib","GSK2110183 IR Tablet|IR Afuresertib|Immediate-release Tablet Afuresertib","An immediate-release (IR) tablet formulation containing afuresertib, an inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Upon oral administration of the IR formulation, afuresertib binds to and inhibits the activity of Akt, which may result in the inhibition of PI3K/Akt signaling pathway, decreased tumor cell proliferation and the induction of tumor cell apoptosis in Akt-expressing tumor cells. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C74044","Immunoadjuvant QS-DG","Immunoadjuvant QS-DG|QS-DG","A synthetic saponin, chemically identical to the natural saponin QS-21, with immunoadjuvant activity. When co-administered with vaccine antigens, immunoadjuvant QS-DG may increase total antitumoral vaccine-specific antibody responses and cytotoxic T-lymphocyte (CTL) responses.","Pharmacologic Substance"]
["C104058","Immunoconjugate RO5479599","Immunoconjugate RO5479599|RO5479599","An immunoconjugate containing a glycoengineered, humanized monoclonal antibody directed against the human epidermal growth factor receptor HER3 (ErbB3), with potential antineoplastic activity. Upon administration, RO5479599 binds to the extracellular domain of HER3 and inhibits HER3 dimerization; thereby, preventing EGFR-dependent signaling. In addition, RO5479599 stimulates the immune system to exert antibody-dependent cellular cytotoxicity (ADCC). This may decrease proliferation of HER3-overexpressing tumor cells. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors; it has no active kinase domain but is activated through heterodimerization with other members of the EGFR receptor family, such as HER2.","Pharmacologic Substance"]
["C97961","Immunocytokine NHS-IL12","Immunocytokine NHS-IL12|NHS-IL12","A fusion protein consisting of the heavy-chains of the human antibody NHS76, raised against DNA released by necrotic tumor cells, and fused to two molecules of a genetically modified human interleukin-12 (IL-12) with potential immunostimulating and antineoplastic activities. Upon administration, the antibody moiety of immunocytokine NHS-IL12 binds to DNA released from necrotic tumor cells located primarily at the core of necrotic solid tumors, thereby delivering the IL-12 moiety. In turn, the IL-12 moiety of this agent stimulates the host immune system to mount an immune response against tumor cells, thereby inhibiting tumor growth. IL-12 is a proinflammatory cytokine with numerous immunoregulatory functions and may augment host immune responses to tumor cells. By targeting tumor cells, NHS-IL-12 may reduce the toxicity associated with systemic administration of recombinant human IL-12.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82411","Immunocytokine NHS-IL2-LT","Ch.14.18-IL2|EMD 521873|Immunocytokine NHS-IL2-LT|Selectikine","A fusion protein consisting of a mouse-human chimeric antibody directed against DNA released by necrotic tumor cells fused to two molecules of a genetically modified human interleukin-2 (IL-2) with potential antineoplastic activity. Upon administration, the antibody moiety of immunocytokine NHS-IL2-LT binds to DNA released by necrotic tumor cells located primarily at the core of necrotic solid tumors, delivering the IL-2 moiety. In turn, the IL-2 moiety of this agent activates the immune system to mount a cytotoxic T lymphocyte response against nearby tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C49092","Immunomodulator OHR/AVR118","AVR118|Immunomodulator OHR/AVR118|Product R","A broad-spectrum peptide nucleic acid formulation comprised of breakdown products of casein, peptone, RNA and serum albumin, with potential anti-inflammatory, immunomodulatory, anti-anorectic and anti-cachexia activities. AVR118 mainly contains two peptides, peptide A and peptide B, in approximately a 1:1 ratio: peptide A (31 a. a.) is derived from bovine casein; peptide B (21 a. a.) is covalently linked via phosphodiester bond to a diadenosine unit. In addition, AVR118 contains nucleosides, nucleoside diphosphates and nucleoside monophosphates. Upon subcutaneous injection of AVR118, this agent affects the synthesis of many pro-inflammatory chemokines and cytokines, especially monocyte chemotactic protein-1 (MCP-1), interleukin (IL)-8, IL-1 beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha). In particular, AVR118 stimulates macrophages to produce these mediators while in highly activated macrophages this agent inhibits their synthesis. This way, AVR118 may prevent the excessive release of cytokines seen during chemotherapy. Controlling the release of pro-inflammatory mediators may ultimately improve appetite and mood, increase strength and weight gain, and decrease fatigue.","Pharmacologic Substance"]
["C101370","Immunomodulatory Agent CC-11006","CC-11006-MDS-001|CC-11006|Immunomodulatory Agent CC-11006","A proprietary, orally available, small molecule and thalidomide analog, with potential immunomodulating and antineoplastic activity. CC-11006 appears to have a similar mechanism to thalidomide and may modulate the expression of proinflammatory and regulatory cytokines.","Pharmacologic Substance"]
["C122922","Immunotherapeutic Combination Product CMB305","CMB 305|CMB305|ID-CMB305|ID-LV305 Plus ID G305|Immunotherapeutic Combination Product CMB305|LV 305 Plus G 305|LV305 Plus G305","An immunotherapeutic combination product composed of LV305, an engineered lentiviral vector that both targets dendritic cells (DCs) and contains nucleic acids encoding the human tumor-associated cancer-testis antigen NY-ESO-1 (CTAG1), and G305, a cancer vaccine comprised of an NY-ESO-1 recombinant protein and glucopyranosyl lipid adjuvant (GLA)-stable emulsion (GLA-SE), with potential synergistic immunostimulatory and antineoplastic activities. Upon intradermal administration of LV305, the DC-targeting lentiviral vector targets and binds to dermal DCs via the DC-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) receptor. Upon internalization of the vector, the NY-ESO-1 protein is expressed, which stimulates DC maturation, and activates the immune system to mount a cytotoxic T-lymphocyte (CTL) response against NY-ESO-1-expressing cells; this may result in tumor cell lysis. Upon the sequential intramuscular injection of G305, the adjuvant portion of G305 binds to toll-like receptor 4 (TLR-4) expressed on various immune cells, including DCs, monocytes, macrophages and B-cells. The activated DCs present the NY-ESO-1 antigen to CD4-positive Th1 T-lymphocytes. The induction of antigen-specific CD4-positive T-lymphocytes further induces a CTL response against NY-ESO-1-expressing tumor cells. In addition, G305 induces an NY-ESO-1-specific antibody response. NY-ESO-1, expressed in normal testes and on the surfaces of various tumor cells, plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C91714","Immunotherapeutic GSK1572932A","GSK1572932A|Immunotherapeutic GSK1572932A","An immunotherapeutic containing a proprietary adjuvant system combined with a melanoma-associated antigen peptide MAGE-A3 epitope with potential immunomodulating and antineoplastic activities. Intramuscular administration with GSK1572932A may stimulate the immune system to exert both humoral and cellular immune responses against MAGE-A3-expressing tumor cells. MAGE-A3, a tumor associated antigen (TAA), is overexpressed in a variety of tumor cell types, including non-small cell lung cancer (NSCLC), melanoma, head and neck cancer, and bladder cancer.","Pharmacologic Substance"]
["C77971","Immunotherapy Regimen MKC-1106-MT","Immunotherapy Regimen MKC-1106-MT|MKC-1106-MT","An immunotherapy regimen containing three components: a plasmid encoding portions of the two melanoma-associated antigens Melan A (also called MART-1) and tyrosinase and two synthetic analogs of Melan-A and tyrosinase antigen epitopes with potential immunostimulating and antitumor activities. First, the plasmid is injected directly into lymph nodes in order to sensitize or prime antigen-presenting cells (APCs) and central memory T cells in lymph nodes to plasmid-expressed Melan A and tyrosinase.  After several priming injections with plasmids, the Melan A and tyrosinase synthetic epitope analogs are injected directly into lymph nodes; upon binding to major histocompatibility complex (MHC) molecules on APC cell surfaces, these synthetic epitope analogs may stimulate a \"primed\" cytotoxic T lymphocyte (CTL) response against melanoma tumor cells, resulting in tumor cell lysis. Melan-A and tyrosinase are overexpressed by melanoma tumor cells.","Pharmacologic Substance"]
["C62480","Immunotoxin CMD-193","Immunotoxin CMD-193","A humanized immunotoxin directed against the Lewis Y antigen conjugated with calicheamicin, a hydrophobic enediyne antibiotic, with potential antineoplastic activity. CMD193 binds to the Lewis Y antigen, a tetrasaccharide expressed on the cell surfaces of many tumor cell types. Upon binding, CMD-193 is internalized, thereby delivering the attached calicheamicin to Lewis Y antigen-expressing tumor cells. Calicheamicin binds non-covalently to the minor groove of DNA and prompts conformational changes and DNA oxidation, thereby inhibiting DNA synthesis and inducing apoptosis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C119739","Immunotoxin D2C7-(scdsFv)-PE38KDEL","D2C7-(scdsFv)-PE38KDEL Immunotoxin|D2C7-(scdsFv)-PE38KDEL|Immunotoxin D2C7-(scdsFv)-PE38KDEL","A recombinant immunotoxin fusion protein consisting of single-chain variable-region antibody fragments (scFvs), which contain disulfide stabilized heavy- (Vh) and light- (Vl) chain variable regions of the monoclonal antibody D2C7 (D2C7-scdsFv), targeting both the wild-type form (EGFRwt) and the in-frame deletion mutant form (EGFRvIII) of epidermal growth factor receptor (EGFR), and fused, via a 15-amino acid peptide linker to domains II and III of the Pseudomonas exotoxin A (PE38KDEL) (D2C7-(scdsFv)-PE38KDEL), with potential antineoplastic activity. Upon intratumoral administration by convection-enhanced delivery, the scFv moiety of immunotoxin anti-EGFR scFv monoclonal antibody fragment immunotoxin D2C7-(scdsFv)-PE38KDEL targets and binds to a specific amino acid epitope present in the extracellular domain of both the EGFRwt and EGFRvIII proteins. This binding facilitates the internalization of the immunotoxin by tumor cells. Inside the cells, the exotoxin portion of the fusion protein binds to translation elongation factor 2 (EF-2), and deactivates EF-2 through ADP ribosylation. This results in the inhibition of protein synthesis, the induction of apoptosis and a reduction in cell proliferation of EGFRwt/EGFRvIII-expressing tumor cells. Compared to intact IgG antibodies and single-chain antibodies, scFvs are smaller with increased tumor-penetrating capacity which may enhance therapeutic efficacy. The EGFR gene, a transmembrane receptor tyrosine kinase, and its mutant form, EGFRvIII, which contains a deletion of exons 2-7 of the EGFR gene, are frequently amplified and overexpressed in a variety of cancers. KDEL increases the toxin's intracellular retention, thereby enhancing its cytotoxicity.","Pharmacologic Substance"]
["C62509","IMP321","IMP321|Immufact","A T-cell immunostimulatory factor, derived from the soluble form of the lymphocyte-activation gene 3 (LAG-3) protein, with potential antineoplastic activity. Upon administration, alone or in combination with tumor antigens, IMP321 binds with high affinity to MHC class II molecules expressed by dendritic cells (DC), potentially resulting in DC maturation, DC migration to lymph nodes, enhanced DC cross-presentation of antigens to T cells, and antitumor cytotoxic T cell responses.","Organic Chemical|Pharmacologic Substance"]
["C77863","IMT-1012 Immunotherapeutic Vaccine","IMT-1012 Immunotherapeutic Vaccine|IMT-1012|OCPM Immunotherapeutic Vaccine","A multi-peptide cancer vaccine with potential immunostimulating and antineoplastic activities. IMT-1012 immunotherapeutic vaccine contains twelve different synthetic peptides or tumor associated antigens (TAAs), including cyclin I (CCNI), cyclin-dependent kinase CDC2, EDDRI and TACE/ADAM17, each of which is involved in a different pathway associated with tumor growth, survival, and metastasis. Each antigen in the vaccine elicits a specific cytotoxic T-lymphocyte (CTL) immune response against tumor cells expressing that antigen. This multi-antigen/multi-pathway targeting strategy provides broad immunotherapeutic coverage with respect to tumor complexity and heterogeneity and may result in enhanced vaccine efficacy.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C29317","Inalimarev","Inalimarev|PANVAC-V|Vaccinia-CEA-MUC1-TRICOM Vaccine|inalimarev|rVaccinia-CEA(D609)/MUC1(L93)/TRICOM Vaccine|recombinant vaccinia-CEA-MUC-1-TRICOM vaccine","A cancer vaccine comprised of a recombinant vaccinia viral vector encoding the carcinoembryonic antigen (CEA), MUC-1 (mucin-1), a transmembrane glycoprotein secreted by glandular tissues, and TRICOM, comprised of the three co-stimulatory molecule transgenes B7-1, ICAM-1 and LFA-3. Upon administration, inalimarev may enhance CEA and MUC-1 presentation to antigen presenting cells (APC) and may activate a cytotoxic T lymphocyte (CTL) response against CEA- and MUC-1-expressing tumor cells.","Pharmacologic Substance|Virus"]
["C1573","Incomplete Freund's Adjuvant","Freund's Incomplete Adjuvant|IFA|ISA-51|Incomplete Freund's Adjuvant|Montanide ISA 51|Montanide ISA-51|incomplete Freund's adjuvant","A water-in-oil emulsion that stimulates the T-cell immune response to antigens and may be used in various types of cancer vaccines. (NCI04)","Pharmacologic Substance"]
["C2454","Incyclinide","4-Dimethlyamino Sancycline|4-Dimethlyaminosancycline|4-dedimethylamino sancycline|6-deoxy, 6-demethyl, 4-de-dimethylamino tetracycline|6-deoxy-6-demethyl-4-dedimethylaminotetracycline|CMT-3|COL 3|COL-3|INCYCLINIDE|Incyclinide|Metastat|Tetracycline CMT-3","A chemically-modified tetracycline with potential antineoplastic activity. Incyclinide inhibits matrix metalloproteinases (MMPs), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis. This agent also causes mitochondrial depolarization in tumor cells and induces both cellular apoptosis and tissue necrosis.","Antibiotic|Organic Chemical|Pharmacologic Substance"]
["C2049","Indibulin","D 24851|D-24851|INDIBULIN|Indibulin|N-(Pyridin-4-yl)-(1-(4-chlorobenzyl)indol-3-yl)glycoxylamide|ZIO-301","A synthetic small molecule with antimitotic and potential antineoplastic activities. Indibulin binds to a site on tubulin that is different from taxane- or Vinca alkaloid-binding sites, destabilizing tubulin polymerization and inducing tumor cell cycle arrest and apoptosis. This agent has been shown to be active against multidrug-resistant (MDR) and taxane- resistant tumor cell lines.","Pharmacologic Substance"]
["C1134","Indicine-N-Oxide","2,3-Dihydroxy-2-(1-methylethyl)butanoic Acid (2,3,5,7a-tetrahydro-1-hydroxy-1H-pyrrolizin-7-yl)methyl Ester N-Oxide|Butanoic Acid, 2,3-Dihydroxy-2-(1-methylethyl)- (2,3,5, 7a-tetrahydro-1-hydroxy-1H-pyrrolizin-7-yl) Methyl Ester, N-Oxide,(1R-(1alpha,7(2R*,3S*),7a-beta))-(9CI)|Butanoic acid, 2,3-dihydroxy-2-(1-methylethyl)- (2,3,5, 7a-tetrahydro-1-hydroxy-1H-pyrrolizin-7-yl) methyl ester, N-oxide, (1R-(1alpha,7(2R*,3S*),7a-beta))-(9CI)|Indicine N-Oxide|Indicine N-oxide|Indicine, N-oxide|Indicine-N-Oxide","A natural pyrrolizidine alkaloid with antineoplastic properties.  Indicine-N-oxide alkylates and crosslinks DNA. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C25797","Indisulam","E7070|INDISULAM|Indisulam|N-(3-Chloro-7-indoyl)-1,4-Benzenedisulfonamide","A novel sulfonamide compound with potential antineoplastic activity. Indisulam inhibits cyclin-dependent kinases (CDK), which regulate cell cycle progression and are usually over-expressed in cancerous cells. Inhibition of CDK results in G1/S phase arrest of the cell cycle, and may lead to induction of apoptosis and inhibition of tumor cell proliferation. In addition, indisulam also inhibits carbonic anhydrases (CA), especially isoforms IX and XII that are involved in aqueous humor production and are highly overexpressed in some types of cancers. Inhibition of CA IX and XII results in interference with ion exchange and pH in hypoxic tumor tissue and preventing chemoresistance to weakly basic antineoplastic agents.","Pharmacologic Substance"]
["C94215","Indoleamine 2,3-dioxygenase Peptide Vaccine","IDO Peptide Vaccine|Indoleamine 2,3-dioxygenase Peptide Vaccine","A peptide vaccine against the immunomodulatory enzyme indoleamine 2,3-dioxygenase (IDO), with potential immunomodulating and antineoplastic activities. Vaccination with indoleamine 2,3-dioxygenase peptide vaccine may activate the immune system to induce an immune response against IDO-expressing cells. This may increase and restore the proliferation and activation of various immune cells, including dendritic cells (DCs), natural killer (NK) cells, and T-lymphocytes, and may eradicate IDO-expressing tumor cells. IDO, a cytosolic enzyme responsible for tryptophan catabolism and conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs) and plays an important role in immunosuppression; Tryptophan depletion inhibits T-lymphocyte proliferation and activation, and suppresses the immune system.","Immunologic Factor|Pharmacologic Substance"]
["C576","Indomethacin","1-(4-chlorobenzoyl)-5-methoxy- 2-methyl-1-H-indole-3-acetic acid|INDOMETHACIN|Indocin|Indometacin|Indomethacin|indomethacin","A synthetic nonsteroidal indole derivative with anti-inflammatory activity and chemopreventive properties. As a nonsteroidal anti-inflammatory drug (NSAID), indomethacin inhibits the enzyme cyclooxygenase, thereby preventing cyclooxygenase-mediated DNA adduct formation by heterocyclic aromatic amines. This agent also may inhibit the expression of multidrug-resistant protein type 1, resulting in increased efficacies of some antineoplastic agents in treating multi-drug resistant tumors. In addition, indomethacin activates phosphatases that inhibit the migration and proliferation of cancer cells and downregulates survivin, which may result in tumor cell apoptosis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1789","Infliximab","Avakine|INFLIXIMAB|Infliximab|Remicade|cA2|infliximab","A recombinant chimeric, mouse-human monoclonal antibody directed against tumor necrosis factor alpha (TNF-alpha), a protein involved in inflammation, cell survival, and apoptosis. Infliximab may be pro- apoptotic or anti-apoptotic, depending on cell type. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48398","Ingenol Mebutate","2-Butenoic acid, 2-methyl-, (1aR,2S,5R,5aS,6S,8aS,9R,10aR)-1a,2,5,5a,6,9,10,10a- octahydro-5,5a-dihydroxy-4-(hydroxymethyl)-1,1,7,9-tetramethyl-11-oxo-1H-2,8a- methanocyclopenta[a]cyclopropa[e]cyclodecen-6-yl ester, (2Z)-|I3A|INGENOL MEBUTATE|Ingenol Mebutate|Ingenol-3-angelate|PEP-005|PEP005","A selective small-molecule activator of protein kinase C (PKC) isolated from the plant Euphorbia peplus with potential antineoplastic activity. Ingenol mebutate activates various protein kinase C (PKC) isoforms, thereby inducing apoptosis in some tumor cells, including myeloid leukemia cells, melanoma cells, and basal cell carcinoma cells. The PKC family consists of signaling isoenzymes that regulate many cell processes including proliferation, differentiation, and apoptosis.","Pharmacologic Substance"]
["C118776","Ingenol Mebutate Gel","Ingenol Mebutate Gel|Ingenol-3-angelate Gel|PEP-005 Topical Gel|PEP005 Gel|Picato","A topical, aqueous gel formulation containing the mebutate salt form of ingenol, a selective small-molecule activator of protein kinase C (PKC) that is isolated from the sap of Euphorbia species, with potential antineoplastic activity. Upon topical application of the ingenol mebutate gel, ingenol activates various PKC isoforms, which induces apoptosis in certain tumor cells, including myeloid leukemia cells, melanoma cells, and basal cell carcinoma cells. The PKC family consists of signaling isoenzymes that regulate many cell processes, including proliferation, differentiation, and apoptosis.","Pharmacologic Substance"]
["C62526","Iniparib","4-Iodo-3-Nitrobenzamide|BSI-201|INIPARIB|Iniparib|PARP-1 Inhibitor BSI-201|PARP-1 inhibitor BSI-201|SAR240550|iniparib","A small molecule iodobenzamide with potential cytotoxic and antineoplastic activities. Although the mechanism of action is unknown, iniparib appears to be cytotoxic in cells with DNA alterations or DNA damage, like that found in tumor cells with mutations in the ataxia telangiectasia mutated (ATM) gene. ATM encodes a serine/threonine protein kinase and mutations of the gene are associated with ataxia telangiectasia and contribute to certain cancers such as T-cell acute lymphoblastic leukemia, B-cell chronic lymphocytic leukemia and B-cell non-Hodgkin lymphomas.","Pharmacologic Substance"]
["C82362","Innate Immunostimulator rBBX-01","Innate Immunostimulator rBBX-01|rBBX-01","A recombinant 19 kDa protein derived from the Apicomplexa protozoan Eimeria with potential immunostimulating and antitumor activities. Upon administration, innate immunostimulator rBBX-01 activates dendritic cells (DCs), stimulates the Toll-like receptor 11 (TLR-11)-mediated release of interleukin-12 (Il-12) from DCs, and induces a T-helper 1 (Th1) type immune response, which may induce an immune response against tumor cells. Infection with Eimeria, a coccidian commonly infecting the intestine, may be negatively correlated with tumorigenesis.","Pharmacologic Substance"]
["C61315","INO-1001","INO 1001|INO-1001","A isoindolinone derivative and potent inhibitor of the nuclear enzyme poly (ADP-ribose) polymerase (PARP) with chemosensitization and radiosensitization properties. INO-1001 inhibits PARP, which may result in inhibition of tumor cell DNA repair mechanisms and, so, tumor cell resistance to chemotherapy and radiation therapy. PARP enzymes are activated by DNA breaks and have been implicated in the repair of DNA single-strand breaks (SSB).","Pharmacologic Substance"]
["C122835","Inosine 5'-monophosphate Dehydrogenase Inhibitor FF-10501-01","FF-10501-01|FF-10501|IMPDH Inhibitor FF-10501|Inosine 5'-monophosphate Dehydrogenase Inhibitor FF-10501-01","An orally bioavailable inhibitor of inosine 5'- monophosphate dehydrogenase (IMPDH), with potential antineoplastic activity. Upon administration, IMPDH inhibitor FF-10501-01 competitively inhibits the enzyme IMPDH, thereby preventing the conversion of inosine monophosphate to xanthosine monophosphate. This inhibits the synthesis of guanine nucleotides, deprives cancer cells of guanosine triphosphate (GTP), disrupts DNA and RNA synthesis, and decreases tumor cell proliferation. Tumor cells are highly susceptible to IMPDH inhibition because they are rapidly dividing cells that are dependent on rapid DNA synthesis, which requires a high concentration of nucleotides. IMPDH, an enzyme that catalyzes the rate-limiting step in the synthesis of guanosine triphosphate (GTP), is overexpressed in numerous tumor cell types.","Pharmacologic Substance"]
["C28163","Inositol","Cyclohexanehexol|INOSITOL|Inositol|cis-1,2,3,5-trans-4,6-Cyclohexanehexol|inositol|myo-Inositol|myoinositol","A natural sugar found in cell membrane phospholipids, plasma lipoproteins, and (as the phosphate form) in the nucleus with potential chemopreventive properties. As one of a number of intracellular phosphate compounds, inositol is involved in cell signaling and may stimulate tumor cell differentiation. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C71542","Inotuzumab Ozogamicin","CMC-544|INOTUZUMAB OZOGAMICIN|Inotuzumab Ozogamicin|WAY-207294|Way 207294","A CD22-targeted cytotoxic immunoconjugate composed of a humanized IgG4 anti-CD22 antibody covalently linked to N-acetyl-gamma-calicheamicin dimethyl hydrazide (CalichDMH) with potential antineoplastic activity. Inotuzumab ozogamicin is rapidly internalized upon binding of the antibody moiety to B cell-specific CD22 receptors, delivering the conjugated CalichDMH intracellularly; the CalichDMH moiety binds to the minor groove of DNA in a sequence-specific manner, resulting in double-strand DNA breaks and apoptosis. CalichDMH is a derivative of gamma calicheamicin, a cytotoxic antibiotic produced by the bacterium Micromonospora echinospora.","Immunologic Factor|Pharmacologic Substance"]
["C65919","Inproquone","INPROQUONE|Inproquone","A benzoquinone-based antineoplastic agent. Inproquone was never marketed.","Pharmacologic Substance"]
["C96223","Integrin Receptor Antagonist GLPG0187","GLPG0187|Integrin Receptor Antagonist GLPG0187","A small molecule integrin receptor antagonist (IRA) with potential antineoplastic activity. Upon administration, GLPG0187 binds to and blocks the activity of 5 RGD-integrin receptor subtypes, including alphavbeta1, alphavbeta3, alphavbeta5, alphavbeta6 and alpha5beta1. This may result in the inhibition of endothelial cell-cell interactions and endothelial cell-matrix interactions, and the prevention of angiogenesis and metastasis in tumor cells expressing these integrin receptors. Integrin receptors are transmembrane glycoproteins expressed on the surface of tumor vessel endothelial cells and some types of cancer cells, and play a crucial role in endothelial cell adhesion and migration.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1766","Interferon Alfacon-1","Advaferon|CIFN|Consensus Interferon|IFN Alfacon-1|INTERFERON ALFACON-1|Infergen|Interferon Alfacon-1|Interferon Consensus, Methionyl|Methionyl Interferon Consensus|Methionyl-Interferon-Consensus|Recombinant Consensus Interferon|Recombinant methionyl human consensus interferon|interferon consensus, methionyl|methionyl interferon consensus|r-metHuIFN-Con1","An analogue of consensus interferon which contains an additional methionyl amino acid residue.  Consensus interferon (also known as interferon alfacon-1, rCon-IFN, and CIFN) is a genetically engineered synthetic interferon created from the most common amino acid sequences from the naturally occurring alpha interferons.  Alpha interferons bind to specific cell-surface receptors, resulting in the transcription and translation of genes whose protein products have antiviral, antiproliferative, anticancer, and immune-modulating effects.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2220","Interferon Alfa-N1","Humoferon|Interferon Alfa-N1|Interferon Alfa|Wellferon","A highly purified alpha interferon produced by a human lymphoid cell line.  Interferon alpha-n1 consists of multiple alpha interferon subtypes, at least two of which are glycosylated.  In contrast, recombinant alpha interferons are individual non-glycosylated proteins produced from individual alpha interferon genes.  Alpha interferons bind to specific cell-surface receptors, resulting in the transcription and translation of genes whose proteins have antiviral, antiproliferative, anticancer, and immune-modulating effects. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C30136","Interferon Alfa-N3","Alfa-N3 Interferon|Alferon N|Altemol|Interferon Alfa-N3","A formulated therapeutic analog of the endogenous alpha interferon containing multiple interferon species with antiviral and antitumor properties.  Interferons bind to specific cell-surface receptors, leading to the transcription and translation of genes with an interferon-specific response element, thereby inducing: antiviral effects (the most important being inhibition of viral protein synthesis); antiproliferative effects (including inhibition of cellular growth and alteration of cellular differentiation); anticancer effects (including interference with oncogene expression); and immune-modulating effects (including activation of natural killer cells, alteration of cell surface antigen expression, and augmentation of lymphocyte and macrophage cytotoxicity). (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1823","Interferon Beta-1A","Avonex|BG9418|INTERFERON BETA-1A|Interferon Beta-1A|Rebif|Recombinant interferon beta-1a","A synthetic version of naturally occurring interferons that have immunomodulatory, antiviral and antiproliferative activities. It may exert antitumor activity by anti-angiogenic and cell differentiation activities. (NCI)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C123724","Interferon Beta-secreting Mesenchymal Stem Cells","IFNb-MSC|IFNb-secreting MSCs|IFNbeta-MSC|Interferon Beta-secreting Mesenchymal Stem Cells|MSC-IFN beta","Human autologous mesenchymal stem cells (MSCs) harvested from the bone marrow of healthy individuals and transduced with a retroviral vector encoding the human cytokine interferon beta (IFNb), with potential immunomodulating and antineoplastic activities. Upon administration of IFNb-secreting MSCs, the cells are attracted and specifically migrate to tumor sites and become part of the tumor microenvironment. Since the MSCs express IFNb, these cells selectively deliver high levels of IFNb to the tumor site. In turn, IFNb binds to IFN-specific cell surface receptors and modulates the transcription and translation of certain genes whose protein products are involved in tumor cell proliferation. This decreases tumor cell growth.","Cell|Pharmacologic Substance"]
["C66972","Interferon-gamma-expressing Adenovirus Vaccine ASN-002","ASN-002|Ad-IFNg|INFg-expressing Ad Vaccine ASN-002|Interferon-gamma-expressing Adenovirus Vaccine ASN-002|TG1042","A replication-defective adenoviral serotype 5 vector encoding a recombinant form of the human cytokine interferon-gamma (IFN-g), with potential antineoplastic and immunoregulatory activities. Upon intratumoral administration, the sustained expression of IFN-g by IFN-g-expressing adenovirus vaccine ASN-002 promotes a T-helper type 1 (Th1) immune response and inhibits the Th2-mediated cytokine production observed in many cutaneous lymphomas. IFN-g also mediates interleukin-12 (IL-12) production by antigen-presenting cells (APCs); activates macrophages, cytotoxic T-cells, and natural killer (NK) cells; upregulates major histocompatibility complex (MHC) molecules; and stimulates antibody-dependent cellular cytotoxicity (ADCC). Altogether, these IFN-g-mediated effects may result in both an inhibition of tumor cell proliferation and tumor cell death. Compared to IFN-g injections, the prolonged local production of IFN-g at the tumor site allows for higher efficacy and a reduction of systemic toxicity.","Pharmacologic Substance"]
["C2222","Interleukin-12 Gene","IL-12 gene|Interleukin-12 Gene|Plasmid DNA Encoding Human Interleukin-12|Plasmid IL-12|pIL-12","The DNA sequence that encodes the protein cytokine interleukin-12 (IL-12). When introduced as the complementary DNA (cDNA) form into tumor cells by, for example, a genetically engineered adenovirus vector, the transfected IL-12 cDNA expresses IL-12 which activates antitumoral natural killer (NK) cells and CD8+ T-cells and stimulates the secretion of interferon-gamma (IFN-gamma), potentially inhibiting tumor cell metastasis. This gene therapy may also result in IL-12-mediated inhibition of vascular endothelial growth factor (VEGF) and enhancement of matrix metalloproteinases (MMPs). (NCI04)","Gene or Genome|Pharmacologic Substance"]
["C2549","Interleukin-2 Gene","IL-2 Gene|Interleukin-2 Gene","The DNA sequence that encodes the protein cytokine interleukin-2 (IL-2). When introduced as the complementary DNA (cDNA) form into tumor cells by, for example, a genetically engineered adenovirus vector, the transfected IL-2 cDNA expresses IL-2 which may activate antitumoral natural killer cells and elicit an antitumoral cytotoxic T-cell response, resulting in an inhibition of tumor progression. (NCI04)","Gene or Genome|Pharmacologic Substance"]
["C2373","Interleukin-2 Liposome","Interleukin-2 Liposome|Liposome encapsulated interleukin-2","A formulation in which liposomes are loaded with the cytokine interleukin-2 (IL-2). By activating cytotoxic T-lymphocytes, such as lymphokine-activated killer cells, and increasing levels of the cytotoxic cytokines interferon-gamma (IFN-gamma) and transforming growth factor-beta (TGF-beta), IL-2 may exhibit antitumoral activity.  Liposomal formulations of IL-2 may promote entry of the cytokine into target tumor cells and may be used as an immunoadjuvant in cancer vaccine therapy. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C128107","Intermediate-affinity Interleukin-2 Receptor Agonist ALKS 4230","ALKS 4230|Intermediate-affinity IL-2R Agonist ALKS 4230|Intermediate-affinity Interleukin-2 Receptor Agonist ALKS 4230|RDB 1450","A selective effector cell activator protein and agonist of the intermediate-affinity interleukin-2 (IL-2) receptor with potential immunostimulating and antineoplastic activity. Upon administration, intermediate-affinity interleukin-2 receptor agonist ALKS 4230 binds to and signals through the intermediate-affinity IL-2 receptor complex; this may selectively stimulate and activate natural killer (NK) cells and memory CD8 T-cells, leading to tumor cell elimination, while circumventing the activation of immunosuppressive cells that may prevent the anti-tumor response. IL-2 is a cytokine signaling molecule that plays a critical role in the immune response.","Pharmacologic Substance"]
["C61070","Intetumumab","CNTO 095|CNTO-95|Human Anti-Alpha-5 Integrin Monoclonal Antibody|Human Monoclonal CNTO 95 gamma1 heavy chain (222-215')-disulfide with Human Monoclonal CNTO 95 kappa light chain dimer (228-228'':231-231'')-bisdisulfide|INTETUMUMAB|Immunoglobulin G1, anti-(human integrin alpha-V (vitronectin receptor subunit alpha or CD51))|Intetumumab","A pan alpha-v human monoclonal antibody that recognizes alpha-v beta-1, alpha-v beta-3, alpha-v beta-5, and alpha-v beta-6 integrins with antiangiogenic and antitumor activities. Intetumumab competitively binds to and blocks both alpha-v beta-3 and alpha-v beta-5 integrins, resulting in inhibition of integrin-mediated tumor angiogenesis and tumor growth. Integrins facilitate the adhesion of stimulated endothelial cells to the extracellular matrix (ECM); trigger the secretion of ECM-rearranging proteases; and propagate signaling events that promote the survival and differentiation of cells in newly formed vasculature.","Amino Acid, Peptide, or Protein"]
["C83820","Intiquinatine","(2R)-2-(4-((7-Bromoquinolin-2-yl)Oxy)Phenoxy)Propanoic Acid|INTIQUINATINE|Intiquinatine|Tiliquinatine","An antineoplastic agent.","Pharmacologic Substance"]
["C1495","Intoplicine","7H-benzo(e)pyrido(4,3-b)indol-3-ol, 11-((3-(dimethylamino)propyl)amino)-8-methyl|INTOPLICINE|Intoplicine|intoplicine","A benzopyridoindole derivative with antineoplastic property. Intoplicine inhibits activities of both topoisomerase I and II via intercalating DNA helix, thereby hindering the movements of enzymes along DNA molecules during DNA transcription and replication, respectively. Furthermore, this agent stabilizes DNA-enzyme complexes during unwinding processes by both topoisomerases, leading to double- and single-stranded DNA breaks. Consequently, these effects bring about cell growth inhibition and apoptosis of tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C61506","Inulin","INULIN|Inulin","A naturally occurring, indigestible and non-absorbable oligosaccharide produced by certain plants with prebiotic and potential anticancer activity. Inulin stimulates the growth of beneficial bacteria in the colon, including Bifidobacteria and Lactobacilli, thereby modulating the composition of microflora. This creates an environment that protects against pathogens, toxins and carcinogens, which can cause inflammation and cancer. In addition, fermentation of inulin leads to an increase in short-chain fatty acids and lactic acid production, thereby reducing colonic pH, which may further control pathogenic bacteria growth and may contribute to inulin's cancer protective properties.","Organic Chemical|Pharmacologic Substance"]
["C970","Iobenguane I-131","(131)I-MIBG|131I-MIBG|I 131 Meta-iodobenzylguanidine|I-131 Metaiodobenzylguanidine|IOBENGUANE I-131|Iobenguane I-131|Iodine I 131 Metaiodobenzylguanidine|MIBG I-131|iodine I 131 metaiodobenzylguanidine","An I 131 radioiodinated synthetic analogue of the neurotransmitter norepinephrine. Iobenguane localizes to adrenergic tissue and, in radioiodinated forms, may be used to image or eradicate tumor cells that take up and metabolize norepinephrine.","Indicator, Reagent, or Diagnostic Aid|Pharmacologic Substance"]
["C2440","Iodine I 124 Monoclonal Antibody A33","I 124 Monoclonal Antibody A33|Iodine I 124 Monoclonal Antibody A33|iodine I 124 MOAB A33","A radioimmunoconjugate of a humanized monoclonal antibody (MoAb) A33 labelled with Iodine 124 (I-124). MoAb A33 recognizes A33 antigen, a 43 KDa transmembrane glycoprotein of the immunoglobulin superfamily, highly and homogenously expressed in 95% of colorectal cancer metastases, with only restricted expression in normal colonic mucosa. I-124 MoAb A33 delivers beta particle emitting I-124 nuclide directly to metastatic colorectal tissues, thereby this agent could be used in kinetics studies or radioimmunotherapy.","Amino Acid, Peptide, or Protein|Indicator, Reagent, or Diagnostic Aid"]
["C74051","Iodine I 125-Anti-EGFR-425 Monoclonal Antibody","Iodine I 125-Anti-EGFR-425 Monoclonal Antibody","A radioimmunoconjugate consisting of a murine IgG2a monoclonal antibody directed against the human epidermal growth factor receptor (EGFR) labeled with iodine I 125 with potential antineoplastic activity. Iodine I 125 anti-EGFR-425 monoclonal antibody binds specifically to the epidermal growth factor receptor (EGFR). Upon binding to EGFR-expressing tumor cells, this agent is internalized, selectively delivering a potentially cytotoxic dose of gamma radiation. EGFR is a receptor tyrosine kinase that may be overexpressed on the cell surfaces of various solid tumors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C91389","Iodine I 131 Anti-Fibronectin Antibody Fragment L19-SIP","Iodine I 131 Anti-Fibronectin Antibody Fragment L19-SIP|L19-SIP","An iodine 131 radioimmunoconjugate of a small immunoprotein (SIP), derived from the variable region fragment of human monoclonal antibody L19, that is directed against the extra-domain B (ED-B) of fibronectin, with potential radioimmunotherapeutic activity. The SIP moiety of iodine I 131 anti-fibronectin antibody fragment L19-SIP binds to the ED-B domain of fibronectin on tumor cells in the tumor neovasculature. Upon internalization, the I 131 radionuclide may selectively detect or deliver cytotoxic radiation to fibronectin-expressing tumor cells. ED-B of fibronectin, a naturally occurring marker of tissue remodeling and angiogenesis, is expressed in the majority of aggressive solid human tumors, whereas it is not detectable in normal vessels and tissues.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2696","Iodine I 131 Ethiodized Oil","131 I-Ethiodized Oil|I 131 Lipiodol|Iodine I 131 Ethiodized Oil|Iodine I 131 Lipiodol|Lipiocis|iodine I 131 Lipiodol|iodine I 131 ethiodized oil","A cytotoxic radioconjugate consisting of lipiodol, an iodinated ethyl ester derived from poppy seed oil, labeled with iodine 131 (I-131).  I-131 Lipiodol accumulates in hepatocellular carcinoma and hepatoblastoma tumor cells, resulting in targeted cytotoxicity to tumor cells while sparing surrounding normal cells and tissues. (NCI04)","Pharmacologic Substance"]
["C2488","Iodine I 131 Monoclonal Antibody 81C6","I 131 Monoclonal Antibody 81C6|Iodine I 131 Monoclonal Antibody 81C6|Neuradiab|iodine I 131 MOAB 81C6","A radioimmunoconjugate consisting of 81C6, a murine IgG2 anti-tenascin monoclonal antibody labeled with iodine 131 (I-131), with radioimaging and radioimmunotherapeutic activities. Using monoclonal antibody 81C6 as a carrier for I-131 results in the targeted imaging and/or destruction of cells expressing tenascin. Tenascin is an extracellular matrix protein which is overexpressed in gliomas and other cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48400","Iodine I 131 Monoclonal Antibody 8H9","Iodine I 131 MOAB 8H9|Iodine I 131 Monoclonal Antibody 8H9","A radioimmunoconjugate consisting of the iodine 131-radiolabeled murine IgG1 monoclonal antibody 8H9 directed against the surface immunomodulatory glycoprotein 4Ig-B7-H3 with potential radioimaging and radioimmunotherapeutic uses. Iodine I 131 monoclonal antibody 8H9 binds to 4Ig-B7-H3 (human B7-H3 with 4 Ig-like domains) and may be used to radioimage and/or destroy tumor cells that express tenascin. 4Ig-B7-H3 inhibits T-cell activation and the production of effector cytokines such as interferon-gamma and interleukin-4; it is expressed on the cell membranes of a wide variety of tumors of neuroectodermal, mesenchymal and epithelial origin and is highly expressed on monocyte-derived dendritic cells (mdDCs). In vitro, it has been shown that monoclonal antibody-mediated masking of 4Ig-B7-H3 on neuroblastoma cells resulted in the enhancement of natural killer (NK)-mediated lysis of target cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2697","Iodine I 131 Monoclonal Antibody CC49-deltaCH2","131I-HuCC49-deltaCH2|131I-MOAB CC49-deltaCH2|I131 MOAB CC49-deltaCH2|Iodine I 131 Monoclonal Antibody CC49-deltaCH2","A radioimmunoconjugate consisting of the humanized CH2 domain-deleted monoclonal antibody CC49 and iodine I 131 with antineoplastic activity. Monoclonal antibody CC49-deltaCH2 targets the tumor-associated glycoprotein 72 (TAG-72) that is expressed by a wide range of human neoplasms including colorectal, gastric, pancreatic, ovarian, endometrial, breast, non-small cell lung, and prostate cancers. Iodine I 131 monoclonal antibody CC49-deltaCH2 binds to tumor cells expressing TAG-72, selectively delivering a cytotoxic dose of beta and gamma radiation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C95025","Iodine I 131 Monoclonal Antibody F16SIP","(131I) Monoclonal Antibody F16SIP|131I-F16SIP|F16-131I|Iodine I 131 Monoclonal Antibody F16SIP|Tenarad","A fully human monoclonal antibody (MoAb) against human A1 domain of tenascin-C, in small immunoprotein (SIP) format conjugated with iodine 131 with potential antineoplastic activity. Iodine I 131 MoAb F16SIP binds to tenascin-C on the vascular tissues and delivers cytotoxic radiation to the tumors, thereby minimizing systemic radiotoxicity. Tenascin-C is a glycoprotein of the extracellular matrix, and the large isoform of this matrix protein is expressed and restricted around vascular structures in the tumor stroma of a variety of different tumors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2449","Iodine I 131 Monoclonal Antibody G-250","I 131 Monoclonal Antibody G-250|Iodine I 131 Monoclonal Antibody G-250|iodine I 131 MOAB G 250|iodine I 131 MOAB G-250|iodine I 131 MOAB G250|iodine I 131 monoclonal antibody G250","A radioimmunoconjugate comprised of the chimeric monoclonal antibody G-250 conjugated with iodine I 131 with potential antineoplastic activity. The antibody moiety of iodine I 131 chimeric monoclonal antibody G-250 binds to G-250, a renal-cell carcinoma-associated antigen, delivering cytotoxic iodine I 131 specifically to renal carcinoma cells that express G-250.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2604","Iodine I 131 Monoclonal Antibody muJ591","Iodine I 131 Monoclonal Antibody muJ591","A radioimmunoconjugate of a mouse monoclonal antibody (MoAb) J591 labeled with Iodine 131 (I-131). MoAb muJ591 recognizes the extracellular domain of the prostate-specific membrane antigen (PSMA) and reacts with tumor vascular endothelium. Using MoAb muJ591 as a carrier for I-131 results in the targeted imaging and/or destruction of cells overexpressed PSM.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2223","Iodine I 131 Monoclonal Antibody TNT-1/B","I 131 MOAB TNT-1/B|I 131 Monoclonal Antibody TNT-1/B|Iodine I 131 Monoclonal Antibody TNT-1/B|iodine I 131 MOAB TNT-1/B","An iodine 131 labeled radioimmunoconjugate of monoclonal antibody (MOAB) TNT-1/B with radioimaging and antineoplastic properties. MOAB TNT-1/B was developed for radioimmunotherapy of solid tumors, designated as Tumor Necrosis Treatment (TNT). TNT exploits the presence of degenerating and necrotic cells within tumors by utilizing MOAbs directed against universal, intracellular nucleosomal determinants consisting of histone H1 and DNA. This MOAB was conjugated with biotin (B) molecules, which increase pharmacokinetic performance of the monoclonal antibody. MOAB TNT-1/B delivers I 131 to tumor cells and results in the targeted imaging and/or destruction of cells with exposed necrotic antigens.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C84879","Iodine I 131 Phospholipid Ether Analogue CLR1404","I-131 PLE Analogue CLR1404|I-131-CLR1404|Iodine I 131 Phospholipid Ether Analogue CLR1404","A small-molecule radiopharmaceutical consisting of the beta-emitting radioisotope iodine I 131 attached to a phospholipid ether (PLE) analogue, comprised of a linear 18 carbon backbone, with potential antineoplastic activity. Iodine I 131 phospholipid ether analogue CLR1404 selectively accumulates in tumor cells, thereby delivering a cytotoxic dose of radiation to cancer cells. Compared to normal cells, tumor cells are unable to metabolize and eliminate PLEs possibly due to deficiency of the enzyme phospholipase-D. In addition, the radioiodine moiety of this agent is resistant to de-iodination.","Pharmacologic Substance"]
["C102981","Iodine I 131 Rituximab","(131)I-Rituximab|131I-Rituxan|Iodine I 131 Rituximab","A radioimmunoconjugate comprised of rituximab, a recombinant chimeric monoclonal antibody directed against the CD20 antigen, and labeled with iodine I 131 with potential antineoplastic activity. The antibody moiety of iodine I 131 rituximab binds to the CD20 antigen thereby delivering cytotoxic iodine I 131 specifically to cancer cells expressing CD20. The CD20 antigen, a hydrophobic transmembrane protein, is expressed on normal pre-B and mature B lymphocytes.","Pharmacologic Substance"]
["C124996","Iodine I 131 Tenatumomab","131I-Tenatumomab|Iodine I 131 Tenatumomab","A radioimmunoconjugate of tenatumomab, a murine monoclonal antibody targeting the tumor-associated antigen (TAA) tenascin-C (TNC), labeled with iodine I 131, with potential antineoplastic activity. The antibody moiety of iodine I 131 tenatumomab binds to TNC, thereby delivering a cytotoxic dose of iodine I 131 specifically to tumors expressing TNC. TNC, an extracellular matrix protein, is upregulated in a variety of tumor cell types; it plays a key role in invasion, tumor cell proliferation and immune evasion.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48263","Iodine I 131 TM-601","131I-Chlorotoxin|131I-TM-601|131I-TM601|I 131 TM-601|Iodine I 131 TM-601","An iodine 131 (I 131) radioconjugate of the synthetic chlorotoxin (CTX) TM-601 with potential antiangiogenic and antineoplastic activities. CTX is a 36 amino acid neurotoxin found in the venom of the giant yellow scorpion Leiurus quinquestriatus that preferentially binds malignant cells of neuroectodermal origin. The recombinant version of this peptide, TM-601, is expressed in and purified from E. coli and then covalently linked to I 131 to produce 131I-TM-601. 131I-TM-601 binds to tumor cells of neuroectodermal origin and is internalized; administered once, it may be used as a radioimaging agent; repeated administration may result in a tumor-specific, cumulative radiocytotoxic dose of I 131. In addition, TM-601 alone, similar to native CTX, may inhibit angiogenesis due to its ability to bind to and inhibit matrix metalloproteinase 2 (MMP-2), an endopeptidase involved in tissue remodeling processes such as angiogenesis.","Pharmacologic Substance"]
["C2444","Iodine I 131 Tositumomab","131-I-Anti-B1 Monoclonal Antibody|I 131 Monoclonal Antibody Anti-B1|I 131 Tositumomab|I131-MOAB-B1|Iodine I 131 MOAB Anti-B1|Iodine I 131 Monoclonal Antibody Anti-B1|Iodine I 131 Tositumomab|Iodine-131 Anti-B1 Antibody|Iodine-131 Anti-CD20 Monoclonal Antibody|Iodine-131 Tositumomab|TOSITUMOMAB I-131|iodine I 131 tositumomab","A monoclonal antibody directed against the CD20 protein expressed on the surface of B-lymphocytes and radiolabeled with the radioisotope iodine I 131 with potential antineoplastic activity. Iodine I 131 tositumomab binds to and selectively delivers cyctotoxic radiation to CD20-expressing B-lymphocytes, thereby minimizing systemic radiotoxicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1639","Iodine I-131","131-Iodine|Bound Iodide I-131|I 131|I-131|IODINE I-131|Iodide I-131|Iodide, I-131|Iodine 131|Iodine I-131|Iodotope|Iodotrope","A radioactive isotope of iodine with an atomic mass of 131, a half life of eight days, and potential antineoplastic activity. Selectively accumulating in the thyroid gland, iodine I 131 emits beta and gamma particles, thereby killing thyroid cells and decreasing thyroid hormone production.","Element, Ion, or Isotope|Indicator, Reagent, or Diagnostic Aid|Pharmacologic Substance"]
["C80056","Ioflubenzamide I-131","IOFLUBENZAMIDE I-131|Ioflubenzamide I-131|MIP-1145|N-(2-(diethylamino)ethyl)-4-((4-fluorobenzoyl)amino)-5-((sup 131)I)iodo-2-methoxybenzamide","An iodine 131-radiolabeled small-molecule benzamide compound with potential antineoplastic activity. The benzamide moiety of 131-I-MIP-1145 binds to melanin, selectively delivering a cyotoxic dose of gamma and beta radiation to melanin-expressing tumor cells. Melanin pigments, polymer derivatives of the amino acid tyrosine, are over-expressed in approximately 40% of melanomas.","Pharmacologic Substance"]
["C596","Ionomycin","Ionomycin|ionomycin","A polyether antibiotic isolated from Streptomyces conglobatus sp. nov. Trejo with antineoplastic activity.  Ionomycin is a calcium ionophore that increases intracellular Ca++ levels, possibly relating to endonuclease activation of lymphocytes and decreased ratio of Bcl-2 to Bax and ultimately apoptosis.  In addition, this agent is used to investigate the role of intracellular calcium in cellular processes. (NCI)","Antibiotic"]
["C102565","Ipafricept","Fusion Protein For Immune Applications (fpia) Comprising Homo Sapiens FZD8 (Frizzled Family Receptor 8, Frizzled-8) Extracellular Domain, Fused With Homo Sapiens Immunoglobulin G1 Fc Fragment|Fzd8-Fc|IPAFRICEPT|Ipafricept|OMP 54F28|OMP-54F28","A proprietary fusion protein comprised of the cysteine-rich domain of frizzled family receptor 8 (Fzd8) fused to the human immunoglobulin Fc domain with potential antineoplastic activity. Upon intravenous administration, ipafricept competes with the membrane-bound Fzd8 receptor for its ligand, Wnt proteins, thereby antagonizing Wnt signaling. This may result in the inhibition of Wnt-driven tumor growth. Fzd8, a member of the Frizzled family of G protein-coupled receptors, is one of the components in the Wnt/beta-catenin signaling pathway that plays key roles in embryogenesis and cancer growth.","Pharmacologic Substance"]
["C91072","Ipatasertib","(2S)-2-(4-chlorophenyl)-1-(4-((5r,7r)-7-hydroxy-5-methyl-6,7-dihydro-5h-cyclopenta(d)pyrimidin-4-yl)piperazin-1-yl(-3-((propan-2-yl)amino)propan-1-one|GDC-0068|IPATASERTIB|Ipatasertib|RG-7440","An orally bioavailable inhibitor of the serine/threonine protein kinase Akt (protein kinase B) with potential antineoplastic activity. Ipatasertib binds to and inhibits the activity of Akt in a non-ATP-competitive manner, which may result in the inhibition of the PI3K/Akt signaling pathway and tumor cell proliferation and the induction of tumor cell apoptosis. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Organic Chemical|Pharmacologic Substance"]
["C60772","IPI-609","IPI-609","A novel proprietary small molecule, and a selective inhibitor of sonic hedgehog signaling pathway, with potential anti-tumor activity. The hedgehog signaling pathway is normally active during neuronal development in embryos and quiescent in adult cells. However, aberrant activation of the hedgehog pathway in adults has been implicated in many cancers, including cancers of the pancreas, prostate, lung (small cell), and brain (glioma). IPI-609 exerts its effect through inhibiting the hedgehog signaling pathway and thereby alters gene expressions of the cancer cells.","Pharmacologic Substance"]
["C2654","Ipilimumab","Anti-Cytotoxic T-Lymphocyte-Associated Antigen-4 Monoclonal Antibody|BMS-734016|IPILIMUMAB|Ipilimumab|MDX-010|MDX-CTLA4|Yervoy|ipilimumab","A recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4), with immune checkpoint inhibitory and antineoplastic activities. Ipilimumab binds to CTLA4 expressed on T-cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C976","Ipomeanol","1-(3-Furanyl)-4-hydroxy-1-pentanone|1-(3-furanyl)-4-hydroxy-1-pentanone|1-Pentanone, 1-(3-furanyl)-4-hydroxy-|4-Ipomeanol|4-ipomeanol|Ipomeanol","A natural toxic furan isolated from a fungus-infected sweet potato (Ipomoea batatas) with potential antineoplastic activity.  Ipomeanol is activated by mixed function oxidases in vivo to its epoxide form, an alkylating agent that covalently binds cell macromolecules. This agent causes cell death by a p53-independent mechanism. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1070","Iproplatin","(OC-6-33)-dichlorodihydroxybis(2-propanamine)platinum|CHIP|Diisopropylammine-trans-dihydroxymalonatoplatinum(IV)|IPROPLATIN|Iproplatin|JM-9|Platinum, dichlorodihydroxybis(2-propanamine)-, (oc-6-33)-","A synthetic second-generation platinum-containing compound related to cisplatin. Iproplatin binds to and forms DNA crosslinks and platinum-DNA adducts, resulting in DNA replication failure and cell death.  Although less prone to glutathione inactivation compared to cisplatin, resistance to this agent has been observed in vitro due to repair of platination damage by tumor cells. (NCI04)","Pharmacologic Substance"]
["C26441","Iratumumab","IRATUMUMAB|Iratumumab|MDX-060|Monoclonal Antibody MDX-060","A fully human monoclonal antibody with potential antineoplastic activity.  MDX-060 is a fully humanized antibody that targets CD30, a member of the tumor necrosis factor receptor superfamily found on activated lymphocytes.  CD30 is over-expressed in various lymphoproliferative disorders, Hodgkin's disease and other lymphomas, and other cancers. (NCI04)","Amino Acid, Peptide, or Protein|Indicator, Reagent, or Diagnostic Aid"]
["C104270","Iridium Ir 192","Ir-192|Iridium Ir 192|Iridium-192","A radioactive isotope of iridium. Iridium-192 emits gamma rays and has a half-life of 74 days. A high dose rate of this radioisotope can be used in brachytherapy to treat tumors by selectively delivering a cytotoxic dose of radiation to the tumor site.","Indicator, Reagent, or Diagnostic Aid"]
["C62040","Irinotecan","(+)-(4S)-4,11-diethyl-4-hydroxy-9-[(4-piperidino-piperidino)carbonyloxy]-1H-pyrano[3',4':6,7]indolizino[1,2-b]quinol-3,14,(4H,12H)-dione|(+)-7-ethyl-10-hydroxycamptothecine 10-[1,4'-bipiperidine]-1'-carboxylate|7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin|IRINOTECAN|Irinotecan|[1,4'-bipiperidine]-1'-carboxylic acid (S)-4,11-diethyl-3,4,12,14-tetrahydro-4-hydroxy-3,14-dioxo-1H-pyrano[3',4':6,7]indolizino[1,2-b]quinolin-9-yl ester|irinotecan","A semisynthetic derivative of camptothecin, a cytotoxic, quinoline-based alkaloid extracted from the Asian tree Camptotheca acuminata.  Irinotecan, a prodrug, is converted to a biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38) by a carboxylesterase-converting enzyme.  One thousand-fold more potent than its parent compound irinotecan, SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death.  Because ongoing DNA synthesis is necessary for irinotecan to exert its cytotoxic effects, it is classified as an S-phase-specific agent.","Organic Chemical|Pharmacologic Substance"]
["C1381","Irinotecan Hydrochloride","CPT 11|CPT-11|Campto|Camptosar|Camptothecin 11|Camptothecin-11|IRINOTECAN HYDROCHLORIDE|Irinomedac|Irinotecan Hydrochloride|U-101440E|irinotecan hydrochloride","The hydrochloride salt of a semisynthetic derivative of camptothecin, a cytotoxic, quinoline-based alkaloid extracted from the Asian tree Camptotheca acuminata.  Irinotecan, a prodrug, is converted to a biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38) by a carboxylesterase-converting enzyme.  One thousand-fold more potent than its parent compound irinotecan, SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death.  Because ongoing DNA synthesis is necessary for irinotecan to exert its cytotoxic effects, it is classified as an S-phase-specific agent.","Organic Chemical|Pharmacologic Substance"]
["C88280","Irinotecan/P-glycoprotein Inhibitor HM30181AK Combination Tablet","Irinotecan/P-glycoprotein Inhibitor HM30181AK Combination Tablet|Oratecan","An orally bioavailable combination tablet containing the semisynthetic camptothecin derivative irinotecan and the multidrug resistance (MDR) efflux pump P-glycoprotein (P-gp) inhibitor HM30181AK, with potential antineoplastic activity. HM30181A binds to P-gp and prevents the P-gp-mediated efflux of irinotecan from tumor cells, which may result in greater intracellular concentrations of irinotecan and enhanced cytotoxicity. Retained intracellularly, the prodrug irinotecan is converted, by a carboxylesterase-converting enzyme, to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38). SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death.  P-gp, encoded by the MDR-1 gene, is a member of the ATP-binding cassette (ABC) superfamily of transmembrane transporters and is overexpressed by some MDR tumors, preventing the intracellular accumulation of various cytotoxic agents.","Pharmacologic Substance"]
["C82682","Irinotecan-Eluting Beads","CM-BC2|Irinotecan Hydrochloride Drug-eluting Beads|Irinotecan-Eluting Beads","Microporous hydrospheres of polyvinylalcohol (PVA) impregnated with irinotecan with potential antineoplastic activity. In transarterial chemoembolization (TACE), irinotecan-eluting beads are administered into blood vessels that feed the tumor, occluding tumor blood vessels and inducing ischemic tumor necrosis while simultaneously delivering high-dose chemotherapy locally. Irinotecan, a semisynthetic derivative of camptothecin, inhibits topoisomerase I activity by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptotic cell death.","Pharmacologic Substance"]
["C1717","Irofulven","(R)-6'-Hydroxy-3'-(hydroxymethyl)-2',4',6'-trimethylspiro(cyclopropane-1,5'(5H)-inden)-7'(6'H)-one|6-Hydroxymethylacylfulvene|6-hydroxymethylacylfulvene|HMAF|Hydroxymethylacylfulvene|IROFULVEN|Irofulven|MGI 114|MGI-114|irofulven","A semisynthetic sesquiterpene derivative of illudin S, a natural toxin isolated from the fungus Omphalotus illudens.  Irofulven alkylates DNA and protein macromolecules, forms adducts, and arrests cells in the S-phase of the cell cycle.  This agent requires NADPH-dependent metabolism by alkenal/one oxidoreductase for activity. Irofulven is more active in vitro against tumor cells of epithelial origin and is more resistant to deactivation by p53 loss and MDR1 than other alkylating agents. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C79827","Irosustat","667 Coumate|BN83495|IROSUSTAT|Irosustat|STX 64|Steroid Sulfatase Inhibitor BN 83495","Steroid sulfatase inhibitor BN 83495 selectively binds to and inhibits steroid sulfatase (STS), which may inhibit the production of locally active estrogens and so inhibit estrogen-dependent cell growth in tumor cells, such as those of the breast, ovary, and endometrium. STS is a cytoplasmic enzyme responsible for the conversion of circulating inactive estrone sulfate and estradiol sulfate to biologically active unconjugated estrone and estradiol, respectively.","Pharmacologic Substance"]
["C53396","IRX-2","IRX-2","A cell-free mixture comprised of a variety of naturally-derived cytokines obtained from normal, unrelated donor lymphocytes with potential immunostimulatory activity. The cytokines in IRX-2, including interleukin (IL)-1, -2, -6, -8, -10, -12, tumor necrosis factor alpha (TNF-a), interferon-gamma (IFN-g) and colony stimulating factors (CSFs), play vital roles in regulating cellular immunity and may synergistically stimulate a cellular immune response against tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2024","ISIS 2503","H-RAS Antisense|ISIS 2503|ISIS-2503","A synthetic oligodeoxynucleotide.  Functioning as an anti-sense agent, it hybridizes to the translation initiation region of the human mRNA for the oncogene H-Ras.  ISIS 2503 selectively inhibits the expression of H-Ras, and may inhibit the growth of some Ras-dependent tumor cells. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1788","ISIS 3521","Affinitac|Affinitak|CGP 64128A|DNA, d(P-thio)(G-T-T-C-T-C-G-C-T-G-G-T-G-A-G-T-T-T-C-A)|DNA, d(P-thio)(GTTCTCGCTGGTGAGTTTCA)|ISIS 3521|LY900003|Protein Kinase C-Alpha Antisense","A synthetic phosphorothioate oligodeoxynucleotide. As an antisense molecule, ISIS 3521 hybridizes to the 3-untranslated region of the human protein kinase C (PKC-alpha) mRNA, thereby inhibiting PKC-alpha expression and growth of PKC-alpha-dependent tumor cells. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1774","Isobrucein B","Isobrucein B","A quassinoid phytochemical isolated from the tropical plant Cedronia granatensis with potential antineoplastic and chemopreventive activities. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C97332","Iso-fludelone","17-Iso-oxazole-26-F3-9,10-dehydro-12,13-desoxy-epothilone B|17-Iso-oxazole-fludelone|Iso-fludelone|KOS-1803","A third-generation epothilone B analogue with potential anti-mitotic and antineoplastic activites. Iso-fludelone binds to tubulin and induces microtubule polymerization and stabilizes microtubules against depolymerization, which may result in the inhibition of cell division, the induction of G2/M arrest, and apoptosis. Compared to other generations of epothilones, iso-fludelone exhibits increased stability, water solubility, potency, duration of action, tumor penetration as well as reduced toxicity. In addition, this agent is a not a substrate of the P-glycoprotein (P-gp), a multidrug resistance pump often overexpressed in cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C603","Isotretinoin","13-cRA|13-cis retinoic acid|13-cis-Retinoate|13-cis-Retinoic Acid|13-cis-Vitamin A Acid|3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)2-cis-4-trans-6-trans-8-trans-nonatetraenoic Acid|Accure|Accutane|Amnesteem|Cistane|Claravis|ISOTRETINOIN|Isotretinoin|Isotretinoinum|Isotrex|Isotrexin|Neovitamin A Acid|Neovitamin A|Oratane|Retinoicacid-13-cis|Ro 4-3780|Ro-4-3780|Roaccutan|Roaccutane|Roacutan|Sotret|cis-Retinoic Acid|isotretinoin","A naturally-occurring retinoic acid with potential antineoplastic activity. Isotretinoin binds to and activates nuclear retinoic acid receptors (RARs); activated RARs serve as transcription factors that promote cell differentiation and apoptosis. This agent also exhibits immunomodulatory and anti-inflammatory responses and inhibits ornithine decarboxylase, thereby decreasing polyamine synthesis and keratinization.","Organic Chemical|Pharmacologic Substance"]
["C38131","Ispinesib","CK0238273|ISPINESIB|Ispinesib|SB-715992|ispinesib","A synthetic small molecule, derived from quinazolinone, with antineoplastic properties. Ispinesib selectively inhibits the mitotic motor protein, kinesin spindle protein (KSP), resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest during the mitotic phase, and cell death in tumor cells that are actively dividing. Because KSP is not involved in nonmitotic processes, such as neuronal transport, ispinesib may be less likely to cause the peripheral neuropathy often associated with the tubulin-targeting agents.","Organic Chemical|Pharmacologic Substance"]
["C77518","Ispinesib Mesylate","ISPINESIB MESYLATE|Ispinesib Mesylate","The mesylate salt form of ispinesib, a synthetic small molecule, derived from quinazolinone, and kinesin spindle protein (KSP) inhibitor, with antineoplastic activity. Ispinesib selectively inhibits KSP and prevents its binding to microtubules, resulting in inhibition of mitotic spindle assembly, induction of cell cycle arrest during the M-phase, and cell death in tumor cells that are actively dividing.","Pharmacologic Substance"]
["C61080","ISS 1018 CpG Oligodeoxynucleotide","ISS 1018 CpG Oligodeoxynucleotide","A short, synthetic, unmethylated CpG motif-based oligodeoxynucleotide (CpG ODN) with immunostimulatory activity. As an immunostimulatory sequence (ISS) that signals through Toll-like receptor 9 (TLR9), ISS 1018 CpG ODN induces the production of immunoglobulin by B cells and interferon (IFN) -alpha, IFN-beta, interleukin (IL) -12, and tumor necrosis factor (TNF) -alpha by plasmacytoid dendritic cells (pDC). pDC, through cell-cell contact, and IFN-alpha and -beta, in turn, induce natural killer (NK) cell proliferation, NK cell production of IFN-gamma, and NK cell-mediated cytotoxicity; secreted IFNs also stimulate bystander T cell activation and differentiation of naive CD4+ T cells into T-helper 1 cells on specific antigen challenge. In addition, ISS 1018 CpG ODN promotes antigen presentation and co-stimulatory molecule expression.","Chemical Viewed Structurally"]
["C104048","Itraconazole Dispersion In Polymer Matrix","Itraconazole Dispersion In Polymer Matrix|SUBA-Itraconazole","A proprietary oral formulation composed of the poorly soluble, synthetic triazole agent, itraconazole, dispersed in a polymer matrix, with antifungal and potential anti-angiogenic activities. Upon oral administration, itraconazole inhibits the enzyme cytochrome P450 lanosterol 14 alpha-demethylase, resulting in a decrease in fungal ergosterol synthesis. Although the exact mechanism through which itraconazole inhibits angiogenesis has yet to be fully elucidated, this agent appears to inhibit the Hedgehog (Hh) signaling pathway, cholesterol synthesis and mammalian target of rapamycin (mTOR) signaling in endothelial cells. This agent may also prevent the activation of and signaling by various angiogenic growth factors. By decreasing the tumor vasculature and nutrient supply, itraconazole ultimately inhibits tumor cell growth. The solid dispersion of itraconazole in the polymer matrix enhances dissolution of itraconazole in the gastrointestinal tract and increases its bioavailability; this allows for the administration of a much lower dose compared to itraconazole alone.","Pharmacologic Substance"]
["C113650","IVAC Mutanome Vaccine","IVAC Mutanome Vaccine","An individualized, poly-neo-epitopic encoding, ribonucleic acid (RNA)-based cancer vaccine that targets a variety of patient-specific, immunogenic mutant epitopes, with potential immunostimulatory and antineoplastic activities. Upon intranodal administration, the RNA in the individualized mutanome vaccine is translated by antigen presenting cells (APCs) and the expressed protein is presented via major histocompatibility complex (MHC) molecules on the surface of the APCs. This leads to an induction of both cytotoxic T-lymphocyte (CTL) and memory T-cell immune responses against the patient-specific neoantigens.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C37452","Ixabepilone","(1S,3S,7S,10R,11S,12S,16R)-7,11-Dihydroxy-8,8,10,12,16-pentamethyl-3-[(1E)-1-methyl-2-(2-methyl-4-thiazolyl)ethenyl]-17-oxa-4-azabicyclo[14.1.0]heptadecane-5,9-dione|Azaepothilone B|BMS 247550|BMS-247550|BMS247550|Epothilone-B BMS 247550|Epothilone|IXABEPILONE|Ixabepilone|Ixempra|ixabepilone","An orally bioavailable semisynthetic analogue of epothilone B with antineoplastic activity. Ixabepilone binds to tubulin and promotes tubulin polymerization and microtubule stabilization, thereby arresting cells in the G2-M phase of the cell cycle and inducing tumor cell apoptosis. This agent demonstrates antineoplastic activity against taxane-resistant cell lines.","Pharmacologic Substance"]
["C97940","Ixazomib","IXAZOMIB|Ixazomib|MLN-2238|MLN2238|{(1R)-1-[(2,5-dichlorobenzamido)acetamido]-3-methylbutyl}boronic Acid","An active metabolite of MLN9708, a second generation, boron containing peptide proteasome inhibitor (PI) with potential antineoplastic activity. Ixazomib binds to and inhibits the 20S catalytic core of the proteasome, thereby blocking the targeted proteolysis normally performed by the proteasome, which results in an accumulation of unwanted or misfolded proteins; disruption of various cell signaling pathways may follow, resulting in the induction of apoptosis. Compared to first generation PIs, second generation PIs may have an improved pharmacokinetic profile with increased potency and less toxicity. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquinated.","Organic Chemical|Pharmacologic Substance"]
["C82653","Ixazomib Citrate","1,3,2-dioxaborinane-4-acetic acid, 4-carboxy-2-((1r)-1-((2-((2,5-dichlorobenzoyl)amino)acetyl)amino)-3-methylbutyl)-6-oxo-|IXAZOMIB CITRATE|Ixazomib Citrate|MLN-9708|MLN9708|Ninlaro","The citrate salt form of ixazomib, an orally bioavailable second generation proteasome inhibitor (PI) with potential antineoplastic activity. Ixazomib inhibits the activity of the proteasome, blocking the targeted proteolysis normally performed by the proteasome, which results in an accumulation of unwanted or misfolded proteins; disruption of various cell signaling pathways may follow, resulting in the induction of apoptosis. Compared to first generation PIs, second generation PIs may have an improved pharmacokinetic profile with increased potency and less toxicity. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquinated.","Organic Chemical|Pharmacologic Substance"]
["C111761","JAK Inhibitor INCB047986","INCB 047986|INCB-047986|INCB047986|JAK Inhibitor INCB047986","An orally bioavailable inhibitor of Janus-associated kinases (JAK), with potential antineoplastic activity. Upon oral administration, INCB047986 specifically binds to and inhibits the phosphorylation of JAK, which affects JAK-dependent signaling and may lead to an inhibition of cellular proliferation in JAK-overexpressing tumor cells. The JAK-STAT (signal transducer and activator of transcription) pathway plays a key role in the signaling of many cytokines and growth factors and is involved in cellular proliferation, growth, hematopoiesis, and the immune response; JAK kinases may be upregulated in inflammatory diseases, myeloproliferative disorders, and various malignancies.","Pharmacologic Substance"]
["C116855","JAK1 Inhibitor INCB039110","INCB039110|JAK1 Inhibitor INCB039110","An orally bioavailable inhibitor of Janus-associated kinase 1 (JAK1) with potential antineoplastic activity. Upon oral administration of JAK1 inhibitor INCB039110, this agent selectively inhibits the phosphorylation and activity of JAK1, which may result in inhibition of JAK1-mediated signaling, induction of apoptosis, and reduction of cell proliferation in JAK1-expressing tumor cells. JAK1 is overexpressed in a variety of tumor cell types and plays a key role in tumor cell proliferation.","Pharmacologic Substance"]
["C118629","JAK1 Inhibitor INCB052793","INCB052793|JAK1 Inhibitor INCB052793","An orally bioavailable inhibitor of Janus-associated kinase 1 (JAK1), with potential antineoplastic activity. Upon oral administration, INCB052793 specifically binds to and inhibits the phosphorylation of JAK1, which interferes with JAK-dependent signaling and may lead to an inhibition of cellular proliferation in JAK1-overexpressing tumor cells. The JAK-STAT (signal transducer and activator of transcription) signaling pathway is a major mediator of cytokine activity and is often dysregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C91394","JAK2 Inhibitor AZD1480","AZD1480|JAK2 Inhibitor AZD1480","An orally bioavailable inhibitor of Janus-associated kinase 2 (JAK2) with potential antineoplastic activity. JAK2 inhibitor AZD1480 inhibits JAK2 activation, leading to the inhibition of the JAK/STAT (signal transducer and activator of transcription) signaling including activation of STAT3. This may lead to induction of tumor cell apoptosis and a decrease in cellular proliferation. JAK2, often upregulated or mutated in a variety of cancer cells, mediates STAT3 activation and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C95702","JAK2 Inhibitor BMS-911543","BMS-911543|JAK2 Inhibitor BMS-911543","An orally available small molecule targeting a subset of Janus-associated kinase (JAK) with potential antineoplastic activity. JAK2 inhibitor BMS-911543 selectively inhibits JAK2, thereby preventing the JAK/STAT (signal transducer and activator of transcription) signaling cascade, including activation of STAT3. This may lead to an induction of tumor cell apoptosis and a decrease in cellular proliferation. JAK2, often upregulated or mutated in a variety of cancer cells, mediates STAT3 activation and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C88293","JAK2 Inhibitor TG101348","JAK2 Inhibitor TG101348|SAR302503|TG101348","An orally bioavailable, small-molecule, ATP-competitive inhibitor of Janus-associated kinase 2 (JAK2) with potential antineoplastic activity. JAK2 inhibitor TG101348 competes with JAK2 as well as the mutated form AK2V617F for ATP binding, which may result in inhibition of JAK2 activation, inhibition of the JAK-STAT signaling pathway, and the induction of tumor cell apoptosis. JAK2 is the most common mutated gene in bcr-abl-negative myeloproliferative disorders (MPDs); the mutated form JAK2V617F has a valine-to-phenylalanine modification at position 617 and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C111042","JAK2 Inhibitor WP1066","(E)-3(6-bromopyridin-2-yl)-2-cyano-N-((S0-1-phenylethyl)acrylamide|JAK2 Inhibitor WP1066|WP1066","An orally bioavailable inhibitor of Janus-associated kinase 2 (JAK2) with potential antineoplastic activity. Upon oral administration, WP1066 specifically binds to both JAK2 and its mutated form JAK2 V617F, and inhibits their phosphorylation and activation. In addition, this agent degrades JAK2 protein. This results in the inhibition of the JAK- signal transducer and activator of transcription (STAT) and phosphoinositide-3-kinase (PI3K)/AKT signaling pathways, resulting in the induction of apoptosis in tumor cells overexpressing JAK2. JAK2, a tyrosine kinase, is overexpressed in a variety of tumor cells and is correlated with increased tumor cell proliferation and survival. The mutated form JAK2 V617F has a valine-to-phenylalanine modification at position 617 and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C90573","JAK2 Inhibitor XL019","JAK2 Inhibitor XL019|XL019","An orally bioavailable inhibitor of Janus-associated kinase 2 (JAK2) with potential antineoplastic activity. XL019 inhibits the activation of JAK2 as well as the mutated form JAK2V617F, which may result in the inhibition of the JAK-STAT signaling pathway and may induce apoptosis. The JAK2 mutated form JAK2V617F has a valine-to-phenylalanine modification at position 617 and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C98109","JAK2/Src Inhibitor NS-018","JAK2/Src Inhibitor NS-018|NS-018","An orally bioavailable, small molecule inhibitor of Janus-associated kinase 2 (JAK2) and Src-family kinases, with potential antineoplastic activity. JAK2 inhibitor NS-018 competes with ATP for binding to JAK2 as well as the mutated form JAK2V617F, thereby inhibiting the activation of JAK2 and downstream molecules in the JAK2/STAT3 (signal transducer and activator of transcription 3) signaling pathway that plays an important role in normal development, particularly hematopoiesis. In addition, NS-018 inhibits the Src family tyrosine kinases. This eventually leads to the induction of tumor cell apoptosis. JAK2 is the most common mutated gene in bcr-abl-negative myeloproliferative disorders (MPDs); JAK2V617F is a constitutively activated kinase that activates the JAK/STAT signaling pathway and dysregulates cell growth and function, and its expression transforms hematopoietic cells to cytokine-independent growth.","Pharmacologic Substance"]
["C61316","Jin Fu Kang","Jin Fu Kang","A traditional Chinese herbal medicine derived from the plant Astragalus membranaceus with potential immunopotentiation activity. Jin Fu Kang may stimulate anti-tumor macrophage and natural killer cell activity and may enhance immune recognition of tumor cells by inhibiting the production of T-helper cell type 2 (Th2) cytokines such as interleukin-4 (IL-4) and interleukin-10 (IL-10).","Pharmacologic Substance"]
["C91705","Kanglaite","Coicis Semen Oil|KLT|Kanglaite","An injectable microemulsion of a purified oil extracted from the seeds of the traditional Chinese medicinal herb Coix lacryma-jobi (Job's tears), with potential antineoplastic activity. Although the exact mechanism of action is unknown, kanglaite exhibits an antineoplastic effect, potentially via interfering with the cell cycle and halting tumor cells in the G2/M phase, which may eventually inhibit mitosis and proliferation of cancer cells.","Pharmacologic Substance"]
["C605","Ketoconazole","Cis-1-Acetyl-4-[4-[[2-(2,4-dichlorophenyl)-2-(1H-imidazole-1-ylmethyl)-1,3-dioxolan-4-yl]methoxy]phenyl]piperazine|Fungarest|Fungoral|KETOCONAZOLE|Ketoconazole|Ketoderm|Ketoisdin|Nizoral|Orifungal M|Panfungol|R-41400|Xolegel|ketoconazole","A synthetic derivative of phenylpiperazine with broad antifungal properties and potential antineoplastic activity.  Ketoconazole inhibits sterol 14-a-dimethylase, a microsomal cytochrome P450-dependent enzyme, thereby disrupting synthesis of ergosterol, an important component of the fungal cell wall. (NCI04)","Antibiotic|Organic Chemical"]
["C77403","Ketotrexate","KETOTREXATE|Ketotrexate","A folic acid antagonist and mammalian dihydrofolate reductase inhibitor with antineoplastic activity. Ketotrexate inhibits dihydrofolate reductase, an enzyme that reduces dihydrofolic acid to tetrahydrofolic acid which is essential for the synthesis of purine nucleotides and thymidylate. By depleting tetrahydrofolic acid availability, DNA synthesis is halted.","Pharmacologic Substance"]
["C124067","KIT/PDGFR Inhibitor DCC-2618","1-N'-[2,5-difluoro-4-[2-(1-methylpyrazol-4-yl)pyridin-4-yl]oxyphenyl]-1-N'-phenylcyclopropane-1,1-dicarboxamide|DCC-2618|DCC2618|KIT/PDGFR Inhibitor DCC-2618","An orally bioavailable switch pocket control inhibitor of wild-type and mutated forms of the tumor-associated antigens (TAA) mast/stem cell factor receptor (SCFR) KIT and platelet-derived growth factor receptor alpha (PDGFR-alpha; PDGFRa), with potential antineoplastic activity. Upon oral administration, DCC-2618 targets and binds to both wild-type and mutant forms of KIT and PDGFRa specifically at their switch pocket binding sites, thereby preventing the switch from inactive to active conformations of these kinases and inactivating their wild-type and mutant forms. This abrogates KIT/PDGFRa-mediated tumor cell signaling and prevents proliferation in KIT/PDGFRa-driven cancers. DCC-2618 also inhibits several other kinases, including vascular endothelial growth factor receptor type 2 (VEGFR2; KDR), angiopoietin-1 receptor (TIE2; TEK), PDGFR-beta and macrophage colony-stimulating factor 1 receptor (FMS; CSF1R), thereby further inhibiting tumor cell growth. KIT and PDGFRa are tyrosine kinase receptors that are upregulated or mutated in a variety of cancer cell types; mutated forms play a key role in the regulation of tumor cell proliferation and resistance to chemotherapy.","Pharmacologic Substance"]
["C2771","KLH-Lymphoma Ig Vaccine","Id KLH Lymphoma|KLH-Lymphoma Ig Vaccine|Lymphoma Ig Vaccine-KLH","A chimeric lymphoma vaccine generated by combining the recipient's Ig idiotype (Id) protein with keyhole limpet hemocyanin (KLH), an immune stimulant, with potential antineoplastic activity.  Vaccination with KLH-Lymphoma Ig Vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against lymphoma cells, resulting in decreased tumor growth. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C1614","KRN5500","6-[4-Deoxy-4-[(2E,4E)-tetradecadienoylglycyl]amino-L-glycero-beta-L-mannohepto-pyranosyl]amino-9H-purine|KRN5500","A semisynthetic derivative of the nucleoside-like antineoplastic antibiotic spicamycin, originally isolated from the bacterium Streptomyces alanosinicus.  KRN 5500 inhibits protein synthesis by interfering with endoplasmic reticulum and Golgi apparatus functions.  This agent also induces cell differentiation and caspase-dependent apoptosis. (NCI04)","Antibiotic|Organic Chemical"]
["C2520","KSA-KLH Conjugate Vaccine","KSA-KLH Conjugate Vaccine|KSA-KLH","A peptide vaccine containing an epitope of human tumor-associated KSA antigen (Ep-CAM) conjugated with keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. KSA antigen, a type-I transmembrane glycoprotein and a cellular adhesion molecule with a molecular mass of 40 kDa, is overexpressed on the majority of epithelial tumor cells. KSA antigen is conjugated with KLH, an immunostimulant and a hapten carrier, to enhance immune recognition. Vaccination with KSA-KLH may result in the production of antibodies as well as eliciting a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the KSA antigen.","Immunologic Factor|Pharmacologic Substance"]
["C68937","KSP Inhibitor ARRY-520","ARRY-520|KSP Inhibitor ARRY-520","A synthetic, small molecule targeting the kinesin spindle protein (KSP) with potential antineoplastic activity. KSP inhibitor ARRY-520 specifically inhibits KSP (kinesin-5 or Eg5), resulting in activation of the spindle assembly checkpoint, induction of cell cycle arrest during the mitotic phase, and consequently cell death in tumor cells that are actively dividing. Because KSP is not involved in postmitotic processes, such as neuronal transport, this agent does not cause the peripheral neuropathy that is often associated with tubulin-targeting agents. KSP is an ATP-dependent microtubule motor protein that is essential for the formation of bipolar spindles and the proper segregation of sister chromatids during mitosis.","Organic Chemical|Pharmacologic Substance"]
["C64522","KSP Inhibitor AZD4877","AZD4877|KSP Inhibitor AZD4877","A synthetic kinesin spindle protein (KSP) inhibitor with potential antineoplastic activity. AZD4877 selectively inhibits microtubule motor protein KSP (also called kinesin-5 or Eg5), which is essential for the formation of bipolar spindles and the proper segregation of sister chromatids during mitosis. Inhibition of KSP results in an inhibition of mitotic spindle assembly, activation of the spindle assembly checkpoint, induction of cell cycle arrest during the mitotic phase, thereby causing cell death in tumor cells that are actively dividing. Because KSP is not involved in postmitotic processes, such as neuronal transport, AZD4877 may be less likely to cause the peripheral neuropathy often associated with the tubulin-targeting agents.","Organic Chemical|Pharmacologic Substance"]
["C67049","Kunecatechins Ointment","Defined Green Tea Catechin Extract OIntment|Kunecatechins Ointment|Polyphenon E Ointment|Polyphenon E Topical Ointment|Veregen","A topical ointment containing a green tea polyphenol mixture (kunecatechins) with potential antiviral, antibacterial, antioxidant, and chemopreventive activities. Kunecatechins is a partially purified fraction of the aqueous extract of green tea leaves from Camellia sinensis and contains catechins and other green tea components. Catechins, polyphenolic antioxidant plant metabolites or flavonoids, comprise most of the drug substance in kunecatechins with epigallocatechin gallate (EGCG) present as the primary catechin. Catechins may inhibit basic functions of human papillomavirus (HPV), counteract specific changes in tumor cells, affect cell signaling, and stimulate the immune system. Topical application of kunecatechins ointment has been reported to reduce HPV-induced genital and anal warts through a not yet fully understood mechanism, which may involve anti-oxidative activity.","Pharmacologic Substance"]
["C1140","KW-2149","7-N-(2-((2-(gamma-L-Glutamylamino)ethyl)dithio)ethyl)mitomycin C|KT6149|KW 2149|KW-2149","A semisynthetic water-soluble disulfide derivative of the antineoplastic antibiotic mitomycin C.  Activated by serum and glutathione, KW-2149 causes interstrand DNA cross-links and DNA-protein cross-links, resulting in single-strand DNA breaks and inhibition of DNA synthesis. (NCI04)","Antibiotic|Organic Chemical"]
["C90546","L19-IL2 Monoclonal Antibody-Cytokine Fusion Protein","L19-IL2 Monoclonal Antibody-Cytokine Fusion Protein|L19-IL2","An immunoconjugate consisting of the recombinant form of the cytokine interleukin-2 (IL-2) fused to a human single-chain Fv (scFv) antibody fragment directed against the extra-domain B (ED-B) of fibronectin (L19), with potential immunopotentiating and antineoplastic activities. The L19 moiety of L19-IL2 monoclonal antibody-cytokine fusion protein binds to the ED-B domain of fibronectin on tumor cells in the tumor neovasculature. In turn, the IL-2 moiety may locally activate natural killer (NK) cells and macrophages, and may induce T cell cytotoxic immune responses against ED-B fibronectin-expressing tumor cells. This may specifically decrease the proliferation of ED-B-expressing tumor cells. ED-B is predominantly expressed during angiogenesis and tumor growth.","Pharmacologic Substance"]
["C1853","L-377,202","L-377,202|L-377202","A prodrug in which a peptide is covalently conjugated with the anthracycline antineoplastic antibiotic doxorubicin.  This complex is hydrolyzed by the enzyme prostate-specific antigen (PSA), resulting in the formation of doxorubicin and leucine-doxorubicin.  Selective targeting of these drugs to prostate tumor cells occurs because the hydrolyzing PSA enzyme is localized to the prostate gland.  Doxorubicin and leucine-doxorubicin intercalate into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.  These agents also produce toxic free-radical intermediates and interact with cell membrane lipids causing lipid peroxidation. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C1840","L-778,123","4-[[5-[[4-(3-Chlorophenyl)-3-oxo-1-piperazinyl]methyl]-1H-imidazol-1-yl]methyl]benzonitrile Monohydrochloride|L 778123|L-778,123|L-778123","A benzonitrile derivative capable of inhibiting some prenyltransferases. L-778,123 is a dual inhibitor of farnesyl:protein and geranylgeranyl:protein transferases; both enzymes catalyze prenylation of oncoprotein KRAS, a prerequisite step in activation of KRAS in signal transduction pathway of apoptosis. Although this agent was developed in part as an anti-KRAS agent, L-778,123 failed in a Phase I trial to inhibit KRAS, which is associated with many types of solid tumors.","Organic Chemical|Pharmacologic Substance"]
["C2722","L-779450","L-779,450|L-779450","A synthetic triarylimidazole with potential antineoplastic activity.  As a Raf kinase inhibitor, L-779450 competes with ATP for binding to the Raf-1 and A-Raf catalytic sites, thus inhibiting their enzymatic activities and blocking various signal transduction pathways that depend on Raf-1 kinase (particularly the Ras-Raf-MEK-ERK cascade which is often up-regulated in neoplasms). (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C95710","Labetuzumab-SN-38 Immunoconjugate IMMU-130","ADC IMMU-130|Antibody-Drug Conjugate IMMU-130|Labetuzumab-SN-38 Immunoconjugate IMMU-130|hMN14-SN38","An antibody-drug conjugate (ADC) containing labetuzumab, a mildly reduced, anti-CEACAM5 humanized monoclonal antibody, conjugated to the potent topoisomerase I inhibitor SN-38, with antineoplastic activity.  The monoclonal antibody moiety of antibody-drug conjugate IMMU-130 selectively binds to carcinoembryonic cell adhesion molecule 5 (CEACAM5), which is abundantly expressed on the surface of a majority of solid tumors. Upon internalization and proteolytic cleavage, SN-38, the active metabolite of irinotecan, inhibits the activity of topoisomerase I in the tumor cells, eventually inhibiting both DNA replication and transcription and leading to tumor cell apoptosis.","Immunologic Factor|Pharmacologic Substance"]
["C90547","Lactoferrin-derived Lytic Peptide LTX-315","LTX-315|Lactoferrin-derived Lytic Peptide LTX-315|Oncopore","A peptide derived from human lactoferrin, with potential lytic and immunostimulating activities. Upon transdermal injection directly into the tumor, LTX315 may bind to the tumor cell membranes and subsequently lyse tumor cells, thereby inducing tumor cell necrosis. In turn, presentation of the tumor antigens to the immune system may induce systemic innate and adaptive immune responses mediated by anti-tumor natural killer (NK) cells, cytotoxic T lymphocytes, and natural killer T (NKT) cells. This may trigger an immune response against tumor associated antigens on tumors distant from the primary tumor. Human lactoferrin, a 692 amino acid glycoprotein, belongs to the transferrin family of metal-binding proteins.","Pharmacologic Substance"]
["C83861","Ladirubicin","LADIRUBICIN|Ladirubicin","An alkylcycline-based anthracycline analogue with antineoplastic activity.","Pharmacologic Substance"]
["C29149","Laetrile","Beta-D-Glucopyranosiduronic acid, alpha-cyanobenzyl|Cyanophenylmethyl-beta-D-glucopyranosiduronic acid|L-Mandelonitrile-beta-glucuronoside|Laetrile|Laetrille|Mandelonitrile-beta-glucuronide|Vitamin B17|laetrile","Originally, the name laetrile was the contraction of laevo-mandelonitrile glucoside, a cyanogenic glycoside found naturally in some plants.  Over the years the meaning of laetrile has changed.  There are now preparations called Laetrile where amygdalin is the major constituent.  Laetrile and amygdalin are often used interchangeably, but are different agents.  Cyanide and benzaldehyde are metabolites of both laetrile and amygdalin.  Both metabolites may possess antineoplastic properties.  Laetrile has been used as an anticancer treatment in humans worldwide, but scientific evidence does not support its effectiveness.  It is not approved for use in the United States. (NCI04)","Pharmacologic Substance"]
["C28698","Laniquidar","LANIQUIDAR|Laniquidar|R101933","A stereoisomer of verapamil and third-generation P-glycoprotein inhibitor. Laniquidar inhibits the drug efflux pump P-glycoprotein, resulting in higher concentrations of antineoplastic agents in tumor cells that are multi-drug resistant due to the overexpression of P-glycoprotein. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C74584","Lanreotide Acetate","AT-1001|L-Threoninamide, 3-(2-naphthalenyl)-D-alanyl-L-cysteinyl-L-tyrosyl-D-tryptophyl-L-lysyl-L-valyl-L-cysteinyl-, cyclic (2-7)-disulfide, acetate|LANREOTIDE ACETATE|Lanreotide Acetate|Somatuline Depot","The acetate salt of a synthetic cyclic octapeptide analogue of somatostatin. Lanreotide binds to somatostatin receptors (SSTR), specifically SSTR-2 and also to SSTR-5 with a lesser affinity. However, compare with octreotide, this agent is less potent in inhibiting the release of growth hormone from the pituitary gland. Furthermore, lanreotide has an acute effect on decreasing circulating total and free insulin-like growth factor 1 (IGF-I).  This agent is usually given as a prolonged-release microparticle or Autogel formulation for the treatment of acromegaly and to relieve the symptoms of neuroendocrine tumors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C28694","Lapachone","3,4-Dihydro-2,2-dimethyl-2H-naphtho(1,2-b)pyran-5,6-dione|ARQ 501|ARQ501|Beta-Lap-WJ|Beta-Lapachone|LAPACHONE|Lapachone|beta-Lapachone","A poorly soluble, ortho-naphthoquinone with potential antineoplastic and radiosensitizing activity. Beta-lapachone (b-lap) is bioactivated by NAD(P)H:quinone oxidoreductase-1 (NQO1), creating a futile oxidoreduction that generates high levels of superoxide. In turn, the highly reactive oxygen species (ROS) interact with DNA, thereby causing single-strand DNA breaks and calcium release from endoplasmic reticulum (ER) stores. Eventually, the extensive DNA damage causes hyperactivation of poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme facilitating DNA repair, accompanied by rapid depletion of NAD+/ATP nucleotide levels. As a result, a caspase-independent and ER-stress induced mu-calpain-mediated cell death occurs in NQO1-overexpressing tumor cells. NQO1, a flavoprotein and two-electron oxidoreductase, is overexpressed in a variety of tumors.","Organic Chemical|Pharmacologic Substance"]
["C26653","Lapatinib","GSK572016|GW 2016|GW2016|GW572016|LAPATINIB|Lapatinib|lapatinib","A synthetic, orally-active quinazoline with potential antineoplastic properties. Lapatinib reversibly blocks phosphorylation of the epidermal growth factor receptor (EGFR), ErbB2, and the Erk-1 and-2 and AKT kinases; it also inhibits cyclin D protein levels in human tumor cell lines and xenografts. EGFR and ErbB2 have been implicated in the growth of various tumor types.","Organic Chemical|Pharmacologic Substance"]
["C66878","Lapatinib Ditosylate","LAPATINIB DITOSYLATE|Lapatinib Ditosylate|Tykerb|lapatinib ditosylate","The ditosylate salt of lapatinib, a synthetic, orally-active quinazoline with potential antineoplastic activity. Lapatinib reversibly blocks phosphorylation of the epidermal growth factor receptor (EGFR), ErbB2, and the Erk-1 and-2 and AKT kinases; it also inhibits cyclin D protein levels in human tumor cell lines and xenografts. EGFR and ErbB2 have been implicated in the growth of various tumor types.","Pharmacologic Substance"]
["C2057","Lapuleucel-T","APC 8024|APC8024|DN24-02|Lapuleucel-T|Neuvenge","A cell-based vaccine targets tumors expressing the HER2/neu marker.  HER-2/neu is a growth factor receptor, and its overexpression has been associated with a number of cancers including breast, ovarian, colon and lung cancers.  APC8024 comprise of autologous antigen-presenting peripheral blood mononuclear cells (APCs) that have been exposed to HER2/neu protein and can be administered to the patient.  These cells may stimulate an antitumor T-cell response to cancer cells expressing HER2/neu. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C2653","Laromustine","1,2-Bis(methylsulfonyl)-1-(2-chloroethyl)-2-(methylaminocarbonyl)hydrazine|101M|Cloretazine|LAROMUSTINE|Laromustine|Onrigin|VNP40101M|laromustine","A sulfonyl hydrazine prodrug with antineoplastic activity. Laromustine releases the DNA chloroethylating agent 90CE after entering the blood stream; 90CE chloroethylates alkylates the O6 position of guanine, resulting in DNA crosslinking, strand breaks, chromosomal aberrations, and disruption of DNA synthesis. Intracellular metabolism of this agent also releases methyl isocyanate which inhibits O6-alkyl-guanine transferase, an enzyme involved with DNA repair.","Organic Chemical|Pharmacologic Substance"]
["C48427","Larotaxel","LAROTAXEL|Larotaxel|RPR 109881A|RPR-109881|Taxoid-109881|XRP9881","A semi-synthetic derivative of the taxane 10-deacetylbaccatin III with potential antineoplastic activities. Larotaxel binds to tubulin, promoting microtubule assembly and stabilization and preventing microtubule depolymerization, thereby inhibiting cell proliferation. As it represents poor substrate for P-glycoprotein-related drug resistance mechanisms, this agent may be useful for treating multi-drug resistant tumors. Larotaxel penetrates the blood brain barrier.","Organic Chemical|Pharmacologic Substance"]
["C1142","Lavendustin A","5-(((2,5-Dihydroxyphenyl)methyl)((2-hydroxyphenyl)methyl)amino)-2-hydroxy Benzoic Acid|Benzoic acid, 5-[[(2, 5-dihydroxyphenyl)methyl][(2-hydroxyphenyl)methyl]amino]-2-hydroxy -|Lavendustin A","A compound isolated from strains of Streptomyces griseolavendus that may exert antitumor activity by inhibition of protein tyrosine kinase and tubulin polymerization. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C97500","Lead Pb 212 TCMC-trastuzumab","Lead Pb 212 TCMC-Herceptin|Lead Pb 212 TCMC-trastuzumab|[212]Pb TCMC-Herceptin|[212]Pb TCMC-trastuzumab","A radioimmunoconjugate containing the recombinant humanized monoclonal antibody trastuzumab conjugated with the bifunctional chelating agent TCMC ((1,4,7,10-Tetra-(2-Carbamoyl Methyl)-Cyclododecane), and radiolabeled with the alpha-emitting isotope lead Pb 212, with potential anti-tumor activity. Upon administration, the antibody moiety of lead Pb 212 TCMC-trastuzumab binds with high affinity to the extracellular domain of human epidermal growth factor receptor 2 (HER2); after internalization, the radioisotope moiety delivers a cytotoxic dose of alpha radiation to the HER2-expressing tumor cells. HER2, a tyrosine kinase receptor, is overexpressed on the cell surface of a variety of cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2668","Lenalidomide","3-(4-Amino-1-oxo-1,3-dihydro-2H-isoindol-2-yl)piperidine-2,6-dione|CC-5013|CC5013|CDC 501|LENALIDOMIDE|Lenalidomide|Revlimid|lenalidomide","A thalidomide analog with potential antineoplastic activity.  Lenalidomide inhibits TNF-alpha production, stimulates T cells, reduces serum levels of the cytokines vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), and inhibits angiogenesis.  This agent also promotes G1 cell cycle arrest and apoptosis of malignant cells.","Organic Chemical|Pharmacologic Substance"]
["C28168","Lentinan","LC-33|LENTINAN|Lentinan|lentinan",null,"Organic Chemical|Pharmacologic Substance"]
["C101371","Lentivirus Vector rHIV7-shI-TAR-CCR5RZ-transduced Hematopoietic Progenitor Cells","Lentivirus Vector rHIV7-shI-TAR-CCR5RZ-transduced Hematopoietic Progenitor Cells","Autologous, CD34-positive hematopoietic progenitor cells (HPCs) transduced with rHIV7-shI-TAR-CCR5RZ, a lentiviral vector encoding three anti-human immunodeficiency virus (HIV) RNA genes, with potential antineoplastic activity. The 3 RNA products produced by the lentilvirus are: a short hairpin RNA (shRNA) targeted to an exon of the HIV-1 genes tat/rev, designated as shI; a decoy for the HIV TAT reactive element, designated as TAR; a ribozyme targeting the host cells CCR5 chemokine receptor, designated as CCR5RZ. Upon administration, lentivirus vector rHIV7-shI-TAR-CCR5RZ-transduced hematopoietic progenitor cells expressing the 3 species of RNAs display 3 seperate mechanims of action: the shRNA blocks the transcription of tat/rev, the TAR decoy binds to the TAT protein that is essential for HIV replication, and CCR5RZ catalyzes CCR5 which is needed for viral attachment and entry into the host cells. Altogether, infusion of these HPCs may ultimately inhibit HIV replication and suppress HIV infection.","Cell|Pharmacologic Substance"]
["C95124","Lenvatinib","6-Quinolinecarboxamide, 4-[3-chloro-4-[[(cyclopropylamino)carbonyl]amino]phenoxy]- 7-methoxy-|E7080|ER-203492-00|LENVATINIB|Lenvatinib|Multi-Kinase Inhibitor E7080","A synthetic, orally available inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2, also known as KDR/FLK-1) tyrosine kinase with potential antineoplastic activity. Lenvatinib blocks VEGFR2 activation by VEGF, resulting in inhibition of the VEGF receptor signal transduction pathway, decreased vascular endothelial cell migration and proliferation, and vascular endothelial cell apoptosis.","Pharmacologic Substance"]
["C48636","Lenvatinib Mesylate","4-[3-Chloro-4-(N'-cyclopropylureido)phenoxy]7-methoxyquinoline-6-carboxamide Mesylate|6-Quinolinecarboxamide, 4-[3-chloro-4-[[(cyclopropylamino)carbonyl]amino]phenoxy]- 7-methoxy-, methanesulfonate (1:1)|E7080|LENVATINIB MESYLATE|Lenvatinib Mesylate|Lenvima|Multi-Kinase Inhibitor E7080","A synthetic, orally available inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2, also known as KDR/FLK-1) tyrosine kinase with potential antineoplastic activity. E7080 blocks VEGFR2 activation by VEGF, resulting in inhibition of the VEGF receptor signal transduction pathway, decreased vascular endothelial cell migration and proliferation, and vascular endothelial cell apoptosis.","Pharmacologic Substance"]
["C125081","Lenzilumab","Immunoglobulin G1-kappa, Anti-(Homo sapiens CSF2 (Colony Stimulating Factor 2 (Granulocyte-Macrophage), Granulocyte Macrophage Colony Stimulating Factor, GM-CSF)), Homo sapiens Monoclonal Antibody|KB 003|KB003|LENZILUMAB|Lenzilumab","A recombinant monoclonal antibody against the cytokine granulocyte macrophage colony-stimulating factor (GM-CSF), with potential immunomodulating activity. Upon administration, lenzilumab binds to and neutralizes GM-CSF. This prevents GM-CSF binding to the GM-CSF receptor, which is a heterodimeric protein expressed on myeloid progenitor cells, and prevents GM-CSF-mediated signaling. This may induce apoptosis in and inhibit proliferation of cancer cells that overproduce GM-CSF. GM-CSF plays a key role in the differentiation and proliferation of monocytes, macrophages and granulocytes; elevated levels of GM-CSF are associated with certain autoimmune diseases, inflammatory diseases, and cancers.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C48402","Lestaurtinib","9,12-Epoxy-1H-diindolo(1,2,3-fg:3',2',1'-kl)pyrrolo(3,4-i)(1,6)benzodiazocin-1-one, 2,3,9,10,11,12-hexahydro-10-hydroxy-10-(hydroxymethyl)-9-methyl-, (9S,10S,12R)-|CEP-701|KT-5555|LESTAURTINIB|Lestaurtinib|SPM-924|lestaurtinib","An orally bioavailable indolocarbazole derivative with antineoplastic properties. Lestaurtinib inhibits autophosphorylation of FMS-like tyrosine kinase 3 (FLT3), resulting in inhibition of FLT3 activity and induction of apoptosis in tumor cells that overexpress FLT3. (NCI05)","Pharmacologic Substance"]
["C1527","Letrozole","4,4'-(1H-1,2,4triazol-1-ylmethylene)dibenzonitrile|CGS 20267|Femara|LETROZOLE|Letrozole|letrozole","A nonsteroidal inhibitor of estrogen synthesis with antineoplastic activity. As a third-generation aromatase inhibitor, letrozole selectively and reversibly inhibits aromatase, which may result in growth inhibition of estrogen-dependent breast cancer cells. Aromatase, a cytochrome P-450 enzyme localized to the endoplasmic reticulum of the cell and found in many tissues including those of the premenopausal ovary, liver, and breast, catalyzes the aromatization of androstenedione and testosterone into estrone and estradiol, the final step in estrogen biosynthesis.","Organic Chemical|Pharmacologic Substance"]
["C607","Leucovorin Calcium","5-Formyl Tetrahydrofolate|5-Formyl-5,6,7,8-tetrahydrofolic Acid|5-Formyl-5,6,7,8-tetrahydropteroyl-L-glutamic Acid|Adinepar|Calcifolin|Calcium (6S)-Folinate|Calcium Folinate|Calcium Leucovorin|Calcium N-(p-((((6RS)-2-amino-5-formyl-5,6,7,8-tetrahydro-4-hydroxy-6-pteridinyl)methyl)amino)benzoyl)-L-glutamate (1:1)|Calfolex|Calinat|Cehafolin|Citofolin|Citrec|Citrovorum Factor|Cromatonbic Folinico|Dalisol|Disintox|Divical|Ecofol|Emovis|FOLI-cell|Factor, Citrovorum|Flynoken A|Folaren|Folaxin|Foliben|Folidan|Folidar|Folinac|Folinate Calcium|Folinic Acid Calcium Salt Pentahydrate|Folinoral|Folinvit|Foliplus|Folix|Imo|LEUCOVORIN CALCIUM|Lederfolat|Lederfolin|Leucosar|Leucovorin Calcium|N-[4-[[(2-Amino-5-formyl-1,4,5,6,7,8-hexahydro-4-oxo-6-pteridinyl)methyl]amnio]benzoyl]-L-glutamic Acid, Calcium Salt (1:1)|N-[p-[[(2-Amino-5-formyl-5,6,7,8-tetrahydro-4-hydroxy-6-pteridinyl)methyl]amino]benzoyl]glutamic Acid|Rescufolin|Rescuvolin|Tonofolin|Wellcovorin|citrovorum factor|folinic acid|leucovorin calcium|leucovorin","An active metabolite of folic acid (also called folinic acid and citrovorum factor), which does not require metabolism by dihydrofolate reductase, the molecular target of folate antagonist-type chemotherapeutic drugs.  Leucovorin calcium counteracts the toxic effects of these medications, 'rescuing' the patient while permitting the antitumor activity of the folate antagonist. This agent also potentiates the effects of fluorouracil and its derivatives by stabilizing the binding of the drug's metabolite to its target enzyme, thus prolonging drug activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C91379","Leukemic Apoptotic Corpse-Pulsed Autologous Dendritic Cells","Leukemic Apoptotic Corpse-Pulsed Autologous Dendritic Cells","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with corpses of apoptotic leukemic cells, with potential immunostimulatory and antineoplastic activities. Upon vaccination, autologous dendritic cells pulsed with leukemic apoptotic corpse may activate the immune system to mount an anti-tumoral cytotoxic T-lymphocyte (CTL) response against leukemic cells expressing leukemia-associated antigens, which may result in leukemic cell lysis and inhibition of tumor cell growth. Apoptotic tumor cell corpses contain an array of tumor associated antigens (TAAs).","Immunologic Factor|Pharmacologic Substance"]
["C62042","Leuprolide","6-D-Leucine-9-(N-ethyl-L-prolinamide)-1-9-luteinizing Hormone-releasing Factor (Pig)|6-D-Leucine-9-(N-ethyl-L-prolinamide)-10-deglycinamide Luteinizing Hormone-Releasing Factor (Pig)|LEUPROLIDE|Leuprolide|Leuprorelin|leuprolide","A synthetic nonapeptide analogue of gonadotropin-releasing hormone. Leuprolide binds to and activates gonadotropin-releasing hormone (GnRH) receptors. Continuous, prolonged administration of leuprolide in males results in pituitary GnRH receptor desensitization and inhibition of pituitary secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to a significant decline in testosterone production; in females, prolonged administration results in a decrease in estradiol production. This agent reduces testosterone production to castration levels and may inhibit androgen receptor-positive tumor progression.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1319","Leuprolide Acetate","6-D-Leucine-9-(N-ethyl-L-prolinamide)-1-9-luteinizing Hormone-releasing Factor (Pig) Monoacetate|6-D-Leucine-9-(N-ethyl-L-prolinamide)-10-deglycinamide Luteinizing Hormone-Releasing Factor (Pig) Monoacetate|A-43818|Abbott 43818|Abbott-43818|Carcinil|Depo-Eligard|Eligard|Enanton|Enantone-Gyn|Enantone|Ginecrin|LEUP|LEUPROLIDE ACETATE|Leuplin|Leuprolide Acetate|Leuprorelin Acetate|Lucrin Depot|Lucrin|Lupron Depot-3 Month|Lupron Depot-4 Month|Lupron Depot-Ped|Lupron Depot|Lupron|Procren|Procrin|Prostap|TAP-144|Trenantone|Uno-Enantone|Viadur|leuprolide acetate","The acetate salt of a synthetic nonapeptide analogue of gonadotropin-releasing hormone. Leuprolide binds to and activates gonadotropin-releasing hormone (GnRH) receptors. Continuous, prolonged administration of leuprolide in males results in pituitary GnRH receptor desensitization and inhibition of pituitary secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH), leading to a significant decline in testosterone production; in females, prolonged administration results in a decrease in estradiol production. This agent reduces testosterone production to castration levels and may inhibit androgen receptor-positive tumor progression.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C118363","Leuprolide Mesylate Injectable Suspension","LMIS|Leuprolide Mesylate Injectable Suspension","A depot suspension for injection composed of the mesylate salt of leuprolide, a synthetic, long-acting nonapeptide analog of the endogenous hormone gonadotropin-releasing hormone (GnRH), with potential antineoplastic activity. Upon subcutaneous injection of the depot suspension, leuprolide binds to and activates the gonadotropin-releasing hormone receptor (GnRHR). The continuous stimulation of GnRHR by leuprolide results in both the desensitization of pituitary GnRHR and the inhibition of pituitary secretion of the gonadotropins follicle stimulating hormone (FSH) and luteinizing hormone (LH). In males, this results in a significant decline in testosterone production to castration levels and may inhibit androgen receptor-positive tumor progression.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C81421","Leurubicin","LEURUBICIN|Leurubicin","An N-L-leucyl prodrug of the anthracycline doxorubicin, with antineoplastic activity. Leurubicin is converted to its active form doxorubicin in or on tumor cells by hydrolytic enzymes.","Pharmacologic Substance"]
["C64621","Lexatumumab","Anti-TRAIL Receptor 2 Monoclonal Antibody HGS-ETR2|HGS-ETR2|HGS1018|LEXATUMUMAB|Lexatumumab|Monoclonal Antibody HGS-ETR2|anti-TRAIL R2 mAb HGS-ETR2|lexatumumab","A fully human monoclonal agonistic antibody directed against tumor necrosis factor-alpha (TNF-alpha)-related apoptosis-inducing ligand receptor-2 (TRAIL-R2) with potential antitumor activity. Mimicking the natural ligand TRAIL, lexatumumab binds to and activates TRAIL-R2, which may trigger apoptosis in and inhibit the growth of TRAIL-R2-expressing tumor cells. TRAIL-R2, also known as death receptor 5 (DR5), is a member of the TNF receptor family and is expressed on many malignant cell types.","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C77882","Lexibulin","1-ethyl-3-(2-methoxy-4-(5-methyl-4-(((1s)-1-(pyridin-3-yl)butyl)amino)pyrimidin-2-yl)phenyl)urea|CYT997|LEXIBULIN|Lexibulin|Tubulin Inhibitor CYT997","An orally bioavailable small-molecule with tubulin-inhibiting, vascular-disrupting, and potential antineoplastic activities. Lexibulin inhibits tubulin polymerization in tumor blood vessel endothelial cells and tumor cells, blocking the formation of the mitotic spindle and leading to cell cycle arrest at the G2/M phase; this may result in disruption of the tumor vasculature and tumor blood flow, and tumor cell death.","Organic Chemical|Pharmacologic Substance"]
["C2062","LGD 1550","(2E,4E,6E)-7-[3,5-Bis(1,1-dimethylethyl)phenyl]-3-methyl-2,4,6-octatrienoic Acid|LGD 1550","An orally-active synthetic aromatic retinoic acid agent with potential antineoplastic and chemopreventive activities.  LGD 1550 selectively binds to all three retinoic acid receptors (RAR-alpha, RAR-beta, and RAR-gamma), resulting in alterations in the expression of genes responsible for cell differentiation and proliferation.  This agent also acts as an inhibitor of activator protein 1 (AP-1), a protein that mediates trophic responses and malignant transformation. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C62178","L-Gossypol","L-Gossypol","The levo-enantiomer of an orally bioavailable polyphenolic aldehyde, derived primarily from unrefined cottonseed oil, with potential antineoplastic activity. Mimicking the inhibitory BH3 (Bcl-2 homology 3) domain of endogenous antagonists of Bcl-2, L-gossypol binds to and inhibits various anti-apoptotic Bcl-2 proteins, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. This agent has greater affinity for Bcl-2 proteins than racemic gossypol.","Organic Chemical|Pharmacologic Substance"]
["C1433","Liarozole","1H-Benzimidazole, 5-((3-chlorophenyl)-1H-imidazol-1-ylmethyl)-|LIAROZOLE|Liarozole|Liazal|R 75251|R-61405|liarozole","An orally-active benzimidazole derivative with potential antineoplastic activity. As a retinoic acid metabolism blocking agent, liarozole inhibits cytochrome P450-dependent all-trans-retinoic acid (ATRA)-4-hydroxylase, resulting in an increase in endogenous ATRA production, inhibition of cell proliferation, and induction of cell differentiation. This agent also inhibits aromatase, the enzyme that catalyzes the final, rate-limiting step in estrogen biosynthesis.","Organic Chemical|Pharmacologic Substance"]
["C1524","Liarozole Fumarate","(+-)-5-(m-Chloro-alpha-imidazol-1-ylbenzyl)benzimidazole Fumarate (2:3)|1H-Benzimidazole, 5-((3-chlorophenyl)-1H-imidazol-1-ylmethyl)-, (+-)-, (E)-2-butenedioate (2:3)|LIAROZOLE FUMARATE|Liarozole Fumarate|R85246","The orally active fumarate salt of the benzimidazole derivative liarozole with potential antineoplastic activity. As a retinoic acid metabolism blocking agent (RAMBA), liarozole inhibits cytochrome P450-dependent all-trans-retinoic acid (ATRA)-4-hydroxylase, resulting in an increase in endogenous ATRA production, inhibition of cell proliferation, and induction of cell differentiation. This agent also inhibits aromatase, the enzyme that catalyzes the final, rate-limiting step in estrogen biosynthesis.","Organic Chemical|Pharmacologic Substance"]
["C80333","Liarozole Hydrochloride","(+-)-5-(m-Chloro-alpha-imidazol-1-ylbenzyl)benzimidazole Monohydrochloride|1H-Benzimidazole, 5-((3-chlorophenyl)-1H-imidazol-1-ylmethyl)-, Monohydrochloride, (+-)-|LIAROZOLE HYDROCHLORIDE|Liarozole HCl|Liarozole Hydrochloride|R 75251","The fumarate salt of an orally-active benzimidazole derivative with potential antineoplastic activity. As a retinoic acid metabolism blocking agent (RAMBA), liarozole inhibits cytochrome P450-dependent all-trans-retinoic acid (ATRA)-4-hydroxylase, resulting in an increase in endogenous ATRA production, inhibition of cell proliferation, and induction of cell differentiation. This agent also inhibits aromatase, the enzyme that catalyzes the final, rate-limiting step in estrogen biosynthesis.","Organic Chemical|Pharmacologic Substance"]
["C104275","Licartin","(131)I-labeled HAb18 F(ab')(2)|Iodine I 131 Metuximab|Iodine[131I] Metuximab|Licartin|[131I] mAb HAb18G/CD147","An immunoradioconjugate containing metuximab, an antibody fragment targeting the hepatocellular cancer (HCC)-associated antigen HAb18G/CD147, that is conjugated to the radioisotope iodine I 131, with potential antineoplastic activity. Upon administration, the metuximab moiety of licartin targets and binds to HAb18G/CD147 on HCC cells; upon internalization, the radioisotope I 131 delivers a cytotoxic dose of gamma radiation, thereby causing selective destruction of HAb18G/CD147-expressing cells. HAb18G/CD147, a member of CD147 family, is overexpressed in HCC and fibroblasts and its expression is associated with cancer cell progression and increased adhesion, invasion and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C61436","Licorice","Glycyrrhiza|Glycyrrhizae Radix|LICORICE|Licorice Root Extract|Licorice|licorice root extract","An herbal extract derived from the root of the plant Glycyrrhiza glabra with potential anti-inflammatory, antioxidant, and antineoplastic activities. Licorice root extract contains glycoside glycyrrhizinic acid and numerous flavonoids. Glycyrrhizinic acid in licorice root extract is hydrolyzed to glycyrrhetic acid (GA); GA inhibits 11 beta-hydroxysteroid dehydrogenase, resulting in inhibition of the conversion of cortisol to the inactive steroid cortisone and elevated cortisol levels. In addition, GA inhibits 17,20-lyase and 17 beta-hydroxysteroid dehydrogenase, resulting in decreased conversions of 17-hydroxyprogesterone to androstenedione and androstenedione to testosterone. The primary antioxidant found in licorice root, the flavonoid glabridin, may inactivate or inhibit the activities of some cytochrome P450 enzymes. In tumor cells, beta-hydroxy-DHP, another flavonoid, may induce Bcl-2 phosphorylation, apoptosis, and G2/M cell cycle arrest.","Pharmacologic Substance"]
["C79833","Light-Emitting Oncolytic Vaccinia Virus GL-ONC1","GL-ONC1|GLV-1h68|Light-Emitting Oncolytic Vaccinia Virus GL-ONC1","An attenuated oncolytic vaccinia virus encoding the light-emitting fusion protein Renilla luciferase-Aequorea green fluorescent protein (RUC-GFP) with potential bioluminescent and antineoplastic activities. Upon administration, light-emitting oncolytic vaccinia virus GL-ONC1 specifically enters tumor cells due to the permeable nature of the tumor vasculature. Once inside the cell, the virus replicates, resulting in tumor cell lysis and the release of mature viral particles into the tumor microenvironment. Released viral particles may then infect and destroy neighboring tumor cells. In addition, the release of tumor-associated antigens (TAAs) by lysed tumor cells into the bloodstream may activate the immune system to mount a cytotoxic T lymphocyte (CTL) response against the tumor. The expression of RUC-GFP by this agent allows for both detection and monitoring of virally infected tumor cells in vivo and vitro with luciferase-mediated bioluminescence imaging and fluorescence imaging techniques.","Pharmacologic Substance"]
["C61714","Limonene, (+)-","(+)-(R)-4-isopropenyl-1-methylcyclohexene|(+)-alpha-Limonene|(+)-limonene|(4R)-1-methyl-4-(1-methylethenyl)cyclohexene|(4R)-1-methyl-4-prop-1-en-2-yl-cyclohexene|(R)-(+)-limonene|(R)-1-Methyl-4-(1-methylethenyl)cyclohexene|(R)-4-isopropenyl-1-methylcyclohexene|1-methyl-4-isopropenyl-1-cyclohexene|Cyclohexene, 1-methyl-4-(1-methylethenyl)-, (4R)-|D-Limonene|LIMONENE, (+)-|Limonene, (+)-|Limonene, D-|Limonene","An oral dietary supplement containing a natural cyclic monoterpene and major component of the oil extracted from citrus peels with potential chemopreventive and antitumor activities. Although the mechanism of action has yet to be fully elucidated, limonene and its metabolites perillic acid, dihydroperillic acid, uroterpenol and limonene 1,2-diol may inhibit tumor growth through inhibition of p21-dependent signaling and may induce apoptosis via the induction of the transforming growth factor beta-signaling pathway. In addition, they inhibit post-translational modification of signal transduction proteins, resulting in G1 cell cycle arrest as well as differential expression of cell cycle- and apoptosis-related genes.","Pharmacologic Substance"]
["C61709","Limonene, (+/-)-","(+/-)-1-methyl-4-(1-methylethenyl)cyclohexene|1-methyl-4-(1-methylethenyl)cyclohexene|1-methyl-4-prop-1-en-2-yl-cyclohexene|Cajeputene|Cinene|DL-Limonene|Dipentene|Eulimen|LIMONENE, (+/-)-|Limonene, (+/-)-|Limonene|Nesol","A racemic mixture of limonene, a natural cyclic monoterpene and major component of the oil extracted from citrus rind with chemo-preventive and antitumor activities. The metabolites of DL-limonene, perillic acid, dihydroperillic acid, uroterpenol and limonene 1,2-diol are suggested to inhibit tumor growth through inhibition of p21-dependent signaling, induce apoptosis via the induction of the transforming growth factor beta-signaling pathway, inhibit post-translational modification of signal transduction proteins, result in G1 cell cycle arrest as well as cause differential expression of cell cycle- and apoptosis-related genes.","Pharmacologic Substance"]
["C71759","Linifanib","ABT-869|LINIFANIB|Linifanib|multitargeted receptor tyrosine kinase inhibitor ABT-869","An orally bioavailable receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Linifanib inhibits members of the vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptor families; it exhibits much less activity against unrelated RTKs, soluble tyrosine kinases, or serine/threonine kinases. This agent does not have a general antiproliferative effect due to its high dose requirement. However, linifanib may exhibit potent antiproliferative and apoptotic effects on tumor cells whose proliferation is dependent on mutant kinases, such as FMS-related tyrosine kinase receptor-3 (FLT3).","Pharmacologic Substance"]
["C101792","Linoleyl Carbonate-paclitaxel","2-Linoleyl Carbonate-paclitaxel|LOC-paclitaxel|Linoleyl Carbonate-paclitaxel","A formulation of the 6-omega fatty acid derivative 2'-linoleyl carbonate (LOC) conjugated to paclitaxel, a taxane compound extracted from the Pacific yew tree Taxus brevifolia, with potential antineoplastic activity. Paclitaxel binds to and stabilizes tubulin, thereby interfering with the dynamics of microtubule assembly/disassembly and resulting in the inhibition of cell division. LOC enhances the uptake of paclitaxel by tumor cells, thereby concentrating this agent in tumor cells compared to normal cells, and may decrease its toxicity profile; fatty acids serve as energy sources and biochemical precursors for the fast growing tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C70982","Linsitinib","Cyclobutanol, 3-[8-amino-1-(2-phenyl-7-quinolinyl)imidazo[1,5-a]pyrazin-3-yl]-1-methyl, cis-|IGF-1R inhibitor OSI-906|LINSITINIB|Linsitinib|OSI-906|OSI-906AA|cis-3-(8-Amino-1-(2-Phenylquinolin-7-yl)Imidazo(1,5-A)Pyrazin-3-yl)-1-Methylcyclobutanol","An orally bioavailable small molecule inhibitor of the insulin-like growth factor 1 receptor (IGF-1R) with potential antineoplastic activity. Linsitinib selectively inhibits IGF-1R, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. Overexpressed in a variety of human cancers, IGF-1R stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis.","Pharmacologic Substance"]
["C1716","Lintuzumab","Hu-M195 monoclonal antibody|HuG1-M195 monoclonal antibody|Lintuzumab|MoAb HuG1-M195|MoAb HuM195|Monoclonal Antibody HuG1-M195|Monoclonal Antibody HuM195|lintuzumab|monoclonal antibody HuM195 HuG1-M195","A humanized recombinant monoclonal antibody directed against CD33, a cell surface antigen found on myeloid leukemia blasts and early hematopoietic progenitor cells. Lintuzumab stimulates antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells expressing CD33, resulting in a decrease in tumor burden. The humanized version of this monoclonal antibody exhibits less immunogenicity and improved binding affinity compared to its murine counterpart.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2396","Liothyronine I-131","I 131 Liothyronine|LIOTHYRONINE I-131|Liothyronine I-131","A radioconjugate of synthetic active thyroid hormone, liothyronine (T3), labeled with Iodine 131. Liothyronine involves many important metabolic functions and is essential to the proper development and differentiation of all cells. I131 liothyronine may be used in radiotherapy in thyroid cancers.","Pharmacologic Substance"]
["C116889","Lipid Encapsulated Anti-PLK1 siRNA TKM-PLK1","Lipid Encapsulated Anti-PLK1 siRNA TKM-PLK1|PLK1 SNALP|PLK1424|TKM-080301|TKM-PLK1","short interfering RNAs (siRNAs) directed against polo-like kinase 1 (PLK1, STPK13), with potential antineoplastic activity. Upon administration of lipid-encapsulated anti-PLK1 siRNA TKM-PLK1, siRNA binds to PLK1 mRNA, which results in the inhibition of both the translation and expression of the PLK1 protein. Blockage of PLK1 expression prevents proper tumor cell mitosis, causes cell cycle arrest and tumor cell apoptosis. This inhibits the proliferation of PLK1-overexpressing tumor cells. PLK1, named after the polo gene of Drosophila melanogaster, is a serine/threonine kinase crucial in the regulation of mitosis; its expression is upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation. The pegylated lipid bilayer of SNALP provides stability and protects siRNA degradation; it facilitates uptake into the cell and release from endosomes.","Pharmacologic Substance"]
["C95718","Liposomal c-raf Antisense Oligonucleotide","LErafAON|Liposomal c-raf Antisense Oligonucleotide|c-raf Antisense Oligodeoxynucleotide Liposome|liposome-encapsulated c-raf Antisense Oligodeoxynucleotide","The liposomal formulation of a c-raf-1 antisense oligonucleotide, with potential antineoplastic activity. Liposomal c-raf antisense oligonucleotide targets the translation initiation site of human c-raf-1 mRNA, thereby blocking the expression and production of Raf-1 protein and thus inhibit tumor cell growth and development. Raf-1 plays a key role in the RAF/MEK/ERK signaling pathway, which regulates mammalian cell proliferation and growth. The liposomal formulation increases the solubility of the c-raf antisense oligonucleotide, thus improving its pharmacodynamic profile.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C116322","Liposomal Curcumin","Curcumin Liposome|Liposomal Curcumin","A liposomal formulation containing curcumin, a poorly water-soluble polylphenol pigment isolated from the plant Curcuma longa, with potential antineoplastic, chemopreventive, antioxidant, anti-angiogenic and anti-inflammatory activities. Upon intravenous administration of liposomal curcumin, this agent blocks the formation of reactive-oxygen species, neutralizes free radicals, and exhibits anti-inflammatory properties as a result of inhibition of cyclooxygenases (COX) and other enzymes involved in inflammation. In addition, curcumin disrupts various cell signal transduction pathways involved in carcinogenesis, inhibits the activity of nuclear factor-kappa B (NF-kB), SRC, and annexin A2 (ANXA2), and reduces the expression of both matrix metalloproteinase-9 (MMP-9) and vascular endothelial growth factor receptor 2 (VEGFR2). This prevents and/or inhibits tumor cell formation and proliferation. Liposome encapsulation of curcumin improves its efficacy, when compared to the administration of unencapsulated curcumin.","Organic Chemical|Pharmacologic Substance"]
["C67504","Liposomal Cytarabine-Daunorubicin CPX-351","CPX-351|Cytarabine-Daunorubicin Liposome for Injection|Liposomal AraC-Daunorubicin CPX-351|Liposomal Cytarabine-Daunorubicin CPX-351","A liposomal formulation containing a fixed combination of the antineoplastic agents cytarabine and daunorubicin in a 5:1 molar ratio. Liposomal cytarabine-daunorubicin CPX-351 has been designed to provide optimal delivery of a specific ratio of cytarabine to daunorubicin, one that has been shown to be synergistic in vitro. The antimetabolite cytarabine competes with cytidine for incorporation into DNA, inhibiting DNA synthesis. This agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Daunorubicin, an intercalator and a topoisomerase II inhibitor, prevents DNA replication and inhibits protein synthesis. This agent also generates oxygen free radicals, resulting in the cytotoxic lipid peroxidation of cell membrane lipids.","Pharmacologic Substance"]
["C2213","Liposomal Daunorubicin Citrate","DaunoXome|Daunorubicin Citrate Liposome Injection|Daunorubicin Liposomal|Liposomal Daunorubicin Citrate|Liposomal Daunorubicin","A liposome-encapsulated form of the citrate salt of the anthracycline antineoplastic antibiotic daunorubicin. Daunorubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. Liposomal delivery of doxorubicin citrate improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic drug effects.","Antibiotic|Organic Chemical"]
["C92581","Liposomal Docetaxel","LE-DT|Liposomal Docetaxel|Liposome Entrapped Docetaxel","A formulation of the poorly soluble, semi-synthetic, second-generation taxane docetaxel encapsulated within liposomes, with antineoplastic activity.  Upon intravenous administration, docetaxel binds to and stabilizes tubulin, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and cell death.  This liposomal formulation solubilizes docetaxel without the use of toxic solvents such as Tween 80, permitting the administration of larger doses of docetaxel while avoiding solvent-associated toxicity, including hypersensitivity reactions. In addition, liposomal delivery of docetaxel improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic drug effects while lowering the toxicity profile.","Pharmacologic Substance"]
["C111899","Liposomal Eribulin Mesylate","E7389 Liposomal Formulation|E7389-LF|Liposomal Eribulin Mesylate","A liposome-encapsulated formulation of the mesylate salt form of eribulin, a synthetic, macrocyclic ketone analogue of halichondrin B, a substance derived from the marine sponge genus Halichondria, with potential antineoplastic activity. Eribulin binds to the vinca domain of tubulin and inhibits both the polymerization of tubulin and the assembly of microtubules. This results in the inhibition of mitotic spindle assembly, the induction of cell cycle arrest at G2/M phase, as well as tumor cell apoptosis. Compared to the administration of eribulin alone, liposomal delivery of eribulin allows for a longer half-life, which allows increased drug concentration in target tissues while decreasing systemic toxicity.","Pharmacologic Substance"]
["C111688","Liposomal HPV-16 E6/E7 Multipeptide Vaccine PDS0101","Liposomal HPV-16 E6/E7 Multipeptide Vaccine PDS0101|PDS0101|mmunoMAPK-RDOTAP /HPV-16 E6/E7 Peptide Antigen Vaccine","A liposomal nanoparticle-based therapeutic vaccine composed of the cationic lipid R-DOTAP (R-enantiomer of 1,2-dioleoyl-3-trimethylammonium-propane chloride) encapsulating six human papillomavirus 16 (HPV-16) E6 and E7 peptides, with potential immunostimulating activity. Upon subcutaneous administration of the liposomal HPV-16 E6 and E7 multipeptide vaccine, the nanoparticles are taken up by antigen presenting cells (APCs), specifically dendritic cells (DCs), which may stimulate the immune system to induce a cytotoxic T-lymphocyte response (CTL) against HPV-16 E6 and E7-expressing tumor cells. HPV-16 E6 and E7 are oncoproteins that play a key role in the tumorigenesis of a variety of cancers.","Immunologic Factor|Pharmacologic Substance"]
["C82676","Liposomal Irinotecan","Irinotecan Liposome|Liposomal Irinotecan|Onivyde|PEP02","A liposomal formulation of the hydrochloride salt of the semisynthetic camptothecin analogue irinotecan with potential antineoplastic activity. During the S phase of the cell cycle, irinotecan selectively stabilizes topoisomerase I-DNA covalent complexes, inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing lethal double-strand DNA breaks when complexes are encountered by the DNA replication machinery. Liposome encapsulation of this agent promotes efficient drug delivery into the cytosol from the endosome compartment of the cell.","Pharmacologic Substance"]
["C116064","Liposomal Mitoxantrone Hydrochloride","Liposomal Mitoxantrone Hydrochloride|Mitoxantrone Hydrochloride Liposome","A formulation composed of the hydrochloride salt form of the anthracenedione antibiotic mitoxantrone encapsulated within liposomes, with potential antineoplastic activity. Upon intravenous administration, mitoxantrone intercalates into and forms crosslinks with DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, which both results in DNA strand breaks and prevents DNA synthesis. This leads to the induction of apoptosis in the rapidly dividing cancer cells. The liposomal delivery of mitoxantrone improves drug penetration into tumors and decreases drug clearance, thereby increasing drug circulation and therapeutic efficacy while lowering the toxic effects.","Organic Chemical|Pharmacologic Substance"]
["C101262","Liposomal MUC1/PET-lipid A Vaccine","Liposomal MUC1/PET-lipid A Vaccine|ONT-10","A cancer vaccine comprised of a 43 amino acid epitope from glycoprotein MUC1 (mucin 1) and the synthetic Toll-like receptor 4 (TLR-4) agonist PET lipid A encapsulated in cholesterol/dipalmitoylphosphatidylcholine (DPPC)/dimyristoylphosphatidylglycerol (DMPG) liposomes, with potential immunostimulatory and antineoplastic activities. The MUC1 epitope is composed of two 20 amino glycosylated VNTR (various number tandem repeats) from human MUC1A and including 6 glycosylated sites modified by Tn (alfa-N-acetyl-D-galactosamine). Immunization of liposomal MUC1/PET-lipid A vaccine results in an antibody as well as a cytotoxic T-lymphocyte (CTL) response against hypoglycosylated MUC1 expressing tumor cells. The tumor associated antigen MUC1, a type I transmembrane protein, is overexpressed and aberrantly glycosylated in a variety of tumor cells. As a vaccine adjuvant, PET lipid A, also known as penta erythritol lipid A, stimulates both cellular and humoral responses to the vaccine antigen.","Immunologic Factor|Pharmacologic Substance"]
["C1383","Liposomal NDDP","Aroplatin|L-NDDP|Liposomal NDDP|Liposomal Neodecanoic Acid Platinum Complex|Liposomal-Cisplatin Analogue|Liposomal-Entrapped Cis-Bis-Neodecanoate-trans-R,R-1,2-Diaminocyclohexane Platinum (II)","A synthetic liposomal formulation of bis-neodecanoate diaminocyclohexane platinum (NDDP), a third-generation platinum complex analogue of cisplatin, with potential antineoplastic activity. After displacement of the 2 long-chain aliphatic leaving groups (neodecanoic acid), platinum diaminocyclohexane (DACH) complexes become highly reactive and alkylate macromolecules, forming both inter- and intra-stranded DNA cross-linkings and inhibiting DNA synthesis, which results in tumor cell cytotoxicity. Because DNA mismatch-repair (MMR) complexes do not recognize DACH-platinum adducts, DNA repair mechanisms are inhibited, overcoming limitations observed with other platinum-based agents. In addition, the liposomal encapsulation improves the bioavailability of NDDP and reduces its toxicity profile.","Organic Chemical|Pharmacologic Substance"]
["C107679","Liposomal Rhenium Re 186","(186)Re-Liposomes|186RNL|Liposomal Rhenium Re 186|Liposomal Rhenium-186|Rhenium-186 Liposome","A therapeutic preparation consisting of the beta-emitting radioisotope rhenium Re 186 encapsulated in a nanoliposome, with potential antineoplastic activity. Upon intratumoral infusion of liposomal rhenium Re 186, the radioisotope releases radiation, which directly kills the tumor cells. The nanoliposomes facilitate the retention of the radioisotope by the tumor cells and localize the radiocytotoxicity to the tumor while sparing surrounding normal, healthy cells. Re-186 has a short half-life and a short path length, which contributes further to limiting the radiotoxicity to the tumor cells.","Pharmacologic Substance"]
["C95717","Liposomal SN-38","7-Ethyl-10-hydroxycamptothecin Liposome|LE-SN38|Liposomal SN-38|SN-38 Liposome","The liposomal formulation of SN-38 (7-ethyl-10-hydroxy-camptothecin), a biologically active metabolite of the prodrug irinotecan, with potential antineoplastic activity. SN-38 binds to and inhibits topoisomerase I by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks, inhibition of DNA replication, and apoptosis. SN-38 has been reported to exhibit up to 1,000-fold more cytotoxic activity against various cancer cells in vitro than irinotecan. The liposomal formulation of SN-38 increases the solubility of SN-38, which is a relatively insoluble compound, and improves the pharmacodynamic profile as compared to SN-38 alone.","Organic Chemical|Pharmacologic Substance"]
["C62790","Liposomal Vinorelbine","Liposomal Vinorelbine","A formulation of the semisynthetic vinca alkaloid, vinorelbine, encapsulated within liposomes, with antineoplastic activity. Vinorelbine binds to tubulin and prevents formation of the mitotic spindle, resulting in cell cycle arrest in metaphase. Like other vinca alkaloids, vinorelbine may also interfere with the metabolism of nucleic acids, lipids, amino acids, cAMP, and glutathione, as well as other biological processes including calmodulin-dependent Ca2+-transport, ATPase activity, or cellular respiration. Liposomal delivery of vinorelbine improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic effects while lowering the toxicity profile.","Organic Chemical|Pharmacologic Substance"]
["C61317","Liposome-Encapsulated Doxorubicin Citrate","Liposome-Encapsulated Doxorubicin Citrate|Myocet|liposome-encapsulated doxorubicin citrate","A formulation of the citrate salt of the antineoplastic anthracycline antibiotic doxorubicin, encapsulated within liposomes, with antitumor activity. Doxorubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and RNA synthesis. This agent also interacts with cell membrane lipids causing lipid peroxidation. Liposomal delivery of doxorubicin improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic drug effects while lowering the toxicity profile.","Pharmacologic Substance"]
["C105802","Liposome-encapsulated miR-34 Mimic MRX34","Liposome-encapsulated miR-34 Mimic MRX34|MRX34","A liposomal formulation containing a nucleotide that mimics the human tumor suppressor microRNA (miRNA) miR-34, with potential antineoplastic activity. Upon administration, liposome-encapsulated MRX34 mimics miR-34 by inhibiting the expression of a variety of oncogenes including MYC, MET, BCL2, and beta-catenin. This induces cell cycle arrest, senescence and apoptosis in susceptible tumor cells. miR-34 is downregulated in most solid and hematologic malignancies and regulates the expression of a variety of genes. This miRNA plays an important role in the inhibition of cancer cell stemness, metastasis and cancer cell survival.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C106271","Liposome-encapsulated RB94 Plasmid DNA Gene Therapy Agent SGT-94","Liposome-encapsulated RB94 Plasmid DNA Gene Therapy Agent SGT-94|SGT-94|TfRscFv/Lip/RB94","A systemic gene therapy anti-cancer agent composed of cationic liposomes, which encapsulates plasmid DNA encoding for the tumor suppressor gene RB94 and is complexed with anti-transferrin receptor single chain antibody fragment (TfRscFv), with potential antineoplastic activity. Upon systemic administration of liposome-encapsulated RB94 plasmid DNA gene therapy agent SGT-94, the TfRscFv portion of this agent selectively targets the tumor cells expressing transferrin receptors. TfRscFv binding to the transferrin receptor allows receptor-mediated endocytosis and transfection, followed by the expression of RB94 gene. This induces tumor cell apoptosis through an as of yet unknown pathway. RB94 is a modified, N-terminal truncated form of the full-length protein retinoblastoma gene RB110, and exerts enhanced antitumor activity. The transferrin receptor (TfR) functions in cellular iron uptake through its interaction with transferrin, and is overexpressed in a variety of tumor types.","Pharmacologic Substance"]
["C91736","Liposome-Incorporated Grb2 Antisense Oligodeoxynucleotide","BP-100-1.01|BP-1001|BP1001|Liposomal Grb2 AS ODN|Liposome-Incorporated Grb2 Antisense Oligodeoxynucleotide","A liposomal formulation containing the antisense oligodeoxynucleotide (ODN) growth factor receptor-bound protein 2 (Grb2), with potential antineoplastic activity. Upon administration, liposome-incorporated Grb2 antisense oligodeoxynucleotide binds directly to and blocks Grb2 mRNA, thereby preventing Grb2 protein synthesis, leading to inhibition of cell proliferation of cancer cells overexpressing Grb2. Grb2, an adaptor protein involved in growth signaling pathways, is upregulated in certain tumor cells.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C103820","Lirilumab","BMS-986015|IPH2102|LIRILUMAB|Lirilumab","A fully humanized monoclonal antibody against killer-cell immunoglobulin-like receptors (KIR), with potential antineoplastic activity. Upon administration, lirilumab binds to KIR, thereby preventing the binding of KIR ligands to KIR on natural killer (NK) cells. By blocking these inhibitory receptors, NK cells become activated and attack cancer cells leading to tumor cell death. KIR, a member of the immunoglobulin superfamily, is expressed on the surface of NK cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C120103","Listeria monocytogenes-LLO-PSA Vaccine ADXS31-142","ADXS-PSA|ADXS31-142|Listeria monocytogenes-LLO-PSA Vaccine ADXS31-142|Lm-LLO-PSA","A cancer vaccine containing a live-attenuated strain of the Gram-positive bacterium Listeria monocytogenes (Lm) encoding a fusion protein composed of the tumor-associated antigen (TAA) human prostate-specific antigen (PSA) fused to a fragment of the immunostimulant listeriolysin O (LLO) protein, with potential immunostimulatory and antineoplastic activities. Upon administration of the Lm-LLO-PSA vaccine ADXS31-142, the expressed LLO-PSA is processed by antigen presenting cells (APCs), presented to the immune system by both major histocompatibility complex (MHC) I and II molecules, and activates the immune system to exert both an innate and adaptive immune response involving the recruitment and activation of T-lymphocytes against PSA-expressing tumor cells as well as the inhibition of tumor-infiltrating T regulatory cells (T regs) and myeloid-derived suppressor cells (MDSCs). This eventually results in tumor cell lysis.","Pharmacologic Substance"]
["C88328","Litronesib","KF89617|LITRONESIB|LY2523355|Litronesib|Propanamide, N-[4-(2,2-dimethyl-1-oxopropyl)-5-[[[[2-(ethylamino)ethyl]sulfonyl] amino]methyl]-4,5-dihydro-5-phenyl-1,3,4-thiadiazol-2-yl]-2,2-dimethyl-, (-)-","An inhibitor of the kinesin-related motor protein Eg5 with potential antineoplastic activity. Litronesib selectively inhibits the activity of Eg5, which may result in mitotic disruption, apoptosis and consequently cell death in tumor cells that are actively dividing. The ATP-dependent Eg5 kinesin-related motor protein (also known as KIF11 or kinesin spindle protein-5) is a plus-end directed kinesin motor protein that plays an essential role during mitosis, particularly in the regulation of spindle dynamics, including assembly and maintenance.","Pharmacologic Substance"]
["C82651","Live Attenuated Measles Virus Vaccine","Live Attenuated Measles Virus Vaccine","A live, attenuated measles vaccine with potential antineoplastic activity. Upon subcutaneous administration, live attenuated measles virus vaccine may activate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against measles-positive tumor cells. Measles virus has been shown to be present in some non-small cell lung cancers.","Pharmacologic Substance|Virus"]
["C61505","Live Freeze-Dried Lactic Acid Bacteria Probiotic","Live Freeze-Dried Lactic Acid Bacteria Probiotic|VSL#3","A probiotic containing live, cultivated, freeze-dried lactic acid bacteria with gastrointestinal (GI) protective, anti-inflammatory, immunomodulating and potential antitumor properties. Oral administration of probiotic bacteria help maintain adequate colonization of the GI tract and modulate the composition of the normal microflora. Upon colonization of the GI tract, the probiotic bacteria form a protective barrier, interfere with the attachment of pathogenic bacteria and other harmful substances and may bind to and degrade carcinogens. This may prevent inflammation and possibly cancer. In addition, these bacteria produce lactic acid, thereby creating an acidic environment that is unfavorable for pathogens.","Bacterium|Pharmacologic Substance"]
["C125631","Live-attenuated Double-deleted Listeria monocytogenes Bacteria JNJ-64041809","ADU-741|JNJ-64041809|LADD Listeria monocytogenes Bacteria JNJ-64041809|Live-attenuated Double-deleted Listeria monocytogenes Bacteria JNJ-64041809","A proprietary, live-attenuated, double-deleted (LADD) strain of the Gram-positive bacterium Listeria monocytogenes (Lm) encoding multiple, as of yet undisclosed, tumor-associated antigens (TAAs), with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, live-attenuated double-deleted Listeria monocytogenes bacteria JNJ-64041809 is taken up by antigen-presenting cells (APCs), including dendritic cells (DCs). The TAAs are subsequently expressed by the APCs and then processed and presented to the immune system by both major histocompatibility complex (MHC) class I and II molecules. This activates the immune system and leads to the recruitment and activation of cytotoxic T-lymphocytes (CTLs) against the TAA-expressing tumor cells, eventually resulting in tumor cell lysis. Two genes contributing to the virulence of Lm have been removed to minimize the risk of infection.","Bacterium"]
["C74055","Live-Attenuated Listeria Encoding Human Mesothelin Vaccine CRS-207","CRS-207|LADD Listeria monocytogenes CRS-207|Live-Attenuated Listeria Encoding Human Mesothelin Vaccine CRS-207","A recombinant Listeria-based cancer vaccine containing a live-attenuated strain of the facultative intracellular bacterium Listeria monocytogenes (Lm) expressing human mesothelin with potential immunostimulatory and antineoplastic activities. Upon administration of this vaccine, Listeria invade professional phagocytes within the immune system and express mesothelin, which may activate a cytotoxic T-lymphocyte (CTL) response against mesothelin-expressing tumor cells, resulting in tumor cell lysis. In addition, the Listeria vector itself may induce a potent innate and adaptive immunity unrelated to mesothelin expression. Mesothelin is a cell surface glycoprotein involved in cell adhesion and is overexpressed in many epithelial-derived cancers, including pancreatic, ovarian and lung cancers, and malignant mesotheliomas.","Pharmacologic Substance"]
["C124843","Live-attenuated Listeria monocytogenes Encoding EGFRvIII-mesothelin Vaccine JNJ-64041757","ADU-214|JNJ-64041757|LADD Listeria monocytogenes JNJ-64041757|Live-attenuated Listeria monocytogenes Encoding EGFRvIII-mesothelin Vaccine JNJ-64041757","A proprietary, live-attenuated, double-deleted (LADD) strain of the Gram-positive bacterium Listeria monocytogenes (Lm) encoding the tumor-associated antigens (TAAs) epidermal growth factor receptor mutant form EGFRvIII and human mesothelin, with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, the live-attenuated Listeria monocytogenes encoding EGFRvIII-mesothelin vaccine JNJ-64041757 is taken up by antigen-presenting cells (APCs), including dendritic cells (DCs). EGFRvIII and mesothelin are subsequently expressed by the APCs and then processed and presented to the immune system by both major histocompatibility complex (MHC) class I and II molecules. This activates the immune system and leads to the recruitment and activation of cytotoxic T-lymphocytes (CTLs) against EGFRvIII- and mesothelin-expressing tumor cells, eventually resulting in tumor cell lysis. EGFRvIII and mesothelin are overexpressed in many types of cancer. Two genes contributing to the virulence of Lm have been removed to minimize the risk of infection.","Bacterium|Pharmacologic Substance"]
["C111998","Live-attenuated Listeria monocytogenes-encoding EGFRvIII-NY-ESO-1 Vaccine ADU-623","ADU-623|Live-attenuated Listeria monocytogenes-encoding EGFRvIII-NY-ESO-1 Vaccine ADU-623","A live-attenuated, double-deleted strain of the Gram-positive bacterium Listeria monocytogenes (Lm) encoding a mutant form of the tumor associated antigens, epidermal growth factor receptor (EGFRvIII) and the cancer/testis antigen NY-ESO-1, with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, live-attenuated Listeria monocytogenes encoding EGFRvIII-NY-ESO-1 vaccine targets dendritic cells and expresses EGFRvIII and NY-ESO-1. This promotes both a potent innate immune response and an adaptive immune response involving the recruitment and activation of T lymphocytes against EGFRvIII and NY-ESO-1-expressing tumor cells, which results in tumor cell lysis.","Bacterium|Pharmacologic Substance"]
["C2499","LMB-1 Immunotoxin","B3-NLysPE38|Immunotoxin LMB-1|LMB-1 Immunotoxin|LMB-1 immunotoxin|LMB-1","A chimeric protein consisting of the Fv portion of a monoclonal antibody attached to a fragment of Pseudomonas exotoxin A without its cell-binding region.  LMB-1 immunotoxin targets B3, a Lewis Y-related carbohydrate epitope found on some solid tumors.  The antibody attaches to the tumor cell and the exotoxin stops protein synthesis by inactivating elongation factor 2. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2513","LMB-2 Immunotoxin","Anti-Tac(Fv)-PE38|Humanized AntiTac Toxin|Immunotoxin LMB-2|LMB-2 (Anti-TAC(FV)-PE-38)|LMB-2 Immunotoxin|LMB-2 immunotoxin|LMB-2","A fusion protein consisting of the Fv portion of a monoclonal antibody attached to a 38-kDa fragment of the Pseudomonas exotoxin A (with amino acids 365-380 deleted).  LMB-2 immunotoxin targets the interleukin 2 receptor (also known as IL-2R or CD25) which is expressed on activated normal T and B cells and macrophages and on the cells of various hematologic malignancies.  The antibody attaches to the IL-2R on the cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1619","LMB-7 Immunotoxin","B3(Fv)-PE38 Immunotoxin|B3(Fv)-PE38|HB21(Fv)PE40|Immunotoxin LMB-7|LMB-7 (Single-Chain Immunotoxin)|LMB-7 Immunotoxin|LMB-7 immunotoxin","A single chain chimeric protein consisting of a monoclonal antibody fragment attached to a portion of the Pseudomonas exotoxin A. LMB-7 immunotoxin attaches to B3, a Lewis Y-related carbohydrate epitope on some solid tumor cells.  The antibody attaches to the cell and the exotoxin inhibits protein synthesis by inactivating elongation factor 2. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2472","LMB-9 Immunotoxin","B3 (dsFv)-PE38|Immunotoxin LMB-9|LMB-9 Immunotoxin|LMB-9 immunotoxin|LMB-9","A recombinant disulfide stabilized anti-Lewis Y IgG immunotoxin containing a 38 KD toxic element derived from the Pseudomonas aeruginosa exotoxin A and a monoclonal antibody fragment, designed to target adenocarcinomas expressing Lewis Y. LMB-9 immunotoxin attaches to tumor cells, facilitating he entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C121541","LmddA-LLO-chHER2 Fusion Protein-secreting Live-attenuated Listeria Cancer Vaccine ADXS31-164","ADXS31-164|LmddA-LLO-chHER2 Fusion Protein-secreting Live-attenuated Listeria Cancer Vaccine ADXS31-164","A cancer vaccine containing a live, highly attenuated strain of the Gram-positive bacterium Listeria monocytogenes (LmddA) encoding a fusion protein composed of a chimeric peptide comprised of three highly immunogenic epitopes of the human tumor-associated antigen (TAA) HER2/neu (chHER2) fused to a non-hemolytic fragment of the immunostimulant listeriolysin O (LLO) protein, with potential immunostimulatory and antineoplastic activities. Upon administration of the LmddA-LLO-chHER2 vaccine ADXS31-142, the LmddA is taken up by phagocytic cells; then the listeriolysin portion of the expressed LLO-chHER2 can form pores in the phagolysosomes and the fusion protein can escape into the cytosol. In turn, the LLO-chHER2 is processed and presented to the immune system by major histocompatibility complex (MHC) I on the phagocytic cells. Antigen presentation activates the immune system to exert an immune response involving the recruitment and activation of T-lymphocytes against HER2-expressing tumor cells, and inhibits tumor-infiltrating T regulatory cells (Tregs) and myeloid-derived suppressor cells (MDSCs). This eventually results in tumor cell lysis. HER2/neu, a tyrosine kinase receptor belonging to the epidermal growth factor receptor (EGFR) family, is overexpressed in various tumor cell types.","Pharmacologic Substance"]
["C107240","L-methylfolate","5-MTHF|5-Methyl terahydrofolic Acid|5-Methyltetrahydrofolate|Deplin|L-Glutamic Acid, N-(4-(((2-amino-1,4,5,6,7,8-hexahydro-5- methyl-4-oxo-6-pteridinyl)methyl)amino)benzoyl)-|L-methylfolate|L-methyltetrahydrofolate","A nutritional supplement containing the biologically active form of the B9 vitamin folate, 5-methyltetrahydrofolate (L-methylfolate), with potential antineoplastic activity. Upon administration, L-methylfolate is able to provide methyl groups allowing an increase in the level of DNA methylation in the promoter regions of certain tumor-promoting genes, thereby reversing the DNA hypomethylation of these genes and inactivating them. This may result in a decrease of both tumor cell proliferation and tumor progression. In addition, administration of L-methylfolate may sensitize tumor cells to the cytotoxic effects of other chemotherapeutic agents. Unlike folic acid, L-methylfolate is able to cross the blood brain barrier and could be beneficial in the treatment of brain tumors. DNA hypomethylation of certain genes leads to chromosome instability and contributes to tumor development.","Pharmacologic Substance"]
["C118956","LMP1/BARF1/EBNA1-specific Cytotoxic T-lymphocytes","LMP1/BARF1/ EBNA1-specific CTLs|LMP1/BARF1/EBNA-1 MABEL CTLs|LMP1/BARF1/EBNA-1 Minimum Anticipated Biological Effect Level Cytotoxic T-lymphocytes|LMP1/BARF1/EBNA1-specific Cytotoxic T-lymphocytes","A preparation of allogeneic cytotoxic T-lymphocytes (CTL) made specifically reactive to three Epstein-Barr virus (EBV) proteins, latent membrane protein (LMP) 1, BamH1-A rightward frame-1 (BARF1) and EBV nuclear antigen 1 (EBNA1), with potential antineoplastic activity. Administration of LMP1/BARF1/ EBNA1-specific CTLs to patients with LMP1/BARF1/EBNA1-positive tumors may result in a specific CTL response against the tumor cells expressing these antigens, which can result in both cell lysis and the inhibition of tumor cell proliferation. LMP1, BARF1 and EBNA1 are expressed in various, EBV-associated malignancies, including nasopharyngeal cancer and EBV-positive Hodgkin lymphoma.","Cell|Pharmacologic Substance"]
["C62767","LMP-2:340-349 Peptide Vaccine","LMP-2:340-349 Peptide Vaccine","A peptide vaccine containing amino acids residues from 340 through 349 of the latent membrane protein-2 (LMP-2) of the Epstein-Barr virus (EBV) with potential immunostimulating and antineoplastic activities. LMP-2, an EBV transmembrane protein, is expressed in various malignancies including nasopharyngeal cancer and EBV-positive Hodgkin's disease. Vaccination with the LMP-2:340-349 peptide may boost the immune system to mount a specific cytotoxic T-lymphocyte (CTL) response against LMP-2 producing cells, resulting in cell lysis and inhibition of cancer cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C62768","LMP-2:419-427 Peptide Vaccine","LMP-2:419-427 Peptide Vaccine","A peptide vaccine containing amino acids residues from 419 through 427 of the latent membrane protein-2 (LMP-2) of the Epstein-Barr virus (EBV) with potential immunostimulating and antineoplastic activities. LMP-2, an EBV transmembrane protein, is expressed in various malignancies including nasopharyngeal cancer and EBV-positive Hodgkin's disease. Vaccination with the LMP-2:49-427 peptide may boost the immune system to mount a specific cytotoxic T-lymphocyte response against LMP-2 producing cells, resulting in cell lysis and inhibition of cancer cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C62784","LMP2A-Specific Cytotoxic T-Lymphocytes","EBV-Specific Cytotoxic T-Lymphocytes|LMP2A-Specific CTL|LMP2A-Specific Cytotoxic T-Lymphocytes","A preparation of cytotoxic T-lymphocytes (CTL), specifically reactive to Epstein-Barr virus (EBV) latent membrane protein-2A (LMP2A), with potential antineoplastic activity. T-lymphocytes are exposed ex vivo to dendritic cells (DCs) transfected with a replication-deficient adenovirus encoding EBV LMP2A. Subsequently, LMP2A-specific CTLs are exposed to EBV infected cells transfected with adenovirus encoding LMP2A, thereby further stimulating CTLs. Administered to patients with EBV-positive tumors, LMP2A-specific CTLs target LMP2A-positive cells, resulting in cell lysis and inhibition of cancer cell proliferation. EBV LMP2A may be expressed in various malignancies, including nasopharyngeal carcinoma and Hodgkin and non-Hodgkin lymphomas.","Cell|Pharmacologic Substance"]
["C124225","LNA-based AntimiR-155 MRG-106","Anti-miR-155 Oligonucleotide MRG-106|LNA AntimiR-155 MRG-106|LNA-based AntimiR-155 MRG-106|MRG-106|MiR-155 Antagonist MRG-106|MicroRNA-155 Antagonist MRG-106","A locked nucleic acid (LNA)-based oligonucleotide inhibitor of microRNA (miRNA) 155 (miR-155), with potential antineoplastic activity. Upon administration, LNA-based anti-miR-155 MRG-106 targets, binds to and inhibits miR-155. This silences miR-155 and prevents the translation of certain tumor promoting genes, which leads to the induction of cancer cell apoptosis and the inhibition of tumor cell growth. miR-155, an oncogenic single-stranded, non-coding RNA that is critical to the regulation of gene expression, is overexpressed in certain tumor cell types. Up-regulation of miR-155 plays a key role in increased tumor cell proliferation and survival. The LNA is an RNA analog in which the ribose ring is locked in a particular confirmation that increases stability. Compared to the unmodified oligonucleotide, the LNA-modified oligonucleotide shows increased affinity for its target miR-155.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1434","Lobaplatin","1,2-diammino-methy lcyclobutane-platinum (II) lactate|D-19466|LOBAPLATIN|Lobaplatin|lobaplatin","A third-generation, water-soluble platinum compound with potential antineoplastic activity. Lobaplatin forms highly reactive, charged, platinum complexes that bind to nucleophilic groups such as GC- and AG-rich sites in DNA, inducing intrastrand DNA cross-links. These cross-links will ultimately result in induction of apoptosis and cell growth inhibition. Compared to first and second generation platinum compounds, lobaplatin appears to be more stable, less toxic, have a better therapeutic index and may overcome tumor resistance.","Inorganic Chemical|Pharmacologic Substance"]
["C979","Lometrexol","(6R)-DDATHF|6R-5,10-Dideazatetrahydrofolate|L-Glutamic acid, N-(4-(2-((6R)-2-amino-1,4,5,6,7,8-hexahydro-4-oxopyrido(2,3-d)pyrimidin-6-yl)ethyl)benzoyl)-|L-Glutamic acid, N-(4-(2-(2-amino-1,4,5,6,7,8-hexahydro-4-oxopyrido(2,3-d)pyrimidin-6-yl)ethyl)benzoyl)-, (R)-|LOMETREXOL|Lometrexol|Pyrido[2,3-d]pyrimidine, L-glutamic acid derivative (9CI)|lometrexol","A folate analog antimetabolite with antineoplastic activity. As the 6R diastereomer of 5,10-dideazatetrahydrofolate, lometrexol inhibits glycinamide ribonucleotide formyltransferase (GARFT), the enzyme that catalyzes the first step in the de novo purine biosynthetic pathway, thereby inhibiting DNA synthesis, arresting cells in the S phase of the cell cycle, and inhibiting tumor cell proliferation.  The agent has been shown to be active against tumors that are resistant to the folate antagonist methotrexate. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C90623","Lometrexol Sodium","LOMETREXOL SODIUM|LY264618 Disodium|Lometrexol Sodium","The sodium salt form of lometrexol, a folate analogue antimetabolite with antineoplastic activity. As the stereoisomer of 5,10-dideazatetrahydrofolate, lometrexol selectively inhibits glycinamide ribonucleotide formyltransferase (GARFT), the enzyme that catalyzes the first step in the de novo purine biosynthetic pathway, thereby inhibiting DNA synthesis and leading to an inhibition of tumor cell proliferation.  The agent has been shown to be active against tumors that are resistant to the folate antagonist methotrexate, but causes severe, dose-limiting toxicities.","Organic Chemical|Pharmacologic Substance"]
["C617","Lomustine","1-(2-Chloroethyl)-3-cyclohexyl-1-nitrosourea|1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea|1-Nitrosourea, 1-(2-chloroethyl)-3-cyclohexyl-|Belustin|Belustine|CCNU|Cecenu|CeeNU|Chloroethylcyclo- hexylnitrosourea|Chloroethylcyclohexylnitrosourea|Citostal|LOMUSTINE|Lomeblastin|Lomustine|Lomustinum|Lucostin|Lucostine|N-(2-Chloroethyl)-N'-cyclohexyl-N-nitrosourea|N-(2-chloroethyl)-N'-cyclohexyl-N-nitrosourea|Prava|RB-1509|WR-139017|lomustine","A nitrosourea with antineoplastic activity. Lomustine alkylates and crosslinks DNA, thereby inhibiting DNA and RNA synthesis.  This agent also carbamoylates DNA and proteins, resulting in inhibition of DNA and RNA synthesis and disruption of RNA processing.  Lomustine is lipophilic and crosses the blood-brain barrier. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1829","Lonafarnib","4-[2-[4-(3,10-Dibromo-8-chloro-6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridin-11-yl)-1-piperidinyl]-2-oxoethyl]-1-piperidinecarboxamide|4-[2-[4-[(11R)-3,10-Dibromo-8-chloro-6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridin-11-yl]-1-piperidinyl]-2-oxoethyl]-1-piperidinecarboxamide|LONAFARNIB|Lonafarnib|SCH 66336|SCH-66336|SCH66336|Sarasar|lonafarnib","A synthetic tricyclic derivative of carboxamide with antineoplastic properties.  Lonarfanib binds to and inhibits farnesyl transferase, an enzyme involved in the post-translational modification and activation of Ras proteins.  Ras proteins participate in numerous signalling pathways (proliferation, cytoskeletal organization), and play an important role in oncogenesis.  Mutated ras proteins have been found in a wide range of human cancers. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C116067","Long Peptide Vaccine 7","LPV7|Long Peptide Vaccine 7","A peptide vaccine consisting of a combination of seven synthetic long peptides (SLPs), which are each about 30 amino acids in size, and derived from cancer-testis antigens (CTA) and melanocytic differentiation proteins (MDP), with potential immunostimulating and antitumor activities. Upon administration, long peptide vaccine 7 may stimulate the host immune system to mount a cytotoxic T-cell lymphocyte (CTL) response against tumor cells expressing these peptides. CTA and MDP are overexpressed in a variety of cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C113656","Long-acting Release Pasireotide","LAR Pasireotide|Long-acting Release Pasireotide|SOM230 LAR","A long-acting release (LAR) formulation containing pasireotide, a synthetic long-acting cyclohexapeptide, with somatostatin-like activity. Upon intramuscular administration of the LAR formulation of pasireotide, this somatostatin analog strongly binds to and activates somatostatin receptor (SSTR) subtypes 1, 2, 3, and 5. This leads to an inhibition in the secretion of human growth hormone (hGH) and results in decreased production of insulin-like growth factor (IGF-1), which may inhibit IGF-1-mediated cell signaling pathways. This may lead to an inhibition in tumor cell growth and an increase in apoptosis in IGF-1-overexpressing tumor cells. In addition, this agent causes a reduction in adrenocorticotropic hormone (ACTH), which leads to an inhibition of cortisol secretion. ACTH-producing tumors cause hypersecretion of cortisol which results in many unwanted symptoms. This agent may also block other key survival pathways such as the phosphatidylinositol 3-kinase (PI3K) and the mitogen-activated protein kinase (MAPK) signaling pathways. Pasireotide also inhibits vascular endothelial growth factor (VEGF) secretion, thereby decreasing angiogenesis and tumor cell growth in VEGF-overexpressing tumor cells. The long-acting form of pasireotide allows for less frequent administration as compared to the original form of this agent. SSTRs are overexpressed by some neuroendocrine and non-neuroendocrine tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C113655","Lorlatinib","2H-4,8-Methenopyrazolo(4,3-H)(2,5,11)benzoxadiazacyclotetradecine-3-carbonitrile, 7-amino-12-fluoro-10,15,16,17-tetrahydro-2,10,16-trimethyl-15-oxo-, (10R)-|7-Amino-12-fluoro-2,10,16-trimethyl-15-oxo-10,15,16,17-tetrahydro-2H-8,4-(metheno)pyrazolo(4,3-h)(2,5,11)benzoxadiazacyclotetradecine-3-carbonitrile|LORLATINIB|Lorlatinib|PF-06463922","An orally available, ATP-competitive inhibitor of the receptor tyrosine kinases, anaplastic lymphoma kinase (ALK) and C-ros oncogene 1 (Ros1), with potential antineoplastic activity. Upon administration, lorlatinib binds to and inhibits both ALK and ROS1 kinases. The kinase inhibition leads to disruption of ALK- and ROS1-mediated signaling and eventually inhibits tumor cell growth in ALK- and ROS1-overexpressing tumor cells. In addition, PF-06463922 is able to cross the blood brain barrier. ALK belongs to the insulin receptor superfamily and plays an important role in nervous system development; ALK dysregulation and gene rearrangements are associated with a series of tumors. ROS1, overexpressed in certain cancer cells, plays a key role in cell growth and survival of cancer cells.","Pharmacologic Substance"]
["C38714","Lorvotuzumab Mertansine","Anti-Human NCAM-1 Monoclonal Antibody N901|BB-10901|IMGN901|LORVOTUZUMAB MERTANSINE|Lorvotuzumab Mertansine|huN901-DM1","An immunoconjugate of a humanized murine monoclonal antibody (huN-901) and DMI, a semi-synthetic derivative of the plant-derived ansa macrolide maytansine. The antibody moiety of BB-10901 selectively attaches to CD56 antigen, a neural cell adhesion molecule (NCAM)) expressed on the surface of cells of small cell lung cancer (SCLC) and other neuroendocrine (NE) tumors. Thus, the DMI conjugate is targeted specifically to CD56-expressing tumor cells, where it inhibits tubulin polymerization and assembly, resulting in inhibition of mitosis and cell cycle arrest in the S phase. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1521","Losoxantrone","Biantrazole|CI-941|DuP 941|LOSOXANTRONE|Losoxantrone|losoxantrone","An anthrapyrazole-based antineoplastic antibiotic. Losoxantrone intercalates into DNA, induces single- and double-stranded DNA breaks and inhibits topoisomerase II, thereby inhibiting DNA replication and repair as well as RNA and protein synthesis. Losoxantrone is less cardiotoxic than doxorubicin.","Organic Chemical|Pharmacologic Substance"]
["C72077","Losoxantrone Hydrochloride","LOSOXANTRONE HYDROCHLORIDE|Losoxantrone Hydrochloride","The hydrochloride salt form of losoxantrone, an anthrapyrazole-based antineoplastic antibiotic. Losoxantrone intercalates into DNA, induces single- and double-stranded DNA breaks and inhibits topoisomerase II, thereby inhibiting DNA replication and repair as well as RNA and protein synthesis. Losoxantrone is less cardiotoxic than doxorubicin.","Pharmacologic Substance"]
["C620","Lovastatin","(2S)-2-Methylbutanoic Acid, (1S,3R,7S,8S,8aR)-1,2,3,7,8,8a-Hexahydro-3,7-dimethyl-8-[2-[(2R,4R)-tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl]ethyl]-1-naphthalenyl Ester|LOVASTATIN|Lovastatin Sodium|Lovastatin|Mevacor|Mevinolin|Monacolin K|lovastatin","A lactone metabolite isolated from the fungus Aspergillus terreus with cholesterol-lowering and potential antineoplastic activities. Lovastatin is hydrolyzed to the active beta-hydroxyacid form, which competitively inhibits 3-hydroxyl-3-methylgutarylcoenzyme A (HMG-CoA) reductase, an enzyme involved in cholesterol biosynthesis. In addition, this agent may induce tumor cell apoptosis and inhibit tumor cell invasiveness, possibly by inhibiting protein farnesylation and protein geranylgeranylation, and may arrest cells in the G1 phase of the cell cycle. The latter effect sensitizes tumor cells to the cytotoxic effects of ionizing radiation.","Organic Chemical|Pharmacologic Substance"]
["C113646","LSD1 Inhibitor GSK2879552","GSK2879552|LSD1 Inhibitor GSK2879552","An orally available, irreversible, inhibitor of lysine specific demethylase 1 (LSD1), with potential antineoplastic activity. Upon administration, GSK2879552 binds to and inhibits LSD1, a demethylase that suppresses the expression of target genes by converting the dimethylated form of lysine at position 4 of histone H3 (H3K4) to mono- and unmethylated H3K4. LSD1 inhibition enhances H3K4 methylation and increases the expression of tumor-suppressor genes. This may lead to an inhibition of cell growth in LSD1-overexpressing tumor cells. LSD1, overexpressed in certain tumor cells, plays a key role in tumor cell growth and survival.","Pharmacologic Substance"]
["C83925","Lucanthone","LUCANTHONE|Lucanthone","An orally available thioxanthone-based DNA intercalator and inhibitor of the DNA repair enzyme apurinic-apyrimidinic endonuclease 1 (APEX1 or APE1), with anti-schistosomal and potential antineoplastic activity. Lucanthone intercalates DNA and interferes with the activity of topoisomerases I and II during replication and transcription, thereby inhibiting the synthesis of macromolecules. In addition, this agent specifically inhibits the endonuclease activity of APE1, without affecting its redox activity, resulting in un-repaired DNA strand breaks which may induce apoptosis. Therefore, lucanthone may sensitize tumor cells to radiation and chemotherapy. Furthermore, lucanthone inhibits autophagy through the disruption of lysosomal function. The multifunctional nuclease APE1 is a key component for DNA repair; its expression is often correlated with tumor cell resistance to radio- and chemotherapy.","Pharmacologic Substance"]
["C48405","Lucatumumab","Anti-CD40 Monoclonal Antibody CHIR-12.12|CHIR-12.12|HCD-122|LUCATUMUMAB|Lucatumumab|Monoclonal Antibody CHIR-12.12","A fully human monoclonal antibody directed against the B-cell surface antigen CD40 with potential antineoplastic activity. Lucatumumab binds to and inhibits CD40, thereby inhibiting CD40 ligand-induced cell proliferation and triggering cell lysis via antibody-dependent cellular cytotoxicity (ADCC) in cells overexpressing CD40. CD40, an integral membrane protein found on the surface of B lymphocytes, is a member of the tumor necrosis factor receptor superfamily and is highly expressed in a number of B-cell malignancies.","Pharmacologic Substance"]
["C95726","Lucitanib","1-Naphthalenecarboxamide, 6-((7-((1-aminocyclopropyl)methoxy)-6-methoxy-4-quinolinyl)oxy)-n-methyl-|AL3810|E-3810|Lucitanib","A novel dual inhibitor targeting human vascular endothelial growth factor receptors (VEGFRs) and fibroblast growth factor receptors (FGFRs) with antiangiogenic activity. Lucitanib inhibits VEGFR-1, -2, -3 and FGFR-1, -2 kinases in the nM range, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. Both VEGFRs and FGFRs belong to the family of receptor tyrosine kinases that may be upregulated in various tumor cell types.","Pharmacologic Substance"]
["C2224","Lung Tumor Associated Antigen","Lung TAA|Lung Tumor Associated Antigen|tumor associated antigen, lung","A tumor associated antigen derived from the cell surface antigen of lung cancer cells. Lung tumor associated antigen could be used as a diagnostic marker or as a form of immunotherapy targeted against lung cancer cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C118623","Lung-targeted Immunomodulator QBKPN","Lung-targeted Immunomodulator QBKPN|QBKPN|SSI QBKPN|Site Specific Immunomodulator QBKPN","A proprietary, lung-targeted, site specific immunomodulator (SSI), with potential immunostimulating and antineoplastic activities. Although the exact type and composition of the lung-targeted immunomodulator QBKPN has yet to be fully disclosed, upon subcutaneous administration, this agent is able to activate a local innate immune response in the lung tissue. This results in an increased number of M1 macrophages, which induces a shift from M2 to M1 macrophage dominance in the tumor microenvironment, and stimulates the recruitment of other immune cells. The M1 macrophages exert antitumor activity and eradicate lung cancer cells through phagocytosis. QBKPN does not induce a systemic immune response or affect other organs or tissues. Altogether, this SSI may decrease tumor cell growth in the lungs. SSIs contain specific, inactivated components of pathogens, such as bacteria and/or viruses, which normally cause an acute infection in the specific organ or tissue of interest.","Pharmacologic Substance"]
["C82382","Lurbinectedin","Lurbinectedin|PM01183","A synthetic tetrahydropyrrolo [4, 3, 2-de]quinolin-8(1H)-one alkaloid analogue with potential antineoplastic activity. Lurbinectedin covalently binds to residues lying in the minor groove of DNA, which may result in delayed progression through S phase, cell cycle arrest in the G2/M phase and cell death.","Organic Chemical|Pharmacologic Substance"]
["C1610","Lurtotecan","7-(4-methylpiperazinomethylene)-10,11-ethylenedioxy-20(S)-camptothecin|GG 211|GI147211|LURTOTECAN|Lurtotecan|lurtotecan","A semisynthetic analogue of camptothecin with antineoplastic activity. Lurtotecan selectively stabilizes the topoisomerase I-DNA covalent complex and forms an enzyme-drug-DNA ternary complex. As a consequence of the formation of this complex, both the initial cleavage reaction and religation steps are inhibited and subsequent collision of the replication fork with the cleaved strand of DNA results in inhibition of DNA replication, double strand DNA breakage and triggering of apoptosis. Independent from DNA replication inhibition, lurtotecan also inhibits RNA synthesis, multi-ubiquitination and degradation of topoisomerase I and chromatin reorganization.","Organic Chemical|Pharmacologic Substance"]
["C1876","Lurtotecan Liposome","Lurtotecan Liposome|NX211|OSI-211|liposomal lurtotecan|liposome, lurtotecan","A liposome-encapsulated formulation of lurtotecan with antineoplastic activity. Lurtotecan, a semisynthetic analogue of camptothecin, selectively stabilizes the topoisomerase I-DNA covalent complex and forms an enzyme-drug-DNA ternary complex during S phase of the cell cycle, thereby inhibiting religation of topoisomerase I-mediated single-stranded DNA breaks. This ultimately results in an inhibition of DNA replication, inducing double-stranded DNA breakages, obstruction of RNA and protein synthesis and triggering apoptosis. Furthermore, this agent also stimulates degradation of topoisomerase I, likely mediated through ubiquitin-proteasomal pathway. Liposomal delivery of lurtotecan improves its penetration and delivery into tumors while lowering systemic side effects.","Organic Chemical|Pharmacologic Substance"]
["C113801","Lutetium Lu 177 DOTA-biotin","177Lu-ST2210|Lutetium Lu 177 DOTA-biotin|[177Lu]DOTA-biotin","A radioconjugate of biotin conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) and labeled with the beta-emitting isotope lutetium Lu 177 (Lu-177) that can be used for radioimmunotherapeutic purposes.  Lutetium Lu 177 DOTA-biotin could be used in pre-targeting radioimmunotherapy, which pretreats the lesion with oxidized avidin that binds to protein amino groups on cells. As avidin binds to biotin, the radioisotope can be selectively delivered to cancer cells leading to tumor cell eradication.","Pharmacologic Substance"]
["C124929","Lutetium Lu 177 DOTA-JR11","177Lu-DOTA-Cpa-c[d-Cys-Aph(Hor)-d-Aph(Cbm)-Lys-Thr-Cys]-d-Tyr-NH2|177Lu-DOTA-JR11|177Lu-DOTA-[Cpa-c(DCys-Aph(Hor)-DAph(Cbm)-Lys-Thr-Cys)-DTyr-NH2]|Lutetium Lu 177 DOTA-JR11","A radioconjugate consisting of the somatostatin antagonistic peptide JR11 that is linked, via the chelating agent dodecanetetraacetic acid (DOTA), to the beta-emitting radioisotope lutetium Lu 177, with potential antineoplastic activity and imaging activity during positron emission tomography/computed tomography (PET/CT). Upon administration, lutetium Lu 177-DOTA-JR11 binds to somatostatin receptors (SSTRs), with high affinity for SSTR2, present on the cell membranes of many types of neuroendocrine tumor (NET) cells. Upon binding and internalization, this radioconjugate specifically delivers a cytotoxic dose of beta radiation to SSTR-positive cells. SSTRs have been shown to be present in large numbers on NETs and their metastases, while most normal tissues express low levels of SSTRs.","Pharmacologic Substance"]
["C105403","Lutetium Lu 177 DOTA-Tetulomab","177Lu-DOTA-HH1|177Lu-Dota-Tetulomab|177Lu-HH1|Lutetium Lu 177 DOTA-Tetulomab","A radioimmunoconjugate, which consists of a monoclonal antibody against the cell-surface antigen CD37 covalently linked, via the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), to the beta-emitting radioisotope lutetium Lu 177, with potential antineoplastic activity. The antibody moiety of lutetium Lu 177 DOTA-tetulomab binds to CD37 on tumor B-cells. Upon internalization, the radioisotope moiety delivers a cytotoxic dose of beta radiation to CD37-expressing tumor cells. CD37, a transmembrane glycoprotein, is overexpressed in B-cell malignancies.","Pharmacologic Substance"]
["C2598","Lutetium Lu 177 Monoclonal Antibody CC49","177 Lu-CC49|Lutetium Lu 177 Monoclonal Antibody CC49","A radioimmunoconjugate of the humanized monoclonal antibody (MoAb) CC49 labeled with lutetium 131 (Lu-177). MoAb CC49 binds to the pancarcinoma tumor-associated glycoprotein (TAG)-72 with high affinity. Lu-177 MoAb CC49 delivers gamma radiation emitting Lu-177 nuclide directly to tumor cells that express TAG-72, and so may be used in radioimmunotherapeutic treatment of cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C38701","Lutetium Lu 177 Monoclonal Antibody J591","Lu 177 MOAB J591|Lutetium Lu 177 Monoclonal Antibody J591","A radioimmunoconjugate consisting of a humanized monoclonal antibody directed against the extracellular domain of prostate-specific membrane antigen linked to a beta-emitting radioisotope (lutetium-177).  This radioimmunoconjugate binds to tumor cells that express the extracellular domain of prostate-specific membrane antigen, delivering beta particle radiation selectively to tumor cells expressing this antigen and so limiting the exposure of normal tissues to ionizing radiation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C114499","Lutetium Lu 177 PP-F11N","177Lu-PP-F11N|Lutetium Lu 177 PP-F11N","A radioconjugate composed of PP-F11N, a gastrin analog, conjugated to the beta-emitting radioisotope lutetium Lu 177, with potential antineoplastic activity and potential use as an imaging agent for scintigraphy. Following intravenous administration, the PP-F11N moiety binds to the cholecystokinin-2 (CCK-2) receptor. Subsequently, the CCK-2 receptor-expressing tumor cells can be visualized scintigraphically. In addition, the radioisotope moiety delivers a cytotoxic dose of beta radiation to CCK-2 receptor-expressing tumor cells. CCK-2 receptors are expressed on a variety of tumor cell types.","Pharmacologic Substance"]
["C82354","Lutetium Lu 177-DOTA-di-HSG Peptide IMP-288","Lu-177-Labeled Di-Histamine-Succinyl-Glycine-DOTA Peptide IMP-288|Lutetium Lu 177-DOTA-di-HSG Peptide IMP-288","A radiolabeled divalent histamine-succinyl-glycine (HSG) hapten-peptide linked with the macrocyclic chelator 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) to the radionuclide lutetium (Lu) 177. After pretargeting with a bispecific monoclonal antibody (BiMoAB) directed against both a tumor associated antigen (TAA) and the HSG hapten-peptide, the HSG portion of administered Lu-177-labeled di-HSG-DOTA peptide IMP-288 binds the anti-HSG portion of the BiMoAB; Lu-177 radioisotopic activity localized to tumor cells bearing the TAA can then be visualized scintigraphically.","Pharmacologic Substance"]
["C95020","Lutetium Lu 177-DOTA-TATE","177 Lu-DOTA-TATE|177 Lu-DOTA-Tyr3-Octreotate|177Lu-DOTA0-Tyr3-Octreotate|DOTATATE LUTENIUM LU-177|Lutathera|Lutetium Lu 177 DOTA(0)-Tyr(3)-Octreotate|Lutetium Lu 177 Dotatate|Lutetium Lu 177-DOTA-TATE|Lutetium Lu 177-DOTA-Tyr3-Octreotate|lutetium Lu 177-DOTATATE","A radioconjugate consisting of the tyrosine-containing somatostatin analog Tyr3-octreotate (TATE) conjugated with the bifunctional, macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) and radiolabeled with the beta-emitting radioisotope lutetium Lu 177, with potential imaging and antineoplastic activities. Lutetium Lu 177-DOTA-TATE binds to somatostatin receptors (SSTRs), with high affinity to type 2 SSTR, present on the cell membranes of many types of neuroendocrine tumor (NET) cells. Upon binding and internalization, this radioconjugate specifically delivers a cytotoxic dose of beta radiation to SSTR-positive cells. Tyr3-octreotate (TATE) is an octreotide derivative in which phenylalanine at position 3 is substituted by tyrosine and position 8 threoninol is replaced with threonine. SSTRs have been shown to be present in large numbers on NET and their metastases, while most other normal tissues express low levels of SSTRs.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C88277","Lutetium Lu 177-Edotreotide","Lutetium Lu 177 DOTA-Tyr3-octreotide|Lutetium Lu 177-Edotreotide|[177LuDOTA]-TOC","A radioconjugate consisting of the somatostatin analogue edotreotide labeled with lutetium Lu 177 with potential antineoplastic activities. Lutetium Lu 177-edotreotide binds to somatostatin receptors (SSTRs), with high affinity to type 2 SSTR, present on the cell membranes of many types of neuroendocrine tumor cells. Upon binding and internalization, this radioconjugate specifically delivers a cytotoxic dose of beta radiation to SSTR-positive cells. Edotreotide is produced by substituting tyrosine for phenylalanine at the 3 position of the somatostatin analogue octreotide (Tyr3-octreotide or TOC) and chelated by the bifunctional, macrocyclic chelating agent dodecanetetraacetic acid (DOTA).","Pharmacologic Substance"]
["C67039","Lutetium Lu-177 Capromab","177Lu-meO-DOTA-7E11|CYT-500|Lutetium Lu 177-Labeled Capromab|Lutetium Lu-177 Capromab","A radioimmunoconjugate consisting of capromab linked to lutetium Lu 177 via the bifunctional macrocyclic chelator methoxy-tetraazacyclododecane-tetraacetic acid (MeO-DOTA) with potential antineoplastic activity. Lutetium Lu 177-capromab binds to human prostate specific membrane antigen (PSMA) expressed on tumor cell surfaces via its capromab moiety and, upon internalization, delivers cytotoxic beta radiation directly to PSMA-expressing tumor cells. PSMA is a cell surface glycoprotein abundantly expressed by prostate epithelium and is typically overexpressed by prostate cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C66978","Lutetium Lu-177 Girentuximab","177Lu-DOTA-cG250|Lutetium Lu-177 Girentuximab|Lutetium Lu-177-DOTA-Chimeric Monoclonal Antibody cG250|Lutetium-177 Labeled cG250","A radioimmunoconjugate consisting of the chimeric monoclonal antibody cG250 linked to the low energy beta-emitting radioisotope Lutetium 177, via the bifunctional macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA), with potential antineoplastic activity. The antibody moiety of lutetium Lu-177-DOTA-chimeric monoclonal antibody cG250 binds to renal cell carcinoma (RCC) cells expressing the RCC-associated antigen G250; a cytotoxic dose of beta radiation is selectively delivered to G250-expressing RCC cells upon internalization of the radioimmunoconjugate.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C78832","LV.IL-2/B7.1-Transduced AML Blast Vaccine","LV.IL-2/B7.1-Transduced AML Blast Vaccine|Lentivirus-transduced AML Blasts Expressing B7.1 and IL-2|RFUSIN2-AML1","A whole-cell cancer vaccine, containing human acute myeloid leukemic (AML) blasts that have been genetically engineered to express a B7.1/IIL-2 fusion protein encoded by a self-inactivating lentiviral vector (LV), with potential antineoplastic and immunomodulating activities. Upon administration, LV.IL-2/B7.1-transduced AML blast vaccine may stimulate a host cytotoxic T lymphocyte (CTL) response against AML cells.  The single fusion protein encoded by the LV is postsynthetically cleaved to produce biologically active membrane-anchored B7.1 and secreted IL-2 in AML blasts; combined expression of IL-2 and the co-stimulatory molecule B7.1 by AML blasts may increase stimulation of both allogeneic and autologous cytotoxic T cells.","Pharmacologic Substance"]
["C74056","LY6K/VEGFR1/VEGFR2 Multipeptide Vaccine","LY6K/VEGFR1/VEGFR2 Multipeptide Vaccine","A multipeptide vaccine consisting of peptides derived from lymphocyte antigen 6 complex locus K (LY6K) and type I and II vascular endothelial growth factor receptors (VEGFRs) with potential antineoplastic activity. Upon administration, LY6K/VEGFR1/VEGFR2 multipeptide vaccine may elicit an antitumor cytotoxic T-lymphocyte (CTL) immune response against LY6K-expressing tumor cells and/or VEGFR-expressing vascular endothelial cells involved in tumor angiogenesis. LY6K is a tumor-associated antigen (TAA) that occurs singly in glycosylphosphatidyl-inositol (GPI)-linked cell-surface glycoproteins or as three-fold repeated domain in the urokinase-type plasminogen activator receptor; VEGFRs are cell surface receptors that stimulate endothelial cell proliferation, invasion, angiogenesis, and vasculogenesis upon ligand binding and receptor activation.","Pharmacologic Substance"]
["C96736","Lymphoma TAA-specific Cytotoxic T Lymphocytes","Lymphoma TAA-specific Cytotoxic T Lymphocytes","A population of autologous cytotoxic T lymphocytes (CTLs) with potential immunomodulating and antitumor activities. White blood cells are grown ex-vivo and are exposed to dendritic cells (DCs) loaded with lymphoma tumor associated antigens (TAAs); the TAA-specific CTLs are further expanded ex-vivo before being introduced into the patient. Upon infusion with TAA-specific CTLs, these CTLs may help activate tumor-specific CTL responses in the patient, thereby specifically killing TAA-expressing cancer cells and eventually inhibiting tumor cell proliferation.","Pharmacologic Substance"]
["C99163","Lyophilized Black Raspberry Lozenge","BRB Confection|Black Raspberry Confection|LBR Lozenge|Lyophilized Black Raspberry Lozenge","A lozenge containing lyophilized black raspberry with potential antioxidant, pro-apoptotic, anti-angiogenic and chemopreventive activities. In addition to vitamins, minerals and phytosterols, black raspberries are rich in phenolic acids, such as gallic acid, ellagic acid, proanthocyanidins, and flavonoids. The anthocyanins appear to contribute significantly to this agent's effects. Anthocyanins inhibit both the activation of several signal transduction pathways, including the mitogen-activated protein kinase-mediated pathways, and certain transcription factors, such as nuclear factor kappa B (NF-kB), activator protein-1 (AP-1) complex, and nuclear factor in activated T-cells (NFAT). This inhibitory activity modulates the expression of downstream target genes that are upregulated in a variety of cancer cell types, including inducible nitric oxide synthase, cyclooxygenase-2, vascular endothelial growth factor and the anti-apoptotic protein survivin.","Pharmacologic Substance"]
["C99164","Lyophilized Black Raspberry Saliva Substitute","LBR Saliva Substitute|Lyophilized Black Raspberry Saliva Substitute","A saliva substitute (or artificial saliva) containing lyophilized black raspberry with potential antioxidant, pro-apoptotic and chemopreventive activities. In addition to vitamins, minerals and phytosterols, black raspberries are rich in flavonols of which the anthocyanins appear to contribute significantly to this agent's chemopreventive effects. Anthocyanins inhibit the activation of several signal transduction pathways, including the mitogen-activated protein kinase-mediated pathways, and certain transcription factors, such as nuclear factor kappa B (NF-kB), activator protein-1 (AP-1) complex, and nuclear factor in activated T-cells (NFAT). This in turn modulates the expression of downstream target genes that are upregulated in a variety of cancer cell types, including inducible nitric oxide synthase, cyclooxygenase-2, vascular endothelial growth factor and the anti-apoptotic protein survivin.","Pharmacologic Substance"]
["C126421","Lysine-specific Demethylase 1 Inhibitor INCB059872","INCB059872|LSD1 Inhibitor INCB059872|Lysine-specific Demethylase 1 Inhibitor INCB059872","An orally available inhibitor of lysine-specific demethylase 1 (LSD1), with potential antineoplastic activity. Upon administration, INCB059872 binds to and inhibits LSD1, a demethylase that suppresses the expression of target genes by converting the di- and mono-methylated forms of lysine at position 4 of histone H3 (H3K4) to mono- and unmethylated H3K4, respectively, through amine oxidation. LSD1 inhibition enhances H3K4 methylation and increases the expression of tumor-suppressor genes. In addition, LSD1 demethylates mono- or di-methylated H3K9 which increases gene expression of tumor promoting genes; inhibition of LSD1 promotes H3K9 methylation and decreases transcription of these genes. Altogether, this may lead to an inhibition of cell growth in LSD1-overexpressing tumor cells. LSD1, an enzyme belonging to the flavin adenine dinucleotide (FAD)-dependent amine oxidase family, is overexpressed in certain tumor cells and plays a key role in the regulation of gene expression and in tumor cell growth and survival.","Pharmacologic Substance"]
["C61571","Lyso-Thermosensitive Liposome Doxorubicin","Heat-Activated Liposomal Doxorubicin Hydrochloride|Lyso-Thermosensitive Liposome Doxorubicin|Temperature Sensitive Liposome Encapsulated Doxorubicin|ThermoDox","A temperature-sensitive liposomal formulation of the anthracycline antibiotic doxorubicin with potential antineoplastic activity. Upon intravenous administration, circulating thermosensitive liposomes are activated locally by increasing the tumor temperature to 40-41 degrees Celsius using an external heat source. The elevated temperature causes compositional changes in the liposomes, creating openings that allow for the release of encapsulated doxorubicin. Compared to non-thermosensitive liposomes, lyso-thermosensitive liposomes deliver higher concentrations of a cytotoxic agent to a heat-treated tumor site while sparing normal tissues unexposed to heat treatment.","Pharmacologic Substance"]
["C95123","Macimorelin","AEZS-130|D-Tryptophanamide,2-methylalanyl-N-[(1R)-1-(formylamino)-2-(1H-indol-3-yl)ethyl]-|EP 1572|JMV 1843|MACIMORELIN|Macimorelin|Solorel","An orally available synthetic mimetic of the growth hormone (GH) secretagogue ghrelin with potential anti-cachexia activity. Upon oral administration, macimorelin mimics endogenous ghrelin by stimulating appetite and binds to the growth hormone secretagogue receptor GHSR in the central nervous system, thereby mimicking the GH-releasing effects of ghrelin from the pituitary gland. Stimulation of GH secretion increases insulin-like growth factor-I (IGF-I) levels which may further stimulate protein synthesis. In addition, ghrelin reduces the production of pro-inflammatory cytokines, which may play a direct role in cancer-related loss of appetite.","Pharmacologic Substance"]
["C1150","Mafosfamide","MAFOSFAMIDE|Mafosfamide|mafosfamide","A synthetic oxazaphosphorine derivative with antineoplastic properties.  Mafosfamide alkylates DNA, forming DNA cross-links and inhibiting DNA synthesis.  Although closely related to cyclophosphamide, mafosfamide, unlike cyclophosphamide, does not require hepatic activation to generate its active metabolite 4-hydroxy-cyclophosphamide; accordingly, mafosfamide is potentially useful in the intrathecal treatment of neoplastic meningitis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C29187","MAGE-1 Vaccinia Contaminated with BVDV","MAGE-1 Vaccinia Contaminated with BVDV","A cancer vaccine consisting of a recombinant vaccinia virus encoding the tumor-associated gene MAGE-1 that is contaminated with bovine viral diarrhea virus (BVDV).  The MAGE-1 gene is a member of the melanoma antigen-encoding gene family which is expressed in various malignant tumors such as hepatocellular carcinoma and germ cell tumors in addition to melanoma.  Vaccination with vaccinia virus expressing human MAGE-1 may generate antitumoral T-cell responses.  BVDV is an RNA pestivirus that may contaminate vaccines due to its presence in the fetal calf serum used as a growth supplement in the tissue culture of mammalian cells used in vaccine production. (NCI04)","Pharmacologic Substance"]
["C2681","MAGE-10.A2","MAGE-10.A2","A synthetic nonapeptide derived from a melanoma-associated antigen. Vaccination with MAGE-10.A2 may stimulate a host cytotoxic T-cell response against tumor cells that express the melanoma-associated antigen, resulting in tumor cell lysis. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2596","MAGE-12 Peptide Vaccine","MAGE-12 Peptide Vaccine","A synthetic vaccine comprised of a peptide consisting of peptide fragments of melanoma-associated antigen 12 (MAGE-12). MAGE-12 has been identified as an epitope recognized by tumor infiltrating lymphocytes (TIL). Vaccination with MAGE-12 peptide stimulates the host immune system to mount a TIL response against tumor cells expressing MAGE-12, potentially resulting in decreased tumor growth.","Immunologic Factor|Pharmacologic Substance"]
["C48632","MAGE-3.A1 Peptide Vaccine","HLA-A1-Restricted MAGE-3 Peptide Vaccine|MAGE-3.A1 Peptide Vaccine|MAGE-3.A1","A synthetic peptide cancer vaccine consisting of human leukocyte antigen HLA-A1-restricted peptide derived from human melanoma antigen 3 (MAGE-3) with potential immunostimulating and antineoplastic activities. Upon administration, MAGE-3.A1 peptide vaccine may stimulate the immune system to mount a cytotoxic T-cell (CTL) response against tumor cells expressing MAGE-3, resulting in tumor cell lysis. MAGE-3, a tumor-associated antigen (TAA), is overexpressed by a variety of cancer cell types.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C62775","MAGE-A1, Her-2/neu, FBP Peptides Cancer Vaccine","MAGE-A1, Her-2/neu, FBP Peptides Cancer Vaccine|MAGE-A1, Her-2/neu, FBP Peptides Ovarian Cancer Vaccine","A synthetic cancer vaccine comprised of multiple peptides derived from MAGE-1A, Her-2/neu, and folate binding protein (FBP), with potential immunostimulating and antineoplastic properties. MAGE-A1, Her-2/neu, and FBP proteins are simultaneously over-expressed in various cancer cell types, such as epithelial ovarian cancer. The MAGE-A1, Her-2/neu, FBP peptides cancer vaccine includes the peptides MAGE-A1:161-169, FBP:191-199, Her-2/neu:369-377, MAGE-A1:96-104, and Her-2/neu:754-762. Vaccination with this cancer vaccine may activate the immune system to mount a cytotoxic T-cell (CTL) response against tumor cells expressing the corresponding antigens, resulting in tumor cell lysis.","Immunologic Factor|Pharmacologic Substance"]
["C84854","MAGE-A1/MAGE-A3/NY-ESO-1 Peptides Vaccine","MAGE-A1/MAGE-A3/NY-ESO-1 Peptides Vaccine","A cancer vaccine comprised of synthetic peptides derived from human melanoma antigen A1 (MAGE-A1), human melanoma antigen A3 (MAGE-A3) and cancer-testis antigen NY-ESO-1 with potential immunostimulating and antineoplastic activities. Upon administration, MAGE-A1/MAGE-A3/NY-ESO-1 peptides vaccine may stimulate the immune system to mount a cytotoxic T-cell (CTL) response against tumor cells expressing MAGE-A1, MAGE-A3 and NY-ESO-1, resulting in tumor cell lysis. The MAGE-A1, MAGE-A3, and NY-ESO-1 tumor-associated antigens (TAAS) are overexpressed by a variety of cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C129968","MAGE-A3 Multipeptide Vaccine GL-0817","GL-0817 Vaccine|GL-0817|GL0817|MAGE-A3 Multipeptide Vaccine GL-0817|MAGE-A3 Peptide Vaccine GL-0817","A proprietary, peptide cancer vaccine comprised of multiple peptides derived from human melanoma antigen A3 (MAGE-A3; MAGEA3), with potential immunostimulating and antineoplastic activities. Upon administration, MAGE-A3 multipeptide vaccine GL-0817 may stimulate the immune system to mount specific responses from B-cells, and CD4-positive and CD8-positive cells against tumor cells expressing MAGE-A3, resulting in tumor cell lysis. MAGE-A3, a tumor-associated antigen (TAA), is overexpressed by a variety of cancer cell types.","Immunologic Factor|Pharmacologic Substance"]
["C91710","MAGE-A3 Peptide Vaccine","MAGE-A3 Peptide Vaccine","A peptide cancer vaccine comprised of a peptide derived from the human melanoma antigen A3 (MAGE-A3), with potential immunostimulating and antineoplastic activities. Upon administration, MAGE-A3 peptide vaccine may stimulate the immune system to mount a cytotoxic T-cell (CTL) response against tumor cells expressing MAGE-A3, resulting in tumor cell lysis. MAGE-A3, a tumor-associated antigen (TAA), is overexpressed by a variety of cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C97035","MAGE-A3 Reactive T Cell Receptor-transduced Autologous T Cells","MAGE-A3 Reactive T Cell Receptor-transduced Autologous T Cells|MAGE-A3 TCR-transduced Autologous T cells","Human autologous T-lymphocytes transduced with a retroviral vector encoding a T cell receptor (TCR) specific for the human melanoma antigen A3 (MAGE-A3), with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the MAGE-A3 reactive TCR-transduced autologous T cells bind to tumor cells expressing MAGE-A3, which may halt the growth of MAGE-A3-expressing cancer cells; the TCR is specific for MAGE-A3:168-176.","Cell|Pharmacologic Substance"]
["C116862","MAGE-A3/12-specific TCR Gene-transduced Autologous PBLs","Anti-MAGE A3/12 TCR PBLs|MAGE-A3/12-specific T Cell Receptor Gene-transduced Autologous Peripheral Blood Lymphocytes|MAGE-A3/12-specific T-Cell Receptor Gene-transduced Autologous Peripheral Blood Lymphocytes|MAGE-A3/12-specific TCR Gene-transduced Autologous PBLs","Human autologous peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding a T-cell receptor (TCR) that recognizes the human melanoma antigens A3 and A12 (MAGE-A3/12), with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the MAGE-A3/12-specific TCR gene-transduced autologous PBLs bind to and lyse tumor cells expressing MAGE-A3/12, which may halt the growth of MAGE-A3/12-expressing cancer cells. MAGE-A3 and MAGE-A12, tumor associated antigens and members of the melanoma-associated antigen gene family, are overexpressed by a variety of cancer cell types.","Cell|Pharmacologic Substance"]
["C61088","MAGE-A3/HPV 16 Peptide Vaccine","MAGE-A3/HPV 16 Peptide Vaccine","A multi-epitope Trojan antigen (TA) construct vaccine consisting of human melanoma antigen A3 (MAGE-A3) and human papillomavirus (HPV) 16 peptide epitopes linked by the furin-sensitive linker peptide RVKR (arginine-serine-lysine-arginine) with immunostimulatory and antitumor activities. The TA construct enters the cytoplasm of antigen-presenting cells (APC) and is processed by the endoplasmic reticulum (ER) and the trans-Golgi network (TGN), where the endopeptidase furin releases the epitopes from the RVKR linker peptide and, together with various exopeptidases, generates MHC class I-binding peptides. Expressed on the cell surfaces of APC, these MHC class I-binding peptides stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells that display the same peptide epitopes on their cell surfaces.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C119614","MAGE-A3-expressing Adenovirus Type 5 Vaccine","AdMA3|Adenovirus/MAGE-A3|MAGE-A3-expressing Adenovirus Type 5 Vaccine","An oncolytic adenoviral vaccine composed of a replication-defective, E1- and E3-deleted adenovirus serotype 5 (Ad5) with a transgene encoding the human melanoma antigen A3 (MAGE-A3), with potential antineoplastic activity. Upon administration, MAGE-A3-expressing adenovirus type 5 vaccine selectively replicates in cancer cells and expresses MAGE-A3. This induces an immune response against tumor cells expressing the MAGE-A3 antigen, which leads to tumor cell death. The tumor-associated antigen MAGE-A3 is overexpressed by a variety of cancer cell types.","Pharmacologic Substance"]
["C114978","MAGE-A4-specific TCR Gene-transduced Autologous T Lymphocytes TBI-1201","MAGE-A4-specific TCR Gene-transduced Autologous T Lymphocytes TBI-1201|TBI-1201","Autologous human T-lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the human melanoma antigen A4 (MAGE-A4), with potential immunostimulatory and antineoplastic activities. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, MAGE-A4-specific TCR gene-transduced T-lymphocytes TBI-1201 binds to tumor cells expressing MAGE-A4. This may result in both an inhibition of growth and increased cell death for MAGE-A4-expressing tumor cells. The tumor-associated antigen MAGE-A4 is overexpressed by a variety of cancer cell types.","Cell|Pharmacologic Substance"]
["C71156","Magnesium Valproate","Magnesium Dipropylacetate|Magnesium Valproate|Pentanoic acid, 2-propyl-, Magnesium Salt|VALPROATE MAGNESIUM|Valproate Magnesium","The magnesium salt of valproic acid (2-propylpentanoic acid) with antiepileptic and potential antineoplastic activities. Magnesium valproate dissociates in the gastrointestinal tract and is absorbed into the circulation as magnesium ions and valproic acid ions; valproic acid may inhibit histone deacetylases, inducing tumor cell differentiation, apoptosis, and growth arrest. In addition, valproic acid exerts an antiepileptic effect, likely by inhibiting enzymes that catabolize the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) catabolism and so increasing concentrations of GABA in the central nervous system (CNS). The presence of the magnesium in this agent may contribute to its anticonvulsant activity and sedative properties.","Pharmacologic Substance"]
["C120555","MAG-Tn3/AS15 Vaccine","MAG-Tn3 Plus AS15 Cancer Vaccine|MAG-Tn3/AS15 Vaccine|MAG-Tn3/AS15","A vaccine containing synthetic multiple antigenic glycopeptide (MAG) composed of tri Tn glycotope (MAG-Tn3), which is comprised of a dendrimeric, nonimmunogenic lysine core linked to a tetravalent peptidic CD4+ T-cell epitope backbone and each attached to three Tn antigens (tri-Tn cluster), combined with the immunoadjuvant AS15, with potential antineoplastic activity. Upon administration of the MAG-Tn3/AS15 vaccine, MAG-Tn3 induces the production of tumor-specific anti-Tn glycosidic antibodies, which results in antibody-dependent cell cytotoxicity (ADCC) against Tn-expressing tumor cells. The Tn carbohydrate antigen, a tumor-associated antigen (TAA), is overexpressed in a number of tumor cell types. The tri-Tn clusters mimic carbohydrate structures found on tumor cells. The T-cell epitope stimulates effective T-cell responses. AS15, a potent adjuvant liposomal formulation that contains CpG 7909, monophosphoryl lipid (MPL), and QS-21, increases the immune response against the Tn antigens.","Pharmacologic Substance"]
["C91082","Maitake Mushroom Extract","Maitake Mushroom Extract","An extract of the edible mushroom Maitaki, Grifola frondosa, rich in glucan polysaccharides, with potential immunostimulating activity. Upon oral ingestion, Maitaki mushroom extract may promote dendritic cell (DC) maturation, increase interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) production, and may enhance natural killer (NK) cell activity, thereby amplifying both innate and T cell-mediated immune responses against cancer cells. In addition, this extract may stimulate the production of granulocyte colony stimulating factor (GCSF) and promote hematopoiesis, and may improve the neutrophil count.","Pharmacologic Substance"]
["C74057","Malignant Glioma Tumor Lysate-Pulsed Autologous Dendritic Cell Vaccine","Malignant Glioma Tumor Lysate-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with lysates from malignant glioma cells with potential immunostimulatory and antineoplastic activities. Upon administration, malignant glioma tumor lysate-pulsed autologous dendritic cell vaccine exposes the immune system to undefined malignant glioma tumor-associated antigens (TAAs), which may result in anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against glioma cells and glioma cell lysis.","Pharmacologic Substance"]
["C82675","Mammaglobin-A DNA Vaccine","MAM-A DNA Vaccine|Mammaglobin-A DNA Vaccine","A cancer vaccine containing a plasmid encoding the mammaglobin-A gene with potential immunostimulating and antineoplastic activities. Upon administration, mammaglobin-A DNA vaccine may induce both humoral and cytotoxic T lymphocyte (CTL) immune responses against tumor cells that express mammaglobin-A, which may result in decreased tumor growth. The 10 kiloDalton (kD) glycoprotein mammglobin-A is expressed in over 80% of human breast cancers.","Pharmacologic Substance"]
["C83904","Mannosulfan","MANNOSULFAN|Mannosulfan","An alkyl sulfonate with potential antineoplastic activity. Mannosulfan alkylates DNA, thereby producing DNA intra- or interstrand crosslinks, and ultimately results in inhibiting DNA replication and cell growth.","Pharmacologic Substance"]
["C1990","Mannosylerythritol Lipid","Mannosylerythritol Lipid","A yeast glycolipid biosurfactant with potential antineoplastic activity.  Mannosylerythritol lipid activates protein kinase signal cascades, resulting in cell differentiation, condensation of chromatin, DNA fragmentation, G1 phase cell-cycle arrest, and apoptosis of tumor cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C61502","Mapatumumab","Anti-TRAIL R1-mAb|HGS-ETR1|Mapatumumab|TRM-1 mAb|anti-TRAIL R1-mAb","A fully human agonistic monoclonal antibody to tumor necrosis factor-related apoptosis-inducing ligand receptor-1 (TRAIL-R1) with apoptosis promoting and potential antitumor activities. TRAIL-R1 is a cell surface receptor expressed on many malignant cell types. Mapatumumab selectively binds to and activates the TRAIL cell receptor, thereby inducing apoptosis and reducing tumor growth.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1152","Marcellomycin","1-Naphthacenecarboxylic acid, 4-[[O-2,6-dideoxy-alpha-L-lyxo-hexopyranosyl-(1-4)-O-2, 6-dideoxy-alpha-L-lyxo-hexopyranosyl-(1-4)-2,3, 6-trideoxy-3-(dimethylamino)-alpha-L-lyxo-hexopyranosyl]oxy]-2-e thyl-1,2,3,4,6,11-hexahydro-2,5,7,10-tetrahydroxy-6,11-dioxo-, methyl ester, (1R-(1alpha,2beta,4beta))- (9CI)|MARCELLOMYCIN|Marcellomycin|Rhodirubin E","An antineoplastic oligosaccharide anthracycline antineoplastic antibiotic isolated from the bacterium Actinosporangium bohemicum.  Marcellomycin intercalates into DNA and induces DNA crosslinks, thereby inhibiting DNA replication and repair and RNA and protein synthesis.  This agent also induces differentiation in HL-60 promyelocytic leukemia cells by interfering with glycoprotein synthesis. (NCI04)","Antibiotic|Organic Chemical"]
["C91733","Margetuximab","Immunoglobulin G1, Anti-(human Neu (Receptor)) (Human-Mus musculus Monoclonal MGAH22 Clone ch4D5 Heavy Chain), Disulfide with Human-Mus musculus Monoclonal MGAH22 Clone ch4D5 Light Chain, Dimer|MARGETUXIMAB|MGAH-22|MGAH22|Margetuximab","A Fc-domain optimized IgG monoclonal antibody directed against the human epidermal growth factor receptor 2 (HER2) with potential immunomodulating and antineoplastic activities. After binding to HER2 on the tumor cell surface, margetuximab may induce an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells overexpressing HER2. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types. Compared to other anti-HER2 monoclonal antibodies, the Fc domain of MGAH22 is optimized with increased binding to the activating Fcgamma receptor IIIA (CD16A), expressed on cells such as natural killer (NK) cells and macrophages, thereby mediating an enhanced ADCC; the Fc domain also shows decreased binding to the inhibitory Fcgamma receptor IIB (CD32B).","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1652","Marimastat","(2S,3R)-3-(((1S)-2,2-Dimethyl-1-(methylcarbamoxy)propyl)carboyl)-2-hydroxy-5-methylhexanohydroxamic Acid|(2S,3R)-3-{(S)-[2,2-Dimethyl-1-(methylcarbamoyl) propyl]carbamoyl}-2-hydroxy-5-methylhexanohydroxamic acid|BB 2516|BB-2516|MARIMASTAT|Marimastat|Marimistat|TA-2516|marimastat","An orally-active synthetic hydroxamate with potential antineoplastic activity.  Marimastat covalently binds to the zinc(II) ion in the active site of matrix metalloproteinases (MMPs), thereby inhibiting the action of MMPs, inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis.  This agent may also inhibit tumor necrosis factor-alpha converting enzyme (TACE), an enzyme involved in tumor necrosis factor alpha (TNF-alpha) production that may play a role in some malignancies as well as in the development of arthritis and sepsis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C64634","Marizomib","(1R,4R,5S)-4-(2-chloroethyl)-1-{(S)-[(1S)-cyclohex-2-en-1-yl]hydroxymethyl}-5-methyl-6-oxa-2-azabicyclo[3.2.0]heptane-3,7-dione|MARIZOMIB|ML 858|Marizomib|NPI-0052|Salinosporamide A|Salinosporin A","A naturally-occurring salinosporamide, isolated from the marine actinomycete Salinospora tropica, with potential antineoplastic activity. Marizomib irreversibly binds to and inhibits the 20S catalytic core subunit of the proteasome by covalently modifying its active site threonine residues; inhibition of ubiquitin-proteasome mediated proteolysis results in an accumulation of poly-ubiquitinated proteins, which may result in the disruption of cellular processes, cell cycle arrest, the induction of apoptosis, and the inhibition of tumor growth and angiogenesis. This agent more may more potent and selective than the proteasome inhibitor bortezomib.","Organic Chemical|Pharmacologic Substance"]
["C2773","MART-1 Adenovirus Vaccine","MART-1 Adenovirus Vaccine","A vaccine consisting of recombinant adenovirus vector encoding MART-1 (melanoma antigen recognized by T-cells 1), an immunogenic protein of unknown function that is expressed by certain types of melanoma.  Vaccination with MART-1 adenovirus vaccine may stimulate the host immune system to direct cytotoxic T lymphocytes (CTL) against MART-1 positive melanoma cells, resulting in an antitumor effect. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C28724","MART-1 Antigen","Antigen LB39-AA|Antigen SK29-AA|MART-1 Antigen|MART-1 Tumor Antigen|MART-1 antigen|MART-1|MART1|MLANA Protein|MLANA|Melan A|Melan-A Protein|Melan-A|Melanoma Antigen Recognized by T-Cells 1","A tumor-associated melanocytic differentiation antigen. Vaccination with MART-1 antigen may stimulate a host cytotoxic T-cell response against tumor cells expressing the melanocytic differentiation antigen, resulting in tumor cell lysis. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C111683","MART-1 Reactive CD8+ T-lymphocytes","MART-1 Reactive CD8+ T-lymphocytes","Human CD8-positive T-lymphocytes that are engineered to recognize melanoma tumor associated antigen MART-1 (Melanoma Antigen Recognized by T cells, also called Melan-A) in a human leukocyte antigen (HLA)-A2-restricted manner, with potential antineoplastic activity. Human peripheral blood lymphocytes (PBLs) are isolated from a melanoma patient, exposed to the MART-1:27-35(27L) peptide and MART-1 specific T-lymphocytes are isolated and expanded. Upon infusion, these lymphocytes recognize and exert a cytotoxic T-cell-mediated immune response against MART-1-expressing melanoma cells. The synthetic MART-1:27-35 HLA-A2-restricted peptide has an amino acid substitution, leucine to alanine at position 27, to increase its immunogenicity.","Cell|Pharmacologic Substance"]
["C107159","MART-1/gp100/Tyrosinase/MAGE-A3 Peptides-loaded Irradiated Allogeneic Plasmacytoid Dendritic Cells","GeniusVac-Mel4|MART-1/gp100/Tyrosinase/MAGE-A3 Peptides-loaded Irradiated Allogeneic Plasmacytoid Dendritic Cells","Irradiated allogeneic, HLA-A*0201 positive, plasmacytoid dendritic cells (pDCs) loaded with 4 melanoma peptides derived from the tumor associated antigens (TAAs) MelA/MART-1, gp100/pmel17, tyrosinase, and MAGE-A3, with potential immunostimulating and antineoplastic activities. Upon subcutaneous administration, the irradiated allogeneic pDCs may trigger functional multi-specific T cells from peripheral blood mononuclear cells and tumor-infiltrating lymphocytes, and activate the immune system to mount a cytotoxic T-lymphocyte response against HLA-A*0201 positive melanoma cancer cells expressing the TAAs MelA/MART-1, gp100/pmel17, tyrosinase, and MAGE-A3. These TAAs are upregulated in a variety of tumor cells. The pDCs are derived from a distinct subset of dendritic cells (DCs) with a plasma cell-like morphology and express a characteristic set of surface markers and may increase the anti-tumor immune responses.","Cell|Pharmacologic Substance"]
["C2772","MART-1:26-35(27L) Peptide Vaccine","MART-1:26-35 (27L)|MART-1:26-35(27L) Peptide Vaccine","A peptide-based cancer vaccine consisting of amino acid residues 26 through 35 of MART-1 (melanoma antigen recognized by T-cells-1) with a leucine substitution at amino acid position 27 to improve immunogenicity. Upon administration, MART-1:26-35(27L) peptide vaccine may induce a cytotoxic T-lymphocyte (CTL) response against MART-1-expressing tumor cells, resulting in decreased tumor growth. The tumor-associated antigen (TAA) MART-1 may be overexpressed on melanoma cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2775","MART-1:27-35 Peptide Vaccine","MART-1:27-35 Peptide Vaccine|MART-1:27-35 Peptide","A natural or synthetic peptide cancer vaccine consisting of amino acid residues 27 through 35 of the melanoma-associated antigen MART-1 with potential antineoplastic activity. Vaccination with MART-1:27-35 peptide may induce cytotoxic host immune responses against melanoma cells that express this peptide.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C79831","Masitinib Mesylate","4-[(4-Methylpiperazin-1-yl)methyl]-N-(4-methyl-3-{[4-(pyridin-3-yl)-1,3-thiazol-2-yl]amino}phenyl)benzamide Mesylate|AB1010|Masitinib Mesylate","The orally bioavailable mesylate salt of masatinib, a multi-targeted protein tyrosine kinase inhibitor with potential antineoplastic activity. Masitinib selectively binds to and inhibits both the wild-type and mutated forms of the stem cell factor receptor (c-Kit; SCFR); platelet-derived growth factor receptor (PDGFR); fibroblast growth factor receptor 3 (FGFR3); and, to a lesser extent, focal adhesion kinase (FAK). As a consequence, tumor cell proliferation may be inhibited in cancer cell types that overexpress these receptor tyrosine kinases (RTKs).","Pharmacologic Substance"]
["C701","Masoprocol","4,4'-(2,3-Dimethyl-1,4-butanediyl)bis[1,2-benzenediol]|Actinex|MASOPROCOL|Masoprocol|NDGA|NDHGA|Nordihydroguaiaretic Acid|Nordihydroguaiaretic acid|masoprocol","A naturally occurring antioxidant dicatechol originally derived from the creosote bush Larrea divaricatta with antipromoter, anti-inflammatory, and antineoplastic activities. Masoprocol directly inhibits activation of two receptor tyrosine kinases (RTKs), the insulin-like growth factor receptor (IGF-1R) and the c-erbB2/HER2/neu receptor, resulting in decreased proliferation of susceptible tumor cell populations. This agent may induce apoptosis in susceptible tumor cell populations as a result of disruption of the actin cytoskeleton in association with the activation of stress activated protein kinases (SAPKs). In addition, masoprocol inhibits arachidonic acid 5-lipoxygenase (5LOX), resulting in diminished synthesis of inflammatory mediators such as prostaglandins and leukotrienes. It may prevent leukocyte infiltration into tissues and the release of reactive oxygen species.","Organic Chemical|Pharmacologic Substance"]
["C2012","Matuzumab","EMD 72000|Matuzumab|matuzumab","A humanized monoclonal antibody with antineoplastic activity. Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and inhibiting receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C626","Maytansine","Alanine, N-acetyl-N-methyl-, 6-ester with 11-chloro-6, 21-dihydroxy-12,20-dimethoxy-2,5,9,16-tetramethyl-4,24-dioxa-9, 22-diazatetracyclo[19.3.1.1(10,24).0(3,5)]hexacosa-10,12,14[26], 16,18-pentaene-8,23-dione|L-Alanine, N-acetyl-N-methyl-, 11-chloro-21-hydroxy-12,20-dimethoxy-2,5,9,16-tetramethyl-8, 23-dioxo-4,24-dioxa-9,22-diazatetracyclo[19.3.1.110,14.03, 5]hexacosa-10,12,14(26),16,18-pentaen-6-yl ester, [1S-(1R*,2S*, 3R*,5R*,6R*,16E,18E,20S*,21R*)]-|L-alanine, N-acetyl-N-methyl-, 11-chloro-21-hydroxy-12,20-dimethoxy-2,5,9,16-tetramethyl-8,23-dioxo-4,24-dioxa-9,22-diazatetracyclo[19.3.1.110,14.03, 5]hexacosa-10,12,14(26),16,18-pentaen-6-yl ester, [1S-(1R*,2S*,3R*,5R*,6R*,16E,18E,20S*,21R*)]|MAYTANSINE|Maitansine|Maysanine|Maytansin|Maytansine|alanine, N-acetyl-N-methyl-, 6-ester with 11-chloro-6, 21-dihydroxy-12,20-dimethoxy-2,5,9,16-tetramethyl-4,24-dioxa-9,22-diazatetracyclo[19.3.1.1(10,24).0(3,5)]hexacosa-10,12,14[26], 16,18-pentaene-8,23-dione","An ansamycin antibiotic originally isolated from the Ethiopian shrub Maytenus serrata. Maytansine binds to tubulin at the rhizoxin binding site, thereby inhibiting microtubule assembly, inducing microtubule disassembly, and disrupting mitosis.  Maytansine exhibits cytotoxicity against many tumor cell lines and may inhibit tumor growth in vivo. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C127817","MCL-1 Inhibitor AMG 176","AMG 176|MCL-1 Inhibitor AMG 176","An inhibitor of induced myeloid leukemia cell differentiation protein MCL-1 (myeloid cell leukemia-1), with potential pro-apoptotic and antineoplastic activities. Upon administration, AMG 176 binds to and inhibits the activity of MCL-1. This disrupts the formation of MCL-1/Bcl-2-like protein 11 (BCL2L11; BIM) complexes and induces apoptosis in tumor cells. MCL-1, an anti-apoptotic protein belonging to the Bcl-2 family of proteins, is upregulated in cancer cells and promotes tumor cell survival.","Pharmacologic Substance"]
["C104009","MCPyV TAg-specific Polyclonal Autologous CD8-positive T Cells","MCPyV TAg-specific Polyclonal Autologous CD8-positive T Cells","A preparation of polyclonal autologous CD8 positive T-lymphocytes specific for the Merkel cell polyomavirus (MCPyV) T antigen (TAg) with potential antineoplastic activity. Peripheral blood lymphocytes from a Merkel cell carcinoma (MCC) patient were obtained and antigen-specific CD8+ T cells targeting a specific MCPyV TAg epitope were derived and expanded ex vivo. Upon infusion of the MCPyV TAg-specific polyclonal autologous CD8-positive T cell vaccine, the T cells recognize the MCPyV antigen and exert a cytotoxic T-lymphocyte response against the MCPyV TAg-expressing MCC cells. MCPyV is expressed in about 80% of MCC and is not expressed in normal, human tissue; the MCPyVTag oncoprotein plays a key role in MCC survival and tumor cell proliferation.","Cell|Pharmacologic Substance"]
["C91724","MDM2 Antagonist RO5045337","MDM2 Antagonist RO5045337|R7112|RO5045337","An MDM2 (human homolog of double minutes-2; HDM2) antagonist with potential antineoplastic activity. RO5045337 binds to MDM2, thereby preventing the binding of the MDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this MDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored, which may result in the restoration of p53 signaling and thus the p53-mediated induction of tumor cell apoptosis. MDM2, a zinc finger protein, is a negative regulator of the p53 pathway; often overexpressed in cancer cells, it has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C114980","MDM2 Antagonist RO6839921","MDM2 Antagonist RO6839921|RO6839921","An MDM2 (human homolog of murine double minute-2; HDM2) antagonist with potential antineoplastic activity. Upon intravenous administration, RO6839921 binds to MDM2 and prevents the binding of the MDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing MDM2-p53 interaction, the proteasome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored. This may result in the restoration of p53 signaling, followed by p53-mediated induction of tumor cell apoptosis. MDM2, a zinc finger protein, is a negative regulator of the p53 pathway and is often overexpressed in cancer cells; p53 inhibition has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C116624","MDM2 Inhibitor AMG-232","AMG 232|AMG-232|MDM2 Inhibitor AMG-232","An orally available, piperidinone inhibitor of MDM2 (murine double minute 2), with potential antineoplastic activity. Upon oral administration, MDM2 inhibitor AMG-232 binds to MDM2 protein and prevents its binding to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this MDM2-p53 interaction, the transcriptional activity of p53 is restored. This leads to p53-mediated induction of tumor cell apoptosis. MDM2, a zinc finger protein and a negative regulator of the p53 pathway, is overexpressed in cancer cells; it plays a key role in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C107384","MDM2 Inhibitor DS-3032b","DS-3032b|HDM2 Inhibitor DS-3032b|MDM2 Inhibitor DS-3032b","An orally available MDM2 (murine double minute 2) antagonist with potential antineoplastic activity. Upon oral administration, MDM2 inhibitor DS-3032b binds to, and prevents the binding of MDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this MDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored. This results in the restoration of p53 signaling and leads to the p53-mediated induction of tumor cell apoptosis. MDM2, a zinc finger protein and a negative regulator of the p53 pathway, is overexpressed in cancer cells; it has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C118669","MDM2/MDMX Inhibitor ALRN-6924","ALRN-6924|MDM2/MDMX Inhibitor ALRN-6924","An orally available inhibitor of both murine double minute 2 (MDM2) and murine double minute X (MDMX), with potential antineoplastic activity. Upon oral administration, ALRN-6924 binds to both MDM2 and MDMX and interferes with their interaction with the transcriptional activation domain of the tumor suppressor protein p53. By preventing MDM2-p53 and MDMX-p53 interactions, p53 activity is restored, which leads to p53-mediated induction of tumor cell apoptosis. MDM2 and MDMX, negative regulators of p53 function, are often overexpressed in cancer cells.","Pharmacologic Substance"]
["C67042","MDR Modulator CBT-1","CBT-1|MDR Modulator CBT-1|MDR modulator CBT-1","A naturally-occurring, orally bioavailable bisbenzylisoquinoline plant alkaloid with potential chemosensitization activity. MDR modulator CBT-1 binds to and inhibits the MDR efflux pump P-glycoprotein (P-gp), which may inhibit the efflux of various chemotherapeutic agents from tumor cells and reverse P-gp-mediated tumor cell MDR. P-gp is a transmembrane ATP-binding cassette (ABC) transporter and is overexpressed by some multidrug resistant tumors.","Pharmacologic Substance"]
["C62056","Mechlorethamine","Bis(2-chloroethyl)methylamine|Chlorethazine|Chlormethine|HN 2|MECHLORETHAMINE|Mechlorethamine|Methylbis(beta-chloroethyl)amine|Mustard|Mustine|Nitrogen Mustard|chlorethazine|chloromethine|ethanamine,2-chloro-N-(2-chloroethyl)-N-methyl|methylchlorethamine","A synthetic agent related to sulphur mustard with antineoplastic and immunosuppressive properties. Nitrogen mustard (a member of a family of chemotherapy agents including cyclophosphamide and chlorambucil) is an irritant and carcinogenic agent metabolized to a highly reactive ethylene immonium derivative; the ethylene immonium derivative alkylates DNA and inhibits DNA replication. This agent also exhibits lympholytic properties. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C627","Mechlorethamine Hydrochloride","Bis(2-chloroethyl)methylamine Hydrochloride|Caryolysine|Chlorethamine HCl|Chlorethazine Hydrochloride|Chlormethine Hydrochloride|Chlormethine hydrochloride|Chloromethine HCl|Chloromethine Hydrochloride|Cloramin|Erasol|HN 2 Hydrochloride|MECHLORETHAMINE HYDROCHLORIDE|Mechlorethamine Hydrochloride|Mechlorethamine hydrochloride|Methylbis(beta-chloroethyl)amine Hydrochloride|Methylchlorethamine Hydrochloride|Mustargen HCl|Mustargen Hydrochloride|Mustargen hydrochloride|Mustargen|Mustine Hydrochloride|Mustine hydrochloride|N-Lost|Onco-Cloramin|WR-147650|chlorethamine hydrochloride|ethanamine,2-chloro-N-(2-chloroethyl)-N-methyl Hydrochloride|mechlorethamine HCl|mechlorethamine hydrochloride|mustine","The hydrochloride salt of mechlorethamine, a nitrogen mustard and an analogue of sulfur mustard, with antineoplastic and immunosuppressive activities. Mechlorethamine is metabolized to an unstable, highly reactive ethyleniminium intermediate that alkylates DNA, particularly the 7 nitrogen of guanine residues, resulting in DNA base pair mismatching, DNA interstrand crosslinking, the inhibition of DNA repair and synthesis, cell-cycle arrest, and apoptosis. This agent also exhibits lympholytic properties.","Organic Chemical|Pharmacologic Substance"]
["C119736","Mechlorethamine Hydrochloride Gel","Mechlorethamine HCl Gel|Mechlorethamine Hydrochloride Gel|Valchlor","A gel formulation composed of the hydrochloride salt form of mechlorethamine, which is a nitrogen mustard alkylating agent and an analog of sulfur mustard, with antineoplastic and immunosuppressive activities. Upon topical application, mechlorethamine is metabolized to an unstable, highly reactive ethyleniminium intermediate that binds to and alkylates DNA, with a high affinity to the N7 nitrogen of guanine residues. This results in DNA base pair mismatching, DNA interstrand crosslinking, the inhibition of DNA repair and synthesis, cell-cycle arrest, and apoptosis.","Pharmacologic Substance"]
["C87599","Medorubicin","(1S,3S)-3-Glycoloyl-1,2,3,4,6,11-Hexahydro-3,5,12-Trihydroxy-6,11-Dioxo-1-Naphthacenyl 3-Amino-2,3,6-Trideoxy-Alpha-L-Lyxo-Hexopyranoside|4-Demethoxydoxorubicin|MEDORUBICIN|Medorubicin","A demethoxy derivative of doxorubicin with antineoplastic activity.","Pharmacologic Substance"]
["C629","Medroxyprogesterone","(6Alpha)-17-hydroxy-6-methylpregn-4-ene-3,20-dione|17Alpha-hydroxy-6alpha-methylprogesterone|6Alpha-methyl-17alpha-hydroxyprogesterone|6Alpha-methyl-4-pregnen-17alpha-ol-3,20-dione|Curretab|MEDROXYPROGESTERONE|Medroxyprogesterone|medroxyprogesterone","A synthetic derivative of progesterone administered as an acetate salt (medroxyprogesterone acetate) with antiestrogenic activity. As a do all progestins, medroxyprogesterone binds to and activates nuclear receptors which subsequently bind to and activate target genes for transcription. As an antiestrogen, this agent may inhibit the growth-stimulating effects of estrogen on estrogen-sensitive tumor cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1156","Megestrol Acetate","(9beta,10alpha)-17-(Acetyloxy)-6-methylpregna-4,6-diene-3,20-dione|17 Alpha-acetoxy-6-methylpregna-4,6-diene-3,20-dione|17-Hydroxy-6-methylpregna-4,6-diene-3,20-dione Acetate|17-Hydroxy-6-methylpregna-4,6-diene-3,20-dione acetate|17.alpha.-Acetoxy-6-methylpregna-4,6-diene-3,20-dione|6-Dehydro-6-methyl-17 alpha-acetoxyprogesterone|6-Dehydro-6-methyl-17.alpha.-acetoxyprogesterone|6-Methyl-6-dehydro-17.alpha.-acetoxyprogesterone|6-Methyl-delta-4,6-pregnadien-17 alpha-ol-3,20-dione Acetate|BDH 1298|BDH-1298|MEGESTROL ACETATE|Maygace|Megace|Megestat|Megestil|Megestrol Acetate|Niagestin|Ovaban|Pallace|SC-10363","The acetate salt form of megestrol, a synthetic derivative of the naturally occurring female sex hormone progesterone with potential anti-estrogenic and antineoplastic activity. Mimicking the action of progesterone, megestrol acetate binds to and activates nuclear progesterone receptors in the reproductive system, and causes the ligand-receptor complex to be translocated to the nucleus where it binds to and promotes expression of target genes. This leads to an alteration in protein synthesis, which modulates cell growth of reproductive tissues. Due to the negative feedback mechanism seen with progesterone, megestrol also blocks luteinizing hormone (LH) release from the pituitary gland, thereby leading to an inhibition of ovulation and an alteration in the cervical mucus and endometrium. Furthermore, without stimulation of LH, estrogen release from the ovaries is stopped, hence impedes the growth of estrogen-sensitive tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C98832","MEK 1/2 Inhibitor AS703988/MSC2015103B","AS703988/MSC2015103B|AS703988|MEK 1/2 Inhibitor AS703988/MSC2015103B|MSC2015103B","An orally bioavailable small-molecule inhibitor of mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK) 1 and 2 with potential antineoplastic activity. MEK1/2 inhibitor AS703988/MSC2015103B selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway that regulates cell growth and are often upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C69143","MEK Inhibitor AZD8330","ARRY-424704|ARRY-704|AZD8330|MEK Inhibitor AZD8330","An orally active, selective MEK inhibitor with potential antineoplastic activity. MEK inhibitor AZD8330 specifically inhibits mitogen-activated protein kinase kinase 1 (MEK or MAP/ERK kinase1), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","Organic Chemical|Pharmacologic Substance"]
["C2670","MEK Inhibitor CI-1040","2-(2-Chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide|CI-1040|MEK Inhibitor CI-1040|PD 184352/CI-1040|PD-184352","An agent that inhibits both mitogen-activated protein kinase kinases 1 and 2 (MEK1 and MEK2), substrates of Raf and phosphorylates extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2), preventing phosphorylation and activation of the Mitogen-Activated Protein Kinase (MAPK) pathways, involved with signal transduction pathways and tumor proliferation.","Pharmacologic Substance"]
["C95738","MEK Inhibitor GDC-0623","GDC-0623|MEK Inhibitor GDC-0623","An orally active, selective MEK inhibitor with potential antineoplastic activity. MEK inhibitor GDC-0623 specifically inhibits mitogen-activated protein kinase kinase (MEK or MAP/ERK kinase), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","Pharmacologic Substance"]
["C82696","MEK Inhibitor RO4987655","MEK Inhibitor RO4987655|RO4987655","An orally active small molecule, targeting mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. MEK inhibitor RO4987655 binds to and inhibits MEK, which may result in the inhibition of MEK-dependent cell signaling and the inhibition of tumor cell proliferation. MEK, a dual specificity threonine/tyrosine kinase, is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","Pharmacologic Substance"]
["C84858","MEK Inhibitor TAK-733","MEK Inhibitor TAK-733|TAK-733","An orally bioavailable small-molecule inhibitor of MEK1 and MEK2 (MEK1/2) with potential antineoplastic activity. MEK inhibitor TAK-733 selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C101532","MEK Inhibitor WX-554","MEK Inhibitor WX-554|WX-554","An orally available small molecule mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK) inhibitor, with potential antineoplastic activity. MEK inhibitor WX-554 selectively binds to and inhibits the activity of MEK, thereby preventing the activation of MEK-dependent effector proteins including some transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a dual-specificity threonine/tyrosine kinase that plays a key role in the activation of the RAS/RAF/MEK/ERK signaling pathway, is frequently upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C106126","MEK/Aurora Kinase Inhibitor BI 847325","BI 847325|MEK/Aurora Kinase Inhibitor BI 847325","An orally available dual inhibitor of mitogen-activated protein kinase kinase (MEK) and Aurora kinases, with potential antineoplastic activity. Upon oral administration, MEK/Aurora kinase inhibitor BI 847325 selectively binds to and inhibits the activity of MEK, which both prevents the activation of MEK-dependent effector proteins and inhibits growth factor-mediated cell signaling. BI 847325 also binds to and inhibits the activity of the Aurora kinases A, B and C which may disrupt the assembly of the mitotic spindle apparatus, prevent chromosome segregation, and inhibit both cellular division and proliferation in Aurora kinase-overexpressing tumor cells.  Altogether, this leads to the inhibition of cell proliferation and tumor growth as well as the induction of tumor regression. MEK, a dual-specificity threonine/tyrosine kinase that plays a key role in the activation of the RAS/RAF/MEK/ERK signaling pathway, is frequently upregulated in a variety of tumor cell types. Aurora kinases are serine-threonine kinases that play essential roles in mitotic checkpoint control and are overexpressed by a wide variety of cancer cell types.","Pharmacologic Substance"]
["C79848","MEK-1/MEKK-1 Inhibitor E6201","E6201|MEK-1/MEKK-1 Inhibitor E6201","A synthetic, fungal metabolite analogue inhibitor of mitogen-activated protein kinase kinase 1 (MEK-1) and mitogen-activated protein kinase kinase kinase 1 (MEKK-1) with potential antipsoriatic and antineoplastic activities. MEK-1/MEKK-1 inhibitor E6201 specifically binds to and inhibits the activities of MEK-1 and MEKK-1, which may result in the inhibition of tumor cell proliferation. MEK-1 and MEKK-1 are key components in the RAS/RAF/MEK/MAPK signaling pathway, which regulates cell proliferation and is frequently activated in human cancers.","Organic Chemical|Pharmacologic Substance"]
["C61495","Melan-A VLP Vaccine","CYT004-MelQbG10|Melan-A VLP Vaccine","A vaccine consisting of the melanocyte differentiation antigen Melan A (also called MART-1) encapsulated in noninfectious virus-like particles (VLP) with potential immunostimulating and antineoplastic activities. Upon administration, Melan-A VLP vaccine may activate the immune system to exert a specific cytotoxic T lymphocyte (CTL) response against cancer cells expressing the Melan A antigen, resulting in tumor cell lysis. Melan A is an antigen that is upregulated in most melanomas. VLP stimulates the immune system and promotes the CTL response.","Immunologic Factor|Pharmacologic Substance"]
["C96041","Melan-A/MAGE-3.DP4 Peptide Vaccine","Melan-A/MAGE-3.DP4 Peptide Vaccine","A cancer vaccine consisting of a peptide derived from the melanocyte differentiation antigen Melan-A (or MART-1) and the human leukocyte antigen HLA-DP4-restricted human melanoma antigen 3 (MAGE-3.DP4), with potential immunostimulating and antineoplastic activities. Upon administration, Melan-A/MAGE-3.DP4 peptide vaccine may stimulate the immune system to mount a cytotoxic T-cell (CTL) response against tumor cells expressing Melan-A and MAGE-3, resulting in tumor cell lysis. The tumor associated antigens Melan-A and MAGE-3 are overexpressed in a variety of cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C38700","Melanoma Helper Peptide Vaccine","MHP VAC|Melanoma Helper Peptide Vaccine","A multivalent vaccine consisting of peptides derived from melanoma-associated antigens and an adjuvant peptide derived from tetanus toxoid. Vaccination with this agent may stimulate a host cytotoxic T-cell response against tumor cells expressing melanoma-associated antigens, resulting in tumor cell lysis. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C29178","Melanoma Monoclonal Antibody hIgG2A","M A IG2A Human Melanoma|Melanoma Monoclonal Antibody hIgG2A","One of a number human monoclonal antibodies of the immunoglobulin subclass IgG2a directed against melanoma antigens with potential antineoplastic activity.  A melanoma monoclonal antibody, subclass IgG2A, may have potential use as a diagnostic agent and, therapeutically, may induce macrophage-mediated cytotoxicity against antibody-bound melanoma cells. (NCI04)","Immunologic Factor"]
["C91380","Melanoma TRP2 CTL Epitope Vaccine SCIB1","Melanoma TRP2 CTL Epitope Vaccine SCIB1|SCIB1","A proprietary DNA-based cancer vaccine that encodes a melanoma antigen tyrosinase-related protein 2 (TRP2) cytotoxic T-lymphocyte (CTL) epitope and a modified monoclonal antibody, a chimera of human IgG1/murine IgG2a with T cell mimotopes expressed within the complementarity-determining regions (CDR) of the antibodies, with potential immunostimulating and antineoplastic activities. Upon intramuscular injection and electroporation, melanoma TRP2 CTL epitope vaccine SCIB1 expresses the modified antibody. Subsequently, the Fc component of the engineered antibody targets and binds to the CD64 receptor on the dendritic cells (DCs); upon processing by DCs, the cellular immune system may be activated to induce helper T-cell and CTL immune responses against tumor cells expressing the TRP2 antigen.","Immunologic Factor|Pharmacologic Substance"]
["C95741","MELITAC 12.1 Peptide Vaccine","MELITAC 12.1 Peptide Vaccine","A peptide cancer vaccine consisting of an emulsion of a mixture of 12 class I MHC-restricted melanoma peptides and a class II MHC-restricted tetanus toxoid helper peptide, with potential immunostimulating and antineoplastic activities. Upon administration, the MELITAC 12.1 peptide vaccine may stimulate the host immune system to mount a cytotoxic T-cell response against tumor cells expressing the melanoma peptide antigens, resulting in tumor cell lysis. The melanoma peptides contained in the vaccine are upregulated in melanoma cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C111569","MELK Inhibitor OTS167","MELK Inhibitor OTS167|OTS167","An orally available inhibitor of maternal embryonic leucine zipper kinase (MELK) with potential antineoplastic activity. Upon administration, OTS167 binds to MELK, which prevents both MELK phosphorylation and activation; thus inhibiting the phosphorylation of downstream MELK substrates. This may lead to an inhibition of both cell proliferation and survival in MELK-expressing tumor cells. MELK, a serine/threonine kinase, is involved in cancer cell survival, invasiveness and cancer-stem cell formation and maintenance; it is highly upregulated in various types of cancer cells and absent in normal, healthy cells.","Organic Chemical|Pharmacologic Substance"]
["C633","Melphalan","4-[bis(2-chloroethyl)amino]-L-phenylalanine|Alanine Nitrogen Mustard|CB-3025|L-PAM|L-Phenylalanine Mustard|L-Phenylalanine mustard|L-Sarcolysin Phenylalanine mustard|L-Sarcolysin|L-Sarcolysine|L-sarcolysin|MELPHALAN|Melphalan|Melphalanum|Phenylalanine Mustard|Phenylalanine Nitrogen Mustard|Phenylalanine nitrogen mustard|Sarcoclorin|Sarkolysin|WR-19813|melphalan|p-di(chloroethyl)amino-L-phenylalanine","A phenylalanine derivative of nitrogen mustard with antineoplastic activity. Melphalan alkylates DNA at the N7 position of guanine and induces DNA inter-strand cross-linkages, resulting in the inhibition of DNA and RNA synthesis and cytotoxicity against both dividing and non-dividing tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C84878","Melphalan Hydrochloride/Sulfobutyl Ether Beta-Cyclodextrin Complex","Captisol-enabled Melphalan IV|Melphalan Hydrochloride/Sulfobutyl Ether Beta-Cyclodextrin Complex","A propylene glycol-free intravenous formulation containing the hydrochloride salt of the nitrogen mustard phenylalanine derivative melphalan complexed with polyanionic sulfobutyl ether beta-cyclodextrin (SBE-CD) with potential antineoplastic activity. Upon administration, melphalan is converted into highly reactive ethylenimmonium intermediates that induce covalent guanine N7-N7 intra- and inter-crosslinks and alkylation of adenine N3 of DNA; RNA and proteins may also be alkylated. Subsequently, RNA transcription and protein synthesis are inhibited, resulting in cell growth arrest. The addition of sulfobutyl ether beta-cyclodextrin to the formulation improves the solubility, stability and ease of use of melphalan; cyclodextrins are cyclic dextrins derived from starch.","Pharmacologic Substance"]
["C107680","Melphalan-Flufenamide Prodrug","J1|L-melphalanyl-p-L-fluorophenylalanine Ethyl Ester|Melphalan-Flufenamide Prodrug","A melphalan prodrug in which the alkylating agent melphalan is bound to flufenamide, with potential antineoplastic and anti-angiogenic activities. Upon administration, the dipeptide bond in the melphalan-flufenamide compound is hydrolyzed by peptidases, which are overexpressed by certain cancer cells. This results in the specific release and accumulation of the active metabolite melphalan in cancer cells. Melphalan alkylates DNA at the N7 position of guanine residues and induces DNA intra- and inter-strand cross-linkages. This results in the inhibition of DNA and RNA synthesis and the induction of apoptosis, thereby inhibiting tumor cell proliferation. The administration of the melphalan-flufenamide prodrug allows for enhanced efficacy and reduced toxicity compared to melphalan alone.","Pharmacologic Substance"]
["C84860","Membrane-Disrupting Peptide EP-100","EP-100|Membrane-Disrupting Peptide EP-100","A water-soluble, positively charged fusion protein consisting of a luteinizing hormone releasing hormone (LHRH) receptor-targeting ligand conjugated to the membrane-disrupting peptide CLIP 71 with membrane-disrupting and potential antineoplastic activities. The LHRH ligand moiety of membrane-disrupting peptide EP-100 specifically binds to LHRH receptors, which are upregulated on a variety of human cancer cell types. Subsequently, the positively charged CLIP 71 moiety of this agent interacts with the negatively charged membrane on the cancer cell surface, which may result in cell membrane disruption and cell lysis.","Pharmacologic Substance"]
["C84863","Menadione Topical Lotion","Menadione Topical Lotion","A topical lotion containing the small organic molecule protein tyrosine phosphatase (PTP) inhibitor menadione (vitamin K3) with potential EGFR- and ErbB2/HER2-activating activities. Upon topical administration, menadione binds to and inhibits the activity of PTPs that dephosphorylate and inactivate EGFR and ErbB2 in human keratinocytes; local reversal of EGFR and ErbB2 inhibition associated with the systemic administration of EGFR inhibitors may help alleviate EGFR inhibitor-mediated skin toxicity. EGFR (epidermal growth factor receptor) and ErbB2/HER2 (erythroblastic leukemia viral oncogene homolog 2/ human epidermal growth factor receptor 2) are cell surface receptors that are upregulated in a number of cancer cells types and play important roles in the growth and maintenance of normal epithelial tissues.","Pharmacologic Substance"]
["C52194","Menatetrenone","2-Methyl-3-trans-tetraprenyl-1,4-naphthoquinone|E0167|MENATETRENONE|Menaquinone K4|Menaquinone-4|Menatetrenone|Vitamin MK 4","A menaquinone compound and form of vitamin K2 with potential antineoplastic activity. Menatetrenone may act by modulating the signalling of certain tyrosine kinases, thereby affecting several transcription factors including c-myc and c-fos. This agent inhibits tumor cell growth by inducing apoptosis and cell cycle arrest.","Pharmacologic Substance"]
["C1389","Menogaril","7(R)-O-Methylnogarol|7-(R)-O-methylnogarol|7-OMEN|7-con-O-Methylnogarol|7-con-O-methylnogarol|7-con-O-methylnorgarol|MEN|MENOGARIL|Menogaril|Menogarol|OMEN,7-|TUT-7|U-52047|[2R-(2alpha,3beta,4alpha,5beta,6alpha,11alpha,13alpha)]-4-(dimethylamino)-3,4,5,6,11,12,13,14-octahydro-3,5,8,10,13-pentahydroxy-11-methoxy-6,13-dimethyl-2,6-epoxy-2H-naphthaceno[1,2-b]oxocin-9,16-dione","A semisynthetic derivative of the anthracycline antineoplastic antibiotic nogalamycin.  Menogaril intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.  This agent is less cardiotoxic than doxorubicin. (NCI04)","Antibiotic|Organic Chemical"]
["C1390","Merbarone","Merbarone","A nonsedating derivative of thiobarbituric acid and a novel catalytic topoisomerase II inhibitor with antineoplastic activity. Merbarone interferes with DNA replication via binding directly to topoisomerase II at a domain that maybe shared by other topoisomerase II cleavage-enhancing agents, ex., etoposide. Its mechanism of action appears to be a novel one, since merbarone does not intercalate DNA nor stabilize DNA-topoisomerase II cleavable complexes.","Organic Chemical|Pharmacologic Substance"]
["C195","Mercaptopurine","1,7-Dihydro-6H-purine-6-thione Monohydrate|1,7-Dihydro-6H-purine-6-thione|3H-Purine-6-thiol|6 MP|6 Thiohypoxanthine|6 Thiopurine|6-MP|6-Mercaptopurine Monohydrate|6-Mercaptopurine|6-Purinethiol|6-Thiopurine|6-Thioxopurine|6H-Purine-6-thione, 1,7-dihydro- (9CI)|7-Mercapto-1,3,4,6-tetrazaindene|Alti-Mercaptopurine|Azathiopurine|BW 57-323H|Bw 57-323H|Flocofil|Ismipur|Leukerin|Leupurin|MERCAPTOPURINE|Mercaleukim|Mercaleukin|Mercaptina|Mercapto-6-purine|Mercaptopurine|Mercaptopurinum|Mercapurin|Mern|NCI-C04886|Puri-Nethol|Purimethol|Purine, 6-mercapto-|Purine-6-thiol (8CI)|Purine-6-thiol Monohydrate|Purine-6-thiol, Monohydrate|Purine-6-thiol, monohydrate|Purinethiol|Purinethol|U-4748|WR-2785|mercaptopurine","A thiopurine-derivative antimetabolite with antineoplastic and immunosuppressive activities.  Produced through the metabolism of mercaptopurine by hypoxanthine-guanine phosphoribosyltransferase (HGPRT), mercaptopurine metabolites 6-thioguanosine-5'-phosphate (6-thioGMP) and 6-thioinosine monophosphate (T-IMP) inhibit nucleotide interconversions and de novo purine synthesis, thereby blocking the formation of purine nucleotides and inhibiting DNA synthesis.  This agent is also incorporated into DNA in the form of deoxythioguanosine, which results in the disruption of DNA replication. In addition, mercaptopurine is converted to 6-methylmercaptopurine ribonucleoside (MMPR) by 6-thiopurine methyltransferase; MMPRs are also potent inhibitors of de novo purine synthesis. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C61832","Mercaptopurine Anhydrous","MERCAPTOPURINE ANHYDROUS|Mercaptopurine Anhydrous","The anhydrous form of mercaptopurine, a thiopurine-derivative antimetabolite with antineoplastic and immunosuppressive activities.  Produced through the metabolism of mercaptopurine by hypoxanthine-guanine phosphoribosyltransferase (HGPRT), mercaptopurine metabolites 6-thioguanosine-5'-phosphate (6-thioGMP) and 6-thioinosine monophosphate (T-IMP) inhibit nucleotide interconversions and de novo purine synthesis, thereby blocking the formation of purine nucleotides and inhibiting DNA synthesis.  This agent is also incorporated into DNA in the form of deoxythioguanosine, which results in the disruption of DNA replication. In addition, mercaptopurine is converted to 6-methylmercaptopurine ribonucleoside (MMPR) by 6-thiopurine methyltransferase; MMPRs are also potent inhibitors of de novo purine synthesis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C111757","Mercaptopurine Oral Suspension","6-MP Oral Suspension|Mercaptopurine Oral Suspension|Purixan|Xaluprine","An oral suspension containing the thiopurine-derivative antimetabolite 6-mercaptopurine, with potential antineoplastic activity. Upon oral administration, mercaptopurine is metabolized by hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) to its active metabolite 6-thioinosine monophosphate (TIMP); TIMP inhibits nucleotide interconversions and de novo purine ribonucleotide synthesis, which both blocks the formation of purine nucleotides and inhibits DNA synthesis. This agent is also incorporated into DNA in the form of deoxythioguanosine, which results in the disruption of DNA replication. By blocking DNA synthesis and replication, cancer cells are unable to proliferate. Compared to the tablet formulation, the liquid is easier to swallow and offers more flexibility and accuracy in dosing, which is beneficial for use in pediatric patients.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C95729","Merestinib","3-Pyridinecarboxamide, N-(3-fluoro-4-((1-methyl-6-(1H-pyrazol-4-yl)-1H-indazol-5-yl)oxy)phenyl)-1-(4-fluorophenyl)-1,2-dihydro-6-methyl-2-oxo-|LY-2801653|LY2801653|MERESTINIB|Merestinib","An orally available, small molecule inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. Merestinib selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. This agent has potent anti-tumor efficacy in mono and combination therapy in a broad range of cancers. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays key roles in tumor cell proliferation, survival, invasion, metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C101773","Mesothelin-specific Chimeric Antigen Receptor-engineered Peripheral Blood Lymphocytes","Anti-mesothelin CAR PBL|Mesothelin-specific Chimeric Antigen Receptor-engineered Peripheral Blood Lymphocytes","A preparation of peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding a T cell chimeric antigen receptor (CAR) specific for mesothelin with potential immunostimulatory and antineoplastic activities. After transduction, expansion in culture, and reintroduction into the patient, the mesothelin-specific chimeric antigen receptor-engineered PBLs bind to tumor cells expressing mesothelin. This may stimulate the secretion of cytokines and result in cell lysis of mesothelin-expressing cancer cells. Mesothelin, a cell surface glycoprotein involved in cell adhesion, is overexpressed in many epithelial-derived cancers.","Cell|Pharmacologic Substance"]
["C78448","Mesothelioma Tumor Lysate-Pulsed Autologous Dendritic Cell Vaccine","Mesothelioma Tumor Lysate-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine consisting of autologous dendritic cells (DCs) pulsed with mesothelioma tumor lysate with potential immunostimulating and antineoplastic activities. Upon administration, mesothelioma tumor lysate-pulsed autologous dendritic cell vaccine may stimulate the host immune system to mount a specific cytotoxic T lymphocyte (CTL) response against mesothelioma tumor cells, resulting in tumor cell lysis.","Cell|Pharmacologic Substance"]
["C74060","MET Tyrosine Kinase Inhibitor BMS-777607","BMS-777607|MET Tyrosine Kinase Inhibitor BMS-777607","An inhibitor of MET tyrosine kinase with potential antineoplastic activity. MET tyrosine kinase inhibitor BMS-777607 binds to c-Met protein, or hepatocyte growth factor receptor (HGFR), preventing binding of hepatocyte growth factor (HGF) and disrupting the MET signaling pathway; this agent may induce cell death in tumor cells expressing c-Met. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays an important role in tumor cell proliferation, survival, invasion, and metastasis, and in tumor angiogenesis.","Pharmacologic Substance"]
["C91097","MET Tyrosine Kinase Inhibitor EMD 1204831","EMD 1204831|MET Tyrosine Kinase Inhibitor EMD 1204831","An inhibitor of the receptor tyrosine kinase Met (hepatocyte growth factor receptor) with potential antineoplastic activity. MET inhibitor EMD 1204831 selectively binds to Met tyrosine kinase, thereby disrupting MET mediated signal transduction pathways. This may induce cell death in tumor cells overexpressing this kinase. MET is overexpressed or mutated in many tumor cell types, and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C78483","MET Tyrosine Kinase Inhibitor PF-04217903","2-(4-(1-(Quinolin-6-ylmethyl)-1H-(1,2,3)triazolo(4,5-b)pyrazin-6-yl)-1H-pyrazol-1-yl)ethanol|MET Tyrosine Kinase Inhibitor PF-04217903|PF-04217903","An orally bioavailabe, small-molecule tyrosine kinase inhibitor with potential antineoplastic activity. MET tyrosine kinase inhibitor PF-04217903 selectively binds to and inhibits c-Met, disrupting the c-Met signaling pathway, which may result in the inhibition of tumor cell growth, migration and invasion of tumor cells, and the induction of death in tumor cells expressing c-Met. The receptor tyrosine kinase c-Met, also known as hepatocyte growth factor (HGF) receptor, is overexpressed or mutated in many tumor cell types, playing an important role in tumor cell proliferation, survival, invasion, and metastasis and angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C97511","MET Tyrosine Kinase Inhibitor SAR125844","MET Tyrosine Kinase Inhibitor SAR125844|SAR125844","An inhibitor of the proto-oncogene c-Met (also known as hepatocyte growth factor receptor (HGFR)) with potential antineoplastic activity. Upon intravenous administration, c-Met inhibitor SAR125844 binds to c-Met, thereby disrupting c-Met-mediated signal transduction pathways. This may result in cell growth inhibition in tumors that overexpress c-Met. c-Met, a receptor tyrosine kinase overexpressed or mutated in a variety of cancers, plays an important role in tumor cell proliferation, survival, invasion, metastasis and tumor angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C74062","MET Tyrosine Kinase Inhibitor SGX523","MET Tyrosine Kinase Inhibitor SGX523|SGX523","An orally bioavailable small molecule, c-Met inhibitor with potential antineoplastic activity. MET receptor tyrosine kinase inhibitor SGX523 specifically binds to c-Met protein, or hepatocyte growth factor receptor (HGFR), preventing binding of hepatocyte growth factor (HGF) and disrupting the MET signaling pathway; this agent may induce cell death in tumor cells expressing c-Met. c-Met, a receptor tyrosine kinase overexpressed or mutated in many tumor cell types, plays an important role in tumor cell proliferation, survival, invasion, and metastasis, and in tumor angiogenesis.","Pharmacologic Substance"]
["C83946","Metamelfalan","METAMELFALAN|Metamelfalan","The meta form of the levo isomer melphalan, an alkylating nitrogen mustard with potential antineoplastic activity. Metamelfalan causes crosslinking of DNA, thereby preventing DNA replication and eventually cellular proliferation.","Pharmacologic Substance"]
["C128030","MetAP2 Inhibitor SDX-7320","MetAP2 Inhibitor SDX-7320|Methionine aminopeptidase type II Inhibitor SDX-7320|SDX-7320","A synthetic copolymer-drug conjugate of a fumagillin-derived methionine aminopeptidase 2 (MetAP2) inhibitor conjugated to the bio-compatible polymer poly(N-(hydroxypropyl)methacrylamide) (HPMA), with potential antineoplastic activity. Upon administration of SDX-7320, the active moiety SDX7539 is released inside the tumor cells. SDX7539 binds to and inhibits MetAP2, which prevents MetAP2-mediated signal transduction pathways and results in tumor cell death. MetAP2, a member of the dimetallohydrolase family upregulated in certain tumor cell types, plays a key role in angiogenesis, proliferation and survival. Polymer conjugation reduces systemic drug exposure and increases this agent's efficacy as compared to non-polymer conjugates.","Pharmacologic Substance"]
["C113294","Metatinib Tromethamine","BCR-ABL Tyrosine Kinase Inhibitor BL001|BL001|Metatinib Tromethamine|Metatinib","An orally bioavailable tyrosine kinase inhibitor of the BCR-ABL fusion oncoprotein, with potential antineoplastic activity. Upon oral administration, BCR-ABL tyrosine kinase inhibitor BL001 may inhibit the BCL-ABL protein, which may lead to decreased proliferation and enhanced apoptosis in tumor cells. BCR-ABL oncoprotein is generated by a reciprocal translocation between chromosome 9 and 22 specifically t(9;22)(q34;q11). The resulting fusion gene produces proteins with constitutively active tyrosine kinase activity, which stimulate both abnormal cell division and increased cellular proliferation. This fusion is associated with both chronic myeloid leukemia and acute lymphoblastic leukemia.","Pharmacologic Substance"]
["C29251","Metformin Hydrochloride","1,1-Dimethylbiguanide Hydrochloride|Cidophage|Dimefor|Glifage|Glucoformin|Glucophage ER|Glucophage|METFORMIN HYDROCHLORIDE|Metformin HCl|Metformin Hydrochloride|N,N-Dimethylimidodicarbonimidic Diamide Monohydrochloride|Riomet|Siofor|metformin hydrochloride","The hydrochloride salt of the biguanide metformin with antihyperglycemic and potential antineoplastic activities. Metformin inhibits complex I (NADPH:ubiquinone oxidoreductase) of the mitochondrial respiratory chain, thereby increasing the cellular AMP to ATP ratio and leading to activation of AMP-activated protein kinase (AMPK) and regulating AMPK-mediated transcription of target genes. This eventually prevents hepatic gluconeogenesis, enhances insulin sensitivity and fatty acid oxidation and ultimately leads to a decrease in glucose levels. Metformin may exert antineoplastic effects through AMPK-mediated or AMPK-independent inhibition of mammalian target of rapamycin (mTOR), which is up-regulated in many cancer tissues. Furthermore, this agent also inhibits tumor cell migration and invasion by inhibiting matrix metalloproteinase-9 (MMP-9) expression which is mediated through the suppression of transcription activator protein-1 (AP-1) activation.","Organic Chemical|Pharmacologic Substance"]
["C1159","Methanol Extraction Residue of BCG","MER BCG|MER of BCG|MER-BCG|Methanol Extraction Residue of BCG|Methanol Extraction Residue of Bacillus Calmette-Guerin","A cell wall fraction of bacillus Calmette-Guerin (BCG) obtained by menthol extraction with immunomodulating properties and potential use in cancer immunotherapy. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C61318","Methazolamide","Glauctabs|METHAZOLAMIDE|MZM|Methazolamide|N-[5-(aminosulfonyl)-3-methyl-1,3,4-thiadiazol-2(3H)-ylidene]-acetamide|Neptazane","A sulfonamide derivate and carbonic anhydrase inhibitor with potential antineoplastic activity. Methazolamide inhibits tumor-associated carbonic anhydrase IX (CAIX), which may result in increased cell death in hypoxic tumors. As a hypoxia-inducible transmembrane glycoprotein, CAIX catalyzes the rapid interconversion of carbon dioxide and water into carbonic acid, protons, and bicarbonate ions, helping to maintain acidification of the tumor microenvironment and enhance resistance to cytotoxic therapy in some hypoxic tumors.","Pharmacologic Substance"]
["C642","Methotrexate","4-Amino-10-methylfolic Acid|4-Amino-4-deoxy-10-methylpteroyl-L-glutamic Acid|Abitrexate|Alpha-Methopterin|Amethopterin|Brimexate|CL 14377|CL-14377|Emtexate|Emthexat|Emthexate|Farmitrexat|Fauldexato|Folex PFS|Folex|Lantarel|Ledertrexate|Lumexon|METHOTREXATE|MTX|Maxtrex|Medsatrexate|Metex|Methoblastin|Methotrexate LPF|Methotrexate Methylaminopterin|Methotrexate|Methotrexatum|Metotrexato|Metrotex|Mexate-AQ|Mexate|N-[4-[[(2,4-Diamino-6-pteridinyl)methyl]methylamino]benzoyl]-L-glutamic Acid|Novatrex|Rheumatrex|Texate|Tremetex|Trexeron|Trixilem|WR-19039|amethopterin|methotrexate","An antimetabolite and antifolate agent with antineoplastic and immunosuppressant activities. Methotrexate binds to and inhibits the enzyme dihydrofolate reductase, resulting in inhibition of purine nucleotide and thymidylate synthesis and, subsequently, inhibition of DNA and RNA syntheses. Methotrexate also exhibits potent immunosuppressant activity although the mechanism(s) of actions is unclear.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1735","Methotrexate Sodium","METHOTREXATE SODIUM|Methotrexate Sodium|Sodium Methotrexate|Trexall","The sodium salt of methotrexate, an antimetabolite with antineoplastic and immunomodulating properties.  Methotrexate binds to and inhibits the enzyme dihydrofolate reductase, resulting in inhibition of purine nucleotide and thymidylate synthesis and, subsequently, inhibition of DNA and RNA syntheses.  Methotrexate also exhibits potent immunosuppressant properties. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C17876","Methotrexate-E Therapeutic Implant","MTX-e TI|MTX/epi gel|Methotrexate-E Therapeutic Implant|Methotrexate-epinephrine therapeutic implant|Methotrexate/epi","An injectable collagen matrix gel containing the antimetabolite methotrexate and the sympathicomimetic agent epinephrine with potential antineoplastic activity. After intratumoral injection, methotrexate binds to and inhibits the enzyme dihydrofolate reductase, resulting in inhibition of purine nucleotide and thymidylate synthesis and, subsequently, inhibition of DNA and RNA syntheses. Epinephrine, a potent vasoconstrictor, is added to the gel to enhance penetration of methotrexate into the tumor tissue and reduce dispersion to the surrounding tissues thereby enhancing the local concentration of methotrexate and increasing its anti-tumor activity. Intratumoral injection of methotrexate combined with epinephrine may potentially increase chemotherapeutic efficacy compared to systemic administration and reduce systemic toxicity and side effects.","Organic Chemical|Pharmacologic Substance"]
["C125656","Methotrexate-Encapsulating Autologous Tumor-Derived Microparticles","MTX-ATMP|Methotrexate-Encapsulating Autologous Tumor-Derived Microparticles","A suspension of autologous tumor-derived microparticles (ATMP), that are harvested from a patient with malignant pleural effusion, encapsulating the antimetabolic drug methotrexate (MTX), with potential anticancer activity. Although the exact mechanism(s) of action through which this agent exerts its effect has yet to be fully elucidated, upon administration of MTX-ATMP, the MTX moiety is released and internalized by tumor cells. It then binds to and inhibits the enzyme dihydrofolate reductase. This results in the inhibition of purine nucleotide synthesis and leads to decreased synthesis of both DNA and RNA, which induces cell death. Presumably, the encapsulation of MTX by the ATMP improves its bioavailability and decreases its toxicity.","Pharmacologic Substance"]
["C78084","Methoxyamine","METHOXYAMINE|Methoxyamine|TRC102","An orally bioavailable small molecule inhibitor with potential adjuvant activity. Methoxyamine covalently binds to apurinic/apyrimidinic (AP) DNA damage sites and inhibits base excision repair (BER), which may result in an increase in DNA strand breaks and apoptosis. This agent may potentiate the anti-tumor activity of alkylating agents.","Organic Chemical|Pharmacologic Substance"]
["C78085","Methoxyamine Hydrochloride","METHOXYAMINE HYDROCHLORIDE|Methoxyamine Hydrochloride|methoxyamine hydrochloride","The hydrochloride salt form of methoxyamine, an alkoxyamine with potential chemotherapeutic adjuvant activity. Methoxyamine covalently binds to apurinic/apyrimidinic DNA damage sites and thereby inhibits base excision repair (BER) process, which may prevent repair of DNA strand breaks and result in an induction of apoptosis. This agent may potentiate the anti-tumor activity of alkylating agents.","Pharmacologic Substance"]
["C2647","Methyl-5-Aminolevulinate Hydrochloride Cream","Methyl Aminolevulinate Hydrochloride Cream|Methyl-5-Aminolevulinate Hydrochloride Cream|Metvix|Metvixia|methyl-5-aminolevulinate","A topical cream formulation containing the hydrochloride salt of methyl-5-aminolevulinate, a lipophilic methyl ester of 5-aminolevulinic acid, with photosensitizer prodrug activity. Upon topical administration, methyl-5-aminolevulinate in the cream is selectively absorbed by tumor cells where it is converted to the photosensitizer protoporphyrin IX (PpIX). Upon photoirradiation, PpIX is activated and transfers energy to oxygen, generating singlet oxygen and superoxide and hydroxyl radicals, which may result in free-radical-mediated DNA damage and cell death.","Pharmacologic Substance"]
["C2352","Methylmercaptopurine Riboside","6-(methylmercapto)purine ribonucleoside|6-(methylthio) inosine|6-(methylthio)purine ribonucleoside|6-(methylthio)purine riboside|6-MMPR|6-methyl MP riboside|6-methylmercaptopurine riboside|6-methylthioinosine|9H-Purine, 6-(methylthio)-9-.beta.-D-ribofuranosyl- (8CI 9CI)|9H-Purine, 6-(methylthio)-9-.beta.-D-ribofuranosyl-, dihydrate|9H-purine, 6-(methylthio)-9-beta-D-ribofuranosyl- (8CI 9CI)|9H-purine, 6-(methylthio)-9-beta-D-ribofuranosyl-, dihydrate|9H-purine, 6-(methylthio)-9beta-D-ribofuranosyl|MMPR|Methylmercaptopurine Riboside|NCI-C04784|SQ 21977|beta-D-ribosyl-6-methylthiopurine|methylthioinosine|purine-6-thiol,6-methyl-9-ribofuranosyl","A purine derivative with antineoplastic and anti-angiogenic properties.  6-methylmercaptopurine riboside (6-MMPR) inhibits amidophosphoribosyltransferase, the first committed step in de novo purine synthesis, and inhibits fibroblast growth factor-2 (FGF2)-induced cell proliferation. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C647","Methylprednisolone","(6alpha,11beta)-11,17,21-Trihydroxy-6-methylpregna-1,4-diene-3,20-dione|6Alpha-Methylprednisolone|Adlone|Caberdelta M|DepMedalone|Depo Moderin|Depo-Nisolone|Duralone|Emmetipi|Esametone|Firmacort|METHYLPREDNISOLONE|Medlone 21|Medrate|Medrol Veriderm|Medrol|Medrone|Mega-Star|Meprolone|Methylprednisolone|Methylprednisolonum|Metilbetasone Solubile|Metrocort|Metypresol|Metysolon|Predni-M-Tablinen|Prednilen|Radilem|Sieropresol|Solpredone|Summicort|Urbason|Veriderm Medrol|Wyacort|methylprednisolone","A synthetic corticosteroid with anti-inflammatory and immunomodulating properties.  Methylprednisolone binds to and activates specific nuclear receptors, resulting in altered gene expression and inhibition of proinflammatory cytokine production.  This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis in sensitive tumor cell populations.","Organic Chemical|Pharmacologic Substance"]
["C1161","Metoprine","BW 197U|DDMP|METOPRINE|Metoprine","A diaminopyrimidine folate antagonist with potential antineoplastic activity.  Metoprine inhibits dihydrofolate reductase, resulting in decreased cellular folate metabolism and cell growth; it also inhibits histamine-N-methyltransferase, resulting in decreased histamine catabolism. Lipid-soluble metoprine is capable of crossing the blood-brain barrier. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2530","MG 98","MG 98|MG-98 oligonucleotide|MG-98|MG98","A second-generation, mixed-backbone, phosphorothioate antisense oligonucleotide (ODN) with potential antitumor activity. MG 98 is a highly specific inhibitor of translation of the mRNA for human DNA (cytosine-5-)-methyltransferase 1 (DNMT1), hybridizing to the 3' un-translated region of DNMT1 mRNA. The silencing of DNMT1 translation by MG 98 may result in the prevention or reversal of abnormal methylation of tumor suppressor genes and ultimately in tumor growth inhibition or tumor regression.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1879","MGN3","Arabinoxylan Compound|Biobran|MGN3","An arabinoxylane polysaccharide composed of the hemicellulose-Beta extract of rice bran, treated with enzymes from Shiitake mushrooms, that exerts antitumor and antiviral activity by increasing the level of natural killer cells activation. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C85476","Micellar Nanoparticle-Encapsulated Cisplatin NC-6004","Micellar Nanoparticle-Encapsulated Cisplatin NC-6004|NC-6004|Nanoplatin","A nanoparticle-based prodrug formulation consisting of polymeric micelles incorporating the inorganic platinum agent cisplatin with potential antineoplastic activity. In micellar nanoparticle-encapsulated cisplatin NC-6004, cisplatin forms a polymer-metal complex with hydrophilic polyethylene glycol poly(glutamic acid) block copolymers by attaching to the micelle inner core consisting of the hydrophobic polyamino acids. Upon cell entry and release from the polymer-metal complex, cisplatin forms highly reactive, charged platinum complexes that bind to nucleophilic groups such as GC-rich sites in DNA, inducing intrastrand and interstrand DNA cross-linking, DNA-protein cross-linking and, subsequently, tumor cell apoptosis and growth inhibition. Due to the hydrophilic nature of polyethylene glycol, this formulation increases the water-solubility of cisplatin and decreases the nephrotoxicity and neurotoxicity associated with the administration of cisplatin alone.","Pharmacologic Substance"]
["C97664","Microtubule-targeted Agent BAL101553","BAL101553|Microtubule-targeted Agent BAL101553","An orally available, highly water-soluble lysine prodrug of the synthetic small molecule BAL27862 with potential antitumor activity. Upon administration of BAL101553 and conversion into the active form BAL27862, this agent binds to tubulin at a site distinct from the vinca-alkaloid-binding site, and prevents tubulin polymerization and destabilizes microtubules, ultimately leading to cell cycle arrest, blockage of cell division and an induction of cell death in cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C1872","Midostaurin","CGP 41251|CGP41251|MIDOSTAURIN|Midostaurin|N-Benzoyl-Staurosporine|N-Benzoylstaurosporine|N-benzoyl-staurosporine|PKC-412|PKC412|midostaurin","A synthetic indolocarbazole multikinase inhibitor with potential antiangiogenic and antineoplastic activities. Midostaurin inhibits protein kinase C alpha (PKCalpha), vascular endothelial growth factor receptor 2 (VEGFR2), c-kit, platelet-derived growth factor receptor (PDGFR) and FMS-like tyrosine kinase 3 (FLT3) tyrosine kinases, which may result in disruption of the cell cycle, inhibition of proliferation, apoptosis, and inhibition of angiogenesis in susceptible tumors.","Organic Chemical|Pharmacologic Substance"]
["C1394","Mifamurtide","CGP 19835A Lipid|Junovan|L-MTP-PE|MEPACT|MIFAMURTIDE|MTP-PE Liposome|Mepact|Mifamurtide|Muramyl Tripeptide Phosphatidylethanolamine Liposome|mifamurtide|muramyl tripeptide phosphatidylethanolamine","A liposomal formulation containing a muramyl dipeptide (MDP) analogue with potential immunomodulatory and antineoplastic activities. Muramyl tripeptide phosphatidylethanolamine (MTP-PE), a derivative of the mycobacterial cell wall component MDP, activates both monocytes and macrophages. Activated macrophages secrete cytokines and induce the recruitment and activation of other immune cells, which may result in indirect tumoricidal effects. Liposomal encapsulation of MTP-PE prolongs its half-life and enhances tissue targeting.","Organic Chemical|Pharmacologic Substance"]
["C123921","MiHA-loaded PD-L1/L2-silenced Dendritic Cell Vaccine","MiHA-loaded PD-L-silenced DC Vaccine|MiHA-loaded PD-L1/L2-silenced Dendritic Cell Vaccine","A dendritic cell (DC)-based vaccine composed of program death ligands 1 and 2 (PDL1/L2)-silenced DCs and loaded with the recipient's minor histocompatibility antigens (MiHA), with potential use for graft-versus-tumor (GVT) induction following allogeneic stem cell transplantation (allo-SCT). Donor DCs are electroporated ex vivo with MiHA mRNA and small interfering RNAs (siRNAs) designed to silence the expression of PD L1/L2. After allo-SCT and upon intravenous administration of the MiHA-loaded PD-L1/L2-silenced DC vaccine, the DCs induce the expansion and activation of MiHA-specific CD8-positive T-cells. These tumor antigen-reactive T-cells exert their GVT effect by killing miHA-positive tumor cells. PD-L1/L2, co-inhibitory ligands expressed on DCs, play key roles in preventing MiHA-specific CD8-positive T-cell expansion; silencing enhances MiHA-specific CD8-positive T-cell expansion and activity and improves the GVT effect. The MiHA are human leukocyte antigen (HLA)-bound peptides and are exclusively expressed by the recipient's hematopoietic tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C66983","Milatuzumab","Humanized Anti-CD74 Monoclonal Antibody hLL1|IMMU-115|MILATUZUMAB|Milatuzumab|Monoclonal Antibody hLL1|hLL1|milatuzumab","A humanized monoclonal antibody directed against human CD74 with potential antineoplastic activity. Milatuzumab specifically binds to CD74 on CD74-positive cells. Although the exact mechanism through which this agent induces apoptosis is unknown, it may involve antibody-dependent cellular cytotoxicity (ADCC) or complement-mediated cytotoxicity (CMC). Alternatively, as CD74 is the cellular receptor for the cytokine migration-inhibitory factor (MIF), the cytotoxicity of this agent may be related to inhibition of CD74 activation by MIF. CD74, an integral membrane protein that functions as an MHC class II chaperone, may also be an accessory-signaling molecule; activation of CD74 may initiate cell survival mechanisms involving induction of a signaling cascade resulting in NFkB activation, entry of stimulated cells into the S phase of the cell cycle, elevation of DNA synthesis, cell division, and augmented expression of Bcl-xL.","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C91086","Milatuzumab-Doxorubicin Antibody-Drug Conjugate","IMMU-110|Milatuzumab-Doxorubicin Antibody-Drug Conjugate|hLL1-DOX","An immunoconjugate consisting of milatuzumab, a humanized monoclonal antibody against CD74, conjugated to the anthracycline antibiotic doxorubicin with potential antineoplastic activity. The milatuzumab moiety of this ADC selectively binds to CD74 on tumor cell surfaces; upon internalization, the doxorubicin moiety is released, where it intercalates between base pairs in the DNA helix and inhibits topoisomerase II, thereby preventing DNA replication and increasing double-strand breakage. As a result, this agent may inhibit the proliferation of cancer cells that overexpress CD74. CD74, an integral membrane protein and tumor associated antigen (TAA), is overexpressed in certain cancer cells and promotes survival in rapidly proliferating tumor cells.","Pharmacologic Substance"]
["C29261","Milk Thistle","Milk Thistle|milk thistle","A substance derived from any of several Old World coarse prickly-leaved shrubs and subshrubs including the plant Silybum marianum.  Milk thistle's active chemical component is silymarin, which is a combination of flavonoids such as silibinin, dehydrosilibinin, silychristin and silydianin.  These compounds are antioxidants and may alter the membrane structure of the liver cell, thereby blocking the absorption of toxins; they may also stimulate the production of new liver cells. In addition, milk thistle may increase cellular adenosine triphosphate (ATP) levels, exhibiting dose-dependent cardiac myocyte cytoprotection against doxorubicin.  The silibinin component of milk thistle has been shown to inhibit growth factor receptor-mediated mitogenic and cell survival signaling, thereby inhibiting tumor growth. (NCI04)","Pharmacologic Substance"]
["C1170","Miltefosine","2-[[(Hexadecycloxy)hydroxyphosphinyl]oxy]-N,N,N-trimethylethanaminium Inner Salt|Choline Phosphate Hexadecyl Ester, Hydroxide, Inner Salt|D-18506|Hexadecyl 2-(N,N,N-trimethylamino)ethyl Phosphate|Hexadecylphosphocholine|MILTEFOSINE|Miltefosin|Miltefosina|Miltefosine|Miltefosinum|Miltex|n-Hexadecylphosphorylcholine","An orally- and topically-active alkyl-phosphocholine compound with potential antineoplastic activity.  Miltefosine targets cellular membranes, modulating cell membrane permeability, membrane lipid composition, phospholipid metabolism, and mitogenic signal transduction, resulting in cell differentiation and inhibition of cell growth.  This agent also inhibits the anti-apoptotic mitogen-activated protein kinase (MAPK) pathway and modulates the balance between the MAPK and pro-apoptotic stress-activated protein kinase (SAPK/JNK) pathways, thereby inducing apoptosis.  As an immunomodulator, miltefosine stimulates T-cells, macrophages and the expression of interleukin 3 (IL-3), granulocyte-macrophage colony stimulating factor (GM-CSF), and interferon gamma (INF-gamma). (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C123381","Mimotope-P10s-PADRE Peptide Vaccine","Mimotope-P10s-PADRE Peptide Vaccine|P10s-PADRE Vaccine|P10s-PADRE","A peptide-based vaccine containing a carbohydrate mimetic peptide (CMP) P10s fused to the pan HLA DR-binding epitope (PADRE) peptide, with immunomoadjuvant activity and potential antineoplastic activity. Upon injection of the mimotope-P10s-PADRE peptide vaccine, the P10s peptide, which mimics gangliosides and other tumor-associated carbohydrate antigens (TACA), both stimulates a cytotoxic T-lymphocyte (CTL) response towards cells expressing TACAs and induces the production of antibodies that are reactive with a broad set of TACAs. Additionally, the anti-TACA antibodies may interfere with cellular pathways involved in tumor cell survival and may induce antibody-dependent cellular cytotoxicity (ADCC) toward cells expressing TACAs. PADRE is a helper T-cell epitope that is able to increase the magnitude and duration of the CTL response.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C90554","Mipsagargin","G-202|MIPSAGARGIN|Mipsagargin","A soluble, thapsigargin prodrug containing the cytotoxic analog of thapsigargin, 8-O-(12Aminododecanoyl)-8-O debutanoylthapsigargin (12-ADT) linked, via a carboxyl group, to the targeting peptide containing aspartic acid with potential antineoplastic activity. Upon intravenous administration, mipsagargin targets prostate specific membrane antigen (PSMA), a type II membrane carboxypeptidase, which is overexpressed in prostate cancer cells and in the neovasculature of most solid tumors but not in normal blood vessels. Mipsagargin is subsequently converted, through hydrolysis, into the active cytotoxic analog of thapsigargin 12-ADT-Asp. 12-ADT binds to and blocks the Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase (SERCA) pump, thereby increasing the concentration of cytosolic calcium which leads to an induction of apoptosis. By preventing nutrient supply to tumor cells, G-202 may be able to inhibit tumor growth. Compared to thapsigargin alone, thapsigargin prodrug G-202 is able to achieve higher concentrations of the active agents at the tumor site while avoiding systemic toxicity.","Pharmacologic Substance"]
["C90633","Mirabegron","2-(2-Aminothiazol-4-yl)-N-[4-(2-{[(2R)-2-hydroxy-2-phenylethyl]amino}ethyl)phenyl] Acetamide|4-Thiazoleacetamide, 2-Amino-N-(4-(2-(((2R)-2-hydroxy-2-phenylethyl)amino)ethyl)phenyl)-|Betanis|MIRABEGRON|Mirabegron|Myrbetriq|YM-178|YM178","An orally bioavailable agonist of the human beta-3 adrenergic receptor (ADRB3), with muscle relaxing, neuroprotective and potential antineoplastic activities.  Upon oral administration, mirabegron binds to and activates ADRB3, which leads to smooth muscle relaxation. Mirabegron also restores sympathetic stimulation in mesenchymal stem cell (MSC) niches, inhibits JAK2-mutated hematopoietic stem cell (HSC) expansion and blocks the progression of myeloproliferative neoplasms (MPNs). Lack of sympathetic stimulation of the MSC and HSC niche is associated with the development of MPNs.","Organic Chemical|Pharmacologic Substance"]
["C102566","Mirvetuximab Soravtansine","IMGN853|M9346A-sulfo-SPDB-DM4|MIRVETUXIMAB SORAVTANSINE|Mirvetuximab Soravtansine","An immunoconjugate consisting of the humanized monoclonal antibody M9346A against folate receptor 1 (FOLR1) conjugated, via the disulfide-containing cleavable linker sulfo-SPDB, to the cytotoxic maytansinoid DM4, with potential antineoplastic activity. The anti-FOLR1 monoclonal antibody moiety of mirvetuximab soravtansine targets and binds to the cell surface antigen FOLR1. After antibody-antigen interaction and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, thereby inhibiting cell division and cell growth of FOLR1-expressing tumor cells. FOLR1, a member of the folate receptor family is overexpressed on a variety of epithelial-derived cancer cells. The sulfo-SPDB linker prevents cleavage in the bloodstream and may improve this agent's efficacy in multidrug resistant tumor cells.","Pharmacologic Substance"]
["C657","Misonidazole","1-(alpha-methoxymethyl ethanol)-2-Nitroimidazole|MISONIDAZOLE|Misonidazole|RO 7-0582|Ro-07-0582|Ro-7-0582","A nitroimidazole with radiosensitizing and antineoplastic properties. Exhibiting high electron affinity, misonidazole induces the formation of free radicals and depletes radioprotective thiols, thereby sensitizing hypoxic cells to the cytotoxic effects of ionizing radiation. This single-strand breaks in DNA induced by this agent result in the inhibition of DNA synthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2703","Mistletoe Extract","Abnobaviscum|Apotheker Bauer's Misteltinktur|Cefalektin|Eurixor|Helixor|Iscador|Isorel|Isugran|Lektinol|Mistel Curarina|Mistel- Krautertabletten|Mistelol-Kapseln|Mistletoe Extract|Plenosol N|VISCUM ALBUM FRUITING TOP|Viscum Album Extract|Viscum album Extract|Viscum|Viscysat|mistletoe lectin","An extract of the whole plant Viscum album (mistletoe) with potential biological response modifier (BRM) activity. Mistletoe extract may both stimulate the antitumoral functions of the immune system and have a direct toxic effect on tumor cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C29195","Mitindomide","4, 8-Ethenopyrrolo[3',4':3,4]cyclobut[1,2-f]isoindole-1,3,5,7(2H, 6H)tetrone, octahydro-|MITINDOMIDE|Mitindomide","A bisdioxopiperazines analog with antineoplastic activity.  Mitinomide inhibits topoisomerase II and slowly promotes DNA-interstrand cross-linking, thereby inhibiting DNA repair, RNA and protein synthesis.  This agent acts without increasing topoisomerase II-DNA covalent cleavable complex formation, as do most topoisomerase inhibitors. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C659","Mitobronitol","1,6-Dibromo-1,6-dideoxy-D-mannitol|DBM|Dibromomannitol|MITOBRONITOL|Mitobronitol|Myelobromol","A brominated analog of mannitol with potential antineoplastic activity. Mitobronitol most likely acts through alkylation via derived epoxide groups.","Organic Chemical|Pharmacologic Substance"]
["C66164","Mitoclomine","MITOCLOMINE|Mitoclomine|N,N-bis(2-chloroethyl)4-amino-2-methyl-1-methoxy-naphthalene","An aromatic nitrogen mustard derivative with potential antineoplastic activity. Mitoclomine alkylates DNA and appears to concentrate primarily in the spleen and thymus where it causes lymphocyte depletion.","Pharmacologic Substance"]
["C1101","Mitoflaxone","2-Phenyl-8-(carboxymethyl)-benzopyran-4-one|4H-1-Benzopyran-8-acetic acid, 4-oxo-2-phenyl-|4H-1-benzopyran-8-acetic Acid, 4-Oxo-2-phenyl|FAA|Flavone Acetic Acid|Flavone acetic acid|Flavone-8-Acetic Acid|LM 975|MITOFLAXONE|Mitoflaxone","A synthetic flavonoid with vascular targeting properties. Flavone acetic acid exhibits an antiproliferative effect on endothelial cells as a result of a superoxide-dependent mechanism, which induces changes in permeability of the vasculature of the tumor. This agent may stimulate tumor necrosis and promote shunting of blood flow to viable regions of the tumor, increasing their oxygenation and rendering them more susceptible to the antitumor effects of hyperthermia and ionizing radiation.  (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C661","Mitoguazone","1,1'-((methylethanediylidene)dinitrilo)diguanidine|2,2\"-(methyl-1,2-ethanediylidene)bis[hydrazinecarboximidamide]|DRG-0223|MGBG|MITOGUAZONE|Me-GAG|Methyl GAG|Methyl-G|Methyl-GAG|Methylglyoxal Bisguanylhydrazone|Methylglyoxal bis(amidinohydrazone)|Mitoguazone|Zyrkamine|methylglyoxal bis(guanylhydrazone)|pyruvaldehyde bis(amidinohydrazone)","A guanylhydrazone with potential antineoplastic activity. Mitoguazone competitively inhibits S-adenosyl-L-methionine decarboxylase (SAMD), an enzyme involved in the synthesis of polyamines, resulting in decreased proliferation of tumor cells, antimitochondrial effects, and p53-independent apoptosis. Polyamines, specifically spermine and spermidine, are essential for thymidine kinase production, DNA synthesis, and cell proliferation. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C91409","Mitoguazone Dihydrochloride","1,1'-((Methylethanediylidene)Dinitrilo)Diguanidine Dihydrochloride|2,2'-(1-Methyl-1,2-Ethanediylidene)Bis(Hydrazinecarboximidamide) Dihydrochloride|MGBG 2HCl|MITOGUAZONE DIHYDROCHLORIDE|Methylglyoxal Bis(amidinohydrazone) Dihydrochloride|Mitoguazone Dihydrochloride|Pyruvaldehyde Bis(amidinohydrazone) Hydrochloride|mitoguazone dihydrochloride","The hydrochloride salt of a guanylhydrazone with potential antineoplastic activity. Mitoguazone competitively inhibits S-adenosyl-L-methionine decarboxylase (SAMD), an enzyme involved in the synthesis of polyamines, resulting in decreased proliferation of tumor cells, antimitochondrial effects, and p53-independent apoptosis. Polyamines, specifically spermine and spermidine, are essential for thymidine kinase production, DNA synthesis, and cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C662","Mitolactol","6-Dibromodideoxydulcitol|6-Dibromodulcitol|DBD|Dibromdicil|Dibromodulcitol|Elobromol|MITOLACTOL|Mitolac|Mitolactol|mitolactol","A synthetic derivative of hexitol with antineoplastic and radiosensitizing properties.  Mitolactol alkylates DNA via actual or derived epoxide groups, resulting in inhibition of DNA and RNA synthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1820","Mitomycin","(1aS,8S,8aR,8bS)-6-Amino-8-[[(aminocarbonyl)oxy]methyl]-1,1a,2,8,8a,8b-hexahydro-8a-methoxy-5-methylazirino[2',3':3,4]pyrrolo[1,2-a]indole-4,7-dione|Ametycine|MITO-C|MITO|MITOMYCIN C|MITOMYCIN|Mito-C|Mito-Medac|Mitocin-C|Mitocin|Mitolem|Mitomycin C|Mitomycin-C|Mitomycin-X|Mitomycin|Mitomycine C|Mitosol|Mitozytrex|Mutamycin|Mutamycine|NCI-C04706|[1aS-(1a alpha,8beta,8a alpha,8b alpha)]-6-amino-8-[[(aminocarbonyl)oxy]methyl]-1,1a,2,8,8a,8b-hexahydro-8a-methoxy-5-methylazirino[2',3':3,4]pyrrolo[1,2-a]indole-4,7-dione","A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus and other Streptomyces bacterial species.  Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis.  Preferentially toxic to hypoxic cells, mitomycin C also inhibits RNA and protein synthesis at high concentrations. (NCI04)","Antibiotic|Organic Chemical"]
["C1164","Mitomycin A","Azirino(2',3':3,4)pyrrolo(1,2-a)indole-4,7-dione, 1,1a,2,8,8a,8b-hexahydro-8-(hydroxymethyl)-6,8a-dimethoxy-5-methyl-, carbamate (ester)|Mitomycin A","A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus.  Bioreduced mitomycin A generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis.  Mitomycin A is more toxic than mitomycin C due to increased and nonselective DNA cross-linking in both aerobic and hypoxic cells. (NCI04)","Antibiotic|Organic Chemical"]
["C1392","Mitomycin B","Azirino(2',3':3,4)pyrrolo(1,2-a)indole-4,7-dione, 1,1a,2,8,8a,8b-hexahydro-8a-hydroxy-8-(hydroxymethyl)-6-methoxy-1,5-dimethyl-, 8-carbamate|MITOMYCIN B|Mitomycin B","A methylazirinopyrroloindoledione antineoplastic antibiotic isolated from the bacterium Streptomyces caespitosus.  Bioreduced mitomycin B generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. (NCI04)","Antibiotic|Organic Chemical"]
["C664","Mitotane","(o,p)-DDD|1, 1-Dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane|1,1-Dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane|1-Chloro-2-[2,2-dichloro-1-(4-chlorophenyl)ethyl]benzene|2, 2-Bis(2-chlorophenyl-4-chlorophenyl)-1,1-dichloroethane|2, 4'-Dichlorodiphenyldichloroethane|2,2-Bis(2-chlorophenyl-4-chlorophenyl)-1,1-dichloroethane|2,4'-Dichlorodiphenyldichloroethane|2-(2-Chlorophenyl)-2-(4-chlorophenyl)-1,1-dichloroethane|CB 313|CB-313|Chloditan|Chlodithane|DDD|Ethane, 2-(o-chlorophenyl)-2-(p-chlorophenyl)-1,1-dichloro-|Khloditan|Lisodren|Lysodren|MITOTANE|Mitotane|Mytotan|Ortho,para-DDD|WR-13045|mitotane|o,p' - DDD|o,p'-DDD","A synthetic derivative of the insecticide dichlorodiphenyl trichloroethane (DDT) with anti-adrenocorticoid properties.  Following its metabolism in the adrenal cortex to a reactive acyl chloride intermediate, mitotane covalently binds to adrenal proteins, specifically inhibiting adrenal cortical hormone production. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C66167","Mitotenamine","MITOTENAMINE|Mitotenamine","A nucleotoxic with potential antineoplastic activity. The mechanism of action through which mitotenamine exerts its effect has yet to be fully elucidated.","Pharmacologic Substance"]
["C62050","Mitoxantrone","1,3-Dihydroxy-5,8-bis[[2-[(2-hydroxyethyl)amino]ethyl]amino]-9, 10-anthracenedione|1,4-Dihydroxy-5,8-bis[[2-[(2-hydroxyethyl)amino]ethyl]amino]-9, 10-anthroquinone|Dihydroxyanthracenedione|MITOXANTRONE|Mitoxantrone|Mitozantrone|mitoxantrone","An anthracenedione antibiotic with antineoplastic activity. Mitoxantrone intercalates into and crosslinks DNA, thereby disrupting DNA and RNA replication.  This agent also binds to topoisomerase II, resulting in DNA strand breaks and inhibition of DNA repair.  Mitoxantrone is less cardiotoxic compared to doxorubicin.","Organic Chemical|Pharmacologic Substance"]
["C665","Mitoxantrone Hydrochloride","1,3-Dihydroxy-5,8-bis[[2-[(2-hydroxyethyl)amino]ethyl]amino]-9, 10-anthracenedione Dihydrochloride|1,4-Dihydroxy-5,8-bis[[2-[(2-hydroxyethyl)amino]ethyl]amino]-9, 10-anthroquinone Dihydrochloride|CL 232315|DHAD|DHAQ|Dihydroxyanthracenedione Dihydrochloride|MITOXANTRONE HYDROCHLORIDE|Mitoxantrone Dihydrochloride|Mitoxantrone Hydrochloride|Mitoxantroni Hydrochloridum|Mitozantrone Hydrochloride|Mitroxone|Neotalem|Novantrone|Onkotrone|Pralifan","The hydrochloride salt of an anthracenedione antibiotic with antineoplastic activity. Mitoxantrone intercalates into and crosslinks DNA, thereby disrupting DNA and RNA replication.  This agent also binds to topoisomerase II, resulting in DNA strand breaks and inhibition of DNA repair.  Mitoxantrone is less cardiotoxic compared to doxorubicin.","Antibiotic|Organic Chemical"]
["C1166","Mitozolomide","Azolastone|Imidazo[5,1-d]-1,2,3,5-tetrazine-8-carboxamide, 3-(2-chloroethyl)-3,4-dihydro-4-oxo-|MITOZOLOMIDE|Mitozolomide|imidazo[5,1-d]-1,2,3,5-tetrazine-8-carboxamide, 3-(2-chloroethyl)-3,4-dihydro-4-oxo","A prodrug of imidazotetrazine alkylating agent with antineoplastic property. Mitozolomide undergoes ring opening upon the nucleophilic attack at C-4 by an activated molecule of water within the major groove of DNA. The resulting bioactive mono-alkyltriazene species are capable of alkylating nucleophilic residues in the immediate vicinity such as N-7 and/or O-6 sites of guanine, thereby causes intra- or inter-stranded DNA cross-links and trigger apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C87698","Mivobulin","Carbamic Acid, (5-Amino-1,2-Dihydro-2-Methyl-3-Phenylpyrido(3,4-B)Pyrazin-7-Yl) Ethyl Ester, (S)-|Ethyl (S)-5-Amino-1,2-Dihydro-2-Methyl-3-Phenylpyrido(3,4-B)Pyrazine-7-Carbamate|MIVOBULIN|Mivobulin","A synthetic, colchicine analogue with potential antineoplastic activity. Mivobulin targets and binds to colchicine-binding site on tubulin, thereby inhibiting microtubule polymerization, the assembly of the mitotic spindle and mitosis. This eventually results in cell cycle arrest, apoptosis and a reduction in cellular proliferation.","Pharmacologic Substance"]
["C1357","Mivobulin Isethionate","CI-980|CI980|MIVOBULIN ISETHIONATE|Mivobulin Isethionate|mivobulin isethionate","The isethionate salt of mivobulin, a synthetic colchicine analogue with potential antineoplastic activity. Mivobulin isethionate binds to tubulin, thereby inhibiting microtubule polymerization and mitosis.","Organic Chemical|Pharmacologic Substance"]
["C74063","Mixed Bacteria Vaccine","Coley's Toxin|MBV|Mixed Bacteria Vaccine","A cancer vaccine containing a mixture of killed bacteria with potential immunostimulatory and antineoplastic activities. Mixed bacteria vaccine (MBV or Coley's toxins) consists of a pyrogenic bacterial lysate derived from Serratia marcescens and Streptococcus pyogenes; the active components in the lysate may be lipopolysaccharide (LPS), a component of the Gram-negative bacterial cell wall of Serratia, and streptokinase, an enzyme produced by Streptococcus pyogenes. LPS has been shown to stimulate the host humoral immune response and induce the release of various antitumor cytokines such as tumor necrosis factor (TNF) and interleukin-12 (IL-12).","Pharmacologic Substance"]
["C49174","MK0731","MK0731","A synthetic small molecule with potential antineoplastic activity. MK0731 selectively inhibits kinesin spindle protein (KSP), which may result in the inhibition of mitotic spindle assembly, induction of cell cycle arrest during the mitotic phase, and apoptosis in tumor cells that overexpress KSP.","Organic Chemical|Pharmacologic Substance"]
["C2507","MKC-1","MKC-1|R440|Ro 31-7453","An orally bioavailable, small-molecule, bisindolylmaleimide cell cycle inhibitor with potential antineoplastic activity. MKC-1 and its metabolites inhibit tubulin polymerization, blocking the formation of the mitotic spindle, which may result in cell cycle arrest at the G2/M phase and apoptosis. In addition, this agent has been shown to inhibit the activities of the oncogenic kinase Akt, the mTOR pathway, and importin-beta, a protein essential to the transport of other proteins from the cytosol into the nucleus.","Organic Chemical|Pharmacologic Substance"]
["C121956","MKNK1 Inhibitor BAY 1143269","BAY 1143269|MKNK1 Inhibitor BAY 1143269","An orally bioavailable inhibitor of mitogen-activated protein kinase interacting serine/threonine-protein kinase 1 (MKNK1), with potential antineoplastic activity. Upon oral administration, MKNK1 inhibitor BAY 1143269 binds to MKNK1, thereby preventing its activation and the downstream MKNK1-mediated phosphorylation and activation of eukaryotic translation initiation factor 4E (eIF4E). As eIF4E enhances the synthesis of oncogenic proteins, preventing eIF4E activity inhibits the synthesis of tumor angiogenic factors and leads to both the inhibition of cellular proliferation and apoptosis in susceptible tumor cells. eIF4E, overexpressed in a variety of cancer cells, plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C26660","MLN2704","MLN2704|MLN591DM1","An immunoconjugate that consists of a humanized monoclonal antibody (MLN591), directed against prostate-specific membrane antigen linked to a maytansinoid (DM1). The monoclonal antibody moiety of MLN2704 binds to tumor cells expressing prostate-specific membrane antigen; MLN274 is then internalized into the tumor cell where the DM1 maytansinoid moiety binds to tubulin and inhibits tubulin polymerization and microtubule assembly, resulting in a disruption of microtubule activity and cell division, and cell death. (NCI04)","Pharmacologic Substance"]
["C2045","MMI270","(2R)-N-Hydroxy-2-[[(4-methoxyphenyl)sulfonyl](3-pyridinylmethyl)amino]-3-methylbutanamide Monohydrochloride|CGS27023|CGS27023A|MMI 270B CGS27023A|MMI270|N-hydroxy-2(R)-[(4-methoxysulfony) (3-picolyl)-amino]-3-metylbutaneamide hydrochloride monohydrate|N-hydroxy-2(R)-[[4- methoxysulfonyl](3-picolyl)amino]-3-methylbutaneamide hydrochloride","An orally-active synthetic hydroxamic acid derivative with potential antineoplastic activity.  MMI270 inhibits a broad spectrum of matrix metalloproteinases (MMPs) (specifically MMP-1, 2, 3, 9, and 13), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis.  This agent may also downregulate lymphangiogenesis, resulting in decreased lymphatic system-related metastasis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C125062","MNK1/2 Inhibitor eFT508","MNK1/2 Inhibitor eFT508|eFT508","An orally bioavailable inhibitor of mitogen-activated protein kinase (MAPK)-interacting serine/threonine-protein kinase 1 (MNK1) and 2 (MNK2), with potential antineoplastic activity. Upon oral administration, MNK1/2 inhibitor eFT508 binds to and inhibits the activity of MNK1 and 2. This prevents MNK1/2-mediated signaling, and inhibits the phosphorylation of certain regulatory proteins, including eukaryotic translation initiation factor 4E (eIF4E), that regulate the translation of messenger RNAs (mRNAs) involved in tumor cell proliferation, angiogenesis, survival and immune signaling. This inhibits tumor cell proliferation in MNK1/2-overexpressing tumor cells. MNK1/2 are overexpressed in a variety of tumor cell types and promote phosphorylation of eIF4E; eIF4E is overexpressed in many tumor cell types and contributes to tumor development, maintenance and resistance.","Pharmacologic Substance"]
["C62521","Mocetinostat","Benzamide, N-(2-aminophenyl)-4-[[[4-(3-pyridinyl)-2-pyrimidinyl]amino]methyl]-|MG-0103|MGCD0103|MOCETINOSTAT|Mocetinostat|N-(2-aminophenyl)-4-((4-pyridin-3-ylpyrimidin-2-ylamino)methyl)benzamide|mocetinostat","A rationally designed, orally available, Class 1-selective, small molecule, 2-aminobenzamide HDAC inhibitor with potential antineoplastic activity. Mocetinostat binds to and inhibits Class 1 isoforms of HDAC, specifically HDAC 1, 2 and 3, which may result in epigenetic changes in tumor cells and so tumor cell death; although the exact mechanism has yet to be defined, tumor cell death may occur through the induction of apoptosis, differentiation, cell cycle arrest, inhibition of DNA repair, upregulation of tumor suppressors, down regulation of growth factors, oxidative stress, and autophagy, among others. Overexpression of Class I HDACs 1, 2 and 3 has been found in many tumors and has been correlated with a poor prognosis.","Organic Chemical|Pharmacologic Substance"]
["C103178","Modified Citrus Pectin Supplement","Modified Citrus Pectin Supplement|PectaSol-C","A dietary supplement containing the modified citrus pectin (MCP) derived from the soluble fiber of citrus fruit peels and a galectin-3 inhibitor with potential antioxidant, hypocholesterolemic, immunostimulatory, metal chelating, and anti-metastatic activities. MCP is a low molecular weight version of pectin composed of short, slightly-branched carbohydrate chains and is modified for enhanced absorbability. The bioactive fragments, most likely the galactan-containing portion, of pectin binds to galectin-3, a carbohydrate-binding protein involved in imflammation, heart disease and is upregulated on the surface of certain types of tumor cells. Binding of MCP may result in the suppression of cancer cell aggregation, adhesion, proliferation and metastasis. In addition, MCP decreases prostate specific antigen (PSA) levels and may remove heavy metals. Also, unsaturated oligogalacturonic acids in MCP may stimulate the immune system through the activation of natural killer cells, cytotoxic T-cells, and B-cells.","Pharmacologic Substance"]
["C71758","Modified Vaccinia Ankara (Bavarian Nordic)-HER2 Vaccine","MVA-BN-HER2|Modified Vaccinia Ankara (Bavarian Nordic)-HER2 Vaccine","A cancer vaccine consisting of a proprietary, recombinant modified vaccinia Ankara (MVA) viral vector encoding an epitope of human epidermal growth factor receptor 2 (HER2) with potential antineoplastic activity. Upon administration, modified vaccinia Ankara (Bavarian Nordic)-HER2 vaccine may stimulate the host immune system to mount humoral and cytotoxic T lymphocyte responses against HER2-expressing tumor cells, resulting in tumor cell lysis. HER2, also known as ErbB-2, is a tyrosine kinase growth factor receptor and a member of the epidermal growth factor receptor family; it plays a significant role in the pathogenesis of some breast cancers.","Pharmacologic Substance"]
["C116868","Modified Vaccinia Virus Ankara Vaccine Expressing p53","MVA-p53 Vaccine|MVA-p53|MVAp53 Vaccine|Modified Vaccinia Virus Ankara Vaccine Expressing p53|p53-MVA Vaccine|p53MVA","A cancer vaccine comprised of a recombinant modified vaccinia Ankara (MVA) viral vector encoding the wild-type form of the tumor protein p53 (wt p53), with potential immunostimulating and antineoplastic activities. Upon subcutaneous vaccination with MVA vaccine expressing p53, the expressed p53 may stimulate the host immune system to mount a p53-specific cytotoxic T-lymphocyte (CTL) response against tumor cells expressing p53, resulting in tumor cell lysis. The MVA viral vector, derived from the replication-competent strain Ankara, is a highly attentuated, replication-defective vaccinia strain and is incapable of virion assembly. The p53 gene, a tumor suppressor gene, is mutated in many cancer cell types.","Pharmacologic Substance"]
["C63667","Mofarotene","(E)-4-[2-[4-[2-(5,6,7,8-Tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl]phenoxy]ethyl]morpholine|MOFAROTENE|Mofarontene|Mofarotene|Ro 40-8757","An arotinoic acid derivative with a morpholine structure in the polar end group with differentiation inducing and antineoplastic activity. Like other retinoic acid agents, mofarotene binds to and activates retinoic acid receptors (RARs), thereby altering the expression of certain genes leading to cell differentiation and decreased cell proliferation in susceptible cells. In addition, this agent is able to inhibit melanoma cell motility.","Pharmacologic Substance"]
["C62510","Mogamulizumab","Immunoglobulin G1, Anti-(CC Chemokine Receptor CCR4) (Human-Mouse Monoclonal KW-0761 Heavy Chain), Disulfide With Human-Mouse Monoclonal KW-0761 Kappa-Chain, Dimer|KM8761|KW-0761|MOGAMULIZUMAB|Mogamulizumab","A humanized monoclonal antibody directed against C-C chemokine receptor 4 (CCR4) with potential anti-inflammatory and antineoplastic activities. Mogamulizumab selectively binds to and blocks the activity of CCR4, which may inhibit CCR4-mediated signal transduction pathways and, so, chemokine-mediated cellular migration and proliferation of T cells, and chemokine-mediated angiogenesis. In addition, this agent may induce antibody-dependent cell-mediated cytotoxicity (ADCC) against CCR4-positive T cells. CCR4, a G-coupled-protein receptor for C-C chemokines such MIP-1, RANTES, TARC and MCP-1, is expressed on the surfaces of some types of T cells, endothelial cells, and some types of neurons. CCR4, also known as CD194, may be overexpressed on adult T-cell lymphoma (ATL) and peripheral T-cell lymphoma (PTCL) cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C88311","Momelotinib","CYT387|GS-0387|MOMELOTINIB|Momelotinib|N-(Cyanomethyl)-4-(2-((4-(morpholin-4-yl)phenyl)amino)pyrimidin-4-yl)benzamide","An orally bioavailable small-molecule inhibitor of Janus kinases 1 and 2 (JAK1/2) with potential antineoplastic activity. JAK1/2 inhibitor CYT387 competes with JAK1/2 for ATP binding, which may result in inhibition of JAK1/2 activation, inhibition of the JAK-STAT signaling pathway, and so the induction of apoptosis and a reduction of tumor cell proliferation in JAK1/2-expressing tumor cells. JAK2 is the most common mutated gene in bcr-abl-negative myeloproliferative disorders; the JAK2V617F gain-of-function mutation involves a valine-to-phenylalanine modification at position 617. The JAK-STAT signaling pathway is a major mediator of cytokine activity and is often dysregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C120208","Monalizumab","IPH-2201|IPH2201|Immunoglobulin G4-kappa, Anti-(Homo sapiens KLRC1 (Killer Cell Lectin-like Receptor Subfamily C Member 1, NKG2-a, NKG2a, CD159A, CD94)), Humanized Monoclonal Antibody|MONALIZUMAB|Monalizumab|NN-8765|NN8765-3658|NN8765","A humanized immunoglobulin G4 (IgG4) monoclonal antibody against the human natural killer (NK) and T-lymphocyte cell checkpoint inhibitor killer cell lectin-like receptor subfamily C member 1 (NKG2A), with potential antineoplastic activity. Upon administration, monalizumab binds to NKG2A and prevents the binding of NKG2A to its ligand human leukocyte antigen-E (HLA-E), which is overexpressed on tumor cells. This blocks the HLA-E-mediated inhibition of NKG2A-positive infiltrating NK and cytotoxic T-lymphocytes (CTLs) and induces a NK and CTL-mediated immune response against the cancer cells leading to their destruction. Human NKG2A, an inhibitory cell surface receptor covalently bound to CD94, is expressed by NK cells and CTLs. Stimulation of the CD94/NKG2A complex inhibits the cytotoxic activity of these cells. HLA-E, a nonclassical HLA class Ib molecule, is often overexpressed on tumor cells and is associated with poor prognosis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C123775","Monoacetyldiglyceride EC-18","1-Palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol|9,12-Octadecadienoic acid (9Z,12Z)-, 1-((Acetyloxy)methyl)-2-((1-oxohexadecyl)oxy)ethyl Ester|EC-18|Monoacetyldiglyceride EC-18","A synthetic version of a monoacetyldiacylglyceride naturally occurring in various seed oils, bovine udder and milk fat, antlers of sika deer, with potential antineoplastic activity. Although the exact mechanism of action through which EC-18 exerts its pharmacological effect has yet to be fully identified, upon administration, EC-18 stimulates calcium influx into T-lymphocytes and increases the production of various cytokines, including interleukin (IL) -2, IL-4, IL-12, interferon-gamma (IFN-g), and granulocyte-macrophage colony-stimulating factor (GM-CSF). This stimulates the proliferation of hematopoietic stem cells, bone marrow stromal cells and immune cells, including T- and B-lymphocytes, dendritic cells (DCs) and macrophages. Therefore, EC18 may stimulate the immune system to target cancer cells. In addition, EC-18 enhances the cytolytic activity of natural killer (NK) cells and suppresses the expression of the transmembrane protein tumor cell toll-like receptor 4 (TLR-4) on cancer cells. As activation of TLR-4 enhances immunosuppression and stimulates cancer cell growth, blocking TLR-4 expression suppresses tumor cell proliferation.","Pharmacologic Substance"]
["C105399","Monocarboxylate Transporter 1 Inhibitor AZD3965","AZD3965|MCT1 Inhibitor AZD3965|Monocarboxylate Transporter 1 Inhibitor AZD3965","An orally available inhibitor of monocarboxylate transporter 1 (MCT1), with potential antineoplastic activity. Upon oral administration, MCT1 inhibitor AZD3965 binds to MCT1 and prevents the transport of lactate into and out of the cell. This leads to an accumulation of lactate, intracellular acidification, and eventually cancer cell death. MCT1, a protein overexpressed on tumor cells, is responsible for the transport of monocarboxylates across the cell membrane and plays a key role in cell metabolism.","Pharmacologic Substance"]
["C2648","Monoclonal Antibody 105AD7 Anti-idiotype Vaccine","Monoclonal Antibody 105AD7 Anti-idiotype Vaccine","A cancer vaccine consisting of a humanized monoclonal antibody that mimics a tumor-associated antigen 791Tgp72 (also known as CD55). Vaccination with this agent may stimulate a host cytotoxic T-cell response against tumor cells expressing CD55, resulting in tumor cell lysis. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2446","Monoclonal Antibody 11D10","11D10|MoAb 11D10|Monoclonal Antibody 11D10","A murine monoclonal anti-idiotype antibody (anti-Id). Anti-Id 11D10 mimics a specific epitope of the high molecular weight human milk fat globule (HMFG) glycoprotein primarily expressed by human breast and some other tumor cells at high density. This specific HMFG epitope is identified by mAb BrE1, which was used as the immunizing antibody, or Ab1 to generate the anti-Id (Ab2) 11D10. Anti-ID 11D10 reacts specifically with breast tumor cells and with minimal reactivity with normal tissues. Vaccination with anti-Id 11D10 induces anti-anti-idiotype antibodies (Ab3) that may react with breast cancer cell lines expressing the HMFG membrane epitope.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2606","Monoclonal Antibody 11D10 Anti-Idiotype Vaccine","11D10 Anti-Idiotype Vaccine|Monoclonal Antibody 11D10 Anti-Idiotype Vaccine|TriAb anti-idiotype antibody|TriAb","A vaccine consisting of a monoclonal antibody (MoAb) directed against an idiotype that mimics a human milk fat globule (HMFG) membrane epitope.  Vaccination with monoclonal antibody 11D10 anti-idiotype vaccine induces anti-anti-idiotype antibodies (Ab3) that may react with breast cancer cell lines expressing the HMFG membrane epitope.","Immunologic Factor|Pharmacologic Substance"]
["C2368","Monoclonal Antibody 14G2A","14G2A, monoclonal antibody|14G2A|Antibody 14G2A, Monoclonal|MoAb 14G2A|Monoclonal Antibody 14G2A","A murine monoclonal antibody directed against the ganglioside GD2 with potential antineoplastic activity. Monoclonal antibody 14G2A binds to the ganglioside GD2 and induces antibody-dependent cell mediated cytotoxicity and complement-dependent cytotoxicity against GD2-expressing tumor cells.  GD2 is overexpressed in malignant melanoma, neuroblastoma, osteosarcoma, and small cell carcinoma of the lung. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C29198","Monoclonal Antibody 1F5","Anti-CD20 Monoclonal Antibody 1F5|MOAB 1F5|Monoclonal Antibody 1F5","A murine monoclonal antibody directed against CD20, a cross-membrane ion channel phosphoprotein expressed by B cells, with potential antineoplastic activity.  MOAB 1F5 binds to CD20, thereby directly inhibiting B-cell proliferation and differentiation. When cross-linked by secondary anti-mouse antibodies or Fc receptor-bearing cells, MOAB 1F5 may induce activation of B-cell protein tyrosine kinases, increases in B-cell intracellular calcium ion concentrations, and B-cell caspase activation, resulting in apoptosis of B cells expressing CD20. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2470","Monoclonal Antibody 3622W94","3622W94|MoAb 3622W94|Monoclonal Antibody 3622W94","A humanized murine monoclonal antibody (MoAb) against the 17-1A antigen, with potential adjuvant therapeutic properties in colorectal cancer. 17-1A antigen (EpCAM), a human epithelial cell adhesion molecule, expresses in a variety of carcinoma tissues, such as those of colon and breast carcinomas. Immunization with MoAb 3622W94 may elicit immune responses, which could result in eradicating tumor cells expressing 17-1A antigen.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2370","Monoclonal Antibody 3F8","3F8 Monoclonal Antibody|3F8|MoAb 3F8|Monoclonal Antibody 3F8|anti-Ganglioside (GD2) Monoclonal Antibody 3F8","A murine monoclonal antibody directed against the cell-surface, tumor-associated antigen ganglioside GD2. Vaccination with monoclonal antibody 3F8 may stimulate a host cytotoxic immune response against tumors that express ganglioside GD2. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2424","Monoclonal Antibody 3H1 Anti-Idiotype Vaccine","CEA-Vac|CeaVac|MoAb 3H1 anti-idiotype vaccine|Monoclonal Antibody 3H1 Anti-Idiotype Vaccine","A recombinant monoclonal antibody in which the heavy and light chain variable domains mimic a specific epitope of the tumor-associated protein carcinoembryonic antigen (CEA).  This agent is used as a cancer vaccine against tumors that express CEA. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C2227","Monoclonal Antibody 4B5 Anti-Idiotype Vaccine","4B5 monoclonal antibody anti-idiotype vaccine|MoAb 4B5 anti-idiotype vaccine|Monoclonal Antibody 4B5 Anti-Idiotype Vaccine","A humanized anti-idiotypic (anti-Id) monoclonal antibody (MoAb) that mimics the disialoganglioside GD2 with potential immunostimulating and antineoplastic activities.  Upon administration, monoclonal antibody 4B5 anti-idiotype vaccine may elicit both cellular and humoral immune responses against GD2- expressing tumor cells. GD2 is a glycosphingolipid (ceramide and oligosaccharide) that may be highly expressed by melanomas and other neuroectodermal tumors, while only minimally expressed by normal tissues.","Immunologic Factor|Pharmacologic Substance"]
["C2739","Monoclonal Antibody 7C11","MoAb 7C11|MoAb IMC-7C11|Monoclonal Antibody 7C11","A murine IgM monoclonal antibody against Fas antigen with antineoplastic property. Fas antigen is a member of tumor necrosis factor family that mediates antibody-triggered apoptosis. Upon binds to Fas, monoclonal antibody 7C11 (MoAb 7C11) induces apoptosis in Fas-expressing cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2436","Monoclonal Antibody A1G4 Anti-Idiotype Vaccine","A1G4 anti-idiotype monoclonal antibody vaccine|Monoclonal Antibody A1G4 Anti-Idiotype Vaccine","An anti-idiotypic (anti-Id) rat monoclonal antibody (MoAb) that mimics the disialoganglioside GD2, a cancer-associated antigen present on melanoma, small cell lung cancer, sarcoma, neuroblastoma, and other malignancies. GD2 is a highly expressed glycosphingolipid by melanoma and other neuroectodermal tumors with only minimal expression on normal tissues. Vaccination with anti-Id A1G4 MoAb may elicit cellular and humoral immune responses against GD2 expression tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C2447","Monoclonal Antibody A27.15","A27.15|ANTI-TRANSFERRIN MOAB 27.15|MoAb A27.15|Monoclonal Antibody A27.15","A murine IgG1 monoclonal antibody directed against the human transferrin (Tf) receptor. Monoclonal antibody A27.15 binds to the Tf receptor, blocking the binding of transferrin to the receptor and resulting in decreased tumor cell growth. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2410","Monoclonal Antibody A33","A33 Monoclonal Antibody|A33|MoAb A33|Monoclonal Antibody A33","A humanized monoclonal antibody directed against the human A33 antigen. Monoclonal antibody A33 recognizes the human A33 antigen, a 43 KDa transmembrane glycoprotein of the immunoglobulin superfamily, which is highly and homogenously expressed in 95% of colorectal cancer metastases with only restricted expression in normal colonic mucosa.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C99162","Monoclonal Antibody AbGn-7","AbGn-7|Monoclonal Antibody AbGn-7","A chimeric monoclonal antibody against a Lewis-A-like glycotope (AbGn-7 antigen) with potential immunomodulating and antineoplastic activities. Monoclonal antibody AbGn-7 targets and binds to the carbohydrate AbGn-7 antigen on the cell surface of tumor cells and may induce complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC), thereby killing AbGn-7-epitope positive tumor cells. AbGn-7 antigen is expressed on a variety of tumor cell types, including human colorectal, pancreatic and gastric tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C129591","Monoclonal Antibody AK002","AK 002|AK002|Monoclonal Antibody AK 002|Monoclonal Antibody AK002","A therapeutic monoclonal antibody against an as of yet unidentified target expressed on mast cells and eosinophils. Upon administration, AK002 targets and binds to a receptor expressed on the surface of mast cells and eosinophils. This may induce antibody-dependent cell-mediated cytotoxicity (ADCC) against cells overexpressing the undisclosed receptor. This may reduce abnormal proliferation of mast cells and eosinophils, which play a key role in allergic and inflammatory responses.","Pharmacologic Substance"]
["C2659","Monoclonal Antibody CAL","Monoclonal Antibody CAL","A humanized monoclonal antibody directed against parathyroid hormone-related protein (PTH-rP). As a poly-hormone with diverse biological roles, PTH-rP is expressed by normal tissues, acting in local tissue environments in a variety of ways; it is commonly overexpressed by breast, prostate, and other cancers, acting systemically by promoting bone resorption, inhibiting calcium excretion from the kidney, inducing hypercalcemia, and possibly playing a role in the formation of bony metastases. By blocking the effects of PTH-rP on calcium metabolism, monoclonal antibody CAL may inhibit cancer-related hypercalcemia. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2567","Monoclonal Antibody CC49","Antibody CC49, Monoclonal|CC-49 Monoclonal Antibody|CC-49|MAb CC49|MOAB CC-49/TAG72 (DW)|MoAb CC49|Monoclonal Antibody CC-49|Monoclonal Antibody CC49","A second-generation murine monoclonal antibody based on the antibody B72.3 that is directed against tumor-associated glycoprotein 72 (TAG72).  TAG72 is expressed by gastric, breast, pancreatic, colorectal, and ovarian carcinoma cells. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2698","Monoclonal Antibody CC49-delta CH2","MOAB CC49-deltaCH2|MOAB HCC49DCH2|MoAb HuCC49DeltaCH2|Monoclonal Antibody CC49-delta CH2|Monoclonal Antibody HCC49DCH2","A humanized CH2 domain-deleted second-generation monoclonal antibody based on the antibody B72.3 that is directed against tumor-associated glycoprotein 72 (TAG72).  TAG72 is expressed by gastric, breast, pancreatic, colorectal, and ovarian carcinoma cells. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C98296","Monoclonal Antibody CEP-37250/KHK2804","CEP-37250/KHK2804|Monoclonal Antibody CEP-37250/KHK2804","A humanized monoclonal antibody targeting glycolipids, with potential immunomodulating and antineoplastic activity. Upon administration, monoclonal antibody CEP-37250/KHK2804 targets and binds to a specific tumor antigen, thereby stimulating the immune system to exert an antibody-dependent cellular cytotoxicity (ADCC) against the tumor associated antigen (TAA)-expressing cancer cells. This agent has shown to be active in both wild-type and mutant K-RAS-expressing colorectal cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2683","Monoclonal Antibody D6.12","MoAb D6.12|MoAb D612|Monoclonal Antibody D6.12","A murine IgG2a monoclonal antibody directed against a 48 kDa antigen expressed on the cell surface of normal and malignant gastrointestinal epithelium. MoAb D6.12 has been shown to induce antibody-dependent cell-mediated cytotoxicity (ADCC). This MoAb, either alone or in combination with other immunotherapeutic agents, may have possible diagnostic or therapeutic applications in gastrointestinal cancers.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2448","Monoclonal Antibody E2.3","Anti-Transferrin MOAB E2.3|E2.3|MoAb E2.3|Monoclonal Antibody E2.3","A murine IgG1 monoclonal antibody directed against the human transferrin (Tf) receptor. Monoclonal antibody E2.3 binds to the Tf receptor, blocking the binding of transferrin to the receptor and resulting in decreased tumor cell growth. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2514","Monoclonal Antibody F19","Anti-F19 Monoclonal Antibody|Anti-FAP (Fibroblast Activation Protein), F19 Epitope, Monoclonal Antibody|F19 monoclonal antibody|MoAb F19|Monoclonal Antibody F19","A murine monoclonal antibody (MoAb) against human fibroblast activation protein (FAP). FAP is a 95 kDa cell surface glycoprotein and an inducible tumour stromal antigen of epithelial cancers and of a subset of soft tissue sarcomas. FAP shows a very limited distribution pattern in normal tissues, thereby MoAb F19 has possible diagnostic and therapeutic applications in epithelial cancers.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C26450","Monoclonal Antibody GD2 Anti-Idiotype Vaccine","Monoclonal Antibody GD2 Anti-Idiotype Vaccine","A class of vaccines that consist of anti-idiotype monoclonal antibodies against the tumor-associated antigen disialoganglioside GD2 with potential antineoplastic activity.  Vaccination with a monoclonal antibody GD2 anti-idiotype vaccine produces an immunoglobulin response against GD2 with subsequent destruction of GD2 positive tumor cells via antibody-dependent cellular cytotoxicity (ADCC).  GD2 is overexpressed in melanoma, neuroblastoma, soft tissue sarcoma, and small cell carcinoma of the lung. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C2505","Monoclonal Antibody HeFi-1","HeFi-1|MoAb HeFi-1|Monoclonal Antibody HeFi-1","A murine monoclonal antibody with potential antineoplastic activity. Monoclonal antibody HeFi-1 binds to CD30, a cell surface antigen found on mitogen-activated B-cells and T-cells, and Reed-Sternberg cells.  Monoclonal antibody HeFi-1 has been shown to arrest tumor growth and prevent metastasis in animal models. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2547","Monoclonal Antibody Hu3S193","Hu3S193|MoAb Hu3S193|Monoclonal Antibody Hu3S193","A humanized monoclonal antibody directed against the Lewis Y antigen, a tumor-associated epithelial antigen, with potential antineoplastic activity. Following binding, monoclonal antibody Hu3S193 triggers an antibody-dependent cell-mediated cytotoxicity in cells expressing Lewis Y antigen. (NCI05)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C48407","Monoclonal Antibody HuAFP31","HuAFP31|MOAB HuAFP31|Monoclonal Antibody HuAFP31|hAFP-31","A humanized monoclonal antibody directed against alpha fetoprotein with potential antineoplastic activity. Upon administration, monoclonal antibody HuAFP31 (mAb HuAFP31) binds to and stimulates a cytotoxic T lymphocyte (CTL) response against tumor cells that express alpha fetoprotein.","Pharmacologic Substance"]
["C38697","Monoclonal Antibody HuHMFG1","AS1402|HuHMFG1|Monoclonal Antibody HuHMFG1|R1550|Therex","A humanized monoclonal antibody directed against MUC1, a mucin glycoprotein overexpressed in breast and other carcinomas.  Monoclonal antibody HuHMFG1 stimulates antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells expressing MUC1, resulting in a decrease in tumor burden. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2652","Monoclonal Antibody huJ591","Monoclonal Antibody huJ591","A humanized monoclonal antibody (MoAb) against the external domain of the Prostate-specific membrane antigen (PSMA), overexpressed in the malignant prostate and its metastases. Although PSMA is not a biomarker of disease progression, over-expression indicates an aggressive phenotype of the prostate cancer. This humanized J591 (huJ591) MoAb was generated by replacing murine Ig sequences with human ones, thereby MoAb huJ591can be administered to patients on multiple occasions over long time periods without inducing an immune response. Radiolabelled MoAb huJ591 may be used in immunotherapy of prostate cancer.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C48408","Monoclonal Antibody HuPAM4","MOAB HuPAM4|Monoclonal Antibody HuPAM4","A humanized monoclonal antibody directed against the pancreatic cancer antigen MUC1 with potential antineoplastic activity. Monoclonal antibody HuPAM4 (mAb HuPAM4) binds to cells expressing MUC1 antigen; mAb HuPAM4 may be useful as a carrier for radioisotopes and other antineoplastic therapeutic agents. (NCI05)","Pharmacologic Substance"]
["C29224","Monoclonal Antibody IMMU-14","MOAB IMMU-14|Monoclonal Antibody IMMU-14","An anti-carcinoembryonic antigen (anti-CEA) murine monoclonal immunoglobulin G (IgG) with potential antineoplastic activity.  CEA is overexpressed in several cancer cell types, including gastrointestinal, breast, and non-small cell lung cancers.  MOAB IMMU-14 can be conjugated with a radioactive element for use in radioimmunotherapy (RIT), a regimen that uses a tumor-specific monoclonal antibody to deliver targeted radiation to cancer cells. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2372","Monoclonal Antibody L6","L6|MoAb L6|Monoclonal Antibody L6","A murine IgG2a monoclonal antibody with potential antineoplastic activity. Monoclonal antibody L6 binds to the L6 antigen, a cell surface glycoprotein overexpressed in many carcinomas, and induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity against L6-expressing tumor cells.  This agent may be conjugated with various toxins in order to target their cytotoxic activity to tumor cells expressing the L6 antigen. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1561","Monoclonal Antibody Lym-1","IgG2a murine monoclonal antibody Lym-1|Lym-1|MoAb Lym-1|Monoclonal Antibody Lym-1, IgG2a Murine|Monoclonal Antibody Lym-1","A murine IgG2a monoclonal antibody directed against the HLA-Dr10 protein, a cell surface marker present on over eighty percent of lymphoma cells.  When conjugated with a radioactive isotope, Lym-1 monoclonal antibody selectively transports the cytotoxic radioisotope to HLA-Dr10-expressing tumor cells, thereby sparing healthy B-cells and normal tissues.  This agent also mediates antibody-dependent cytotoxicity thereby promoting Raji B-lymphoid cell lysis by human neutrophils. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1959","Monoclonal Antibody m170","Monoclonal Antibody 170|Monoclonal Antibody M170|Monoclonal Antibody m170","A panadenocarcinoma murine monoclonal antibody (MoAb) with potential antineoplastic activity. MoAb m170 recognizes MUC-1 antigen present on the surface of many adenocarcinomas. It may be conjugated with a radioactive element and used in radioimmunotherapy (RIT), a procedure that uses a tumor-specific monoclonal antibody to target radiation to cancer cells.","Amino Acid, Peptide, or Protein|Immunologic Factor|Indicator, Reagent, or Diagnostic Aid"]
["C2409","Monoclonal Antibody Me1-14 F(ab')2","Me1-14 F(ab')2 monoclonal antibody|Me1-14 F(ab')2|MoAb Me1-14 F(ab')2|Monoclonal Antibody Me1-14 F(ab')2","The F(ab)2 fragment of Me1-14, a murine IgG2a monoclonal antibody directed against proteoglycan chondroitin sulfate-associated protein expressed by gliomas and melanomas.  By binding to proteoglycan chondroitin sulfate-associated protein, monoclonal antibody Me1-14 F(ab')2 conjugated to a radioisotope may localize gliomas and melanomas when used as a tracer in radioimaging applications; in radioimmunotherapeutic applications, this agent conjugated to a radioisotope may be used to deliver targeted radiotoxicity to these tumors.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C97510","Monoclonal Antibody MGA271","MGA271|Monoclonal Antibody MGA271","An Fc-domain optimized, humanized monoclonal antibody directed against cancer stem cells (CSCs), with potential immunomodulating and antineoplastic activities. After binding of monoclonal antibody MGA271 to an as of yet not elucidated target expressed on CSCs and differentiated tumor cells, this agent may induce an antibody-dependent cell-mediated cytotoxicity (ADCC) against CSCs. CSCs are tumor initiating cells that are able to self-renew and are responsible for tumor cell growth and resistance.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2476","Monoclonal Antibody muJ591","MoAb muJ591|Monoclonal Antibody muJ591|muJ591 Monoclonal Antibody|muJ591","A murine IgG monoclonal antibody against the external domain of the prostate-specific membrane antigen (PSMA), overexpressed in the malignant prostate and its metastases. Although PSMA is not a biomarker of disease progression, over-expression indicates an aggressive phenotype of the prostate cancer. Radiolabelled MoAb muJ591 may be used in prostate cancer diagnosis and therapy.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2417","Monoclonal Antibody MX35 F(ab')2","MX35 F(ab')2 monoclonal antibody|MX35 F(ab')2|MoAb MX35 F(ab')2|Monoclonal Antibody MX35 F(ab')2","The F(ab)2 fragment of monoclonal antibody (MoAb) MX35 that recognizes a 95 kD glycoprotein with homogeneous distribution on 80% of ovarian tumor specimens. When radiolabeled, this MoAb has potential use in the radioimaging or may induce a cytotoxic T-cell response against tumor cells that express this glycoprotein. Containing only the antigen-binding fragment of the Ig molecule, MoAb MX35 F(ab')2 offers the advantages of smaller size and lower cross-reactivity compared to complete antibodies.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2349","Monoclonal Antibody R24","MoAb R24|Monoclonal Antibody R24|R24","An IgG murine monoclonal antibody directed against the ganglioside GD3 glycolipid, located in the cell membranes of some tumor cells.  Monoclonal antibody R24 binds to GD3-positive cells, thereby initiating antibody-dependent cytotoxicity against GD3-positive cells. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C48409","Monoclonal Antibody RAV12","Monoclonal Antibody RAV12|RAV12|anti-RAAG12 MOAB","A chimeric monoclonal antibody directed against a primate-restricted N-linked carbohydrate epitope (glycotope) expressed on various human carcinomas with potential antineoplastic activity. Following binding, monoclonal antibody RAV12 disrupts sodium channels of tumor cells expressing this glycotope, resulting in cell and organelle swelling, loss of membrane integrity, and cell death. (NCI05)","Pharmacologic Substance"]
["C2005","Monoclonal Antibody SGN-14","Monoclonal Antibody SGN-14|SGN-14","A humanized monoclonal antibody targeting the CD40 antigen with potential antineoplastic activity. CD-40, an integral membrane protein found on the surface of B lymphocytes and member of the tumor necrosis factor receptor super-family, is highly overexpressed on the cell surface of a number of B-cell malignancies. Monoclonal antibody SGN-14 specifically binds to and inhibits CD-40, thereby inhibiting cell proliferation and inducing cell lysis via antibody-dependent cellular cytotoxicity (ADCC) in cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2007","Monoclonal Antibody SGN-30","Anti-CD30 Monoclonal Antibody|Monoclonal Antibody SGN-30|SGN-30","A genetically-engineered, chimeric mouse-human, anti-CD30 monoclonal antibody with potential antineoplastic activity. Monoclonal antibody SGN-30 specifically binds to the receptor CD-30, a member of the tumor necrosis factor receptor super-family, which may be overexpressed on the surfaces of Hodgkin lymphoma cells and anaplastic-large cell lymphoma cells. After binding to CD30, this agent interferes with the G1 phase of the cell cycle, thereby inducing growth arrest and apoptosis in susceptible tumor cell populations.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C94208","Monoclonal T-cell Receptor Anti-CD3 scFv Fusion Protein IMCgp100","IMCgp100|ImmTAC-gp100|Monoclonal T-cell Receptor Anti-CD3 scFv Fusion Protein IMCgp100","A fusion protein containing a modified form of human T-cell receptor (TCR) specific for the gp100 antigen and fused to an anti-CD3 single-chain antibody fragment, with potential antineoplastic activity. Upon direct intratumoral administration of IMCgp100 into the melanoma lesion, the TCR moiety of this agent targets and binds to the tumor associated antigen (TAA) gp100 presented on the melanoma tumor cell; the anti-CD3 fragment moiety binds to CD3- expressing T lymphocytes, thereby selectively cross-linking tumor cells and T-lymphocytes. This may lead to the recruitment of cytotoxic T lymphocytes (CTL) to the T lymphocyte/tumor cell aggregates and result in CTL-mediated death of gp100-expressing melanoma cancer cells.","Immunologic Factor|Pharmacologic Substance"]
["C122637","Monomethyl Auristatin E","(S)-N-((3R,4S,5S)-1-((S)-2-((1R,2R)-3-(((1S,2R)-1-hydroxy-1-phenylpropan-2-yl)amino)-1-methoxy-2-methyl-3-oxopropyl)pyrrolidin-1-yl)-3-methoxy-5-methyl-1-oxoheptan-4-yl)-N,3-dimethyl-2-((S)-3-methyl-2-(methylamino)butanamido)butanamide|L-Valinamide, N-methyl-L-valyl-N-((1S,2R)-4-((2S)-2-((1R,2R)-3-(((1R,2S)-2-hydroxy-1- methyl-2-phenylethyl)amino)-1-methoxy-2-methyl-3-oxopropyl)-1-pyrrolidinyl)-2- methoxy-1-((1S)-1-methylpropyl)-4-oxobutyl)-N-methyl-|MMAE|Monomethyl Auristatin E|Monomethylauristatin E|N(sup 2)-(N-methyl-L-valyl)-N(sup 1)-((1S,2R)-4-((2S)-2-((1R,2R)-3-(((1R,2S)-2-hydroxy-1-methyl-2- phenylethyl)amino)-1-methoxy-2-methyl-3-oxopropyl)pyrrolidin-1-yl)-2-methoxy-1-((1S)-1-methylpropyl)-4-oxobutyl)-N(sup 1)-methyl-L-valinamide","A dolastatin-10 peptide derivative with potent antimitotic activity and potential antineoplastic activity as part of an antibody-drug conjugate (ADC). Monomethyl auristatin E (MMAE) binds to tubulin, blocks tubulin polymerization, and inhibits microtubule formation, which results in both disruption of mitotic spindle assembly and arrest of tumor cells in the M phase of the cell cycle. To minimize toxicity and maximize efficacy, MMAE is conjugated, via a cleavable peptide linker, to a monoclonal antibody that specifically targets a patient's tumor. The linker is stable in the extracellular milieu but is readily cleaved to release MMAE following binding and internalization of the ADC by the target cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C97330","Montanide ISA 720","ISA 720|Montanide ISA 720","A proprietary adjuvant, applicable for water-in-oil (W/O; 30/70 v/v) vaccine emulsion, with potential immunoadjuvant activity. Montanide ISA 720 is made of natural metabolizable non-mineral oil and a highly refined emulsifier from the mannide mono-oleate family; it is rapidly metabolized and eliminated, and may be used in various vaccines, including cancer vaccines. Upon administration, Montanide ISA 720 forms a depot at the injection site and is therefore capable of slowly releasing the antigen(s) from the injection site. This may result in enhanced cellular and humoral immune responses to the antigen vaccine.","Pharmacologic Substance"]
["C131215","Montanide ISA-51 VG/KLH/NY-ESO-1/MART-1 Peptide Vaccine","Montanide ISA-51 VG/KLH/NY-ESO-1/MART-1 Peptide Vaccine|Montanide ISA-51 VG/KLH/NY-ESO-1/MART-1 Vaccine|NY-ESO-1/MART-1/KLH/Montanide ISA-51 VG Vaccine","A cancer vaccine consisting of two immunogenic peptides derived from the cancer-testis antigen NY-ESO-1 and the melanoma differentiation antigen Melan-A (MART-1; Melanoma Antigen Recognized by T cells 1), which are conjugated with the immunostimulant keyhole limpet hemocyanin (KLH) and emulsified in the immunoadjuvant Montanide ISA-51 VG, with potential immunomodulating and antineoplastic activities. Upon subcutaneous vaccination, the Montanide ISA-51 VG/KLH/NY-ESO-1/MART-1 peptide vaccine stimulates the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing the NY-ESO-1 and Melan-A antigens, resulting in tumor cell lysis. NY-ESO-1 and Melan-A are overexpressed in a variety of tumor cell types. The surfactant mannide monooleate in Montanide ISA 51 VG is derived from vegetable-grade (VG) oleic acid that was purified from olive oil. KLH is a hapten carrier and serves as an immunostimulant to improve immune recognition.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C26662","Morinda Citrifolia Fruit Extract","Indian Mulberry Extract|Morinda Citrifolia Fruit Extract|Morinda citrifolia Extract|Noni Extract|Noni Juice|Noni","An extract prepared from the fruit of Morinda citrifolia, a plant that yields various herbal preparations. Morinda citrifolia fruit juice has antioxidant properties and may prevent tumorigenesis via inhibition of DNA-carcinogen adduct formation.","Plant"]
["C1442","Morpholinodoxorubicin","5,12-Naphthacenedione, 7, 8, 9, 10-tetrahydro-6, 8, 11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-10-[[2, 3, 6-trideoxy-3-(4-morpholinyl)-alpha-L-lyxo-hexopyranosyl] oxy]-, hydrochloride, (8S-cis)-|Morpholinodoxorubicin|morpholino-ADR|morpholino-adriamycin","A semisynthetic derivative of the anthracycline antineoplastic antibiotic doxorubicin.  As an antineoplastic agent, morpholinodoxorubicin is more potent than doxorubicin.  Similar to doxorubicin, morpholinodoxorubicin intercalates into DNA and causes single- and double-strand breaks in DNA via inhibition of topoisomerase I and II.  Unlike doxorubicin, this agent is metabolized in vivo to a DNA-alkylating derivative that forms DNA interstrand cross-links, thereby potentiating its doxorubicin-like cytotoxicity. (NCI04)","Antibiotic|Organic Chemical"]
["C71896","Motesanib","MOTESANIB|Motesanib","An orally bioavailable receptor tyrosine kinase inhibitor with potential antineoplastic activity. AMG 706 selectively targets and inhibits vascular endothelial growth factor (VEGFR), platelet-derived growth factor (PDGFR), Kit, and Ret receptors, thereby inhibiting angiogenesis and cellular proliferation.","Pharmacologic Substance"]
["C48374","Motesanib Diphosphate","3-Pyridinecarboxamide, N-(2,3-dihydro-3,3-dimethyl-1H-indol-6-yl)-2-((4-pyridinylmethyl)amino)-, phosphate (1:2)|AMG 706|MOTESANIB DIPHOSPHATE|Motesanib Diphosphate","The orally bioavailable diphosphate salt of a multiple-receptor tyrosine kinase inhibitor with potential antineoplastic activity. Motesanib selectively targets and inhibits vascular endothelial growth factor (VEGFR), platelet-derived growth factor (PDGFR), kit, and Ret receptors, thereby inhibiting angiogenesis and cellular proliferation.","Pharmacologic Substance"]
["C1651","Motexafin Lutetium","Antrin|Lu tex|Lu-Tex|Lutetium Texaphrin|Lutetium Texaphyrin|Lutetium texaphyrin|Lutex|Lutrin|MOTEXAFIN LUTETIUM|Motexafin Lutetium|Optrin|PCI-0123|lutetium texaphyrin|motexafin lutetium","A pentadentate aromatic metallotexaphyrin with photosensitizing properties. Motexafin lutetium preferentially accumulates in tumor cells due to their increased rates of metabolism and absorbs light, forming an extended high energy conformational state that produces high quantum yields of singlet oxygen, resulting in local cytotoxic effects. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C48410","Mouse gp100 Plasmid DNA Vaccine","Mouse gp100 Plasmid DNA Vaccine","A vaccine consisting of a plasmid DNA encoding the murine melanoma-associated antigen gp100. Upon administration, expressed gp100 antigen may stimulate a cytotoxic T cell HLA-A2.1-restricted immune response against tumor cells that express the gp100 antigen, resulting in tumor cell lysis. (NCI05)","Pharmacologic Substance"]
["C48411","Mouse Prostate-Specific Membrane Antigen Plasmid DNA Vaccine","Mouse PSMA DNA Vaccine|Mouse Prostate-Specific Membrane Antigen Plasmid DNA Vaccine","A vaccine consisting of a plasmid DNA encoding the murine prostate-specific membrane antigen (PSMA). Upon administration, expressed PSMA may stimulate a cytotoxic T cell response against tumor cells that express PSMA, resulting in tumor cell lysis. (NCI05)","Pharmacologic Substance"]
["C91713","Mouse Renal Adenocarcinoma Cell-Encapsulated Agarose-Agarose Macrobeads","Mouse Renal Adenocarcinoma Cell-Encapsulated Agarose-Agarose Macrobeads|RENCA Macrobead","An agarose matrix containing mouse renal adenocarcinoma (RENCA) cells, with potential antineoplastic activity. The agarose-agarose macrobeads consist of two spherical agarose layers; the mouse RENCA cells are contained within the inner agarose layer. Upon placement into the abdominal cavity, the restricted mouse renal adenocarcinoma cells in the agarose macrobeads produce and release certain growth-retarding factors that inhibit the proliferation of the RENCA cells; Upon diffusion of these growth-slowing factors out of the agarose layers, these substances may inhibit cancer cell proliferation of proliferating tumors.","Pharmacologic Substance"]
["C2638","MOv-gamma Chimeric Receptor Gene","MOv-gamma Chimeric Receptor Gene|MOv-gamma","A recombinant engineered chimeric gene derived from the murine gene encoding the variable region of monoclonal antibody MOv18 against folate-binding protein, which is often overexpressed in human ovarian cancer cells, and the gene encoding the Fc receptor for the gamma subunit of human IgG and IgE. Peripheral blood lymphocytes expressing the MOv-gamma gene may be used in the immunotherapeutic treatment of ovarian cancer. (NCI04)","Gene or Genome|Pharmacologic Substance"]
["C68819","Moxetumomab Pasudotox","Anti-CD22 Immunotoxin CAT-8015|CAT-8015|GCR-8015|HA22|Immunotoxin CAT-8015|MOXETUMOMAB PASUDOTOX|Moxetumomab Pasudotox|anti-CD22 immunotoxin CAT-8015","A recombinant immunotoxin consisting of the Fv portion of the anti-CD22 antibody covalently fused to a 38 KDa fragment of Pseudomonas exotoxin-A (PE38) with potential antineoplastic activity. The Fv portion of anti-CD22 immunotoxin CAT-8015 binds to CD22, a cell surface receptor expressed on a variety of malignant B-cells, thereby delivering the toxin moiety PE38 directly to tumor cells. Once internalized, PE38 induces caspase-mediated apoptosis via a mechanism involving mitochondrial damage and blocks translational elongation by binding to elongation factor 2 (EF-2). Anti-CD22 immunotoxin CAT-8015 exhibits a greater affinity for CD22 than its predecessor, anti-CD22 immunotoxin CAT-3888 (BL22 immunotoxin), and hence may be more effective against tumor cells expressing lower levels of CD22.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C122707","Mps1 Inhibitor BAY 1217389","BAY 1217389|Mps1 Inhibitor BAY 1217389","An orally bioavailable, selective inhibitor of the serine/threonine kinase monopolar spindle 1 (Mps1, TTK), with potential antineoplastic activity. Upon administration, the Mps1 inhibitor BAY 1217389 selectively binds to and inhibits the activity of Mps1. This inactivates the spindle assembly checkpoint (SAC), accelerates mitosis, causes chromosomal misalignment and missegregation, and mitotic checkpoint complex destabilization. This induces cell death in Mps1-overexpressing cancer cells. Mps1, a kinase expressed in proliferating normal tissues and aberrantly overexpressed in a wide range of human tumors, is activated during mitosis and is essential for proper SAC functioning and chromosome alignment.","Pharmacologic Substance"]
["C116074","Mps1 Kinase Inhibitor BAY1161909","BAY116-1909|BAY1161909|Mps1 Kinase Inhibitor BAY1161909","An orally bioavailable, selective inhibitor of the serine/threonine monopolar spindle 1 (Mps1) kinase, with potential antineoplastic activity. Upon administration, the Mps1 kinase inhibitor BAY1161909 binds to and inhibits the activity of Mps1. This causes inactivation of the spindle assembly checkpoint (SAC), accelerated mitosis, chromosomal misalignment, chromosomal missegregation, mitotic checkpoint complex destabilization, and increased aneuploidy. This leads to the induction of cell death in cancer cells overexpressing Mps1. Mps1, a kinase expressed in proliferating normal tissues and aberrantly overexpressed in a wide range of human tumors, is activated during mitosis and is essential for SAC functioning and controls chromosome alignment.","Pharmacologic Substance"]
["C111574","mRNA-derived Lung Cancer Vaccine CV9202","CV9202|mRNA-derived Lung Cancer Vaccine CV9202","A non-small cell lung cancer (NSCLC) vaccine containing six modified mRNAs, which encode six different NSCLC associated antigens, with potential antitumor and immunomodulatory activities. Upon intradermal administration, mRNA-derived lung cancer vaccine CV9202 may stimulate the immune system to mount both humoral and cellular responses against NSCLC cells. The six tumor-associated antigens (TAAs) encoded by these mRNAs are frequently expressed by NSCLC cells and are minimally expressed or absent in normal, healthy cells.","Immunologic Factor|Pharmacologic Substance"]
["C82654","mRNA-Derived Prostate Cancer Vaccine CV9103","CV9103|Messenger RNA-Derived Prostate Cancer Vaccine CV9103|mRNA-Derived Prostate Cancer Vaccine CV9103","A prostate cancer vaccine containing mRNAs encoding prostate specific antigen (PSA), prostate specific membrane antigen (PSMA), prostate stem cell antigen (PSCA) and six-transmembrane epithelial antigen of the prostate (STEAP), with potential antitumor activity. Upon administration, mRNA-derived prostate cancer vaccine CV9103 may stimulate the immune system to mount a cytotoxic T lymphocyte response (CTL) against PSA-, PSMA-, PSCA- and STEAP-expressing prostate tumor cells. The mRNA used in this vaccine is modified and formulated to have enhanced translational potency and adjuvant activities. PSA, PSMA, PSCA and STEAP may be upregulated in prostate cancer cells; their expression in prostate cancer has been correlated with disease progression.","Pharmacologic Substance"]
["C106231","mRNA-derived Prostate Cancer Vaccine CV9104","CV9104|RNActive-derived Prostate Cancer Vaccine CV9104|mRNA-derived Prostate Cancer Vaccine CV9104","A prostate cancer vaccine containing six messenger RNAs (mRNAs) encoding for antigens upregulated in prostate cancer, including mRNAs for prostate specific antigen (PSA), prostate specific membrane antigen (PSMA), prostatic acid phosphatase (PAP), and mucin 1 (MUC1), with potential antineoplastic and immunomodulating activities. Upon intradermal administration of mRNA-derived prostate cancer vaccine CV9104, this agent enters cells, the mRNAs are translated into the respective prostate specific antigens and may cause the immune system to mount a cytotoxic T lymphocyte response (CTL) against PSA-, PSMA-, PAP- and MUC1-expressing prostate tumor cells. The mRNAs used in this vaccine are modified to have enhanced translational potency and adjuvant activities. PSA, PSMA, PAP and MUC1 are frequently upregulated in prostate cancer cells; their expression in prostate cancer has been correlated with disease progression.","Pharmacologic Substance"]
["C95724","MTF-1 Inhibitor APTO-253 HCl","2-(6-Fluoro-2-methyl-1H-indol-3-yl)-1H-imidazo[4,5-f][1,10]phenanthroline Hydrochloride|APTO-253 HCl|LOR-253 HCl|LT-253 HCl|MTF-1 Inhibitor APTO-253 HCl","The hydrochloride salt of a small molecule inhibitor of human metal-regulatory transcription factor 1 (MTF-1) with potential antitumor activity. MTF-1 inhibitor APTO-253 inhibits MTF-1 activity and thereby induces the expression of MTF-1 dependent tumor suppressor factor Kruppel like factor 4 (KLF4). This subsequently leads to the downregulation of cyclin D1, blocking cell cycle progression and proliferation. This agent also causes decreased expression of genes involved in tumor hypoxia and angiogenesis.","Pharmacologic Substance"]
["C78856","mTOR Kinase Inhibitor AZD8055","AZD8055|mTOR Kinase Inhibitor AZD8055","An inhibitor of the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. mTOR kinase inhibitor AZD8055 inhibits the serine/threonine kinase activity of mTOR, resulting in decreased expression of mRNAs necessary for cell cycle progression, which may induce cell cycle arrest and tumor cell apoptosis. mTOR phosphorylates transcription factors, such as S6K1 and 4E-BP1, which stimulate protein synthesis and regulate cell growth, proliferation, motility, and survival.","Pharmacologic Substance"]
["C92575","mTOR Kinase Inhibitor CC-223","CC-223|TORKi|mTOR Kinase Inhibitor CC-223","An orally available inhibitor of the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. mTOR kinase inhibitor CC-223 inhibits the activity of mTOR, which may result in the induction of tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR, a serine/threonine kinase that is upregulated in a variety of tumors, plays an important role downstream in the PI3K/AKT/mTOR signaling pathway, which is frequently dysregulated in human cancers.","Pharmacologic Substance"]
["C78476","mTOR Kinase Inhibitor OSI-027","Mammalian Target of Rapamycin Kinase Inhibitor OSI-027|OSI-027|mTOR Kinase Inhibitor OSI-027","An orally bioavailable mammalian target of rapamycin (mTOR) kinase inhibitor with potential antineoplastic activity. mTOR kinase inhibitor OSI-027 binds to and inhibits both the raptor-mTOR (TOR complex 1 or TORC1) and the rictor-mTOR (TOR complex 2 or TORC2) complexes of mTOR, which may result in tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR is a serine/threonine kinase that is upregulated in some tumors and plays an important role downstream in the PI3K/Akt/mTOR signaling pathway.","Organic Chemical|Pharmacologic Substance"]
["C128632","mTOR Kinase Inhibitor PP242","2-(4-Amino-1-isopropyl-1H-pyrazolo(3,4-d)pyrimidin-3-yl)-1H-indol-5-ol|PP-242|PP242|mTOR Kinase Inhibitor PP242",null,"Organic Chemical|Pharmacologic Substance"]
["C101132","mTOR1/2 Kinase Inhibitor ME-344","ME-344|mTOR1/2 Kinase Inhibitor ME-344","An active metabolite of NV-128, a novel flavonoid small molecule inhibitor of the mammalian Target of Rapamycin (mTOR), with potential antineoplastic activity. Upon administration, mTOR1/2 Kinase inhibitor ME-344 downregulates the PIK3/AKT/mTOR pathway and results in chromatin condensation in the absence of caspase activation. Consequently, this agent induces caspase-independent cell death in tumor cells with a de-regulated PIK3/AKT/mTOR pathway or chemotherapeutic resistant cells.","Pharmacologic Substance"]
["C122836","mTORC1/2 Kinase Inhibitor BI 860585","BI 860585|mTORC1/2 Kinase Inhibitor BI 860585","An orally bioavailable inhibitor of raptor-mammalian target of rapamycin (mTOR) complex 1 (mTOR complex 1; mTORC1) and rictor-mTOR complex 2 (mTOR complex 2; mTORC2), with potential antineoplastic activity. Upon oral administration, mTORC1/2 kinase inhibitor BI 860585 binds to the kinase domain of mTOR and inhibits both mTORC1 and mTORC2, in an ATP-competitive manner. This inhibits mTOR-mediated signaling and leads to both an induction of apoptosis and a decrease in the proliferation of mTORC1/2-expressing tumor cells. mTOR is a serine/threonine kinase that is upregulated in certain tumor cell types. It plays an important role in the PI3K/Akt/mTOR signaling pathway, which is often deregulated in cancer cells and promotes cell growth, survival, and resistance to chemotherapy and radiotherapy.","Pharmacologic Substance"]
["C117290","mTORC1/mTORC2/DHFR Inhibitor ABTL0812","ABTL0812|mTORC1/mTORC2/DHFR Inhibitor ABTL0812","An orally bioavailable, lipid analogue and inhibitor of raptor-mammalian target of rapamycin (mTOR) (mTOR complex 1; mTORC1), rictor-mTOR (mTOR complex 2; mTORC2) and dihydrofolate reductase (DHFR) with potential antineoplastic activity. Upon oral administration, mTORC1/mTORC2/DHFR inhibitor ABTL0812 binds to and inhibits both mTORC1 and mTORC2, which may result in apoptosis and a decrease in proliferation in mTORC1/2-expressing tumor cells. mTOR is a serine/threonine kinase that is upregulated in some tumors; it plays an important role in the PI3K/Akt/mTOR signaling pathway which is often deregulated in cancer cells. In addition, ABTL0812 inhibits DHFR, an enzyme that reduces dihydrofolic acid to tetrahydrofolic acid, thereby blocking tetrahydrofolate synthesis, and resulting in both the depletion of nucleotide precursors and the inhibition of DNA, RNA and protein synthesis. This induces autophagy-induced cell death and further inhibition of cell proliferation.","Pharmacologic Substance"]
["C53290","MUC-1 Peptide Vaccine","MUC-1 Peptide Vaccine|MUC1 Peptide Vaccine","A cancer vaccine comprised of a synthetic peptide derived from the mucin 1 (MUC1) antigen with potential antineoplastic activity. Upon administration, MUC1 peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for the MUC1 antigen, resulting in decreased tumor growth. Overexpressed on many tumor cells, MUC1 antigen, a mammary-type apomucin, is a high-molecular-weight transmembrane glycoprotein.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82417","MUC1 Peptide-Poly-ICLC Vaccine","MUC1 Peptide-Poly-ICLC Vaccine","A vaccine preparation containing mucus 1 (MUC1) peptide and the adjuvant poly-ICLC with potential immunostimulatory and antineoplastic activities. Upon administration, MUC1 peptide-poly-ICLC adjuvant vaccine may induce the host immune system to mount a cytotoxic T cell response against MUC1-expressing tumor cells. MUC1, a tumor associated antigen normally present on the lining of the human colon, may be overexpressed and/or mutated in a variety of cancer cell types. The adjuvant poly-ICLC, a ligand for toll-like receptor-3, induces the release of cytokines which may help boost the immune response against MUC1.","Pharmacologic Substance"]
["C106119","MUC16-targeted Antibody-Drug Conjugate DMUC5754A","DMUC5754A|MUC16-targeted Antibody-Drug Conjugate DMUC5754A","An antibody drug conjugate (ADC) consisting of a humanized IgG1 monoclonal antibody targeting the MUC16 protein (CA-125) conjugated to, via a cleavable linker, the antimicrotubulin agent monomethyl auristatin E (MMAE), with potential antineoplastic activity. The monoclonal antibody moiety of DMUC5754A selectively binds to MUC16. After internalization of the drug conjugate and proteolytic cleavage of the linker, MMAE binds to tubulin and inhibits its polymerization, which results in G2/M-phase growth arrest and tumor cell apoptosis. MUC16, a transmembrane protein, is overexpressed on the cell surface of more than 80 percent of ovarian cancer cells but not on healthy cells.","Pharmacologic Substance"]
["C2232","MUC1-KLH Conjugate Vaccine","MUC-1 KLH Vaccine|MUC-1-KLH vaccine|MUC1-KLH Conjugate Vaccine|MUC1-KLH VAC","A peptide vaccine, containing human tumor-associated epithelial mucin (MUC1) conjugated with keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Vaccination with MUC1-KLH conjugate vaccine may stimulate humoral and cytotoxic T-lymphocyte (CTL) responses against tumor cells expressing the MUC1 antigen. In this vaccine, MUC1 antigen is conjugated with KLH, an immunostimulant and a hapten carrier, to enhance immune recognition. MUC1 antigen, a membrane-bound glycoprotein expressed by most glandular and ductal epithelial cells, is overexpressed in an aberrant or deglycosylated form in various cancers such as those of the breast, prostate, and ovary.","Immunologic Factor|Pharmacologic Substance"]
["C11845","MUC1-KLH Vaccine/QS21","MUC1-KLH Vaccine/QS21","A peptide vaccine containing the human tumor-associated antigen epithelial mucin (MUC1 antigen) conjugated with keyhole limpet hemocyanin (KLH) and combined with the nonspecific immunoadjuvant QS21, with potential antineoplastic activity.  MUC1 antigen is linked with KLH, an immunostimulant and a hapten carrier, in order to enhance immune recognition; the co-administration of saponin-derived QS21 potentially amplifies the total immune response to the MUC1 antigen.  Administration of MUC1-KLH vaccine/QS21 may result in both the production of antitumor antibodies and the stimulation of a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the MUC1 antigen. MUC1 antigen, a membrane-bound glycoprotein expressed by most glandular and ductal epithelial cells, is overexpressed as an aberrant or deglycosylated form in various cancers such as breast, prostate and ovarian cancers.","Therapeutic or Preventive Procedure"]
["C95722","MUC1-targeted Peptide GO-203-2C","GO-203-2C|MUC1-targeted Peptide GO-203-2C","An optimized small peptide drug candidate targeting epithelial mucin (MUC1) with antineoplastic activity. MUC1-targeted peptide GO-203-2C interacts with oncoprotein MUC1 C-terminal subunit on the cell surface, thereby impeding cell-cell interactions, signaling, and metastasis. MUC1 antigen, a membrane bound glycoprotein expressed by most glandular and ductal epithelial cells, is over-expressed in many diverse human carcinomas including those of the breast, prostate, lung, colon, pancreas, and ovary, and has been associated with poor prognosis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2465","MUC-2-KLH Vaccine","MUC-2-KLH Vaccine|MUC-2-KLH|vaccine, MUC-2-KLH","A peptide vaccine containing human mucin 2 (MUC2) protein conjugated with keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. MUC2, a secretory or gel forming glycoprotein expressed predominantly in goblet cells of the gastrointestinal and respiratory tracts, is overexpressed as an aberrant or deglycosylated form in various tumors such as gastric carcinomas and some hormone-refractory prostate cancers. MUC2 protein is conjugated with KLH, an immunostimulant and a hapten carrier, to enhance immune recognition. Vaccination with MUC2-KLH may result in the production of antibodies as well as elicit a cytotoxic T- lymphocyte (CTL) response against tumor cells expressing MUC2.","Immunologic Factor|Pharmacologic Substance"]
["C107188","Mucoadhesive Paclitaxel Formulation","DHP107|Mucoadhesive Paclitaxel Formulation","An orally available, mucoadhesive lipid preparation consisting of paclitaxel, a compound extracted from the Pacific yew tree Taxus brevifolia, in a formulation that is comprised of a mixture of monoolein, tricarprylin, and Tween 80, with potential antineoplastic activity. Upon oral administration, DHP107 forms droplets and micelles in the intestine; these adhere to mucoepithelial cells in the gastrointestinal tract and are absorbed through lipid-based uptake mechanisms. Upon absorption, paclitaxel binds to and stabilizes tubulin molecules, which results in the inhibition of both microtubule depolymerization and cell division. This agent also induces apoptosis by both binding to and blocking the function of the apoptosis inhibitor protein B-cell Leukemia 2 (Bcl-2).The mucoadhesive paclitaxel formulation does not contain P-glycoprotein inhibitors, the solvent cremophor or any other toxic solvent.","Pharmacologic Substance"]
["C101786","Multi-AGC Kinase Inhibitor AT13148","AT13148|Multi-AGC Kinase Inhibitor AT13148","An orally available, small molecule inhibitor of AGC group kinases, with potential antineoplastic activity. AT13148 inhibits, in an ATP-competitive manner, the enzymatic activity of two AGC kinases, protein kinase B (PKB or AKT) and p70S6K which play key roles in the PI3K/PKB/mTOR signaling pathway. Blockade of this pathway leads to an inhibition of cell growth and the induction of apoptosis in susceptible tumor cells. PI3K/PKB/mTOR pathway is dysregulated in greater than 50% of tumors, and is often correlated with resistance and increased tumor survival. AGC group kinases are serine/threonine kinases that are regulated by secondary messengers such as cyclic AMP and lipids.","Pharmacologic Substance"]
["C128898","Multi-epitope Anti-folate Receptor Peptide Vaccine TPIV 200","Multi-epitope Anti-folate Receptor Peptide Vaccine TPIV 200|TPIV 200 Vaccine|TPIV 200|TPIV-200|TPIV200/huFR-1|TPIV200","A peptide vaccine containing five immunogenic peptide epitopes of the human folate receptor 1 (FOLR1; FR-alpha), with potential immunomodulating and antineoplastic activities. Upon intradermal administration, multi-epitope anti-folate receptor peptide vaccine TPIV 200 may induce a cytotoxic T-lymphocyte (CTL) response against FR-alpha-overexpressing tumor cells. FR-alpha is a high-affinity folate-binding protein and a member of the folate receptor family; this receptor is overexpressed in various cancer cell types.","Pharmacologic Substance"]
["C101777","Multi-epitope Folate Receptor Alpha Peptide Vaccine","FR Alpha Peptide Vaccine|Multi-epitope Folate Receptor Alpha Peptide Vaccine","A peptide vaccine containing five immunogenic peptide epitopes of the human folate receptor alpha (FR alpha or FOLR1), including FR30, FR56, FR76, FR113, and FR238, with potential immunomodulating and antineoplastic activity. Upon administration, the multi-epitope FR alpha peptide vaccine may induce a cytotoxic T-lymphocyte (CTL) response against FR alpha-overexpressing tumor cells. FR alpha is a high-affinity folate-binding protein and a member of the folate receptor family; this receptor is overexpressed in a majority of ovarian cancers and in about 50% of breast cancers.","Immunologic Factor|Pharmacologic Substance"]
["C114990","Multi-epitope Folate Receptor Alpha-loaded Dendritic Cell Vaccine","FRaDC Vaccine|FRalphaDC Vaccine|Multi-epitope Folate Receptor Alpha-loaded Dendritic Cell Vaccine","A cell-based vaccine composed of autologous-monocyte-derived dendritic cells (DCs) loaded with five immunogenic peptide epitopes, derived from the tumor-associated antigen human folate receptor alpha (FR alpha or FOLR1), including FR30, FR56, FR76, FR113, and FR238, with potential immunomodulatory and antineoplastic activity. Ex vivo treatment of the DCs with a p38 inhibitor decreases p38-mediated signaling and enhances ERK activation. This may allow, upon intradermal administration of the multi-epitope FR alpha-loaded DC vaccine into the patient, for decreased activation and expansion of CD4+ regulatory T-cells (Tregs), increased differentiation and expansion of interleukin-17 secreting T helper cells (Th17) and activation of CD8+ CTLs, which induces a strong anti-tumor T-cell immune response against FR alpha-overexpressing tumor cells. FR alpha is a high-affinity folate-binding protein and a member of the folate receptor family; this receptor is overexpressed in the majority of ovarian cancers and in about approximately 50% of breast cancers.","Cell|Pharmacologic Substance"]
["C38695","Multi-epitope Melanoma Peptide Vaccine","MULTI-EP MP VAC|Multi-epitope Melanoma Peptide Vaccine","A peptide cancer vaccine consisting of a combination of peptides derived form several melanoma epitopes. Vaccination with multi-epitope melanoma peptide vaccine stimulates the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing the corresponding antigens, resulting in tumor cell lysis.  This vaccine may stimulate a broader CTL response compared to single-antigen vaccines. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C101260","Multifunctional/Multitargeted Anticancer Agent OMN54","Aneustat|MFMT OMN54|Multifunctional/Multitargeted Anticancer Agent OMN54|OMN54","An orally available, multivalent herbal formulation containing a novel mixture of whole extracts from three commonly used Chinese medicinal herbs Ganoderma lucidum (lingzhi mushroom), Salvia miltiorrhiza (Chinese sage, or danshen) and Scutellaria barbata (ban zhi lian), with potential immunomodulating, antiangiogenic, anti-inflammatory, antiproliferative and antiviral activities. Although the exact mechanism of action remains to be fully elucidated due to the complexity of the multiple phytochemicals, multifunctional/multitargeted anticancer agent OMN54 appears to work in an additive and synergistic manner by acting on a variety of signaling pathways and on multiple targets, such as vascular endothelial growth factor, nuclear factor kappa B, interleukin-1beta, fibroblast growth factor, and epidermal growth factor.","Pharmacologic Substance"]
["C124054","Multi-glioblastoma-peptide-targeting Autologous Dendritic Cell Vaccine ICT-107","ICT-107|Multi-glioblastoma-peptide-pulsed Autologous DC Vaccine ICT-107|Multi-glioblastoma-peptide-targeting Autologous DC Vaccine ICT-107|Multi-glioblastoma-peptide-targeting Autologous Dendritic Cell Vaccine ICT-107","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with six synthetic glioblastoma (GBM) peptides: absent in melanoma 2 (AIM-2), melanoma-associated antigen 1 (MAGE-1), tyrosinase-related protein 2 (TRP-2), glycoprotein 100 (gp100), epidermal growth factor receptor 2 (HER-2), interleukin-13 receptor subunit alpha-2 (IL-13Ra2), with potential immunostimulatory and antineoplastic activities. Mononuclear cells obtained via leukapheresis are differentiated into DCs, and pulsed with the GBM-associated peptides. Upon administration, multi-glioblastoma-peptide-targeting autologous DC vaccine ICT-107 exposes the immune system to GBM-associated antigens, which activates a specific cytotoxic T-lymphocyte (CTL) response against GBM cells. This leads to GBM cell lysis. The six peptides are derived from tumor associated antigens (TAA) expressed on GBM cells and cancer stem cells (CSCs). GBM stem-like cells contain a specific range of antigens that are essential for the neoplastic growth and survival of GBM cells.","Cell|Pharmacologic Substance"]
["C90553","Multikinase Inhibitor 4SC-203","4SC-203|Multikinase Inhibitor 4SC-203","A multikinase inhibitor with potential antineoplastic activity. Multikinase inhibitor 4SC-203 selectively inhibits FMS-related tyrosine kinase 3 (FLT3/STK1), FLT3 mutated forms, and vascular endothelial growth factor receptors (VEGFRs). This may result in the inhibition of angiogenesis and cell proliferation in tumor cells in which these kinases are upregulated. FLT3 (FLK2), a class III tyrosine kinase receptor, is overexpressed or mutated in most B lineage and acute myeloid leukemias (AML). VEGFRs, tyrosine kinase receptors, are overexpressed in a variety of tumor cell types and play key roles in angiogenesis.","Pharmacologic Substance"]
["C85481","Multikinase Inhibitor ARRY614","ARRY-614|Multikinase Inhibitor ARRY614","An orally bioavailable small-molecule inhibitor of p38 and Tie2 kinases with potential antineoplastic, anti-inflammatory and antiangiogenic activities. p38/Tie2 kinase inhibitor Arry-614 binds to and inhibits the activities of p38 and Tie2 kinases, which may inhibit the production of proinflammatory cytokines and may decrease tumor angiogenesis and tumor cell growth and survival. p38 is a MAP kinase that is often upregulated in cancer cells, playing a crucial part in the production of a variety of cytokines involved in inflammation and cellular proliferation such as tumor necrosis factor (TNF) and interleukin (IL)-1 and -6. Tie2 is an endothelial cell specific receptor that is activated by angiopoietins, growth factors required for angiogenesis. This agent has also been reported to inhibit other kinases including vascular endothelial growth factor receptor (VEGFR2) and Src tyrosine kinases.","Pharmacologic Substance"]
["C66947","Multikinase Inhibitor AT9283","AT9283|Aurora kinase inhibitor AT9283|Multikinase Inhibitor AT9283","A small synthetic molecule and aurora kinase (AK) inhibitor with potential antineoplastic activity. AT9283 selectively binds to and inhibits AKs A and B, which are serine-threonine kinases that play essential roles in mitotic checkpoint control during mitosis. Inhibition of these kinases results in an inhibition of cellular division and proliferation in tumor cells that overexpress AKs.","Pharmacologic Substance"]
["C88278","Multikinase Inhibitor SAR103168","Multikinase Inhibitor SAR103168|SAR103168","A multikinase inhibitor with potential antineoplastic activity. Upon intravenous infusion, multikinase inhibitor SAR103168 may, through the inhibition of multiple kinases, inhibit the phosphorylation and activation of signal transducer and activator of transcription 5 (STAT5). STAT5, a protein often upregulated in cancer cells, plays a key role in signal transduction pathways and the suppression of apoptosis.","Pharmacologic Substance"]
["C111036","Multi-peptide CMV-Modified Vaccinia Ankara Vaccine","CMV-MVA Triplex Vaccine|Multi-peptide CMV-Modified Vaccinia Ankara Vaccine","A vaccine consisting of an inactivated, Modified Vaccinia Ankara (MVA) viral vector encoding three herpes virus cytomegalovirus (CMV) tumor-associated antigens (TAAs), including UL83 (pp65), UL123 (IE1) and UL122 (IE2), with potential immunostimulating activity. The viral peptides expressed after administration of the multi-peptide CMV-MVA vaccine, may stimulate the immune system to mount both cytotoxic T-lymphocyte (CTL) and helper T-cell responses against CMV-infected cells. This results in cell lysis and prevents viral replication and the development of CMV disease. This vaccine also provides active immunization and protective immunity against CMV infection in CMV-negative patients. CMV infection can cause serious complications in patients receiving either allogeneic hematopoietic cell transplants (HCT) or solid organ transplants.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C125692","Multipeptide Vaccine S-588210","Multipeptide Vaccine S-588210|S-488210/S-488211|S-588210","A cancer vaccine composed of a combination of the injectable formulations S-488210, which contains the three HLA-A*02:01-restricted peptides up-regulated lung cancer 10 (lymphocyte antigen 6K; LY6K; URLC10), cell division cycle-associated protein 1 (kinetochore protein Nuf2; NUF2; CDCA1) and insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3; KOC1) and S-488211, which contains the two HLA-A*02:01-restricted peptides DEP domain-containing protein 1A (DEPDC1) and M-phase phosphoprotein 1 (kinesin-like protein KIF20B; MPHOSPH1), with potential immunostimulatory and antitumor activities. Upon administration, multipeptide vaccine S-588210 may stimulate a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing KOC1, CDCA1, URLC10, DEPDC1 or MPHOSPH1 peptides, resulting in tumor cell lysis and decreased tumor growth.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C97509","Multi-subtype Natural Human Leukocyte Interferon Alpha","Multi-subtype Natural Human Leukocyte Interferon Alpha|Multiferon|Multisubtype Natural Human Interferon Alpha","A preparation containing a mixture of multiple naturally occurring, active subtypes 1, 2, 8, 10, 14 and 21 of interferon alpha (IFN-alpha) with immunomodulating, anti-viral and anti-cancer activities. Multi-subtype natural human leukocyte IFN-alpha is purified from the leukocyte fraction of human blood challenged with Sendai virus. Upon administration, IFN-alpha subtypes bind to cell surface IFN-alpha receptors (IFNARs), resulting in an upregulation of interferon stimulated genes and related protein products. This ultimately leads to the proliferation of human B cells, activation of natural killer (NK) cells and dendritic cells (DCs), an increase in HLA-I and HLA-II expression and activation of CD8-lymphocytes. Compared to single-subtype IFN, multi-subtypes act synergistically.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77866","Multitargeted Tyrosine Kinase Inhibitor JNJ-26483327","JNJ-26483327|Multitargeted Tyrosine Kinase Inhibitor JNJ-26483327|TKI JNJ-26483327","An orally bioavailable, small-molecule, multitargeted reversible tyrosine kinase inhibitor with potential antineoplastic activity. Multitargeted tyrosine kinase inhibitor JNJ-26483327 binds to and inhibits several members of the epidermal growth factor receptor (EGFR) family, including EGFR, HER2 and HER4; Src family kinases (Lyn, Yes, Fyn, Lck and Src); and vascular endothelial growth factor receptor type 3 (VEGFR3). By inhibiting several different signaling molecules that play crucial roles at various stages in tumorigenesis, this agent may inhibit tumor growth, invasion, migration and metastasis. In addition, JNJ-26483327 crosses the blood-brain barrier (BBB).","Organic Chemical|Pharmacologic Substance"]
["C2234","Mureletecan","MAG-CPT|MAG-Camptothecin|MURELETECAN|Mureletecan|PNU 166148|PNU166148","A water-soluble prodrug, consisting of camptothecin covalently linked to polymeric backbone methacryloylglycynamide, with potential antineoplastic activity. After entering tumor cells, the active moiety camptothecin is slowly released from mureletecan via hydrolysis of the ester linkage. Camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, binds to and stabilizes the topoisomerase I-DNA covalent complex. This inhibits the religation of topoisomerase I-mediated single-stranded DNA breaks and produces potentially lethal double-stranded DNA breaks when encountered by the DNA replication machinery, resulting in the inhibition of DNA replication and apoptosis. Compared to camtpothecin, this prodrug formulation increases camptothecin drug delivery to the tumor site while reducing systemic toxicity.","Organic Chemical|Pharmacologic Substance"]
["C77877","Murine TYRP2 Plasmid DNA Vaccine","Murine TYRP2 Plasmid DNA Vaccine","A plasmid DNA vaccine encoding the mouse tumor associated antigen tyrosinase-related protein-2 (TYRP2) with potential immunostimulating and antineoplastic activities. Upon administration, murine TYRP2 plasmid DNA vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing TYRP2; this vaccine may also induce an immune response against tyrosinase-related protein-1 (TYRP1). TYRP2 and TYRP1, melanosomal membrane glycoproteins upregulated in melanoma cells, are involved in melanin synthesis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C96231","Muscadine Grape Skin Extract","MSKE|Muscadine Grape Skin Extract","A nutritional supplement containing an extract of the skin of Muscadine grape (Vitis rotundifolia), with anti-inflammatory, antioxidant and potential chemopreventive activities. The skin extract of the muscadine grape contains numerous phytochemicals including hydrolyzable tannins and flavonoids, such as anthocyanin 3,5-diglucosides, quercetin, myricetin, and kaempferol glycosides. Upon administration, muscadine grape skin extract (MSKE) appears to inhibit PI3K/Akt and MAPK signaling, eventually leading to apoptosis and a reduction in tumor cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C121951","Mutant p53 Activator COTI-2","COTI2|Coti-2|Mutant p53 Activator COTI-2","An orally available third generation thiosemicarbazone and activator of mutant forms of the p53 protein, with potential antineoplastic activity. Upon oral administration, mutant p53 activator COTI-2 targets and binds to the misfolded mutant forms of the p53 protein, which induces a conformational change that normalizes p53 and restores its activity. This induces apoptosis in tumor cells in which the p53 protein is mutated. In addition, COTI-2 inhibits the activation of Akt2 and prevents the activation of the PI3K/AKT/mTOR pathway, thereby inducing apoptosis in cancer cells in which this pathway is overexpressed. p53, a tumor suppressor protein, plays a key role in controlling cellular proliferation and survival. High levels of mutant p53 are seen in many cancers and are associated with uncontrolled cellular growth.","Pharmacologic Substance"]
["C2540","Mutant p53 Peptide Pulsed Dendritic Cell Vaccine","Mutant p53 Peptide Pulsed Dendritic Cell Vaccine|dendritic cell vaccine, mutant p53 peptide pulsed|mutant p53 peptide pulsed DC vaccine","A cancer vaccine consisting of autologous dendritic cells which have been pulsed with a mutant p53 peptide. Vaccination with mutant p53 peptide pulsed dendritic cells may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing mutant p53, resulting in tumor cell lysis. Many tumor cells overexpress mutant p53 proteins, resulting in the loss of apoptosis regulation and abnormal cell proliferation. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C119624","Mutant-selective EGFR Inhibitor PF-06459988","Mutant-selective EGFR Inhibitor PF-06459988|PF-06459988","An orally available, small molecule, third-generation, irreversible inhibitor of epidermal growth factor receptor (EGFR) mutant (EGFRm) forms with potential antineoplastic activity. EGFR inhibitor PF-06459988 specifically binds to and inhibits mutant forms of EGFR, including the secondary acquired resistance mutation T790M, which prevents EGFR-mediated signaling and leads to cell death in EGFRm-expressing tumor cells. Compared to some other EGFR inhibitors, PF-06459988 may have therapeutic benefits in tumors with T790M-mediated drug resistance. This agent shows minimal activity against wild-type EGFR (WT EGFR), and does not cause dose-limiting toxicities that are seen with the use of non-selective EGFR inhibitors, which also inhibit WT EGFR. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.","Pharmacologic Substance"]
["C91076","MVA-EBNA1/LMP2 Vaccine","MVA-EBNA1/LMP2 Vaccine","A cancer vaccine consisting of a recombinant modified vaccinia Ankara (MVA) viral vector encoding the gene for the CD4 epitope-rich C-terminal domain of the Epstein Barr Virus (EBV) antigen EBNA1 and fused to the full-length of the EBV-associated antigen latent membrane protein 2 (LMP2), with potential immunostimulatory and antineoplastic activities. Upon administration, MVA EBNA1/LMP2 vaccine may elicit a cytotoxic T-cell immune response against cancer cells expressing EBNA1 and LMP2. Multi-antigen vaccine therapy may be more efficacious than single-antigen therapy vaccine therapy. EBNA1, a sequence-specific DNA binding protein, plays an important role in EBV episomal genome maintenance and gene transactivation.","Immunologic Factor|Pharmacologic Substance"]
["C88279","MVA-FCU1 TG4023","MVA-FCU1 TG4023|Modified Ankara Virus-Mediated Suicide Gene Delivery Vector TG4023|TG4023","A cancer vaccine comprised of a recombinant modified vaccinia Ankara (MVA) viral vector encoding the suicide gene FCU1 with potential antineoplastic activity. FCU1 is a bifunctional yeast cytosine deaminase (CD) / uracil phosphoribosyltransferase (UPRT) fusion gene. Upon intratumoral administration, MVA-FCU1TG4023 enters tumor cells where FCU1 is expressed. Subsequently, the noncytotoxic prodrug 5-fluorocytosine (5-FC) is administered systemically and is deaminated by CD in FCU1- transduced tumor cells into 5-fluorouracil (5-FU), which is then directly metabolized to 5-fluoro-uridine monophosphate (5-FUMP) by UPRT; 5-FUMP may then be further transformed to 5-fluoro-deoxyuridine monophosphate (5-FdUMP), an irreversible inhibitor of thymidylate synthase and, so, DNA synthesis through deprivation of deoxythymidine triphosphate (dTTP). 5-FU and its active metabolites may then selectively kill tumor cells, avoiding toxicity in nonmalignant cells. The MVA viral vector, derived from the replication-competent strain Ankara, is a highly attenuated, replication-defective vaccinia strain incapable of virion assembly.","Pharmacologic Substance"]
["C2241","MVA-MUC1-IL2 Vaccine","MVA-MUC1-IL2 Vaccine|MVA-MUC1-IL2|Modified Vaccinia Ankara Encoding Human MUC-1 Antigen and Interleukin-2 Suspension|TG4010","A bivalent cancer vaccine comprised of a modified vaccinia virus Ankara (MVA) strain encoding human mucin 1 (MUC1) and interleukin-2 (IL-2) with potential immunostimulating and antineoplastic activities. Originally developed for the eradication of smallpox, MVA is a highly attenuated and replication-defective strain incapable of virion assembly and exerts potent immunostimulatory activity against antigens. Vaccination with MVA-MUC1-IL2 vaccine may stimulate the host immune system to mount a humoral and cytotoxic T lymphocyte (CTL) responses against tumor cells expressing MUC1, a tumor associated antigen, resulting in tumor cell lysis. Expression of IL-2 augments the specific CTL response against MUC1 expressing cells.","Immunologic Factor|Pharmacologic Substance"]
["C74064","MVA-PSA/PAP Prostate Cancer Vaccine","MVA-BN-PRO|MVA-PSA/PAP Prostate Cancer Vaccine|Modified Vaccinia Ankara (Bavarian Nordic) Prostate Cancer Vaccine","A cancer vaccine consisting of a recombinant modified vaccinia Ankara (MVA) viral vector encoding genes for prostate specific antigen (PSA) and prostate acid phosphatase (PAP) with potential immunostimulatory and antineoplastic activities. Upon administration, MVA-PSA-PAP prostate cancer vaccine expresses PSA and PAP peptides, which may elicit humoral and cellular immune responses against prostate cancer cells expressing PSA and PAP. Multi-antigen vaccine therapy may be more efficacious than single-antigen therapy vaccine therapy.","Pharmacologic Substance"]
["C97344","MVF-HER-2(597-626)/MVF-HER-2 (266-296) Peptide Vaccine","MVF-HER-2(597-626)/MVF-HER-2 (266-296) Peptide Vaccine","A combination peptide vaccine of 2 chimeric peptides of the promiscuous T cell epitope derived from measles virus fusion protein (MVF; amino acid residues 288-302) co-synthesized with B-cell epitopes derived from the HER-2/neu a.a. 597-626 and HER-2/neu a.a. 266-296, with potential antineoplastic activity. Vaccination with MVF-HER-2(597-626)/MVF-HER-2(266-296) peptide vaccine may be capable of inducing an active specific immune response, mounting a cytotoxic T-lymphocyte (CTL) response and an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells that overexpress the HER-2 protein. The oncogenic protein HER-2, a member of the human epidermal growth factor receptor (EGFR) family of tyrosine kinases, is overexpressed in a variety of cancers and is correlated with increased tumor growth, progression and a poor prognosis. HER-2(597-626) corresponds to the binding site of trastuzumab on the extracellular domain IV of HER-2; HER-2 (266-296) corresponds to the binding site of pertuzumab on the dimerization loop of domain II of HER-2.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2637","MVF-HER-2(628-647)-CRL 1005 Vaccine","MVF-HER-2(628-647)-CRL 1005 Vaccine","A chimeric peptide immunogen of human epidermal growth factor-2 (HER-2) with antineoplastic property. HER-2 protein is a receptor tyrosine kinase and a tumor-associated antigen (TAA) that is overexpressed in a variety of cancers. MVF-HER-2(628-647)-CRL 1005 vaccine, coated with poloxamer CRL-1005 to form microparticles, consists of a mutated HER-2 B-cell epitope, HER-2(628-647), and a promiscuous T cell epitope (amino acid sequence 288-302) of the measles virus fusion protein (MVF). Vaccination with this immunogen may stimulate the host immune response to mount a cytotoxic T-lymphocyte response against tumor cells that overexpress the HER2 protein, resulting in tumor cell lysis.","Immunologic Factor|Pharmacologic Substance"]
["C123382","MVX-1-loaded Macrocapsule/autologous Tumor Cell Vaccine MVX-ONCO-1","MVX-1-loaded Macrocapsule/autologous Tumor Cell Vaccine MVX-ONCO-1|MVX-ONCO-1","A two-component, anti-cancer vaccine containing irradiated tumor cells from a patient, and a capsule implanted with a genetically modified allogeneic cell line that continuously releases granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immune-protective and -boosting activities. Upon subcutaneous injection of MVX-1-loaded macrocapsule/autologous tumor cell vaccine MVX-ONCO-1, the GM-CSF-secreting allogeneic cell capsules and the autologous irradiated cells isolated from the patient's tumor are co-localized in the patient's tissue. This permits the production of GM-CSF and exposes the immune system to the tumor-associated antigens (TAA) expressed by the autologous tumor cells at the injection site. Local expression of GM-CSF recruits and activates antigen-presenting cells (APC), which induces both antibody-dependent cell-mediated cytotoxicity (ADCC) and cytotoxic T-lymphocyte responses at the site of the injection and systemically. This may lead to tumor regression. By using the patient's own irradiated cancer cells as vaccine antigens, the patient's immune system is exposed to the entire repertoire of this individual's TAAs. The encapsulated cell technology (ECT) of GM-CSF-secreting allogeneic cell capsules ensures the continuous release of GM-CSF. GM-CSF, a monomeric glycoprotein that functions as a cytokine, is a strong immune booster and plays an important role in the activation of immune system.","Immunologic Factor|Pharmacologic Substance"]
["C64765","Mycobacterial Cell Wall-DNA Complex","MCC|Mycobacterial Cell Wall-DNA Complex","A proprietary preparation of mycobacterial DNA oligonucleotides embedded in mycobacterial cell wall fragments derived from cultures of Mycobacterium phlei, with potential immunomodulatory and antineoplastic activities. DNA oligonucleotides in the mycobacterial cell wall-DNA complex (MCC) are capable of inducing apoptosis by increasing BAX protein levels, releasing cytochrome C from mitochondria, and activating caspase-3 and -7. This leads to the cleavage of poly (ADP-ribose) polymerase and the release of nuclear matrix proteins (NuMA). In addition to its pro-apoptotic effect, MCC activates monocytes and macrophages to produce various cytokines, including interleukin 6 (IL-6), IL-8, IL-12, IL-18, and tumor necrosis factor alpha (TNF-a). This leads to an activation of natural killer cells and cytotoxic T lymphocytes and to interferon gamma (INF-g) synthesis, thereby attaining an anti-angiogenic effect.","Bacterium|Pharmacologic Substance"]
["C118445","Mycobacterium tuberculosis Arabinomannan Z-100","Mycobacterium tuberculosis Arabinomannan Z-100|Z-100","An extract from Mycobacterium tuberculosis (M. tuberculosis) containing the polysaccharide arabinomannan, with potential immunostimulating activity. Upon administration of M. tuberculosis arabinomannan Z-100, this agent may activate the immune system by increasing the expression of various cytokines, such as interferon-gamma (IFNg) and interleukin-12. This inhibits the activity of suppressor T-cells, increases T helper 1 cell (Th1) activity and may restore the balance between Th1/Th2 cells. Additionally, Z-100 may inhibit metastasis and tumor cell proliferation.","Pharmacologic Substance"]
["C70969","Mycobacterium w","Immuvac|Mycobacterium w","An attenuated strain of Mycobacterium w, a non-pathogenic, rapidly growing, atypical mycobacterium, with non-specific immunopotentiating properties. In addition to sharing a number of common B and T cell determinants with Mycobacterium leprae and Mycobacterium tuberculosis, Mycobacterium w (Mw) also shares an immunogenic determinant with prostate specific antigen (PSA). In vitro and in vivo studies have shown that heat-killed Mw can induce significant T-cell responses. This agent may induce host T-cell responses against tumor cells expressing PSA. PSA is a glycoprotein secreted by prostatic epithelial and ductal cells and may be overexpressed in prostate cancer cells.","Bacterium|Immunologic Factor"]
["C673","Mycophenolic Acid","4-Hexenoic acid, 6-(1,3-dihydro-4-hydroxy-6-methoxy-7-methyl-3-oxo-5-isobenzofuranyl)-4-methyl-, (E)-|4-Hexenoic acid, 6-(4-hydroxy-6-methoxy-7-methyl-3-oxo-5-phthalanyl)-4-methyl-, (E)-|Acide mycophenolique|Acido micofenolico|Acidum mycophenolicum|Lilly-68618|Ly 68618|MPA|MYCOPHENOLIC ACID|Mycophenolic Acid|Myfortic","An antineoplastic antibiotic derived from various Penicillium fungal species.  Mycophenolic acid is an active metabolite of the prodrug mycophenolate mofetil.  Mycophenolic acid inhibits inosine monophosphate dehydrogenase (IMPDH), preventing the formation of guanosine monophosphate and synthesis of lymphocyte DNA that results in inhibition of lymphocyte proliferation, antibody production, cellular adhesion, and migration of T and B lymphocytes.  Mycophenolic acid also has antibacterial, antifungal, and antiviral activities. (NCI04)","Antibiotic|Organic Chemical"]
["C115108","MYC-targeting siRNA DCR-MYC","DCR-M1711|DCR-MYC|MYC-targeting siRNA DCR-MYC","A lipid nanoparticle-based formulation consisting of small-interfering RNAs (siRNAs) directed against the oncogene c-Myc encapsulated in lipids with potential antineoplastic activity. Upon intravenous administration of MYC-targeting siRNA DCR-MYC, the lipid formulation promotes the uptake by tumor cells where the siRNAs moieties are subsequently released. The siRNAs bind to c-Myc mRNAs, which may result in the inhibition of translation and expression of the c-Myc protein and leads to growth inhibition for tumor cells that are overexpressing c-Myc. c-Myc, a proto-oncogene overexpressed in a variety of cancers, is involved in cellular proliferation, differentiation, and apoptosis.","Pharmacologic Substance"]
["C2782","Myeloma Ig Id-KLH Conjugate Vaccine","Id KLH Myeloma|Idiotype KLH Myeloma Vaccine|Myeloma Ig Id-KLH Conjugate Vaccine","A vaccine consisting of myeloma-specific immunoglobulin conjugated to keyhole limpet hemocyanin (KLH), an immune stimulant, with potential antineoplastic activity.  Vaccination with myeloma Ig Id-KLH conjugate vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against myeloma cells, resulting in decreased tumor growth. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C44168","N-(5-tert-butyl-3-isoxazolyl)-N-(4-(4-pyridinyl)oxyphenyl) Urea","N-(5-tert-butyl-3-isoxazolyl)-N-(4-(4-pyridinyl)oxyphenyl) Urea|N-(5-tert-butyl-3-isoxazolyl)-N-(4-(4-pyridinyl)oxyphenyl)urea","An orally available isoxazole urea with potential anti-tumor activity.  In preclinical trials, N-(5-tert-butyl-3-isoxazolyl)-N-(4-(4-pyridinyl)oxyphenyl)urea inhibited raf kinase, an enzyme capable of reversing the phenotype of ras-transformed cells and blocking tumor growth. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C2084","N,N-Dibenzyl Daunomycin","N,N-Dibenzyl Daunomycin|N,N-dibenzyl daunorubicin|N,N-dibenzyldaunomycin|N,N-dibenzyldaunorubicin","The N-alkylated analogue of the anthracycline antineoplastic antibiotic daunomycin.  N,N-Dibenzyl Daunomycin interacts with topoisomerase II, thereby inhibiting DNA replication and repair and promoting DNA fragmentation.  This agent is less cardiotoxic than daunomycin. (NCI04)","Antibiotic|Organic Chemical"]
["C2680","NA17.A2 Peptide Vaccine","NA17.A2 Peptide Vaccine|NA17.A2","A peptide cancer vaccine comprised of human leukocyte antigen HLA-A2-restricted peptide derived from a metastatic melanoma cell line of patient NA17, with potential immunomodulating and antineoplastic activity. NA17.A2 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumors that express this antigen, which may result in a reduction in tumor size. This NA17 specific antigen, encoded by an intron sequence of N-acetylglucosaminyltransferase V (GnT-V) gene, is expressed in about 50% of melanomas.","Amino Acid, Peptide, or Protein"]
["C96042","NA-17/MAGE-3.A2/NY-ESO-1 Peptide Vaccine","NA-17/MAGE-3.A2/NY-ESO-1 Peptide Vaccine","A peptide cancer vaccine consisting of peptides derived from the melanoma antigen NA-17, the human leukocyte antigen HLA-A2-restricted human melanoma antigen 3 (MAGE-3.A2) and the cancer-testis antigen (NY-ESO-1), with potential immunostimulating and antineoplastic activities. Upon administration, the NA-17/MAGE-3.A2/NY-ESO-1 peptide vaccine may stimulate the immune system to mount a cytotoxic T-cell (CTL) response against tumor cells expressing NA-17, MAGE-3.A2 and NY-ESO-1, resulting in tumor cell lysis. The tumor-associated antigens (TAAs) NA-17, MAGE-3.A2 and NY-ESO-1 are overexpressed in a variety of cancer cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C37450","NA17-A Antigen","NA17-A Antigen|NA17-A","A specific melanoma antigen protein derived from a patient (NA17) with cutaneous melanoma metastases. When administered in a vaccine formulation, NA17-A antigen may stimulate a cytotoxic T lymphocyte (CTL) response against tumors that express this antigen, which may result in a reduction in tumor size. The NA17-A antigen is part of the enzyme N-acetyl glucosaminyltransferase V (GnT-V). Approximately half of melanomas have been found to express significant levels of this atypical protein, which is not expressed by normal tissues.","Immunologic Factor"]
["C131213","Nab-paclitaxel/Rituximab-coated Nanoparticle AR160","AR160|Abraxane Coated with Rituximab 160nm Nanoparticle|Abraxane coated with Rituximab|Abraxane/Rituxan 160 Complex|Nab-paclitaxel/Rituximab-coated Nanoparticle AR160","A formulation composed of nanoparticle albumin-bound (nab) paclitaxel, which is an albumin-stabilized nanoparticle containing the natural taxane paclitaxel, non-covalently coated with rituximab, a recombinant chimeric murine/human antibody directed against the CD20 antigen found on B-lymphocytes, with potential antineoplastic activity. Upon administration of nab-paclitaxel/rituximab nanoparticle AR160, the rituximab moiety specifically binds to CD20 and targets this formulation to CD20-positive tumor cells. Paclitaxel binds to and stabilizes microtubules, which prevents depolymerization and inhibits cellular motility, mitosis, and replication. This leads to cell death of the CD20-expressing tumor cells that were targeted by this agent. The combination of albumin-stabilization and rituximab-targeting allows for higher efficacy and decreased paclitaxel-induced toxicity as it specifically targets CD20-expressing tumor cells. Rituximab may also induce complement-dependent cytotoxicity and antibody-dependent cellular toxicity.","Pharmacologic Substance"]
["C83981","Namirotene","NAMIROTENE|Namirotene","A synthetic analogue of retinoic acid with differentiation inducing and potential antineoplastic activities. Like other retinoic acid agents, namirotene binds to and activates retinoic acid receptors (RARs), thereby altering the expression of certain genes leading to cell differentiation and decreased cell proliferation in susceptible cells.","Pharmacologic Substance"]
["C72594","Nanafrocin","(1S,3R)-3,4,5,10-Tetrahydro-9-hydroxy-1-methyl-5,10-dioxo-1H-naphtho[2,3-c]pyran-3-acetic Acid|NANAFROCIN|Nanafrocin|Nanaomycin A|OS 3966-A","A quinone antibiotic isolated from Streptomyces rosa var. notoensis with activity against gram-positive bacteria, mycoplasmas and fungi. Within an organism, nanaomycin A is first reduced by flavin or NADH dehydrogenase then rapidly autooxidized leading to the production of singlet molecular oxygen (O2-). The increase in intracellular O2- results in inhibition of DNA, RNA and cell-wall peptidoglycan synthesis. Further, nanaomycin A may have antineoplastic properties resulting from a reduction in DNA methylation by inhibiting DNA methyltransferase 3B (DNMT3B) and reactivating the tumor suppressor gene RASSF1A.","Pharmacologic Substance"]
["C121214","Nanocell-encapsulated miR-16-based microRNA Mimic","Nanocell-encapsulated miR-16-based microRNA Mimic|TargomiRs","A nanoparticle-based formulation composed of a microRNA 16 (miR-16) mimic, a double-stranded, 23 base pair, synthetic RNA molecule, encapsulated in nonliving bacterial minicells and coated with anti-epidermal growth factor receptor (EGFR) antibodies, with potential antineoplastic activity. Upon intravenous administration and subsequent transfection, nanocell-encapsulated miR-16-based microRNA mimic targets EGFR-expressing tumor cells and facilitates the restoration of expression of the miR-16 family. This leads to the downregulation of the expression of tumor promoting genes and the inhibition of tumor cell growth. In addition, restoration of miR-16 expression sensitizes the tumor cell to certain chemotherapeutic agents. miR-16, a family of microRNAs, is critical to the regulation of gene expression and appears to have a tumor suppressor function; its expression is downregulated in various cancer cell types.","Pharmacologic Substance"]
["C71696","Nanoparticle Albumin-Bound Docetaxel","ABI-008|Nab-Docetaxel|Nanoparticle Albumin-Bound Docetaxel","A nanoparticle albumin-bound formulation of the taxane docetaxel with antineoplastic activity. Docetaxel is a semi-synthetic, second-generation taxane derived from a compound found in the European yew tree Taxus baccata. Docetaxel binds to and stabilizes tubulin, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and cell death. This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and displays immunomodulatory and pro-inflammatory properties by inducing various mediators of the inflammatory response. This nanoparticle albumin-bound formulation solubilizes docetaxel without the use of the nonionic solubilizer Cremophor ELP, permitting the administration of larger doses of docetaxel while avoiding Cremophor ELP-associated toxicity.","Pharmacologic Substance"]
["C74065","Nanoparticle Albumin-Bound Rapamycin","ABI-009|Nab-Rapamycin|Nanoparticle Albumin-Bound Rapamycin","The macrolide antibiotic rapamycin bound to nanoparticle albumin with immunosuppressant (see sirolimus) and potential antiangiogenic and antineoplastic activities. Rapamycin binds to the immunophilin FK Binding Protein-12 (FKBP-12) to generate a complex that binds to and inhibits the activation of the mammalian Target Of Rapamycin (mTOR), a key regulatory kinase. In turn, inhibition of mTOR may result in the inhibition of the phosphatidylinositol 3 (PI-3) kinase/Akt pathway and vascular endothelial cell growth factor (VEGF) secretion, which may result in decreased tumor cell proliferation and tumor angiogenesis. The binding of water-insoluble rapamycin to nanoparticle albumin permits the albumin-mediated endocytosis of rapamycin by tumor cells and endothelial cells.","Pharmacologic Substance"]
["C116890","Nanoparticle Albumin-bound Thiocolchicine Dimer nab-5404","ABI-011|IDN 5404|NTB-011|Nanoparticle Albumin-bound Thiocolchicine Dimer nab-5404|nab-5404|nab-Thiocolchicine Dimer","A nanoparticle albumin-bound formulation of a thiocolchicine dimer, an inhibitor of both microtubule and topoisomerase I (TOP1), with antineoplastic and vascular disrupting activities. Upon administration of nanoparticle albumin-bound thiocolchicine dimer nab-5404, this agent binds to tubulin and inhibits its polymerization, which blocks mitotic spindle formation and leads to cell cycle arrest and tumor endothelial cell apoptosis. This disrupts the tumor vasculature and leads to tumor necrosis. In addition, nab-5404 binds to topoisomerase I (TOPI) and inhibits its activity. This results in the inhibition of the repair of single-strand DNA breaks, DNA replication, and tumor cell growth in susceptible tumor cell populations. The nanoparticle albumin-based formulation permits the albumin-mediated endocytosis of the thiocolchicine dimer by tumor cells and endothelial cells.","Pharmacologic Substance"]
["C121961","Nanoparticle-encapsulated Docetaxel","CriPec (R) Docetaxel|Nanoparticle-encapsulated Docetaxel","A nanoparticle-based formulation containing the poorly water-soluble, second-generation taxane analog docetaxel covalently conjugated to proprietary and as of yet undisclosed degradable linkers and encapsulated in polymers, with antineoplastic activity. Upon intravenous administration of nanoparticle-encapsulated docetaxel, the nanoparticles are able to accumulate at the tumor site due to the unique characteristics of the tumor's vasculature, while avoiding normal, healthy tissue. Docetaxel is released and becomes active upon cleavage from various linkers at a predetermined and controlled rate which is dependent on the properties of the proprietary linkers. In turn, active, unconjugated docetaxel binds to the beta-subunit of tubulin, stabilizes microtubules and inhibits microtubule disassembly. This prevents mitosis and results in tumor cell death. Compared to the administration of docetaxel alone, this formulation is able to increase docetaxel's efficacy while avoiding systemic exposure, which minimizes its toxicity. By using different linkers, docetaxel can be released at various rates.","Organic Chemical|Pharmacologic Substance"]
["C102875","Nanoparticle-encapsulated Doxorubicin Hydrochloride","BA-003|Doxorubicin Transdrug|Livatag|Nanoparticle-encapsulated Doxorubicin Hydrochloride","A formulation of nanoparticles encapsulating the hydrochloride salt form of the anthracycline antibiotic doxorubicin, with potential antitumor activity. Upon intravenous administration, doxorubicin intercalates DNA, interferes with the activity of topoisomerase II, and causes DNA adducts and other DNA damage, resulting in tumor cell growth inhibition and apoptosis. This agent also interacts with cell membrane lipids causing lipid peroxidation. Delivery of doxorubicin in nanoparticles may improve drug penetration into tumors and may circumvent the tumor cells multidrug resistance mechanisms and may therefore be effective in chemoresistant tumor cells.","Pharmacologic Substance"]
["C111570","Nanosomal Docetaxel Lipid Suspension","DTX-LNS|NDLS|Nanosomal Docetaxel Lipid Suspension","A lipid-based nanosomal formulation of the poorly soluble, semi-synthetic, second-generation taxane docetaxel, with potential antineoplastic activity. Upon intravenous injection, docetaxel binds to and stabilizes tubulin, which inhibits microtubule disassembly and results in both cell cycle arrest at the G2/M phase and cell death. This liposomal formulation solubilizes docetaxel without the use of toxic solvents, such as polysorbate 80. This permits the administration of larger doses of docetaxel and improves the drug's safety profile by avoiding solvent-associated toxicities, such as hypersensitivity reactions and neurotoxicity. In addition, the nanosomal lipid-based delivery of docetaxel improves drug penetration into tumors and decreases drug clearance, all of which prolong the duration of docetaxel's therapeutic effects.","Pharmacologic Substance"]
["C96429","Napabucasin","2-Acetylnaphtho(2,3-b)furan-4,9-dione|BB608|BBI-608|BBI608|NAPABUCASIN|Napabucasin","An orally available cancer cell stemness inhibitor with potential antineoplastic activity. Even though the exact target has yet to be fully elucidated, napabucasin appears to target and inhibit multiple pathways involved in cancer cell stemness. This may ultimately inhibit cancer stemness cell (CSC) growth as well as heterogeneous cancer cell growth. CSCs, self-replicating cells that are able to differentiate into heterogeneous cancer cells, appear to be responsible for the malignant growth, recurrence and resistance to conventional chemotherapies.","Pharmacologic Substance"]
["C102850","Naphthalimide Analogue UNBS5162","1-(2-(2-(Dimethylamino)ethyl)-1,3-dioxo-2,3-dihydro-1H-benzo[de]isoquinolin-5-yl)urea|Naphthalimide Analogue UNBS5162|UNBS5162","An amonafide (naphthalimide) derivative and pan-antagonist of chemokine ligand (CXCL) expression, with potential anti-angiogenic activity. Although UNBS5162 is a derivative of amonafide, this agent appears to have a different profile to that of amonafide and its exact mechanism of action remains to be fully elucidated. This agent seems to decrease the expression of various proangiogenic CXCL chemokines in vitro and may have synergistic effects with radiotherapy or chemotherapy. CXCLs are small cytokines in the CXC chemokine family that are overexpressed in certain cancers; CXCL-mediated signaling plays a key role in angiogenesis and tumor progression.","Pharmacologic Substance"]
["C95789","Naptumomab Estafenatox","NAPTUMOMAB ESTAFENATOX|Naptumomab Estafenatox","A recombinant fusion protein consisting of the antigen-binding fragment of a monoclonal antibody directed towards the tumor-associated oncofetal trophoblast glycoprotein antigen 5T4 attached to a mutated form of superantigen staphylococcal enterotoxin E (SEA/E-120), with immunomodulating and antineoplastic activities. The Fab moiety of naptumomab estafenatox binds to 5T4, an antigen expressed by various tumor cells. In turn, the superantigen binds to both major histocompatibility complex class II molecules and to the T-cell receptor beta chain, which results in a massive activation of T lymphocytes and induces a potent T-cell-mediated killing of tumor cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C91382","Narnatumab","Anti-RON Monoclonal Antibody IMC-RON8|IMC-RON8|NARNATUMAB|Narnatumab","A fully human monoclonal antibody against RON (recepteur d'origine nantais; macrophage stimulating 1 receptor), with potential antineoplastic activity. Anti-RON monoclonal antibody IMC-RON8 binds to RON, thereby preventing binding of its ligand hepatocyte growth factor-like protein (HGFL or macrophage-stimulating protein (MSP)). This may prevent RON receptor-mediated signaling and may prevent cellular proliferation in tumor cells overexpressing RON. RON, a receptor tyrosine kinase, is overexpressed in a variety of epithelial cancer cell types and plays an important role in cellular proliferation, migration and invasion.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77862","Natalizumab","AN100226|Antegren|Anti-VLA4|Anti-alph4 Integrin Monoclonal Antibody AN100226|NATALIZUMAB|Natalizumab|Tysabri","A humanized recombinant IgG4 monoclonal antibody directed against the alpha4 subunit of the integrins alpha4beta1and alpha4beta7 with immunomodulating, anti-inflammatory, and potential antineoplastic activities.  Natalizumab binds to the alpha4-subunit of alpha4beta1 and alpha4beta7 integrins expressed on the surface of all leukocytes except neutrophils, inhibiting the alpha4-mediated adhesion of leukocytes to counter-receptor(s) such as vascular cell adhesion molecule-1 (VCAM-1); natalizumab-mediated disruption of VCAM-1 binding by these integrins may prevent the transmigration of leukocytes across the endothelium into inflamed parenchymal tissue.  Integrins are cellular adhesion molecules (CAMs) that are upregulated in various types of cancer and some autoimmune diseases; alpha4beta1 integrin (VLA4) has been implicated in the survival of myeloma cells, possibly by mediating their adhesion to stromal cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C71159","Natural IFN-alpha OPC-18","Natural IFN-alpha OPC-18|OPC-18|nIFN-alpha OPC-18","A proprietary preparation of natural human interferon alpha (IFN alpha) with potential immunomodulatory and antineoplastic activities. Natural human interferon alpha OPC-18 binds to cell-surface IFN alpha receptors (IFNARs), resulting in the transcription and translation of genes whose products mediate antiviral, antiproliferative, and immune-modulating effects. IFN alpha is a type I interferon produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products and is the primary interferon produced by virus-induced leukocyte cultures. In addition to its pronounced antiviral activity, it activates NK cells.","Pharmacologic Substance"]
["C85466","Natural Killer Cells ZRx101","NK Cells ZRx101|Natural Killer Cells ZRx101","A population of activated, immortalized, interleukin-2 (IL-2)-dependent, cytotoxic natural killer (NK) cells with potential antitumor activity. Natural killer cells ZRx101 are derived from NK-92 cells, having been modified to target tumor-associated antigens (TAAs) upregulated in certain types of cancer. The NK-92 cell line was originally isolated from a patient with large granular lymphocytic (LGL) leukemia/lymphoma.","Cell|Pharmacologic Substance"]
["C64776","Navitoclax","A-855071.0|ABT-263|BcI-2 Family Protein Inhibitor ABT-263|NAVITOCLAX|Navitoclax|navitoclax","An orally active, synthetic small molecule and an antagonist of a subset of the B-cell leukemia 2 (Bcl-2) family of proteins with potential antineoplastic activity. Navitoclax selectively binds to apoptosis suppressor proteins Bcl-2, Bcl-XL, and Bcl-w, which are frequently overexpressed in a wide variety of cancers, including those of the lymph, breast, lung, prostate, and colon, and are linked to tumor drug resistance. Inhibition of these apoptosis suppressors prevents their binding to the apoptotic effectors Bax and Bak proteins, thereby triggering apoptotic processes in cells overexpressing Bcl-2, Bcl-XL, and Bcl-w. This eventually reduces tumor cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C111687","Navy Bean Powder","Navy Bean Powder","The powder form of the cooked navy bean with potential antioxidant and chemopreventive activities. Navy beans are rich in fiber, minerals, vitamins, and phytochemicals such as flavonoids and phytosterols. They appear to prevent carcinogenesis by inducing tumor cell apoptosis. Intake of navy bean powder may have a beneficial effect on intestinal microflora.","Pharmacologic Substance"]
["C123825","ncmtRNA Oligonucleotide Andes-1537","Andes-1537|ncmtRNA Oligonucleotide Andes-1537","A proprietary antisense oligonucleotide targeting a novel non-coding mitochondrial RNA (ncmtRNA), with potential antineoplastic activity. Upon administration, Andes-1537 binds to ncmtRNA, which is overexpressed in rapidly proliferating cells, such as cancer cells, and not expressed in resting cells. This may decrease the expression of the ncmtRNA, which may inhibit cell proliferation and eventually induce apoptosis in susceptible cancer cells. The proprietary mitochondrial RNA (mtRNA) belongs to the family of non-coding RNAs (ncRNA); it contains an inverted repeat (IR) of 815 nucleotides (nt), which can form a covalent link to the 5' end of the mitochondrial 16S ribosomal RNA (16S mtrRNA).","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C88281","Necitumumab","Anti-Epidermal Growth Factor Receptor Monoclonal Antibody IMC-11F8|IMC-11F8|Immunoglobulin G1, Anti-(Human Epidermal Growth Factor Receptor (Receptor Tyrosine-Protein Kinase ErbB-1, EC 2.7.10.1)); Human Monoclonal IMC-11F8 Gamma1 Heavy Chain (224-214')-Disulfide with Human Monoclonal IMC-11F8 Kappa Light Chain, Dimer (230- 230'':233-233'')-Bisdisulfide|NECITUMUMAB|Necitumumab|Portrazza","A fully human IgG1 monoclonal antibody directed against the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Necitumumab binds to and blocks the ligand binding site of EGFR, thereby preventing the activation and subsequent dimerization of the receptor. This may lead to an inhibition of EGFR-dependent downstream pathways and so inhibition of EGFR-dependent tumor cell proliferation and metastasis.  EGFR, a member of the epidermal growth factor family of extracellular protein ligands, may be overexpressed on the cell surfaces of various tumor cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C61099","Nedaplatin","(Glycolato-O,O')diammineplatinum(II)|254-S|CDGP|NDP|NEDAPLATIN|Nedaplatin|cis-Diammine(glucolato)platinum","A second-generation cisplatin analogue with antineoplastic activity. Containing a novel ring structure in which glycolate is bound to the platinum by a bidentate ligand, nedaplatin forms reactive platinum complexes that bind to nucelophillic groups in DNA, resulting in intrastrand and interstrand DNA cross-links, apoptosis and cell death. This agent appears to be less nephrotoxic and neurotoxic compared to both cisplatin and carboplatin.","Inorganic Chemical|Pharmacologic Substance"]
["C1704","Nelarabine","2-Amino, 6-Methoxypurine Arabinoside|2-Amino-6-methoxypurine arabinoside|2-Amino-9-beta-D-arabinofuranosyl-6-methoxy-9H-purine|506U78|Arranon|Compound 506U78|GW506U78|NELARABINE|Nelarabine|nelarabine","An arabinonucleoside antimetabolite with antineoplastic activity. Nelarabine is demethoxylated by adenosine deaminase to become biologically active 9-beta-D-arabinosylguanine (ara-G); ara-G incorporates into DNA, thereby inhibiting DNA synthesis and inducing an S phase-dependent apoptosis of tumor cells. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C117985","Nelipepimut-S","E75 Peptide|Human Receptor Tyrosine-Protein Kinase erbB-2 (Proto-Oncogene Neu, Tyrosine Kinase- type Cell Surface Receptor HER2, CD340)-(347-355)-Peptide|L-Leucine, L-lysyl-L-isoleucyl-L-phenylalanylglycyl-L-seryl-L-leucyl-L-alanyl-L- phenylalanyl-|NELIPEPIMUT-S|Nelipepimut S|Nelipepimut-S|NeuVax","A cancer vaccine comprised of a human leukocyte antigen (HLA) A2/A3 restricted HER2/neu (human epidermal growth factor receptor 2; ErbB2) nonapeptide derived from the extracellular domain of the HER2 protein, with potential immunomodulating and antineoplastic activities. Upon intradermal injection, nelipepimut-S may induce a specific cytotoxic T-lymphocyte (CTL) response against HER2/neu-expressing tumor cells. HER2/neu, a tumor-associated antigen and a member of the epidermal growth factor receptor family of tyrosine kinases, is overexpressed in various tumor cell types and plays a key role in tumorigenesis.","Immunologic Factor|Pharmacologic Substance"]
["C99228","Nelipepimut-S Plus GM-CSF Vaccine","E75 Plus GM-CSF|E75 Vaccine Plus GM-CSF|HLA A2/A3-Restricted HER-2/neu Peptide Vaccine Plus GM-CSF|Nelipepimut-S Plus GM-CSF Vaccine|Nelipepimut-S Plus Sargramostim|NeuVax Plus GM-CSF","A cancer peptide vaccine comprised of a human leukocyte antigen (HLA) A2/A3 restricted HER2/neu (ERBB2) peptide from the extracellular domain of the HER2 protein (E75 peptide) and combined with the immunoadjuvant granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential immunomodulating and antineoplastic activity. Upon intradermal injection, nelipepimut-S plus GM-CSF vaccine may induce a specific cytotoxic T-lymphocyte (CTL) response against HER2/neu-expressing tumor cell types. HER2/neu, a tumor-associated antigen and a member of the epidermal growth factor receptor family of tyrosine kinases, is overexpressed in various tumor cell types. GM-CSF potentiates the antitumor immune response.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C83999","Nemorubicin","NEMORUBICIN|Nemorubicin","A morpholinyl analogue of the anthracycline doxorubicin with antineoplastic activity. Nemorubicin is metabolized via the P450 CYP3A enzyme to a highly cytotoxic derivative. Unlike most anthracyclines, nemorubicin is a topoisomerase I inhibitor and appears to exert its effect through the nucleotide excision repair (NER) system. In addition, this agent does not show cross-resistance with other anthracyclines.","Pharmacologic Substance"]
["C84000","Nemorubicin Hydrochloride","5,12-Naphthacenedione, 7,8,9,10-Tetrahydro-6,8,11-Trihydroxy-8-(Hydroxyacetyl)-1-Methoxy-10-((2,3,6-Trideoxy-3-((2S)-2-Methoxy-4-Morpholinyl)-Alpha-L-Lyxo-Hexopyranosyl)Oxy)-, Hydrochloride, (8S,10S)-|NEMORUBICIN HYDROCHLORIDE|Nemorubicin Hydrochloride","The hydrochloride salt form of nemorubicin, a morpholinyl analogue of the anthracycline doxorubicin with antineoplastic activity. Nemorubicin is metabolized via the P450 CYP3A enzyme to a highly cytotoxic derivative. Unlike most anthracyclines, nemorubicin is a topoisomerase I inhibitor and appears to exert its effect through the nucleotide excision repair (NER) system. In addition, this agent does not show cross-resistance with other anthracyclines.","Pharmacologic Substance"]
["C118960","Neoantigen-based Glioblastoma Vaccine","NeoVax (TM) Glioblastoma Vaccine|Neoantigen-based Glioblastoma Vaccine|Personalized Neoantigen Glioblastoma Vaccine","A peptide-based, personalized glioblastoma cancer vaccine consisting of patient-specific glioblastoma derived immunogenic mutated epitopes (neoantigens), with potential immunomodulating and antineoplastic activities. Vaccination with the neoantigen-based glioblastoma vaccine stimulates the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis. Neoantigens are tumor-specific antigens derived from mutated proteins that are present only in a specific tumor.","Immunologic Factor|Pharmacologic Substance"]
["C112003","Neoantigen-based Melanoma-Poly-ICLC Vaccine","NeoVax Melanoma Vaccine|Neoantigen-based Melanoma-Poly-ICLC Vaccine","A peptide-based melanoma cancer vaccine consisting of neoantigens and peptides derived from patient-specific melanoma immunogenic epitopes, combined with the immunostimulant poly-ICLC with potential immunomodulating and antineoplastic activities. Vaccination with the neoantigen-based melanoma vaccine stimulates the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis. The adjuvant poly-ICLC, composed of double-stranded RNA molecules of polyinosinic-polycytidylic acid stabilized with poly L-lysine in carboxymethylcellulose, is a ligand for toll-like receptor-3 (TLR3) and induces the release of cytokines which may help to boost the immune response against the selected neoantigens.","Immunologic Factor|Pharmacologic Substance"]
["C49094","Neratinib","HKI-272|NERATINIB|Neratinib","An orally available, 6,7-disubstituted-4-anilinoquinoline-3-carbonitrile irreversible inhibitor of the HER-2 receptor tyrosine kinase with potential antineoplastic activity. Neratinib binds to the HER-2 receptor irreversibly, thereby reducing autophosphorylation in cells, apparently by targeting a cysteine residue in the ATP-binding pocket of the receptor. Treatment of cells with this agent results in inhibition of downstream signal transduction events and cell cycle regulatory pathways; arrest at the G1-S (Gap 1/DNA synthesis)-phase transition of the cell division cycle; and ultimately decreased cellular proliferation. Neratinib also inhibits the epidermal growth factor receptor (EGFR) kinase and the proliferation of EGFR-dependent cells.","Pharmacologic Substance"]
["C95712","Nesvacumab","Anti-ANG2 MOAB REGN910|Nesvacumab|REGN910|SAR307746","A fully human monoclonal antibody directed against angiopoietin 2 (ANG2) with potential antiangiogenic and antineoplastic activities. Nesvacumab binds to ANG2 and interferes with the interaction between Ang2 and its receptor TEK tyrosine kinase (Tie2), which may inhibit tumor cell angiogenesis and tumor cell proliferation. ANG2 is upregulated in a variety of cancer cell types and plays a crucial role in angiogenesis.","Immunologic Factor|Pharmacologic Substance"]
["C96232","NG-nitro-L-arginine","L-NNA|NG-nitro-L-arginine|NOLA","An amino acid derivative and nitric oxide synthase (NOS) inhibitor with potential antineoplastic and antiangiogenic activities. Upon administration, NG-nitro-L-arginine inhibits the enzyme nitric oxide synthase, thereby preventing the formation of nitric oxide (NO). By preventing NO generation, the vasodilatory effects of NO are abrogated leading to vasoconstriction, reduction in vascular permeability and an inhibition of angiogenesis. As blood flow to tumors is restricted, this may result in an inhibition of tumor cell proliferation. NO plays an important role in tumor blood flow and stimulation of angiogenesis, tumor progression, survival, migration and invasiveness.","Pharmacologic Substance"]
["C2327","Niacinamide","3-Pyridinecarboxamide|NIACINAMIDE|Niacinamide|Nicamid|Nicosedine|Nicotinamide|Nicotinamidum|Nicotinic Acid Amide|Nicotinic acid amide|Nicotylamide|Pellagra-Preventing Factor|Vitamin PP|niacinamide|nicotinamide","The active form of vitamin B3 and a component of the coenzyme nicotinamide adenine dinucleotide (NAD). Niacinamide acts as a chemo- and radio-sensitizing agent by enhancing tumor blood flow, thereby reducing tumor hypoxia.  This agent also inhibits poly(ADP-ribose) polymerases, enzymes involved in the rejoining of DNA strand breaks induced by radiation or chemotherapy.","Organic Chemical|Vitamin"]
["C66240","Niclosamide","Benzamide, 5-Chloro-N-(2-chloro-4-nitrophenyl)-2-hydroxy-|NICLOSAMIDE|Niclosamide|Salicylanilide, 2',5-Dichloro-4'-nitro-","An orally bioavailable chlorinated salicylanilide, with anthelmintic and potential antineoplastic activity. Upon oral administration, niclosamide specifically induces degradation of the androgen receptor (AR) variant V7 (AR-V7) through the proteasome-mediated pathway. This downregulates the expression of the AR variant, inhibits AR-V7-mediated transcriptional activity, and reduces AR-V7 recruitment to the prostate-specific antigen (PSA) gene promoter. Niclosamide also prevents AR-V7-mediated STAT3 phosphorylation and activation. This inhibits AR/STAT3-mediated signaling and prevents expression of STAT3 target genes. Altogether, this may inhibit growth of AR-V7-overexpressing cancer cells. The AR-V7 variant, which is encoded by contiguous splicing of AR exons 1/2/3/CE3, is upregulated in a variety of cancer cell types, and is associated with both cancer progression and resistance to AR-targeted therapies.","Pharmacologic Substance"]
["C71734","Nifurtimox","4-((5-Nitrofurfurylidene)amino)-3-methylthiomorpholine-1,1-dioxide|BAY 2502|BAYER 2502|Lampit|NIFURTIMOX|Nifurtimox","A nitrofuran derivative with antiprotozoal and potential antineoplastic activities. Nifurtimox is reduced by cytosol enzymes or flavin-containing microsomal enzymes to a highly reactive nitro anion free radical; autooxidation of the nitro anion free radical generates cytotoxic superoxide anion (02-). In addition, nifurtimox-derived nitro anion free radicals may alkylate macromolecules such as nucleic acids and proteins, resulting in the disruption of their structure and function.","Pharmacologic Substance"]
["C48375","Nilotinib","4-Methyl-3-((4-(3-pyridinyl)-2-pyrimidinyl)amino)-N-(5-(4-methyl-1H-imidazol-1-yl)-3-(trifluoromethyl)phenyl)benzamide|AMN 107|NILOTINIB|Nilotinib|Tasigna|nilotinib","An orally bioavailable aminopyrimidine-derivative Bcr-Abl tyrosine kinase inhibitor with antineoplastic activity. Designed to overcome imatinib resistance, nilotinib binds to and stabilizes the inactive conformation of the kinase domain of the Abl protein of the Bcr-Abl fusion protein, resulting in the inhibition of the Bcr-Abl-mediated proliferation of Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML) cells. This agent also inhibits the receptor tyrosine kinases platelet-derived growth factor receptor (PDGF-R) and c-kit, a receptor tyrosine kinase mutated and constitutively activated in most gastrointestinal stromal tumors (GISTs). With a binding mode that is energetically more favorable than that of imatinib, nilotinib has been shown to have an approximately 20-fold increased potency in kinase and proliferation assays compared to imatinib.","Pharmacologic Substance"]
["C95223","Nilotinib Hydrochloride Anhydrous","NILOTINIB HYDROCHLORIDE ANHYDROUS|Nilotinib Hydrochloride Anhydrous","The hydrochloride salt of nilotinib, an orally bioavailable aminopyrimidine-derivative Bcr-Abl tyrosine kinase inhibitor with antineoplastic activity. Designed to overcome imatinib resistance, nilotinib binds to and stabilizes the inactive conformation of the kinase domain of the Abl protein of the Bcr-Abl fusion protein, resulting in the inhibition of the Bcr-Abl-mediated proliferation of Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML) cells. This agent also inhibits the receptor tyrosine kinases platelet-derived growth factor receptor (PDGF-R) and c-kit, a receptor tyrosine kinase mutated and constitutively activated in most gastrointestinal stromal tumors (GISTs). With a binding mode that is energetically more favorable than that of imatinib, nilotinib has been shown to have an approximately 20-fold increased potency in kinase and proliferation assays compared to imatinib.","Pharmacologic Substance"]
["C1173","Nilutamide","1-(3'-Trifluoromethyl-4'-nitrophenyl)-4,4-dimethylimidazoline-3,5-dione|5,5-Dimethyl-3-[4-nitro-3-(trifluoro-methyl)phenyl]-2,4-imidazolidinedione|Anandron|NILUTAMIDE|Nilandron|Nilutamide|RU-23908|nilutamide","A synthetic, nonsteroidal agent with antiandrogenic properties. Nilutamide preferentially binds to androgen receptors and blocks androgen receptor activation by testosterone and other androgens; this agent may inhibit androgen-dependent growth of normal and neoplastic prostate cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C692","Nimodipine","NIMO|NIMODIPINE|Nimodipine|Nimotop|nimodipine","A dihydropyridine derivative and an analogue of the calcium channel blocker nifedipine, with antihypertensive activity. Nimodipine inhibits the transmembrane influx of calcium ions in response to depolarization in smooth muscle cells, thereby inhibiting vascular smooth muscle contraction and inducing vasodilatation. Nimodipine has a greater effect on cerebral arteries than on peripheral smooth muscle cells and myocardial cells, probably because this agent can cross the blood brain barrier due to its lipophilic nature. Furthermore, this agent also inhibits the drug efflux pump P-glycoprotein, which is overexpressed in some multi-drug resistant tumors, and may improve the efficacy of some antineoplastic agents.","Organic Chemical|Pharmacologic Substance"]
["C2733","Nimotuzumab","NIMOTUZUMAB|Nimotuzumab|Thera-CIM-hr3|TheraCim hR3|Theraloc|nimotuzumab","A humanized monoclonal antibody directed against the epidermal growth factor receptor (EGFR) with potential antineoplastic activity. Nimotuzumab binds to and inhibits EGFR, resulting in growth inhibition of tumor cells that overexpress EGFR. This agent may act synergistically with radiation therapy.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C693","Nimustine","3-((4-Amino-2-Methyl-5-Pyrimidinyl)Methyl)-1-(2-Chloroethyl)-1-Nitrosourea|ACNU|N'-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-N-(2-chloroethyl)-N-nitrosourea|NIMUSTINE|Nidran|Nimustine|nimustine","A nitrosourea with antineoplastic activity. Nimustine alkylates and crosslinks DNA, thereby causing DNA fragmentation, inhibition of protein synthesis, and cell death. (NCI05)","Organic Chemical|Pharmacologic Substance"]
["C95325","Nimustine Hydrochloride","3-((4-Amino-2-Methyl-5-Pyrimidinyl)Methyl)-1-(2-Chloroethyl)-1-Nitrosourea Hydrochloride|ACNU HCl|CS 439 HCl|N'-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-N-(2-chloroethyl)-N-nitrosourea Hydrochloride|NIMUSTINE HYDROCHLORIDE|Nidran HCl|Nimustine Hydrochloride|Nimustine hydrochloride","The hydrochloride salt of nimustine, a nitrosourea with antineoplastic activity. Nimustine alkylates and crosslinks DNA, thereby causing DNA fragmentation, inhibition of protein synthesis, and cell death.","Organic Chemical|Pharmacologic Substance"]
["C62765","Nintedanib","BIBF 1120|BIBF-1120|Intedanib|Methyl (3Z)-3-(((4-(N-methyl-2-(4-methylpiperazin-1-yl)acetamido)phenyl)amino)(phenyl)methylidene)-2-oxo-2,3-dihydro-1H-indole-6-carboxylate|Multitargeted Tyrosine Kinase Inhibitor BIBF 1120|NINTEDANIB|Nintedanib|Vargatef|tyrosine kinase inhibitor BIBF 1120","An orally bioavailable, indolinone-derived, receptor tyrosine kinase (RTK) inhibitor with potential antiangiogenic and antineoplastic activities. Multitargeted tyrosine kinase inhibitor BIBF 1120 selectively binds to and inhibits vascular endothelial growth factor receptor (VEGFR), fibroblast growth factor receptor (FGFR) and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, which may result in the induction of endothelial cell apoptosis; a reduction in tumor vasculature; and the inhibition of tumor cell proliferation and migration. In addition, this agent also inhibits members of the Src family of tyrosine kinases, including Src, Lck, Lyn, and FLT-3 (fms-like tyrosine kinase 3). VEGFR, FGFR and PDGFR RTKs play key roles in tumor angiogenesis.","Pharmacologic Substance"]
["C80059","Niraparib","MK-4827|MK4827|NIRAPARIB|Niraparib","An inhibitor of poly (ADP-ribose) polymerase (PARP) with potential antineoplastic activity. Niraparib inhibits PARP activity, enhancing the accumulation of DNA strand breaks and promoting genomic instability and apoptosis. The PARP family of proteins detect and repair single strand DNA breaks by the base-excision repair (BER) pathway. The specific PARP family member target for PARP inhibitor MK4827 is unknown.","Pharmacologic Substance"]
["C61499","Nitric Oxide-Releasing Acetylsalicylic Acid Derivative","Benzoic Acid, 2-(Acetyl-oxy)-3-[(nitrooxy)methyl]phenyl Ester|NCX 4016|Nitric Oxide-Releasing Acetylsalicylic Acid Derivative|Nitric Oxide-Releasing Aspirin Derivative|Nitroaspirin|nitric oxide-releasing acetylsalicylic acid derivative","A nitric oxide (NO) donating derivative of acetylsalicylic acid with anti-inflammatory, analgesic, antipyretic, antithrombotic, gastroprotective and potential antitumor activities. The acetylsalicylic acid derivative moiety of this agent inhibits the activities of cyclooxygenase (COX) I and II, preventing the formation of prostaglandins and thromboxanes. A reduction in prostaglandin synthesis accounts for this agent's anti-inflammatory, anti-pyretic and analgesic activities; a reduction in thromboxane A2 synthesis results in an irreversible inhibition of platelet aggregation. NO donation by this agent, after cleavage from the acetylsalicylic acid derivative in vivo, may protect the gastric mucosa against the damaging effects of the aspirin derivative by modulating prostaglandins. In tumor cells, the NO donating moiety may block the cell cycle in the G1 and G2 phases and may induce apoptosis through caspase-mediated mechanisms.","Organic Chemical|Pharmacologic Substance"]
["C103272","Nitroglycerin Transdermal Patch","GTN Transdermal Patch|Glyceryl Trinitrate Transdermal Patch|Minitran|Nitroglycerin Transdermal Patch","A sustained release transdermal patch containing the organic nitrate nitroglycerin, with vasodilator and potential immunomodulating activities. Upon application to the skin, nitroglycerin is continuously released from the patch and absorbed. In turn, nitroglycerin is converted into nitric oxide (NO), which activates guanylyl cyclase, increasing cyclic guanosine monophosphate concentration thus resulting in smooth muscle relaxation. In addition, activation of NO-mediated signaling pathways may inhibit hypoxia-induced tumor cell invasiveness, chemoresistance, evasion of immune cell recognition and cancer cell progression. Particularly, reactivation of NO-mediated signaling appears to inhibit the increased tumor cell shedding of the major histocompatibility complex class I chain-related (MIC) molecules MICA and MICB as is seen in hypoxic tumor environments; MIC molecules play key roles in tumor cell immune surveillance through their interaction with the C-type lectin-like NKG2D receptor on natural killer, lymphokine-activated killer and effector T cells.","Pharmacologic Substance"]
["C68814","Nivolumab","BMS-936558|MDX-1106|NIVO|NIVOLUMAB|Nivolumab|ONO-4538|Opdivo","A fully human immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1,PCD-1,) with immune checkpoint inhibitory and antineoplastic activities. Nivolumab binds to and blocks the activation of PD-1, an Ig superfamily transmembrane protein, by its ligands programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. This results in the activation of T-cells and cell-mediated immune responses against tumor cells or pathogens. Activated PD-1 negatively regulates T-cell activation and and plays a key role in in tumor evasion from host immunity.","Amino Acid, Peptide, or Protein|Indicator, Reagent, or Diagnostic Aid"]
["C1888","NM-3","NM-3","An orally bioavailable antiangiogenic isocoumarin with potential antineoplastic activity.  NM-3 inhibits vascular endothelial growth factor (VEGF), a pro-angiogenic growth factor, thereby inhibiting endothelial cell proliferation.  This agent also induces apoptosis by a mechanism involving reactive oxygen species. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1163","N-Methylformamide","EK 7011|Formamide, N-methyl|Monomethylformamide|N-METHYLFORMAMIDE|N-Methylformamide|NMF|X 188|formylmethylamine|monomethylformamide","A water-soluble organic solvent.  As an adjuvant antineoplastic agent, N-methylformamide depletes cellular glutathione, a key molecule involved in the antioxidation of reactive oxygen species (ROS) and other free radicals, thereby enhancing ionizing radiation-induced DNA cross-linking in and terminal differentiation of tumor cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C75228","Nocodazole","Methyl (5-(2-thienylcarbonyl))-1H-benzimidazol-2-yl|NOCODAZOLE|Nocodazole","A synthetic tubulin-binding agent with antineoplastic activity. Nocodazole binds to beta-tubulin and disrupts microtubule assembly/disassembly dynamics. This prevents mitosis and induces apoptosis in tumor cells. Although nocodazole binding site overlaps with that of colchicine, the two agents are structurally quite different.","Pharmacologic Substance"]
["C700","Nogalamycin","Antibiotic 205T3|NOGALAMYCIN|Nogalamycin|U 15167|U-15167|[2R-(2alpha,3beta,4alpha,5beta,6alpha,11beta,13alpha,14alpha)]-11-[(6-deoxy-3-C-methyl-2,3,4-tri-O-methyl-alpha-L-mannopyranosyl)oxy]-4(dimethylamino)-3,4,5,6,9,11,12,13,14,16-decahydro-3,5,8,10,13-pentahydroxy-6,13-dimethyl-9,16-dioxo-2,6-epoxy-2H-naphthaceno[1,2-b]oxocin-14-carboxylic acid methyl ester","An anthracycline antineoplastic antibiotic isolated from the bacterium Streptomyces nogalater.  Nogalamycin intercalates into DNA and interacts with topoisomerase I, thereby inhibiting DNA replication and repair and RNA and protein synthesis. (NCI04)","Antibiotic|Organic Chemical"]
["C1577","Nolatrexed Dihydrochloride","3,4-Dihydro-2-amino-6-methyl-4-oxy-5-(4-pyridylthio)-quinazoline Dihydrochloride|AG-337|AG337|NOLATREXED DIHYDROCHLORIDE|Nolatrexed Dihydrochloride|Nolatrexed Hydrochloride|Thymitaq|nolatrexed","The dihydrochloride salt of nolatrexed, a water-soluble lipophilic quinazoline folate analog with antineoplastic activity. Nolatrexed occupies the folate binding site of thymidylate synthase, resulting in inhibition of thymidylate synthase activity and thymine nucleotide synthesis with subsequent inhibition of DNA replication, DNA damage, S-phase cell cycle arrest, and caspase-dependent apoptosis. This agent also exhibits radiosensitizing activity.","Organic Chemical|Pharmacologic Substance"]
["C84872","Non-Small Cell Lung Cancer mRNA-Derived Vaccine CV9201","CV9201|Non-Small Cell Lung Cancer mRNA-Derived Vaccine CV9201","A non-small cell lung cancer (NSCLC) vaccine containing modified mRNAs encoding cancer-testis antigen NY-ESO-1, melanoma-associated antigens C1 (MAGE-C1/CT7) and C2 (MAGE-C2/CT10), survivin, and the oncofetal antigen 5T4 with potential antitumor and immunomodulatory activities. Upon subcutaneous administration, non-small cell lung cancer mRNA-derived vaccine CV9201 may stimulate the immune system to mount a cytotoxic, antigen-specific T lymphocyte response (CTL) against NSCLC cells. The modified mRNAs in this vaccine are taken up by cells after injection and exhibit enhanced translational potency. The five tumor-associated antigens (TAAs) encoded by these mRNAs are frequently expressed by NSCLC cells.","Immunologic Factor|Pharmacologic Substance"]
["C703","Norgestrel","(+/-)-13-Ethyl-17alpha-hydroxy-18,19-dinorpregn-4-en-20-yne-3-one|(17alpha)-(+/-)-13-Ethyl-17-hydroxy-18,19-dinorpregn-4-en-20-yne-3-one|NORGESTREL|Neogest|Norgestrel|Ovrette|Wy-3707","A synthetic progestin commonly used alone or in combination with an estrogen for contraception.  Norgestrel suppresses the secretion of luteinizing and follicle-stimulating hormones (LH and FSH), thickens cervical mucus, and slows the transit of ova through the fallopian tubes.  This agent also exhibits antiproliferative activity in endometrial tissue and may exhibit chemopreventive and antineoplastic activities in endometrial carcinoma. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C99122","North American Ginseng Extract AFX-2","AFX-2|COLD-fX|CVT-E002|North American Ginseng Extract AFX-2|Panax quinquefolius Extract AFX-2","An orally available proprietary aqueous extract from the North American ginseng (Panax quinquefolius) dried root, primarily containing poly-furanosyl-pyranosyl-saccharides, with potential immunostimulating activity. Upon administration, North American ginseng extract AFX-2 may stimulate the proliferation and activation of B-lymphocytes and stimulates IgG production by B cells. Also, this agent induces maturation of dendritic cells, induces T cell proliferation and activates peritoneal exudate macrophages leading to an increase in the production of the cytokines interleukin -1 and -6, tumor necrosis factor-alpha, interferon-gamma and nitric oxide.","Pharmacologic Substance|Plant"]
["C81423","Nortopixantrone","NORTOPIXANTRONE|Nortopixantrone","A 9-aza-anthrapyrazole-based antineoplastic antibiotic. Nortopixantrone intercalates into DNA, induces single- and double-stranded DNA breaks and inhibits topoisomerase II, thereby inhibiting DNA replication and repair as well as RNA and protein synthesis. Nortopixantrone is less cardiotoxicity than anthracyclines.","Pharmacologic Substance"]
["C80589","Noscapine","NOSCAPINE|Noscapine","A phthalide isoquinoline non-narcotic alkaloid derived from the opium poppy Papaver somniferum, with mild analgesic, antitussive, and potential antineoplastic activities. Noscapine exerts its antitussive effects through the activation of sigma opioid receptors. This agent appears to exert its antimitotic effect by binding to tubulin, resulting in a disruption of microtubule assembly dynamics and subsequently, the inhibition of mitosis and tumor cell death.","Pharmacologic Substance"]
["C61103","Noscapine Hydrochloride","1(3H)Isobenzofuranone,6,7-dimethoxy-3-(5,6,7,8-tetrahydro-4-methoxy-6-methyl-1,3,-dioxolo(4,5-g)isoquinolin-5-yl)-hydrochloride|NOSCAPINE HYDROCHLORIDE|Narcotine hydrochloride|Noscapine HCl|Noscapine Hydrochloride","The orally available hydrochloride salt of the opioid agonist noscapine, a phthalideisoquinoline alkaloid derived from the opium poppy Papaver somniferum, with mild analgesic, antitussive, and potential antineoplastic activities. Noscapine binds to tubulin and alters its conformation, resulting in a disruption of the dynamics of microtubule assembly (by increasing the time that microtubules spend idle in a paused state) and subsequently, the inhibition of mitosis and tumor cell death. Unlike other tubulin inhibitors such as the taxanes and vinca alkaloids, noscapine does not affect microtubule polymerization.","Organic Chemical|Pharmacologic Substance"]
["C49175","Notch Signaling Pathway Inhibitor MK0752","MK0752|Notch Signaling Pathway Inhibitor MK0752","A synthetic small molecule with potential antineoplastic activity. MK0752 inhibits the Notch signaling pathway, which may result in induction of growth arrest and apoptosis in tumor cells in which the Notch signaling pathway is overactivated. The Notch signaling pathway plays an important role in cell-fate determination, cell survival, and cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C91738","NSCLC Antigen-Loaded Dendritic Cell-derived Exosomes","NSCLC Antigen-Loaded Dendritic Cell-derived Exosomes","Exosomes loaded with non-small cell lung cancer (NSCLC)-specific antigens, with potential immunostimulating and antineoplastic activities. Exosomes derived from autologous maturing dendritic cells (DCs) are pulsed with HLA-DP04-restricted MAGE-3, and HLA-A02-restricted peptides NY-ESO-1, MAGE-1, MAGE-3, and MART-1. Upon vaccination, these exosomes may stimulate natural killer (NK) cell activation and proliferation, restoration of NKG2D expression on NK cells, and antigen-specific T-cell responses. This may eventually lead to inhibition of tumor cell proliferation in NSCLC expressing these specific tumor antigens. These exosomes, nanovesicles secreted from DCs, are embedded with molecules necessary for potent immune responses on the exosomal surface, such as MHC class II molecules, CD40, ICAM-1, IL-15Ralpha, and NKG2D ligands.","Pharmacologic Substance"]
["C118948","NTRK/ROS1 Inhibitor DS-6051b","DS-6051b|NTRK/ROS1 Inhibitor DS-6051b","An orally available inhibitor of the receptor tyrosine kinases C-ros oncogene 1 (ROS1) and the neurotrophic tyrosine receptor kinase (NTRK) types 1, 2 and 3, with potential antineoplastic activity. Upon oral administration, DS-6051b binds to and inhibits ROS1 and the NTRK family members. This inhibition leads to a disruption of ROS1- and NTRK-mediated signaling and eventually inhibits the growth of tumor cells that are overexpressing ROS1 and/or NTRKs. ROS1, overexpressed in certain cancer cells, plays a key role in cell growth and survival of cancer cells. NTRK mutations or rearrangements play a key role in cancer progression.","Organic Chemical|Pharmacologic Substance"]
["C103297","Nucleolin Antagonist IPP-204106N","IPP-204106|N6L|Nucleolin Antagonist IPP-204106N","A synthetic, multivalent, lysine-rich, pseudopeptide and nucleolin antagonist with potential anti-angiogenic, antineoplastic and pro-apoptotic activities. Upon administration, IPP-204106N antagonizes nucleolin leading to a downregulation of cell-surface nucleolin; preventing the binding of certain growth promoting ligands to nucleolin may suppress tumor cell proliferation and angiogenesis. In addition, IPP-204106N is able to translocate to the nucleolus and bind to nucleolar nucleolin. This prevents nucleolin from binding to and stabilizing mRNA of the anti-apoptotic Bcl2; destabilizing Bcl2 mRNA leads to a reduction in Bcl2 protein synthesis and induces apoptosis. Further, this agent can antagonize nucleophosmin. Nucleolin, a nucleolar phosphoprotein, is overexpressed on the cell surface of certain cancer cells and binds ligands involved in cell proliferation, adhesion and angiogenesis.","Pharmacologic Substance"]
["C116744","Nucleoside Analog DFP-10917","2'-C-cyano-2'-deoxy-1-beta-D-arabino-pentofuranosylcytosine|CNDAC|DFP-10917|Nucleoside Analog DFP-10917","A deoxycytosine analog with potential antineoplastic activity. Upon administration, DFP-10917 is phosphorylated to generate its nucleotide form that functions as a deoxycytosine mimic and is incorporated into DNA in tumor cells. This causes DNA strand breaks during polymerization due to beta-elimination during the fidelity checkpoint, which results in G2/M phase-arrest and tumor cell apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C71742","Nucleotide Analogue GS 9219","9-(2-phosphonylmethoxyethyl)guanine nucleotide analogue prodrug GS 9219|GS9219|Nucleotide Analogue GS 9219","A prodrug of the acyclic nucleoside phosphonate analogue 9-(2-phosphonylmethoxyethyl)guanine (PMEG) with potential antineoplastic activity. Formulated to selectively accumulate in lymphocytes, nucleotide analogue GS 9219 is converted to its active metabolite, PMEG diphosphate (PMEGpp), via enzymatic hydrolysis, deamination, and phosphorylation; subsequently, PMEGpp is incorporated into nascent DNA chains by DNA polymerases, which may result in the termination of DNA synthesis, S-phase cell cycle arrest, and the induction of apoptosis in susceptible lymphoma cell populations.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C74594","Nutlin-3a","Nutlin-3a","A small molecule and MDM2 (murine double minute 2) inhibitor, with potential antineoplastic activity. In cancer cells, nutlin-3a antagonizes the binding of MDM2 to p53, thereby preventing MDM2-mediated p53 degradation. This results in stabilizing and activating p53-dependent cell cycle arrest and apoptosis. The protein MDM2, a negative regulator of p53 activity, is overexpressed in many cancer cell types; the tumor suppressor p53 is mutated or deleted in about 50% of all cancers but active in the other 50%.","Organic Chemical|Pharmacologic Substance"]
["C96036","Nutraceutical TBL-12","Nutraceutical TBL-12|TBL-12","An orally available nutritional supplement and proprietary formulation containing extracts from the sea cucumber, sea sponge, shark fin, sea urchin and the marine grass Sargassum, with potential antioxidant, antitumor, anti-angiogenic and immunomodulating activities. TBL-12 contains various amino acids, minerals, vitamins and omega-3 fatty acids.","Pharmacologic Substance"]
["C2623","NV1020","NV1020","A genetically engineered oncolytic virus with potential antineoplastic property. NV1020 is constructed from the herpes simplex virus 1 (HSV-1) by the deletion of a single copy of the gamma (1)34.5 gene and the substitution of the UL23 region of the thymidine kinase (tk) gene with a DNA fragment from HSV-2, thereby resulting in a replication-competent, attenuated virus. This modified virus preferentially transfects rapidly dividing cells, which causes cell lysis in tumor cells. NV1020 has shown reduced virulence against normal tissues and a decreased neurovirulence in comparison with some other modified HSV strains.","Pharmacologic Substance|Virus"]
["C2657","NY-ESO-1 Peptide Vaccine","ESO-1 Peptide Vaccine|NY-ESO-1 Peptide Vaccine","A cancer vaccine consisting of an immunogenic peptide derived from the cancer-testis antigen (NY-ESO-1), an antigen found in normal testis and various tumors. Vaccination with NY-ESO-1 peptide vaccine may stimulate the host immune system to mount a humoral and cytotoxic T lymphocyte (CTL) response to cells expressing NY-ESO-1 antigen, resulting in tumor cell lysis.","Immunologic Factor|Pharmacologic Substance"]
["C62452","NY-ESO-1 Plasmid DNA Cancer Vaccine","NY-ESO-1 Plasmid DNA Cancer Vaccine|pPJV7611 Vaccine|pPJV7611","A plasmid DNA encoding an immunogenic peptide derived from the cancer-testis antigen NY-ESO-1 with potential immunostimulating and antitumor activities. Upon administration, NY-ESO-1 plasmid DNA cancer vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing the NY-ESO-1 antigen, resulting in tumor cell lysis. NY-ESO-1 is a tumor associated antigen (TAA) found in normal testes and expressed on the surfaces of various tumor cells, including melanoma, breast, bladder, prostate, lung, ovarian, and hepatocellular tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C128887","NY-ESO-1 Protein/Microparticle MDP/Bacterial DNA-containing MIS416 Vaccine","NY-ESO-1 Protein with MIS416|NY-ESO-1 Protein/MIS416|NY-ESO-1 Protein/Microparticle MDP/Bacterial DNA-containing MIS416 Vaccine","A combination preparation composed of a protein derived from the human tumor-associated antigen (TAA) cancer-testis antigen 1 (NY-ESO-1) and a microparticle combining two immune-modifying components derived from the bacterium Propionibacterium acnes, a bacterial cell wall component that is rich in muramyl dipeptide (MDP) and bacteria-derived single-stranded DNA fragments, with potential immunomodulating, immunoadjuvant and antineoplastic activities. Upon administration of NY-ESO-1 protein/microparticle MDP/bacterial DNA-containing MIS416 vaccine, MIS416 localizes in and is taken up mainly by the liver, thereby forming a liver depot. MIS416 is then taken up by immune cells, such as monocytes and dendritic cells (DCs), where MDP and the bacterial DNA target and bind to the cytosolic innate pattern recognition receptors (PRRs) nucleotide-binding oligomerization domain-containing protein 2 (NOD2), and toll-like receptor 9 (TLR9), respectively. The simultaneous binding and activation of both NOD2 and TLR9, leads to activation of both NOD2 and TLR9 signaling pathways. This stimulates the innate immune system, induces secretion of cytokines, particularly interferon (IFN), and modulates the activation of various immune cells. In the presence of the NY-ESO-1 peptide, MIS416 enhances the cytotoxic T-lymphocyte (CTL)-mediated immune response against NY-ESO-1, resulting in an increased anti-tumor immune response. NY-ESO-1 is expressed in normal testes and on the surfaces of various tumor cells, and plays a key role in tumor cell proliferation and survival.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C90559","NY-ESO-1 Reactive TCR Retroviral Vector Transduced Autologous PBL","Anti-NY-ESO-1 TCR Retroviral Vector Transduced Autologous PBL|NY-ESO-1 Reactive TCR Retroviral Vector Transduced Autologous PBL","Human autologous peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding a T cell receptor (TCR) specific for the cancer-testis antigen NY-ESO-1, with potential antineoplastic activity. Upon isolation, transduction, expansion ex vivo, and reintroduction into the patient, the NY-ESO-1 reactive TCR-transduced autologous PBLs bind to NY-ESO-1-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL) killing of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types; the TCR is specific for NY-ESO-1:157-165.","Cell|Pharmacologic Substance"]
["C114380","NY-ESO-1(157-165) Peptide-pulsed Autologous Dendritic Cell Vaccine","Autologous NY-ESO-1 (157-165) Peptide-pulsed DC Vaccine|NY-ESO-1(157-165) Peptide-pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with a peptide derived from the tumor associated antigen human cancer-testis antigen NY-ESO-1 (NY-ESO-1(157-165)), with potential immunostimulatory and antineoplastic activities. Upon administration, the NY-ESO-1(157-165) peptide-pulsed autologous dendritic cell vaccine may stimulate the immune system to mount both an anti-tumoral cytotoxic T-lymphocyte (CTL)- and an antibody-mediated immune response against NY-ESO-1-expressing tumor cells, which may result in tumor cell lysis. NY-ESO-1 is expressed both in normal testes and on the surfaces of various tumor cells, and plays a key role in tumor cell proliferation and survival.","Cell|Pharmacologic Substance"]
["C113432","NY-ESO-1/GLA-SE Vaccine ID-G305","ID-G305|IDC-G305|NY-ESO-1/GLA-SE Vaccine ID-G305","A cancer vaccine composed of a recombinant form of the tumor antigen NY-ESO-1 and glucopyranosyl lipid adjuvant (GLA)-stable emulsion (GLA-SE), with potential antineoplastic and immunomodulating activities. Upon intramuscular injection, the adjuvant portion of the NY-ESO-1/GLA-SE vaccine ID-G30 binds to toll-like receptor subtype 4 (TLR-4) expressed on dendritic cells (DCs), monocytes, macrophages and B cells. The activated DCs present the NY-ESO-1 antigen to Th1 CD4 T-lymphocytes. This leads to the induction of cytotoxic T lymphocytes (CTLs) and the killing of NY-ESO-1-expressing tumor cells. This vaccine also induces specific antibody responses and increases the production of inflammatory cytokines.","Pharmacologic Substance"]
["C74066","NY-ESO-1/LAGE-1 Peptide Vaccine","NY-ESO-1/LAGE-1 HLA Class I/II Peptide Vaccine|NY-ESO-1/LAGE-1 Peptide Vaccine","A cancer vaccine containing HLA class I- and II-binding peptides derived from the NY-ESO-1/LAGE-1 cancer/testis antigen with potential immunostimulatory and antineoplastic activities. Upon administration, NY-ESO-1/LAGE-1 HLA class I/II peptide vaccine may induce a cytotoxic immune response against tumor cells that over-express NY-ESO-1/LAGE-1. Rarely expressed by normal cells, the NY-ESO-1/LAGE-1 cancer/testis antigen has been shown to be preferentially expressed on the surface of some cancer cell types.","Pharmacologic Substance"]
["C118367","NY-ESO-1/MAGE-A4/PRAME/Survivin/SSX-specific Autologous Cytotoxic T Lymphocytes","NY-ESO-1/MAGE-A4/PRAME/Survivin/SSX-specific Autologous CTLs|NY-ESO-1/MAGE-A4/PRAME/Survivin/SSX-specific Autologous Cytotoxic T Lymphocytes","A preparation of cytotoxic T-lymphocytes (CTL), specifically reactive to the tumor-associated antigens (TAAs) survivin, melanoma-associated antigen 4 (MAGE-A4), synovial sarcoma X (SSX2), preferentially expressed antigen in melanoma (PRAME) and the cancer-testis antigen NY-ESO-1, with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMC) are collected, exposed ex vivo to dendritic cells (DCs) pulsed with multiple peptides for survivin, MAGE-A4, SSX2, PRAME and NY-ESO-1, and subsequently treated with the Th1-polarizing and pro-proliferative cytokines interleukin (IL) 12 (IL-12), IL-7, and IL-15. The treated cells are expanded in culture. Administration of the TAA specific CTLs results in a targeted CTL response against tumor cells expressing these TAAs, which leads to cell lysis and inhibition of cell proliferation in susceptible tumor cells. These TAAs are absent or minimally expressed on normal, healthy human cells and play a key role in tumor cell proliferation.","Cell|Pharmacologic Substance"]
["C120129","NY-ESO-1/MART-1 Peptide-pulsed Dendritic Cell Vaccine","NY-ESO-1/MART-1 Peptide-pulsed DC Vaccine|NY-ESO-1/MART-1 Peptide-pulsed Dendritic Cell Vaccine","A cell-based cancer vaccine composed of dendritic cells (DC) pulsed with peptides derived from the tumor-associated antigens human cancer/testis antigen NY-ESO-1 and melanoma antigen recognized by T-cells (MART-1/Melan-A), with potential immunostimulatory and antineoplastic activities. Upon administration, the NY-ESO-1/MART-1-peptide pulsed DC vaccine may stimulate the immune system to mount an anti-tumor cytotoxic T-lymphocyte (CTL) response against NY-ESO-1/MART-1-expressing tumor cells, which may result in tumor cell lysis. NY-ESO-1 is expressed both in normal testes and on the surfaces of various tumor cells. MART-1 is expressed by melanoma cells.","Pharmacologic Substance"]
["C127125","NY-ESO-1/PRAME/MAGE-A3/WT-1 Peptide Vaccine","NPMW-peptide Vaccine|NY-ESO-1/PRAME/MAGE-A3/WT-1 Peptide Vaccine","A peptide-based cancer vaccine comprised of synthetic peptides derived from the cancer-testis antigen NY-ESO-1, preferentially expressed antigen in melanoma (PRAME), human melanoma antigen A3 (MAGE-A3) and the human Wilms tumor protein-1 (WT-1), with potential immunostimulating and antineoplastic activities. Upon administration, NY-ESO-1/PRAME/MAGE-A3/WT-1 peptide vaccine may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing NY-ESO-1, PRAME, MAGE-A3 and WT-1, resulting in tumor cell lysis. The NY-ESO-1, PRAME, MAGE-A3 and WT-1 peptides, tumor-associated antigens (TAAs) overexpressed in a variety of cancer cell types, play a key role in tumor cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C68999","NY-ESO-1b Peptide Vaccine","NY-ESO-1b Peptide (p157-165)|NY-ESO-1b Peptide Vaccine","A recombinant nonapeptide used as an antineoplastic vaccine. NY-ESO-1b peptide vaccine contains the amino acid sequence SLLMWITQC, derived from the cancer-testis tumor antigen (NY-ESO-1), which is expressed on tumor cells of many different types, including melanomas. Vaccination with this peptide vaccine may elicit strong humoral and cellular immune responses to NY-ESO-1-expressing cancers.","Immunologic Factor|Pharmacologic Substance"]
["C117724","NY-ESO-1-specific CD4-positive T Lymphocytes","CD4+ NY-ESO-1-specific T Cells|NY-ESO-1-specific CD4-positive T Lymphocytes","A preparation of autologous CD4+ T-lymphocytes sensitized to cancer-testis antigen NY-ESO-1, with potential immunostimulating and antineoplastic activities. CD4-positive T-lymphocytes are exposed to a NY-ESO-1 peptide ex vivo, expanded, and introduced into the patient. The NY-ESO-1-specific CD4-positive T-lymphocytes may stimulate the host immune system to produce a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the NY-ESO-1 antigen, which results in tumor cell lysis. NY-ESO-1, an antigen found in normal testis, may be upregulated in various cancers.","Cell|Pharmacologic Substance"]
["C120557","NY-ESO-1-specific TCR Gene-transduced T Lymphocytes TBI-1301","NY-ESO-1-specific TCR Gene-transduced T Lymphocytes TBI-1301|NY-ESO-1-specific TCR Gene-transduced T Lymphocytes|TBI-1301","Human peripheral blood T-lymphocytes transduced with a retroviral vector encoding a T-cell receptor (TCR) specific for the cancer-testis antigen NY-ESO-1, with potential antineoplastic activity. Following leukapheresis, isolation of lymphocytes, expansion ex vivo, transduction, and introduction into the patient, the NY-ESO-1-specific TCR gene-transduced T lymphocytes TBI-1301 bind to NY-ESO-1 on tumor cells. This may result in cytotoxic T-lymphocyte (CTL)-mediated elimination of NY-ESO-1-positive cancer cells. NY-ESO-1, a tumor-associated antigen (TAA), is found in normal testis and on the surface of various tumor cell types.","Pharmacologic Substance"]
["C26680","NY-ESO-B","NY-ESO-B","A tumor-associated antigen belonging to the family of immunogenic testicular proteins that are aberrantly expressed in human cancers in a lineage-nonspecific fashion. Reverse transcription-PCR analysis showed NY-ESO-1 mRNA expression in a variable proportion of a wide array of human cancers, including melanoma, breast cancer, bladder cancer, prostate cancer, and hepatocellular carcinoma; and restricted expression in normal tissues, with high-level mRNA expression found only in testis and ovary tissues. The gene for NY-ESO-1 maps to Xq28 and codes for an 18-kDa protein having no homology with any known protein. NY-ESO-1 elicits a strong, integrated humoral and cellular immune response in a high proportion of patients with NY-ESO-1-expressing tumors and is under investigation as a cancer immunotherapy agent.","Immunologic Factor"]
["C1306","O6-Benzylguanine","2-amino-6-(benzyloxy)purine|2-amino-6-(phenylmethoxy)-9h-purine|6-O-BENZYLGUANINE|6-O-Benzylguanine|O(6)-Benzylguanine|O(6)-benzylguanine|O-6-Benzylguanine|O6-Benzylguanine","A guanine analogue with antineoplastic activity. O6-benzylguanine binds the DNA repair enzyme O(6)-alkylguanine DNA alkyltransferase (AGT), transferring the benzyl moiety to the active-site cysteine and resulting in inhibition of AGT-mediated DNA repair. Co-administration of this agent potentiates the effects of other chemotherapeutic agents that damage DNA. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C62771","Obatoclax Mesylate","2-(2-[(3,5-Dimethyl-1H-pyrrol-2-yl)methylidene]-3-methoxy-2H-pyrrol-5-yl)-1H-indole Monomethanesulfonate|GX15-070MS|OBATOCLAX MESYLATE|Obatoclax Mesylate|obatoclax mesylate","The mesylate salt of obatoclax, a synthetic small-molecule inhibitor of the bcl-2 family of proteins with potential pro-apoptotic and antineoplastic activities. Obatoclax binds to members of the Bcl-2 protein family, preventing the binding of these anti-apoptotic proteins to the pro-apoptotic proteins Bax and Bak and so promoting the activation of the apoptotic pathway in Bcl-2-overexpressing cells. The Bcl-2 family of proteins (bcl-2, bcl-xl, bcl-w, and Mcl-1) are overexpressed in a wide variety of cancers, including those of the lymphatic system, breast, lung, prostate, and colon.","Pharmacologic Substance"]
["C70741","Obinutuzumab","Afutuzumab|Anti-CD20 Monoclonal Antibody R7159|GA-101|GA101|Gazyva|OBINUTUZUMAB|Obinutuzumab|R7159|RO 5072759|huMAB(CD20)","A glycoengineered, humanized IgG1 monoclonal antibody with potential antineoplastic activity. Obinutuzumab, a third generation type II anti-CD20 antibody, selectivity binds to the extracellular domain of the human CD20 antigen on malignant human B cells. The Fc region carbohydrates of the antibody, enriched in bisected non-fucosylated glycosylation variants, contribute to its higher binding affinity for human FcgammaRIII receptors compared to non-glycoengineered antibodies, resulting in enhanced antibody-dependent cellular cytotoxicity (ADCC) and caspase-independent apoptosis. In addition, modification of elbow hinge sequences within the antibody variable framework regions may account for the strong apoptosis-inducing activity of R7159 upon binding to CD20 on target cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C66722","Oblimersen Sodium","Anticode G3139|Augmerosen|BCL-2 Antisense Oligodeoxynucleotide G3139|BCL-2 Antisense/G3139|G3139 Antisense Oligonucleotide|G3139 BCL-2 Antisense Oligo|G3139 BCL-2 Antisense Oligodeoxynucleotide|G3139 BCL-2 Antisense Oligonucleotide|G3139|Genasense|OBLIMERSEN SODIUM|Oblimersen Sodium|augmerosen|bcl-2 antisense oligodeoxynucleotide G3139|oblimersen sodium","The sodium salt of a phosphorothioate antisense oligonucleotide targeted to the initiation codon region of mRNA for the anti-apoptotic gene Bcl-2. Oblimersen inhibits Bcl-2 mRNA translation, which may result in decreased expression of the Bcl-2 protein and tumor cell apoptosis. This agent may enhance the efficacy of standard cytotoxic chemotherapy. The anti-apoptotic bcl-2 protein is an integral outer mitochondrial membrane protein (OMMP) that is overexpressed in some cancer cell types and is linked to tumor drug resistance.","Pharmacologic Substance"]
["C2524","Ocaratuzumab","AME-133v|Anti-CD20 Monoclonal Antibody AME-133v|LY 2469298|MoAb CD20|Ocaratuzumab|monoclonal antibody, CD20","An Fc-engineered monoclonal antibody directed against human CD20 with potential antineoplastic activity. Ocaratuzumab specifically binds to CD20 antigen (B1), preventing mitogen-induced B-cell proliferation; inhibiting B-cell differentiation; and promoting antibody-dependent cell-mediated cytotoxicity (ADCC) and apoptosis of B cells expressing CD20. The Fc portion of this monoclonal antibody has been engineered to possess a higher binding affinity for variant Fc receptors on T helper cells, resulting in an augmentation of the anti-tumor immune response. Because of Fc engineering, this agent may be significantly more potent than rituximab in inducing B cell-directed ADCC. CD20 is a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B cell development.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1298","O-Chloroacetylcarbamoylfumagillol","(3R,4S,5S,6R)-5-Methoxy-4- [(2R,3R)-2-methyl-3-(3-methyl-2-butenyl) -oxiranyl]-1-oxaspiro [2,5] oct-6-yl(chloroacetyl) Carbamate|5-methoxy-4-(2-methyl-3-(3-methyl-2-butenyl)oxiranyl)-1-oxaspiro(2,5)oct-6-yl(chloroacetyl) carbamate|AGM-1470|O-Chloroacetylcarbamoylfumagillol|TNP-470|[3R-[3alpha,4alpha(2R*,3R*),5beta,6beta]]-5-Methoxy-4-[2-methyl-3-(3-methyl-2-butenyl)oxiranyl]-1-oxaspiro[2.5]oct-6-yl (chloroacetyl)carbamate","A synthetic analog of fumagillin, an antibiotic isolated from the fungus Aspergillus fumigatus fresenius with antineoplastic activity.  TNP-470 binds to and irreversibly inactivates methionine aminopeptidase-2 (MetAP2), resulting in endothelial cell cycle arrest late in the G1 phase and inhibition of tumor angiogenesis.  This agent may also induce the p53 pathway, thereby stimulating the production of cyclin-dependent kinase inhibitor p21 and inhibiting angiogenesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C66250","Ocrelizumab","OCRELIZUMAB|Ocrelizumab|PR070769|PRO-70769|PRO70769|RO4964913|rhuMAb 2H7","A Fc-modified, humanized monoclonal antibody directed against the B-cell CD20 cell surface antigen, with immunosuppressive activity. Ocrelizumab binds to CD20 on the surfaces of B-cells, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) of B-cells overexpressing CD20. The CD20 antigen, a non-glycosylated cell surface phosphoprotein that acts as a calcium ion channel, is found on over 90% of B-cells, B-cell lymphomas, and other lymphoid tumor cells of B-cell origin; it plays an important role in B-cell functioning.","Pharmacologic Substance"]
["C711","Octreotide","D-Phenylalanyl-L-cysteinyl-L-phenyl-alanyl-D-tryptophyl-L-lysyl-L-threonyl-N-[2-hydroxy-1-(hydroxymethyl)propyl]-L-cysteinamide Cyclic (2->7)-Disulfide|D-Phenylalanyl-L-cysteinyl-L-phenylalanyl-D-tryptophyl-L-lysyl-L-threonyl-L-cysteinyl-L-threoninol Cyclic (2->7)-Disulfide|D-Phenylalanyl-L-cysteinyl-L-phenylalanyl-D-tryptophyl-L-lysyl-L-threonyl-N-[(1R,2R)-2-hydroxy-1-(hyroxymethyl)propyl]-L-cysteinamide, Cyclic (2->7)-disulfide|OCTREOTIDE|Octreotide|SMS-201-995|octreotide","A synthetic long-acting cyclic octapeptide with pharmacologic properties mimicking those of the natural hormone somatostatin. Octreotide is a more potent inhibitor of growth hormone, glucagon, and insulin than somatostatin. Similar to somatostatin, this agent also suppresses the luteinizing hormone response to gonadotropin-releasing hormone, decreases splanchnic blood flow, and inhibits the release of serotonin, gastrin, vasoactive intestinal peptide (VIP), secretin, motilin, pancreatic polypeptide, and thyroid stimulating hormone.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2402","Octreotide Pamoate","OCTREOTIDE PAMOATE|OP LAR|Octreotide Embpnate|Octreotide Pamoate|Octreotide pamoate|OncoLar|SMS 201-995 PA|SMS 201-995 pa LAR","A synthetic long-acting octapeptide analogue of endogenous somatostatin.  Octreotide pamoate binds to somatostatin receptors expressed by some neuroendocrine and non-neuroendocrine tumor cells, thereby initiating somatostatin receptor-mediated apoptosis. Other possible antineoplastic activities of this agent include suppression of tumor angiogenesis and tumor growth-promoting insulin-like growth factor 1 (IGF-1).  (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C66952","Ofatumumab","Arzerra|GSK1841157|HuMax-CD20, 2F2|HuMax-CD20|OFATUMUMAB|Ofatumumab|ofatumumab","A fully human, high-affinity IgG1 monoclonal antibody directed against the B cell CD20 cell surface antigen with potential antineoplastic activity. Ofatumumab binds specifically to CD20 on the surfaces of B cells, triggering complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) of B cells overexpressing CD20. The CD20 antigen, found on over 90% of B cells, B cell lymphomas, and other B cells of lymphoid tumors of B cell origin, is a non-glycosylated cell surface phosphoprotein that acts as a calcium ion channel; it is exclusively expressed on B cells during most stages of B cell development.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2558","Oglufanide Disodium","Glufanide Disodium|IM 862|IM-862|IM862|L-Tryptophan, L-alpha-glutamyl-, disodium salt|OGLUFANIDE DISODIUM|Oglufanide Disodium|Thymogen","The disodium salt of a synthetic form of a naturally-occurring dipeptide consisting of L-glutamic acid and L-tryptophan with potential antiangiogenic and potential immunomodulating activities. Oglufanide inhibits vascular endothelial growth factor (VEGF), which may inhibit angiogenesis. This agent has also been reported to stimulate the immune response to hepatitic C virus and intracellular bacterial infections.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C71721","Olaparib","AZD2281|KU-0059436|Lynparza|OLAPARIB|Olaparib|PARP Inhibitor AZD2281|PARP inhibitor AZD2281|olaparib","A small molecule inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemosensitizing, radiosensitizing, and antineoplastic activities. Olaparib selectively binds to and inhibits PARP, inhibiting PARP-mediated repair of single strand DNA breaks; PARP inhibition may enhance the cytotoxicity of DNA-damaging agents and may reverse tumor cell chemoresistance and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins and can be activated by single-stranded DNA breaks.","Pharmacologic Substance"]
["C79825","Olaratumab","Anti-PDGFR alpha Monoclonal Antibody IMC-3G3|Anti-Platelet-Derived Growth Factor Receptor alpha Monoclonal Antibody IMC-3G3|IMC-3G3|Lartruvo|OLARATUMAB|Olaratumab|anti-PDGFR alpha monoclonal antibody IMC-3G3|anti-platelet-derived growth factor receptor alpha monoclonal antibody IMC-3G3","A fully human IgG1 monoclonal antibody directed against the platelet-derived growth factor receptor alpha (PDGFR alpha) with potential antineoplastic activity. Anti-PDGFR alpha monoclonal antibody IMC-3G3 selectively binds to PDGFR alpha, .blocking the binding of its ligand, PDGF; signal transduction downstream of PDGFR through the MAPK and PI3K pathways is inhibited, which may result in inhibition of angiogenesis and tumor cell proliferation. Overexpressed by various cancer cell types, PDGFR is a transmembrane protein tyrosine kinase receptor, consisting of isoforms A and B that is important in regulating cellular growth and differentiation and angiogenesis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C90586","Oleandrin","Oleandrin|PBI-05204","A lipid soluble cardiac glycoside with potential antineoplastic activity. Upon administration, oleandrin specifically binds to and inhibits the alpha3 subunit of the Na/K-ATPase pump in human cancer cells. This may inhibit the phosphorylation of Akt, upregulate MAPK, inhibit NF-kb activation and inhibit FGF-2 export and may downregulate mTOR thereby inhibiting p70S6K and S6 protein expression. All of this may lead to an induction of apoptosis. As cancer cells with relatively higher expression of the alpha3 subunit and with limited expression of the alpha1 subunit are more sensitive to oleandrin, one may predict the tumor response to treatment with lipid-soluble cardiac glycosides such as oleandrin based on the tumors Na/K-ATPase pump protein subunit expression. Overexpression of the alpha3 subunit in tumor cells correlates with tumor proliferation.","Pharmacologic Substance"]
["C61325","Oligonucleotide SPC2996","Oligonucleotide SPC2996","A synthetic antisense oligonucleotide against Bcl-2 messenger RNA with potential antitumor activity. Oligonucleotide SPC2996 binds to and inactivates Bcl-2 mRNA, thereby inhibiting the expression of Bcl-2 protein, promoting tumor cell apoptosis, and potentially enhancing the efficacy of standard cytotoxic chemotherapy. Linked to tumor drug resistance, the antiapoptotic protein Bcl-2 is upregulated in several types of cancers.","Pharmacologic Substance"]
["C106234","Olive Oil Extract/Curcumin-based Capsule","Olive Oil Extract/Curcumin-based Capsule|PhytoMed Medical Food Suppement","A capsule containing an extract of olive oil, rich in polyphenols, and curcumin, the polyphenol derived from the plant Curcuma longa, also known as turmeric, with potential anti-neoplastic, -angiogenic, -inflammatory, -oxidant and chemopreventive activities. The olive oil extract/curcumin-based capsule is rich in phytonutrients, especially polyphenols. Upon oral administration, the polyphenols, and other active ingredients in this supplement may exert anti-inflammatory activity by decreasing the production of inflammation mediators, such as TNF-alpha, interleukin (IL) 1-beta, IL-6, IL-10, interferon gamma, thromboxane B2, and leukotriene B4. They also inhibit a variety of pro-inflammatory enzymes, such as cyclooxygenase 1 (COX-1) and COX-2, block the formation of reactive-oxygen species and neutralize free radicals. In addition, curcumin and some other polyphenols disrupt cell signal transduction pathways involved in carcinogenesis. Specifically, curcumin inhibits cell invasion by inhibiting matrix metalloproteinase-9 (MMP-9) expression by suppressing NF-kB and AP-1 activation.","Pharmacologic Substance"]
["C111896","Olive Oil/Soya Oil/Egg Lecithin-based Emulsion","ClinOleic|Olive Oil/Soya Oil/Egg Lecithin-based Emulsion","An injectable, isotonic, nutritional lipid emulsion composed of approximately 80% refined olive oil and 20% refined soybean oil, used for parenteral nutrition. The olive oil/soya oil/egg lecithin emulsion provides about 15% of saturated fatty acids (SFA), 65% of mono-unsaturated fatty acids (MUFA) and 20% of essential poly-unsaturated fatty acids (EPUFA). Upon parenteral administration, the emulsion supplies calories, for energy, and essential fatty acids that can be incorporated into cell membranes. The fatty acids may decrease the production of certain pro-inflammatory cytokines, including interleukin 1 (IL-1), IL-6 and tumor necrosis factor (TNF). In addition to olive oil and soya oil, this lipid emulsion contains egg lecithin and provides phosphorus and choline, which are needed to maintain cell membrane integrity.","Pharmacologic Substance"]
["C715","Olivomycin","OLIVOMYCIN|Oligomycin A, mixt. with oligomycin B|Olivomycin|Olivomycins|Toyomycin R","A preparation containing a mixture of glycosidic antibiotics isolated from Streptomyces olivoreticuli with fluorescent microscopy applications and potential antineoplastic activities. Olivomycin preferentially binds to DNA and can be utilized as a fluorescent marker during the characterization of heterochromatin. Additionally, binding to DNA inhibits both RNA transcription and RNA elongation by RNA polymerase; therefore protein synthesis is inhibited. In addition, olivomycin antibiotics are able to induce apoptosis in tumor cells through a mechanism that has not yet been fully elucidated.","Antibiotic"]
["C1177","Oltipraz","3H-1,2-Dithiole-3-thione, 4-methyl-5-pyrazinyl-|3H-1,2-Dithiole-3-thione,4-methyl-5-pyrazinyl|4-Methyl-5-(pyrazinyl)-3H-1,2-dithiole-3-thione|4-Methyl-5-pyrazinyl-3H-1,2-dithiole-3-thione|5-(2-Pyrazinyl)-4-methyl-1,2-dithiol-3-thione|5-[2-Pyrazinyl]-4-methyl-1,2-3-thione|OLTIPRAZ|Oltipraz|RP-35,972|oltipraz","A synthetic dithiolethione with potential chemopreventive and anti-angiogenic properties. Oltipraz induces phase II detoxification enzymes, such as glutathione S transferase (GST) and NAD(P)H:quinone oxidoreductase 1 (NQO1). The induction of detoxification enzymes enhances the detoxification of certain cancer-causing agents, thereby enhancing their elimination and preventing carcinogen-induced DNA damages. Although the exact mechanism through which the anti-angiogenesis effect remains to be fully elucidated, oltipraz maybe able to modulate the expression of a number of angiogenic factors, thereby blocking the sustained and focal neovascularization in multiple tumor cell types.","Organic Chemical|Pharmacologic Substance"]
["C1127","Omacetaxine Mepesuccinate","CGX-635|Ceflatonin|Cephalotaxine, 4-Methyl 2-hydroxy-2-(4-hydroxy-4-methylpentyl)butanedioate (Ester), [3(R)]- (9CI)|Cephalotaxine, 4-Methyl 2-hydroxy-2-(4-hydroxy-4-methylpentyl)butanedioate (Ester)|Cephalotaxine, 4-methyl 2-hydroxy-2-(4-hydroxy-4-methylpentyl)butanedioate (ester), [3(R)]- (9CI)|HHT|OMACETAXINE MEPESUCCINATE|Omacetaxine Mepesuccinate|Synribo|homoharringtonine","A semisynthetic formulation of the cytotoxic plant alkaloid homoharringtonine isolated from the evergreen tree Cephalotaxus with potential antineoplastic activity. Omacetaxine mepesuccinate binds to the 80S ribosome in eukaryotic cells and inhibits protein synthesis by interfering with chain elongation. This agent also induces differentiation and apoptosis in some cancer cell types.","Organic Chemical|Pharmacologic Substance"]
["C78480","Ombrabulin","(2S)-2-amino-3-hydroxy-n-(2-methoxy-5-((1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl)phenyl)propanamide|AC7700|AVE8062|Combretastatin A4 Analogue AVE8062|OMBRABULIN|Ombrabulin","A synthetic water-soluble analogue of combretastatin A4, derived from the South African willow bush (Combretum caffrum), with potential vascular-disrupting and antineoplastic activities. Ombrabulin binds to the colchicine binding site of endothelial cell tubulin, inhibiting tubulin polymerization and inducing mitotic arrest and apoptosis in endothelial cells. As apoptotic endothelial cells detach from their substrata, tumor blood vessels collapse; the acute disruption of tumor blood flow may result in tumor necrosis.","Organic Chemical|Pharmacologic Substance"]
["C85454","Onalespib","(2,4-Dihydroxy-5-isopropylphenyl)-(5-(4-methylpiperazin-1-ylmethyl)-1,3-dihydroisoindol-2-yl)methanone|AT 13387|AT-13387|AT13387|ONALESPIB|Onalespib","A synthetic, orally bioavailable, small-molecule inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Onalespib selectively binds to Hsp90, thereby inhibiting its chaperone function and promoting the degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival. Hsp90, a chaperone protein upregulated in a variety of tumor cells, regulates the folding, stability and degradation of many oncogenic signaling proteins.","Pharmacologic Substance"]
["C129425","Onalespib Lactate","AT-13387 Lactate|ATI-13387A|ATI-13387AU|ONALESPIB LACTATE|Onalespib Lactate|Propanoic Acid, 2-Hydroxy-, (2S)-, Compound with (1,3-Dihydro-5-((4-methyl-1-piperazinyl)methyl)-2H-isoindol-2-yl)(2,4-dihydroxy-5-(1-methylethyl)phenyl)methanone (1:1)","The lactate form of onalespib, a synthetic, orally bioavailable, small-molecule inhibitor of heat shock protein 90 (Hsp90) with potential antineoplastic activity. Onalespib selectively binds to Hsp90, thereby inhibiting its chaperone function and promoting the degradation of oncogenic signaling proteins involved in tumor cell proliferation and survival. Hsp90, a chaperone protein upregulated in a variety of tumor cells, regulates the folding, stability and degradation of many oncogenic signaling proteins.","Pharmacologic Substance"]
["C82348","Onartuzumab","Anti-MET Monoclonal Antibody MetMAb|MetMAb|OA-5D5|ONARTUZUMAB|Onartuzumab|PRO 143966","A humanized monovalent monoclonal antibody directed against the hepatocyte growth factor receptor (c-Met) with potential antineoplastic activity. Anti-MET monoclonal antibody MetMAb binds to the extracellular domain of c-Met, preventing the binding of its ligand, hepatocyte growth factor (HGF); the activation of the c-Met signaling pathway is thus inhibited, which may result in cell death in c-Met-expressing tumor cells. c-Met, a receptor tyrosine kinase, is overexpressed on the cell surfaces of a variety of cancer cell types and may play a key role in their proliferation, invasion and survival.","Pharmacologic Substance"]
["C74067","Oncolytic Adenovirus Ad5-DNX-2401","Ad5-Delta24RGD|DNX-2401|DNX2401|Oncolytic Ad5-Delta 24RGD|Oncolytic Adenovirus Ad5-DNX-2401|Oncolytic Adenovirus Ad5-Delta 24RGD","An adenovirus serotype 5 strain, selectively replication competent in cells defective in the Rb/p16 tumor suppressor pathway, with potential oncolytic activity. Oncolytic adenovirus Ad5-DNX2401 contains an integrin binding RGD-4C motif, allowing Coxsackie adenovirus receptor-independent infection of tumor cells, which are often deficient for Coxsackie and adenovirus receptors (CARs). Selectively replication competent in cells that are defective in retinoblastoma gene (Rb) or cyclin-dependent kinase inhibitor-2A (p16), active replication of oncolytic adenovirus Ad5-Delta 24RGD in tumor cells may induce oncolysis or cell lysis. As integral components of the late G1 restriction point, the Rb gene product and p16 are negative regulators of the cell cycle; ovarian cancer cells and non-small cell lung cancer cells may be defective in the Rb/p16 pathway.","Pharmacologic Substance"]
["C48412","Oncolytic Adenovirus Encoding GM-CSF","CG0070|Oncolytic Adenovirus Encoding GM-CSF","A recombinant oncolytic adenovirus encoding the immunohematopoietic cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with potential antineoplastic activity. Upon administration, the oncolytic adenovirus selectively infects and replicates in tumor cells, which may result in tumor cells lysis. Synergistically, GM-CSF (sargramostim) expressed by the oncolytic adenovirus may promote a cytotoxic T cell response against tumor cells harboring the oncolytic adenovirus, resulting in an immune-mediated tumor cell death.","Pharmacologic Substance"]
["C107160","Oncolytic Adenovirus ICOVIR5-infected Autologous Mesenchymal Stem Cells","Celyvir|Oncolytic Adenovirus ICOVIR5-infected Autologous Mesenchymal Stem Cells","Bone marrow-derived autologous mesenchymal stem cells (MSCs) infected with the oncolytic, replication-competent adenovirus ICOVIR5, with potential antineoplastic activity. Upon infusion of the oncolytic adenovirus ICOVIR5-infected autologous MSCs, these cells target the adenovirus to tumors. The oncolytic virus then selectively transfects and replicates in the tumor cells causing a direct cytotoxic effect and lysis of the tumor cells. In addition, the viral infection may stimulate an immune response against the virally-infected tumor cells. This may lead to an inhibition of cancer cell proliferation. ICOVIR-5, a virus derived from wild-type human adenovirus serotype 5 (Had5), has been modified to selectively replicate in tumor cells that have a deregulated retinoblastoma/E2F pathway.","Cell|Pharmacologic Substance"]
["C111893","Oncolytic Herpes Simplex Virus-1-encoding GM-CSF","HSV-encoding GM-CSF|Oncolytic Herpes Simplex Virus-1-encoding GM-CSF|OrienX010|Recombinant hGM-CSF","An ICP34.5-, ICP47-deleted, oncolytic herpes simplex type-1 virus (HSV-1) isolated from the mouth of an HSV-1-infected patient of Chinese Han ethnicity, and encoding the immunostimulating factor cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with potential immunostimulating and antineoplastic activities. Upon administration, the recombinant human GM-CSF HSV-1 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, GM-CSF attracts dendritic cells (DCs) and may stimulate a cytotoxic T cell response against tumor cells, which results in immune-mediated tumor cell death. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Additionally, deletion of ICP47 causes increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and oncolysis of tumor cells. Interruption of the ICP6 gene, which encodes the large subunit of the viral ribonucleotide reductase, in the viral vector also enhances selective replication in tumor cells.","Pharmacologic Substance"]
["C90563","Oncolytic HSV-1 rRp450","Oncolytic HSV-1 rRp450|rRp450","A gene therapy agent containing an attenuated, replication-competent, genetically engineered mutant form of the Herpes simplex virus 1 (HSV-1) strain KOS with potential antineoplastic activity. Upon infusion into the hepatic artery, oncolytic HSV-1 rRp450 replicates in hepatocellular carcinoma (HCC) cells and exerts direct cytotoxic effects eventually disrupting cancer cell membranes and liberating progeny virions thereby infecting adjacent tumor cells. In addition, rRp450 expresses the cytochrome P450 transgene that activates oxazaphosphorines, such as cyclophosphamide (CPA). Therefore, CPA can become activated in the presence of rRp450 and exert its antineoplastic effect. rRp450 is deleted for the HSV-1 gene UL39, encoding the viral ribonucleotide reductase large subunit infected cell protein 6 (ICP6), thereby disrupting the activity of viral ribonucleotide reductase and resulting in the inhibition of nucleotide metabolism and viral DNA synthesis in nondividing cells but not in dividing cells. UL39 is replaced by the rat CYP2B1 gene, encoding a cytochrome P450 enzyme that activates oxazaphosphorines. rRp450 also expresses viral thymidine kinase, which activates the cancer prodrug ganciclovir.","Pharmacologic Substance"]
["C84840","Oncolytic HSV1716","HSV1716|Oncolytic HSV1716","A neuroattenuated, replication-restricted, ICP34.5 deleted (RL1 gene)-mutant herpes simplex virus (HSV) type I, constructed from wild-type strain 17, with potential oncolytic activity. Upon intratumoral injection, oncolytic HSV1716 transfects, replicates in, and lyses rapidly dividing cells such as tumor cells. Because the RL1 gene is deleted, HSV1716 is unable to replicate in non-dividing cells.","Immunologic Factor|Pharmacologic Substance"]
["C66942","Oncolytic Measles Virus Encoding Thyroidal Sodium Iodide Symporter","MV-NIS|Oncolytic Measles Virus Encoding Thyroidal Sodium Iodide Symporter","An attenuated oncolytic Edmonston (Ed) strain of measles virus encoding the human thyroidal sodium iodide symporter (MV-NIS) with potential antineoplastic activity. The cellular receptor of MV is human CD46 antigen, a type 1 integral membrane glycoprotein found on nearly all human tissues and overexpressed on many cancer cell types. After attachment to and fusion of host cell membranes, MV-NIS induces syncytia and cell lysis. When combined with radioiodine 123 (I-123), expressed NIS facilitates uptake of I-123 into MV-infected cells, thereby allowing for noninvasive imaging of viral gene expression. MV-NIS also enhances the oncolytic activity of MV against radiosensitive tumor cells by additional destruction of the MV-infected cells when using iodine-131.","Pharmacologic Substance|Virus"]
["C91700","Oncolytic Newcastle Disease Virus","MTH-68H|Oncolytic NDV|Oncolytic Newcastle Disease Virus","An oncolytic viral agent containing the oncolytic, live-attenuated strain of the paramyxovirus Newcastle disease virus (NDV), with potential antineoplastic activity. Upon administration, NDV specifically infects and replicates in cancer cells. This may result in a direct cytotoxic effect involving the lysis of tumor cells via apoptotic mechanisms and may eventually lead to an inhibition of cancer cell proliferation.","Pharmacologic Substance|Virus"]
["C2830","ONYX-015","CI-1042|E1B 55kDa mutant adenovirus dl1520|E1B-Attenuated Adenovirus|ONYX-015","An E1B-55kDa-deleted adenovirus that is able to selectively replicate in and lyse TP53-deficient human tumor cells. After tumor cell lysis, released viruses infect neighboring tumor cells, tripping a chain of ONYX-015-mediated tumor cell cytotoxicity. (NCI04)","Pharmacologic Substance"]
["C90545","OPCs/Green Tea/Spirullina/Curcumin/Antrodia Camphorate/Fermented Soymilk Extract Capsule","MB-6|OPCs/Green Tea/Spirullina/Curcumin/Antrodia Camphorate/Fermented Soymilk Extract Capsule|Oligomeric Proanthocyanidins/Green Tea/Spirullina/Curcumin/Antrodia Camphorate/Fermented Soymilk Extract Capsule","A capsule containing a fermented soymilk extract and oligomeric proanthocyanidins (OPCs), green tea, spirullina, curcumin and antrodia camphorate powder, with potential antioxidant, immunomodulating, anti-infective and anti-cancer activities. OPCs/green tea/spirullina/curcumin/antrodia camphorate/fermented soymilk extract capsule may boost the immune system and may alleviate fatigue and poor appetite in cancer chemotherapy patients.","Pharmacologic Substance"]
["C48413","Opioid Growth Factor","OGF|Opioid Growth Factor|opioid growth factor","An endogenous pentapeptide with potential antineoplastic and antiangiogenic activities. Opioid growth factor (OGF) binds to and activates the OGF receptor, present on some tumor cells and vascular cells, thereby inhibiting tumor cell proliferation and angiogenesis. (NCI05)","Pharmacologic Substance"]
["C91388","Oprozomib","O-methyl-N-((2-methylthiazol-5-yl)carbonyl)-l-seryl-O-methyl-N-((1S)-1-benzyl-2-((2R)-2-methyloxiran-2-yl)-2-oxoethyl)-l-serinamide|OPROZOMIB|Oprozomib|PR-047|Proteasome Inhibitor ONX 0912","An orally bioavailable proteasome inhibitor with potential antineoplastic activity. Proteasome inhibitor ONX 0912 inhibits the activity of the proteasome, thereby blocking the targeted proteolysis normally performed by the proteasome; this may result in an accumulation of unwanted or misfolded proteins. Disruption of various cell signaling pathways may follow, eventually leading to the induction of apoptosis and inhibition of tumor growth. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquitinated.","Pharmacologic Substance"]
["C99763","Oral Aminolevulinic Acid Hydrochloride","5-Aminolevulinic Acid Hydrochloride, Oral|Gliolan|Oral 5-ALA|Oral Aminolevulinic Acid Hydrochloride","A powder for an oral solution comprised of the hydrochloride salt of 5-aminolevulinic acid (ALA) with a potential application for photodynamic therapy. After oral administration, ALA is converted intracellularly into the photosensitizer protoporphyrin IX (PpIX). Upon exposure to light of appropriate wavelength (violet to blue range), excited PpIX emits a characteristic red fluorescence which could facilitate guided resection, and generates excited singlet oxygen molecules that could kill cells when appropriate laser dosage is applied. ALA is preferentially taken up by and accumulates in many types of cancer cells compared to normal, healthy cells. Consequently, cancer cells can be visualized and can be distinguished from normal, healthy cells.","Pharmacologic Substance"]
["C118288","Oral Azacitidine","CC-486|Oral Azacitidine","An orally bioavailable formulation of azacitidine, a pyrimidine nucleoside analogue of cytidine, with antineoplastic activity. Upon oral administration, azacitidine is taken up by cells and metabolized to 5-azadeoxycitidine triphosphate. The incorporation of 5-azadeoxycitidine triphosphate into DNA reversibly inhibits DNA methyltransferase, and blocks DNA methylation. Hypomethylation of DNA by azacitidine may re-activate tumor suppressor genes previously silenced by hypermethylation, resulting in an antitumor effect. In addition, the incorporation of 5-azacitidine triphosphate into RNA disrupts normal RNA function and impairs tRNA (cytosine-5)-methyltransferase activity, resulting in an inhibition of RNA and protein synthesis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C64338","Oral Fludarabine Phosphate","Fludara Oral|Oral Fludarabine Phosphate","An oral formulation of the phosphate salt of fludarabine, a synthetic purine nucleoside analogue antimetabolite with antineoplastic activity. Fudarabine is preferentially transported into malignant cells and metabolized by deoxycytidine kinase to its active form, 2-fluoro-ara-ATP; 2-fluoro-ara-ATP competes directly with deoxyadenosine triphosphate (dATP) and inhibits alpha DNA polymerase, RNA reductase, and DNA primase, which may result in inhibition of DNA synthesis and cell death.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C78843","Oral Hsp90 Inhibitor IPI-493","17-Aminodemethoxygeldanamycin|17-Aminogeldanamycin|Heat Shock Protein 90 Inhibitor IPI-493|IPI-493|Oral Hsp90 Inhibitor IPI-493","An orally bioavailable formulation of the ansamycin derivative 17-amino-17-demethoxygeldanamycin (17-AG) with potential antineoplastic activity. Oral Hsp90 inhibitor IPI-493 binds to and inhibits Hsp90, which may result the in growth inhibition in sensitive tumor cell populations. Hsp90, a 90 kDa molecular chaperone, may be highly expressed in tumor cells, playing a key role in the conformational maturation, stability and function of other substrate or \"client\" proteins within the cell; many of these client proteins are involved in signal transduction, cell cycle regulation and apoptosis, and may include kinases, transcription factors and hormone receptors.","Pharmacologic Substance"]
["C63478","Oral Ixabepilone","Oral Ixabepilone","An enteric-coated formulation of ixabepilone, a semisynthetic analogue of epothilone B and a non-taxane tubulin inhibitor, with antineoplastic activity. Ixabepilone binds to and stabilizes tubulin molecules, thereby interfering with the dynamics of microtubule assembly/disassembly. This results in cell cycle arrest at the G2-M phase and leads to apoptosis within fast growing tumor cells. This agent demonstrates antineoplastic activity against taxane-resistant cell lines. Compared to intravenously administered ixabepilone, the oral formulation provides a more manageable way to administer this agent.","Organic Chemical|Pharmacologic Substance"]
["C71132","Oral Microencapsulated Diindolylmethane","BR-DIM|BioResponse DIM|Oral Microencapsulated Diindolylmethane","An orally bioavailable microencapsulated formulation of diindolylmethane, an indole phytonutrient found in cruciferous vegetables, with estrogen-modulating, antiandrogenic, and potential antineoplastic activities. As a dimer of indole-3-carbinol, diindolylmethane (DIM) modulates estrogen balance by reducing the levels of 16-hydroxy estrogen metabolites and increasing the formation of beneficial 2-hydroxy estrogen metabolites. DIM also antagonizes androgen receptor activity, which may result in diminished cell proliferation and apoptosis in susceptible tumor cell populations. Pure DIM, which is relatively hydrophobic, is poorly absorbed after oral administration. This oral formulation, which consists of DIM, d-alpha-tocopheryl acid succinate, phosphatidylcholine, and silica microencapsulated in starch, significantly improves the gastrointestinal absorption of DIM.","Organic Chemical|Pharmacologic Substance"]
["C77880","Oral Milataxel","Oral Milataxel|TL-00139|TL139","An orally bioavailable taxane with potential antineoplastic activity. Upon oral administration, milataxel and its major active metabolite M-10 bind to and stabilize tubulin, resulting in the inhibition of microtubule depolymerization and cell division, cell cycle arrest in the G2/M phase, and the inhibition of tumor cell proliferation. Unlike other taxane compounds, milataxel appears to be a poor substrate for the multidrug resistance (MDR) membrane-associated P-glycoprotein (P-gp) efflux pump and may be useful for treating multidrug-resistant tumors.","Organic Chemical|Pharmacologic Substance"]
["C68924","Oral Picoplatin","Oral Picoplatin|Picoplatin (Oral)","An oral preparation of picoplatin, a third generation platinum compound with antineoplastic activity. Designed to overcome platinum drug resistance, picoplatin alkylates DNA, forming both inter- and intra-strand cross-linkages, resulting in inhibition of DNA replication and RNA transcription and the induction of apoptosis. Because of the increase in steric bulk around the platinum center, there is a relative reduction in the inactivation of picoplatin by thiol-containing species such as glutathione and metallothionein in comparison to cisplatin.","Inorganic Chemical|Pharmacologic Substance"]
["C67083","Oral Sodium Phenylbutyrate","Oral Sodium Phenylbutyrate","An orally active derivative of the short-chain fatty acid butyrate with potential antineoplastic activity. 4-Phenylbutyrate inhibits histone deacetylase, resulting in cell cycle gene expression modulation, reduced cell proliferation, increased cell differentiation, and apoptosis. This agent also initiates fragmentation of genomic DNA, resulting in decreased DNA synthesis and the inhibition of tumor cell migration and invasion.","Pharmacologic Substance"]
["C63477","Oral Topotecan Hydrochloride","(S)-10-[(dimethylamino)methyl]-4-ethyl-4,9-dihydroxy-1H-pyrano[3',4'; 6,7] indolizino[1,2-b] quinoline-3,14-(4H,12H)-dione monohydrochloride|Oral Hycamtin|Oral Topotecan Hydrochloride","An oral formulation of the hydrochloride salt of topotecan, a semisynthetic derivative of the quinoline alkaloid camptothecin, with potential antineoplastic activity. Topotecan selectively inhibits topoisomerase I activity by stabilizing topoisomerase I-DNA covalent complexes during the S phase of the cell cycle, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery.","Organic Chemical|Pharmacologic Substance"]
["C112000","Oraxol","Oraxol|Paclitaxel-HM30181 Methanesulfonate Monohydrate|Paclitaxel/HM30181A","A combination formulation composed of a capsule containing the taxane compound paclitaxel and a tablet containing the multidrug resistance (MDR) efflux pump P-glycoprotein (P-gp) inhibitor HM30181A, with potential antineoplastic activity. Upon oral administration of oraxol, the HM30181A moiety binds to and inhibits P-gp, which prevents P-gp-mediated efflux of paclitaxel, therefore enhancing its oral bioavailability. In turn, paclitaxel binds to and stabilizes microtubules, preventing their depolymerization, which results in the inhibition of cellular motility, mitosis, and replication. Altogether, this may result in greater intracellular concentration of paclitaxel, and enhanced cytotoxicity against tumor cells, when compared to the administration of paclitaxel alone.  P-gp, encoded by the MDR-1 gene, is a member of the ATP-binding cassette (ABC) superfamily of transmembrane transporters; it prevents the intestinal uptake and intracellular accumulation of various cytotoxic agents.","Pharmacologic Substance"]
["C1784","Oregovomab","B43.13|MoAb B43.13|Monoclonal Antibody B43.13|OREGOVOMAB|Oregovomab|OvaRex Monoclonal Antibody B43.13|OvaRex|oregovomab","A murine monoclonal antibody that attaches to the tumor-associated antigen CA125. Vaccination with monoclonal antibody B43.13 may stimulate a host cytotoxic immune response against tumor cells that express CA125. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1250","Ormaplatin","ORMAPLATIN|Ormaplatin|Platinum, tetrachloro(1,2-cyclohexanediamine-N,N')-, (OC-6-22-(trans))-|Tetraplatin|tetrachloro(1,2-cyclohexanediamine-N,N')-, (OC-6-22-(trans))Platinum","A platinum(IV) analogue with antineoplastic activity. Ormaplatin alkylates DNA, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity.","Inorganic Chemical|Pharmacologic Substance"]
["C1867","Ortataxel","BAY 59-8862|Bay 59-8862|IDN5109|Ortataxel|SB-T-101131","A semisynthetic, second-generation taxane derivative with potential antineoplastic activity. Ortataxel binds to and stabilizes tubulin molecules, thereby interfering with the dynamics of microtubule assembly/disassembly. This results in the inhibition of cell division and cellular proliferation. As it represents a poor substrate for P-glycoprotein (P-gp), multi-drug resistance protein (MRP-1) and breast cancer resistance protein (BCRP) mediated efflux, ortataxel modulates multi-drug resistance mechanisms and may be useful for treating multi-drug resistant tumors that express Pgp, MRP-1 and BCRP.","Organic Chemical|Pharmacologic Substance"]
["C90582","Orteronel","6-((7S)-7-hydroxy-6,7-dihydro-5h-pyrrolo(1,2-c)imidazol-7-yl)-N-methyl-2-naphthalenecarboxamide|Androgen Synthesis Inhibitor TAK-700|CYP17A1 Lyase Inhibitor TAK-700|ORTERONEL|Orteronel|TAK-700","An orally bioavailable non-steroidal androgen synthesis inhibitor of steroid 17alpha-monooxygenase (17,20 lyase) with potential antiandrogen activity. TAK-700 binds to and inhibits the steroid 17alpha-monooxygenase in both the testes and adrenal glands, thereby inhibiting androgen production. This may decrease androgen-dependent growth signaling and may inhibit cell proliferation of androgen-dependent tumor cells. The cytochrome P450 enzyme CYP17A1 (P450C17), localized to the endoplasmic reticulum (ER), exhibits both 17alpha-hydroxylase and 17,20-lyase activities, and plays a key role in the steroidogenic pathway that produces steroidal hormones, such as progestins, mineralocorticoids, glucocorticoids, androgens, and estrogens.","Pharmacologic Substance"]
["C26645","OSE 2101","EP-2101|EP2101|IDM2101|OSE 2101|OSE-2101|Tedopi","A proprietary cancer DNA vaccine that contains multiple natural and modified epitopes derived from the four tumor associated antigens, CEA, HER2/neu, p53, and MAGE 2/3. EP-2101 also includes CAP1-6D, a heteroclitic CEA analog, and PADRE, a proprietary universal T-cell epitope that serves to enhance the immunogenicity of the epitopes.  This agent has been shown to elicit cytotoxic T-lymphocyte responses against tumor cells expressing these multiple epitopes. (NCI04)","Pharmacologic Substance"]
["C38694","OSI-7904L","GS7904L|OSI-7904L","A liposome-encapsulated formulation of the benzoquinazoline folate analog OSI-7904 with antineoplastic activity. As a thymidylate synthase inhibitor, OSI-7904 noncompetitively binds to thymidylate synthase, resulting in inhibition of thymine nucleotide synthesis and DNA replication. Liposome encapsulation improves the efficacy and increases the half-life of OSI-7904. (NCI04)","Pharmacologic Substance"]
["C116377","Osimertinib","2-Propenamide, N-(2-((2-(dimethylamino)ethyl)methylamino)-4-methoxy-5-((4-(1-methyl-1H-indol-3-yl)-2-pyrimidinyl)amino)phenyl)-|AZD-9291|AZD9291|Mereletinib|OSIMERTINIB|Osimertinib|Tagrisso","A third-generation, orally available, irreversible, mutant-selective, epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, osimertinib covalently binds to and inhibits the activity of mutant forms of EGFR, including the T790M EGFR mutant, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization. AZD9291 preferentially inhibits mutated forms of EGFR including T790M, a secondarily-acquired resistance mutation, and may have enhanced anti-tumor effects in tumors with T790M-mediated resistance when compared to other EGFR tyrosine kinase inhibitors. As this agent is selective towards mutant forms of EGFR, its toxicity profile may be reduced when compared to non-selective EGFR inhibitors which also inhibit wild-type EGFR.","Pharmacologic Substance"]
["C74006","Otlertuzumab","Otlertuzumab|TRU-016","A recombinant single-chain polypeptide engineered to exhibit the full binding and activity of an anti-CD37 monoclonal antibody with potential immunostimulatory and antineoplastic activities. Otlertuzumab binds to CD37 on B-cells, which may result in antibody-dependent cell-mediated cytotoxicity (ADCC) and apoptosis. CD37 is a transmembrane glycoprotein expressed at high-levels on B cells and to a lesser extent on T cells and myeloid cells. This agent may have a longer half-life in vivo than conventional monoclonal antibodies.","Pharmacologic Substance"]
["C2546","OVA BiP Peptide","OVA BiP Peptide|OVA-BiP Hybrid Peptide","A 19 amino-acid hybrid peptide antigen with immune adjuvant property. OVA-BiP peptide consists of 8 amino acids from ovalbumin joined via a tripeptide linker to a stretch of 8 amino acids, the minimum binding domain of BiP (immunoglobulin heavy chain-binding protein, aka grp78), a member of the heat shock protein (hsp) 70 family. As a chaperon, BiP binds to newly synthesized, unfolded mu immnoglobulin heavy chains prior to its assembly with light chains in the endoplasmic reticulum. In conjunction with a tumor antigen, this hybrid peptide is used to potentiate antigen presentation and consequently prime cytotoxic T lymphocyte responses.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C113651","Ovapuldencel-T","Ovapuldencel-T","A cancer vaccine consisting of autologous dendritic cells (DCs) loaded with autologous, lethally irradiated cancer cells and mixed with the cytokine granulocyte-macrophage colony stimulating factor (GM-CSF), with potential immunostimulatory and antineoplastic activities. Upon vaccination, ovapuldencel-T may stimulate the immune system to exert a cytotoxic T-lymphocyte (CTL) immune response against the repertoire of tumor associated antigens (TAAs) found in the irradiated cancer cells. GM-CSF enhances the activation of dendritic cells (DCs) and promotes antigen presentation to both B- and T-lymphocytes.","Cell|Pharmacologic Substance"]
["C48414","Ovarian Cancer Peptide Vaccine","OC-PEP-VAC|Ovarian Cancer Peptide Vaccine","A cancer vaccine comprised of synthetic peptides corresponding to naturally-occurring peptides derived from ovarian cancer cell antigens. Ovarian cancer peptide vaccine may elicit a cytotoxic T-cell response against tumor cells expressing the related ovarian cancer cell antigens. (NCI05)","Pharmacologic Substance"]
["C96739","Ovarian Cancer Stem Cell/hTERT/Survivin mRNAs-loaded Autologous Dendritic Cell Vaccine","DC-006 Vaccine|DC-006|Ovarian Cancer Stem Cell/hTERT/Survivin mRNAs-loaded Autologous Dendritic Cell Vaccine","A cancer vaccine containing autologous dendritic cells (DCs) that are transfected with mRNAs extracted from amplified ovarian cancer stem cells, and mRNAs of the universal tumor antigens human telomerase reverse transcriptase (hTERT) and survivin with potential immunostimulatory and antineoplastic activities. Upon administration, ovarian cancer stem cell/hTERT/survivin mRNAs-loaded autologous DC-006 vaccine may elicit a highly specific cytotoxic T-cell (CTL) response against ovarian cancer cells expressing hTERT, survivin, and specific ovarian cancer stem cell antigens. hTERT, the catalytic subunit of human telomerase, and survivin, a member of the inhibitor of apoptosis (IAP) family of proteins, may be upregulated in certain tumor cell types, playing key roles in tumor cell growth and survival. Ovarian cancer stem cells contain a specific range of antigens that are essential for the neoplastic growth and survival of ovarian cancer cells.","Immunologic Factor|Pharmacologic Substance"]
["C115105","Ovarian Tumor Antigen-activated Autologous Dendritic Cell Vaccine","DCVAC/OvCa|Ovarian Tumor Antigen-activated Autologous Dendritic Cell Vaccine","A dendritic cell (DC)-based cancer vaccine composed of autologous dendritic cells (DCs) activated with an ovarian tumor cell lysate containing tumor-associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, the ovarian tumor antigen-activated autologous DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against ovarian cancer cells expressing ovarian tumor cell-specific antigens, which may result in ovarian tumor cell lysis.","Cell|Pharmacologic Substance"]
["C2350","Ovine Submaxillary Mucin","Ovine Sialomucin|Ovine Submaxillary Mucin","A naturally occurring mucin glycoprotein. Ovine submaxillary mucin (OSM), extracted from an ovine submaxillary gland, provides a rich source of the sialylated Tn antigen (sTn), which is a carbohydrate antigen found on mucins of many epithelial tumors. Vaccination with OSM may result in the production of antibodies as well as elicitation of a cytotoxic T- lymphocyte (CTL) response against tumor cells expressing sTn, thereby results in decreased tumor cell growth.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1181","Oxaliplatin","1-OHP|Ai Heng|Aiheng|DACPLAT|Dacotin|Dacplat|Diaminocyclohexane Oxalatoplatinum|ELOXATIN|Eloxatin|Eloxatine|JM-83|OXALIPLATIN|Oxalatoplatin|Oxalatoplatinum|Oxaliplatin|RP 54780|RP-54780|SR-96669|[(1R,-2R)-1,2-cyclohexanediamine-N,N'][oxalato (2--)-O,O']platinum|[SP-4-2-(1R-trans)]-(1,2,cyclohexanediamine-N,N')[ethanedioato(2--)-O,O']platinum|oxalato (1R,2R-cyclohexanediamine)platinum(II)|oxalato (trans-l-1,2-diaminocyclohexane)platinum(II)|oxaliplatin|trans-l DACH oxalatoplatinum|trans-l diaminocyclohexane oxalatoplatinum","An organoplatinum complex in which the platinum atom is complexed with 1,2-diaminocyclohexane (DACH) and with an oxalate ligand as a 'leaving group.' A 'leaving group' is an atom or a group of atoms that is displaced as a stable species taking with it the bonding electrons. After displacement of the labile oxalate ligand leaving group, active oxaliplatin derivatives, such as monoaquo and diaquo DACH platinum, alkylate macromolecules, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity. The DACH side chain appears to inhibit alkylating-agent resistance. (NCI04)","Pharmacologic Substance"]
["C91074","Oxaliplatin-Encapsulated Transferrin-Conjugated N-glutaryl Phosphatidylethanolamine Liposome","MBP-426|Oxaliplatin-Encapsulated Tf-Conjugated NGPE-Liposome|Oxaliplatin-Encapsulated Transferrin-Conjugated N-glutaryl Phosphatidylethanolamine Liposome","A nanoparticle formulation containing N-glutaryl phosphatidylethanolamine (NGPE)-liposomes encapsulating oxaliplatin and conjugated to the human transferrin (Tf) ligand, with potential antineoplastic activity. Upon infusion of oxaliplatin-encapsulated transferrin-conjugated NGPE liposomes, the transferrin moiety targets and binds to the Tf receptor, which is overexpressed on a variety of human cancer cells. Upon binding and internalization, oxaliplatin is released and its active derivatives alkylate macromolecules, forming both inter- and intra-strand platinum-DNA crosslinks, which results in an inhibition of DNA replication and transcription. By extending the circulation time and specifically targeting transferrin receptors, this formulation may improve the efficacy and safety of oxaliplatin therapy, compared to administration of oxaliplatin alone. NGPE, a reactive phospholipid, is used as a linker to attach the Tf ligand, to the liposome.","Pharmacologic Substance"]
["C130012","Oxidative Phosphorylation Inhibitor IACS-010759","IACS-010759|OXPHOS Inhibitor IACS-010759|Oxidative Phosphorylation Inhibitor IACS-010759","An orally bioavailable oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. Upon administration of the OxPhos inhibitor IACS-010759, this agent binds to and inhibits complex I of the electron transport chain (NADH ubiquinone oxidoreductase), thereby selectively depriving tumor cells of nutrients, and energy, and inhibiting nucleotide and amino acid production, which induces autophagy, causes tumor cell death and inhibits cell proliferation. Mitochondrial complex I, which is hyperactivated in cancer cells to meet their increased demands for energy, plays a key role in the promotion of cancer cell proliferation.","Pharmacologic Substance"]
["C1316","Oxidopamine","2,4,5-Trihydroxyphenethylamine|5-(2-Aminoethyl)-1,2,4-benzenetriol|6-Hydroxydopamine|6-OHDA|OXIDOPAMINE|Oxidopamine","An antagonist of the neurotransmitter dopamine with potential antineoplastic activity. 6-Hydroxydopamine (6-HOD) can be taken up by selective adrenergic terminals, thereby causing acute degeneration of adrenergic terminals that leads to depletion of norepinephrine, and of dopamine in the dopamine-sensitive sites. This agent is auto-oxidated at physiological pH that leads to the formation of reactive free radicals, thereby leading to cytotoxicity in neural cells.  6-Hydroxydopamine is often used to induce CNS and sympathetic neural lesions that model aging and various nervous disorders in animal systems.","Organic Chemical|Pharmacologic Substance"]
["C118283","OxPhos Inhibitor VLX600","1-(2-Pyridinyl)ethanone(6-methyl-5H-[1,2,4]triazino[5,6-b]indol-3-yl)hydrazone|OxPhos Inhibitor VLX600|VLX-600","A lipophilic cation-based triazinoindolyl-hydrazone compound and mitochondrial oxidative phosphorylation (OxPhos) inhibitor, with potential antineoplastic activity. Upon infusion, in normal cells and proliferating tumor cells where glucose is readily available, inhibition of OxPhos by VLX600 induces a hypoxia-inducible factor 1-alpha (HIF-1alpha)-dependent shift to, and an increase in glycolysis. Glycolysis alone does not produce enough energy to support the growth of tumor cells in this environment, and the induction of autophagy occurs. In the metabolically compromised tumor microenvironment, the availability of oxygen and glucose is limited due to poor vascularization and perfusion of tumor micro-areas. Tumor cells growing in this environment are thus unable to compensate for decreased mitochondrial function by increasing glycolysis. This leads to nutrient depletion, decreased energy production, induction of autophagy, tumor cell death and an inhibition of cell proliferation in quiescent tumor cells. Mitochondrial OxPhos, which is hyperactivated in cancer cells, plays a key role in the promotion of cancer cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C95214","Ozarelix","D 63153|D-63 153|LHRH antagonist SPI-153|Ozarelix|SPI-153","A highly modified, fourth generation linear decapeptide with gonadotropin-releasing hormone (GnRH or LHRH) antagonizing properties. Ozarelix competitively binds to and blocks the gonadotropin releasing hormone receptor in the anterior pituitary gland, thereby inhibiting the secretion and release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone. As a result, this may relieve symptoms associated with hormonally dependent disease states such as hormone-dependent prostate cancer.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C96738","p.DOM-WT1-126 DNA Vaccine","p.DOM-WT1-126 DNA Vaccine","A fusion DNA vaccine containing the first domain of fragment C (FrC) of tetanus toxin (TT865-1120) (p.DOM) fused to the human Wilms' Tumor gene-1 (WT1)-derived MHC class I-binding epitope WT1.126, with potential antitumor activity. Upon vaccination with p.DOM-WT1-126 DNA and subsequent electroporation, this vaccine may induce a WT1 epitope-specific cytotoxic T-lymphocyte (CTL) response against WT1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation in WT1-overexpressing cancer cells. WT1, a tumor associated antigen, is overexpressed in most types of leukemia and in a variety of solid cancers. The FrC of tetanus toxin contains the MHC II-binding sequence, p30, which induces T-helper cell activation for long-lasting immunity.","Pharmacologic Substance"]
["C96737","p.DOM-WT1-37 DNA Vaccine","p.DOM-WT1-37 DNA Vaccine","A fusion DNA vaccine containing the first domain of fragment C (FrC) of tetanus toxin (TT865-1120) (p.DOM) fused to the human Wilms' Tumor gene-1 (WT1)-derived MHC class I-binding epitope WT1.37, with potential antitumor activity. Upon vaccination with p.DOM-WT1-37 DNA and subsequent electroporation, this vaccine may induce a WT1 epitope-specific cytotoxic T-lymphocyte (CTL) response against WT1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation in WT1-overexpressing cancer cells. WT1, a tumor associated antigen, is overexpressed in most types of leukemia and in a variety of solid cancers. The FrC of tetanus toxin contains the MHC II-binding sequence, p30, which induces T-helper cell activation for long-lasting immunity.","Pharmacologic Substance"]
["C103277","p110beta/delta PI3K Inhibitor GS-9820","CAL-120|GS-9820|p110beta/delta PI3K Inhibitor GS-9820","An inhibitor of the beta and delta isoforms of the 110 kDa catalytic subunit of class IA phosphoinositide-3 kinases (PI3K) with potential immunomodulating and antineoplastic activities. p110beta/delta PI3K inhibitor GS-9820 inhibits the activity of PI3K, thereby preventing the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3), which decreases tumor cell proliferation and induces cell death. PI3K-mediated signaling is often dysregulated in cancer cells; the targeted inhibition of PI3K is designed to preserve PI3K signaling in normal, non-neoplastic cells.","Pharmacologic Substance"]
["C99134","p38 MAPK Inhibitor LY3007113","LY3007113|p38 MAPK Inhibitor LY3007113","An orally active p38 mitogen-activated protein kinase (MAPK) inhibitor with potential immunomodulating, anti-inflammatory, and antineoplastic activity. Upon administration, LY3007113 inhibits the activity of p38, thereby preventing p38 MAPK-mediated signaling. This may result in the inhibition of the production of proinflammatory cytokines and the induction of tumor cell apoptosis. p38 MAPK, a serine/threonine protein kinase often upregulated in cancer cells, plays a crucial part in the production of a variety of cytokines involved in inflammation and cellular proliferation such as tumor necrosis factor (TNF) and interleukin (IL)-1 and -6.","Pharmacologic Substance"]
["C1986","p53 Peptide Vaccine","MPS-128|PR-147|p53 Peptide Vaccine|p53:264-272 Peptide","A peptide-based cancer vaccine composed of amino acids 264 to 272 of the wild-type protein encoded by the P53 gene. p53 peptide vaccine may elicit an HLA-A2.1-restricted cytotoxic T lymphocyte immune response against tumor cells that overexpress p53 protein. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C104280","p53/HDM2 Interaction Inhibitor CGM097","CGM097|HDM2/p53 Inhibitor CGM097|p53/HDM2 Interaction Inhibitor CGM097","An orally bioavailable HDM2 (human homolog of double minute 2) antagonist with potential antineoplastic activity. Upon oral administration, p53/HDM2 interaction inhibitor CGM097 inhibits the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited, which may result in the restoration of p53 signaling and, thus, the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger nuclear phosphoprotein, is a negative regulator of the p53 pathway, often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C106120","p53-HDM2 Interaction Inhibitor MI-773","MI-773|SAR405838|p53-HDM2 Interaction Inhibitor MI-773|p53-MDM2 Interaction Inhibitor MI-773","An orally available spiro-oxindole HDM2 (human double minute 2) antagonist with potential antineoplastic activity. Upon oral administration, the p53-HDM2 protein-protein interaction inhibitor MI-773 binds to HDM2, preventing the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored, which may result in the restoration of p53 signaling and lead to the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger protein and a negative regulator of the p53 pathway, is often overexpressed in cancer cells. It has been implicated in cancer cell proliferation and survival.","Pharmacologic Substance"]
["C82420","P53-Synthetic Long Peptides Vaccine","P53-SLP (70-251) Vaccine|P53-Synthetic Long Peptides (70-251) Vaccine|P53-Synthetic Long Peptides Vaccine","A peptide vaccine consisting of 10 synthetic long peptides (SLPs), 25-30 amino acids in size and derived from the middle portion of p53 (amino acids 70-251), mixed with the adjuvant Montanide ISA-51 with potential immunostimulatory and antitumor activities. Upon administration, p53 synthetic long peptide (70-251) vaccine may stimulate the host immune system to mount a cytotoxic T-cell lymphocyte (CTL) response against p53-expressing tumor cells. p53, a tumor associated antigen (TAA), may be overexpressed in variety of cancer cell types.","Immunologic Factor|Pharmacologic Substance"]
["C91393","p70S6K Inhibitor LY2584702","LY2584702|p70S6K Inhibitor LY2584702","An orally available inhibitor of p70S6K signaling, with potential antineoplastic activity. p70S6K inhibitor LY2584702 inhibits ribosomal protein S6 Kinase (p70S6K), and prevents phosphorylation of the S6 subunit of ribosomes, thereby inhibiting normal ribosomal function within tumor cells leading to a decrease in protein synthesis and in cellular proliferation. P70S6K, a serine/threonine kinase, acts downstream of PIP3 and phosphoinositide-dependent kinase-1 in the PI3 kinase pathway, is often upregulated in a variety of cancer cells, and is involved in the regulation of cell growth, proliferation, motility, and survival.","Pharmacologic Substance"]
["C112004","p70S6K/Akt Inhibitor MSC2363318A","MSC2363318A|p70S6K/Akt Inhibitor MSC2363318A","An orally available inhibitor of the serine/threonine protein kinases ribosomal protein S6 Kinase (p70S6K) and Akt (protein kinase B), with potential antineoplastic activity. Upon administration, p70S6K/Akt inhibitor MSC2363318A binds to and inhibits the activity of p70S6K and Akt. This prevents the activation of the PI3K/Akt/p70S6K signaling pathway and inhibits tumor cell proliferation in cancer cells that have an overactivated PI3K/Akt/p70S6K signaling pathway. Constitutive activation and dysregulated signaling of the PI3K/Akt/p70S6K pathway are frequently associated with tumorigenesis of many tumor types; targeting multiple kinases in this pathway is more efficacious than targeting a single kinase.","Organic Chemical|Pharmacologic Substance"]
["C118287","p97 Inhibitor CB-5083","CB-5083|p97 Inhibitor CB-5083","An orally bioavailable inhibitor of valosin-containing protein (VCP) p97, with potential antineoplastic activity. Upon oral administration, CB-5083 specifically binds to and inhibits the activity of p97. This prevents ubiquitin-dependent protein degradation and causes cellular accumulation of poly-ubiquitinated proteins. The inhibition of endoplasmic reticulum (ER)-associated protein degradation activates the ER-dependent stress response pathway, and leads to both an induction of apoptosis and inhibition of cell proliferation in susceptible tumor cells. p97, a type II AAA ATPase, plays a key role in cellular protein homeostasis. Its overexpression in many tumor cell types is associated with increased tumor cell proliferation and survival.","Pharmacologic Substance"]
["C2428","PA-1-STK Ovarian Carcinoma Vaccine","PA-1-STK Ovarian Carcinoma Vaccine","A cell-based cancer vaccine with potential antineoplastic activity. PA-1-STK ovarian carcinoma vaccine is produced by transducing the ovarian cancer cell line, PA-1, with the herpes simplex thymidine kinase (HSV-tk) gene, resulting in a cell line, PA-1-STK, that permanently expresses the HSV tk gene. Upon transfection into malignant cells, this vaccine is capable of sensitizing tumor cells in response to an antiviral drug such as ganciclovir, which is readily phosphorylated by the TK enzyme to its active form. Administration of ganciclovir following PA-1 STK transfection results in enhanced cytotoxicity of the transfected tumor cells. Additionally, adjacent non-transfected cells are also killed by the activated antiviral drug, a phenomenon referred to as the bystander effect that occurs with this type of suicide-gene transfer technique.","Immunologic Factor|Pharmacologic Substance"]
["C1411","Paclitaxel","5Beta,20-epoxy-1,2alpha,4,7beta,10beta,13alpha-hexahydroxytax-11-en-9-one, 4,10-Diacetate 2-Benzoate 13-Ester with (2R,3S)-N-Benzoyl-3-phenylisoserine|Anzatax|Asotax|Bristaxol|PACLITAXEL|Paclitaxel|Praxel|Taxol Konzentrat|Taxol|[2aR-[2a Alpha,4beta,4a beta,6beta,9alpha(alphaR*,betaS*),-11alpha,12alpha,12a alpha,12b alpha]]-beta-(benzoylamino)-alpha-hydroxybenzene-propanoic acid 6,12b-bis(acetyloxy)-12-(benzoyloxy)-1a,33,4,-41,5,6,9,10,11,12,12a,12b-dodecahydro-4,11-dihydroxy-41,8,-12,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca[3,4]benz[1,2-b]oxet-9-yl Ester|paclitaxel","A compound extracted from the Pacific yew tree Taxus brevifolia with antineoplastic activity.  Paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division.  This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2). (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2688","Paclitaxel Albumin-Stabilized Nanoparticle Formulation","ABI 007|ABI-007|Abraxane|Albumin-Stabilized Nanoparticle Paclitaxel|Albumin-bound Paclitaxel|Nanoparticle Albumin-bound Paclitaxel|Nanoparticle Paclitaxel|Paclitaxel Albumin-Stabilized Nanoparticle Formulation|nab-paclitaxel|nanoparticle paclitaxel|paclitaxel albumin-stabilized nanoparticle formulation|protein-bound paclitaxel","A Cremophor EL-free, albumin-stabilized nanoparticle formulation of the natural taxane paclitaxel with antineoplastic activity. Paclitaxel binds to and stabilizes microtubules, preventing their depolymerization and so inhibiting cellular motility, mitosis, and replication. This formulation solubilizes paclitaxel without the use of the solvent Cremophor, thereby permitting the administration of larger doses of paclitaxel while avoiding the toxic effects associated with Cremophor.","Pharmacologic Substance"]
["C96934","Paclitaxel Ceribate","7beta-((2RS)-2,3-dihydroxypropoxycarbonyloxy)-1-hydroxy-9-oxo-5beta,20-epoxytax-11-ene-2alpha,4,10beta,13alpha-tetrayl 4,10-diacetate 2-benzoate 13-((2R,3S)-3-benzamido-2-hydroxy-3-phenylpropanoate)|PACLITAXEL CERIBATE|Paclitaxel Ceribate","The ceribate ester form of paclitaxel, a compound extracted from the Pacific yew tree Taxus brevifolia with antineoplastic activity. Paclitaxel binds to and stabilizes tubulin thereby inhibiting the disassembly of microtubules, resulting in the inhibition of cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein B-cell Leukemia 2 (BCL2).","Organic Chemical|Pharmacologic Substance"]
["C96037","Paclitaxel Injection Concentrate for Nanodispersion","PICN|Paclitaxel Injection Concentrate for Nanodispersion","A nanoparticle-based injectable concentrate containing the water-insoluble taxane paclitaxel, with potential antineoplastic activity.  Upon reconstitution and administration, paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. Compared to paclitaxel alone, the nanodispersion-based formulation uses less toxic solvents and allows for administration of higher doses resulting in higher concentrations of paclitaxel at the tumor site, and an increased safety profile.","Pharmacologic Substance"]
["C2631","Paclitaxel Liposome","LEP-ETU|LipoTaxen|Liposome-Encapsulated Paclitaxel|PNU-93914|Paclitaxel Liposome|liposomal paclitaxel|paclitaxel liposome","A liposome-encapsulated formulation of paclitaxel, a taxoid compound extracted from the Pacific yew tree Taxus brevifolia, with antineoplastic property. Paclitaxel binds to tubulin and interferes with the assembly/disassembly dynamics of microtubules, thereby resulting in the inhibition of cell division. This agent also induces apoptosis via inactivation of the apoptosis inhibitor, B-cell Leukemia 2 (Bcl-2) protein. Paclitaxel liposome formulation potentially enhances delivery of higher doses of paclitaxel to the target tissues and exhibits lower systemic toxicity.","Pharmacologic Substance"]
["C1795","Paclitaxel Poliglumex","CT-2103|PACLITAXEL POLIGLUMEX|PG-TXL|Paclitaxel Poliglumex|Paclitaxel Polyglutamate|Paclitaxel-Polyglutamate Polymer|Poly-L-Glutamic acid-Paclitaxel Conjugate|Polyglutamic Acid Paclitaxel|Xyotax|paclitaxel poliglumex|paclitaxel polyglutamate","The agent paclitaxel linked to a biodegradable, water-soluble polyglutamate polymer with antineoplastic properties. The polyglutamate residue increases the water solubility of paclitaxel and allows delivery of higher doses than those achievable with paclitaxel alone. Paclitaxel promotes microtubule assembly and prevents microtubule depolymerization, thus interfering with normal mitosis.","Organic Chemical|Pharmacologic Substance"]
["C2785","Paclitaxel PPE Microspheres","Paclimer Microspheres (Polilactofate/Paclitaxel)|Paclimer Microspheres|Paclitaxel Biopolymer Formulation|Paclitaxel PPE Microspheres","A paclitaxel formulation containing paclitaxel incorporated in biodegradable polyphosphoester (PPE) polymer form with potential antineoplastic activity. Upon intraperitoneal delivery, paclitaxel PPE microspheres slowly and continuously dissolve and deliver paclitaxel to the tumor site, where it binds to tubulin and inhibits the dynamics of disassembly-assembly of microtubules. As a result, this formulation induces cell cycle arrest and leads to cell death.","Pharmacologic Substance"]
["C99461","Paclitaxel Trevatide","ANG-1005|ANG1005|GRN1005|PACLITAXEL TREVATIDE|Paclitaxel Trevatide","A peptide-drug conjugate containing the taxane paclitaxel covalently linked to the proprietary 19 amino acid peptide angiopep-2, in a 3:1 ratio, with potential antineoplastic activity. Upon administration, paclitaxel trevatide, via angiopep-2 moiety, binds to LRP-1 (low density lipoprotein receptor-related protein 1), which is highly expressed in blood brain barrier (BBB) and glioma cells. This binding allows the transcytosis of the agent across the BBB and the delivery of the cytotoxic agent paclitaxel. Compared to paclitaxel alone, GRN1005 is able to increase the concentration of paclitaxel in the brain and is also able to specifically deliver paclitaxel to LRP-1-overexpressing tumor cells, both in the brain and in the periphery.","Pharmacologic Substance"]
["C61079","Paclitaxel Vitamin E-Based Emulsion","PIE|Paclitaxel Injectable Emulsion|Paclitaxel Vitamin E-Based Emulsion|S-8184|Tocosol","A cremophor-free, P-glycoprotein-inhibiting, vitamin E-based emulsion particle formulation of paclitaxel with antineoplastic activity. Paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein B-cell Leukemia 2 (Bcl-2). The vitamin-E based emulsion allows bolus infusion without steroid premedication and may diminish hypersensitivity reactions. The tumor tissue may be passively targeted due to preferential deposition of emulsion particles while an emulsion formulation component inhibits the P-glycoprotein drug efflux pump.","Chemical Viewed Functionally"]
["C48415","Paclitaxel-Loaded Polymeric Micelle","Cynviloq TM|Genexol PM|IG-001|Paclitaxel-Loaded Polymeric Micelle|paclitaxel-loaded polymeric micelle","A biodegradable poly(ethylene glycol)-poly(D,L-lactide) copolymer micelle nanoparticle-entrapped formulation of paclitaxel with antineoplastic activity. Paclitaxel promotes microtubule assembly and prevents depolymerization, thus interfering with normal mitosis. The copolymer residue increases the water-solubility of paclitaxel and allows delivery of higher doses than those achievable with paclitaxel alone.","Pharmacologic Substance"]
["C78837","Pacritinib","Oral JAK2 Inhibitor SB1518|PACRITINIB|Pacritinib|SB1518","An orally bioavailable inhibitor of Janus kinase 2 (JAK2) and the JAK2 mutant JAK2V617F with potential antineoplastic activity. Oral JAK2 inhibitor SB1518 competes with JAK2 for ATP binding, which may result in inhibition of JAK2 activation, inhibition of the JAK-STAT signaling pathway, and so caspase-dependent apoptosis. JAK2 is the most common mutated gene in bcr-abl-negative myeloproliferative disorders; the JAK2V617F gain-of-function mutation involves a valine-to-phenylalanine modification at position 617. The JAK-STAT signaling pathway is a major mediator of cytokine activity.","Pharmacologic Substance"]
["C78481","Padeliporfin","PADELIPORFIN|Padeliporfin|Palladium-Bacteriochlorophyll Derivative WST11|WST11","A vascular-acting photosensitizer consisting of a water-soluble, palladium-substituted bacteriochlorophyll derivative with potential antineoplastic activity. Upon administration, paldeliporfin is activated locally when the tumor bed is exposed to low-power laser light; reactive oxygen species (ROS) are formed upon activation and ROS-mediated necrosis may occur at the site of interaction between the photosensitizer, light and oxygen. Vascular-targeted photodynamic therapy (VTP) with padeliporfin may allow tumor-site specific cytotoxicity while sparing adjacent normal tissues.","Organic Chemical|Pharmacologic Substance"]
["C84841","PAK4 Inhibitor PF-03758309","PAK4 Inhibitor PF-03758309|PF-03758309","An orally bioavailable small-molecule inhibitor of p21-activated kinase 4 (PAK4) with potential antineoplastic activity. PAK4 inhibitor PF-03758309 binds to PAK4, inhibiting PAK4 activity and cancer cell growth. PAK4, a serine/threonine kinase belonging to the p21-activated kinase (PAK) family, is often upregulated in a variety of cancer cell types and plays an important role in cancer cell motility, proliferation, and survival.","Pharmacologic Substance"]
["C126646","PAK4/NAMPT Inhibitor KPT-9274","KCP-9274|KPT-9274|PAK4/NAMPT Inhibitor KPT-9274","An orally bioavailable inhibitor of both the serine/threonine kinase P21-activated kinase 4 (PAK4) and the nicotinamide adenine dinucleotide (NAD)-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT; NAMPRTase), with potential antineoplastic activity. Upon administration, KPT-9274 allosterically binds to, destabilizes and causes degradation of PAK4. This inhibits PAK4-mediated signaling, induces cell death in, and inhibits the proliferation of PAK4-overexpressing tumor cells. In addition, KPT-9274 binds to and inhibits the activity of NAMPT. This depletes cellular NAD and inhibits NAD-dependent enzymes, both of which are needed for rapid cell proliferation; this results in tumor cell death in NAMPT-overexpressing cancer cells. PAK4, a serine/threonine kinase and member of the PAK family of proteins upregulated in various cancer cell types, regulates cell motility, proliferation and survival. NAMPT, an enzyme that is responsible for maintaining the intracellular NAD pool, plays a key role in the regulation of cellular metabolism and has cytokine-like activities. NAMPT is often overexpressed in a variety of cancers and metabolic disorders and tumor cells rely on NAMPT activity for their NAD supply.","Pharmacologic Substance"]
["C49176","Palbociclib","6-Acetyl-8-cyclopentyl-5-methyl-2-((5-(piperazin-1-yl)pyridin-2-yl)amino)-8h-pyrido(2,3-d)pyrimidin-7-one|Ibrance|PALBOCICLIB|PD-0332991|PD-332991|Palbociclib","An orally available cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. Palbociclib selectively inhibits cyclin-dependent kinase 4 (CDK4) and 6 (CDK6), thereby inhibiting retinoblastoma (Rb) protein phosphorylation early in the G1 phase leading to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of cell cycle progression.","Organic Chemical|Pharmacologic Substance"]
["C120259","Palbociclib Isethionate","6-Acetyl-8-cyclopentyl-5-methyl-2-((5-(piperazin-1-yl)pyridin-2-yl)amino(pyrido(2,3-d)pyrimidin-7(8h)-one mono(2-hydroxyethanesulfonate)|PALBOCICLIB ISETHIONATE|PD 0332991-0054|PF-00080665-73|Palbociclib Isethionate","The isethionate salt form of palbociclib, an orally available cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. Palbociclib selectively inhibits cyclin-dependent kinase 4 (CDK4) and 6 (CDK6), thereby inhibiting retinoblastoma (Rb) protein phosphorylation early in the G1 phase leading to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of cell cycle progression.","Organic Chemical|Pharmacologic Substance"]
["C66990","Palifosfamide","IPM-Lysine|Isophosphoramide Mustard-Lysine|N,N'-Di-(2-chloroethyl)phosphorodiamidic Acid|PALIFOSFAMIDE|Palifosfamide|ZIO-201","A synthetic mustard compound with potential antineoplastic activity. An active metabolite of ifosfamide covalently linked to the amino acid lysine for stability, palifosfamide irreversibly alkylates and cross-links DNA through GC base pairs, resulting in irreparable 7-atom inter-strand cross-links; inhibition of DNA replication and cell death follow. Unlike ifosfamide, this agent is not metabolized to acrolein or chloroacetaldehyde, metabolites associated with bladder and CNS toxicities. In addition, because palifosfamide does not require activation by aldehyde dehydrogenase, it may overcome the tumor resistance seen with ifosfamide.","Organic Chemical|Pharmacologic Substance"]
["C95703","Palifosfamide Tromethamine","Palifosfamide Tris|Palifosfamide Tromethamine","A synthetic mustard compound of the tromethamine (tris) salt of palifosfamide (Isophosphamide mustard), with potential antineoplastic activity. As the stabilized active metabolite of ifosfamide, palifosfamide irreversibly alkylates and crosslinks DNA through GC base pairs, resulting in irreparable 7-atom interstrand crosslinks. This leads to an inhibition of DNA replication and ultimately cell death. Unlike ifosfamide, this agent is not metabolized to acrolein or chloroacetaldehyde, metabolites associated with bladder and CNS toxicities. In addition, because palifosfamide does not require activation by aldehyde dehydrogenase, it may overcome the tumor resistance seen with ifosfamide. Stabilization with tris instead of lysine further increases stability and may further decrease nephrotoxicity.","Organic Chemical|Pharmacologic Substance"]
["C2550","Palladium Pd-103","Palladium Pd 103|Palladium Pd-103|Palladium-103|Pd 103|radioactive palladium","A radioisotope of the metal palladium used in brachytherapy implants or 'seed'. With a half-life of 17 days, palladium 103 administered with brachytherapy allows continuous, tumor-site specific low-energy irradiation to the tumor cell population while sparing normal adjacent tissues from radiotoxicity. (NCI04)","Element, Ion, or Isotope"]
["C61321","Palladium-Bacteriopheophorbide","Palladium-Bacteriopheophorbide|Tookad|WST09","A novel palladium-substituted bacteriochlorophyll derivative and photosensitizer with potential antitumor activity. Upon administration, inactive palladium-bacteriopheophorbide is activated locally when the tumor bed is exposed to photoirradiation; the activated form induces local cytotoxic processes, resulting in local tissue damage, disruption of tumor vasculature, and tumor hypoxia and necrosis.","Pharmacologic Substance"]
["C104267","pan FGFR Inhibitor ARQ 087","ARQ 087|pan FGFR Inhibitor ARQ 087","An orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) with potential antineoplastic activity. FGFR inhibitor ARQ 087 binds to and potently inhibits the activity of FGFR subtypes 1, 2 and 3. This may result in the inhibition of FGFR-mediated signal transduction pathways, tumor cell proliferation, tumor angiogenesis and tumor cell death in FGFR-overexpressing tumor cells. FGFR, a receptor tyrosine kinase, is upregulated in many tumor cell types and plays a key role in tumor cellular proliferation, differentiation, angiogenesis and survival.","Pharmacologic Substance"]
["C124931","pan FGFR Inhibitor PRN1371","FGFR 1-4 Inhibitor PRN1371|PRN 1371|PRN1371|Pan-FGFR Tyrosine Kinase Inhibitor PRN1371|pan FGFR Inhibitor PRN1371","A highly specific covalent inhibitor of human fibroblast growth factor receptor types 1, 2, 3 and 4 (FGFR1-4) with potential antiangiogenic and antineoplastic activities. FGFR1-4 tyrosine kinase inhibitor PRN1371 specifically binds to a conserved cysteine residue in the glycine-rich loop in FGFRs and inhibits their tyrosine kinase activity, which may result in the inhibition of both tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. FGFRs are a family of receptor tyrosine kinases, which may be upregulated in various tumor cell types and may be involved in tumor cell differentiation, proliferation and survival, and in tumor angiogenesis. This agent potently inhibits FGFR1-4 but does not inhibit other tyrosine kinases, even those that share the conserved cysteine, which may improve therapeutic responses and decrease toxicity when compared with less selective inhibitors.","Chemical Viewed Functionally|Organic Chemical|Pharmacologic Substance"]
["C88302","pan FGFR Kinase Inhibitor BGJ398","BGJ398|pan FGFR Kinase Inhibitor BGJ398","An orally bioavailable pan inhibitor of human fibroblast growth factor receptors (FGFRs) with potential antiangiogenic and antineoplastic activities. pan FGFR kinase inhibitor BGJ398 selectively binds to and inhibits the activities of FGFRs, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. FGFRs are a family of receptor tyrosine kinases which may be upregulated in various tumor cell types and may be involved in tumor cell differentiation and proliferation, tumor angiogenesis, and tumor cell survival.","Pharmacologic Substance"]
["C68832","Pan HER/VEGFR2 Receptor Tyrosine Kinase Inhibitor BMS-690514","BMS-690514|Pan HER/VEGFR2 Receptor Tyrosine Kinase Inhibitor BMS-690514","A pyrrolotriazine-based compound and a pan inhibitor of receptor tyrosine kinases with potential antineoplastic activity. Pan HER/VEGFR2 receptor tyrosine kinase inhibitor BMS-690514 binds to human epidermal growth factor receptors (EGFR) 1, 2 and 4 (HER1, HER2 and HER4) and vascular endothelial growth factor receptor 1, 2 and 3 (VEGFR-1, -2 and -3), all of which are frequently overexpressed by a variety of tumor types. Binding of this agent to these receptors may result in the inhibition of tumor cell proliferation; the inhibition of endothelial cell migration and proliferation and angiogenesis; and tumor cell death.","Pharmacologic Substance"]
["C128250","Pan-AKT Inhibitor ARQ751","AKT Inhibitor ARQ751|ARQ 751|ARQ751|Pan-AKT Inhibitor ARQ751","An orally bioavailable pan inhibitor of the serine/threonine protein kinase AKT (protein kinase B) enzyme family with potential antineoplastic activity. Upon oral administration, AKT inhibitor ARQ 751 selectively binds to and inhibits the activity of the AKT isoforms 1, 2 and 3, which may result in the inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. This may lead to a reduction in tumor cell proliferation and the induction of tumor cell apoptosis. The AKT signaling pathway is often deregulated in cancer and is associated with tumor cell proliferation, survival and migration.","Organic Chemical|Pharmacologic Substance"]
["C71711","Pan-AKT Kinase Inhibitor GSK690693","GSK690693|Pan-AKT Kinase Inhibitor GSK690693","An aminofurazan-derived inhibitor of Akt kinases with potential antineoplastic activity. Pan-AKT kinase inhibitor GSK-690693 binds to and inhibits Akt kinases 1, 2, and 3, which may result in the inhibition of protein phosphorylation events downstream from Akt kinases in the PI3K/Akt signaling pathway, and, subsequently, the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. In addition, this agent may inhibit other protein kinases including protein kinase C (PKC) and protein kinase A (PKA). As serine/threonine protein kinases which are involved in a number of biological processes, AKT kinases promote cell survival by inhibiting apoptosis and are required for glucose transport.","Pharmacologic Substance"]
["C1184","Pancratistatin","Pancratistatin","A isoquinoline alkaloid from amaryllis with antineoplastic activity.","Organic Chemical|Pharmacologic Substance"]
["C112205","Pan-FGFR Tyrosine Kinase Inhibitor BAY1163877","BAY1163877|Pan-FGFR Tyrosine Kinase Inhibitor BAY1163877","A pan inhibitor of human fibroblast growth factor receptors (FGFRs) with potential antiangiogenic and antineoplastic activities. Pan-FGFR kinase inhibitor BAY1163877 inhibits the activities of FGFRs, which may result in the inhibition of both tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. FGFRs are a family of receptor tyrosine kinases, which may be upregulated in various tumor cell types and may be involved in tumor cell differentiation and proliferation, tumor angiogenesis, and tumor cell survival.","Pharmacologic Substance"]
["C103273","pan-FGFR Tyrosine Kinase Inhibitor JNJ-42756493","JNJ-42756493|pan-FGFR Tyrosine Kinase Inhibitor JNJ-42756493","An orally bioavailable, pan fibroblast growth factor receptor (FGFR) inhibitor with potential antineoplastic activity. Upon oral administration, JNJ-42756493 binds to and inhibits FGFR, which may result in the inhibition of FGFR-related signal transduction pathways and thus the inhibition of tumor cell proliferation and tumor cell death in FGFR-overexpressing tumor cells. FGFR, upregulated in many tumor cell types, is a receptor tyrosine kinase essential to tumor cell proliferation, differentiation and survival.","Pharmacologic Substance"]
["C48380","pan-HER Kinase Inhibitor AC480","AC480|BMS-599626|pan-HER Kinase Inhibitor AC480","An orally bioavailable pan-HER tyrosine kinase inhibitor with potential antineoplastic activity. BMS-599626 inhibits human epidermal growth factor receptors (HER) HER1, HER2 and HER4, thereby inhibiting the proliferation of tumor cells that overexpress these receptors. (NCI05)","Pharmacologic Substance"]
["C122874","Pan-IDH Mutant Inhibitor AG-881","AG-881|AG881|IDH1/2 Mutant Inhibitor AG-881|Pan IDH Mutant Inhibitor AG-881|Pan-IDH Mutant Inhibitor AG-881","An orally available inhibitor of mutated forms of both isocitrate dehydrogenase type 1 (IDH1, IDH1 [NADP+] soluble) in the cytoplasm and type 2 (IDH2, isocitrate dehydrogenase [NADP+], mitochondrial) in the mitochondria, with potential antineoplastic activity. Upon administration, pan-IDH mutant inhibitor AG-881 specifically inhibits mutant forms of IDH1 and IDH2, thereby inhibiting the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing IDH mutations. In addition, AG-881 is able to penetrate the blood-brain barrier (BBB). IDH1 and 2, metabolic enzymes that catalyze the conversion of isocitrate into a-KG, play key roles in energy production and are mutated in a variety of cancer cell types. In addition, mutant forms of IDH1 and 2 catalyze the formation of 2HG and drive cancer growth by blocking cellular differentiation and inducing cellular proliferation.","Pharmacologic Substance"]
["C1857","Panitumumab","ABX-EGF Monoclonal Antibody|ABX-EGF, Clone E7.6.3|ABX-EGF|MoAb ABX-EGF|Monoclonal Antibody ABX-EGF|PANITUMUMAB|Panitumumab|Vectibix|panitumumab","A human monoclonal antibody produced in transgenic mice that attaches to the transmembrane epidermal growth factor (EGF) receptor. Panitumumab may inhibit autocrine EGF stimulation of tumor cells that express the EGF receptor, thereby inhibiting tumor cell proliferation.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C66948","Panobinostat","(2E)-N-hydroxy-3-(4-(((2-(2-methyl-1h-indol-3-yl)ethyl)amino)methyl)phenyl)prop-2-enamide|Faridak|Farydak|LBH589|PANOBINOSTAT|Panobinostat|panobinostat","A cinnamic hydroxamic acid analogue with potential antineoplastic activity. Panobinostat selectively inhibits histone deacetylase (HDAC), inducing hyperacetylation of core histone proteins, which may result in modulation of cell cycle protein expression, cell cycle arrest in the G2/M phase and apoptosis. In addition, this agent appears to modulate the expression of angiogenesis-related genes, such as hypoxia-inducible factor-1alpha (HIF-1a) and vascular endothelial growth factor (VEGF), thus impairing endothelial cell chemotaxis and invasion. HDAC is an enzyme that deacetylates chromatin histone proteins.","Organic Chemical|Pharmacologic Substance"]
["C117230","pan-PI3K Inhibitor CLR457","CLR457|pan-PI3K Inhibitor CLR457","An orally bioavailable pan inhibitor of phosphatidylinositol-3-kinase (PI3K), with potential antineoplastic activity. Upon oral administration, pan-PI3K inhibitor CLR457 inhibits all of the PI3K kinase isoforms, which may result in apoptosis and growth inhibition in tumor cells overexpressing PI3K. Activation of the PI3K pathway promotes cell growth, survival, and resistance to both chemotherapy and radiotherapy.","Pharmacologic Substance"]
["C111898","pan-PI3K/mTOR Inhibitor PQR309","PQR309|pan-PI3K/mTOR Inhibitor PQR309","An orally bioavailable pan inhibitor of phosphoinositide-3-kinases (PI3K) and inhibitor of the mammalian target of rapamycin (mTOR), with potential antineoplastic activity. PI3K/mTOR kinase inhibitor PQR309 inhibits the PI3K kinase isoforms alpha, beta, gamma and delta and, to a lesser extent, mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to both chemotherapy and radiotherapy. As mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase. By inhibiting mTOR to a lesser extent than PI3K, PQR309 does not interfere with the mTOR-mediated negative feedback loop on PI3K signaling. Blocking the negative feedback loop would potentially increase PI3K signaling and decrease therapeutic efficacy.","Pharmacologic Substance"]
["C85469","pan-PI3K/mTOR Inhibitor SF1126","SF1126|pan-PI3K/mTOR Inhibitor SF1126","A water soluble, small-molecule prodrug containing the pan-PI3K/mTOR inhibitor LY294002/SF1101 conjugated to the RGD-containing tetra-peptide SF1174 with potential antineoplastic and antiangiogenic activities. The targeting peptide SF1174 moiety of pan-PI3K/mTOR inhibitor SF1126 selectively binds to cell surface integrins and, upon cell entry, the agent is hydrolyzed to the active drug SF1101; SF1101 selectively inhibits all isoforms of phosphoinositide-3-kinase (PI3K) and other members of the PI3K superfamily, such as the mammalian target of rapamycin (mTOR) and DNA-PK. By inhibiting the PI3K signaling pathway, this agent may inhibit tumor cell and tumor endothelial cell proliferation and survival.","Pharmacologic Substance"]
["C124226","Pan-PIM Inhibitor INCB053914","INCB 053914|INCB053914|INCB53914|Pan-PIM Inhibitor INCB053914|Pan-PIM Kinase Inhibitor INCB053914","An orally available, small molecule and selective ATP-competitive pan-inhibitor of proviral integration sites for Moloney murine leukemia virus (PIM) kinases, with potential antineoplastic activity. Upon oral administration, pan-PIM kinase inhibitor INCB053914 binds to and inhibits the activities of the three PIM isoforms, PIM1, PIM2 and PIM3. This prevents phosphorylation of their downstream targets and inhibits proliferation in cells that overexpress PIMs. PIMs, constitutively active proto-oncogenic serine/threonine kinases upregulated in various types of cancers, play key roles in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C99380","pan-PIM Kinase Inhibitor AZD1208","AZD1208|pan-PIM Kinase Inhibitor AZD1208","An orally available, small molecule inhibitor of PIM kinases with potential antineoplastic activity. Pan-PIM kinase inhibitor AZD1208 inhibits the activities of PIM1, PIM2 and PIM3 serine/threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, thereby causing cell cycle arrest and inducing apoptosis in cells that overexpress PIMs. The growth inhibition of several leukemia cell lines by this agent is correlated with the expression levels of PIM1, which is the substrate of STAT transcription factors. PIM kinases are downstream effectors of many cytokine and growth factor signaling pathways and are upregulated in various malignancies.","Pharmacologic Substance"]
["C125003","pan-RAF Inhibitor LXH254","LXH 254|LXH-254|LXH254|Raf Family Kinase Inhibitor LXH254|pan-RAF Inhibitor LXH254|pan-RAF Kinase Inhibitor LXH254","An orally available inhibitor of all members of the serine/threonine protein kinase Raf family, with potential antineoplastic activity. Upon administration, pan-RAF inhibitor LXH254 binds to Raf proteins and inhibits Raf-mediated signal transduction pathways. This inhibits proliferation of Raf-overexpressing tumor cells. Raf protein kinases are critical enzymes in the Ras/Raf/MEK/ERK signaling pathway and are upregulated in a variety of cancer cell types. They play key roles in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C116861","Pan-RAF Inhibitor LY3009120","DP-4978|LY3009120|Pan-RAF Inhibitor LY3009120","An orally available inhibitor of all members of the serine/threonine protein kinase Raf family, including A-Raf, B-Raf and C-Raf protein kinases, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor LY3009120 inhibits Raf-mediated signal transduction pathways, which may inhibit tumor cell growth. Raf protein kinases play a key role in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C121952","pan-RAF Kinase Inhibitor CCT3833","BAL3833|CCT3833|pan-RAF Kinase Inhibitor CCT3833","An orally available inhibitor of the serine/threonine protein kinase family Raf, including A-Raf, B-Raf and C-Raf, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor CCT3833 inhibits Raf-mediated signal transduction pathways, which may inhibit the proliferation of Raf-overexpressing tumor cells. Raf protein kinases play a key role in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C106254","pan-RAF Kinase Inhibitor TAK-580","(R)-2-(1-(6-amino-5-chloropyrimidine-4-carboxamido)ethyl)-N-(5-chloro-4-(trifluoromethyl)pyridin-2-yl)thiazole-5-carboxamide|BIIB-024|MLN-2480|MLN2480|TAK-580|TAK580|pan-RAF Kinase Inhibitor TAK-580","An orally available inhibitor of A-Raf, B-Raf and C-Raf protein kinases, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor TAK-580 inhibits Raf-mediated signal transduction pathways, which may lead to an inhibition of tumor cell growth. Raf protein kinases play a key role in the RAF/MEK/ERK signaling pathway, which is often deregulated in human cancers and plays a key role in tumor cell proliferation and survival.","Pharmacologic Substance"]
["C82379","Pan-VEGFR/TIE2 Tyrosine Kinase Inhibitor CEP-11981","CEP-11981|Pan-VEGFR/TIE2 Tyrosine Kinase Inhibitor CEP-11981","An orally bioavailable inhibitor of vascular endothelial growth factor receptor (VEGFR) and Tie2 receptor tyrosine kinases with potential antiangiogenic and antineoplastic activities. Pan-VEGFR/Tie2 tyrosine kinase inhibitor CEP-11981 selectively binds to VEGFR and Tie2 receptor tyrosine kinases, which may result in the inhibition of endothelial cell migration, proliferation and survival and the inhibition of tumor cell proliferation and tumor cell death. VEGFR and Tie2 are frequently overexpressed by a variety of tumor cell types and play crucial roles in the regulation of angiogenesis and the maintenance of tumor blood vessels. Tie2 (tyrosine kinase with immunoglobulin-like and EGF-like domains) is activated by angiopoietin-1 (Ang-1).","Pharmacologic Substance"]
["C38693","Paricalcitol","(7e,22e)-19-Nor-9,10-Secoergosta-5,7,22-Triene-1Alpha,3Beta,25-Triol|Compound 49510|PARICALCITOL|Paricalcitol|Zemplar|paricalcitol","A synthetic noncalcemic, nonphosphatemic vitamin D analogue.  Paricalcitol binds to the vitamin D receptor and has been shown to reduce parathyroid hormone (PTH) levels. This agent also increases the expression of PTEN ('Phosphatase and Tensin homolog deleted on chromosome Ten'), a tumor-suppressor gene, in leukemic cells and cyclin-dependent kinase inhibitors, resulting in tumor cell apoptosis and tumor cell differentiation into normal phenotypes. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C102746","PARP 1/2 Inhibitor E7449","E7449|PARP 1/2 Inhibitor E7449","An orally available small molecule inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration, E7449 selectively binds to PARP 1 and 2, thereby preventing the repair of damaged DNA via the base excision repair (BER) pathway. This agent enhances the accumulation of single and double strand DNA breaks and promotes genomic instability eventually leading to apoptosis. PARP 1/2 inhibitor E7449 may enhance the cytotoxicity of DNA-damaging agents and of radiotherapy. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA.","Pharmacologic Substance"]
["C95201","PARP Inhibitor AZD2461","AZD2461|PARP Inhibitor AZD2461","An orally bioavailable inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential antineoplastic activity. PARP inhibitor AZD2461 selectively binds to PARP and prevents PARP-mediated DNA repair of single strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability and eventually leads to apoptosis. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by single-strand DNA breaks.","Pharmacologic Substance"]
["C120553","PARP Inhibitor BGB-290","BGB-290|PARP Inhibitor BGB-290","An orally bioavailable inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP), with potential antineoplastic activity. PARP inhibitor BGB-290 selectively binds to PARP and prevents PARP-mediated repair of single-strand DNA breaks via the base-excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks, promotes genomic instability, and eventually leads to apoptosis. PARP is activated by single-strand DNA breaks and, subsequently, catalyzes post-translational ADP-ribosylation of nuclear proteins which then transduce signals to recruit other proteins to repair damaged DNA. BGB-290 may both potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance.","Pharmacologic Substance"]
["C84880","PARP Inhibitor CEP-9722","CEP-9722|PARP Inhibitor CEP-9722","A small-molecule prodrug of CEP-8983, a novel 4-methoxy-carbazole inhibitor of the nuclear enzymes poly(ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration and conversion from CEP-9722, CEP-8983 selectively binds to PARP 1 and 2, preventing repair of damaged DNA via base excision repair (BER). This agent enhances the accumulation of DNA strand breaks and promotes genomic instability and apoptosis. CEP-8983 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and can be activated by single strand breaks in DNA.","Pharmacologic Substance"]
["C91387","PARP Inhibitor E7016","E7016|PARP Inhibitor E7016","An inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemo- and/or radiosensitizing activity. PARP inhibitor E7016 selectively binds to PARP and prevents PARP mediated DNA repair of single strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability and eventually leads to apoptosis. In addition, this agent may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapy and radiation therapy. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by single-strand DNA breaks.","Pharmacologic Substance"]
["C96795","PARP-1/2 Inhibitor ABT-767","ABT-767|PARP-1/2 Inhibitor ABT-767","An orally available inhibitor of the nuclear enzymes poly(ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration, ABT-767 selectively binds to PARP 1 and 2, thereby preventing repair of damaged DNA via the base excision repair (BER) pathway. This agent enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. ABT-767 may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and can be activated by single strand DNA (ssDNA) breaks.","Pharmacologic Substance"]
["C90567","Parsatuzumab","Anti-Epidermal Growth Factor-like Domain 7 Monoclonal Antibody MEGF0444A|MEGF 0444A|MEGF0444A|PARSATUZUMAB|Parsatuzumab|RG 7414|RG7414","A humanized IgG1 monoclonal antibody directed against the epidermal growth factor-like domain multiple 7 (EGFL7) with potential antineoplastic activity. Parsatuzumab binds to EGFL7, thereby preventing the activities of EGFL7 on endothelial cells and inhibiting the survival and migration of endothelial cells during angiogenesis. EGFL7, a vascular-restricted extracellular matrix protein which is upregulated during angiogenesis and which regulates vascular development, may be overexpressed on the cell surfaces of various solid tumor cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C96229","Parvovirus H-1","H-1PV|ParvOryx|Parvovirus H-1","A replication-competent oncolytic parvovirus with potential antineoplastic activity. Upon infection of host cells, parvovirus H-1 preferentially replicates in tumor cells compared to healthy normal cells, thereby potentially resulting in tumor cell lysis and leading to an inhibition of tumor cell proliferation. In addition, H1-infected tumor cells strongly induce the release of the inducible heat shock protein 72 (Hsp72i), which chaperone tumor associated antigens in the H1-mediated tumor lysates and may activate antigen presenting cells (APCs), thereby leading to antitumor immune responses. Parvovirus H-1 does not cause any pathogenic effect in normal, healthy cells and is able to cross the blood brain barrier (BBB).","Pharmacologic Substance|Virus"]
["C78853","Patritumab","AMG 888|Patritumab|U3-1287","A fully human monoclonal antibody directed against the membrane-bound receptor HER3 (ERBB3) with potential antineoplastic activity. Patritumab binds to and inhibits HER3 activation, which may result in inhibition of HER3-dependent PI3K/Akt signaling and so inhibition of cellular proliferation and differentiation. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in solid tumors, including breast, lung, and colorectal tumors of epithelial origin; it has no active kinase domain itself but is activated through heterodimerization with other members of the EGFR receptor family that do.","Pharmacologic Substance"]
["C74547","Pazopanib","Benzenesulfonamide, 5-((4-((2,3-dimethyl-2H-indazol-6-yl)methylamino)-2-pyrimidinyl)amino)-2-methyl-|GW786034|PAZOPANIB|Pazopanib","A small molecule inhibitor of multiple protein tyrosine kinases with potential antineoplastic activity. Pazopanib selectively inhibits vascular endothelial growth factor receptors (VEGFR)-1, -2 and -3, c-kit and platelet derived growth factor receptor (PDGF-R), which may result in inhibition of angiogenesis in tumors in which these receptors are upregulated.","Pharmacologic Substance"]
["C60779","Pazopanib Hydrochloride","5-((4-((2,3-Dimethyl-2h-Indazol-6-Yl)Methylamino)Pyrimidin-2-yl)Amino)-2-Methylbenzenesulfonamide Monohydrochloride|GW786034B|PAZOPANIB HYDROCHLORIDE|Pazopanib Hydrochloride|Votrient|pazopanib hydrochloride","The hydrochloride salt of a small molecule inhibitor of multiple protein tyrosine kinases with potential antineoplastic activity. Pazopanib selectively inhibits vascular endothelial growth factor receptors (VEGFR)-1, -2 and -3, c-kit and platelet derived growth factor receptor (PDGF-R), which may result in inhibition of angiogenesis in tumors in which these receptors are upregulated.","Pharmacologic Substance"]
["C107166","pBCAR3 Phosphopeptide-tetanus Peptide Vaccine","pBCAR3 Phosphopeptide-tetanus Peptide Vaccine|pBCAR3-phosphopeptide Plus Tet Vaccine","A vaccine composed of a phosphorylated peptide from the tumor associated antigen breast cancer anti-estrogen resistance-3 (BCAR3) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pBCAR3 phosphopeptide-tetanus peptide vaccine, the pBCAR3 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against phosphopeptide-containing tumor cells. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response, which may help stimulate an immune response against the pBCAR3-expressing melanoma tumor cells. BCAR3 is upregulated in a variety of cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C107168","pBCAR3/pIRS2-Phosphopeptide-tetanus Peptide Vaccine","2-MpP Phosphopeptide-tetanus Peptide Vaccine|pBCAR3/pIRS2-Phosphopeptide-tetanus Peptide Vaccine","A vaccine composed of phosphorylated peptides from the tumor associated antigens breast cancer anti-estrogen resistance-3 (BCAR3) and insulin receptor substrate-2 (IRS2) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pBCAR3/pIRS2 phosphopeptide-tetanus peptide vaccine, the pBCAR3/pIRS2 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing either phosphopeptide. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response which may help stimulate an immune response against pBCAR3 and pIRS2-expressing melanoma tumor cells. BCAR3 and IRS2 are upregulated in a variety of cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C99639","pbi-shRNA STMN1 Lipoplex","pbi-shRNA STMN1 LP|pbi-shRNA STMN1 Lipoplex","A proprietary RNA interference construct consisting of bifunctional short hairpin RNAs (shRNA) against human stathmin 1 (STMN1) encapsulated in the cationic bilamellar invaginated vesicle lipoplex (LP) with potential antineoplastic activity. pbi-shRNA STMN1 LP contains 2 stem-loop structures encoded by a plasmid vector. Upon intratumoral administration, one shRNA unit with a perfectly matched sequence renders the suppression of STMN1 mRNA translation (mRNA sequestration and cleavage-independent degradation) while the other unit with an imperfectly matched sequence renders STMN1 mRNA degradation via RNase H-like cleavage (cleavage-dependent mRNA silencing). The suppression of STMN1 expression in tumor cells result in a reduction of tumor cell proliferation. STMN1, a ubiquitous cytosolic phosphoprotein and tubulin modulator that plays a key role in mitosis, is overexpressed in a variety of tumors and correlates with poor prognosis.","Pharmacologic Substance"]
["C102983","PBN Derivative OKN-007","2,4-Disulfonyl PBN|2,4-Disulfophenyl-tert-butylnitrone|NXY-059|OKN-007|OKN007|PBN Derivative OKN-007","A disulfonyl derivative of phenyl-tert-butyl nitrone (PBN), with potential anti-glioma activity. Although the exact mechanism(s) of action of OKN007 are still largely unknown, this agent appears to inhibit cancer cell proliferation and migration. This agent appears to inhibit the activity of sulfatase 2 (SULF2), a highly specific endoglucosamine-6-sulfatase that is overexpressed in the extracellular matrix of cancer cells and catalyzes the removal of sulfate from the 6-O-sulfate esters of heparin. In addition, OKN007 may induce changes in tumor metabolism and scavenge free radicals.","Pharmacologic Substance"]
["C106429","PBTL CD19CAR-28/CD137/zeta","CD19CAR/28137-bearing ATLs|PBTL CD19CAR-28/CD137/zeta","Peripheral blood T-lymphocytes (PBTLs) transduced with a retroviral vector expressing a chimeric antigen receptor (CAR) consisting of an anti-CD19 scFv (single chain variable fragment) coupled to the costimulatory signaling domain CD28, the signaling domain of 4-1BB (CD137), and the zeta chain of the T-cell receptor (TCR), with potential immunomodulating and antineoplastic activities. Upon transfusion, PBTL CD19CAR-28/CD137zeta directs the T-lymphocytes to CD19-expressing tumor cells and induces selective toxicity in CD19-expressing tumor cells. CD28, a T-cell surface-associated co-stimulatory molecule, is required for full T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of CD19. Furthermore, inclusion of the 4-1BB signaling domain may increase the antitumor activity compared to the inclusion of the CD28 costimulatory domain and TCR zeta chain alone. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies.","Pharmacologic Substance"]
["C91723","P-cadherin Antagonist PF-03732010","P-cadherin Antagonist PF-03732010|PF-03732010","An agent that inhibits P-cadherin (cdh3), with potential antineoplastic activity. PF-03732010 binds to and inhibits the activity of p-cadherin. Inhibition of the activity of p-cadherin may inhibit tumor cell invasion and proliferation in p-cadherin expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of solid tumors, and plays a role in cell adhesion, motility, invasion and proliferation.","Pharmacologic Substance"]
["C121216","P-cadherin Inhibitor PCA062","P-CAD Inhibitor PCA062|P-cadherin Antagonist PCA062|P-cadherin Inhibitor PCA062|PCA062","An agent that inhibits p-cadherin, with potential antineoplastic activity. Upon intravenous infusion, PCA062 binds to and inhibits the activity of p-cadherin. Inhibition of the activity of p-cadherin may inhibit both invasion and proliferation of p-cadherin expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation.","Pharmacologic Substance"]
["C125607","P-cadherin-targeting Agent PF-06671008","P-cadherin-targeting Agent PF-06671008|PF-06671008","An agent that targets p-cadherin (CDH3), with potential antineoplastic activity. Upon administration, PF-06671008 binds to and inhibits the activity of p-cadherin; this may inhibit both invasion and proliferation of p-cadherin expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation.","Pharmacologic Substance"]
["C1186","PCNU","1-(2-Chloroethyl)-3-(2,6-Dioxo-3-Piperidyl)-1-Nitrourea|PCNU","A chloroethylnitrosourea compound and an alkylating agent with antineoplastic property. PCNU inhibits DNA synthesis by alkylating DNA and causing DNA cross links, thereby inducing apoptosis. In addition, this agent may be associated with pulmonary, hepatic, and hematologic toxicities. Unlike other nitrosoureas, PCNU has strong alkylating while weak carbamoylating activity.","Organic Chemical|Pharmacologic Substance"]
["C1828","PC-SPES","PC-SPES","An herbal mixture with potential antineoplastic effects. PC-SPES, an herbal supplement containing extracts from 8 herbs including Chrysanthemum morifolium, Ganoderma lucidum (a root fungus), Glycyrrhiza glabra (Spanish liquorice), Isatis indigotica, Panax pseudoginseng, Rabdosia rubescens, Scutellaria baicalensis, and Serona repens (saw palmetto), with potential antineoplastic and antiproliferative effects, specifically in prostate cancer cells. Its exact pharmacology is not fully understood due to the complexity of the herbal mixture and may involve multiple metabolic pathways. Exposure to PC-SPES in vitro has resulted in a decreased expression of genes encoding cell cycle regulatory proteins as well as an upregulation of genes that modulate apoptosis in both androgen-dependent and androgen-independent cells. The PC in the acronym PC-SPES stands for Prostate Cancer, while SPES is the Latin word for hope.","Organic Chemical|Pharmacologic Substance"]
["C52195","PD0325901","PD-0325901|PD0325901","An orally bioavailable, synthetic organic molecule targeting mitogen-activated protein kinase kinase (MAPK/ERK kinase or MEK) with potential antineoplastic activity. MEK inhibitor PD325901, a derivative of MEK inhibitor CI-1040, selectively binds to and inhibits MEK, which may result in the inhibition of the phosphorylation and activation of MAPK/ERK and the inhibition of tumor cell proliferation. The dual specific threonine/tyrosine kinase MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors.","Pharmacologic Substance"]
["C2727","PD-168393","4-[(3-Bromophenyl)amino]-6-Acrylamidoquinazoline|PD 168 393|PD-168393","A quinazolone compound with anti-tumor activity. PD-168393 is a cell-permeable, irreversible, and selective inhibitor of ligand-dependent epidermal growth factor (EGF) receptor (EGFR). This agent binds to the catalytic domain of EGFR with a 1:1 stoichiometry and inactivates the EGFR tyrosine kinase activity through alkylation of a cystine residue (Cys-773) within the ATP-binding pocket, thereby inhibiting proliferation of EGFR-expressing tumor cells.","Pharmacologic Substance"]
["C128281","PDCD-1 Knockout Autologous T-lymphocytes","PD-1 Knockout Autologous T-cells|PD-1-disrupted Autologous T-lymphocytes|PDCD-1 Knockout Autologous T Lymphocytes|PDCD-1 Knockout Autologous T-lymphocytes|PDCD1 Gene Knockout Autologous T-cells","A population of engineered autologous T-lymphocytes in which the gene encoding for the programmed cell death protein 1 (PDCD-1) is deleted, with potential immunomodulating activity. Following collection of peripheral blood lymphocytes and selection of T-cells, the PDCD-1 gene was knocked out and the T-cells were expanded. Upon reinfusion of the PDCD-1 knockout T-lymphocytes, these T-cells target and lyse cancer cells. The PDCD-1 protein, found on activated T-cells and often overexpressed on T-cells in cancer patients, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. PDCD-1 knockout enhances cytotoxicity and T-cell-mediated anti-tumor immune responses.","Cell|Pharmacologic Substance"]
["C123827","PDGFR alpha/KIT Mutant-specific Inhibitor BLU-285","BLU-285|PDGFR alpha/KIT Mutant-specific Inhibitor BLU-285","An orally bioavailable inhibitor of specific mutated forms of platelet-derived growth factor receptor alpha (PDGFR alpha; PDGFRa) and mast/stem cell factor receptor c-Kit (SCFR), with potential antineoplastic activity. Upon oral administration, BLU-285 specifically binds to and inhibits specific mutant forms of PDGFRa and c-Kit, including the PDGFRa D842V mutant and various KIT exon 17 mutants. This results in the inhibition of PDGFRa- and c-Kit-mediated signal transduction pathways and the inhibition of proliferation in tumor cells that express these PDGFRa and c-Kit mutants. PDGFRa and c-Kit, protein tyrosine kinases and tumor-associated antigens (TAAs), are mutated in various tumor cell types; they play key roles in the regulation of cellular proliferation.","Pharmacologic Substance"]
["C88271","PDK1 Inhibitor AR-12","AR-12|PDK1 Inhibitor AR-12","An orally bioavailable, small-molecule, celecoxib-derived inhibitor of phosphoinositide-dependent kinase-1 (PDK1) with potential antineoplastic activity. Devoid of any COX inhibiting activity, PDK1 inhibitor AR-12 binds to and inhibits the phosphorylation of 3-phosphoinositide-dependent kinase-1 (PDK-1).; subsequently, the phosphorylation and activation of the serine/threonine protein kinase Akt (protein kinase B or PKB) is inhibited, which may result in inhibition of the PI3K/Akt signaling pathway, inhibition of tumor cell proliferation, and the induction of tumor cell apoptosis.  In addition, this agent appears to induce the activity of protein kinase R-like endoplasmic reticulum kinase (PERK), which plays a key role in the endoplasmic reticulum stress pathway. Activation and dysregulation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C129594","PD-L1/PD-L2/VISTA Antagonist CA-170","AUPM 170|CA-170|PD-L1/PD-L2/VISTA Antagonist CA-170|PD-L1/PD-L2/VISTA Checkpoint Antagonist CA-170","An orally bioavailable small molecule inhibitor of the immune checkpoint regulatory proteins programmed cell death ligand-1 (PD-L1; B7-H1; CD274), PD-L2, and V-domain immunoglobulin (Ig) suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative immune checkpoint regulatory and antineoplastic activities. Upon oral administration, PD-L1/PD-L2/VISTA antagonist CA-170 targets and binds to PD-L1, PD-L2 and VISTA. This inhibits PD-L1/PD-L2/VISTA-mediated signaling, abrogates the PD-L1-, PD-L2- and VISTA-induced suppression of T-lymphocyte immune responses, enhances cytotoxic T-cell proliferation and activation against tumor cells, increases cytokine production by T-cells, and inhibits tumor cell growth. PD-L1, PD-L2 and VISTA, negative checkpoint molecules of immune activation, play key roles in the suppression of T-cell functions.","Pharmacologic Substance"]
["C126276","PE/HPV16 E7/KDEL Fusion Protein TVGV-1","PE-E7-KDEL TVGV-1|PE/HPV16 E7/KDEL Fusion Protein TVGV-1|TVGV-1 Vaccine|TVGV-1","A fusion protein consisting of a peptide sequence of human papillomavirus (HPV) type 16 E7 nuclear protein and fused to the Pseudomonas aeruginosa exotoxin A (PE) and a endoplasmic reticulum (ER) retention signal (KDEL), with potential antineoplastic activity. Upon administration of PE/HPV16 E7/KDEL fusion protein TVGV-1, the PE moiety binds to CD91 (LRP1) expressed on a variety of cells, including antigen-presenting cells such as dendritic cells (DCs), which facilitates the internalization, through endocytosis, of TVGV-1. Following endocytosis, this agent is proteolytically cleaved by the proteosome and the epitopes from the HPV E7 protein become bound to MHC-I molecules and are presented on the DC-cell surface. This facilitates a cytotoxic T-cell- mediated immune response against HPV16 E7 expressing-tumor cells. KDEL targets the fusion protein to the ER, which increases this agent's potential to be bound by MHC-I molecules; this increases the immune response against HPV16 E7-expressing cancer cells.","Pharmacologic Substance"]
["C1200","Pegaspargase","(Monomethoxypolyethylene Glycol Succinimidyl)74-L-Asparaginase|L-Asparaginase with Polyethylene Glycol|Oncaspar|PEG-Asparaginase|PEG-L-Asparaginase (Enzon - Kyowa Hakko)|PEG-L-Asparaginase|PEG-asparaginase|PEGASPARGASE|PEGLA|Pegaspargase|Polyethylene Glycol L-Asparaginase|Polyethylene Glycol-L-Asparaginase|pegaspargase","A complex of polyethylene glycol conjugated with L-asparaginase.  Asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting these cells of asparagine and blocking protein synthesis and tumor cell proliferation, especially in the G1 phase of the cell cycle.  The agent also induces apoptosis in tumor cells. Pegylation decreases the enzyme's antigenicity. Asparagine is critical to protein synthesis in leukemic cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C62791","Pegdinetanib","Angiocept|BMS-844203|CT-322|PEGDINETANIB|Pegdinetanib|VEGFR-2 inhibitor CT-322","A pegylated form of a thermostable and protease resistant peptide targeting human vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antiangiogenic activity. Derived from the 10th type III domain of human fibronectin and one of the natural ligands, pegdinetanib binds to VEGFR-2 and prevents activation of VEGFR-2 by other activating ligands. This may inhibit the growth of new tumor blood vessels.","Pharmacologic Substance"]
["C33987","Peginterferon Alfa-2a","PEG-Interferon Alfa-2a|PEG-interferon alfa-2a|PEGINTERFERON ALFA-2A|Pegasys|Peginterferon Alfa-2a","A covalent conjugate of recombinant interferon alfa, subtype 2a, and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha-2a protein moiety. Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha-2a, thereby extending the duration of its therapeutic effects, but may also reduce interferon-mediated stimulation of an immune response. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1845","Peginterferon Alfa-2b","PEG Interferon Alpha-2b|PEG Intron|PEG-IFN Alfa-2b|PEG-IFN-a 2b|PEG-Interferon Alfa-2b|PEG-Intron|PEG-interferon alfa-2b|PEGINTERFERON ALFA-2B|Peginterferon Alfa-2b|Pegylated Interferon Alpha-2b|Polyethylene Glycol IFN-A2b|Polyethylene Glycol Interferon Alfa-2b|SCH 54031|Sylatron","A covalent conjugate of recombinant interferon alpha, subtype 2b, and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha-2b protein moiety. Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha-2b, thereby extending the duration of its therapeutic effects, but may also reduce the interferon-mediated stimulation of an immune response. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1304","PEG-interleukin-2","PEG-IL-2|PEG-interleukin-2|Polyethylene Glycol-Modified Recombinant Interleukin-2","A complex of polyethylene glycol conjugated with human recombinant cytokine interleukin-2 (IL-2) with antineoplastic activity. PEG-interleukin-2 induces natural killer (NK) cell activity and the production of interferon-gamma (IFN-gamma), and enhances T cell-mediated cytotoxicity. Pegylation of IL-2 protects the cytokine from degradation. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C49178","PEG-PEI-cholesterol Lipopolymer-encased IL-12 DNA Plasmid Vector GEN-1","GEN-1|IL-12 Plasmid Formulated With PEG-PEI-Cholesterol Lipopolymer|Nanoparticle-encased IL-12 DNA Plasmid Vector|PEG-PEI-cholesterol Lipopolymer-encased IL-12 DNA Plasmid Vector GEN-1|phIL-12-005","A nanoparticle-based formulation composed of a non-viral plasmid DNA vector encoding the human pro-inflammatory cytokine interleukin-12 (IL-12) encapsulated in a biodegradable, biocompatible lipoplex composed of polyethylene glycol (PEG), polyethylenimine (PEI), and cholesterol, with potential immunoactivating and antineoplastic activities. Upon intraperitoneal (IP) delivery of the PEG-PEI-cholesterol lipopolymer-encased IL-12 DNA plasmid vector GEN-1, the lipoplex is endocytosed by nearby cells, and the plasmid DNA is transported into the nucleus, which leads to local expresssion of IL-12. In turn, the increased IL-12 production at the tumor site activates the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma (IFN-g) and promoting cytotoxic T-cell responses against tumor cells.","Pharmacologic Substance"]
["C111892","PEG-Proline-Interferon Alfa-2b","AOP2014|P1101|PEG-P-IFN-Alfa-2b|PEG-P-IFN-Alpha-2b|PEG-Proline-Interferon Alfa-2b","A long-acting formulation of recombinant interferon alpha subtype 2b (IFN-a2b) protein, in which IFN-a2b is coupled, via proline, to polyethylene glycol (PEG), with antiviral, immunomodulating and antineoplastic activities. Upon subcutaneous administration, IFN-a2b binds to specific interferon cell-surface receptors. This activates interferon-mediated signal transduction pathways and induces the transcription and translation of genes with interferon-specific response elements (ISREs); the protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects. The PEG moiety inhibits proteolytic breakdown and clearance of IFN-a2b, which prolongs its half-life, extends the duration of its therapeutic effects and allows less frequent dosing. The proline linker facilitates the synthesis of a predominant (90%) positional isomer which allows for further increases in stability and a longer half-life than previous PEG conjugates.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C61881","Pegvisomant","PEGVISOMANT|Pegvisomant|Somatotropin (18-Aspartic Acid, 21-Asparagine, 120-Lysine, 167-Asparagine, 168-Alanine, 171-Serine, 172-Arginine, 174-Serine, 179-Threonine) (Human), Pegylated|Somavert|Trovert","A pegylated, recombinant, human growth hormone (GH) structural analog with GH receptor antagonist activity. As a GH analog, the structure of pegvisomant is similar to that of native GH with the exception of 9 amino acid substitutions. Pegvisomant selectively binds to GH receptors on cell surfaces, interfering with endogenous GH receptor binding and so GH signal transduction. Inhibition of GH signal transduction results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and other GH-responsive serum proteins, including IGF binding protein-3 (IGFBP-3) and the acid-labile subunit (ALS), and may inhibit the growth of cancers in which IGF-1 is upregulated.","Pharmacologic Substance"]
["C61438","Pegylated Anti-GFR Antibody Fragment","CDP-791|Pegylated Anti-GFR Antibody Fragment","A pegylated, cross-linked, humanized divalent-Fab' antibody fragment directed against vascular endothelial growth factor receptor-2 (VEGFR-2) with potential antiangiogenic and antitumor activities. Pegylated anti-GFR antibody fragment binds to and inhibits VEGFR-2, which may inhibit angiogenesis and tumor cell proliferation. Multivalent Fab' antibody fragments may exhibit improved retention and internalization properties compared to their parent IgGs.","Pharmacologic Substance"]
["C91702","Pegylated Arginine Deiminase","ADI-PEG 20|Pegylated Arginine Deiminase|pegylated arginine deiminase","An agent consisting of the arginine-degrading enzyme arginine deiminase combined with polyethylene glycol (20,000 MW) (ADI-PEG 20) with potential antineoplastic activity. Upon administration, arginine deiminase breaks down the amino acid arginine into citrulline. Although arginine is a nonessential amino acid for normal human cells, certain cancer cells are autotrophic for arginine and need arginine in order to survive. Depletion of arginine may lead to an inhibition of cellular proliferation in those cancer cells. ADI is coupled to PEG in order to enhance this agent's half-life.","Pharmacologic Substance"]
["C125143","Pegylated Human Recombinant Arginase 1 AEB1102","AEB1102|Co-ArgI-PEG|Pegylated Human Recombinant Arginase 1 AEB1102|Pegylated Recombinant Arginase AEB1102","A recombinant modified form of the human enzyme arginase 1 (ARG1), in which cobalt is substituted for manganese as a cofactor, covalently attached to polyethylene glycol (PEG), with potential arginine degrading and antineoplastic activities. Upon intravenous administration of pegylated recombinant human ARG1 AEB1102, ARG1 metabolizes the amino acid arginine to ornithine and urea, thereby lowering blood arginine levels. This normalizes blood arginine levels in patients with ARG1 deficiency and prevents hyperargininemia. This also inhibits the proliferation of cancer cells that are dependent on extracellular arginine uptake for their proliferation. In normal, healthy cells, arginine is synthesized intracellularly by the enzymes ornithine transcarbamylase (OTC), argininosuccinate synthase (ASS), and argininosuccinate lyase (ASL); thus they are not dependent on extracellular arginine for survival. In cancer cells these enzymes are disabled; therefore, this agent may inhibit proliferation and survival of these cells by depleting extracellular arginine. Pegylation improves blood circulation times and cobalt substitution increases the catalytic activity of ARG1.","Enzyme|Pharmacologic Substance"]
["C2491","Pegylated Interferon Alfa","PEG-IFN-a|PEG-interferon alfa|Pegylated Interferon Alfa","A covalent conjugate of recombinant interferon alpha and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha protein moiety.  Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha, thereby extending the duration of its therapeutic effects, but may also reduce interferon-mediated stimulation of an immune response. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C74069","Pegylated Irinotecan","NKTR 102|PEG-Irinotecan|Pegylated Irinotecan","A formulation of polyethylene glycol (PEG)-encapsulated irinotecan with antineoplastic activity. The prodrug irinotecan, a semisynthetic derivative of camptothecin, is converted to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin by a carboxylesterase-converting enzyme. One thousand-fold more potent than its parent compound irinotecan, 7-ethyl-10-hydroxy-camptothecin inhibits topoisomerase I activity by stabilizing the cleavable complex of topoisomerase I and DNA, resulting in DNA breaks that inhibit DNA replication and trigger apoptosis. Pegylation provides improved drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic effects while lowering the toxicity profile.","Pharmacologic Substance"]
["C61437","Pegylated Liposomal Belotecan","Pegylated Liposomal Belotecan|S-CKD602|STEALTH Liposomal Belotecan","A sterically stabilized, pegylated liposomal formulation containing belotecan, a semi-synthetic analogue of campthotecin with potential antitumor activity. Belotecan inhibits the action of topoisomerase I, an enzyme that produces reversible single-strand breaks in DNA during DNA replication. This agent stabilizes the topoisomerase I and DNA complex, resulting in the inhibition of religation of DNA breaks, inhibition of DNA replication, and apoptotic cell death. The polyethylene glycol coating allows for greater plasma circulation time, thus enhancing the concentration of belotecan at the tumor site. Encapsulation of belotecan preserves the active lactone form, resulting in an increased cytotoxic effect of belotecan.","Pharmacologic Substance"]
["C1555","Pegylated Liposomal Doxorubicin Hydrochloride","(8S-cis)-8-Acetyl-10-[(3-amino-2,3,6-trideoxy-a-L-lyxo-hexopyranosyl)oxy]-7,8,9,10-tetrahydro-6,8,11-tri-hydroxy-1-methoxy-5,12-naphthacenedione Hydrochloride|ATI-0918|Caelyx|DOX-SL|DOXIL|Dox-SL|Doxil|Doxilen|Doxorubicin HCl Liposome|Doxorubicin Hydrochloride Liposome|Duomeisu|Evacet|LipoDox|Liposomal Adriamycin|Liposomal Doxorubicin Hydrochloride|Liposomal-Encapsulated Doxorubicin|Pegylated Doxorubicin HCl Liposome|Pegylated Liposomal Doxorubicin Hydrochloride|S-Liposomal Doxorubicin|Stealth Liposomal Doxorubicin|TLC D-99|doxorubicin hydrochloride liposome|liposomal doxorubicin hydrochloride","A liposome-encapsulated preparation of the hydrochloride salt of the anthracycline antineoplastic antibiotic doxorubicin. Doxorubicin intercalates between DNA base pairs, thereby hinders the movement of replication machinery along DNA strands, as well as blocks the activity of topoisomerase II during replication. As a result, this agent causes DNA adducts formation, renders single- and double-stranded DNA breakages that induce DNA repair and or apoptotic processes. Doxorubicin also generates reactive oxygen species that leads to cytotoxicity secondary to lipid peroxidation of cell membrane lipids. Liposomal delivery of doxorubicin HCl improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic drug effects. A liposomal formulation of doxorubicin also modulates toxicity, specifically the cardiac effects commonly seen with anthracycline antitumor drugs.","Pharmacologic Substance"]
["C62789","Pegylated Liposomal Irinotecan","IHL-305|Pegylated Liposomal Irinotecan","A formulation of polyethylene glycol (PEG)-modified liposomes encapsulating the semisynthetic derivative of camptothecin irinotecan, with antineoplastic activity. As a prodrug, irinotecan is converted to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38) by a carboxylesterase-converting enzyme. In turn, SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex of topoisomerase I and DNA, resulting in DNA breaks. This results in an inhibition of DNA replication and an induction of apoptosis. Pegylated liposomal delivery of irinotecan improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of exposure while lowering systemic toxicity.","Organic Chemical|Pharmacologic Substance"]
["C103276","Pegylated Liposomal Mitomycin C Lipid-based Prodrug","PL-MLP|Pegylated Liposomal Mitomycin C Lipid-based Prodrug|Promitil","A pegylated liposomal formulation comprised of a lipophilic prodrug of the antineoplastic antibiotic mitomycin C containing a cleavable disulfide bond (PL-MLP), with potential antineoplastic activity. Upon administration of the pegylated liposomal mitomycin C lipid-based prodrug, the MLP moiety becomes activated upon thiolysis at the tumor site, thereby releasing mitomycin C. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis.  The thiolytic environment and upregulated expression of thioredoxins at the tumor site allow for the activation and release of mitomycin C. This prodrug formulation allows for greater circulation time, less systemic toxicity and increased accumulation of mitomycin C at the tumor site.","Antibiotic|Organic Chemical"]
["C116869","Pegylated Liposomal Nanoparticle-based Docetaxel Prodrug MNK-010","MNK-010|MP-3549-1|Pegylated Liposomal Docetaxel Prodrug MNK-010|Pegylated Liposomal Nanoparticle-based Docetaxel Prodrug MNK-010","A formulation containing pegylated liposomal nanoparticles encapsulating a prodrug of the poorly water-soluble, second-generation taxane analog docetaxel, with potential antineoplastic activity. Upon intravenous administration of the liposomal docetaxel prodrug MNK-010, docetaxel is slowly released into the systemic circulation and accumulates at the tumor site due to the unique characteristics of the tumor's vasculature. In turn, docetaxel is taken up by tumor cells, and subsequently binds to and stabilizes the beta-subunit of tubulin, thereby stabilizing microtubules and inhibiting microtubule disassembly. This results in cell cycle arrest and induces cell death. Compared to the administration of docetaxel alone, this formulation is able to increase the delivery of docetaxel into tumors, thereby increasing docetaxel's efficacy while minimizing its toxicity. In addition, this formulation solubilizes docetaxel without the use of toxic solvents, thereby permitting the administration of larger doses of docetaxel while avoiding solvent-associated toxicity.","Pharmacologic Substance"]
["C63476","Pegylated Paclitaxel","Pegylated Paclitaxel","A formulation of polyethylene glycol (PEG) conjugated paclitaxel, a compound extracted from the Pacific yew tree Taxus brevifolia, with antineoplastic activity. Paclitaxel binds to and stabilizes tubulin molecules, thereby interfering with the dynamics of microtubule assembly/disassembly and resulting in the inhibition of cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein B-cell Leukemia 2 (Bcl-2). Compared to paclitaxel alone, pegylated paclitaxel has an enhanced water solubility leading to an increase in bioavailability, and decreases its toxicity profile. Therefore, the pegylated formulation potentially supports delivery of higher doses of paclitaxel to the specific site.","Pharmacologic Substance"]
["C88286","Pegylated Recombinant Human Arginase I BCT-100","BCT-100|Pegylated Recombinant Human Arginase I BCT-100|rhArgIpeg5000","A recombinant human arginase I (liver arginase) covalently attached, via a succinamide propionic acid (SPA) linker, to a polyethylene glycol (PEG) of molecular weight 5,000 [rhArg-peg(5,000mw)] with potential antineoplastic activity. Upon intravenous administration of pegylated recombinant human arginase I BCT-100, arginase metabolizes the amino acid arginine to ornithine and urea, depleting intracellular arginine, which may inhibit proliferation of cells that are auxotrophic for arginine such as hepatocellular carcinoma (HCC) cells.  This agent may also work synergistically with various cytotoxic agents.","Pharmacologic Substance"]
["C82659","Pegylated Recombinant Human Hyaluronidase PH20","PEGPH20|PH20|Pegylated Recombinant Human Hyaluronidase PH20|Pegylated Recombinant Human PH20|Pegylated rHuPH20","A pegylated formulation of a recombinant form of human hyaluronidase with potential antitumor activity. Upon intravenous administration, pegylated recombinant human PH20 degrades hyaluronic acid (HA) coating tumor cells, which may result in the inhibition of tumor cell growth. In addition, the degradation of HA may result in a lowering of the interstitial fluid pressure (IFP), allowing better penetration of chemotherapeutic agents into the tumor bed. HA is a glycosaminoglycan found in the extracellular matrix (ECM) that is frequently overproduced by various tumor cell types. The presence of HA in tumors correlates with increased tumor cell growth, metastatic potential, tumor progression, increased resistance to chemotherapeutic agents, and an elevation in tumor IFP.","Pharmacologic Substance"]
["C113295","Pegylated Recombinant Human Interleukin-10 AM0010","AM0010|PEG-rHuIL-10 AM0010|Pegylated Recombinant Human Interleukin-10 AM0010","A covalent conjugate of recombinant human interleukin-10 (IL-10) and polyethylene glycol (PEG), with potential anti-fibrotic, anti-inflammatory, immunomodulating and antineoplastic activities. Upon subcutaneous administration, pegylated recombinant human interleukin-10 AM0010 may activate cell-mediated immunity against cancer cells by stimulating the differentiation and expansion of tumor specific cytotoxic CD8+ T cells. This agent may also lower serum cholesterol levels and reduce atherosclerotic plaques by inhibiting the synthesis of pro-inflammatory cytokines, such as Interferon-gamma, IL-2, IL-3, TNF-alpha, and GM-CSF. The PEG moiety inhibits proteolytic breakdown and clearance of AM0010, which prolongs its half-life, extends the duration of its therapeutic effects and allows less frequent dosing.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C101259","Pegylated Recombinant L-asparaginase Erwinia chrysanthemi","Asparec|Pegylated Recombinant L-asparaginase Erwinia chrysanthemi|mPEG-R-crisantaspase","A pegylated, recombinant form of L-asparaginase derived from the bacterium Erwinia chrysanthemi (mPEG-R-Crisantaspase), with potential antineoplastic activity. Upon intravenous administration of pegylated recombinant L-asparaginase Erwinia chrysanthemi, asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting cancer cells of asparagine thus blocking protein synthesis and tumor cell proliferation. Asparagine is critical to protein synthesis in cancer cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. Compared to other available Erwinia chrysanthemi derived L-asparaginase agents, the pegylated form is longer acting and less immunogenic.","Enzyme|Pharmacologic Substance"]
["C1650","Peldesine","4H-Pyrrolo(3,2-d)pyrimidin-4-one,1,5-dihydro-2-amino-7-(3-pyridinylmethyl)|9-(3-Pyridinylmethyl)-7H-9-deazaguanine|BCX-34|PELDESINE|Peldesina|Peldesine|peldesine","A pyrimidine analogue and purine nucleoside phosphorylase inhibitor with immunosuppressive and antineoplastic properties. Peldesine inhibits purine nucleoside phosphorylase (PNP) that plays a pivotal role in T-cell proliferation and is responsible for the catalysis of the reversible phosphorolytic cleavage of purine ribonucleosides and 2'-deoxyribonucleosides. Inhibition of PNP results in accumulation of dGTP and the subsequent failure of DNA synthesis. This agent maybe used in T-cell related autoimmune diseases including psoriasis, rheumatoid arthritis and Crohn s disease and T-cell cancers","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C2713","Pelitinib","(2E)-N-(4-((3-Chloro-4-fluorophenyl)amino)-3-cyano-7-ethoxyquinolin-6-yl)-4-(dimethylamino)but-2-enamide|EKB 569|EKB-569|PELITINIB|Pelitinib|WAY-EKB 569","A 3-cyanoquinoline pan-ErbB tyrosine kinase inhibitor with potential antineoplastic activity.  Pelitinib irreversibly binds covalently to epidermal growth factor receptors (EGFR) ErbB-1, -2 and -4, thereby inhibiting receptor phosphorylation and signal transduction and resulting in apoptosis and suppression of proliferation in tumor cells that overexpress these receptors.","Organic Chemical|Pharmacologic Substance"]
["C2633","Pelitrexol","(2S)-2-(((5-(2-((6S)-2-Amino-4-oxo-1,4,5,6,7,8-hexahydropyrido(2,3-d)pyrimidin-6-yl)ethyl)-4-methylthiophen-2-yl)carbonyl)amino)pentanedioic Acid|(2S)-2-[[[5-[2-[(6S)-2-amino-4-oxo-1,4,5,6,7,8-hexahydropyrido[2,3-d]pyrimidin-6-yl]ethyl]-4-methylthiophen-2-yl]carbonyl]amino]pentanedioic Acid|AG2037|PELITREXOL|Pelitrexol","A water soluble antifolate with anti-proliferative activity. Pelitrexol inhibits activity of glycinamide ribonucleotide formyltransferase (GARFT), the first folate-dependent enzyme of the de novo purine synthesis pathway essential for cell proliferation. Enzyme inhibition reduces the purine nucleotides pool required for DNA replication and RNA transcription. As a result, this agent causes cell cycle arrest in S-phase, and ultimately inhibits tumor cell proliferation","Pharmacologic Substance"]
["C106432","Pembrolizumab","Immunoglobulin G4, Anti-(Human Programmed Cell Death 1); Humanized Mouse Monoclonal (228-L-proline(H10-S>P))gamma 4 Heavy Chain (134-218')-disulfide with Humanized Mouse Monoclonal Kappa Light Chain Dimer (226-226'':229-229'')-bisdisulfide|Keytruda|Lambrolizumab|MK-3475|PEMBROLIZUMAB|Pembrolizumab|SCH 900475","A humanized monoclonal immunoglobulin (Ig) G4 antibody directed against human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C61614","Pemetrexed","L-Glutamic Acid, N-(4-(2-(2-Amino-4,7-dihydro-4-oxo-1H-pyrrolo(2,3-d)pyrimidin-5-yl)ethyl)benzoyl)|MTA|Multitargeted Antifolate|PEMETREXED|Pemetrexed","A synthetic pyrimidine-based antifolate. Pemetrexed binds to and inhibits the enzyme thymidylate synthase (TS), which catalyses the methylation of 2'-deoxyuridine-5'-monophosphate (dUMP) to 2'-deoxythymidine-5'-monophosphate (dTMP), an essential precursor in DNA synthesis.","Organic Chemical|Pharmacologic Substance"]
["C1533","Pemetrexed Disodium","Alimta|LY231514|N-[4-[2-(2-Amino-4,7-dihydro-4-oxo-1H-pyrrolo[2,3-d]pyrimidin-5-yl)ethyl]benzoyl]-L-glutamic Acid Disodium Salt|PEMETREXED DISODIUM|Pemetrexed Disodium|pemetrexed disodium","The disodium salt of a synthetic pyrimidine-based antifolate. Pemetrexed binds to and inhibits the enzyme thymidylate synthase (TS) which catalyses the methylation of 2'-deoxyuridine-5'-monophosphate (dUMP) to 2'-deoxythymidine-5'-monophosphate (dTMP), an essential precursor in DNA synthesis.","Organic Chemical|Pharmacologic Substance"]
["C1187","Penberol","Penberol|cis-beta-4-pentoxy-benzoyl-beta-bromoacrylic acid|cis-beta-4-pentoxybenzoyl-beta-bromoacrylic acid","A derivative of bromoacrylic acid with cytostatic activity. Although the mechanism of action is unclear, penberol might inhibit tumor growth mediated through inhibition of the cell energetic metabolism.","Organic Chemical|Pharmacologic Substance"]
["C1188","Penclomedine","3,5-dichloro-2,4-dimethoxy-6-(trichloromethyl) pyridine|CRC 88-04|PEN|PENCLOMEDINE|Penclomedine|Pyridine, 3,5-dichloro-2,4-dimethoxy-6-(trichloromethyl)-|penclomedine","A synthetic derivative of pyrimidine with antineoplastic activity. Penclomedine alkylates and crosslinks DNA, resulting in DNA strand breaks and inhibition of DNA and RNA synthesis. This agent is more active against tumor cells that are defective in p53 function. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C729","Penicillamine",".beta.,.beta.-Dimethylcysteine|3-Mercapto-D-valine|Alpha-amino-beta-methyl-beta-mercaptobutyric Acid|Atamir|Beta,Beta-dimethylcysteine|Beta-thiovaline|Cuprenil|Cuprimine|Cupripen|D-Mercaptovaline|D-Penicillamine|Depamine|Depen|Distamine|Kelatin|Mercaptyl|Metalcaptase|PENICILLAMINE|Pendramine|Penicillamine|Perdolat|Sufortan|Trolovol|penicillamine","A beta dimethyl analog of the amino acid cysteine.  As a degradation product of penicillin antibiotics, penicillamine chelates with heavy metals and increases their urinary excretion.  Possessing antineoplastic properties, penicillamine induces apoptosis by a p53-mediated mechanism and inhibits angiogenesis by chelating with copper, a cofactor for angiogenesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1189","Pentamethylmelamine","1,3,5-Triazine-2,4,6-triamine, N,N,N',N', N''-pentamethyl-, monohydrochloride (9CI)|Melamine, N2,N2,N4,N4,N6-pentamethyl-, monohydrochloride|Melamine|N,N,N',N',N\"-pentamethyl-1,3,5-triazine|PMM|Pentamethylmelamine MonoHCl|Pentamethylmelamine Monohydrochloride|Pentamethylmelamine monoHCl|Pentamethylmelamine monohydrochloride|Pentamethylmelamine|melamine, N2,N2,N4,N4,N6-pentamethyl-, monohydrochloride","A principal metabolite of hexamethylmelamine with antineoplastic activity.  Pentamethylmelamine alkylates DNA and other macromolecules and forms DNA intrastrand and DNA-protein crosslinks, thereby preventing DNA replication. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C66341","Pentamustine","1-(2-Chloroethyl)-3-neopentyl-1-nitrosourea|NCNU|Neptamustine|PENTAMUSTINE|Pentamustine|Salisburystin","A (2-chloroethy1)nitrosourea compound with antineoplastic activity. Petamustine was never marketed.","Pharmacologic Substance"]
["C97034","Pentavalent KLH Conjugate Vaccine","Pentavalent KLH Conjugate Vaccine","A pentavalent vaccine comprised of the epitope antigens of the ganglioside lactones GD2L and GD3L, Globo H hexasaccharide 1 (Globo H), fucosyl GM1 and N-propionylated polysialic acid conjugated with the immunostimulant keyhole limpet hemocyanin (KLH), with potential immunostimulating and antineoplastic activity. Vaccination with the pentavalent KLH conjugate vaccine may induce production of IgG and IgM antibodies as well as an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumors expressing any of these antigens. The antigens included in the pentavalent KLH conjugate vaccine are upregulated in a variety of cancer cells. KLH, a natural protein isolated from the marine mollusk keyhole limpet, is an immunostimulant carrier protein.","Immunologic Factor|Pharmacologic Substance"]
["C732","Pentostatin","(R)-3-(2-Deoxy-.beta.-D-erythro-pentofuranosyl)-3,6,7, 8-tetrahydroimidazo[4,5-d][1,3]diazepin-8-ol|(R)-3-(2-Deoxy-beta-D-erythro-pentofuranosyl)-3,6,7,8-tetrahydroimidazo[4,5-d][1,3]diazepin-8-ol|2'-Deoxycoformycin|CI-825|Co-Vidarabine|Co-vidarabine|Covidarabine|DCF|Deoxycoformycin|Nipent|PD-81565|PENTOSTATIN|Pentostatin|Pentostatine|pentostatin","A purine nucleotide analogue antibiotic isolated from the bacterium Streptomyces antibioticus. Also known as 2'-deoxycoformycin, pentostatin binds to and inhibits adenine deaminase (ADA), an enzyme essential to purine metabolism; ADA activity is greatest in cells of the lymphoid system with T-cells having higher activity than B-cells and T-cell malignancies higher ADA activity than B-cell malignancies. Pentostatin inhibition of ADA appears to result in elevated intracellular levels of dATP which may block DNA synthesis through the inhibition of ribonucleotide reductase. This agent may also inhibit RNA synthesis and may selectively deplete CD26+ lymphocytes. (NCI04)","Antibiotic|Nucleic Acid, Nucleoside, or Nucleotide"]
["C733","Pentoxifylline","3,7-Dihydro-3,7-dimethyl-1-(5-oxohexyl)-1H-purine-2,6-dione|Oxpentifylline|PENTOXIFYLLINE|PTX|Pentoxifylline|Pentoxyphylline|Trental|pentoxifylline","A methylxanthine derivative with hemorrheologic and immunomodulating properties. Pentoxifylline inhibits phosphodiesterase, resulting in increased levels of cyclic adenosine monophosphate (cAMP) in erythrocytes, endothelium, and the surrounding tissues. This leads to vasodilation, improves erythrocyte flexibility, and enhances blood flow. In addition, the increased level of cAMP in platelets inhibits platelet aggregation, which may contribute to a reduction in blood viscosity. This agent also inhibits production of tumor necrosis factor-alpha and interferon-gamma, while it induces Th2-like (T-helper 2) cytokine production, thereby inhibiting Th1-mediated (T-helper 1) inflammatory and autoimmune responses.","Organic Chemical|Pharmacologic Substance"]
["C74070","PEP-3-KLH Conjugate Vaccine","PEP-3-KLH Conjugate Vaccine|PEP-3-KLH","A cancer vaccine consisting of PEP-3, a synthetic peptide encompassing a tumor-specific mutated segment of the epidermal growth factor receptor type vIII (EGFRvIII), conjugated to the naturally-occurring immunoadjuvant keyhole limpet hemocyanin (KLH) with potential immunostimulating and antineoplastic activities. Upon administration, PEP-3-KLH conjugate vaccine may induce a cytotoxic immune response against tumor cells that overexpress EGFRvIII; this antitumoral immune response may involve antibody-dependent cellular cytotoxicity (ADCC).","Pharmacologic Substance"]
["C107243","PEP-CMV Vaccine","PEP-CMV Vaccine","A peptide vaccine derived from cytomegalovirus (CMV) antigens with potential immunostimulating activity. Intradermal administration of the PEP-CMV vaccine may stimulate the immune system to mount a specific helper and cytotoxic T-lymphocyte (CTL) response against CMV-infected tumor cells. Infection with the herpesvirus CMV may play a significant role in tumor cell initiation and progression as well as chemoresistance.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1399","Peplomycin","(S)-n1-[3-[(1-phenylethyl)amino]propyl]bleomycinamide|PEP|PEPLEOMYCIN|PEPLOMYCIN|Pepleomycin|Peplomycin|n1-[3[[(S)-alpha-methylbenzyl]amino]propyl]bleomycinamide","A semisynthetic analog of Bleomycin, a mixture of several basic glycopeptide antineoplastic antibiotics isolated from Streptomyces verticillus.  Peplomycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals that cause single- and double-stranded breaks in DNA.  This agent appears to show greater antitumor activity than bleomycin; its use is limited due to pulmonary toxicity. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C1400","Peplomycin Sulfate","N1-(3-(((S)-(alpha-methylbenzyl))amino)propyl)bleomycinamide Sulfate (1:1) (Salt)|NK-631|PEPLOMYCIN SULFATE|Pepleo|Peplomycin Sulfate","The sulfate salt of the bleomycin analogue peplomycin.  Peplomycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals that cause single- and double-stranded breaks in DNA.  This agent appears to show greater antitumor activity than bleomycin; its use is limited due to pulmonary toxicity. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C734","Peptichemio","Multialchilpeptide|PTC|Peptichemio|peptide bound m-L-sarcolysin","A mixture of six synthetic oligopeptides in which the peptides are conjugated to metamelphalan, with alkylating and potential antineoplastic activity. Peptichemio causes crosslinking of DNA, thereby preventing DNA replication and eventually cellular proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2466","Peptide 946 Melanoma Vaccine","Peptide 946 Melanoma Vaccine","A melanoma peptide vaccine with potential antineoplastic activity. Peptide 946 melanoma vaccine contains one of the peptide sequences for a melanoma-specific epitope that is recognized by melanoma-specific cytotoxic T lymphocytes (CTL). This vaccine contains a peptide sequence homologous to the native epitope and is often formulated with an adjuvant such as QS-21 or Montanide ISA-51 to boost its immune stimulation. Vaccination with peptide 946 vaccine may produce antibodies as well as elicit a cytotoxic T- lymphocyte (CTL) response against cells expressing this antigen, resulting in decreased tumor cell growth.","Immunologic Factor|Pharmacologic Substance"]
["C2467","Peptide 946-Tetanus Peptide Conjugate Melanoma Vaccine","Peptide 946-Tetanus Peptide Conjugate Melanoma Vaccine","A melanoma peptide vaccine complexed with tetanus toxoid with potential antineoplastic activity. Peptide 946 contains a melanoma-specific epitope recognized by melanoma-specific cytotoxic T lymphocytes (CTL). In addition to the peptide 946 sequence, this vaccine contains tetanus toxin, a protein known to stimulate the induction of CD4+ T lymphocytes; it thereby enhances antigen processing and presentation. Vaccination with the peptide 946-tetanus conjugate melanoma vaccine may produce antibodies as well as elicit a cytotoxic T lymphocyte (CTL) response in tumor cells expressing the 946 epitope, thereby decreasing tumor cell growth.","Immunologic Factor|Pharmacologic Substance"]
["C87202","Peretinoin","(2E,4E,6E,10E)-3,7,11,15-Tetramethylhexadeca-2,4,6,10,14-Pentaenoic Acid|NIK-333|PERETINOIN|Peretinoin","An orally available, acyclic retinoid with potential antineoplastic and chemopreventive activities. Peretinoin binds to and activates nuclear retinoic acid receptors (RAR), which in turn recruit coactivator proteins and promote, with other transcriptional complexes, the transcription of target genes. As a result, this agent may modulate the expression of genes involved in the regulation of cell proliferation, cell differentiation, and apoptosis of both normal and tumor cells.","Pharmacologic Substance"]
["C116804","Perflenapent Emulsion","DDFP LIquid Emulsion|Dodecafluoropentane Emulsion|NVX-108|Perflenapent Emulsion","An oil-in-water nano-emulsion composed of the perfluorocarbon perflenapent, that has oxygen-carrying capacity, can be used as a contrast agent and has potential antihypoxic and radiosensitizing activities. Upon intravenous administration of the perflenapent emulsion, this agent increases the oxygen-carrying capacity of blood, enhances the transport of oxygen to hypoxic and ischemic tissues and increases the oxygen concentration in these tissues. Hypoxic tumors are correlated with increased resistance to radiation treatment; therefore, since perflenapent may increase tumor oxygenation, it may improve the tumor's sensitivity to radiation therapy.","Pharmacologic Substance"]
["C1423","Perfosfamide","2-[bis(2-chloroethyl)amino]-4-hydroperoxytetrahydro-2H-1,3,2-oxazaphosphorine 2-oxide|4'-Hydroperoxycyclophosphamide|4-HC|4-Hydroperoxycyclophosphamide|4-Pergamid|Hydroperoxycyclophosphamide|PERFOSFAMIDE|Perfosfamide|Pergamid|cis-2-[bis(2-chloroethyl)amino]tetrahydro-3H-1,3,2-oxazaphosphorin-4-yl hydroperoxide P-oxide|cis-4-hydroperoxycyclophosphamide","The active metabolite of the nitrogen mustard cyclophosphamide with potent antineoplastic and immunosuppressive properties. Perfosfamide alkylates DNA, thereby inhibiting DNA replication and RNA and protein synthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1727","Perifosine","4-[[Hydroxy(octadecyloxy)phosphinyl]oxy]-1,1-dimethylpiperidinium, Inner Salt|D21266|Octadecyl-(N,N-dimethylpiperidino-4-yl)phosphate|Octadecylphosphopiperidine|PERIFOSINE|Perifosine|perifosine","An orally active alkyl-phosphocholine compound with potential antineoplastic activity.  Targeting cellular membranes, perifosine modulates membrane permeability, membrane lipid composition, phospholipid metabolism, and mitogenic signal transduction, resulting in cell differentiation and inhibition of cell growth.  This agent also inhibits the anti-apoptotic mitogen-activated protein kinase (MAPK) pathway and modulates the balance between the MAPK and pro-apoptotic stress-activated protein kinase (SAPK/JNK) pathways, thereby inducing apoptosis.  Perifosine has a lower gastrointestinal toxicity profile than the related agent miltefosine. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1461","Perillyl Alcohol","(S)-(-)-Perillyl Alcohol|(S)-(-)-Perillyl alcohol|(S)-4-Isopropenyl-1-cyclohexenylmethanol|1-Cyclohexene-1-methanol|4-(1-Methylethenyl)-1-cyclohexene-1-methanol|4-(1-Methylethenyl)|4-Isopropenylcyclohex-1-ene-1-methanol|Dihydrocuminyl Alcohol|NEO100|PERILLYL ALCOHOL|POH|Perilla Alcohol|Perilla alcohol|Perillic Alcohol|Perillic alcohol|Perillol|Perillyl Alcohol|[(4S)-4-prop-1-en-2-yl-1-cyclohexenyl]methanol|p-Mentha-1,8-dien-7-ol|perillyl alcohol","A naturally occurring monoterpene related to limonene with antineoplastic activity. Perillyl alcohol inhibits farnesyl transferase and geranylgeranyl transferase, thereby preventing post-translational protein farnesylation and isoprenylation and activation of oncoproteins such as p21-ras, and arresting tumor cells in the G1 phase of the cell cycle. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C129935","Personalized Peptide Cancer Vaccine NEO-PV-01","NEO PV 01|NEO-PV 01|NEO-PV-01|Neoantigen-based Anticancer Vaccine NEO-PV-01|Neoantigen-based Peptide Vaccine NEO-PV-01|Personalized Peptide Cancer Vaccine NEO-PV-01","A synthetic peptide-based, personalized cancer vaccine consisting of patient-specific mutated peptide epitopes, which are immunogenic and unique to the patient's tumor, with potential immunomodulating and antineoplastic activities. Vaccination with the neoantigen-based anti-cancer vaccine NEO-PV-01 stimulates the host immune system to mount a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis.","Immunologic Factor|Pharmacologic Substance"]
["C120306","Personalized Polyepitope Plasmid DNA Breast Cancer Vaccine","Personalized Polyepitope Plasmid DNA Breast Cancer Vaccine","A polyepitope DNA vaccine composed of a DNA plasmid encoding multiple, highly immunogenic tumor associated antigens (TAAs) that are specifically selected after genome profiling of the patient's breast cancer cells, with potential immunostimulatory and antineoplastic activities. Upon intramuscular administration and electroporation of the personalized polyepitope plasmid DNA breast cancer vaccine, the expressed TAAs induce cytotoxic T-lymphocyte (CTL) immune responses against tumor cells expressing the TAAs.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C121947","Personalized Synthetic Long Peptide Breast Cancer Vaccine","Personalized Synthetic Long Peptide Breast Cancer Vaccine","A cancer vaccine consisting of one or more long, synthetic peptides derived from patient-specific breast cancer tumor-associated antigens (TAAs), with potential immunomodulating and antineoplastic activities. Upon intramuscular administration of the personalized synthetic long peptide breast cancer vaccine, the peptides stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the TAAs, which results in tumor cell lysis.","Pharmacologic Substance"]
["C38692","Pertuzumab","2C4 Antibody|2C4|Immunoglobulin G1, Anti-(Human V (Receptor)) (Human-Mouse Monoclonal 2C4 Heavy Chain), Disulfide with Human-Mouse Monoclonal 2C4 Kappa-Chain, Dimer|MoAb 2C4|Monoclonal Antibody 2C4|PERTUZUMAB|Perjeta|Pertuzumab|RO4368451|pertuzumab|rhuMAb2C4","A humanized recombinant monoclonal antibody directed against the extracellular dimerization domain of the HER-2 tyrosine kinase receptor. Binding of the antibody to the dimerization domain of the HER-2 tyrosine kinase receptor protein directly inhibits the ability of the HER-2 tyrosine kinase receptor protein (the most common pairing partner) to dimerize with other HER tyrosine kinase receptor proteins; inhibiting receptor protein dimerization prevents the activation of HER signaling pathways, resulting in tumor cell apoptosis. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C77906","Pevonedistat","((1S,2S,4R)-4-(4-((1S)-2,3-Dihydro-1H-inden-1-ylamino)-7H-pyrrolo(2,3-d)pyrimidin-7-yl)-2-hydroxycyclopentyl)methyl Sulphamate|MLN4924|Nedd8-Activating Enzyme Inhibitor MLN4924|PEVONEDISTAT|Pevonedistat","A small molecule inhibitor of Nedd8 activating enzyme (NAE) with potential antineoplastic activity. Pevonedistat binds to and inhibits NAE, which may result in the inhibition of tumor cell proliferation and survival. NAE activates Nedd8 (Neural precursor cell expressed, developmentally down-regulated 8), an ubiquitin-like (UBL) protein that modifies cellular targets in a pathway that is parallel to but distinct from the ubiquitin-proteasome pathway (UPP). Functioning in diverse regulatory activities, proteins conjugated to UBLs like Nedd8 typically are not targeted for proteasomal degradation.","Organic Chemical|Pharmacologic Substance"]
["C71533","Pexastimogene-devacirepvec","JX-594|Pexastimogene-devacirepvec|Thymidine Kinase-(-) Vaccinia-GM-CSF JX-594 Vaccine","A thymidine kinase-deleted vaccinia virus expressing human GM-CSF (hGM-CSF) with oncolytic activity. Upon intratumoral or intravenous administration, pexastimogene-devacirepvec may selectively infect and lyse tumor cells. While vaccinia displays a natural tumor cell tropism, deletion of the thymidine kinase gene increases the tumor selectivity of vaccinia by limiting viral replication to transformed cells. hGM-CSF expression by this agent may help recruit antigen processing cells (APCs), such as denritic cells and macrophages, to virally infected tumor cells, initiating a systemic antitumoral immune response.","Pharmacologic Substance"]
["C88303","Pexidartinib","3-Pyridinemethanamine, N-(5-((5-chloro-1H-pyrrolo(2,3-b)pyridin-3-yl)methyl)-2-pyridinyl)-6-(trifluoromethyl)-|PEXIDARTINIB|PLX3397|Pexidartinib","A capsule formulation containing a small-molecule receptor tyrosine kinase (RTK) inhibitor of KIT, CSF1R and FLT3 with potential antineoplastic activity. Pexidartinib binds to and inhibits phosphorylation of stem cell factor receptor (KIT), colony-stimulating factor-1 receptor (CSF1R) and FMS-like tyrosine kinase 3 (FLT3), which may result in the inhibition of tumor cell proliferation and down-modulation of macrophages, osteoclasts and mast cells involved in the osteolytic metastatic disease. FLT3, CSF1R and FLT3 are overexpressed or mutated in many cancer cell types and play major roles in tumor cell proliferation and metastasis.","Pharmacologic Substance"]
["C78463","PGG Beta-Glucan","Imprime PGG|PGG Beta-Glucan|Poly-(1-6)-beta-glucotriosyl-(1-3)-beta-glucopyranose Beta-glucan","An injectable formulation of the polysaccharide beta 1,3/1,6 glucan derived from the cell wall of the yeast Saccharomyces cerevisiae with potential immunomodulating and antineoplastic activities. PGG beta-glucan binds to an alternate site on the neutrophil complement receptor 3 (CR3), priming the neurophil to become cytotoxic when binding to complement on tumor cells via CR3. This agent has been reported to selectively activate immune cells without inducing pro-inflammatory cytokines, potentially reducing potential side effects observed with the induction of broad innate immune repsonses. In addition, PGG beta-glucan may induce hematopoietic progenitor cell (HPC) mobilization.","Organic Chemical|Pharmacologic Substance"]
["C71692","PGLA/PEG Copolymer-Based Paclitaxel","OncoGel|PGLA/PEG Copolymer-Based Paclitaxel","A controlled-release, intratumoral paclitaxel formulation in which paclitaxel is incorporated into a thermosensitive, biodegradable triblock copolymer consisting of poly(lactide-co-glycolide) (PLGA) and polyethylene glycol (PEG). Upon intratumoral injection, paclitaxel is released slowly and continuously into tumor tissues from the gelled thermosensitive triblock copolymer over a period of 4 to 6 weeks; in tumor cells, paclitaxel binds to tubulin and inhibits the disassembly-assembly dynamics of microtubules, resulting in cell cycle arrest and cell death. The thermosensitive triblock copolymer component of this formulation transforms from a water-soluble polymer at room temperature to a water-insoluble, biodegradable gel depot at body temperature; intratumoral controlled-release of paclitaxel from the gel minimizes systemic exposure to paclitaxel and the paclitaxel toxicity profile.","Pharmacologic Substance"]
["C113790","PH20 Hyaluronidase-expressing Adenovirus VCN-01","Genetically Modified Adenovirus-encoding Human PH20 Hyaluronidase VCN-01|PH20 Hyaluronidase-expressing Adenovirus VCN-01|VCN-01","An oncolytic, replication-competent adenovirus encoding the human glycosylphosphatidylinositol-anchored enzyme PH20 hyaluronidase with potential antitumor activity. After intratumoral administration, PH20 hyaluronidase-expressing adenovirus VCN-01 selectively replicates in tumor cells, which may both cause oncolytic virus-induced cell death and induce the infection of adjacent tumor cells. In addition, the virus expresses hyaluronidase, which hydrolyzes and degrades the hyaluronic acid (HA) that coats tumor cells. The degradation of HA may result in a decrease for both the viscosity of the interstitial space and the tumor's interstitial fluid pressure (IFP). This increases viral spread and may result in the inhibition of tumor cell growth. In addition, HA degradation facilitates the penetration of chemotherapeutic agents into the tumor. HA is a glycosaminoglycan found in the extracellular matrix (ECM) and is frequently overproduced by various tumor cell types. The presence of HA in tumors correlates with increases in tumor cell growth, metastatic potential, tumor progression and resistance to chemotherapeutic agents.","Pharmacologic Substance"]
["C91739","Phaleria macrocarpa Extract DLBS-1425","DLBS-1425|Phaleria macrocarpa Extract DLBS-1425","An extract of the flesh from the fruit of Phaleria macrocarpa, an Indonesian herbal medicine, with potential antineoplastic activity. Although the active ingredients and exact components are unclear, gallic acid and its derivatives in DLBS-1425 appear to inhibit the phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT) signaling pathway by reducing PI3K transcription followed by a reduction in AKT phosphorylation. This extract also appears to induce apoptosis through induction of pro-apoptotic genes such as BAX, BAD and PUMA and inhibition of the apoptosis suppressor Bcl-2.","Pharmacologic Substance"]
["C103230","Phellodendron amurense Bark Extract","Nexrutine|Phellodendron amurense Bark Extract","A proprietary formulation consisting of a Phellodendron amurense (Amur cork tree) bark extract, often used in traditional Chinese medicine, with anti-inflammatory, anti-oxidant and potential chemopreventive and antineoplastic activities. Phellodendron amurense bark extract contains certain isoquinoline alkaloids, flavone glycosides and phenolic compounds. Upon administration of Phellodendron amurense bark extract, the various phytochemicals in this formulation modulate multiple signal transduction pathways. This agent appears to block the activation of the transcription factor cAMP response binding protein (CREB) and inhibits Akt signaling, thereby inhibiting tumor cell growth and inducing apoptosis in Akt- and CREB-overexpressing cancer cells. In addition, this agent inhibits cyclooxygenase type 2 (COX-2), nuclear factor kappa b (NF-kB) and tumor necrosis factor alpha (TNF-a)-mediated signaling; COX-2, NF-kB and TNF-a are upregulated in certain types of cancer and during inflammation.","Pharmacologic Substance"]
["C1190","Phenesterin","(3-beta)-cholest-5-en-3-ol 4-(bis(2-chloroethyl)amino)benzeneacetate|(4-(bis(2-chloroethyl)amino)phenyl)acetic acid cholesteryl ester|(p-(bis(2-chloroethyl)amino)phenyl) acetate cholesterol|(p-(bis(2-chloroethyl)amino)phenyl)acetic acid cholesteryl ester|5-Cholesten-3-beta-ol 3-(p-(bis(2-chloroethyl)amino)phenyl)acetate|Cholest-5-en-3-ol, (3.beta.)-, 4-[bis(2-chloroethyl)amino]benzeneacetate|Cholest-5-en-3beta-ol 4-(bis(2-chloroethyl)amino)benzeneacetate|Cholesteryl p-bis(2-chloroethyl)aminophenylacetate|Fenesterin|Fenestrin|NCI-C01558|Phenesterin|Phenesterine|p-bis(2-chloroethyl)amino phenylacetate cholesterol","A steroidal nitrogen mustard with antineoplastic and mutagenic activities. After attachment to cell-surface steroid receptors and uptake, phenesterin enters the nucleus where it alkylates macromolecules, resulting in decreased cell proliferation. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2233","Phenethyl Isothiocyanate","(2-Isothiocyanatoethyl)benzene|2-Phenylethyl Isothiocyanate|PEITC|PHENETHYL ISOTHIOCYANATE|Phenethyl Isothiocyanate|Phenethyl isothiocyanate|phenethyl isothiocyanate","An isothiocyanate found in cruciferous vegetables with chemopreventive and potential antitumor activities. Although the mechanism of action is unclear, phenethyl Isothiocyanate (PEITC) was shown to induce apoptosis in tumor cells, possibly mediated through its metabolic intermediates, reactive oxygen species (ROS). PEITC also is able to activate ERK and JNK signal transduction, which in turn induces expression of stress-responsive genes. Specifically, this agent has been shown to reactivate gene expression of a detoxification enzyme, glutathione S-transferase that is silenced in prostate carcinoma.","Organic Chemical|Pharmacologic Substance"]
["C105392","Phenethyl Isothiocyanate-containing Watercress Juice","PEITC-containing Watercress Juice|Phenethyl Isothiocyanate-containing Watercress Juice","A juice extracted from watercress containing high amounts of phenethyl isothiocyanate (PEITC), with potential chemopreventive and antitumor activities. Although the mechanism(s) of action through which PEITC exerts its effect(s) has yet to be fully elucidated, PEITC is able to induce apoptosis in tumor cells through the induction of reactive oxygen species (ROS). Additionally, PEITC is able to modulate extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase (MAPK) signal transduction pathways, activating the expression of stress-responsive genes and eventually inducing apoptosis. PEITC also inhibits the expression of genes involved in tumor progression such as HIF, STAT-3, HER2, BCL-XL, and XIAP and induces the expression of genes involved in tumor suppression such as p53, ATF-2, and p57. Furthermore, this agent has been shown to reactivate the gene expression of certain detoxification enzymes.","Pharmacologic Substance"]
["C1501","Phenyl Acetate","Acetic Acid Phenyl Ester|Acetylphenol|PHENYL ACETATE|Phenyl Acetate|Phenyl acetate|phenylacetate","An aromatic fatty acid metabolite of phenylalanine with potential antineoplastic activity.  Naturally occurring in mammals, phenylacetate induces differentiation, growth inhibition, and apoptosis in tumor cells.  Implicated mechanisms of action include decreased protein prenylation, activation of the peroxisome proliferation-activated receptors, inhibition of DNA methylation, and depletion of glutamine. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C71883","Phosphatidylcholine-Bound Silybin","Phosphatidylcholine-Bound Silybin|Silybin-Phytosome","An oral preparation of the flavonoid silybin with potential antioxidant and chemopreventive activities. Silybin, also known as silibinin, is a mixture of two stereoisomers, denoted silybin A and silybin B, and is the major active constituent of silymarin, a mixture of flavonolignans extracted from blessed milk thistle (Silybum marianum). Silybin modulates P-glycoprotein (P-gp)-mediated cellular efflux; has oxygen radical-scavenging effects; inhibits the arachidonic acid pathway; and inhibits various cytochrome P450 enzymes. This agent may also exhibit anti-angiogenic activity, possibly by inducing endothelial cell apoptosis via modulation of the transcription factor NF-kB, the Bcl-2 family of proteins, and caspases. Complexing silybin with phosphatidylcholine increases its bioavailability.","Organic Chemical|Pharmacologic Substance"]
["C38690","Phosphomannopentaose Sulfate","PI-88|Phosphomannopentaose Sulfate","A mixture of highly sulfated, monophosphorylated mannose oligosaccharides, derived from the extracellular phosphomannan of the yeast Pichia (Hansenula) holstii, with potential antiangiogenic activity. Phosphomannopentaose sulfate inhibits the endo-beta-D-glucuronidase heparanase, which may interfere with the heparanase-mediated degradation of heparan-sulfate proteoglycans in extracellular matrices, an important step in the metastatic process. This agent may also bind with high affinity to the heparan sulfate-binding domains of vascular endothelial growth factor (VEGF) and fibroblast growth factors 1 and 2, thereby reducing their functional activities and inhibiting VEGF and FGF stimulation of tumor angiogenesis. Increased heparanase activity has been implicated in tumor angiogenesis and metastasis.","Pharmacologic Substance"]
["C29322","Phosphoramide Mustard","Phosphoramide Mustard","One of a number of chemically-related alkylating agents with antineoplastic properties.  The prototype of this group of agents is cyclophosphamide.  Most phosphoramide mustards are administered as prodrugs that undergo reductive activation in hypoxic environments to yield cytotoxic metabolites. These agents alkylate and crosslink DNA, resulting in inhibition of DNA replication. Phosphoramide mustards are also immunosuppressants, mutagens and teratogens. (NCI04)","Chemical Viewed Structurally"]
["C62518","Phosphorodiamidate Morpholino Oligomer AVI-4126","AVI-4126|PMO AVI-4126|Phosphorodiamidate Morpholino Oligomer AVI-4126","A c-Myc antisense phosphorodiamidate morpholino oligomer (PMO) with potential antineoplastic activity. Phosphorodiamidate morpholino oligomer AVI-4126 binds to c-Myc mRNA and blocks its translation, which may result in the death of tumor cells overexpressing c-Myc. Differing from traditional antisense oligodeoxynucleotides (ODNs), neutrally charged PMOs are composed of subunits of nucleic acid bases linked to a synthetic backbone and, so, are less prone to enzymatic degradation. c-Myc, a proto-oncogene overexpressed in a variety of cancers, is involved in cellular proliferation, differentiation, and apoptosis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1698","Phosphorus P-32","P-32|P32|PHOSPHORUS P-32|Phosphorus P 32|Phosphorus P-32|phosphorus-32","A radioactive isotope of phosphorus with beta particle-emitting radiocytotoxic activity. Emitted by phosphorus P32, beta particles directly damage cellular DNA and, by ionizing intracellular water to produce several types of cytotoxic free radicals and superoxides, indirectly damage intracellular biological macromolecules, resulting in tumor cell death.","Indicator, Reagent, or Diagnostic Aid"]
["C114382","Photosensitizer LUZ 11","LUZ 11|Photosensitizer LUZ 11","A bacteriochlorin-based photosensitizer, with antineoplastic activity upon photodynamic therapy (PDT). Following intravenous administration, the photosensitizer LUZ 11 preferentially accumulates in hyperproliferative tissues, such as tumors. Local application of laser light at the tumor site results in the absorption of light by this agent and a photodynamic reaction between LUZ 11 and oxygen. This results in the production of reactive oxygen species (ROS), which includes singlet oxygen molecules, the superoxide ion, and other cytotoxic free radicals. The formation of ROS induces free radical-mediated DNA damage and cell death.","Pharmacologic Substance"]
["C126802","Phytochlorin Sodium-Polyvinylpyrrolidone Complex","BLC-1013|Chlorin E6-PVP|Chlorin E6-polyvinylpyrrolidone|Chlorin E6/PVP|Fotolon|Photolon|Phytochlorin Sodium-Polyvinylpyrrolidone Complex","A photosensitizer composed of the sodium salt form of chlorin e6 and its derivatives complexed with a low-molecular weight polyvinylpyrrolidone (PVP) polymer component, with diagnostic and antineoplastic activities upon photodynamic therapy (PDT). Upon intravenous administration, the photosensitizer phytochlorin-PVP sodium complex preferentially accumulates in hyperproliferative tissues, such as tumors. Local application of light with a certain wavelength to the tumor site results in the absorption of light by this agent leading to its photoactivation. This results in a photodynamic reaction between phytochlorin and oxygen, which causes the production of reactive oxygen species (ROS), including singlet oxygen molecules, the superoxide ion, and other cytotoxic free radicals. The formation of ROS induces free radical-mediated oxidative DNA damage followed by apoptosis of tumor cells. Chlorin e6-PVP is able to penetrate deeply into tissues and is therefore able to treat hard-to-reach tumors.","Pharmacologic Substance"]
["C98844","PI3K alpha Inhibitor MLN1117","INK1117|MLN-1117|MLN1117|PI3K alpha Inhibitor MLN1117|TAK 117|TAK-117","An orally bioavailable inhibitor of the class I phosphoinositide 3-kinase (PI3K) alpha isoform with potential antineoplastic activity. PI3K alpha inhibitor MLN1117 selectively inhibits PI3K alpha kinase, including mutations of PIK3CA, in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K alpha-expressing tumor cells. By specifically targeting class I PI3K alpha, this agent may be more efficacious and less toxic than pan PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and results in promoting tumor cell growth, survival, and resistance to chemotherapy and radiotherapy; PIK3CA, one of the most highly mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.","Pharmacologic Substance"]
["C103861","PI3K Alpha/Beta Inhibitor BAY1082439","BAY1082439|PI3K Alpha/Beta Inhibitor BAY1082439","An orally bioavailable inhibitor of the class I phosphoinositide 3-kinase (PI3K) alpha and beta isoforms with potential antineoplastic activity. PI3K alpha/beta inhibitor BAY1082439 selectively inhibits both PI3K alpha, including mutated forms of PIK3CA, and PI3K beta in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K-expressing and/or PTEN-driven tumor cells. By specifically targeting class I PI3K alpha and beta, this agent may be more efficacious and less toxic than pan PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and results in increased tumor cell growth, survival, and resistance to chemotherapy and radiotherapy. PIK3CA, one of the most highly mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells.","Pharmacologic Substance"]
["C97915","PI3K Alpha/mTOR Inhibitor PWT33597 Mesylate","PI3K Alpha/mTOR Inhibitor PWT33597 Mesylate|PWT33597 Mesylate","The mesylate salt form of PWT33597, an orally bioavailable dual inhibitor of phosphatidylinositide 3-kinase (PI3K) alpha and mammalian target of rapamycin (mTOR) kinase with potential antineoplastic activity. PI3K alpha/mTOR dual inhibitor PWT33597 selectively inhibits both PI3K alpha kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in PI3K/mTOR-overexpressing tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.","Pharmacologic Substance"]
["C99225","PI3K delta/gamma Inhibitor IPI-145","IPI-145|PI3K delta/gamma Inhibitor IPI-145","An orally bioavailable, highly selective and potent small molecule inhibitor of the delta and gamma isoforms of phosphoinositide-3 kinase (PI3K) with potential immunomodulating and antineoplastic activities. Upon administration, PI3K delta/gamma inhibitor IPI 145 prevents the activation of the PI3K delta/gamma-mediated signaling pathways which may lead to a reduction in cellular proliferation in PI3K delta/gamma-expressing tumor cells. Unlike other isoforms of PI3K, the delta and gamma isoforms are overexpressed primarily in hematologic malignancies and inflammatory and autoimmune diseases. By selectively targeting these PI3K isoforms, PI3K signaling in normal, non-neoplastic cells is minimally or not affected which would result in a more favorable side effect profile.","Pharmacologic Substance"]
["C113433","PI3K Delta/Gamma Inhibitor RP6530","PI3K Delta/Gamma Inhibitor RP6530|RP 6530|RP-6530|RP6530","An orally active, highly selective, small molecule inhibitor of the delta and gamma isoforms of phosphoinositide-3 kinase (PI3K) with potential immunomodulating and antineoplastic activities. Upon administration, PI3K delta/gamma inhibitor RP6530 inhibits the PI3K delta and gamma isoforms and prevents the activation of the PI3K/AKT-mediated signaling pathway. This may lead to a reduction in cellular proliferation in PI3K delta/gamma-expressing tumor cells. In addition, this agent modulates inflammatory responses through various mechanisms, including the inhibition of both the release of reactive oxygen species (ROS) from neutrophils and tumor necrosis factor (TNF)-alpha activity. Unlike other isoforms of PI3K, the delta and gamma isoforms are overexpressed primarily in hematologic malignancies and in inflammatory and autoimmune diseases. By selectively targeting these isoforms, PI3K signaling in normal, non-neoplastic cells is minimally impacted or not affected at all, which minimizes the side effect profile for this agent.","Pharmacologic Substance"]
["C71705","PI3K Family Kinase Inhibitor XL147","PI3K Family Kinase Inhibitor XL147|XL147","An orally bioavailable small molecule, targeting the class I phosphatidylinositol 3 kinase (PI3K) family of lipid kinases, with potential antineoplastic activity. Class 1 PI3K kinase family inhibitor XL147 reversibly binds to class 1 PI3Ks in an ATP-competitive manner, inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K signaling pathway; this may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents including genotoxic agents and receptor tyrosine kinase inhibitors.","Pharmacologic Substance"]
["C118568","PI3K Inhibitor ACP-319","ACP-319|PI3K Inhibitor ACP-319","An orally available inhibitor of phosphatidylinositol 3-kinase (PI3K), with potential antineoplastic activity. PI3K inhibitor ACP-319 inhibits PI3K, which prevents the activation of the PI3K/AKT (protein kinase B)-mediated signaling pathway. This results in the inhibition of growth and survival of PI3K-overexpressing tumor cells. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis.","Pharmacologic Substance"]
["C74073","PI3K Inhibitor BGT226","BGT226|PI3K Inhibitor BGT226","A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor BGT226 specifically inhibits PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane, increasing mitochondrial membrane permeability; apoptotic cell death may ensue. Bax is a member of the proapoptotic Bcl2 family of proteins.","Pharmacologic Substance"]
["C116877","PI3K Inhibitor GDC-0084","GDC-0084|GDC0084|PI3K Inhibitor GDC-0084","A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor GDC-0084 specifically inhibits PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway, thereby inhibiting the activation of the PI3K signaling pathway. This may result in the inhibition of both cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C82380","PI3K Inhibitor GDC-0941 Bismesylate","2-(1H-indazol-4-yl)-6-(4-methanesulfonyl-piperazin-1- ylmethyl)-4-morpholin-4-yl-thieno[3,2-d]pyrimidine, bimesylate salt|GDC-0941 Bismesylate|PI3K Inhibitor GDC-0941 Bismesylate","The orally bioavailable bismesylate salt of a potent small-molecule thieno[3,2-d]pyrimidine inhibitor of the class I phosphatidylinositol 3 kinase (PI3K) isoforms p100alpha and p100delta with potential antineoplastic activity. PI3K inhibitor GDC-0941 selectively binds to PI3K isoforms in an ATP-competitive manner, inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K/Akt signaling pathway; inhibition of tumor cell growth, motility and survival in susceptible tumor cell populations may result. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis; dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C78470","PI3K Inhibitor GSK1059615","GSK1059615|PI3K Inhibitor GSK1059615","A phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor GSK1059615 inhibits PI3K in the PI3K/AKT kinase signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane and an increase in mitochondrial membrane permeability, followed by apoptosis. Bax is a member of the proapoptotic Bcl-2 family of proteins. PI3K, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.","Organic Chemical|Pharmacologic Substance"]
["C88270","PI3K Inhibitor GSK2126458","GSK2126458|PI3K Inhibitor GSK2126458","A small-molecule pyridylsulfonamide inhibitor of phosphatidylinositol 3-kinase (PI3K) with potential antineoplastic activity. PI3K inhibitor GSK2126458 binds to and inhibits PI3K in the PI3K/mTOR signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane, increasing mitochondrial membrane permeability and inducing apoptotic cell death. Bax is a member of the proapoptotic Bcl2 family of proteins. PI3K, often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.","Pharmacologic Substance"]
["C78848","PI3K Inhibitor PX-866","PI3K Inhibitor PX-866|PX-866|acetic acid (1S,4E,10R,11R,13S,14R)-4-diallylaminomethylene-6-hydroxy-1-methoxymethyl-10,13-dimethyl-3,7,17-trioxo-1,3,4,7,10,11,12,13,14,15,16,17-dodecahydro-2-oxa-cyclopenta[a]phenanthren-11-yl ester|acetic acid 4-diallylaminomethylene-6-hydroxy-1-alpha 12-methoxymethyl-10beta,13beta-dimethyl-3,7,17-trioxo-1,3,4,7,10,11beta,12,13,14alpha,15,16,17-dodecahydro-2-oxa-cyclopenta[a]phenanthren-11-yl ester","A small-molecule wortmannin analogue inhibitor of the alpha, gamma, and delta isoforms of phosphoinositide 3-kinase (PI3K) with potential antineoplastic activity. PI3K inhibitor PX-866 inhibits the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K/Akt signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C107386","PI3K Inhibitor WX-037","PI3K Inhibitor WX-037|WX-037","A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor WX-037 specifically inhibits PI3K, which prevents the activation of the PI3K/protein kinase B-mediated signaling pathway. This may result in the inhibition of both tumor cell growth and survival in PI3K-overexpressing tumor cells. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C95723","PI3K Inhibitor ZSTK474","PI3K Inhibitor ZSTK474|Phosphatidylinositol 3-kinase Inhibitor ZSTK474|ZSTK474","An orally available, s-triazine derivative, ATP-competitive phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor ZSTK474 inhibits all four PI3K isoforms. Inhibiting the activation of the PI3K/AKT kinase (or protein kinase B) signaling pathway results in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents. This agent does not induce apoptosis but rather induces strong G(0)/G(1) arrest, which might contribute to its favorable efficacy in tumor cells.","Pharmacologic Substance"]
["C126271","PI3K p110beta/delta Inhibitor KA2237","KA 2237|KA2237|PI3 Kinase b/d Inhibitor KA2237|PI3K p110beta/delta Inhibitor KA2237","A dual selective inhibitor of the beta and delta isoforms of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinase (PI3K-beta/delta), with potential antineoplastic activity. PI3K-beta/delta inhibitor KA2237 selectively inhibits the PI3K-beta and -delta isoforms and prevents their activation, which inhibits PI3K-beta/delta-mediated signal transduction pathways. This decreases proliferation and induces cell death in susceptible tumor cells. Unlike other isoforms of PI3K, PI3K-beta and -delta are overexpressed primarily in solid and hematological tumor cells and play crucial roles in tumor cell survival, and immunoregulation. The targeted inhibition of these PI3Ks allows this agent to potentially be more efficacious and less toxic than pan PI3K inhibitors, which also affect normal, healthy cells.","Pharmacologic Substance"]
["C104008","PI3K/HDAC Inhibitor CUDC-907","CUDC-907|PI3K/HDAC Inhibitor CUDC-907","An orally bioavailable inhibitor of both phosphoinositide 3-kinase (PI3K) class I and pan histone deacetylase (HDAC) enzymes, with potential antineoplastic activity. Upon oral administration, CUDC-907 inhibits the activity of both PI3K class I isoforms and HDAC, thereby preventing the activation of the PI3K-AKT-mTOR signal transduction pathway that is often overactivated in many cancer cell types. This may prevent growth of PI3K and/or HDAC-expressing tumor cells. CUDC-907 shows an increased inhibition of tumor cell growth and induction of apoptosis when compared to inhibitors that target either PI3K or HDAC.","Pharmacologic Substance"]
["C74072","PI3K/mTOR Inhibitor BEZ235","BEZ235|PI3K/mTOR Inhibitor BEZ235","An orally bioavailable imidazoquinoline targeting the phosphatidylinositol 3 kinase (PI3K) and the mammalian target of rapamycin (mTOR), with potential antineoplastic activity. PI3K/mTOR inhibitor BEZ235 inhibits PI3K kinase and mTOR kinase in the PI3K/AKT/mTOR kinase signaling pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K/mTOR-overexpressing tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.","Pharmacologic Substance"]
["C97254","PI3K/mTOR Kinase Inhibitor DS-7423","DS-7423|Dual PI3 Kinase/mTOR Inhibitor DS-7423|PI3K/mTOR Kinase Inhibitor DS-7423","An orally bioavailable inhibitor of phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinase in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor DS-7423 inhibits both PI3K kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in susceptible tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K. Consequently, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase.","Pharmacologic Substance"]
["C84837","PI3K/mTOR Kinase Inhibitor PF-04691502","PF-04691502|PI3K/mTOR Kinase Inhibitor PF-04691502","An agent targeting the phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor PF-04691502 inhibits both PI3K and mTOR kinases, which may result in apoptosis and growth inhibition of cancer cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.","Pharmacologic Substance"]
["C112497","PI3K/mTOR Kinase Inhibitor VS-5584","2-Pyrimidinamine, 5-[8-Methyl-9-(1-Methylethyl)-2-(4-Morpholinyl)-9H-Purin-6-Yl]-2-|5-[8-Methyl-9-(1-Methylethyl)-2-(4-Morpholinyl)-9H-Purin-6-Yl]-2-Pyrimidinamine|PI3K/mTOR Inhibitor VS-5584|PI3K/mTOR Kinase Inhibitor VS-5584|SB 2343|SB-2343|SB2343|VS 5584|VS-5584|VS5584","A potent and selective inhibitor of both phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinase in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor VS-5584 inhibits mTOR kinase and all class I PI3K isoforms. Consequently, this disrupts phosphorylation of substrates downstream of PI3K and mTOR and may result in apoptosis and growth inhibition in susceptible tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy. mTOR is a serine/threonine kinase downstream of PI3K, which also has PI3K-independent activity. Consequently, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase.","Pharmacologic Substance"]
["C104292","PI3K/mTOR/ALK-1/DNA-PK Inhibitor P7170","P7170|PI3K/mTOR/ALK-1/DNA-PK Inhibitor P7170","An orally bioavailable inhibitor of phosphoinositide 3-kinase (PI3K), mammalian target of rapamycin (mTOR), activin receptor-like kinase 1 (ALK-1) and DNA-dependent protein kinase (DNA-PK), with potential anti-angiogenic and antineoplastic activities. Upon oral administration, PI3K/mTOR/ALK-1/DNA-PK inhibitor P7170 inhibits the activity of all four kinases. This prevents PI3K/mTOR and ALK-1-mediated signaling pathways and may lead to the inhibition of cancer cell growth in PI3K/mTOR-overexpressing tumor cells and angiogenesis in ALK-1-overexpressing endothelial cells. Also, by inhibiting DNA-PK, this agent inhibits the ability of tumor cells to repair damaged DNA. The PI3K/mTOR pathway is upregulated in a variety of tumors and plays an important role in regulating cancer cell proliferation, growth, and survival. ALK-1, a member of the transforming growth factor beta (TGF-b) type I receptor family, is overexpressed on endothelial cells in a variety of tumor types and increases endothelial cell proliferation and migration. DNA-PK is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks.","Pharmacologic Substance"]
["C116351","PI3K/mTORC1/mTORC2 Inhibitor DCBCI0901","DCBCI0901|PI3K/mTORC1/mTORC2 Inhibitor DCBCI0901","An inhibitor of phosphatidylinositide 3-kinase (PI3K), raptor-mTOR (mTOR complex 1 or mTORC1) and rictor-mTOR (mTOR complex 2 or mTORC2) with potential antineoplastic activity. Upon intravenous infusion, PI3K/mTORC1/mTORC2 inhibitor DCBCI0901 binds to and inhibits PI3K as well as both mTORC1 and mTORC2, which may result in both apoptosis and a decrease in cell proliferation in tumor cells overexpressing PI3K, mTORC1, and mTORC2. Activation of the PI3K/mTOR signaling pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.","Pharmacologic Substance"]
["C90291","PI3Ka/mTOR Inhibitor PKI-179","PI3Ka/mTOR Inhibitor PKI-179|PKI-179","A second generation, small-molecule mimetic of ATP that targets the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. PKI-179 selectively inhibits mTOR and phosphoinositide-3-kinase (PI3K) alpha. By inhibiting the PI3K/mTOR signaling pathway, this agent may inhibit tumor cell proliferation and survival.","Pharmacologic Substance"]
["C118624","PI3Kalpha Inhibitor AZD8835","AZD8835|PI3Kalpha Inhibitor AZD8835","An orally bioavailable inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (PIK3CA), with potential antineoplastic activity. PI3K alpha inhibitor AZD8835 selectively binds to and inhibits PIK3CA and its mutated forms, in the PI3K/Akt (protein kinase B) /mammalian target of rapamycin (mTOR) pathway. This results in both apoptosis and growth inhibition in PIK3CA-expressing tumor cells. By specifically targeting PIK3CA, this agent may be more efficacious and less toxic than pan-PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.","Pharmacologic Substance"]
["C107684","PI3Kbeta Inhibitor AZD8186","AZD-8186|AZD8186|PI3Kbeta Inhibitor AZD8186","An inhibitor of the beta isoform of phosphoinositide-3 kinase (PI3K), with potential antineoplastic activity. Upon administration, PI3Kbeta inhibitor AZD8186 selectively inhibits the activity of PI3Kbeta in the PI3K/Akt/mTOR signaling pathway, which may result in a decrease of tumor cell proliferation and induces cell death in PI3K-expressing cancer cells. By specifically targeting class I PI3K beta, this agent may be more efficacious and less toxic than pan PI3K inhibitors. PI3K-mediated signaling is often dysregulated in cancer cells and contributes to increased tumor cell growth, survival, and tumor resistance to a variety of antineoplastic agents.","Pharmacologic Substance"]
["C106261","PI3K-beta Inhibitor GSK2636771","GSK2636771|PI3K-beta Inhibitor GSK2636771","An orally bioavailable, substituted benzimidazole inhibitor of the class I phosphoinositide 3-kinase (PI3K) beta isoform with potential antineoplastic activity. PI3K beta inhibitor GSK2636771 selectively inhibits PI3K beta kinase activity in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K beta-expressing and/or PTEN-driven tumor cells. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to both chemotherapy and radiotherapy. PI3K beta is the p110-beta catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells.","Pharmacologic Substance"]
["C116882","PI3K-beta Inhibitor SAR260301","(S)-2-(2-(2-Methylindolin-1-yl)-2-oxoethyl)-6-morpholinopyrimidin-4(3H)-one|PI3K-beta Inhibitor SAR260301|SAR 260301|SAR-260301|SAR260301","An orally bioavailable inhibitor of the class I phosphatidylinositol 3-kinase (PI3K) beta isoform with potential antineoplastic activity. PI3K beta inhibitor SAR260301 selectively inhibits PI3K beta kinase activity in the PI3K/Akt/mTOR pathway, which may result in apoptosis and growth inhibition in PI3K beta-expressing and/or phosphatase and tensin homolog (PTEN)-deficient tumor cells. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and contributes to increased tumor cell growth, tumor cell survival, and resistance to both chemotherapy and radiotherapy. PI3K beta is the p110-beta catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells. By specifically targeting class I PI3K beta, this agent may be more efficacious and less toxic than pan-PI3K inhibitors.","Pharmacologic Substance"]
["C95891","PI3K-delta Inhibitor AMG 319","AMG 319|PI3K-delta Inhibitor AMG 319","A highly selective, potent, and orally bioavailable small molecule inhibitor of the delta isoform of the 110 kDa catalytic subunit of class IA phosphoinositide-3 kinases (PI3K) with potential immunomodulating and antineoplastic activities.  PI3K-delta inhibitor AMG 319 prevents the activation of the PI3K signaling pathway through inhibition of the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3), thus decreasing proliferation and inducing cell death.  Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in hematopoietic lineages. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells.","Pharmacologic Substance"]
["C107686","PI3Kdelta Inhibitor INCB040093","INCB040093|PI3Kdelta Inhibitor INCB040093","An orally bioavailable, selective inhibitor of the delta isoform of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinases (PI3K) with potential antineoplastic activity.  PI3Kdelta inhibitor INCB040093 specifically inhibits PI3Kdelta, which prevents both the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and the activation of the PI3K/AKT kinase signaling pathway. This decreases proliferation and induces cell death in PI3K-overexpressing tumor cells. Unlike other isoforms of PI3K, PI3Kdelta is often overexpressed in tumor cells, especially those of hematologic origin, and plays a crucial role in tumor cell regulation and survival. The targeted inhibition of PI3Kdelta allows for PI3K signaling in normal, non-neoplastic cells.","Pharmacologic Substance"]
["C113434","PI3K-delta Inhibitor INCB050465","INCB050465|PI3K-delta Inhibitor INCB050465","An inhibitor of the delta isoform of phosphoinositide-3 kinase (PI3K) with potential antineoplastic activity.  PI3K-delta inhibitor INCB050465 inhibits the delta isoform of PI3K and prevents the activation of the PI3K/AKT signaling pathway. This both decreases proliferation and induces cell death in PI3K-delta-overexpressing tumor cells. Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in hematopoietic disease and cell lineages. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells. PI3K, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.","Pharmacologic Substance"]
["C123925","PI3K-delta Inhibitor PWT143","PI3K-delta Inhibitor PWT143|PWT-143|PWT143","An orally bioavailable inhibitor of the delta isoform of phosphatidylinositide 3-kinase (PI3K), with potential antineoplastic activity. Upon oral administration, PI3K-delta inhibitor PWT143 selectively inhibits the delta isoform of PI3K and prevents the activation of the PI3K/AKT signaling pathway. This both decreases proliferation and induces cell death in PI3K-delta-overexpressing tumor cells. PI3K-delta plays a key role in the proliferation and survival of hematologic cancer cells. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells. PI3K, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.","Pharmacologic Substance"]
["C104413","PI3K-delta Inhibitor TGR-1202","PI3K-delta Inhibitor TGR-1202|RP5264|TGR-1202","An orally bioavailable, selective inhibitor of the delta isoform of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinases (PI3K) with potential antineoplastic activity.  PI3K-delta inhibitor TGR-1202 inhibits PI3K and prevents the activation of the PI3K/AKT kinase signaling pathway. This decreases proliferation and induces cell death in susceptible tumor cells.  Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in tumor cells and cells of the hematopoietic lineage. The targeted inhibition of PI3K-delta allows for PI3K signaling in normal, non-neoplastic cells. PI3K, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.","Pharmacologic Substance"]
["C125471","PI3K-gamma Inhibitor IPI-549","IPI 549|IPI-549|PI3K-gamma Inhibitor IPI-549","An orally bioavailable, highly selective small molecule inhibitor of the gamma isoform of phosphoinositide-3 kinase (PI3K-gamma) with potential immunomodulating and antineoplastic activities. Upon administration, IPI-549 prevents the activation of the PI3K-gamma-mediated signaling pathways, which may lead to a reduction in cellular proliferation in PI3K-gamma-expressing tumor cells. In addition, this agent is able to modulate anti-tumor immune responses and inhibit tumor-mediated immunosuppression. Unlike other isoforms of PI3K, the gamma isoform is overexpressed in certain tumor cell types and immune cells; its expression increases tumor cell proliferation and survival. By selectively targeting the gamma isoform, PI3K signaling in normal, non-neoplastic cells is minimally or not affected, which results in a reduced side effect profile.","Pharmacologic Substance"]
["C546","Pibenzimol","Bisbenzimidazole|HOE 33258|Hoe 33258|Hoechst 33258|Hoechst Dye 33258|Hoechst dye 33258|PIBENZIMOL|Phenol, 4-(5-(4-methyl-1-piperazinyl)(2,5'-bi-1H-benzimidazol)-2'-yl)-, Trihydrochloride|Phenol, p-[5-[5-(4-methyl-1-piperazinyl)-2-benzimidazolyl]-2- benzimidazolyl]-, Trihydrochloride|Pibenzimol Hydrochloride|Pibenzimol","A fluorescent dye of benzimidazole derivative.  Pibenzimol binds to AT-specific sites in the minor groove of duplex DNA and inhibits topoisomerase I, and DNA polymerase, thereby preventing DNA replication. This agent prolongs the G2 phase of the cell cycle and initiates apoptosis in tumor cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1542","Pibrozelesin","Benzo(1,2-b:4,3-b')dipyrrole-1-carboxylic Acid, 8-(bromomethyl)-3,6,7,8-tetrahydro-2-methy-4-(((4-methyl-1-piperazinyl)carbonyl)oxy)-6-((5,6,7,-trimethoxy-1H-indol-2-yl)carbonyl)-, Methyl Ester (S)|Duocamycin B2 Analog|KW 2189|KW-2189|KW2189|PIBROZELESIN|Pibrozelesin","A semisynthetic water-soluble derivative of the antineoplastic antibiotic duocarmycin B2.  Activated by carboxyl esterase, pibrozelesin alkylates DNA by binding to adenine-thymine (A-T)-rich sequences in the minor groove of DNA, thereby inhibiting DNA replication and inducing apoptosis.","Antibiotic|Organic Chemical|Pharmacologic Substance"]
["C73816","Pibrozelesin Hydrobromide","PIBROZELESIN HYDROBROMIDE|Pibrozelesin Hydrobromide","The hydrobromide salt form of pibrozelesin, a semisynthetic water-soluble derivative of the antineoplastic antibiotic duocarmycin B2, with antineoplastic activity. Activated by carboxyl esterase, pibrozelesin alkylates DNA by binding to adenine-thymine (A-T)-rich sequences in the minor groove of DNA, thereby inhibiting DNA replication and inducing apoptosis.","Pharmacologic Substance"]
["C745","Picibanil","OK-432|Picibanil","A lyophilized formulation containing cultures of a low-virulent strain of Streptococcus pyogenes, treated and killed with pencillin G, with potential sclerosing, immunostimulating and antineoplastic activity. Besides from picibanil's direct damaging effect as a sclerosing agent, it seems to have multiple effects on the immune system as a non-specific immunostimulant.  Picibanil activates the host immune system by stimulating the activity of natural killer cells, macrophages and lymphocytes, and by enhancing the production of several key immune mediators, including interleukins and tumor necrosis factor.","Organic Chemical|Pharmacologic Substance"]
["C48416","Picoplatin","AMD473|Cis-Amminedichloro (2-Methylpyridine) Platinum (II)|JM473|NX-473|PICOPLATIN|Picoplatin|Platinum, Amminedichloro(2-methylpyridine)-, (SP-4-3)-|ZD0473","A new generation organic platinum analog with an extended spectrum of antineoplastic activity. Designed to overcome platinum drug resistance, picoplatin alkylates DNA, forming both inter- and intra-strand cross-linkages, resulting in inhibition of DNA replication and transcription, and the induction of apoptosis.","Inorganic Chemical|Pharmacologic Substance"]
["C1771","Picrasinoside H","Picras-2-en-1-one, 13-(acetyloxy)-16-(beta-D-glucopyranosyloxy)-2-methoxy-11,12-(methylenebis(oxy))-, (11alpha,12beta,16alpha)-|Picrasinoside H","A quassinoid glycoside phytochemical isolated from the plant Picrasma ailanthoides with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C87736","Picropodophyllin","AXL1717|Furo(3',4':6,7)naphtho(2,3-d)-1,3-dioxol-6(5aH)-one,5,8,8a,9-tetrahydro-9-hydroxy-5-(3,4,5-trimethoxyphenyl)-,(5R-(5-alpha,5a-alpha,8a-alpha,9-alpha))-|PICROPODOPHYLLIN|Picropodophyllin|Picropodophyllotoxin","A cyclolignan alkaloid found in the mayapple plant family (Podophyllum peltatum), and a small molecule inhibitor of the insulin-like growth factor 1 receptor (IGF1R) with potential antineoplastic activity. Picropodophyllin specifically inhibits the activity and downregulates the cellular expression of IGF1R without interfering with activities of other growth factor receptors, such as receptors for insulin, epidermal growth factor, platelet-derived growth factor, fibroblast growth factor and mast/stem cell growth factor (KIT). This agent shows potent activity in the suppression o f tumor cell proliferation and the induction of tumor cell apoptosis. IGF1R, a receptor tyrosine kinase overexpressed in a variety of human cancers, plays a critical role in the growth and survival of many types of cancer cells.","Pharmacologic Substance"]
["C71014","Pidilizumab","CT 011|CT-011|Immunoglobulin G1, Anti-(Human Programmed Cell Death 1); Humanized Mouse Monoclonal CT-011 Gamma1 Heavy Chain (220-213')-disulfide with Humanized Mouse Monoclonal CT-011 Kappa Light Chain Dimer (226-226'':229-229'')-bisdisulfide, Glycosylated (CT-011 is Expressed in NSO Cells)|MDV9300|PIDILIZUMAB|Pidilizumab","A humanized monoclonal antibody directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. Pidilizumab blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues.","Amino Acid, Peptide, or Protein|Indicator, Reagent, or Diagnostic Aid"]
["C106259","PIM Kinase Inhibitor LGH447","LGH447|PIM Kinase Inhibitor LGH447","An orally available pan-PIM protein kinase inhibitor with potential antineoplastic activity. PIM kinase inhibitor LGH447 binds to and inhibits the activities of PIM-1, -2 and -3 serine/threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, the expression of the pro-apoptotic Bcl2 protein and tumor cell apoptosis in cells that overexpress PIMs. PIM kinases, downstream effectors of many cytokine and growth factor signaling pathways, play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies.","Pharmacologic Substance"]
["C82404","PIM Kinase Inhibitor SGI-1776","PIM Kinase Inhibitor SGI-1776|SGI-1776","A small-molecule pan-PIM protein kinase inhibitor with potential antineoplastic activity. PIM kinase inhibitor SGI-1776 binds to and inhibits the activities of PIM-1, -2 and -3 serine/threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, the expression of pro-apoptotic Bcl2 proteins and tumor cell apoptosis. PIM kinases play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies.","Pharmacologic Substance"]
["C84864","Pimasertib","AS703026|EMD 1036239|MSC1936369|N-[(2S)-2,3-dihydroxypropyl]-3-[(2-fluoro-4- iodophenyl)amino]isonicotinamide Hydrochloride|PIMASERTIB|Pimasertib","An orally bioavailable small-molecule inhibitor of MEK1 and MEK2 (MEK1/2) with potential antineoplastic activity. Pimasertib selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C1279","Pingyangmycin","Bleomycetin|Bleomycin A5|N1-(3-((4-Aminobutyl)amino)propyl)bleomycinamide|Pingyangmycin|Zhengguangmycin A5","The naturally-occurring bleomycin antineoplastic antibiotic isolated from the bacterium Streptomyces pingyangensisn.  Pingyangmycin induces tumor cell apoptosis, possibly via a mechanism mediated by the mitogen-activated protein kinase (MAPK) pathway. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C71633","Pioglitazone","PIOGLITAZONE|Pioglitazone|pioglitazone","An orally-active thiazolidinedione with antidiabetic properties and potential antineoplastic activity. Pioglitazone activates peroxisome proliferator-activated receptor gamma (PPAR-gamma), a ligand-activated transcription factor, thereby inducing cell differentiation and inhibiting cell growth and angiogenesis. This agent also modulates the transcription of insulin-responsive genes, inhibits macrophage and monocyte activation, and stimulates adipocyte differentiation.","Organic Chemical|Pharmacologic Substance"]
["C29367","Pioglitazone Hydrochloride","Actos|PIOGLITAZONE HYDROCHLORIDE|Pioglitazone Hydrochloride|Pioglitazone.HCl","The hydrochloride salt of an orally-active thiazolidinedione with antidiabetic properties and potential antineoplastic activity. Pioglitazone activates peroxisome proliferator-activated receptor gamma (PPAR-gamma), a ligand-activated transcription factor, thereby inducing cell differentiation and inhibiting cell growth and angiogenesis. This agent also modulates the transcription of insulin-responsive genes, inhibits macrophage and monocyte activation, and stimulates adipocyte differentiation. (NCI05)","Organic Chemical|Pharmacologic Substance"]
["C1874","Pipendoxifene","2-(4-Hydroxyphenyl)-3-methyl-1-[4-(2-piperidin-1-ylethoxy)benzyl]-1H-indol-5-ol Hydrochloride|ERA 923|ERA-923|PIPENDOXIFENE|Pipendoxifene","A nonsteroidal 2-phenyl indole and a selective estrogen receptor modulator (SERM) with potential antineoplastic activity. Pipendoxifene antagonizes binding of estradiol to estrogen receptor alpha (ER alpha), thereby inhibiting ER alpha-mediated gene expression, interfering with estrogen activity and inhibiting estrogen-stimulated growth in estrogen-dependent breast cancer. In addition, this agent also exerts intrinsic estrogenic activity depending on the tissue types.","Organic Chemical|Pharmacologic Substance"]
["C1401","Piperazinedione","2, 5-Piperazinedione, 3,6-bis-(5-chloro-2-piperidyl)-, dihydrochloride|2, 5-piperazinedione, 3,6-bis-(5-chloro-2-piperidyl)-, dihydrochloride|2,5-Piperazinedione, 3, 6-bis(5-chloro-2-piperidinyl)-, dihydrochloride, [3S-[3.alpha.(2S*,5R*),6.alpha.(2S*,5R*)]]- (9CI)|2,5-piperazinedione, 3, 6-bis(5-chloro-2-piperidinyl)-, dihydrochloride, [3S-[3alpha(2S*,5R*),6alpha(2S*,5R*)]]- (9CI)|593A|Compound 593A|Merck Compound 593A|PZD dihydrochloride, 3,6-bis(5-chloro-2-piperidinyl)-, dihydrochloride|PZD|Piperazinedione","A crystalline antibiotic fermentation product isolated from the bacterium Streptomyces griseoluteus with antineoplastic activity. Piperazinedione alkylates DNA at the N-7 position of guanine, inhibiting DNA replication and inducing cell cycle arrest.","Antibiotic|Organic Chemical"]
["C48417","Piperine Extract (Standardized)","Bioperine|Piperine Extract (Standardized)|Standardized Piperine Extract","A standardized extract containing the active alkaloid piperine, derived from the fruit of the plant Piper nigrum (black pepper) and/or the plant Piper longum L. (long pepper), with thermogenic properties. Co-ingestion of piperidine enhances the bioavailability of various nutrients, including beta-carotene, curcumin, selenium, pyridoxine and coenzyme Q10. In addition, this agent may exert anti-inflammatory and anti-tumor activities and may enhance the production of serotonin.","Pharmacologic Substance"]
["C750","Pipobroman","Amedel|PIPOBROMAN|Pipobroman|Vercyte","A piperazine derivative with potential antineoplastic alkyating activity. Although the exact mechanism of action of pipobroman has yet to be fully elucidated, this agent appears to act by alkylating DNA, leading to disruption of DNA replication and eventually cell death.","Organic Chemical|Pharmacologic Substance"]
["C1783","Piposulfan","A 20968|A-20968|PIPOSULFAN|Piposulfan","An alkyl sulfonate with potential antineoplastic activity.  Piposulfan alkylates DNA, thereby producing DNA interstrand crosslinks and DNA strand breaks and inhibiting DNA replication.  This agent has been shown to exhibit antitumor activity in an animal model of prostate cancer. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1197","Pirarubicin","(2\"R)-4'-O-Tetrahydropyranyladriamycin|(8S,10S)-10-[[3-Amino-2,3,6-trideoxy-4-O-(tetrahydro-2H-pyran-3-yl)-alpha-L-lyxo-hexopyranosyl]oxy]-8-glycoloyl-7,8,9,10-tetrahydro-6,8,11-trihydroxy-1-methoxy-5,12-naphthacenedione|1609RB|4'-O-Tetrahydropyranyl Doxorubicin|PIRARUBICIN|Pinorubicin|Pirarubicin|THP-ADM|THP-Adriamycin|THP-DOX|THP-Doxorubicin|Tepirubicin|Tetrahydropyranyl-Doxorubicin|Theprubicin|Theprubicine|Therarubicin|[8S-[8Alpha,10alpha(S*)]]-10-[[3-amino-2,3,6-trideoxy-4-O-(tetrahydro-2H-pyran-2-yl)-alpha-L-lyxo-hexopyranosyl]oxy]-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-5,12-naphthacenedione","An analogue of the anthracycline antineoplastic antibiotic doxorubicin.  Pirarubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.  This agent is less cardiotoxic than doxorubicin and exhibits activity against some doxorubicin-resistant cell lines. (NCI04)","Antibiotic|Organic Chemical"]
["C95319","Pirarubicin Hydrochloride","(2\"R)-4'-O-Tetrahydropyranyladriamycin Hydrochloride|4'-O-Tetrahydropyranyl Doxorubicin HCl|PIRARUBICIN HYDROCHLORIDE|Pirarubicin Hydrochloride|THP-ADM|THP-adriamycin Hydrochloride","The hydrochloride salt form of pirarubicin, an analogue of the anthracycline antineoplastic antibiotic doxorubicin with antineoplastic activity. Pirarubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair as well as RNA and protein synthesis. This agent is less cardiotoxic than doxorubicin and exhibits activity against some doxorubicin-resistant cell lines.","Antibiotic|Organic Chemical"]
["C2635","Pirfenidone","PIRFENIDONE|Pirfenidone|pirfenidone","An orally active synthetic antifibrotic agent structurally similar to pyridine 2,4-dicarboxylate. Pirfenidone inhibits fibroblast, epidermal, platelet-derived, and transforming beta-1 growth factors, thereby slowing tumor cell proliferation. This agent also inhibits DNA synthesis and the production of mRNA for collagen types I and III, resulting in a reduction in radiation-induced fibrosis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1031","Piritrexim","2,4-Diamino-6-(2,5-dimethoxybenzyl)-5-methylpyrido[2,3-d]pyrimidine|6-((2,5-Dimethoxyphenyl)methyl)-5-methylpyrido(2,3-d)pyrimidine-2,4-diamine|6-[(2,5-Dimethoxyphenyl)methyl]-5-methylpyrido[2,3-d]pyrimidine-2,4-diamine|BW 301U|BW-301U|PIRITREXIM|Piritrexim|piritrexim","A synthetic antifolate agent with antiparasitic, antipsoriatic and antitumor properties. Piritrexim inhibits the enzyme dihydrofolate reductase enzyme, thereby disrupting folate metabolism and DNA synthesis and cell division. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C91407","Piritrexim Isethionate","2,4-Diamino-6-(2,5-dimethoxybenzyl)-5-methylpyrido(2,3-d)pyrimidine mono(2-hydroxyethanesulfonate)|BW-301U Isethionate|PIRITREXIM ISETHIONATE|Piritrexim Isethionate|Piritrexim isethionate","The isethionate salt of piritrexim, a synthetic antifolate agent with antiparasitic, antipsoriatic and antitumor properties. Piritrexim inhibits the enzyme dihydrofolate reductase enzyme, thereby disrupting folate metabolism and DNA synthesis and cell division.","Organic Chemical|Pharmacologic Substance"]
["C121960","Pirotinib","KBP-5209|KBP5209|Pirotinib","An orally bioavailable inhibitor of the receptor tyrosine kinase (RTK) epidermal growth factor receptor (ErbB; EGFR) family, with potential antineoplastic activity. Upon administration, pirotinib selectively and irreversibly binds to and inhibits the epidermal growth factor receptors 1 (ErbB1; EGFR), 2 (ErbB2; HER2), and 4 (ErbB4; HER4). This may result in the inhibition of cell growth and angiogenesis in tumors overexpressing these RTKs. EGFRs play major roles in both tumor cell proliferation and tumor vascularization, and are overexpressed in many cancer cell types.","Pharmacologic Substance"]
["C1182","Piroxantrone","Anthra(1,9-cd)pyrazol-6(2H)-one, 5-((3-aminopropyl)amino)-7,10-dihydroxy-2-(2-((2-hydroxyethyl)amino)ethyl)|CI-942|Oxanthrazole|Oxantrazole|PD-111815|PIROXANTRONE|Piroxantrone HCl|Piroxantrone","An anthrapyrazole antineoplastic antibiotic.  Piroxantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.  Although less cardiotoxic than doxorubicin, this agent exhibits a narrow spectrum of antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C72829","Piroxantrone Hydrochloride","PIROXANTRONE HYDROCHLORIDE|Piroxantrone Hydrochloride","The hydrochloride salt form of piroxantrone, an anthrapyrazole antineoplastic antibiotic. Piroxantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair as well as RNA and protein synthesis. Although less cardiotoxic than doxorubicin, this agent exhibits a narrow spectrum of antineoplastic activity.","Pharmacologic Substance"]
["C107167","pIRS2 Phosphopeptide-tetanus Peptide Vaccine","pIRS2 Phosphopeptide-tetanus Peptide Vaccine|pIRS2-phosphopeptide Plus Tet Vaccine","A vaccine composed of a phosphorylated peptide from the tumor associated antigen insulin receptor substrate-2 (IRS2) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pIRS2 phosphopeptide-tetanus peptide vaccine, the pIRS2 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against phosphopeptide-containing tumor cells. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response which may help stimulate an immune response against the pIRS2-expressing melanoma tumor cells. IRS2 is upregulated in a variety of cancer cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C26663","Pixantrone","6,9-Bis((2-aminoethyl)amino)benzo(g)isoquinoline-5,10-dione|PIXANTRONE|Pixantrone|pixantrone","A synthetic, noncardiotoxic aza-anthracenedione analogue with potential antineoplastic activity. Pixantrone intercalates into DNA and induces topoisomerase II-mediated DNA strand crosslinks, resulting in inhibition of DNA replication and tumor cell cytotoxicity.","Pharmacologic Substance"]
["C82398","Pixantrone Dimaleate","6,9-Bis((2-Aminoethyl)Amino)Benzo(g)Isoquinoline-5,10-Dione (2z)-But-2-Enedioate (1:2)|BBR 2778|Benz(g)Isoquinoline-5,10-Dione, 6,9-Bis((2-Aminoethyl)Amino)-, (2z)-2-Butenedioate (1:2)|Benz(g)isoquinoline-5,10-dione, 6,9-bis((2-aminoethyl)amino)-, (2Z)-2-butenedioate (1:2)|PIXANTRONE DIMALEATE|Pixantrone Dimaleate|Pixantrone Maleate","The dimaleate salt of a synthetic, noncardiotoxic aza-anthracenedione analogue with potential antineoplastic activity. Pixantrone intercalates into DNA and induces topoisomerase II-mediated DNA strand crosslinks, resulting in inhibition of DNA replication and tumor cell cytotoxicity.","Pharmacologic Substance"]
["C1871","PKI166","CGP 75166/PKI166|CGP 75166|PKI166","A pyrrolo-pyrimidine epidermal growth factor receptor (EGFR) protein kinase inhibitor with anti-tumor activity.PKI-166 reversibly inhibits HER1 and HER2 tyrosine kinases, belong to the epidermal growth factor receptor family, thereby inhibiting tumor growth and metastasis.","Organic Chemical|Pharmacologic Substance"]
["C69005","Pladienolide Derivative E7107","E7107|Pladienolide Derivative E7107","A synthetic urethane derivative of pladienolide D with potential antineoplastic activity. Pladienolide derivative E7107 is generated from the 12-membered macrolide pladienolide D, one of several macrolides derived from the bacterium Streptomyces platensis Mer-11107. This agent appears to bind to the 130-kDa subunit 3 (spliceosome-associated protein 130; SAP130) of the splicing factor 3b (SF3b), resulting in inhibition of pre-messenger RNA splicing and the arrest of cell-cycle progression. The splicing factor SF3b is a multiprotein complex integral to the accurate excision of introns from pre-messenger RNA; the subunit SAP130 associates with U2 snRNP and is recruited to prespliceosomal complexes.","Pharmacologic Substance"]
["C103192","Plasmacytoid Dendritic Cell Vaccine","Plasmacytoid Dendritic Cell Vaccine|pDC Vaccine","A whole cell vaccine derived from a distinct subset of dendritic cells (DCs) with a plasma cell-like morphology that exhibits immunomodulating activity. Plasmacytoid dendritic cells (pDCs) express a characteristic set of surface markers, such as CD123 (interleukin-3 receptor alpha chain), BDCA-2 (blood dendritic cell antigen 2; CD303) and BDCA-4 (CD304), as well as intracellular toll-like receptors 7 and 9. Upon stimulation, the activated pDCs produce substantial amounts of interferon (IFN) alpha, and to a lesser degree IFN-beta, as well as other cytokines and chemokines, such as tumor necrosis factor alpha and interleukins 1, 6 and 8. In addition, these pDCs, directly or indirectly stimulate T-cells, B-cells and natural killer cells. This may potentially lead to increased immunity against tumor cells.","Pharmacologic Substance"]
["C90537","Plasmid Encoding Antiangiogenic Metargidin Peptide","AMEP|Peptide AMEP|Plasmid Encoding Antiangiogenic Metargidin Peptide","A plasmid encoding the protein antiangiogenic metargidin plasmid (AMEP), the disintegrin domain of ADAM-15 (metargidin), with potential antiangiogenic and antimetastatic activities. Upon intratumoral electrotransfer of plasmid encoding AMEP, AMEP binds to cellular integrin receptors alpha-v-beta-3 (avb3) and alpha-5-beta-1 (a5b1), which are upregulated on activated endothelial cells and a variety of tumor cells. Binding to the integrin receptors may inhibit angiogenesis and may inhibit tumor cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C97956","Pleiotropic Pathway Modifier CC-122 Hydrochloride","CC-122 Hydrochloride|Pleiotropic Pathway Modifier CC-122 Hydrochloride","The hydrochloride salt form of CC-122, an orally available pleiotropic pathway modulator with potential antineoplastic activity.","Pharmacologic Substance"]
["C1629","Plevitrexed","(alphaS)-alpha-[[4-[[(1,4-Dihydro-2,7-dimethyl-4-oxo-6-quinazolinyl)methyl]-2-propynylamino]-2-fluorobenzoyl]amino]-1H-tetrazole-5-butanoic Acid|BGC 9331|PLEVITREXED|Plevitrexed|Vamidex|Vamydex|ZD9331","An orally bioavailable, small molecule, non-polyglutamatable, antifolate quinazoline derivative thymidine synthetase inhibitor with potential antineoplastic activity. Plevitrexed is transported into the cell via the physiological reduced folate carrier (RFC) system. Intracellularly, this agent selectively binds to the folate binding site of thymidylate synthase and inhibits thymidine synthesis, which may result in DNA synthesis inhibition and apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C658","Plicamycin","A-2371|Aureolic acid|MTH|Mithracin|Mithracine|Mithramycin|PA-144|PLICAMYCIN|Plicamycin|mithramycin|plicamycin","An antibiotic isolated from the bacterium Streptomyces plicatus with antineoplastic activity. Plicamycin, also known as mithramycin, binds to the minor groove of DNA at GC-rich sites, resulting in inhibition of RNA synthesis; this agent also inhibits mRNA expression, resulting in a reduction in protein synthesis. In addition, plicamycin may inhibit bone resorption by down regulating transcription of c-src, an oncogene involved in bone metabolism and resorption. (NCI04)","Antibiotic|Organic Chemical"]
["C62444","Plinabulin","(3Z,6Z)-6-benzylidene-3-{[5-(1,1-dimethylethyl)-1H-imidazol-4-yl]methylidene}piperazine-2,5-dione|NPI-2358|PLINABULIN|Plinabulin","An orally active diketopiperazine derivative with potential antineoplastic activity. Plinabulin selectively targets and binds to the colchicine-binding site of tubulin, thereby interrupting equilibrium of microtubule dynamics. This disrupts mitotic spindle assembly leading to cell cycle arrest at M phase and blockage of cell division. In addition, plinabulin may also inhibit growth of proliferating vascular endothelial cells, thereby disrupting the function of tumor vasculature that further contributes to a decrease in tumor cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C1689","Plitidepsin","APLD|Aplidin|Aplidine|DDB|Dehydrodemnin B|Dehydrodidemnin B|N-[1-(1,2-Dioxopropyl)-L-prolyl]didemnin A|PLITIDEPSIN|Plitidepsin|aplidine","A cyclic depsipeptide isolated from the marine tunicate Aplidium albicans. Plitidepsin displays a broad spectrum of antitumor activities, inducing apoptosis by triggering mitochondrial cytochrome c release, initiating the Fas/DC95, JNK pathway and activating caspase 3 activation. This agent also inhibits elongation factor 1-a, thereby interfering with protein synthesis, and induces G1 arrest and G2 blockade, thereby inhibiting tumor cell growth.","Amino Acid, Peptide, or Protein|Antibiotic"]
["C92587","PLK1 Inhibitor TAK-960","PLK1 Inhibitor TAK-960|Polo-like Kinase 1 Inhibitor TAK-960|TAK-960","An orally available, Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor TAK-960 selectively inhibits PLK1, inducing selective G2/M cell-cycle arrest followed by apoptosis in a variety of tumor cells while causing reversible cell-cycle arrest at the G1 and G2 stages without apoptosis in normal cells. PLK1 inhibition may result in the inhibition of proliferation in PLK1-overexpressed tumor cells. PLK1, named after the polo gene of Drosophila melanogaster, is a serine/threonine kinase crucial in the regulation of mitosis.","Pharmacologic Substance"]
["C88308","Plozalizumab","Immunoglobulin G1, Anti-(Human CC Chemokine Receptor CCR2) (Human-mus musculus Monoclonal 1d9 Heavy Chain), Disulfide with Human-mus musculus Monoclonal 1d9 kappa-chain, Dimer|MLN1202|PLOZALIZUMAB|Plozalizumab|anti-CCR2 monoclonal antibody MLN1202","A humanized monoclonal antibody directed against the human chemokine receptor 2 (CCR2), with potential antiangiogenic, immunomodulating, antimetastatic, and antineoplastic activities. Plozalizumab binds to CCR2 and prevents binding of the endothelium-derived CLL2 (monocyte chemoattractant protein-1 or MCP1) to its receptor CCR2, which may result in inhibition of CCR2 activation and so inhibition of angiogenesis, tumor cell migration, and tumor cell proliferation. In addition, this agent may reduce levels of C-reactive protein (CRP). The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, stimulates the migration and infiltration of these cell types, and plays an important role in inflammation, angiogenesis, and tumor cell migration and proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C62763","PM00104","PM00104|Zalypsis","A synthetic alkaloid compound, related to natural alkaloid compounds, found in molluscs (jorumycin) and sponges (renieramycins), with potential antineoplastic activity. PM00104 reversibly binds to DNA, thereby inducing cytotoxicity due to its interference with DNA replication, transcription, and translation processes. DNA binding by this agent does not trigger DNA damage checkpoint responses, hence PM00104 demonstrates a manageable and reversible cytotoxicity as part of its antitumor activity.","Pharmacologic Substance"]
["C61146","pNGVL3-hICD Vaccine","pNGVL3-hHER2 Intracellular Domain Plasmid DNA Vaccine|pNGVL3-hICD Vaccine","A plasmid DNA cancer vaccine encoding the intracellular domain (ICD) of the HER-2/neu proto-oncogene. Upon administration and after cellular uptake by skin or muscle cells, the pNGVL3-hICD vaccine plasmid expresses the HER-2/neu protein, which, after intracellular processing, may elicit both antigen-specific cytotoxic T-lymphocyte (CTL) and humoral immune responses against tumor cells expressing HER-2. The HER-2/neu ICD protein is highly immunogenic and, as a subdominant epitope, may be associated with decreased immune tolerance.","Immunologic Factor|Pharmacologic Substance"]
["C88289","pNGVL4a-CRT/E7(detox) DNA Vaccine","pNGVL4a-CRT/E7(detox) DNA Vaccine","A cancer vaccine consisting of the DNA plasmid pNGVL4a-A encoding calreticulin (CRT) linked to a detox form of human papillomavirus (HPV) type 16 E7 antigen, with potential immunomodulating and antineoplastic activities. Upon administration, this vaccine may generate a potent cytotoxic T-lymphocyte (CTL) response against E7-expressing tumor cells, resulting in tumor cell death. For E7(detox), the amino acids in E7 at positions 24 (cysteine to glycine) and 26 (glutamic acid to glycine) were substituted. CRT, a 46 kDa protein located in the lumen of the cell's endoplasmic reticulum (ER), may potentiate MHC class I presentation of HPV-16 E7 to E7-specific CD8-positive T cells. In addition, pNGVL4a-A contains two short immunostimulatory DNA sequences (ISS) in the noncoding region, which may elicit the production of IFN- and IL-12 in transfected keratinocytes and dermal antigen presenting cells (APCs), resulting in a potent T helper cell type 1 response.","Pharmacologic Substance"]
["C48418","pNGVL4a-Sig/E7(detox)/HSP70 DNA Vaccine","pNGVL4a-Sig/E7(detox)/HSP70 DNA Vaccine","An antigen-specific DNA cancer vaccine consisting of the coding sequences of a signal peptide (pNGVL4a-Sig), a detox form of the human papillomavirus type 16 (HPV-16) antigen E7, and the heat shock protein 70 (HSP70). Upon administration, this vaccine may generate potent cytotoxic CD8(+) T-cell responses against E7-expressing tumor cells, resulting in tumor cell death.","Pharmacologic Substance"]
["C126798","Pol I Inhibitor CX5461","2-(4-Methyl-1,4-diazepan-1-yl)-N-((5-methylpyrazin-2-yl)methyl)-5-oxo-5H-benzo[4,5]thiazolo[3,2-a][1,8]naphthyridine-6-carboxamide|2-(4-Methyl-1,4-diazepan-1-yl)-N-[(5-methylpyrazin-2-yl)methyl]-5-oxo-[1,3]benzothiazolo[3,2-a][1,8]naphthyridine-6-carboxamide|5H-Benzothiazolo[3,2-a][1,8]naphthyridine-6-carboxamide, 2-(hexahydro-4-methyl-1H-1,4-diazepin-1-yl)-N-[(5-methyl-2-pyrazinyl)methyl]-5-oxo-|CX-5461|CX5461|Pol I Inhibitor CX5461|RNA Pol I Inhibitor CX5461","An orally bioavailable inhibitor of RNA polymerase I (Pol I), with potential antineoplastic activity. Upon oral administration, CX-5461 selectively binds to and inhibits Pol I, prevents Pol I-mediated ribosomal RNA (rRNA) synthesis, induces apoptosis, and inhibits tumor cell growth. Pol I, the multiprotein complex that synthesizes rRNA, is upregulated in cancer cells and plays a key role in cell proliferation and survival. Hyperactivated rRNA transcription is associated with uncontrolled cancer cell proliferation.","Pharmacologic Substance"]
["C104153","Polatuzumab Vedotin","ADC DCDS4501A|Antibody-Drug Conjugate DCDS4501A|DCDS4501A|FCU 2711|POLATUZUMAB VEDOTIN|Polatuzumab Vedotin|RG7596|Ro 5541077-000","An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against B-cell antigen receptor complex-associated protein beta chain (CD79B) conjugated, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity.  Upon administration, the monoclonal antibody moiety of polatuzumab vedotin selectively binds to CD79B, a protein which is abundantly expressed on the surface of B-cells. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. CD79B, a component of the B-cell receptor (BCR), plays a key role in B-cell receptor signaling and is expressed on the surface of almost all types of malignant B-cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2487","Polifeprosan 20 with Carmustine Implant","Carmustine Copolymer|Gliadel Wafer|Polifeprosan 20 with Carmustine Implant|polifeprosan 20 carmustine implant","A synthetic, biodegradable wafer containing the agent carmustine with antineoplastic activity. Used to deliver drug directly into a brain tumor site and typically implanted post-surgically, the wafer is made of a biodegradable poly-anhydride copolymer and contains the nitrosourea carmustine.  As an antineoplastic nitrosourea, carmustine alkylates and cross-links DNA during all phases of the cell cycle, resulting in disruption of DNA function, cell cycle arrest, and apoptosis.  Carmustine also carbamoylates proteins, including DNA repair enzymes, resulting in an enhanced cytotoxic effect.  Carmustine is highly lipophilic and crosses the blood-brain barrier readily. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C70948","Polo-like Kinase 1 Inhibitor GSK461364","GSK461364|Polo-like Kinase 1 Inhibitor GSK461364","A small molecule Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor GSK461364 selectively inhibits Plk1, inducing selective G2/M arrest followed by apoptosis in a variety of tumor cells while causing reversible cell arrest at the G1 and G2 stage without apoptosis in normal cells. Plk1, named after the polo gene of Drosophila melanogaster, is a serine/threonine protein kinase involved in regulating mitotic spindle function in a non-ATP competitive manner.","Pharmacologic Substance"]
["C82389","Polo-like Kinase 1 Inhibitor MK1496","MK1496|PLK1 Inhibitor MK1496|Polo-like Kinase 1 Inhibitor MK1496","An orally bioavailable Polo-like kinase 1 (Plk1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor MK1496 selectively inhibits Plk1, inducing selective G2/M arrest followed by apoptosis in a variety of tumor cells while causing reversible cell arrest at the G1 and G2 stage without apoptosis in normal cells. Plk1, named after the polo gene of Drosophila melanogaster, is a serine/threonine protein kinase involved in regulating mitotic spindle function in a non-ATP competitive manner.","Pharmacologic Substance"]
["C88313","Polo-like Kinase 1 Inhibitor NMS-1286937","NMS-1286937|Polo-like Kinase 1 Inhibitor NMS-1286937","An orally bioavailable, small-molecule Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor NMS-1286937 selectively inhibits PLK1, inducing selective G2/M cell-cycle arrest followed by apoptosis in a variety of tumor cells while causing reversible cell-cycle arrest at the G1 and G2 stages without apoptosis in normal cells. PLK1 inhibition may result in the inhibition of proliferation in PLK1-overexpressing tumor cells. PLK1 is a serine/threonine protein kinase crucial in the regulation of mitosis.","Pharmacologic Substance"]
["C111990","Polo-like Kinase 4 Inhibitor CFI-400945 Fumarate","CFI-400945 Fumarate|PLK4 Inhibitor CFI-400945 Fumarate|Polo-like Kinase 4 Inhibitor CFI-400945 Fumarate","An orally available fumarate salt form of CFI-400945, a polo-like kinase 4 (PLK4) inhibitor with potential antineoplastic activity. Upon oral administration, polo-like kinase 4 inhibitor CFI-400945 selectively inhibits PLK4, which results in the disruption of mitosis and the induction of apoptosis. PLK4 inhibition also prevents cell division and inhibits proliferation of PLK4-overexpressing tumor cells. PLK4, a member of the polo family of serine/threonine kinases overexpressed in a variety of cancer cell types, plays a crucial role in the regulation of centriole duplication during the cell cycle.","Pharmacologic Substance"]
["C757","Poly AU","Poly A:U|Poly AU|Polyadenylic Polyuridylic Acid","A synthetic polyadenylic-polyuridylic acid double-stranded RNA. Poly AU may stimulate the release of cytotoxic cytokines and, by inducing the production of interferon, may increase the number and tumoricidal activities of various immunohematopoietic cells. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C758","Poly IC","5'-Inosinic Acid, Homopolymer Complex with 5'-Cytidylic Acid Homopolymer|Poly C poly I|Poly I:C|Poly I:poly C|Poly IC|Poly rI:poly rC|Poly(I).poly(C)|Poly(rI)-poly(rC)|Poly(rI).poly(rC)|Polyinosinic acid.polycytidylic acid|Polyinosinic acid:polycytidylic acid|Polyinosinic-polycytidylic Acid|poly (I)-poly (C)|poly (I).poly (C)|poly (rI)- poly (rC)|poly (rI). poly (rC)|poly I-poly C|poly I.poly C|polyinosate-polycytidylate|polyinosate.polycytidylate|polyinosinic acid-polycytidylic acid|polyinosinic acid.polycytidylic acid","A synthetic polyinosinic-polycytidylic acid double-stranded RNA. Poly IC may stimulate the release of cytotoxic cytokines and, by inducing interferon-gamma production, may increase the number and tumoricidal activities of various immunohematopoietic cells. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1198","Poly ICLC","Hiltonol|Poly I:Poly C with Poly-L-Lysine Stabilizer|Poly ICLC|PolyI:PolyC with Poly-L-Lysine Stabilizer|Polyinosinic-Polycytidylic Acid Stabilized with Polylysine and Carboxymethylcellulose|Polyriboinosinic-Polyribocytidylic Acid-Polylysine Carboxymethylcellulose|Stabilized Polyriboinosinic/Polyribocytidylic Acid|poly-ICLC","A synthetic complex of carboxymethylcellulose, polyinosinic-polycytidylic acid, and poly-L-lysine double-stranded RNA. Poly ICLC may stimulate the release of cytotoxic cytokines and, by inducing interferon-gamma production, may increase the tumoricidal activities of various immunohematopoietic cells. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C101894","Poly-alendronate Dextran-Guanidine Conjugate","Dextran/Alendronate/Guanidine-containing Polybisphosphonate|ODX|Osteodex|Poly-alendronate Dextran-Guanidine Conjugate","A polybisphosphonate dextran-guanidine conjugate with potential anti-resorptive and antineoplastic activities. Alendronic acid and aminoguanidine were conjugated sequentially to oxidized dextran resulting in an average of 8 alendronate and 50 guanidine groups coupled to the dextran backbone. Upon administration, the poly-alendronate dextran-guanidine conjugate inhibits the mevalonate pathway by inhibiting farnesyl diphosphate synthase (FDPS) which leads to a reduction in protein prenylation and to the loss of downstream metabolites essential for osteoclast function. This eventually leads to the induction of apoptosis in osteoclasts. Also, by preventing osteoclast-mediated bone resorption, this agent decreases bone turnover and stabilizes the bone matrix. The guanidine moiety increases the nitrogen content and possibly the activity of the bisphosphonate and its ability to inhibit FDPS. In addition, the guanidine moiety facilitates cell internalization and may contribute to this agent's cytotoxicity.","Organic Chemical|Pharmacologic Substance"]
["C60816","Polyamine Analogue PG11047","BESpm|CGC-11047|N(1),-N(12)-bis(ethyl)-cis-6,7-dehydrospermine tetrahydrochloride|N(1),-N(12)-bis(ethyl)-cis-6,7-dehydrospermine|N(1),N(12)-bisethylspermine|PG11047|Polyamine Analogue PG11047|SL-11047|SL11047","A second generation polyamine analogue, synthesized through the restriction of molecular conformations of parent polyamine compounds, with potential antineoplastic activity. Polyamine analogue PG11047 may displace endogenous polyamines from DNA binding sites, thereby interfering with cell cycle processes dependent upon polyamine binding and function, and resulting in cell-cycle arrest, induction of apoptosis, depletion of polyamines, and interference with gene and ligand-receptor activities involved with cell growth. This agent may exhibit decreased toxicity and enhanced cytotoxicity profiles compared to first-generation polyamine compounds. In tumor cells, there is an increase dependence on polyamines as well as a dysregulated polyamine metabolic pathway resulting in abnormal or sustained tumor growth.","Organic Chemical|Pharmacologic Substance"]
["C1628","Polyandrol","Polyandrol","A quassinoid phytochemical isolated from Castela polyandra and other plant species with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C92583","Polyethylene Glycol Recombinant Endostatin","M2ES|Polyethylene Glycol Recombinant Endostatin","A formulation containing recombinant endostatin attached to polyethylene glycol (PEG), with potential anti-angiogenic and antineoplastic activities. Endostatin, a 20 kDa C-terminal proteolytic fragment of collagen XVIII, induces microvascular endothelial cell apoptosis and inhibits endothelial proliferation and angiogenesis, which may result in a reduction of tumor cell growth. Modification with PEG extends the circulation half-life of endostatin, improves stability and increases solubility in organic solvents.","Pharmacologic Substance"]
["C125243","Polyethyleneglycol-7-ethyl-10-hydroxycamptothecin DFP-13318","DFP-13318|PEG SN38 DFP-13318|PL 0264|PL-0264|PLX-0264|Polyethyleneglycol-7-ethyl-10-hydroxycamptothecin DFP-13318|Polyethyleneglycol-7-ethyl-10-hydroxycamptothecin|Ultra-Long-Acting-PEG-SN-38|Ultra-long Acting PEG-SN38","A long-acting formulation composed of 7-ethyl-10-hydroxycamptothecin (SN38), a camptothecin derivative and active metabolite of irinotecan conjugated to polyethylene glycol (PEG), via a proprietary, cleavable linker, with potential antineoplastic activity. Upon administration, the proprietary linkage system allows for very slow release of SN38 from the formulation. Upon release, SN38 selectively stabilizes covalent topoisomerase I-DNA complexes, and results in single-stranded and double-stranded DNA breaks, the inhibition of DNA replication, and the induction of apoptosis. This agent is designed to deliver the active metabolite to tumor cells without the need for conversion as is the case with irinotecan. Compared to other PEG-SN38-based formulations, the linker system in DFP-13318 increases its half-life and the exposure time for tumor cells, while decreasing both blood plasma concentrations and exposure to off-target organs; this results in increased efficacy.","Organic Chemical|Pharmacologic Substance"]
["C106124","Poly-gamma Glutamic Acid","Gamma-polyglutamic Acid|Poly-gamma Glutamic Acid|Poly-gamma-glutamate|gamma-PGA","A water-soluble and biodegradable polymer naturally synthesized by various strains of Bacillus and composed of D- and L-glutamic acid polymerized via gamma-amide linkages, with potential antineoplastic activity. Upon administration, poly-gamma glutamic acid may augment the immune response by increasing the production of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) and inducing the activation of macrophage and natural killer (NK) cells. IFN-gamma is a major mediator of innate and adaptive immunity against viral and intracellular bacterial infections as well as for tumor control. TNF-alpha is a cytokine involved in systemic inflammation, which is capable of inducing apoptotic cell death and exhibits anti-tumoral effects.","Pharmacologic Substance"]
["C69079","Polymeric Camptothecin Prodrug XMT-1001","MER-1001|Polymeric Camptothecin Prodrug XMT-1001|XMT-1001","A polymeric prodrug of camptothecin (CPT) with potential antineoplastic activity. Polymeric camptothecin prodrug XMT-1001 consists of CPT conjugated to the 60-70 kDa, inert, bio-degradable, hydrophilic copolymer poly[1-hydroxymethylene hydroxymethyl formal] (PHF). Through a dual-phase, non-enzymatic release mechanism, CPT is first released in plasma from XMT-1001 as the lipophilic prodrugs CPT-SI (a succinimidoglycinate derivative) and CPT-SA (a succinamidoyl glycinate derivative), which are then hydrolyzed within tissues to release the lactone form of CPT. CPT inhibits the catalytic activity of DNA topoisomerase I, thereby inhibiting DNA replication and inducing apoptosis. This agent may exhibit a more favorable pharmacokinetic profile than other agents in the same class.","Organic Chemical|Pharmacologic Substance"]
["C129595","Polypodium leucotomos Extract","Fernblock|PL Extract|PLE|Polypodium leucotomos Extract","A nutritional supplement composed of an aqueous extract derived from the leaves of the tropical fern belonging to the Polypodiaceae family, Polypodium leucotomos (PL; Phlebodium aureum), with potential photoprotective, skin protective, anti-inflammatory, immunomodulating and antioxidant activities. This extract contains many phenolic compounds, such as ferulic, caffeic, coumaric and vanillic acid, which are mainly responsible for this extract's effects. Upon administration, Polypodium leucotomos extract (PLE) exerts antioxidant activity by scavenging free radicals and inhibiting the generation and release of reactive oxygen species (ROS), thereby preventing ultraviolet (UV)-induced as well as ROS-induced DNA damage. In addition, the chemicals in this extract protect antioxidant enzymes and modulate expression of cancer and inflammation-related genes, including the induction of the expression of tumor suppressor genes and the inhibition of the expression of pro-inflammatory cytokines and inflammatory enzymes, thereby inhibiting the activation of signal transduction pathways involved in carcinogenesis and inflammation, respectively. PLE also stimulates tissue inhibitors of metalloproteinases (TIMPs) and inhibits matrix metalloproteinases (MMPs).","Pharmacologic Substance"]
["C1204","Polysaccharide-K","Glycoproteins|KS-2|Krestin|PSK|Polysaccharide-K","A protein-bound polysaccharide derived from the mushroom Trametes versicolor (Turkey Tail) with immunoadjuvant and potential antitumor activities. Although its mechanism of action has yet to be fully elucidated, in vitro and in vivo studies indicate that polysaccharide-K induces peripheral blood monocyte secretion of IL-8 and TNF-alpha, induces T cell proliferation, and prevents cyclophosphamide-induced immunosuppression. This agent has also been reported to stimulate macrophages to produce reactive nitrogen intermediates and superoxide anions and to promote apoptosis in the promyelocytic leukemia cell line HL-60.","Organic Chemical|Pharmacologic Substance"]
["C1201","Polysialic Acid","Polysialic Acid","A highly negative-charged carbohydrate composed of a linear polymer of alpha 2,8-linked sialic acid residue with potential immunotherapeutic activity. Polysialic acid (PSA) is mainly attached to the neural cell adhesion molecule (NCAM), a membrane-bound glycoprotein overexpressed in certain types of cancers. In embryonic tissue PSA-NCAM is abundantly expressed and PSA plays an important role in formation and remodeling of the neural system through modulation of the adhesive properties of NCAM, thereby reducing cell-cell interactions and promoting cellular mobility. In adult tissue however, the expression of PSA-NCAM is associated with a variety of malignant tumors, signifying its potential role in tumor metastasis. When administered in a vaccine formulation, PSA may stimulate a cytotoxic T cell response against tumors expressing PSA, thereby resulting in a reduction in tumor size.","Organic Chemical"]
["C67038","Polyunsaturated Fatty Acid","Fatty Acid, Total Polyunsaturated|PUFA|Polyunsaturated Fatty Acid|Polyunsaturated Fatty Acids","A fatty acid containing more than one double bond (C=C). The essential fatty acids omega-3 and omega-6 are polyunsaturated fatty acids (PUFAs) that contain 2 or more cis double bonds. Dietary intake of some PUFAs may have beneficial effects on blood pressure, serum lipds, and inflammation. Some PUFAs, such as omega-3 PUFAs, may have antineoplastic or chemopreventive activities.","Organic Chemical"]
["C77870","Polyvalent Antigen-KLH Conjugate Vaccine","Polyvalent Antigen-KLH Conjugate Vaccine","A multivalent cancer vaccine comprised of the five tumor-associated antigens (TAAs) globo H, GM2 ganglioside, Tn-MUC1, TF, and sTn conjugated with the immunoadjuvant keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Upon administration, polyvalent antigen-KLH conjugate vaccine may induce production of IgG and IgM antibodies and antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells expressing these TAAs, resulting in tumor cell death and tumor growth inhibition. Globo H (globo H hexasaccharide 1); GM2 ganglioside; Tn-MUC1 (human tumor-associated epithelial mucin 1 carrying the tumor-specific glycan Tn); TF (Thompson-Friedreich); and sTn (sialyl-Tn) are overexpressed in a variety of cancer cells. KLH is a hapten carrier and serves as an immunostimulant to improve immune recognition of antigens.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1633","Polyvalent Melanoma Vaccine","PMCV|Polyvalent Melanoma Cell Vaccine|Polyvalent Melanoma Vaccine","A cancer vaccine consisting of whole irradiated heterologous melanoma cells which express multiple melanoma-related antigens.  Polyvalent melanoma vaccine may stimulate an antitumoral cytotoxic T-cell immune response in the host, resulting in inhibition of tumor cell proliferation and tumor cell death. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C72560","Pomalidomide","3-Amino-N-(2,6-dioxo-3-piperidyl)phthalimide|4-Amino-2-(2,6-dioxo-3-piperidyl)isoindoline-1,3-dione|4-Aminothalidomide|Actimid|CC-4047|Imnovid|POMALIDOMIDE|Pomalidomide|Pomalyst|pomalidomide","An orally bioavailable derivative of thalidomide with potential immunomodulating, antiangiogenic and antineoplastic activities. Although its exact mechanism of action has yet to be fully elucidated, pomalidomide appears to inhibit TNF-alpha production, enhance the activity of T cells and natural killer (NK) cells and enhance antibody-dependent cellular cytotoxicity (ADCC). In addition, pomalidomide may inhibit tumor angiogenesis, promote cell cycle arrest in susceptible tumor cell populations, and stimulate erythropoeisis.","Organic Chemical|Pharmacologic Substance"]
["C26665","Pomegranate Juice","POMEGRANATE JUICE|Pomegranate Juice","A natural juice isolated from the fruit of the plant Punica granatum with antioxidant, potential antineoplastic, and chemopreventive activities.  Pomegranate juice contains flavonoids which promote differentiation and apoptosis in tumor cells by down-regulating vascular endothelial growth factor (VEGF) and stimulating migration inhibitory factor (MIF), thereby inhibiting angiogenesis. The flavonoids in pomegranate juice also scavenge reactive oxygen species (ROS) and, in some cell types, may prevent ROS-mediated cell injury and death. (NCI04)","Food"]
["C78866","Pomegranate Liquid Extract","Dadima Fruit Water|POMEGRANATE FRUIT VOLATILE OIL|Pomegranate Liquid Extract|Punica granatum Fruit Volatile Oil","A liquid extract preparation derived from pomegranate (Punica granatum) seeds with antioxidant, and potential antineoplastic and chemopreventive activities. Pomegranate liquid extract contains flavonoids which may promote differentiation and apoptosis in tumor cells by down-regulating vascular endothelial growth factor (VEGF) and stimulating migration inhibitory factor (MIF), thus inhibiting angiogenesis. Pomegranate liquid extract flavanoids also scavenge reactive oxygen species (ROS) and, in some cell types, may prevent ROS-mediated cell injury and death.","Pharmacologic Substance"]
["C95777","Ponatinib","AP-24534|AP24534|Benzamide, 3-(2-Imidazo(1,2-B)Pyridazin-3-Ylethynyl)-4-Methyl-N-(4-((4-Methyl-1- Piperazinyl)Methyl)-3-(Trifluoromethyl)Phenyl)|PONATINIB|Ponatinib","An orally bioavailable multitargeted receptor tyrosine kinase (RTK) inhibitor with potential antiangiogenic and antineoplastic activities. Ponatinib inhibits unmutated and all mutated forms of Bcr-Abl, including T315I, the highly drug therapy-resistant missense mutation of Bcr-Abl. This agent also inhibits other tyrosine kinases including those associated with vascular endothelial growth factor receptors (VEGFRs) and fibroblast growth factor receptors (FGFRs); in addition, it inhibits the tyrosine kinase receptor TIE2 and FMS-related tyrosine kinase receptor-3 (Flt3). RTK inhibition by ponatinib may result in the inhibition of cellular proliferation and angiogenesis and may induce cell death. Bcr-Abl is a fusion tyrosine kinase encoded by the Philadelphia chromosome.","Organic Chemical|Pharmacologic Substance"]
["C78194","Ponatinib Hydrochloride","AP24534 HCl|Benzamide, 3-(2-Imidazo(1,2-B)Pyridazin-3-Ylethynyl)-4-Methyl-N-(4-((4-Methyl-1- Piperazinyl)Methyl)-3-(Trifluoromethyl)Phenyl)-, Hydrochloride (1:1)|Iclusig|PONATINIB HYDROCHLORIDE|Ponatinib Hydrochloride","The hydrochloride salt form of an orally bioavailable multitargeted receptor tyrosine kinase (RTK) inhibitor with potential antiangiogenic and antineoplastic activities. Ponatinib inhibits unmutated and all mutated forms of Bcr-Abl, including T315I, the highly drug therapy-resistant missense mutation of Bcr-Abl. This agent also inhibits other tyrosine kinases including those associated with vascular endothelial growth factor receptors (VEGFRs) and fibroblast growth factor receptors (FGFRs); in addition, it inhibits the tyrosine kinase receptor TIE2 and FMS-related tyrosine kinase receptor-3 (Flt3). RTK inhibition by ponatinib may result in the inhibition of cellular proliferation and angiogenesis and may induce cell death. Bcr-Abl is a fusion tyrosine kinase encoded by the Philadelphia chromosome.","Organic Chemical|Pharmacologic Substance"]
["C123830","Porcupine Inhibitor ETC-1922159","ETC-159|ETC-1922159|PORCN Inhibitor ETC-1922159|Porcupine Inhibitor ETC-1922159","An orally bioavailable inhibitor of the membrane-bound O-acyltransferase (MBOAT) porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, ETC-1922159 binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational palmitoylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. Porcupine catalyzes the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion. Wnt signaling is dysregulated in a variety of cancers.","Pharmacologic Substance"]
["C116860","Porcupine Inhibitor WNT974","2-(2,3-Dimethyl-[2,4-bipyridin]-5-yl)-N-(5-(pyrazin-2-yl)pyridin-2-yl)acetamide|LGK974|PORCN inhibitor LGK974|Porcupine Inhibitor WNT974|WNT974","An orally available inhibitor of porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, WNT974 binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational acylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. Porcupine, a membrane-bound O-acyltransferase (MBOAT), is required for the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion and activity. Wnt signaling is dysregulated in a variety of cancers.","Pharmacologic Substance"]
["C1071","Porfimer Sodium","CL-184116|DHE|Dihematoporphyrin Ester|Dihematoporphyrin Ether|PORFIMER SODIUM|Photofrin II|Porfimer Sodium|dihematoporphyrin ether|porfimer sodium","The sodium salt of a mixture of oligomers formed by ether and ester linkages of up to eight porphyrin units with photodynamic activity. Absorbed selectively by tumor cells, porfimer produces oxygen radicals after activation by 630 nm wavelength laser light, resulting in tumor cell cytotoxicity. In addition, tumor cell death may occur due to ischemic necrosis secondary to vascular occlusion that appears to be partly mediated by the release of thromboxane A2.","Organic Chemical|Pharmacologic Substance"]
["C763","Porfiromycin","Azirino[2',3':3,4]pyrrolo[1, 2-a]indole-4,7-dione, 6-amino-1,1a,2,8,8a, 8b-hexahydro-8-(hydroxymethyl)-8a- methoxy-1,5-dimethyl-, carbamate (ester) (8CI)|Azirino[2',3':3,4]pyrrolo[1, 2-a]indole-4,7-dione, 6-amino-1,1a,2,8,8a, 8b-hexahydro-8-(hydroxymethyl)-8a- methoxy-1,5-dimethyl-, carbamate (ester)(8CI)|Azirino[2',3':3,4]pyrrolo[1,2-a]indole-4,7-dione, 6-amino-8-[[(aminocarbonyl)oxy]methyl]-1,1a,2,8,8a,8b- hexahydro-8a-methoxy-1,5-dimethyl-,[1aR-(1a.alpha.,8.beta., 8a.alpha.,8b.alpha.)]- (9CI)|Azirino[2',3':3,4]pyrrolo[1,2-a]indole-4,7-dione, 6-amino-8-[[(aminocarbonyl)oxy]methyl]-1,1a,2,8,8a,8b-hexahydro-8a-methoxy-1,5-dimethyl-,[1aR-(1a-alpha,8beta, 8a-alpha,8b-alpha)]- (9CI)|ENT-50825|MITOMYCIN, METHYL|Methyl Mitomycin C|Methyl Mitomycin|Methyl mitomycin C|Methylmitomycin|Mitomycin, methyl-|N-Methylmitomycin C|N-methylmitomycin C|PORFIROMYCIN|Porfiromycin|Porfiromycine|Porphyromycin|Promycin|U-14,743|U-14743|[1aS-(1a alpha,8beta,8a alpha,8b alpha)]-6-amino-8-[[(aminocarbonyl)oxy]methyl]-1,1a,2,8,8a,8b-hexahydro-8a-methoxy-1,5-dimethylazirino[2',3':3,4]pyrrolo[1,2-a]indole-4,7-dione|porfiromycin","An N-methyl derivative of the antineoplastic antibiotic mitomycin C isolated from the bacterium Streptomyces ardus and other Streptomyces bacterial species.  Bioreduced porfiromycin generates oxygen radicals and alkylates DNA, producing interstrand cross-links and single-strand breaks, thereby inhibiting DNA synthesis.  Porfiromycin is preferentially toxic to hypoxic cells. (NCI04)","Antibiotic|Organic Chemical"]
["C98838","Poziotinib","HM781-36B|NOV120101|Poziotinib","An orally bioavailable, quinazoline-based, mall-molecular and irreversible pan-epidermal growth factor receptor (EGFR or HER) inhibitor with potential antineoplastic activity. Poziotinib inhibits EGFR (HER1 or ErbB1), HER2, HER4 and EGFR mutants, thereby inhibiting the proliferation of tumor cells that overexpress these receptors. EGFRs, cell surface receptor tyrosine kinases, are often upregulated in a variety of cancer cell types and play key roles in cellular proliferation and survival.","Pharmacologic Substance"]
["C113293","P-p68 Inhibitor RX-5902","P-p68 Inhibitor RX-5902|RX-5902|Supinoxin","An orally bioavailable small molecule inhibitor of phosphorylated-p68 RNA helicase (P-p68), with potential anti-proliferative and antineoplastic activity. Upon oral administration, P-p68 inhibitor RX-5902 may both inhibit the activity of the anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein and facilitate the induction of cyclin-dependent kinase inhibitor 1 (p21). This may prevent G2/M cell cycle progression and lead to growth inhibition in tumor cells. P-p68 is overexpressed in various types of solid tumors but absent in normal tissues, and plays a role in tumor progression and metastasis. p21 is a potent cyclin-dependent kinase inhibitor which regulates cell cycle progression and mediates both growth arrest and cellular senescence.","Pharmacologic Substance"]
["C38129","PPI-2458","PPI-2458","A synthetic derivative of fumagillin with antineoplastic and cytotoxic properties.  PPI-2458 irreversibly inhibits the enzyme methionine aminopeptidase type 2 (MetAP2), thereby preventing abnormal cell growth and angiogenesis. PPI-2458 is reported to have a better toxicity profile compared to other agents of its class. (NCI04)","Pharmacologic Substance"]
["C2235","PR1 Leukemia Peptide Vaccine","Leukemia Peptide Vaccine, PR1|PR1 Leukemia Peptide Vaccine|Proteinase 3:PR1 Peptide","A cancer vaccine containing PR1, a 9 amino-acid human leukocyte antigen (HLA)-A2 restricted peptide derived from proteinase 3, with potential immunotherapeutic activity. Vaccination with PR1 leukemia peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing proteinase 3, resulting in tumor cell lysis. Often overexpressed in leukemic cells, proteinase 3 is a serine proteinase that activates progelatinase A and is involved in angiogenesis and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C61590","PR-104","((2-Bromoethyl)-2,4-dinitro-6-(((2-(phosphonooxy)ethyl)amino)-carbonyl)anilino)ethyl Methanesulphonate|PR-104|PR104","A non-toxic, small-molecule, hypoxia-activated, 3,5-dinitrobenzamide nitrogen mustard pre-prodrug with potential antitumor activity. Upon intravenous administration, PR-104 is converted by systemic phosphatases to the alcohol intermediate PR-104A, which is reduced to form the active DNA-crosslinking mustard species hydroxylamine PR-104H intracellularly under hypoxic conditions. PR-104H specifically crosslinks hypoxic tumor cell DNA, resulting in the inhibition of DNA repair and synthesis, cell-cycle arrest, and apoptosis in susceptible hypoxic tumor cell populations while sparing normoxic tissues.","Pharmacologic Substance"]
["C71708","Pracinostat","2-propenamide, 3-(2-butyl-1-(2-(diethylamino)ethyl)-1h-benzimidazol-5-yl)-N-hydroxy-, (2E)-|HDAC Inhibitor SB939|PRACINOSTAT|Pracinostat|SB939|kaempferol 3-o-beta-d-(6-E-P-coumaroylglucoside)","An orally available, small-molecule histone deacetylase (HDAC) inhibitor with potential antineoplastic activity. Pracinostat inhibits HDACs, which may result in the accumulation of highly acetylated histones, followed by the induction of chromatin remodeling; the selective transcription of tumor suppressor genes; the tumor suppressor protein-mediated inhibition of tumor cell division; and, finally, the induction of tumor cell apoptosis. This agent may possess improved metabolic, pharmacokinetic and pharmacological properties compared to other HDAC inhibitors.","Pharmacologic Substance"]
["C2250","Pralatrexate","(2S)-2-[[4-[(1RS)-1-[(2, 4-Diaminopteridin-6-yl)methyl]but-3-ynyl]benzoyl]amino]pentanedioic Acid|10-Propargyl-10-Deazaaminopterin|10-propargyl-10-deazaaminopterin|FOLOTYN|Folotyn|N-(4-{1-[(2,4-Diaminopteridin-6-yl)methyl]but-3-yn-1-yl}benzoyl)-L-glutamic Acid|PDX|PRALATREXATE|Pralatrexate|pralatrexate","A folate analogue inhibitor of dihydrofolate reductase (DHFR) exhibiting high affinity for reduced folate carrier-1 (RFC-1) with antineoplastic and immunosuppressive activities. Pralatrexate selectively enters cells expressing RFC-1; intracellularly, this agent is highly polyglutamylated and competes for the folate binding site of DHFR, blocking tetrahydrofolate synthesis, which may result in depletion of nucleotide precursors; inhibition of DNA, RNA and protein synthesis; and apoptotic tumor cell death. Efficient intracellular polyglutamylation of pralatrexate results in higher intracellular concentrations compared to non-polyglutamylated pralatrexate, which is more readily effuxed by the MRP (multidrug resistance protein) drug efflux pump. RFC-1, an oncofetal protein expressed at highest levels during embryonic development, may be over-expressed on the cell surfaces of various cancer cell types.","Organic Chemical|Pharmacologic Substance"]
["C128029","PRAME-targeting T-cell Receptor/Inducible Caspase 9 BPX-701","BPX-701|CaspaCID-based PRAME-TCR Allogeneic T-lymphocytes BPX-701|PRAME-targeting T-cell Receptor/Inducible Caspase 9 BPX-701","Human allogeneic T-lymphocytes transduced with a retroviral vector encoding a high-affinity T-cell receptor (TCR) specific for human leukocyte antigen (HLA)-A2-01-restricted, preferentially-expressed antigen in melanoma (PRAME) and containing the chemical induction of dimerization (CID) suicide/safety switch, composed of a drug binding domain coupled to the signaling domain of the suicide enzyme caspase-9, with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with an anti-PRAME-HLA-A2 restricted TCR, expanded ex vivo, and reintroduced into the HLA-A2-positive patient. Upon reintroduction, PRAME-targeting T-cell receptor-based therapy BPX-701 binds to tumor cells expressing PRAME, which may induce cell death in and halt the growth of PRAME-expressing cancer cells. The tumor-associated antigen PRAME is overexpressed by a variety of cancer cell types. If potential T-cell toxicity due to graft-versus-host disease (GvHD) occurs, the chemical dimerizer rimiducid (AP1903) can be adminstered. Rimiducid binds to the drug binding domain expressed by the BPX-701 T-cells, and triggers activation of the caspase-9 domain, which leads to caspase 9-mediated signaling, the induction of apoptosis and to selective and complete elimination of BPX-701 cells.","Cell|Pharmacologic Substance"]
["C29375","Pravastatin Sodium","PRAVASTATIN SODIUM|Pravastatin Sodium|pravastatin sodium","The sodium salt of pravastatin with cholesterol-lowering and potential antineoplastic activities. Pravastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. In addition, pravastatin, like other statins, exhibits pro-apoptotic, growth inhibitory, and pro-differentiation activities in a variety of tumor cells; these antineoplastic activities may be due, in part, to inhibition of the isoprenylation of Ras and Rho GTPases and related signaling cascades.","Organic Chemical|Pharmacologic Substance"]
["C768","Prednimustine","11beta,17,21-trihydroxypregna-1,4-diene-3,20-dione 21-[4-[p-[bis(3-chloroethyl)amino]phenyl]butyrate]|11beta-21-[4-[4-[bis(2-chloroethyl)amino]phenyl]-1-oxobutoxy]-11,17-dihydroxypregna-1,4-diene-3,20-dione|Chlorambucil Prednisolone Ester|LEO-1031|Leo 1031|PREDNIMUSTINE|Prednimustine|Pregna-1,4-diene-3,20-dione, 11-beta,17,21-trihydroxy-,21-(4-(p-(bis(2-chloroethyl)amino)phenyl)butyrate)|Sterecyt|Stereocyt","The prednisolone ester of chlorambucil and nitrogen mustard alkylating agent with antineoplastic activity. Prednimustine itself is not cytotoxic, however, it becomes cytotoxic upon hydrolysis by serum esterases to chlorambucil. Therefore, the increased potency of prednimustine is linked to the prolonged availability of free chlorambucil.","Organic Chemical|Pharmacologic Substance"]
["C769","Prednisolone","(11beta)-11,17,21-Trihydroxypregna-1,4-diene-3,20-dione|.delta.1-Hydrocortisone|1,2-Dehydrohydrocortisone|Adnisolone|Aprednislon|Capsoid|Cortalone|Cortisolone|Dacortin H|Decaprednil|Decortin H|Delta(1)Hydrocortisone|Delta- Cortef|Delta-Cortef|Delta-Diona|Delta-F|Delta-Phoricol|Delta1-dehydro-hydrocortisone|Deltacortril|Deltahydrocortisone|Deltasolone|Deltidrosol|Dhasolone|Di-Adreson-F|Dontisolon D|Estilsona|Fisopred|Frisolona|Gupisone|Hostacortin H|Hydeltra|Hydeltrasol|Klismacort|Kuhlprednon|Lenisolone|Lepi-Cortinolo|Linola-H N|Linola-H-Fett N|Longiprednil|Metacortandralone|Meti Derm|Meticortelone|Opredsone|PREDNISOLONE|Panafcortelone|Precortisyl|Pred-Clysma|Predeltilone|Predni-Coelin|Predni-Helvacort|Prednicortelone|Prednisolone|Prednisolonum|Prelone|Prenilone|Sterane|prednisolone","A synthetic glucocorticoid with anti-inflammatory and immunomodulating properties.  After cell surface receptor attachment and cell entry, prednisolone enters the nucleus where it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production.  This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis in sensitive tumor cells populations. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C770","Prednisone",".delta.1-Cortisone|1, 2-Dehydrocortisone|1,2-Dehydrocortisone|17,21-Dihydroxypregna-1,4-diene-3,11,20-trione|Adasone|Cortancyl|Dacortin|DeCortin|Decortisyl|Decorton|Delta 1-Cortisone|Delta-Dome|Deltacortene|Deltacortisone|Deltadehydrocortisone|Deltasone|Deltison|Deltra|Econosone|Liquid Pred|Lisacort|Meprosona-F|Metacortandracin|Meticorten|Ofisolona|Orasone|PRED|PREDNISONE|Panafcort|Panasol-S|Paracort|Predeltin|Predicor|Predicorten|Prednicen-M|Prednicort|Prednidib|Prednilonga|Predniment|Prednisone|Prednisonum|Prednitone|Promifen|SK-Prednisone|Servisone|Sk-Prednisone|Sterapred|prednisone","A synthetic glucocorticoid with anti-inflammatory and immunomodulating properties.  After cell surface receptor attachment and cell entry, prednisone enters the nucleus where it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production.  This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis in sensitive tumor cell populations.","Organic Chemical|Pharmacologic Substance"]
["C91392","Prexasertib","2-Pyrazinecarbonitrile, 5-((5-(2-(3-Aminopropoxy)-6-methoxyphenyl)-1H-pyrazol-3-yl)amino)-|LY2606368|PREXASERTIB|Prexasertib","An inhibitor of checkpoint kinase 1 (chk1) with potential antineoplastic activity. Upon administration, prexasertib selectively binds to chk1, thereby preventing activity of chk1 and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA and may promote genomic instability and apoptosis. Prexasertib may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, a serine/threonine kinase, mediates cell cycle checkpoint control and is essential for DNA repair and plays a key role in resistance to chemotherapeutic agents.","Pharmacologic Substance"]
["C85465","PRIMA-1 Analog APR-246","APR-246|PRIMA-1 Analog APR-246|PRIMA-1MET","A methylated derivative and structural analog of PRIMA-1 (p53 re-activation and induction of massive apoptosis), with potential antineoplastic activity. Upon administration, PRIMA-1 analog APR-246 covalently modifies the core domain of mutated forms of cellular tumor antigen p53 (p53) through the alkylation of thiol groups. These modifications restore both the wild-type conformation and function to mutant p53, which reconstitutes endogenous p53 activity, leading to cell cycle arrest and apoptosis in tumor cells. This agent may work synergistically with other antineoplastic agents. p53, a tumor suppressor and transcription factor normally activated upon DNA damage, is frequently mutated and overexpressed in cancer cells; it plays a key role in both DNA repair and the induction of apoptosis.","Pharmacologic Substance"]
["C95771","Primary Prostate Cancer Tissue/hTERT/Survivin mRNA-loaded Autologous Dendritic Cell Vaccine","Primary Prostate Cancer Tissue/hTERT/Survivin mRNA-loaded Autologous Dendritic Cell Vaccine","An autologous dendritic cells (DCs) vaccine targeting prostate cancer with immunostimulating activity. The autologous DC vaccine is prepared via transfecting DCs with mRNAs extracted from primary prostate cancer tissue, and mRNAs of human telomerase reverse transcriptase (hTERT) and survivin. Upon administration, this DC vaccine may elicit a potent cytotoxic T-cell (CTL) response against prostate cancer cells, resulting in tumor cell death. Both hTERT and survivin are essential in neoplastic growth, and are considered to be universal tumor antigens.","Pharmacologic Substance"]
["C1811","Prinomastat","(3S)-N-Hydroxy-2,2-dimethyl-4-{{4-(4-piridinyloxy)phenyl}sulfonyl}-3-thiomorpholinecarboxamide|AG3340|PRINOMASTAT|Prinomastat|prinomastat","A synthetic hydroxamic acid derivative with potential antineoplastic activity.  Prinomastat inhibits matrix metalloproteinases (MMPs) (specifically, MMP-2, 9, 13, and 14), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis.  As a lipophilic agent, prinomastat crosses the blood-brain barrier. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C62072","Procarbazine","Benzethyzin|Ibenzmethyzin|N-(1-methylethyl)-4-[(2-methylhydrazino)methyl]benzamide|N-4-isopropylcarbamoylbenzyl-N'-methylhydrazine|N-Methylhydrazine|N-isopropyl-alpha-(2-methylhydrazino)-p-toluamide|PROCARBAZINE|Procarbazin|Procarbazine|p-(N'-methylhydrazinomethyl)-N-isopropylbenzamide|procarbazine","A methylhydrazine derivative with antineoplastic and mutagenic activities. Although the exact mode of cytotoxicity has not been elucidated, procarbazine, after metabolic activation, appears to inhibit the trans-methylation of methionine into transfer RNA (t-RNA), thereby preventing protein synthesis and consequently DNA and RNA synthesis. This agent may also undergo auto-oxidation, resulting in the formation of cytotoxic free radicals which damage DNA through an alkylation reaction.","Organic Chemical|Pharmacologic Substance"]
["C773","Procarbazine Hydrochloride","Benzamide, N-(1-methylethyl)-4-[(2-methylhydrazino) methyl]-, monohydrochloride (9CI)|Ibenzmethyzine hydrochloride|MIH hydrochloride|Matulane|N-(1-methylethyl)-4-[(2-methylhydrazino)methyl]benzamide Hydrochloride|N-4-isopropylcarbamoylbenzyl-N'-methylhydrazine Hydrochloride|N-isopropyl-alpha-(2-methylhydrazino)-p-toluamide Hydrochloride|NCI-C01810|Natulan|Natulanar|Natunalar|PCB Hydrochloride|PCB hydrochloride|PCB|PCZ|PROCARBAZINE HYDROCHLORIDE|Procarbazine Hydrochloride|Ro 4 6467/1|Ro 4-6467/1|benzamide, N-(1-methylethyl)-4-[(2-methylhydrazino) methyl]-, monohydrochloride (9CI)|p-(N'-methylhydrazinomethyl)-N-isopropylbenzamide hydrochloride|p-Toluamide, N-isopropyl-.alpha.-(2-methylhydrazino)-, monohydrochloride (8CI)|p-toluamide, N-isopropyl-alpha-(2-methylhydrazino)-, monohydrochloride (8CI)|procarbazine hydrochloride","The hydrochloride salt of a methylhydrazine derivative with antineoplastic and mutagenic activities. Although the exact mode of cytotoxicity has not been elucidated, procarbazine, after metabolic activation, appears to inhibit the trans-methylation of methionine into transfer RNA (t-RNA), thereby preventing protein synthesis and consequently DNA and RNA synthesis. This agent may also undergo auto-oxidation, resulting in the formation of cytotoxic free radicals which damage DNA through an alkylation reaction.","Organic Chemical|Pharmacologic Substance"]
["C120318","Procaspase Activating Compound-1 VO-100","PAC-1 VO-100|PAC-1|Procaspase Activating Compound-1 VO-100|VO-100","An orally bioavailable procaspase activating compound-1 (PAC-1), with potential proapoptotic and antineoplastic activities. Upon administration, VO-100 binds to and forms a chelating complex with zinc (Zn) ions inside cells, which prevents the binding of Zn ions to procaspase-3 (PC3) and abrogates the Zn-mediated inhibition of PC3. This allows for the proteolytic autoactivation of PC3 into the active form caspase-3. This results in the selective caspase-3-mediated induction of apoptosis and cell death in cancer cells. In addition, VO-100 is able to cross the blood-brain-barrier (BBB). PC3, a Zn-inhibited proenzyme, is upregulated in a variety of cancer cell types, while its expression is minimal in normal healthy cells.","Pharmacologic Substance"]
["C95709","Prohibitin-Targeting Peptide 1","Prohibitin-TP01|Prohibitin-Targeting Peptide 1|TP01","A chimeric, 25-mer peptide that targets prohibitin, with potential antineoplastic activity. Prohibitin-targeting peptide 1 (prohibitin-TP01) consists of a fat-targeting motif (CKGGRAKDC), two repeats of a proapoptotic peptide motif (KLAKLAK) and a GG linker. This peptide binds specifically to prohibitin in the white adipose vasculature; upon receptor-mediated cell internalization, the ligand/receptor complex triggers apoptosis and results in ablation of white fat. Destruction of white fat may potentially have positive consequences for men with prostate cancer since a high level of white fat has been implicated as a critical contributing factor in poor prostate cancer outcome. Prohibitin, a multifunctional membrane-associated protein that is thought to regulate cell survival and growth, has been shown by immunohistochemical analysis to be expressed in the membrane of endothelial cells in white adipose tissue.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C129689","Prostaglandin E2 EP4 Receptor Inhibitor E7046","E 7046|E-7046|E7046|EP4 Antagonist E7046|EP4 Inhibitor E7046|Prostaglandin E EP4 Receptor Antagonist E7046|Prostaglandin E2 EP4 Receptor Inhibitor E7046","An orally bioavailable antagonist of the prostaglandin E2 (PGE2) receptor type 4 (EP4; EP-4), with potential immunomodulating and antineoplastic activities. Upon oral administration, E7046 selectively targets, binds to and blocks the activity of immunosuppressive tumor-associated myeloid cells (TAMCs) in the microenvironment. This abolishes TAMC-dependent immunosuppression and reduces tumor cell proliferation. The presence of immunosuppressive myeloid cells in certain tumors is associated with a poor prognosis.","Pharmacologic Substance"]
["C71723","Prostate Cancer Vaccine ONY-P1","ONY-P1|Onyvax-P|Prostate Cancer Vaccine ONY-P1","A cell-based vaccine derived from prostate cancer with potential immunopotentiating and antineoplastic activities. Prostate cancer vaccine ONY-P1 is derived from three irradiated allogeneic prostate cancer cell lines that represent different stages of prostate cancer and express a broad range of prostate and prostate cancer antigens. Upon administration, this vaccine may stimulate a host immune response against prostate cancer cells; in the vaccination schedule, the first two vaccinations are co-administered with bacillus Calmette-Guerin (BCG) as an adjuvant.","Pharmacologic Substance"]
["C77860","Prostate Health Cocktail Dietary Supplement","Cholecalciferol/d-Alpha Tocopherol/L-Selenomethionine/Green Tea Extract/Saw Palmetto Berry Extract/Daidzein/Genistein/Lycopene Prostate Health Supplement|PHC|Prostate Health Cocktail Dietary Supplement|Prostate Health Cocktail","A dietary supplement consisting of a blend of 8 natural ingredients with potential antineoplastic and chemopreventive activities. This dietary supplement contains vitamin D3 (as cholecalciferol), vitamin E (as d-alpha tocopherol), selenium (as L-selenomethionine), epigallocatechin (green tea extract), saw palmetto (berry extract), lycopene, and the isoflavonoids daidzein and genistein. This combination preparation may decrease prostate cell growth and inhibit prostate carcinogenesis.","Pharmacologic Substance"]
["C115106","Prostate Tumor Antigen-activated Autologous Dendritic Cell Vaccine","DCVAC/PCa|Prostate Tumor Antigen-activated Autologous Dendritic Cell Vaccine","A dendritic cell (DC)-based cancer vaccine composed of autologous dendritic cells (DCs) activated with a prostate tumor cell lysate containing tumor-associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, the prostate tumor antigen-activated autologous DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against prostate cancer cells expressing prostate tumor cell-specific antigens, which may result in prostate tumor cell lysis.","Cell|Pharmacologic Substance"]
["C2548","Prostatic Acid Phosphatase-Sargramostim Fusion Protein","PA2024|PROSTATIC ACID PHOSPHATASE (PAP)-GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR (GM-CSF) FUSION PROTEIN|Prostatic Acid Phosphatase-Sargramostim Fusion Protein","A genetically-engineered protein formed by the fusion of prostatic acid phosphatase (PAP) and sargramostim (GM-CSF). Vaccination with antigen-presenting cells (APC) loaded with prostatic acid phosphatase-sargramostim fusion protein may elicit a cytotoxic T-cell response against tumor cells that express PAP. (NCI05)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C124796","Protein Kinase C Inhibitor LXS196","LXS196|PKC Inhibitor LXS196|Protein Kinase C Inhibitor LXS196","An orally available protein kinase C (PKC) inhibitor with potential immunosuppressive and antineoplastic activities. Upon oral administration, protein kinase C inhibitor LXS196 binds to and inhibits PKC, which prevents the activation of PKC-mediated signaling pathways. This may lead to the induction of cell cycle arrest and apoptosis in susceptible tumor cells. PKC, a serine/threonine protein kinase overexpressed in certain types of cancer cells, is involved in tumor cell differentiation, proliferation, invasion and survival.","Pharmacologic Substance"]
["C106430","Protein Phosphatase 2A Inhibitor LB-100","LB-100|PP2A Inhibitor LB-100|Protein Phosphatase 2A Inhibitor LB-100","A water soluble inhibitor of the protein phosphatase 2A (PP2A), with potential chemo- and radiotherapy enhancing activity. Upon injection, PP2A inhibitor LB-100 inhibits the removal of phosphate groups from proteins essential for cell cycle progression. When used with radio- or chemotherapy treatment, this agent prevents the activation of PP2A-mediated repair mechanisms and allows for malignant cells to progress through the cell cycle without having their damaged DNA repaired. This enhances the cytotoxic effect of the chemotherapeutic or radiotherapeutic agent and results in tumor cell apoptosis. PP2A, a serine/threonine phosphatase that plays a key role in the control of cell growth and DNA damage repair.","Pharmacologic Substance"]
["C90534","Protein Stabilized Liposomal Docetaxel Nanoparticles","ATI-1123|Protein Stabilized Liposomal Docetaxel Nanoparticles","A formulation containing protein-stabilized liposome nanoparticles encapsulating the poorly water-soluble, second-generation taxane analog docetaxel with antineoplastic activity. Docetaxel binds to and stabilizes the beta-tubulin subunit, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and cell death. This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and displays immunomodulatory and pro-inflammatory properties by inducing various mediators of the inflammatory response. Compared to the use of toxic carriers to increase solubilization of docetaxel, protein-stabilized liposomal docetaxel improves drug solubility while avoiding carrier-associated toxicity.","Pharmacologic Substance"]
["C130036","Proxalutamide","GT-0918|GT0918|Proxalutamide","An orally bioavailable androgen receptor (AR) antagonist with potential antineoplastic activity. Upon oral administration, proxalutamide binds to AR in target tissues, inhibits androgen-induced receptor activation, and facilitates the formation of inactive complexes that cannot translocate to the nucleus. This prevents binding to and transcription of AR-responsive genes that regulate prostate cancer cell proliferation. In addition, proxalutamide induces AR downregulation, thereby further preventing AR-mediated signaling. This ultimately leads to an inhibition of growth in AR-expressing prostate cancer cells. AR is overexpressed in prostate cancer and plays a key role in prostate cancer cell proliferation.","Pharmacologic Substance"]
["C2497","PSA Prostate Cancer Vaccine","OncoVax-PR|PSA Prostate Cancer Vaccine","A peptide vaccine containing the prostate specific antigen (PSA) with potential antineoplastic activity. PSA, a glycoprotein secreted by prostatic epithelial and ductal cells, is overexpressed in prostate cancer cells and is used as a tumor marker for both diagnosis and treatment evaluation. Vaccination with PSA peptide vaccine may produce anti-PSA antibodies as well as elicit a cytotoxic T-cell (CTL) response against prostate cancer cells expressing this antigen, thereby decreasing tumor cell growth.","Immunologic Factor|Pharmacologic Substance"]
["C2236","PSA RNA-Pulsed Dendritic Cell Vaccine","PSA RNA-Pulsed Dendritic Cell Vaccine","An autologous dendritic cell vaccine with potential immunostimulatory activity. Dendritic cells harvested from a prostate cancer patient are transfected with the mRNA encoding for prostate specific antigen (PSA), a tumor marker secreted by prostatic epithelial and ductal cells. When reintroduced back to the patient, these PSA RNA pulsed autologous dendritic cells may elicit a cytotoxic T-cell (CTL) response against PSA-positive prostate cancer cells.","Immunologic Factor|Pharmacologic Substance"]
["C114289","PSA/IL-2/GM-CSF Vaccine","PSA/IL-2/GM-CSF Vaccine|Prostatac","A prostate cancer vaccine containing prostate specific antigen (PSA) combined with the cytokines, interleukin-2 (IL-2) and granulocyte macrophage-colony-stimulating factor (GM-CSF), with potential antineoplastic activity. Upon intradermal vaccination, PSA/IL-2/GM-CSF vaccine may activate the immune system to induce a cytotoxic T-cell (CTL) response against prostate cancer cells expressing this antigen, thereby decreasing tumor cell growth. PSA, a glycoprotein secreted by prostatic epithelial and ductal cells, is overexpressed by prostate cancer cells. IL-2 stimulates natural killer (NK) cells and cytotoxic T-cells against the PSA-expressing tumor cells. GM-CSF promotes antigen presentation to dendritic cells and further stimulates a tumor-specific cytotoxic T-lymphocyte (CTL) response.","Pharmacologic Substance"]
["C123283","PSA/PSMA DNA Plasmid INO-5150","INO 5150|INO-5150|PSA/PSMA DNA Plasmid INO-5150|PSA/PSMA Synthetic DNA Vaccine INO-5150|PSA/PSMA-encoding DNA Plasmid INO-5150","A plasmid DNA vaccine encoding the tumor-associated antigens (TAAs) prostate-specific antigen (PSA) and prostate-specific membrane antigen (PSMA), with potential immunoactivating and antineoplastic activities. Upon intramuscular delivery and electroporation of the PSA/PSMA DNA plasmid INO-5150, both PSA and PSMA are translated in cells which then activate the immune system. This induces cytotoxic T-lymphocyte (CTL) responses against tumor cells expressing PSA and PSMA. This may result in both immune-mediated tumor cell death and the inhibition of tumor cell proliferation. PSA and PSMA are overexpressed on a variety of cancer cell types. The DNA encoding the TAAs in INO-5150 is based on both human and other primate antigen gene sequences. As the plasmid genes differ from the human gene sequences encoding these antigens, INO-5150 may overcome immune tolerance to human TAAs.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C29338","PSA:154-163(155L) Peptide Vaccine","PSA PEP VAC|PSA-3A|PSA:154-163(155L) Peptide Vaccine|PSA:154-163(155L) Peptide","A cancer vaccine comprised of a synthetic peptide with an amino acid sequence corresponding to positions 154-163 of the amino acid sequence for prostate-specific antigen (PSA) with a leucine substitution at position 155. Upon administration, PSA:154-163 (155L) peptide vaccine may elicit a cytotoxic T-cell response against tumor cells that express PSA. (NCI05)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C29337","PSA-OP Peptide Vaccine","PSA-OP Peptide Vaccine","A 30-residue prostate specific antigen (PSA) oligoepitope peptide (OP) vaccine with potential antineoplastic activity.  PSA-OP peptide vaccine contains the PSA-1 and PSA-3 HLA-A2 epitopes and the PSA-9 HLA-class I-A3 epitope joined by peptide linker sequences.  In an animal model, vaccination with this agent has been shown to elicit a cytotoxic T-lymphocyte immune response. (NCI04)","Pharmacologic Substance"]
["C92573","PSA-PAP/KLH-pulsed Autologous Dendritic Cell Vaccine","CreaVax-PC|PSA-PAP/KLH-pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with the prostate-specific tumor associated antigens (TAAs) prostate specific antigen (PSA) and prostate acid phosphatase (PAP), and conjugated to the immunostimulant Keyhole limpet hemocyanin (KLH), with potential immunostimulatory and antineoplastic activities. Upon administration, prostate cancer antigen/KLH-pulsed autologous dendritic cell vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against prostate cancer cells expressing PSA and PAP, which may result in prostate cancer cell lysis. KLH is an immunogenic carrier and serves as an immunostimulant to improve antigenic immune recognition and T-cell responses and can be used to evaluate vaccine efficacy.","Cell|Pharmacologic Substance"]
["C87389","Pseudoisocytidine","4(1H)-Pyrimidinone, 2-Amino-5-Beta-D-Ribofuranosyl-|5-(Beta-D-Ribofuranosyl)Isocytosine|PSEUDOISOCYTIDINE|Pseudoisocytidine|psi Icyd","A synthetic, pyrimidine C-5 nucleoside with antineoplastic activity. Pseudoisocytidine, after conversion into pseudoisocytidine triphosphate, is incorporated into DNA and RNA eventually halting tumor cell proliferation. Compared to 5-azacytidine and cytarabine, this agent shows enhanced stability and resistance to enzymatic deamination.","Pharmacologic Substance"]
["C97662","Pseudomonas aeruginosa Preparation","Pseudomonas aeruginosa Preparation","A preparation containing the inactivated Pseudomonas aeruginosa with potential immunomodulating activity. Upon inoculation, Pseudomonas aeruginosa preparation may stimulate the immune system, increasing macrophage and natural killer cell activity; it may be used thereby in cancer adjuvant treatments, and it may reduce the incidence of infection.","Pharmacologic Substance"]
["C78819","PSMA/TARP Peptide Vaccine","PSMA/TARP Peptide Vaccine","A peptide-based cancer vaccine containing epitopes of T cell receptor gamma-chain alternate reading frame protein (TARP) and prostate-specific membrane antigen (PSMA) in combination with a Poly IC-LC immunoadjuvant, with potential antineoplastic activity. Upon administration, PSMA/TARP peptide vaccine may stimulate a host cytotoxic T-cell (CTL) response against TARP- and PSMA-expressing tumor cells, resulting in tumor cell cytotoxicity. The nuclear protein TARP and PSMA are commonly expressed in prostate cancer cells.","Pharmacologic Substance"]
["C95892","PSMA-targeted Docetaxel Nanoparticles BIND-014","BIND-014|PSMA-targeted Docetaxel Nanoparticles BIND-014","A proprietary preparation of polymeric nanoparticles containing the second-generation taxane docetaxel, targeted to prostate-specific membrane antigen (PSMA), with antineoplastic activity. PSMA-targeted docetaxel nanoparticles BIND-014 carry docetaxel within a matrix of polylactic acid covered with a coating of polyethylene glycol; embedded on the surface of the polyethylene glycol coating are ligands targeted to PSMA. BIND-014 allows gradual release of docetaxel upon degradation of the polylactic acid, and the PEG encapsulation escapes the host immune response while PSMA ligands on the surface restrict the cytotoxic effect to PSMA-expressing cells. Docetaxel binds to and stabilizes the beta-tubulin subunit, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and cell death. PSMA is a cell-surface antigen that is abundantly present on the surface of cancer cells and on the neovasculature that feeds a wide variety of tumor types.","Organic Chemical|Pharmacologic Substance"]
["C117291","PSMA-targeted Tubulysin B-containing Conjugate EC1169","EC1169|EC1719|PSMA-targeted Tubulysin B-containing Conjugate EC1169","An injectable, water soluble, small molecule drug conjugate (SMDC) containing a ligand specific for prostate-specific membrane antigen (PSMA), conjugated via a stable, enzyme-cleavable linker to the cytotoxic agent tubulysin B hydrazide (TubBH), with potential antineoplastic activity. Upon administration of PSMA-targeted tubulysin B-containing conjugate EC1169, the PSMA ligand specifically targets and binds to PSMA, a protein which is abundantly expressed on the surface of metastatic and hormone-refractory prostate cancer cells as well as on the neovasculature of many solid tumors. This allows for the specific delivery of TubBH to PSMA-expressing cancer cells. Upon internalization and cleavage, tubulysin B binds to tubulin and inhibits microtubule polymerization, which blocks cell division and results in G2/M phase arrest, tumor cell apoptosis and a decrease in PSMA-expressing tumor cells.","Chemical|Indicator, Reagent, or Diagnostic Aid"]
["C82407","pTVG-HP Plasmid DNA Vaccine","pTVG-HP Plasmid DNA Vaccine","A cancer vaccine containing plasmid DNA encoding human prostatic acid phosphatase (PAP) (pTVG-HP) with potential immunostimulatory and antineoplastic activities. Upon administration, pTVG-HP plasmid DNA vaccine may stimulate the host immune system to generate a cytotoxic T lymphocyte (CTL) response against PAP-expressing prostate cancer cells. PAP or prostatic specific acid phosphatase (PSAP) is a tumor associated antigen (TAA) that may be overexpressed in prostate cancer.","Pharmacologic Substance"]
["C73239","Pumitepa","Fopurin|PUMITEPA|Pumitepa","A thiotepa derivative with potential antineoplastic alkylating activity. Although the exact mechanism of action of pumitepa has yet to be fully elucidated, this agent appears to work through alkylation, thereby causing DNA damage and cell cycle arrest.","Pharmacologic Substance"]
["C95727","pUMVC3-hIGFBP-2 Multi-Epitope Plasmid DNA Vaccine","pUMVC3-hIGFBP-2 Multi-Epitope Plasmid DNA Vaccine","A recombinant plasmid DNA vaccine containing mammalian expression vector, pUMVC3, encoding epitopes of human Insulin-Like Growth Factor-Binding Protein 2 (hIGFBP-2) with potential antineoplastic activity. Upon vaccination, pUMVC3-hIGFBP-2 multi-epitope plasmid DNA vaccine may produce IGFBP-2 that binds to cell surface, likely via integrin complexes. This results in the dephosphorylation of the focal adhesion-kinase (FAK) and of the p42/44 MAP-kinases, thereby inactivating them; both kinases are involved in cell growth regulation. Furthermore, IGFBP-2 promotes de-adhesion of the cells in a dose-dependent manner, hence impeding cell proliferation. The primary effect of IGFBPs appears to be modulation of IGF activity and control of IGF-mediated cell growth and metabolism.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C127910","pUMVC3-IGFBP2-HER2-IGF1R Plasmid DNA Vaccine","WOKVAC Vaccine|WOKVAC|pUMVC3-IGFBP2-HER2-IGF1R Plasmid DNA Vaccine|pUMVC3-IGFBP2-HER2-IGF1R Vaccine|pUMVC3-IGFBP2-HER2-IGF1R","A polyepitope plasmid DNA vaccine containing the mammalian expression vector pUMVC3 encoding epitopes derived from three tumor-associated antigens (TAAs): human insulin-like growth factor-binding protein 2 (IGFBP2), human epidermal growth factor receptor 2 (HER2; ERBB2) and insulin-like growth factor 1 receptor (IGF1R), with potential immunostimulating and antineoplastic activities. Upon intradermal vaccination, pUMVC3-IGFBP2-HER2-IGF1R plasmid DNA vaccine transfects local keratinocytes, which process the plasmid, express the epitopes and present them to antigen-presenting cells (APCs). This activates the immune system to mount a combined response from specific T helper type 1 (Th1) cells, memory T-cells and cytotoxic T-lymphocytes (CTL) against IGFBP2-, HER2-, and IGF1R-expressing tumor cells. IGFBP2, HER2, and IGF1R are tumor-associated proteins overexpressed in certain tumor cell types, and play key roles in cellular proliferation and survival.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C787","Puromycin","Adenosine, 3'-((2-amino-3-(4-methoxyphenyl)-1-oxopropyl)amino)-3'-deoxy-N,N-dimethyl-, (S)-|Adenosine, 3'-(alpha-amino-p-methoxyhydrocinnamamido)-3'-deoxy-N,N-dimethyl-, L-|CL 16536|L-3'-(alpha-Amino-p-methoxyhydrocinnamamido)-3'-deoxy-N,N-dimethyladenosine|P-638|PUROMYCIN|Puromicina|Puromycin|Puromycine|Puromycinum|Stillomycin|Stylomycin","An aminoglycoside antibiotic isolated from the bacterium Streptomyces alboniger.  Acting as an analog of the 3' terminal end of aminoacyl-tRNA, puromycin incorporates itself into a growing polypeptide chain and causes its premature termination, thereby inhibiting protein synthesis.  This agent has antimicrobial, antitrypanosomal, and antineoplastic properties; it is used as an antibiotic in cell culture. (NCI04)","Antibiotic|Nucleic Acid, Nucleoside, or Nucleotide"]
["C75148","Puromycin Hydrochloride","PUROMYCIN HYDROCHLORIDE|Puromycin Hydrochloride","The hydrochloride salt form of puromycin, an aminoglycoside antibiotic isolated from the bacterium Streptomyces alboniger. Acting as an analog of the 3' terminal end of aminoacyl-tRNA, puromycin incorporates itself into a growing polypeptide chain and causes its premature termination, thereby inhibiting protein synthesis. This agent has antimicrobial, antitrypanosomal, and antineoplastic properties; it is used as an antibiotic in cell culture.","Pharmacologic Substance"]
["C53412","PV-10","4,5,6,7-Tetrachloro-2',4',5',7'-tetraiodofluorescein Disodium Salt|Injectable Rose Bengal 10%|PV-10|Provecta|Rose Bengal Disodium 10%","An injectable ten percent solution of rose bengal disodium, an iodinated fluorescein derivative, with potential antineoplastic and radiosensitizing activities. When injected into tumor tissue, PV-10 specifically targets and concentrates in tumor cells, producing cytotoxic singlet oxygen when exposed to ionizing radiation. In addition, PV-10 may stimulate an anti-tumor immune response.","Organic Chemical|Pharmacologic Substance"]
["C2799","PV701","PV701","An attenuated, replication-competent, oncolytic strain of Newcastle disease virus. PV701 selectively lyses tumor cells. The selectivity of this agent is related to defects in the interferon-mediated antiviral response found in tumor cells. (NCI04)","Pharmacologic Substance|Virus"]
["C71149","PVA Microporous Hydrospheres/Doxorubicin Hydrochloride","HepaSphere Microspheres/Doxorubicin Hydrochloride|PVA Microporous Hydrospheres/Doxorubicin Hydrochloride|QuadraSphere Microspheres/Doxorubicin Hydrochloride","An embolic material composed of microspheres of polyvinyl alcohol (PVA) polymers loaded with doxorubicin hydrochloride with antineoplastic activity. Doxorubicin hydrochloride-loaded microspheres may be used as a drug delivery vehicle during embolization of tumor vasculature. Doxorubicin intercalates DNA, interferes with catalytic activity of topoisomerase II, and causes DNA adducts and other DNA damage, resulting in tumor cell growth inhibition and apoptosis. When used in tumor vasculature embolization, this preparation may provide more tumor-specific treatment with doxorubicin compared to the systemic administration of doxorubicin, thereby reducing the systemic toxicity of doxorubicin.","Pharmacologic Substance"]
["C82352","pVAXrcPSAv53l DNA Vaccine","pVAXrcPSAv53l (DNA Encoding Rhesus PSA)|pVAXrcPSAv53l DNA Vaccine|pVAXrcPSAv53l","A cancer vaccine containing xenogenic DNA from rhesus macaque (Macaca mulatta) that encodes prostate specific antigen (PSA) with potential immunostimulating and antineoplastic activities. Upon repeated intradermal administration via electroporation, pVAXrcPSAv53l vaccine may induce a cytotoxic T-lymphocyte (CTL) response against PSA-expressing prostate cancer cells. Rhesus PSA is 89% homologous to human PSA.","Pharmacologic Substance"]
["C1852","Pyridyl Cyanoguanidine CHS 828","CHS 828|CHS-828|N-(6-(4-Chlorophenoxy)hexyl)-N'-Cyano-N''-4-Pyridylcyanoguanidine|Pyridyl Cyanoguanidine CHS 828","A pyridyl cyanoguanidine that exhibits antitumor activity by an unknown mechanism. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C111895","Pyrotinib","Pyrotinib","An orally bioavailable, dual kinase inhibitor of the epidermal growth factor receptor (EGFR or HER-1) and the human epidermal growth factor receptor 2 (ErbB2 or HER-2), with potential antineoplastic activity. Upon oral administration, pyrotinib binds to and inhibits both EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumor cells. EGFR and HER2 are receptor tyrosine kinases that are upregulated in various tumor cell types and play major roles in tumor cell proliferation and tumor vascularization.","Pharmacologic Substance"]
["C2801","Pyroxamide","Pyroxamide|Suberoyl-3-aminopyridineamide Hydroxamic Acid|pyroxamide","A synthetic derivative of hydroxamic acid with antineoplastic properties, Pyroxamide inhibits histone deacetylases involved in transcription; induces hyperacetylation of core histones, modulating chromatin structure and affecting transcription of some genes that inhibit tumor growth; and induces growth arrest and apoptosis. Pyroxamide is used in clinical studies for cancer chemotherapy. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C67087","Pyruvate Kinase Inhibitor TLN-232","CAP-232|Pyruvate Kinase Inhibitor TLN-232","A synthetic cyclic heptapeptide with potential antineoplastic activity. Pyruvate kinase (PK) inhibitor TLN-232 targets pyruvate kinase M2 (M2PK), which may disrupt tumor cell anaerobic glycolysis. M2PK is a dimeric isoform of PK and the predominant PK isoform found in tumor cells","Pharmacologic Substance"]
["C61087","Quadrivalent Human Papillomavirus (types 6, 11, 16, 18) Recombinant Vaccine","Gardasil|Quadrivalent HPV [Type 6, 11, 16 and 18] L1 Virus-Like Particle vaccine|Quadrivalent Human Papillomavirus (types 6, 11, 16, 18) Recombinant Vaccine|Recombinant Human Papillomavirus (HPV) Quadrivalent Vaccine|V501|quadrivalent human papillomavirus (types 6, 11, 16, and 18) recombinant vaccine","A non-infectious recombinant, quadrivalent vaccine prepared from the highly purified virus-like particles (VLPs) of the major capsid (L1) protein of human papillomavirus (HPV) types 6, 11, 16, and 18 with immunoprophylactic activity. L1 proteins are produced by separate fermentations in recombinant Saccharomyces cerevisiae, self-assembled into VLPs, and adsorbed onto amorphous aluminium hydroxyphosphate sulfate adjuvant following purification. The immunoprophylactic efficacy of L1 VLP vaccines, such as quadrivalent human papillomavirus (types 6,11,16,18) recombinant vaccine, appear to be mediated by the development of humoral immune responses. HPV Types 16 and 18 account for approximately 70% of cervical cancers and HPV Types 6 and 11 account for approximately 90% of genital warts.","Chemical Viewed Functionally"]
["C71726","Quarfloxin","3H-Benzo(b)pyrido(3,2,1-kl)phenoxazine-2-carboxamide, 5-fluoro-N-(2-((2S)- 1-methyl-2-pyrrolidinyl)ethyl)-3-oxo-6-(3-pyrazinyl-1-pyrrolidinyl)-|5-Fluoro-N-(2-((2S)-1-methylpyrrolidin-2-yl)ethyl)-3-oxo-6-(3-(pyrazin-2- yl)pyrrolidin-1-yl)-3H-benzo(b)pyrido(3,2,1-kl)phenoxazine-2-carboxamide|CX-3543|QUARFLOXIN|Quarfloxacin|Quarfloxin","A fluoroquinolone derivative with antineoplastic activity. Quarfloxin disrupts the interaction between the nucleolin protein and a G-quadruplex DNA structure in the ribosomal DNA (rDNA) template, a critical interaction for rRNA biogenesis that is overexpressed in cancer cells; disruption of this G-quadruplex DNA:protein interaction in aberrant rRNA biogenesis may result in the inhibition of ribosome synthesis and tumor cell apoptosis.","Pharmacologic Substance"]
["C67059","Quinacrine Hydrochloride","6-Chloro-9-((4-(diethylamino)-1-methylbutyl)amino)-2-methoxyacridine Dihydrochloride|Atabrine Dihydrochloride|Mepacrine Dihydrochloride|QUINACRINE HYDROCHLORIDE|Quinacrine Dihydrochloride|Quinacrine Hydrochloride|SN 390","The dihydrochloride salt of the 9-aminoacridine derivative quinacrine with potential antineoplastic and antiparasitic activities. Quinacrine may inhibit the transcription and activity of both basal and inducible nuclear factor-kappaB (NF-kappaB), which may result in the induction of tumor suppressor p53 transcription, the restoration of p53-dependent apoptotic pathways, and tumor cell apoptosis. Continuous NF-kappaB signaling, present in many tumors and in chronic inflammatory processes, promotes the expression of antiapoptotic proteins and cytokines while downregulating the expression of proapoptotic proteins, such as p53.","Pharmacologic Substance"]
["C794","Quinine","(-)-Quinine|QUIN|QUININE|Quinine","A quinidine alkaloid isolated from the bark of the cinchona tree. Quinine has many mechanisms of action, including reduction of oxygen intake and carbohydrate metabolism; disruption of DNA replication and transcription via DNA intercalation; and reduction of the excitability of muscle fibers via alteration of calcium distribution.  This agent also inhibits the drug efflux pump P-glycoprotein which is overexpressed in multi-drug resistant tumors and may improve the efficacy of some antineoplastic agents. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C77912","Quisinostat","HDAC Inhibitor JNJ-26481585|JNJ-26481585|QUISINOSTAT|Quisinostat","An orally bioavailable, second-generation, hydroxamic acid-based inhibitor of histone deacetylase (HDAC) with potential antineoplastic activity. HDAC inhibitor JNJ-26481585 inhibits HDAC leading to an accumulation of highly acetylated histones, which may result in an induction of chromatin remodeling; inhibition of the transcription of tumor suppressor genes; inhibition of tumor cell division; and the induction of tumor cell apoptosis. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins. Compared to some first generation HDAC inhibitors, JNJ-26481585 may induce superior HSP70 upregulation and bcl-2 downregulation.","Organic Chemical|Pharmacologic Substance"]
["C68936","Quizartinib","(2E)-N-(4-(3-Chloro-4-Fluoroanilino)-7-(((3S)-Oxolan-3-Yl)Oxy)Quinoxazolin-6-yl)-4-(Dimethylamino)but-2-Enamide|AC-220|AC010220|AC220|N-(5-tert-butyl-isoxazol-3-yl)-N'-{4-[7-(2-morpholin-4-yl-ethoxy)imidazo [2,1-b] [1,3] benzothiazol 2-yl]phenyl}urea|QUIZARTINIB|Quizartinib","An orally available small molecule with potential antineoplastic activity. Quizartinib selectively inhibits class III receptor tyrosine kinases, including FMS-related tyrosine kinase 3 (FLT3/STK1), colony-stimulating factor 1 receptor (CSF1R/FMS), stem cell factor receptor (SCFR/KIT), and platelet derived growth factor receptors (PDGFRs), resulting in inhibition of ligand-independent leukemic cell proliferation and apoptosis. Mutations in FLT3, resulting in constitutive activation, are the most frequent genetic alterations in acute myeloid leukemia (AML) and occur in approximately one-third of AML cases.","Pharmacologic Substance"]
["C78348","R-(-)-Gossypol Acetic Acid","(-)-Gossypol Acetic Acid|(2,2'-Binaphthalene)-8,8'-dicarboxaldehyde, 1,1',6,6',7,7'-hexahydroxy-3,3'-dimethyl-(R)-5,5'-bis(1-methylethyl)-, (2R)-, compd. with acetic acid (1:1)|AT-101|GOSSYPOL ACETIC ACID, (R)-|R-(-)-Gossypol Acetic Acid","The orally bioavailable solvate of the R-(-) enantiomer of gossypol and acetic acid with potential antineoplastic activity. As a BH3 mimetic, R-(-)-gossypol binds to the hydrophobic surface binding groove BH3 of the anti-apoptotic proteins Bcl-2 and Bcl-xL, blocking their heterodimerization with pro-apoptotic members of the Bcl-2 family of proteins such as Bad, Bid, and Bim; this may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. Racemic gossypol is a polyphenolic compound isolated from cottonseed.","Organic Chemical|Pharmacologic Substance"]
["C2662","R(+)XK469","2-{4-[(7-chloro-2-quinoxalinyl)oxy]phenoxy}propionic acid|Propanoic acid, 2-[4-[(7-chloro-2-quinoxalinyl)oxy]phenoxy]-, (+ )-(R)-|R(+)XK469|XK469","The R-isomer of a synthetic quinoxaline phenoxypropionic acid derivative with proapoptotic and antiproliferative activities. R(+)XK469 selectively inhibits topoisomerase II-beta, blocks activation of MEK/MAPK signaling kinases, stimulates caspases, and upregulates p53-dependent proteins, including cyclins A and B1, thereby arresting cancer cells in the G2/M phase of the cell cycle. Both R(+) and S(-) isomers of this agent are cytotoxic, although the R-isomer is more potent. (NCI05)","Pharmacologic Substance"]
["C81937","Rabusertib","1-[5-bromo-4-methyl-2-S-(morpholin-2-yl-methoxy)-phenyl]-3-(5-methyl-pyrazin-2-yl)-urea|Checkpoint Kinase 2 Inhibitor LY2603618|LY2603618|RABUSERTIB|Rabusertib","An inhibitor of the cell cycle checkpoint kinase 2 (chk2) with potential chemopotentiating activity. Rabusertib binds to and inhibits the activity of chk2, which may prevent the repair of DNA caused by DNA-damaging agents, thus potentiating the antitumor efficacies of various chemotherapeutic agents. Chk2, an ATP-dependent serine-threonine kinase, is a key component in the DNA replication-monitoring checkpoint system and is activated by double-stranded breaks (DSBs); activated chk2 is overexpressed by a variety of cancer cell types.","Pharmacologic Substance"]
["C2825","Racemic XK469","Propanoic acid, 2-[4-[(7-chloro-2-quinoxalinyl)oxy]-phenoxy]-, (+ /-)-|Racemic XK469|XK469 Racemic|XK469R","The racemic form of a synthetic quinoxaline phenoxypropionic acid derivative with antineoplastic properties. XK469R selectively inhibits topoisomerase II by stabilizing the enzyme-DNA intermediates in which topoisomerase subunits are covalently linked to DNA through 5-phosphotyrosyl linkages, thereby interfering with DNA repair and replication, RNA and protein synthesis. This agent possesses unusual solid tumor selectivity and activity against multidrug-resistant cancer cells. XK469R is more water soluble and active than the pure isomers, R(+)XK469 and S(-)XK469. (NCI05)","Organic Chemical|Pharmacologic Substance"]
["C95024","Racotumomab","Anti-P3 Antibody Idiotype Monoclonal Antibody 1E10|MoAb 1E10|RACOTUMOMAB|Racotumomab","An anti-idiotype murine monoclonal antibody (MoAb) specific to P3 MoAb with anti-metastatic effect. Racotumomab binds to the idiotype region of P3 MoAb and functionally mimics the three-dimensional structure of N-glycolyl ceramides of mono-sialyl lactose, the antigenic target of P3. As a result, this anti-idiotype antibody may stimulate the host immune system to elicit humoral and cellular immune responses against tumor cells expressing NeuGc-GM3 gangliosides, which are expressed in a wide variety of tumor cells.","Immunologic Factor|Pharmacologic Substance"]
["C2729","Radiolabeled CC49","Radiolabeled CC49","A radioimmunoconjugate comprised of a humanized monoclonal antibody with antitumor activity. The monoclonal antibody CC49 is developed from the murine monoclonal antibody B72.3 and is humanized by grafting the hypervariable regions onto the variable light (VL) and variable heavy (VH) frameworks of the monoclonal antibodies LEN and 21/28' CL. The resultant antibody binds the pancarcinoma tumor-associated glycoprotein (TAG)-72 with high affinity. Furthermore, the antibody is commonly radiolabeled resulting in an effective agent for use in radioimmunotherapy for treatment of cancer.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C62535","Radium Ra 223 Dichloride","Alpharadin|BAY 88-8223|BAY88-8223|RADIUM CHLORIDE RA-223|Radium 223 Dichloride|Radium Ra 223 Dichloride|Radium-223 Dichloride|Xofigo","A radiopharmaceutical composed of the dichloride salt of the alpha-emitting isotope radium Ra 223, with antineoplastic activity. Like calcium, radium targets bone tissue and preferentially accumulates in osteoblastic lesions, such as those seen in areas of bone metastases. Radium Ra 223 forms complexes with hydroxyapatite and becomes incorporated into the bone matrix. The radioisotope Ra 223 kills bone cancer cells through local emission of high energy alpha particles, causing DNA double-strand breaks and tumor regression in the skeleton. The short range effects of alpha emission allows for localized DNA damage with limited toxicity to nearby healthy bone tissue.","Element, Ion, or Isotope|Pharmacologic Substance"]
["C113297","Radix Angelicae Sinensis/Radix Astragali Herbal Supplement","DB1|Danggui Buxue Decoction No.1|Radix Angelicae Sinensis/Radix Astragali Herbal Supplement","A traditional Chinese medicine comprising of Radix Angelicae Sinensis (RAS) and Radix Astragali (RA), with potential anti-inflammatory, immunostimulatory, neuroprotective, anti-hepatotoxic and antineoplastic activities. The main chemical constituents of RAS include ferulic acid, Z-ligustilide, butylidenephthalide and various polysaccharides. RA is the dried root of Astragalus membranaceus with primary constituents such polysaccharides, triterpenoids as well as isoflavones. Though their mechanisms of action remain largely elusive, Radix Angelicae Sinensis/Radix Astragali herbal supplements are commonly used for the treatment of various health conditions affecting women including premenstrual syndrome, dysmenorrhea, pelvic pain, recovery from childbirth and menopausal symptoms. These agents are also used for alleviating constipation, preventing and treating anemia and allergic attacks, and for the management of hypertension, joint pain and ulcers.","Pharmacologic Substance"]
["C99644","Radotinib Hydrochloride","4-Methyl-N-(3-(4-methylimidazol-1-yl)-5-trifluoromethylphenyl)-3-(4-(pyrazin-2-yl)pyrimidin-2-ylamino)benzamide Hydrochloride|IY5511HCl|Radotinib Hydrochloride","An orally available, hydrochloride salt form of radotinib, a second-generation tyrosine kinase inhibitor of Bcr-Abl fusion protein and the platelet-derived growth factor receptor (PDGFR), with potential antineoplastic activity. Upon administration, radotinib specifically inhibits the Bcr-Abl fusion protein, an abnormal enzyme expressed in Philadelphia chromosome positive chronic myeloid leukemia (CML) cells. In addition, this agent also inhibits PDGFR thereby blocking PDGFR-mediated signal transduction pathways. The inhibitory effect of radotinib on these specific tyrosine kinases may decrease cellular proliferation and inhibit angiogenesis. This agent has shown potent efficacy in CML cells that are resistant to the first-generation standard tyrosine kinase inhibitors, such as imatinib, nilotinib and dasatinib. PDGFR, upregulated in many tumor cell types, is a receptor tyrosine kinase essential to cell migration and the development of the microvasculature.","Pharmacologic Substance"]
["C121646","Raf Kinase Inhibitor HM95573","HM95573|Raf Kinase Inhibitor HM95573","An orally available inhibitor of members of the Raf family of serine/threonine protein kinases, with potential antineoplastic activity. Upon administration, Raf kinase inhibitor HM95573 binds to and inhibits the B-Raf mutant V600E and C-Raf. This inhibits B-Raf V600E- and C-Raf-mediated signal transduction pathways, thereby inhibiting tumor cell growth of susceptible tumor cells. In addition, HM95573 may also inhibit mutated Ras proteins. Raf protein kinases play a key role in the Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. The Raf mutation B-Raf V600E, where the valine at residue 600 is substituted for glutamic acid, is frequently overexpressed in a variety of human tumors and results in the constitutive activation of the Raf/MEK/ERK signaling pathway.","Pharmacologic Substance"]
["C69135","RAF Kinase Inhibitor XL281","RAF Kinase Inhibitor XL281|XL281","An orally active, small molecule with potential antineoplastic activity. XL281 specifically inhibits RAF kinases, located downstream from RAS in the RAS/RAF/MEK/ERK kinase signaling pathway, which may result in reduced proliferation of tumor cells. RAS mutations may result in constitutive activation of the RAS/RAF/MEK/ERK kinase signaling pathway, and have been found to occur frequently in human tumors.","Pharmacologic Substance"]
["C105853","Ralimetinib Mesylate","3H-Imidazo(4,5-b)pyridin-2-amine, 5-(2-(1,1-dimethylethyl)-4-(4-fluorophenyl)-1H-imidazol-5-yl)-3-(2,2-dimethylpropyl)-, Methanesulfonate (1:2)|LY-2228820|LY2228820 Dimesylate|LY2228820|RALIMETINIB MESYLATE|Ralimetinib Dimesylate|Ralimetinib Mesylate","The dimesylate salt form of LY2228820, a tri-substituted imidazole derivative and orally available, p38 mitogen-activated protein kinase (MAPK) inhibitor with potential anti-inflammatory and antineoplastic activities. Upon administration, ralimetinib inhibits the activity of p38, particularly the alpha and beta isoforms, thereby inhibiting MAPKAPK2 phosphorylation and preventing p38 MAPK-mediated signaling. This may inhibit the production of a variety of cytokines involved in inflammation, cellular proliferation and angiogenesis such as tumor necrosis factor alpha (TNFa), interleukin (IL)-1, -6 and -8, vascular endothelial growth factor, and macrophage inflammatory protein-1 alpha. Ultimately this induces apoptosis and reduces tumor cell proliferation. In addition, inhibition of the p38 MAPK pathway by LY2228820 increases the antineoplastic activity of certain chemotherapeutic agents. p38 MAPK, a serine/threonine protein kinase that is often upregulated in cancer cells, plays a crucial role in tumor cell proliferation, angiogenesis and metastasis.","Pharmacologic Substance"]
["C1804","Raltitrexed","D1694|ICI D1694|N-(5-[N-(3,4-Dihydro-2-methyl-4-oxoquinazolin-6-ylmethyl)-N-methylamino]-2-thenoyl)-L-glutamic Acid|N-[[5-[[(1,4-Dihydro-2-methyl-4-oxo-6-quinazolinyl)methyl]methylamino]-2-thienyl]carbonyl]-L-glutamic Acid|RALTITREXED|Raltitrexed|Tomudex|ZD1694|raltitrexed","A quinazoline folate analogue with antineoplastic activity.  After transport into cells via the reduced folate carrier, raltitrexed undergoes intracellular polyglutamation and blocks the folate-binding site of thymidylate synthase, thereby inhibiting tetrahydrofolate activity and DNA replication and repair and resulting in cytotoxicity. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C70792","Ramucirumab","Anti-VEGFR-2 Fully Human Monoclonal Antibody IMC-1121B|Cyramza|IMC-1121B|LY3009806|Monoclonal Antibody HGS-ETR2|RAMUCIRUMAB|Ramucirumab|anti-VEGFR-2 fully human monoclonal antibody IMC-1121B|ramucirumab","A recombinant, fully human monoclonal antibody directed against human vascular endothelial growth factor receptor 2 (VEGFR-2) with antiangiogenesis activity. Ramucirumab specifically binds to and inhibits VEGFR-2, which may result in an inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR-2 is a pro-angiogenic growth factor receptor tyrosine kinase expressed by endothelial cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C67562","Ranibizumab","Immunoglobulin G1, Anti-(Human Vascular Endothelial Growth Factor) Fab Fragment (Human-Mouse Monoclonal rhuFab V2 Gamma1 Chain), Disulfide With Human-Mouse Monoclonal rhuFab V2 Light Chain|Lucentis|RANIBIZUMAB|Ranibizumab","A second-generation, recombinant humanized IgG1 kappa monoclonal antibody fragment directed against human vascular endothelial growth factor (VEGF) alpha. Ranibizumab binds to VEGF alpha and inhibits VEGF alpha binding to its receptors, VEGFR1 and VEGFR2, thereby preventing the growth and maintenance of tumor blood vessels. The molecular weight of this agent (48 kD) is much smaller than the molecular weight of bevacizumab (MW ~149 kD), allowing complete penetration of the retina and the subretinal space following intravitreal injection. In contrast to other anti-VEGF aptamers such as pegaptanib, ranibizumab has a high specificity and affinity for all soluble human isoforms of VEGF.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1515","Ranimustine","Cymer|Cymerin|MCNU|RANIMUSTINE|Ranimustine|Ranomustine|alpha-D-glucopyranoside, methyl 6-((((2-chloroethyl)nitrosoamino)carbonyl)amino)-6-deoxy-|methyl 6-((((2-chloroethyl)nitrosoamino)carbonyl) amino)-6-deoxy-alpha-D-glucopyranoside|methyl 6-(3-(2-chloroethyl)-3-nitrosoiureido)-6-deoxy-alpha-D-glucopyranoside|methyl 6-(3-(2-chloroethyl)-3-nitrosoureido)-6-deoxy-alpha-D-glucopyranoside","A chloroethylnitrosourea derivative that inhibits proliferation and growth of tumor cells by alkylation and cross-linkage of DNA strands of tumor cells. (NCI)","Organic Chemical|Pharmacologic Substance"]
["C66507","Ranolazine","1-Piperazineacetamide, N-(2,6-dimethylphenyl)-4-(2-hydroxy- 3-(2-methoxyphenoxy)propyl)-|RANOLAZINE|Ranexa|Ranolazine","An orally available, piperazine derivative with anti-anginal and potential antineoplastic activities. Ranolazine's mechanism of action for its anti-ischemic effects has yet to be fully elucidated but may involve the alteration of the trans-cellular late sodium current in the ischemic myocyte. By preventing the rise of intracellular sodium levels, ranolazine may affect the transport activity of sodium-dependent calcium channels and prevent the calcium overload during myocardial ischemia, thereby preventing cellular injury. Ranolazine's potential antineoplastic effect may depend on its inhibitory effect on fatty acid oxidation, which may sensitize tumor cells to apoptosis and decrease tumor cell proliferation; fatty acid oxidation provides energy and promotes tumor cell proliferation and survival.","Pharmacologic Substance"]
["C1183","Ranpirnase","Onconase|P-30 Protein|P-30 protein|P-30|P30 Protein|P30|Ranpirnase","A natural homologue of ribonuclease A isolated from the eggs of the frog Rana pipiens.  Ranpirnase primarily degrades cellular transfer RNA with a substrate specificity for uridine-guanidine base-pair sequences, resulting in inhibition of protein synthesis and cytotoxicity. This agent also activates caspase-9 in mitochondria, resulting in tumor cell apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2802","Ras Peptide ASP","Ras Peptide ASP","A synthetic form of the ras peptide containing a point mutation at position 12 (glycine to aspartic acid) with potential antineoplastic activity.  Vaccination with ras peptide Asp may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for this ras mutation, resulting in decreased tumor growth. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2438","RAS Peptide Cancer Vaccine","RAS Peptide Cancer Vaccine","A cancer vaccine containing a RAS oncogene-encoded peptide with potential antineoplastic activity.  RAS peptide cancer vaccine may stimulate a RAS peptide-specific antitumoral T-cell cytotoxic immune response, resulting in an inhibition of tumor cell proliferation and tumor cell death. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C2803","Ras Peptide CYS","Ras (sub 5-17) Peptide (C12)|Ras Peptide CYS","A synthetic form of the Ras peptide containing a point mutation at position 12 (glycine to cysteine) with potential antineoplastic activity.  Vaccination with this peptide may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for this Ras mutation, resulting in decreased tumor growth. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2804","Ras Peptide VAL","Ras Peptide VAL","A synthetic form of the Ras peptide containing a point mutation at position 12 (glycine to valine) with potential antineoplastic activity.  Vaccination with this peptide may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for this Ras mutation, resulting in decreased tumor growth. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C801","Razoxane","ICI 59118|ICRF 159|ICRF-159|ICRF159|RAZOXANE|Razoxane|Razoxin","An orally bioavailable bis-dioxopiperazine and a derivative of the chelating agent ethylenediaminetetraacetic acid (EDTA) with antineoplastic, antiangiogenic, and antimetastatic activities. Razoxane specifically inhibits the enzyme topoisomerase II without inducing DNA strand breaks, which may result in the inhibition of DNA synthesis and cell division in the premitotic and early mitotic phases of the cell cycle. This agent may also exhibit antiangiogenic and antimetastatic activities although the precise molecular mechanisms of these actions are unknown.","Organic Chemical|Pharmacologic Substance"]
["C117289","Realgar-Indigo naturalis Formulation","RIF Formula|RIF|Realgar-Indigo naturalis Formulation","An orally bioavailable, traditional Chinese medicine (TCM)-based formulation composed of Realgar-Indigo naturalis formula (RIF) with potential antineoplastic activity. The main constituents in RIF are realgar, Indigo naturalis, and Salvia miltiorrhiza, with tetraarsenic tetrasulfide (As4S4), indirubin and tanshinone IIA as the main active ingredients, respectively, which appear to exert synergistic effects on cancer cells. Tetraarsenic tetrasulfide specifically induces the ubiquitination and degradation of promyelocytic leukemia retinoic acid receptor alpha (PML-RARalpha) oncoprotein. In addition, the active ingredients in the Realgar-Indigo naturalis formulation enhance the expression of myeloid differentiation genes, and induce G(1)/G(0) cell cycle arrest. PML-RARalpha, an acute promyelocytic leukemia (APL)-specific fusion gene, inhibits differentiation and promotes survival of myeloid precursor cells","Pharmacologic Substance"]
["C82693","Rebastinib Tosylate","DCC-2036|DP-1919.TO|Rebastinib Tosylate","The tosylate salt of rebastinib, an orally bioavailable small-molecule inhibitor of multiple tyrosine kinases with potential antineoplastic activity. Rebastinib binds to and inhibits the Bcr-Abl fusion oncoprotein by changing the conformation of the folded protein to disallow ligand-dependent and ligand-independent activation; in addition, this agent binds to and inhibits Src family kinases LYN, HCK and FGR and the receptor tyrosine kinases TIE-2 and VEGFR-2. Rebastinib may exhibit more potent activity against T315I Bcr-Abl gatekeeper mutant kinases than other Bcr-Abl kinase inhibitors. The TIE-2 and VEGFR-2 receptor tyrosine kinases regulate angiogenesis, respectively, while the Src family kinases Abl, LYN, and HCK Src regulate a variety of cellular responses including differentiation, division, adhesion, and the stress response.","Pharmacologic Substance"]
["C1213","Rebeccamycin","5H-Indolo[2, 3-a]pyrrolo[3,4-c]carbazole-5,7(6H)-dione, 1,11-dichloro-12, 13-dihydro-12-(4-O-methyl-.beta.-D-glucopyranosyl)-|5H-indolo(2,3-a)pyrrolo(3,4-c)carbazole-5,7(6H)-dione,1,11-dichloro-12,13-dihydro-12-(4-O-methyl-beta-D-glucopyranosyl)|BRN 4732638|Rebeccamycin|rebeccamycin","An indolocarbazole glycoside antineoplastic antibiotic isolated from the bacterium Saccharothrix aerocolonigenes.  Rebeccamycin intercalates into DNA and stabilizes the DNA-topoisomerase I complex, thereby interfering with the topoisomerase I-catalyzed DNA breakage-reunion reaction and initiating DNA cleavage and apoptosis. (NCI04)","Antibiotic|Organic Chemical"]
["C1875","Rebimastat","BMS-275291|D2163|N-((2S)-2-Mercapto-1-oxo-4-(3,4,4-trimethyl-2,5-dioxo-1-imidazolidinyl)butyl)-L-leucyl-N,3-dimethyl-L-valinamide|REBIMASTAT|Rebimastat","A sulfhydryl-based second-generation matrix metalloproteinase (MMP) inhibitor with potential antineoplastic activity. Rebimastat selectively inhibits several MMPs (MMP 1, 2, 8, 9, and 14), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis.","Pharmacologic Substance"]
["C71710","Receptor Tyrosine Kinase Inhibitor R1530","MAI R1530|R1530|Receptor Tyrosine Kinase Inhibitor R1530","A pyrazolobenzodiazepine small molecule with potential antiangiogenesis and antineoplastic activities. Mitosis-angiogenesis inhibitor (MAI) R1530 inhibits multiple receptor tyrosine kinases involved in angiogenesis, such as vascular endothelial growth factor receptor (VEGFR)-1, -2, -3, platelet-derived growth factor receptor (PDGFR) beta, FMS-like tyrosine kinase (Flt)-3, and fibroblast growth factor receptor (FGFR) -1, -2. In addition, this agents exhibits anti-proliferative activity by initiating mitotic arrest and inducing apoptosis.","Pharmacologic Substance"]
["C28696","Recombinant 70-kD Heat-Shock Protein","70-kD Heat-Shock Protein|HSP70|Heat Shock Protein 70|Recombinant 70-kD Heat-Shock Protein","A recombinant peptide that is chemically identical to or similar to the endogenous 70-kD heat shock protein (HSP70).  HSP70 is a molecular chaperone that prevents physiologic stress-induced cell death by inhibiting both caspase-dependent and caspase-independent apoptosis.  Because this peptide is often overexpressed in tumor cells, autologous vaccination with HSP70 derived from tumor cells may stimulate the host immune system to mount a tumoricidal cytotoxic T lymphocyte (CTL) response. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116879","Recombinant Adenovirus 5 Encoding Tumor Necrosis Factor-related Apoptosis-Inducing Ligand","Ad5-TNFSF10|Ad5-TRAIL|Recombinant Adenovirus 5 Encoding Tumor Necrosis Factor-related Apoptosis-Inducing Ligand","An adenovirus type 5 (Ad5) encoding human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), with potential apoptosis-inducing and antineoplastic activities. Upon administration of recombinant Ad5 encoding TRAIL, the adenovirus selectively infects tumor cells and expresses TRAIL. The virally expressed TRAIL binds to and activates its receptors TRAIL receptor-1 (TRAIL-R1, death receptor 4, DR4) and TRAIL receptor-2 (TRAIL-R2, death receptor 5, DR5), which subsequently activate caspases and induce apoptosis in TRAIL-R1/R2-expressing tumor cells. The pro-apoptotic cell surface receptors TRAIL-R1 and -R2, members of the TNF receptor family, are overexpressed by a variety of cancer cell types.","Pharmacologic Substance"]
["C85485","Recombinant Adenovirus Encoding p53","Gendicine|Genkaxin|Recombinant Adenovirus Encoding p53|rAd-p53","A replication-defective, recombinant adenoviral vector encoding the wild-type human tumor-suppressor protein p53 gene with potential antineoplastic activity. Upon intratumoral administration, rAD-p53 binds to the coxsackie-and-adenovirus receptor (CAR) on tumor cells and enters cells selectively via receptor-mediated endocytosis, which may result in the overexpression of wild-type p53 intracellularly and p53-mediated tumor regression. In addition, this agent may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) immune response against tumor cells, may activate natural killer (NK) cells to exert antitumor 'bystander effects' and may downregulate the expression of various oncogenes. The p53 protein blocks tumor cell cycle progression and directly initiates apoptosis; the p53 gene, a tumor suppressor gene, is deleted or mutated in a significant number of cancers.","Pharmacologic Substance"]
["C28550","Recombinant Adenovirus-hIFN-beta","Ad-hIFN-beta|BG00001|Recombinant Adenovirus-hIFN-beta","A recombinant replication-defective adenovirus which encodes the gene for the cytokine human interferon-beta (IFN-beta). Once inserted into and replicating in host tumor cells, recombinant adenovirus-hIFN-beta expresses human IFN-beta, which may stimulate an antiproliferative natural killer (NK) cell response against tumor cells and induce caspase-mediated tumor cell apoptosis. (NCI04)","Pharmacologic Substance"]
["C71011","Recombinant Adenovirus-Interferon SCH 721015","Recombinant Adenovirus-Interferon SCH 721015|SCH 721015|rAd-IFN SCH 721015","A replication-deficient recombinant adenovirus encoding human interferon alpha-2b with potential antineoplastic activity. Upon intravesical administration, recombinant adenovirus-interferon SCH 721015 infects nearby tumor cells and expresses INF alpha-2b intracellularly which activates the transcription and translation of genes whose products mediate antiviral, antiproliferative, antitumor, and immune-modulating effects.","Pharmacologic Substance"]
["C104743","Recombinant Adenovirus-Interferon/Syn3","Instiladrin|Recombinant Adenovirus-Interferon With Syn3|Recombinant Adenovirus-Interferon/Syn3|rAd-IFN/Syn3","A non-replicating recombinant adenovirus type 5 (Ad5)-vector encoding the gene for interferon alpha-2b (IFN alpha-2b) and the gene transfer enhancement agent Syn 3, with potential antineoplastic activity. Upon intravesical administration, recombinant adenovirus-interferon with Syn3 transfects both cancerous and normal bladder cells, and the adenovirus secretes interferon (IFN alpha-2b) into the bladder. IFN exerts a direct antitumor killing effect and a bystander effect, thereby killing adjacent, non-transfected cancerous bladder cells. Syn 3 enhances the ability of the adenoviral vector to transfect cells.","Pharmacologic Substance"]
["C49289","Recombinant Adenovirus-L523S Vaccine","Ad/L523S|Recombinant Adenovirus-L523S Vaccine","A replication-defective adenovirus containing a gene that encodes the human protein L523S with potential antineoplastic activity. Upon administration, recombinant adenovirus-L523S vaccine expresses L523S, which may stimulate antibody and cytotoxic T lymphocyte (CTL) responses against tumor cells expressing L523S. L523S is an RNA-binding protein that belongs to the KOC (K homology domain containing protein over-expressed in cancer) family of proteins. As an oncofetal protein, L523S is normally expressed in early embryonic tissues and certain normal adult tissues such as colon, fallopian tube, gall bladder, and ovary tissues but may be overexpressed in squamous cell cancers of the lung.","Pharmacologic Substance"]
["C2423","Recombinant Adenovirus-p53 SCH-58500","ACN53|Recombinant Adenovirus-p53 SCH-58500|SCH 58500|SCH-58500|rAd/p53|recombinant adenovirus-p53","A genetically-engineered adenovirus that contains the gene that encodes the human tumor-suppressor protein p53 with potential antineoplastic activity. Recombinant adenovirus-p53 SCH-58500 delivers p53 into tumor cells, which may result in p53-mediated cell cycle arrest and apoptosis.","Pharmacologic Substance"]
["C116880","Recombinant Anti-WT1 Immunotherapeutic GSK2302024A","ASCI GSK2302024A|GSK2302024A|Recombinant Anti-WT1 Immunotherapeutic GSK2302024A","An immunotherapeutic composed of the Wilms tumor 1 (WT1) and an as of yet undisclosed adjuvant, with potential antineoplastic activity. Upon administration, the immune system may be stimulated to exert a cytotoxic T-lymphocyte (CTL) response against WT1-expressing tumor cells. The adjuvant stimulates the immune system's response to WT1. WT1, a tumor-associated antigen (TAA) and transcription factor, is overexpressed in a variety of tumor cell types.","Pharmacologic Substance"]
["C91096","Recombinant Attenuated Salmonella typhimurium Expressing IL-2","Recombinant Attenuated Salmonella typhimurium Expressing IL-2","An orally available, genetically engineered Salmonella typhimurium strain expressing a truncated form of the human cytokine interleukin-2 (IL-2) gene, with antitumor activity. Upon administration of recombinant attenuated S. typhimurium expressing IL-2 (SalpIL2), this Salmonella strain may selectively accumulate and divide in a variety of tumor types, and express IL-2. In turn, IL-2 may induce natural killer (NK) cell proliferation thereby enhancing their activity. This may inhibit the growth of tumor cells.","Bacterium|Pharmacologic Substance"]
["C96735","Recombinant B. pertussis Adenylate Cyclase Toxin-Tyrosinase A2 Epitope Vaccine","Recombinant B. pertussis Adenylate Cyclase Toxin-Tyrosinase A2 Epitope Vaccine|Recombinant Bordetella pertussis Adenylate Cyclase Toxin-Tyrosinase.A2 Epitope YMDGTMSQV Vaccine","A recombinant vaccine containing a genetically detoxified adenylate cyclase toxin (CyaA) of Bordetella pertussis coupled, through its catalytic site, to the melanoma tyrosinase A2 epitope YMDGTMSQV, with potential antineoplastic activity. Via the toxin moiety, the recombinant B. pertussis adenylate cyclase toxin-tyrosinase A2 epitope specifically binds to the alphaMbeta2 integrin (CD11b/CD18) located on CD11b-positive antigen-presenting cells (APC). Upon processing and presentation of the melanoma-specific epitope by MHC class I molecules to the surface of these APCs, a specific cytotoxic T-cell (CTL) response against tumor cells expressing tyrosinase may be initiated, resulting in decreased tumor growth and cell lysis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C60882","Recombinant Bispecific Single-Chain Antibody rM28","Recombinant Bispecific Single-Chain Antibody rM28|rM28","A recombinant, bispecific, single-chain antibody directed against both the T-cell surface-associated costimulatory molecule CD28 and a melanoma-associated proteoglycan (MAPG) with potential antitumor activity. By targeting both CD28 and MAPG, recombinant bispecific single-chain antibody rM28 enhances cytotoxic T-cell recognition of melanoma cells, which may result in immune effector cell-mediated tumor cell death and a decrease in distant metastases. This agent appears to have a long serum half-life secondary to the formation of dimers. When activated, CD28 facilitates interactions between T-cells and other immune effector cells resulting in cytotoxic T-lymphocyte responses; MAPG is a surface antigen expressed on the majority of melanomas, including primary cutaneous, ocular, and metastatic melanomas.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1437","Recombinant CD40-Ligand","CD154 antigen|CD40L|Recombinant CD40-Ligand|T-BAM|T-Cell Antigen gp39|TNF-Related Activation Protein|TRAP Ligand|gp39|rhu CD40L","A recombinant therapeutic agent which is chemically identical to or similar to CD40-ligand. CD40-ligand, also known as CD40L/TRAP and CD154, is a type II membrane protein which binds to CD40, a cell surface receptor that belongs to the tumor necrosis factor receptor family; CD40 is expressed on B lymphocytes, monocytes, dendritic cells (DC), hematopoietic progenitors, endothelial cells and epithelial cells. Recombinant CD40-ligand may be used to activate DC ex vivo via CD40 binding; CD40-ligand-activated DC may provide or augment a protective antitumor immunity when administered in dendritic cell cancer vaccines. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C49177","Recombinant dHER2 Vaccine","Recombinant dHER2 Vaccine","A cancer vaccine consisting of a truncated recombinant HER2 peptide (dHER2) with potential antineoplastic activity. Upon administration, recombinant dHER2 vaccine may stimulate the host immune response to mount a cytotoxic T-lymphocyte response against tumor cells that overexpress the HER2 protein, resulting in tumor cell lysis. The HER2 protein is a tumor-associated antigen (TAA) that is overexpressed in a variety of cancers. dHER2 includes the extracellular domain (ECD) and a part of the intracellular domain (ICD) of the HER2 protein.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C49290","Recombinant DNA-L523S Vaccine","Recombinant DNA-L523S Vaccine|pVAX/L523S","A plasmid DNA encoding human L523S, an RNA-binding protein that belongs to the KOC (K homology domain containing protein overexpressed in cancer) family, with potential antineoplastic activity. Vaccination with L523S DNA may stimulate a cytotoxic T lymphocytes (CTL) response against tumor cells that express the L523S protein. As an oncofetal protein, L523S is normally expressed in early embryonic tissue, but is overexpressed in certain cancer cell types.","Pharmacologic Substance"]
["C102569","Recombinant EphB4-HSA Fusion Protein","Recombinant EphB4-HSA Fusion Protein|sEphB4-HSA","A recombinant fusion protein composed of the full-length extracellular domain (soluble) of human receptor tyrosine kinase ephrin type-B receptor 4 (sEphB4) and fused, at its C-terminus, to full-length human serum albumin (HSA), with potential antineoplastic and anti-angiogenic activities. sEphB4-HSA functions as a decoy receptor for the membrane-bound ligand Ephrin-B2 (Efnb2) and interferes with the binding of Efnb2 to its native receptors, including EphB4 and EphA3. This may result in a reduction of angiogenesis and a reduction in cell growth of Efnb2 and/or EphB4 over-expressing tumor cells. In addition, this agent also prevents the angiogenic effects of numerous growth factors due to interactions between Efnb2 and EphB4. Efnb2 and EphB4 are overexpressed in a variety of tumor cell types; the bi-directional signaling of Efnb2-EphB4 plays an important role in angiogenesis and tumor cell migration, invasion, and proliferation. Albumin reduces this agent's degradation, improves circulation time and may thus improve efficacy.","Pharmacologic Substance"]
["C1538","Recombinant Fas Ligand","FAS-Ligand|Fas Ligand|Fas-L|Recombinant Fas Ligand","A recombinant agent, which is chemically identical to or similar to the endogenous protein Fas ligand, a protein related to tumor necrosis factor (TNF) with potential antineoplastic activity.  Fas ligand binds to the Fas receptor, thereby activating caspases and inducing apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2686","Recombinant Fowlpox GM-CSF Vaccine Adjuvant","Fowlpox-Sargramostim|Recombinant Fowlpox GM-CSF Vaccine Adjuvant|rF-GM-CSF|rF-Sargramostim","A cancer vaccine adjuvant consisting of a recombinant fowlpox virus encoding human granulocyte-macrophage colony-stimulating factor (GM-CSF). GM-CSF binds to specific cell surface receptors on various immuno-hematopoietic cell types, enhancing their proliferation and differentiation and stimulating macrophage and dendritic cell functions in antigen presentation and antitumor cell-mediated immunity. Administration of recombinant fowlpox GM-CSF vaccine adjuvant may induce an immune response against tumor cells. Fowlpox virus is an attractive vector because its genome is easy to manipulate and it is replication incompetent in mammalian cells.","Pharmacologic Substance|Virus"]
["C2666","Recombinant Fowlpox-B7.1 Vaccine","Recombinant Fowlpox-B7.1 Vaccine|Recombinant Fowlpox-B7.1|rF-B7.1 Vaccine|rF-B7.1","A cancer vaccine comprised of a recombinant fowlpox virus vector encoding the stimulatory molecule transgene B7-1. Recombinant fowlpox-B7.1 vaccine may enhance antigen presentation and activate antitumoral cytotoxic T-cells. (NCI04)","Pharmacologic Substance|Virus"]
["C2620","Recombinant Fowlpox-CEA(6D)/TRICOM Vaccine","Recombinant Fowlpox-CEA(6D)/TRICOM Vaccine|Recombinant Fowlpox-CEA-TRICOM Vaccine|fowlpox-CEA-B7.1/ICAM-1/LFA-3|rF-CEA(6D)TRICOM","A cancer vaccine comprised of a recombinant fowlpox virus vector encoding the carcinoembryonic antigen (CEA) and a TRIad of COstimulatory Molecules (B7-1, ICAM-1 and LFA-3) (TRICOM). This agent may enhance CEA presentation to antigen presenting cells (APC) and activate cytotoxic T-cells against CEA-expressing tumors. (NCI04)","Pharmacologic Substance|Virus"]
["C2805","Recombinant Fowlpox-Mgp100 Vaccine","Recombinant Fowlpox-Mgp100 Vaccine|rF-Mgp100 Vaccine","A vaccine consisting of a replication-defective recombinant fowlpox virus that encodes for the murine melanoma antigen glycoprotein 100 (mgp100) with potential antineoplastic activity.  Vaccination with recombinant fowlpox-mgp100 vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for the gp100 antigen, resulting in decreased tumor growth. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C2675","Recombinant Fowlpox-Prostate Specific Antigen Vaccine","Fowlpox-PSA Vaccine|Recombinant Fowlpox-PSA Vaccine|Recombinant Fowlpox-PSA|Recombinant Fowlpox-Prostate Specific Antigen Vaccine|Recombinant Fowlpox-Prostate Specific Antigen|rF-PSA","A cancer vaccine consisting of a recombinant fowlpox virus encoding human prostate-specific antigen (PSA). Administration of this agent may stimulate a cytotoxic T cell response against PSA-expressing tumor cells. Fowlpox virus is an attractive vector because its genome is easy to manipulate and it is replication incompetent in mammalian cells. (NCI04)","Immunologic Factor|Pharmacologic Substance|Virus"]
["C29560","Recombinant Fowlpox-PSA(L155)/TRICOM Vaccine","PROSTVAC-F|Recombinant Fowlpox-PSA(L155)/TRICOM Vaccine|rFowlpox-PSA(L155)/TRICOM Vaccine","A cancer vaccine consisting of a recombinant fowlpox virus encoding fragment of human prostate-specific antigen (PSA), PSA:154-163 (155L), and a TRIad of COstimulatory Molecules (B7-1, ICAM-1 and LFA-3) (TRICOM).  Administration of this agent may induce a cytotoxic T cell response against PSA-expressing tumor cells. Dendritic cells infected with TRICOM vectors greatly enhance naive T-cell activation and peptide-specific T-cell stimulation. Fowlpox virus is an attractive vector because its genome is easy to manipulate and it is replication incompetent in mammalian cells.","Pharmacologic Substance"]
["C2807","Recombinant Fowlpox-Tyrosinase Vaccine","Recombinant Fowlpox-Tyrosinase Vaccine|Tyrosinase-Fowl Pox|rF-TYR vaccine|rF-TYR","A recombinant fowlpox virus vaccine with potential antineoplastic activity. Binding to the melanoma antigen tyrosinase, recombinant fowlpox-tyrosinase vaccine generates cellular immune responses against melanoma cells expressing the tyrosinase antigen; this effect is enhanced by the co-administration of interleukin 2 (IL-2). Fowlpox virus is an attractive vector because its genome is easy to manipulate and it is replication incompetent in mammalian cells.","Pharmacologic Substance|Virus"]
["C2257","Recombinant Fractalkine","CX3CL1|Fractalkine|Neurotactin|Recombinant Fractalkine","A pro-inflammatory delta chemokine with potential antineoplastic activity.  Fractalkine induces the adhesion and migration of T lymphocytes, monocytes and natural killer (NK) cells.  In lymphomas, this agent may promote cell-mediated lympholysis by recruiting activated NK cells. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1792","Recombinant Human 6Ckine","6ckine|CCL21|Exodus-2|Recombinant Human 6Ckine|Recombinant Secondary Lymphoid-Tissue Chemokine|Secondary Lymphoid-Tissue Chemokine|TCA4|ck beta 9","A therapeutic recombinant analogue of a member of the endogenous CC chemokines with potential antineoplastic activity. Expressed by various lymphoid tissues, endogenous 6Ckine is chemotactic for B and T lymphocytes and dendritic cells.","Immunologic Factor|Pharmacologic Substance"]
["C107504","Recombinant Human Adenovirus Type 5 H101","H101|Oncorine|Recombinant Human Adenovirus Type 5 H101|rAd5 H101","A replication selective, recombinant, E1B and partial E3 gene deleted form of human adenovirus type 5, with potential antineoplastic activity. Upon intratumoral injection of recombinant human adenovirus type 5, the adenovirus selectively replicates in cancer cells while preventing viral replication in normal, healthy cells. This induces a selective adenovirus-mediated cytotoxicity in cancer cells, which leads to cancer cell lysis. In addition, viral spread to adjacent cells, following lysis of infected cells, may activate the immune system to kill the infected tumor cells. The E1B protein causes p53 inactivation, which promotes viral replication; deletion of E1B allows for p53 activation in normal cells, which prevents viral replication in normal, healthy cells. The mutation and subsequent inactivation of p53 in cancer cells enables the E1B-deleted adenovirus to selectively replicate in cancer cells. Partial deletion of E3, encoding the adenovirus death protein, enhances the safety profile of the administered adenovirus.","Pharmacologic Substance"]
["C85447","Recombinant Human Angiotensin Converting Enzyme 2 APN01","APN01|Recombinant Human Angiotensin Converting Enzyme 2 APN01|rhACE2 APN01","A recombinant, soluble glycosylated form of human angiotensin converting enzyme 2 (rhACE2) with antihypertensive and potential antineoplastic activities. Recombinant human angiotensin converting enzyme 2 APN01 may normalize ACE2 levels, cleaving angiotensin II to create angiotensin-(1-7) and restoring the function of the renin-angiotensin system (RAS). ACE2, a homolog of ACE1, appears to function as a negative regulator of the RAS system by converting angiotensin II to angiotensin-(1-7), a peptide with actions that counteract the cardiovascular actions of angiotensin II. In addition, angiotensin-(1-7) may inhibit cyclooxygenase 2 (COX-2) and the production of proinflammatory prostaglandins and may activate the angiotensin-(1-7) G protein-coupled receptor Mas, resulting in diminished tumor cell proliferation. ACE2 levels may be reduced in malignancy and diabetes and in liver, cardiovascular and lung diseases.","Pharmacologic Substance"]
["C84873","Recombinant Human Anti-TGF-beta Monoclonal Antibody","GC1008|Recombinant Human Anti-TGF-beta Monoclonal Antibody|Recombinant Human Anti-Transforming Growth Factor-beta Monoclonal Antibody","A recombinant human IgG4 monoclonal antibody directed against transforming growth factor-beta (TGFb) with potential antineoplastic activity. Recombinant human anti-TGF-beta monoclonal antibody specifically targets and binds to all 3 isoforms of TGFb, thereby neutralizing TGFb isoforms 1, 2 and 3. This prevents activation of TGFb-mediated signaling pathways. TGFb, a pleiotropic cytokine, is often overexpressed in a number of cancer cell types and is involved in cancer cell proliferation, differentiation, migration, invasion and angiogenesis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116864","Recombinant Human Apolipoprotein(a) Kringle V MG1102","MG1102|Recombinant Human Apo (a) Kringle V MG1102|Recombinant Human Apolipoprotein(a) Kringle V MG1102","An 86 amino-acid long polypeptide fragment of a recombinant form of human apolipoprotein (a) (apo(a)) kringle V, with potential anti-angiogenic and antineoplastic activities. Although the exact mechanism of action has yet to be fully elucidated, upon administration, recombinant human apo(a) kringle V MG1102 inhibits the fibronectin-mediated migration of endothelial cells, binds to and blocks the activity of alpha 3 beta 1 integrin (a3b1 integrin), inhibits the activation of focal adhesion kinase (FAK) and FAK-mediated signaling, and leads to the inhibition of the p130 Crk-associated substrate (p130CAS)-c-Jun NH2-terminal kinase (JNK) pathway. This inhibits tumor angiogenesis, induces mitochondrial-mediated apoptosis of tumor cells and tumor-associated endothelial cells, and suppresses tumor growth and metastasis. Apo(a), a glycoprotein component of human lipoprotein(a), contains repeated kringle domains; certain kringle domains of apo(a), including the plasminogen kringle V homolog (KV), have anti-angiogenic effects.","Pharmacologic Substance"]
["C70674","Recombinant Human EGF-rP64K/Montanide ISA 51 Vaccine","CIMAvax EGF|CIMAvax Epidermal Growth Factor Vaccine|CIMAvax-EGF|Center of Molecular Immunology (CIMA) Epidermal Growth Factor (EGF) Vaccine|Center of Molecular Immunology Epidermal Growth Factor Vaccine|CimaVax|Cimavax|Recombinant Human EGF-P64K/Montanide Vaccine|Recombinant Human EGF-rP64K/Montanide ISA 51 Vaccine","A peptide vaccine preparation, containing recombinant human epidermal growth factor (rEGF) linked to the Neisseria meningitidis-derived recombinant immunogenic carrier protein P64k (rP64k) and mixed with the immunoadjuvant Montanide ISA 51, with potential active immunotherapy activity. Recombinant human EGF-rP64K/Montanide ISA 51 vaccine may trigger a humoral immune response against vaccine rEGF and rP64K and, so, against endogenous EGF. Antibody-mediated inhibition of endogenous EGF binding to its receptor, epithelial growth factor receptor (EGFR), may result in the inhibition of tumor cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C45515","Recombinant Human Endostatin","Endostar|Endostatin|Recombinant Endostatin|Recombinant Human Endostatin|endostatin|rhEndostatin","A recombinant human proteolytic fragment of the C-terminal end of type XVIII collagen. Endostatin induces microvascular endothelial cell apoptosis and inhibits endothelial proliferation and angiogenesis, which may result in a reduction in tumor burden. This agent also may decrease hepatic metastasis by inhibiting proinflammatory cytokines and vascular cell adhesion molecule (VCAM)-dependent cell attachment to the hepatic microvasculature.  (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C94210","Recombinant Human Fusion Protein L19TNFalpha","L19-TNF-alpha|Recombinant Human Fusion Protein L19TNFalpha","An immunocytokine consisting of human pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) fused to a human single-chain variable fragment (scFv) directed against the extra-domain B (ED-B) of fibronectin (L19), with potential immunopotentiating and antineoplastic activities. The L19 moiety of recombinant human fusion protein L19TNFalpha binds to the ED-B domain of fibronectin on tumor cells in the tumor neovasculature. In turn, the TNFalpha moiety may locally induce an immune response against ED-B fibronectin-expressing tumor cells and may specifically decrease the proliferation of ED-B-expressing tumor cells. ED-B is predominantly expressed during angiogenesis and tumor growth.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C103830","Recombinant Human Hsp110-gp100 Chaperone Complex Vaccine","Recombinant Human Hsp110-gp100 Chaperone Complex Vaccine","A recombinant chaperone-peptide complex-based vaccine composed of a complex between heat shock protein hsp110 and the human melanoma-associated antigen gp100, with potential antineoplastic activity. Upon vaccination, recombinant hsp110-gp100 chaperone complex activates the immune system to exert a cytotoxic T cell immune response and antigen-specific interferon-gamma production against gp100-overexpressing cancer cells. Gp100, is overexpressed in a variety of cancer cell types. Hsp110, binds to and chaperones full-length proteins during heat shock; as an immunoadjuvant it is able to enhance an immune response against antigen(s) and stimulate T-lymphocyte activation.","Pharmacologic Substance"]
["C102782","Recombinant Human MUC1-Oxidized Polymannose-pulsed Autologous Dendritic Cell Vaccine","Recombinant Human MUC1-Oxidized Polymannose-pulsed Autologous Dendritic Cell Vaccine","A cancer vaccine containing autologous dendritic cells pulsed with a fusion product of an epitope of human tumor-associated epithelial mucin 1 (MUC1) antigen and the vaccine adjuvant mannan (oxidized mannose), with potential antineoplastic activity. When the modified dendritic cells are returned to the patient, they may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells positive for the MUC1 antigen, resulting in tumor cell lysis. Addition of manna in this vaccine, enhances immune recognition. MUC1 antigen, a high-molecular-weight transmembrane glycoprotein, is overexpressed on many tumor cells.","Cell|Pharmacologic Substance"]
["C119664","Recombinant Human Papillomavirus Nonavalent Vaccine","Gardasil 9|Nonavalent HPV VLP Vaccine|Recombinant HPV Nonavalent Vaccine|Recombinant Human Papillomavirus 9-valent Vaccine|Recombinant Human Papillomavirus Nonavalent Vaccine","A non-infectious, recombinant, nonavalent vaccine prepared from highly purified virus-like particles (VLPs) comprised of the major capsid (L1) proteins from human papillomavirus (HPV) types 6, 11, 16, 18, 31, 33, 45, 52, and 58, with active immunizing activity. Upon administration, the recombinant HPV nonavalent vaccine activates the immune system to produce antibodies against the 9 HPV types. This protects against HPV infection and HPV-related cancers. Altogether, HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58 account for the majority of the HPV types that cause cervical, vulvar, vaginal and anal cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C584","Recombinant Interferon","Human Leukocyte Interferon|Human Lymphoblastoid Interferon|Human lymphoblastoid interferon|IFN|Interferons|Recombinant Interferon","One of a group of recombinant therapeutic glycoprotein cytokines with antiviral, anti-proliferative, and immunomodulating activities. Interferons bind to specific cell-surface receptors, leading to the transcription and translation of genes with interferon-specific response elements (ISREs). The resultant proteins mediate many complex effects, ultimately leading to inhibition of viral protein synthesis and cellular growth, alteration of cellular differentiation, interference with oncogene expression, activation of natural killer cells, alteration of cell surface antigen expression, and augmentation of lymphocyte and macrophage cytotoxicity. The production of endogenous interferons is induced in response to foreign agents such as bacteria, viruses and parasites and to tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C225","Recombinant Interferon Alfa","Alferon|Alpha Interferon|Interferon Alfa|Leukocyte Interferon|Lymphoblast Interferon|Lymphoblastoid Interferon|Recombinant Interferon Alfa|alpha-Interferon","A class of naturally-isolated or recombinant therapeutic peptides used as antiviral and anti-tumor agents.  Alpha interferons are cytokines produced by nucleated cells (predominantly natural killer (NK) leukocytes) upon exposure to live or inactivated virus, double-stranded RNA or bacterial products.  These agents bind to specific cell-surface receptors, resulting in the transcription and translation of genes containing an interferon-specific response element.  The proteins so produced mediate many complex effects, including antiviral effects (viral protein synthesis); antiproliferative effects (cellular growth inhibition and alteration of cellular differentiation); anticancer effects (interference with oncogene expression); and immune-modulating effects (natural killer cell activation, alteration of cell surface antigen expression, and augmentation of lymphocyte and macrophage cytotoxicity). (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C53411","Recombinant Interferon Alfa-1b","IFN-alfa-1b|INTERFERON ALFA-1B|Interferon Alfa-1b|Recombinant Interferon Alfa-1b|Recombinant Interferon Alpha-1b","The non-glycosylated recombinant interferon alpha, subtype 1b, with immunostimulatory and antineoplastic activities. Alpha interferon-1b binds to specific cell-surface receptors, resulting in the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1952","Recombinant Interferon Alfa-2a","Alpha 2 Interferon|IFN alpha-2A|IFN-Alpha 2|INTERFERON ALFA-2A|Interferon alfa 2a|Laroferon|Recombinant Interferon Alfa-2a|Recombinant Interferon Alpha-2a|Roceron-A|Roferon A|rHuIFN-a 2a","A non-glycosylated recombinant human alpha interferon, subtype 2a, produced in the bacterium E. coli.  Interferon alpha-2a binds to its specific cell-surface receptor, resulting in the transcription and translation of genes whose protein products have antiviral, antiproliferative, anticancer, and immune modulating effects. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1953","Recombinant Interferon Alfa-2b","Alfatronol|Glucoferon|Heberon Alfa|IFN alpha-2B|INTERFERON ALFA-2B|Interferon Alfa-2B|Interferon Alpha-2b|Interferon alfa 2b|Intron A|Recombinant Interferon Alfa-2b|Sch 30500|Urifron|Viraferon|interferon alfa-2b|recombinant interferon alfa-2b","A non-glycosylated recombinant interferon with antiviral and antineoplastic activities. Alfa interferons bind to specific cell-surface receptors, resulting in the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C97503","Recombinant Interferon Alpha 2b-like Protein","Novaferon|Recombinant IFN Alfa-2b-like Protein|Recombinant Interferon Alpha 2b-like Protein","A proprietary recombinant protein highly resembling human interferon alpha 2b (IFN-a2b), with potential anti-tumor, anti-inflammatory, immunomodulating and antiviral activities. Upon injection, recombinant IFN alpha 2b-like protein binds to specific IFN alpha cell surface receptors. This activates interferon-mediated signal transduction pathways and induces the transcription and translation of genes with interferon-specific response elements (ISREs). This may activate the immune system, including the activation of natural killer cells (NKs) and may result in an inhibition of tumor cell proliferation, tumor angiogenesis, metastasis and an induction of apoptosis. Compared to human IFN-a2b (HuINF-a2b), this agent exhibits enhanced antiviral and antiproliferative activities. In addition, this agent exhibits antiviral activity against a variety of viruses, including hepatitis B and C viruses, human immunodeficiency virus (HIV) and Avian Influenza.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C495","Recombinant Interferon Beta","Beta Interferon|Betantrone|Feron|Human Interferon Beta|Interferon Beta|Interferon, Beta|Interferon-B|Interferon-beta|Naferon|Recombinant Interferon Beta","A recombinant protein which is chemically identical to or similar to endogenous interferon beta with antiviral and anti-tumor activities. Endogenous interferons beta are cytokines produced by nucleated cells (predominantly natural killer cells) upon exposure to live or inactivated virus, double-stranded RNA or bacterial products. These agents bind to specific cell-surface receptors, resulting in the transcription and translation of genes with an interferon-specific response element. The proteins so produced mediate many complex effects, including antiviral (the most important being inhibition of viral protein synthesis), antiproliferative and immune modulating effects. The recombinant therapeutic forms of interferon beta are interferon beta 1-a and interferon beta 1-b. (NCI05)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C583","Recombinant Interferon Gamma","Gamma Interferon (GEN)|Gamma Interferon-SCH|Gamma-Interferon|Ginterferon|IFN-g|Interferon Gamma (BIO)|Interferon Gamma|Interferon, Gamma|Recombinant Interferon Gamma","A recombinant therapeutic agent which is chemically identical to or similar to the endogenous lymphokine interferon gamma (IFN-gamma) with antineoplastic, immunoregulatory, and antiviral activities. Therapeutic IFN-gamma binds to and activates the cell-surface IFN-gamma receptor, stimulating antibody-dependent cytotoxicity and enhances natural killer cell attachment to tumor cells. This agent also activates caspases, thereby inducing apoptosis in malignant cells. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1380","Recombinant Interleukin-12","Cytotoxic Lymphocyte Maturation Factor|IL-12|Interleukin 12|Interleukin-12|NM-IL-12|Natural Killer Cell Stimulatory Factor|Recombinant Interleukin-12|Recombinant human interleukin-12 (IL-12) cytokine|Ro 24-7472|interleukin-12","A recombinant form of the endogenous heterodimeric cytokine interleukin-12 with potential antineoplastic activity.  Recombinant interleukin-12 binds to and activates its cell-surface receptor, stimulating the production of interferon-gamma (IFN) which, in turn, induces IFN-gamma-inducible protein-10 (IP-10) and so inhibits tumor angiogenesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1489","Recombinant Interleukin-13","IL-13|Interleukin 13|Recombinant Interleukin-13","The recombinant analogue of an endogenous cytokine interleukin 13 with potential antineoplastic activity. Produced by lymphocytes and exhibiting a variety of functions, interleukin-13 (therapeutic) inhibits DNA synthesis and regulates inflammatory and immune responses. In animal models, this agent has been shown to kill tumor cells both directly and indirectly by activating the host immune system at the tumor site. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1680","Recombinant Interleukin-18","IFN-Gamma-Inducing Factor|IL-18|Interferon-Gamma-Inducing Factor|Interleukin-18|Recombinant Interleukin-18","A recombinant therapeutic agent which is chemically identical to or similar to the endogenous cytokine interleukin-18 (IL-18). Produced primarily by macrophages, IL-18 induces the production of interferon-gamma (IFN-gamma), and enhances the activity of natural killer (NK) and cytotoxic T lymphocytes (CTL).  As a potential immunotherapeutic agent, IL-18 displays antitumor effects in vitro and in animal models. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C591","Recombinant Interleukin-6","B Cell Differentiation Factor 2|B-Cell Stimulatory Factor-2|HPGF|HSF|Hepatocyte Stimulating Factor|Hybridoma Growth Factor|IFN Beta 2|IL-6|Interleukin-6|Myeloid Differentiation Inducing Protein|Plasmacytoma Growth Factor|Recombinant Interleukin-6|Sigosix","A recombinant therapeutic agent which is chemically identical to or similar to the endogenous cytokine interleukin-6 (IL-6) with antiapoptotic, proinflammatory, antiinflammatory, proproliferative and proangiogenic activities. IL-6 binds to its receptor (IL-6R), activating a receptor-CD130 receptor complex; the CD130 portion of the complex is a signal transduction protein that activates JAK kinases and Ras-mediated signaling pathways, which in turn activate downstream signaling pathways, resulting in the activation of various transcription factors (STAT, ELK-1, NF-IL-6, etc.) and gene transcription. The physiological effects of IL-6 are complex and varied and include hematopoietic, pyrogenic and thermogenic, proinflammatory, antiinflammatory, proproliferative (anti-apoptotic), and angiogenic effects.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C28721","Recombinant KSA Glycoprotein","CO17-1A|EGP|Ep-CAM|GA733|KSA Glycoprotein|Recombinant KSA Glycoprotein","A recombinant counterpart of tumor-associated KSA antigen (Ep-CAM), a type-I transmembrane glycoprotein cellular adhesion molecule with a molecular mass of 40 kDa, overexpressed on the majority of tumor cells of most human epithelia in a of variety of tumor tissues such as stomach, colon, pancreas, gall bladder, bile duct, mammary gland, breast, and lung carcinoma. It has been suggested to be involved in the differentiation, growth, and organization of epithelial cells within tissues under normal physiological conditions. The antigen has been used as a target for diagnosis and for passive and active immunotherapy of colorectal cancer. Immunization with KSA Glycoprotein elicits both humoral and Th1-associated cellular immune responses.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2413","Recombinant Leukocyte Interleukin","BC-IL|Buffy Coat Interleukin|Leukocyte Interleukin, Inj.|Multikine|Recombinant Leukocyte Interleukin","A cocktail preparation of synthetic interleukin (IL) -1, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, interferon gamma and other cytokines that are chemically identical to or similar to signaling molecules secreted by leukocyte cells. Leukocyte interleukins are essential in many immune responses, such as antibodies production, modulating secretion of other cytokines, and activation of bone marrow stem cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1143","Recombinant Leukoregulin","Recombinant Leukoregulin","A formulated therapeutic analog of the endogenous lymphokine leukoregulin with potential antineoplastic activity.  Leukoregulin displays direct and indirect cytotoxicity through tumor cell lysis and enhancing tumor cell susceptibility to natural killer cell-mediated cytotoxicity.  This agent enhances membrane permeability and decreases p-glycoprotein expression, thereby promoting cytotoxic drug uptake into tumor cells.  Leukoregulin also induces the synthesis of collagenase and hyaluronan, expression and secretion of interleukin-8, and upregulates stromelysin-1 gene expression in human fibroblasts, thereby regulating extracellular matrix degradation. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1290","Recombinant Macrophage Colony-Stimulating Factor","Macrophage Colony Stimulating Factor|Recombinant Colony Stimulating Factor 1|Recombinant Macrophage Colony-Stimulating Factor|rM-CSF","A recombinant therapeutic agent which is chemically identical to or similar to the endogenous protein cytokine macrophage colony-stimulating factor (M-CSF). Synthesized endogenously by mesenchymal cells, M-CSF stimulates the survival, proliferation, and differentiation of hematopoietic cells of the monocyte-macrophage series and can reverse treatment-related neutropenias. Recombinant M-CSF may also enhance antigen presentation and activate antitumoral cytotoxic T-cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C38724","Recombinant MAGE-3.1 Antigen","MAGE-3.1|MAGE-3|Recombinant MAGE-3.1 Antigen","A recombinant tumor-specific melanoma antigen. Vaccination with recombinant MAGE-3.1 antigen may induce a host immune response against MAGE-expressing cells, resulting in antitumoral T cell-mediated cytotoxicity. MAGE-expressing cells are found in melanoma, non-small-cell lung carcinoma (NSCLC), head and neck squamous cell carcinoma, transitional cell carcinoma of the bladder, and esophageal carcinoma. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C98294","Recombinant MIP1-alpha Variant ECI301","ECI301|Recombinant MIP1-alpha Variant ECI301|eMIP","A recombinant form of a human macrophage inflammatory protein-1 alpha (MIP1-alpha) with a substitution of aspartate to alanine at position 26, with potential immunomodulating and radiotherapy potentiating activity. Intravenous administration of recombinant MIP1-alpha variant ECI301 after local tumor irradiation enhances the anti-tumor effect of ionizing radiation at the irradiated site as well as the antitumor effect at non-irradiated tumor sites (known as the abscopal effect). The abscopal effect appears to be attributed to this agent's ability to recruit and activate leukocytes, such as monocytes, dendritic cells, natural killer cells and T lymphocytes, thereby initiating an anti-tumor immune response against cancer cells. MIP1-alpha, also known as chemokine (C-C motif) ligand 3, is a ligand for the chemokine receptors CCR1, CCR4 and CCR5 that are involved in immune and inflammatory responses.","Pharmacologic Substance"]
["C49087","Recombinant Modified Vaccinia Ankara-5T4 Vaccine","Recombinant MVA-5T4 Vaccine|Recombinant Modified Vaccinia Ankara-5T4 Vaccine|Recombinant Pox Virus Encoding 5T4 Vaccine|TroVax","A cancer vaccine comprised of a recombinant modified vaccinia Ankara (MVA) viral vector encoding the 5T4 fetal oncoprotein (MVA-h5T4). Vaccination with recombinant modified vaccinia Ankara-5T4 vaccine may stimulate the host immune system to mount a humoral and cytotoxic T lymphocyte (CTL) response against tumor cells expressing 5T4 fetal oncoprotein antigen, resulting in tumor cell lysis. The MVA viral vector, derived from the replication-competent strain Ankara, is a highly attenuated, replication-defective vaccinia strain incapable of virion assembly.","Pharmacologic Substance"]
["C69129","Recombinant Nematode Anticoagulant Protein c2","Recombinant Nematode Anticoagulant Protein c2|rNAPc2","An 85-amino acid recombinant peptide derived from protein c2 of the hemophagocytic hookworm Ancylostoma caninum (a common canine parasite) with anticoagulant activity. Recombinant nematode anticoagulant protein c2 (rNAPc2) binds to circulating activated factor X (FXa) or zymogen factor X (FX) to form a binary complex which subsequently binds to and inhibits membrane-bound activated factor VII/tissue factor complex (FVIIa/TF). When administered prophylactically, this agent may reduce the incidence of deep venous thrombosis without hemostatic compromise. Because rNAPc2 inhibits the formation of the FVIIa/TF protease complex, which may play a role in the cellular signaling of both metastatic and angiogenic processes, it may impede tumor progression.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C99459","Recombinant Oncolytic Poliovirus PVS-RIPO","PVS-RIPO|PVSRIPO|Recombinant Oncolytic Poliovirus PVS-RIPO","A recombinant, live attenuated, nonpathogenic oncolytic virus containing the oral poliovirus Sabin type 1 in which the internal ribosomal entry site (IRES) is replaced with the IRES from human rhinovirus type 2 (HRV2), with potential antineoplastic activity. Upon intratumoral administration of recombinant oncolytic poliovirus PVS-RIPO, the poliovirus is selectively taken up by and replicates in tumor cells expressing CD155 (poliovirus receptor, PVR or NECL5) eventually causing tumor cell lysis. CD155, an oncofetal cell adhesion molecule and tumor antigen, is ectopically expressed in certain cancers, such as glioblastoma multiforme (GMB), and plays an important role in tumor cell migration, invasion, and metastasis. Due to the heterologous HRV2 IRES in this recombinant virus, PVS-RIPO only propagates in susceptible, nonneuronal cells (e.g., GBM).","Pharmacologic Substance|Virus"]
["C2251","Recombinant Platelet Factor 4","CXCL4|Platelet Factor 4|Recombinant Platelet Factor 4|rPF4|rhPF4","A recombinant form of the endogenous chemokine platelet factor 4 with potential antiangiogenesis and antineoplastic activities. As a heparin-binding tetramer, recombinant platelet factor 4 inhibits growth factor-stimulated endothelial cell proliferation, migration, and angiogenesis; it has been shown that this agent inhibits fibroblast growth factor 2 (FGF2) angiogenic activity downstream from the FGF2 receptor. Its activity is antagonized by heparin. Recombinant platelet factor 4 may also directly inhibit the proliferation of some tumor cell types.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C92586","Recombinant PRAME Protein Plus AS15 Adjuvant GSK2302025A","Recombinant PRAME Protein Plus AS15 Adjuvant GSK2302025A","A recombinant form of the human PRAME (Preferentially Expressed Antigen of Melanoma) protein combined with the AS15 adjuvant, with potential immunostimulatory and antineoplastic activities. Upon intramuscular administration, GSK2302025A may stimulate the host immune response to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells that overexpress the PRAME protein, resulting in tumor cell lysis. The tumor-associated antigen PRAME is often overexpressed by a variety of tumor cell types. AS15 is an potent adjuvant liposomal formulation that contains CpG 7909, monophosphoryl lipid, and QS-21.","Pharmacologic Substance"]
["C82371","Recombinant Saccharomyces Cerevisia-CEA(610D)-Expressing Vaccine GI-6207","GI-6207|Recombinant Saccharomyces Cerevisia-CEA(610D)-Expressing Vaccine GI-6207","A whole, heat-killed, recombinant Saccharomyces cerevisiae yeast-based vaccine genetically altered to express the carcinoembryonic antigen (CEA) peptide 610D with potential immunostimulating and antineoplastic activities. Upon administration, recombinant Saccharomyces cerevisia-CEA(610D) vaccine GI-6207 may stimulate a host cytotoxic T-lymphocyte (CTL) response against CEA-expressing tumor cells, which may result in tumor cell lysis. CEA, a tumor associated antigen, is overexpressed on a wide variety of human cancer cells including colorectal, gastric, lung, breast and pancreatic cancer cells. CEA 610D encodes for 9 amino acids (605-613) in which aspartate is substituted for asparagine at position 610 (610D) in order to strengthen the induction of the CTL response against CEA-expressing tumor cells.","Chemical Viewed Functionally"]
["C121542","Recombinant Super-compound Interferon","Recombinant Super Compound Interferon|Recombinant Super-compound Interferon|rSIFN-co","A recombinant form of the naturally-occurring cytokine interferon-alpha (IFN-a) that has a modified spatial configuration, with immunomodulating, antiviral and antineoplastic activities. Upon administration of recombinant super-compound interferon (rSIFN-co), this agent binds to IFN-specific cell surface receptors, resulting in the transcription and translation of genes whose protein products have antiviral, antiproliferative, anticancer, and immune-modulating effects. The 3-dimensional conformational change improves efficacy and causes less side effects compared to IFN-a.","Organic Chemical|Pharmacologic Substance"]
["C884","Recombinant Thyroglobulin","Proloid|Recombinant Thyroglobulin|THYROGLOBULIN|Therapeutic TG|Thyroglobulin","A recombinant form of thyroglobulin identical to or similar to the endogenous iodine-containing glycoprotein. Thyroglobulin is synthesized in the thyroid follicular cell, and is the precursor of thyroid hormones T3 and T4. Thyroglobulin levels can serve as a tumor marker for monitoring the status of differentiated thyroid carcinomas.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C61322","Recombinant Thyrotropin Alfa","Recombinant TSH Alpha|Recombinant Thyrotropin Alfa|Recombinant Thyrotropin Alpha|THYROTROPIN ALFA|TSH-alpha|Thyrogen|Thyroid Stimulating Hormone Alpha|Thyrotropin Alfa|thyrotropin alfa","A recombinant form of the human anterior pituitary glycoprotein thyroid stimulating hormone (TSH) with use in the diagnostic setting. With an amino acid sequence identical to that of human TSH, thyrotropin alfa binds to TSH receptors on normal thyroid epithelial cells or well-differentiated thyroid cancer cells, stimulating iodine uptake and organification, synthesis and secretion of thyroglobulin (Tg), triiodothyronine (T3), and thyroxine (T4).","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C898","Recombinant Transforming Growth Factor-Beta","Bone-Derived Transforming Growth Factor|Recombinant Transforming Growth Factor-Beta|TGF-Beta|Therapeutic Milk Growth Factor|Therapeutic TGF B|Therapeutic TGF-Beta|rTGF-Beta","A recombinant therapeutic agent which is chemically identical to or similar to the endogenous cytokine transforming growth factor-beta (TGF-beta) with proapoptotic and antineoplastic properties. TGF-beta may suppress tumor cell growth by decreasing the expression of cyclin D1, a cell cycle regulatory protein, and downregulating the expression of the oncogene c-myc. This agent is also involved in T cell-mediated immunosuppression by CD4+CD25+ T cells, which permits cancer cells to evade immune surveillance. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1286","Recombinant Transforming Growth Factor-Beta-2","Cartilage-Inducing Factor-B|Glioblastoma-Derived T-Cell Suppressor Factor|Recombinant Transforming Growth Factor-Beta-2|TGF-Beta 2|Transforming Growth Factor-Beta 2","A recombinant polypeptide chemically identical to or similar to the endogenous cytokine transforming growth factor-beta-2 (TGF-beta-2). TGF-beta-2 modulates cell growth and immune function and may promote or inhibit tumor growth, depending on the tumor cell type. TGF-beta-2 may also suppress host immune system recognition of and/or response to tumor cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1941","Recombinant Tumor Necrosis Factor Family Protein","Recombinant Tumor Necrosis Factor Family Protein|TNF|Tumor Necrosis Factor Family Protein|Tumor Necrosis Factors|tumor necrosis factor","A recombinant therapeutic agent which is chemically identical to or similar to one of a number of endogenous tumor necrosis factor (TNF) proteins. TNF family cytokines bind to and activate specific cell-surface receptors, thereby mediating inflammatory processes, cell proliferation, immunity, angiogenesis, and tumor cell cytotoxicity. One primary antitumor effect of TNFs involves stimulation of T cell-mediated antitumor cytotoxicity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C913","Recombinant Tumor Necrosis Factor-Alpha","Cachectin|Recombinant Tumor Necrosis Factor-Alpha|TNF-Alpha|TNFA|TUMOR NECROSIS FACTOR-.ALPHA. HUMAN (SOLUBLE FORM)|Tumor Necrosis Factor (TNF-alpha)","A recombinant therapeutic agent which is chemically identical to or similar to the endogenous cytokine tumor necrosis factor-alpha with antineoplastic properties.  Tumor necrosis factor-alpha binds to and activates \"death receptors\" on the cell surface, resulting in apoptosis and cell death by the p53-independent extrinsic pathway. This agent also disrupts tumor vascularization. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C38682","Recombinant Tyrosinase-Related Protein-2","Recombinant Tyrosinase-Related Protein-2|TRP-2|Tyrosinase-Related Protein-2","A recombinant therapeutic agent which is chemically identical to or similar to an endogenous non-mutated melanocyte differentiation antigen expressed by both normal and malignant melanocytes. Vaccinations with recombinant tyrosinase-related protein-2 may elicit an antitumoral cytotoxic T-cell response against tumor cells and some normal cells that express tyrosinase-related protein-2. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2510","Recombinant Vaccinia DF3/MUC1 Vaccine","Recombinant Vaccinia DF3/MUC1 Vaccine|rV-DF3/MUC1","A vaccinia virus based vaccine expressing human tumor associated epithelial mucin (DF3 antigen; MUC1). MUC1 antigen, a membrane bound glycoprotein expressed by most glandular and ductal epithelial cells, is overexpressed in various tumors such as breast, prostate, and ovarian cancers. This vaccine could be used in development of immunotherapeutics against cancers expressing MUC1.","Immunologic Factor|Pharmacologic Substance"]
["C2433","Recombinant Vaccinia PSA Vaccine","PSA Vaccinia (CV1-produced), THERION|PSA Vaccinia (chick embryo dermo cell-produced) THERION|Prostate Specific Antigen Expressing Vaccinia Virus Vaccine|RV-PSA (RECOMB VACCINIA/PSA-CV-1)|Recombinant Vaccinia PSA Vaccine|Vaccinia PSA Vaccine|Vaccinia-PSA Vaccine|Vaccinia-Prostate-Specific Antigen Vaccine|rV-PSA Vaccine|rV-PSA","A vaccine consisting of recombinant vaccinia virus encoding prostate specific antigen (PSA). Vaccination with recombinant vaccinia prostate-specific antigen vaccine stimulates the host immune system to mount a cytotoxic T-cell response against tumor cells expressing PSA.","Pharmacologic Substance|Virus"]
["C88326","Recombinant Vaccinia Viral Vector RO5217790","RO5217790|Recombinant Vaccinia Viral Vector RO5217790","A vaccine consisting of recombinant modified vaccinia Ankara (MVA) viral vector encoding mutated forms of the genes for the viral oncoproteins E6 and E7 derived from the human papillomavirus (HPV) type 16 and the human cytokine interleukin-2 (hIL2), with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration, recombinant vaccinia viral vector RO5217790 may stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against cells expressing HPV E6 and E7, resulting in tumor cell lysis. Oncoproteins E6 and E7 have been implicated in the tumorigenesis of cervical carcinoma.","Pharmacologic Substance"]
["C2237","Recombinant Vaccinia-B7.1 Vaccine","Recombinant Vaccinia-B7.1 Vaccine|Recombinant Vaccinia-B7.1|rV-B7 (Recomb Vaccinia/B7)|rV-B7.1 Vaccine|rV-B7.1","A recombinant vaccinia virus encoding the T-cell co-stimulatory molecule B7-1. Co-administration of recombinant vaccinia-B7.1 and a tumor-associated antigen vaccine may enhance tumor-associated antigen-specific T-cell responses. (NCI04)","Pharmacologic Substance|Virus"]
["C2619","Recombinant Vaccinia-CEA(6D)-TRICOM Vaccine","Recombinant Vaccinia-CEA(6D)-TRICOM Vaccine|Vaccinia-CEA-TRICOM Vaccine|rV-CEA(6D)-TRICOM","A vaccine consisting of recombinant vaccinia virus encoding the tumor-associated antigen carcinoembryonic antigen (CEA) and a TRIad of COstimulatory Molecules (B7-1, ICAM-1, and LFA-3; also called TRICOM). Vaccination with recombinant vaccinia-CEA(6D)-TRICOM vaccine stimulates the host immune system to mount a T-cell response against tumor cells expressing the CEA antigen. The use of TRICOM in the vaccine may elicit a greater antitumor cytotoxic T lymphocyte (CTL) immune response compared to the use of vaccinia-CEA alone.","Pharmacologic Substance|Virus"]
["C2732","Recombinant Vaccinia-MUC-1 Vaccine","Recombinant Vaccinia MUC-1|Recombinant Vaccinia-MUC-1 Vaccine|rV-MUC-1 Vaccine","A vaccine containing a recombinant vaccinia virus that encodes the gene for human mucin-1, a tumor-associated antigen. Upon administration, recombinant vaccinia-MUC-1 vaccine may elicit a MUC-1-specific cytotoxic T cell response against tumor cells bearing MUC-1.","Pharmacologic Substance|Virus"]
["C48638","Recombinant Vaccinia-Multiepitope Melanoma Peptides-B7.1-B7.2 Vaccine","Recombinant Vaccinia-Multiepitope Melanoma Peptides-B7.1-B7.2 Vaccine","A cancer vaccine consisting of an inactivated recombinant vaccinia virus encoding epitope peptides derived from melanoma-related HLA-A2-restricted tumor-associated antigens (TAAs), including Melan-A(27-35), gp100(280-288) and tyrosinase(1-9), and two co-stimulatory B7 proteins, B7.1 (CD80) and B7.2 (CD86). Upon administration, recombinant vaccinia-multiepitope melanoma peptides-B7.1-B7.2 vaccine may stimulate a cytotoxic T-lymphocyte response against melanoma cells that express TAAs which share epitopes with the epitope peptides expressed by the vaccine viral vector, resulting in tumor cell lysis; vaccine viral vector-expressed co-stimulatory proteins B7.1 and B7.2 may enhance the cytotoxic T-lymphocyte immune response to the TAAs.","Pharmacologic Substance"]
["C48419","Recombinant Vaccinia-NY-ESO-1 Vaccine","Recombinant Vaccinia-NY-ESO-1 Vaccine|rV-NY-ESO-1","A cancer vaccine consisting of a recombinant vaccinia viral vector encoding an immunogenic peptide derived from the cancer-testis antigen NY-ESO-1, an antigen found in normal testis and various tumors, including bladder, breast, hepatocellular, melanoma, and prostate cancers. Vaccination with recombinant vaccinia NY-ESO-1 peptide vaccine may stimulate the host immune system to mount a humoral and cytotoxic T lymphocyte (CTL) response against tumor cells expressing NY-ESO-1 antigen, resulting in tumor cell lysis. (NCI05)","Pharmacologic Substance"]
["C2685","Recombinant Vaccinia-TRICOM Vaccine","Recombinant Vaccinia-TRICOM Vaccine|Vaccinia-TRICOM|rV-TRICOM|recombinant vaccinia-TRICOM vaccine|vaccinia-TRICOM vaccine","A vaccine consisting of recombinant vaccinia virus encoding a TRIad of COstimulatory Molecules (B7-1, ICAM-1, and LFA-3; also called TRICOM). Vaccination with recombinant vaccinia-TRICOM vaccine stimulates the host immune system to mount a non-specific T-cell response. With the addition of a tumor-associated antigen peptide, this vaccine may enhance a tumor-specific immune response.","Pharmacologic Substance|Virus"]
["C102545","Recombinant Vesicular Stomatitis Virus-expressing Interferon-beta","Recombinant VSV-IFN-beta|Recombinant Vesicular Stomatitis Virus-expressing Interferon-beta|VSV-hIFN-b","A recombinant, replicating oncolytic vesicular stomatitis virus (VSV) carrying the human interferon-beta (IFN-b) gene, with potential immunomodulating and antineoplastic activities. Upon intratumoral administration, recombinant VSV expressing IFN-b replicates in the tumor environment specifically, partially due to defective innate antiviral host defense mechanisms in tumor cells, involving type I IFNs, and exerts its cytolytic activity towards the tumor cells. By expressing human IFN-b, an INF-b-mediated antiviral immune response in surrounding normal cells is activated which protects normal cells against virus replication and VSV-mediated cell lysis. However, tumor cells have a defective IFN-b-mediated innate antiviral immune response allowing for VSV to replicate in these cells without interference. In addition, the IFN-b produced by VSV may activate an immune response in surrounding normal cells and may activate T-lymphocytes, dendritic cells and natural killer cells; thus, inducing an anti-tumor immune response against the tumor cells. VSV, a single-stranded RNA virus belonging to the genus Vesiculovirus of the family Rhabdoviridae, is relatively nonpathogenic to healthy humans.","Virus"]
["C74059","Refametinib","BAY 869766|BAY86-9766|MEK Inhibitor RDEA119|RDEA119|REFAMETINIB|Refametinib","An orally bioavailable selective MEK inhibitor with potential antineoplastic activity. Refametinib specifically inhibits mitogen-activated protein kinase kinase 1 (MAP2K1 or MAPK/ERK kinase 1), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a dual specificity threonine/tyrosine kinase, is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","Pharmacologic Substance"]
["C78204","Regorafenib","4-(4-(((4-chloro-3-(trifluoromethyl)phenyl)carbamoyl)amino)-3-fluorophenoxy)-N-methylpyridine-2-carboxamide|BAY 73-4506|REGORAFENIB|Regorafenib|Stivarga","An orally bioavailable small molecule with potential antiangiogenic and antineoplastic activities. Regorafenib binds to and inhibits vascular endothelial growth factor receptors (VEGFRs) 2 and 3, and Ret, Kit, PDGFR and Raf kinases, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation. VEGFRs are receptor tyrosine kinases that play important roles in tumor angiogenesis; the receptor tyrosine kinases RET, KIT, and PDGFR, and the serine/threonine-specific Raf kinase are involved in tumor cell signaling.","Organic Chemical|Pharmacologic Substance"]
["C70968","Renal Cell Carcinoma Peptides Vaccine IMA901","IMA901|Renal Cell Carcinoma Peptides Vaccine IMA901","A multipeptide cancer vaccine targeting renal cell carcinoma with potential immunopotentiating activity. Renal cell carcinoma peptides vaccine IMA901 consists of 10 different synthetic tumor-associated peptide (TUMAP) antigens (9 HLA-class I-binding and 1 HLA class II-binding); endogenously, these TUMAPs are expressed by the majority of renal cell carcinomas. Vaccination with this agent may significantly increase host cytotoxic T-lymphocyte (CTL) immune responses against tumor cells expressing these peptide antigens.","Immunologic Factor|Pharmacologic Substance"]
["C77907","Renal Cell Carcinoma/CD40L RNA-Transfected Autologous Dendritic Cell Vaccine AGS-003","AGS-003|Renal Cell Carcinoma/CD40L RNA-Transfected Autologous Dendritic Cell Vaccine AGS-003","A cancer vaccine in which autologous dendritic cells are transfected with patient-specific renal cell carcinoma (RCC) RNA and a synthetic, truncated human CD40 ligand (CD40L) RNA with potential immunostimulatory and antineoplastic activities. Individual RCC-specific RNA, encoding a unique repertoire of tumor-associated antigens (TAAs) (including telomerase reverse transcriptase, G250, and oncofetal antigen) is electroporated into autologous dendritic cells (DCs), transfected with synthetic RNA that encodes a truncated version of the T-cell protein CD40L; the transfected autologous DCs express and process both patient-specific RCC TAAs and the truncated CD40L protein. When reintroduced back to the patient, renal cell carcinoma/CD40L RNA-transfected autologous dendritic cell vaccine AGS-003 may elicit a highly specific cytotoxic T-cell (CTL) response against RCC cells expressing the patient-specific RCC TAA repertoire. The signal cascade initiated by stimulation of the truncated, ectopically expressed co-stimulatory molecule CD40L results in the secretion of the inflammatory cytokine IL-12 downstream.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C66515","Reparixin","2-(4-Isobutylphenyl)propionylmethanesulfonamide|Benzeneacetamide, Alpha-methyl-4-(2-methylpropyl)-N- (methylsulfonyl)- (alphaR)-|DF 1681Y|REPARIXIN|Reparixin|Repertaxin","An orally available inhibitor of CXC chemokine receptor types 1 (CXCR1) and 2 (CXCR2), with potential antineoplastic activity. Upon administration, reparixin allosterically binds to CXCR1 and prevents CXCR1 activation by its ligand interleukin 8 (IL-8 or CXCL8). This may cause cancer stem cell (CSC) apoptosis and may inhibit tumor cell progression and metastasis. CXCR1, overexpressed on CSCs, plays a key role in CSC survival and the ability of CSC to self-renew; it is also linked to tumor resistance to chemotherapy. Inhibition of the IL-8/CXCR1 interaction also potentiates the cytotoxic effect of chemotherapeutic agents. In addition, reparixin inhibits CXCR2 activation and may reduce both neutrophil recruitment and vascular permeability during inflammation or injury.","Pharmacologic Substance"]
["C94233","Resistant Starch","RS|Resistant Starch","A form of dietary fiber that resists degradation in the small intestine by gastrointestinal (GI) enzymes with potential chemopreventive and prebiotic activity. Upon consumption of resistant starch, the fiber is not metabolized or absorbed in the small intestine and enters the colon unaltered. Once in the colon, the starch is fermented by anaerobic colonic bacteria and produces short-chain fatty acids (SCFA), including butyrate, which has anti-inflammatory and immunoregulatory activities. In addition, butyrate appears to exert antitumor effects by inhibiting tumor cell proliferation, inducing tumor cell differentiation and apoptosis in colorectal cancer cells.","Organic Chemical"]
["C84856","Resminostat","4SC-201|RESMINOSTAT|Resminostat","An orally bioavailable inhibitor of histone deacetylases (HDACs) with potential antineoplastic activity. Resminostat binds to and inhibits HDACs leading to an accumulation of highly acetylated histones. This may result in an induction of chromatin remodeling, inhibition of the transcription of tumor suppressor genes, inhibition of tumor cell division and the induction of tumor cell apoptosis. HDACs, upregulated in many tumor types, are a class of enzymes that deacetylate chromatin histone proteins.","Pharmacologic Substance"]
["C85484","Resveratrol Formulation SRT501","Resveratrol Formulation SRT501|SRT501","A proprietary formulation of resveratrol, a polyphenolic phytoalexin derived from grapes and other food products with potential antioxidant, anti-obesity, antidiabetic and chemopreventive activities. Resveratrol may activate sirtuin subtype 1 (SIRT-1). SIRT1 activation has been reported to inhibit tumorigenesis and tumor cell proliferation. SIRT-1 is a member of the silent information regulator 2 (SIR2) (or sirtuin) family of enzymes that plays an important role in mitochondrial activity and acts as a protein deacetylase. SIRT1 appears to be involved in the regulation of numerous transcription factors such as NF-kB and p53.","Pharmacologic Substance"]
["C80378","Retaspimycin","17-Allylamino-17-demethoxygeldanamycin Hydroquinone|Geldanamycin, 18,21-didehydro-17-demethoxy-18,21-dideoxo-18,21-dihydroxy-17-(2-propenylamino)-|RETASPIMYCIN|Retaspimycin","A small-molecule inhibitor of heat shock protein 90 (HSP90) with antiproliferative and antineoplastic activities. Retaspimycin binds to and inhibits the cytosolic chaperone functions of HSP90, which maintains the stability and functional shape of many oncogenic signaling proteins and may be overexpressed or overactive in tumor cells. Retaspimycin-mediated inhibition of HSP90 promotes the proteasomal degradation of oncogenic signaling proteins in susceptible tumor cell populations, which may result in the induction of apoptosis.","Pharmacologic Substance"]
["C48401","Retaspimycin Hydrochloride","17-Allylamino-17-demethoxygeldanamycin hydroquinone hydrochloride|Geldanamycin, 18,21-didehydro-17-demethoxy-18,21-dideoxo-18,21-dihydroxy-17-(2-propenylamino)-, monohydrochloride|IPI-504|RETASPIMYCIN HYDROCHLORIDE|Retaspimycin Hydrochloride","The hydrochloride salt of a small-molecule inhibitor of heat shock protein 90 (HSP90) with antiproliferative and antineoplastic activities. Retaspimycin binds to and inhibits the cytosolic chaperone functions of HSP90, which maintains the stability and functional shape of many oncogenic signaling proteins and may be overexpressed or overactive in tumor cells. Retaspimycin-mediated inhibition of HSP90 promotes the proteasomal degradation of oncogenic signaling proteins in susceptible tumor cell populations, which may result in the induction of apoptosis.","Pharmacologic Substance"]
["C73241","Retelliptine","1-((3-(Diethylamino)propyl)amino)-5,11-dimethyl-9-methoxy-6H-pyrido(4,3-b)carbazole|RETELLIPTINE|Retelliptine","An ellipticine derivative and topoisomerase II inhibitor with antineoplastic activity. Retelliptine intercalates with DNA and inhibits topoisomerase II during DNA replication. In addition, this agent appears to induce cell cycle arrest at G2/M phase and apoptosis mediated through the Fas/Fas ligand death receptor and the mitochondrial pathway.","Pharmacologic Substance"]
["C80061","Retinoid 9cUAB30","9cUAB30|Retinoid 9cUAB30","A synthetic analogue of 9-cis retinoic acid with potential antineoplastic and chemopreventive activities. Retinoid 9cUAB30 binds to and activates retinoid X receptor (RXR) homodimers and/or and retinoic acid receptor (RAR)/RXR heterodimers, which may result in the dissociation of corepressor protein and the recruitment of coactivator protein, followed by transcription of downstream target genes into mRNAs and protein translation. Gene transcription regulated by these transcription factors may result in inhibition of cell proliferation, induction of cell differentiation, and apoptosis of both normal cells and tumor cells.","Pharmacologic Substance"]
["C77899","Retinoid Analogue NRX 195183","NRX 195183|RAR Alpha Agonist NRX 195183|Retinoid Acid Receptor Alpha Agonist NRX 195183|Retinoid Analogue NRX 195183","An orally bioavailable retinoid acid receptor (RAR) alpha agonist with potential antineoplastic activity. Retinoid analogue NRX 195183 binds to and activates RAR alpha, modulating the transcription of genes responsible for cell differentiation and proliferation, which may result in cell differentiation, decreased cell proliferation, and the inhibition of tumorigenesis. Encoded by the RARA gene, RAR alpha is a nuclear receptor and a member of the steroid receptor superfamily.","Organic Chemical|Pharmacologic Substance"]
["C68302","Retinol","3,7-Dimethyl-9-(2,6, 6-trimethyl-1-cyclohexen-1-yl)-2,4,6,8-nonatetraen-1-ol|3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)-2,4,6,8-nonatetraen-1-ol|3,7-dimethyl-9-(2,6,6-trimethyl-1-cyclohexenyl)-nona-2,4,6,8-tetraen-1-ol|All Trans Retinol|RETINOL|Retinol|retinol","The fat soluble vitamin retinol. Vitamin A binds to and activates retinoid receptors (RARs), thereby inducing cell differentiation and apoptosis of some cancer cell types and inhibiting carcinogenesis. Vitamin A plays an essential role in many physiologic processes, including proper functioning of the retina, growth and differentiation of target tissues, proper functioning of the reproductive organs, and modulation of immune function.","Vitamin"]
["C1216","Retinyl Acetate","Retinol Acetate|Retinyl Acetate|Retinyl acetate|VITAMIN A ACETATE|Vitamin A, acetate|vitamin A acetate","A naturally-occurring fatty acid ester form of retinol (vitamin A) with potential antineoplastic and chemopreventive activities.  Retinyl acetate binds to and activates retinoid receptors, inducing cell differentiation and decreasing cell proliferation.  This agent also inhibits carcinogen-induced neoplastic transformation in some cancer cell types and exhibits immunomodulatory properties. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1217","Retinyl Palmitate","Palmitate-1-14C|Retinol Hexadecanoate|Retinol Palmitate|Retinol-15-3H|Retinyl Palmitate|Retinyl-10,11-14C2|VITAMIN A PALMITATE|Vitamin A Palmitate|retinyl palmitate","A naturally-occurring phenyl analogue of retinol (vitamin A) with potential antineoplastic and chemopreventive activities.  As the most common form of vitamin A taken for dietary supplementation, retinyl palmitate binds to and activates retinoid receptors, thereby inducing cell differentiation and decreasing cell proliferation.  This agent also inhibits carcinogen-induced neoplastic transformation, induces apoptosis in some cancer cell types, and exhibits immunomodulatory properties. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C49082","Retrovector Encoding Mutant Anti-Cyclin G1","Mx-dnG1|REXIN-G|Retrovector Encoding Mutant Anti-Cyclin G1","A replication-incompetent, pathotropic, tumor matrix (collagen)-targeted, retroviral vector encoding an N-terminal deletion mutant form of the cyclin G1 gene with potential antineoplastic activity. Under the control of a hybrid long-terminal repeat/cytomegalovirus (CMV) promoter, retrovector encoding mutant anti-cyclin G expresses the mutant cyclin G1 construct, resulting in disruption of tumor cell cyclin G1 activity and decreased cellular proliferation and angiogenesis. This agent preferentially targets collagen of the tumor matrix because of the incorporation of the collagen-binding domain of von Willebrand factor (vWF) on the retrovector surface. Exploiting the collagen-targeting mechanism of vWF permits delivery of the retrovector to tumor sites where angiogenesis and collagen matrix exposure occur.","Pharmacologic Substance"]
["C74076","Rexinoid NRX 194204","AGN194204|NRX194204|Rexinoid NRX 194204","An orally bioavailable synthetic retinoid X receptor (RXR) agonist with potential antineoplastic and anti-inflammatory activities. Rexinoid NRX 194204 selectively binds to and activates RXRs. Because RXRs can form heterodimers with several nuclear receptors (NRs), RXR activation by this agent may result in a broad range of gene expression depending on the effector DNA response elements activated. Rexinoid NRX 194204 may inhibit the tumor-necrosis factor (TNF)-mediated release of nitric oxide (NO) and interleukin 6 (IL6) and may inhibit tumor cell proliferation. This agent appears to be less toxic than RAR-selective ligands.","Pharmacologic Substance"]
["C61498","RFT5-dgA Immunotoxin","Anti-CD25 Immunotoxin IMTOX25|IMTOX25|IgG-RFT5-dgA|RFT5-dgA Immunotoxin|RFT5-dgA immunotoxin","A recombinant immunotoxin consisting of the anti-CD25 monoclonal antibody RFT5 fused to the deglycosylated ricin A-chain (dgA) with potential antitumor activity.  The monoclonal antibody moiety of RFT5-dgA immunotoxin attaches to CD25 (the alpha chain of the IL-2 receptor complex) on the cell membrane; after internalization, the dgA moiety cleaves the N-glycosidic bond between the ribose and adenine base at position 4324 in 28S ribosomal RNA, resulting in ribosome inactivation, inhibition of protein synthesis, and cell death.  CD25 is expressed on activated normal T and B cells and macrophages and is frequently upregulated in many hematologic malignancies.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C118670","Rhenium Re 188 BMEDA-labeled Liposomes","(188) Re-BMEDA-liposomes|188Re-BMEDA-liposomes|188Re-N,N-bis (2-Mercaptoethyl)-N',N'-diethylethylenediamine-labeled Liposomes|Rhenium Re 188 BMEDA-labeled Liposomes","A liposome-based preparation consisting of the beta- and gamma-emitting radionuclide rhenium Re 188 (Re 188) linked to the chelator N,N-bis (2-mercaptoethyl)-N',N'-diethylethylenediamine (BMEDA) and encapsulated in liposomes, with potential tumor imaging and antineoplastic activities. Upon intravenous infusion of rhenium Re 188 BMEDA-labeled liposomes, the liposomes selectively target tumor cells, facilitate the retention of the radioisotope by those cells, and cause localized antitumor radiocytotoxicity while sparing surrounding normal, healthy cells. In addition, Re 188 BMEDA-labeled liposomes can be used for imaging purposes. Re 188 has a short half-life and a short path length, which further contribute to limiting the radiotoxicity to the tumor cells.","Pharmacologic Substance"]
["C1562","Rhenium Re-186 Hydroxyethylidene Diphosphonate","186Re-Etidronate|Re 186 Hydroxyethylidene Diphosphonate|Re-186 HEDP|Re-186 Hydroxyethylidene Diphosphonate|Rhenium Re 186 Etidronate|Rhenium Re-186 Hydroxyethylidene Diphosphonate|Rhenium-186 HEDP","An synthetic compound containing the organic phosphonate hydroxyethylidene diphosphonate (HEDP) labeled with the radioisotope rhenium Re 186. Re-186 hydroxyethylidene diphosphonate binds to hydroxyapatite in bone, delivering a cytotoxic dose of beta radiation to primary and metastatic bone tumors. Re-186 is a beta emitter with a short half-life, a radioisotope profile that provides localized antitumor radiocytotoxicity while sparing extramedullary bone marrow tissues.","Organic Chemical|Pharmacologic Substance"]
["C91390","Rhenium Re-188 Ethiodized Oil","Rhenium Re 188 Lipiodol|Rhenium Re-188 Ethiodized Oil","A rhenium (Re) 188 conjugate of ethiodized oil (lipiodol), an iodinated ethyl ester derived from poppy seed oil, with potential antineoplastic activity. Upon hepatic intra-arterial injection rhenium Re 188 ethiodized oil accumulates in hepatocellular carcinoma (HCC) tumor cells, thereby delivering a cytotoxic dose of radiation through Re 188 directly to the tumor cells. This may kill tumor cells while sparing surrounding normal cells and tissues. Compared to iodine I 131, Re 188 has a shorter half-life.","Pharmacologic Substance"]
["C1218","Rhizoxin","Rhizoxin|WF-1360|rhizoxin","A macrocyclic lactone. Rhizoxin binds to tubulin and inhibits microtubule assembly, thereby inducing cytotoxicity. This agent also may inhibit endothelial cell-induced angiogenic activity, which may result in decreased tumor cell proliferation. (NCI04)","Antibiotic|Organic Chemical"]
["C95701","Ribociclib","7-Cyclopentyl-N,N-dimethyl-2-((5-(piperazin-1-yl)pyridin-2-yl)amino)-7H-pyrrolo[2,3-d]pyrimidine-6-carboxamide|LEE-011|LEE011|RIBOCICLIB|Ribociclib","An orally available cyclin-dependent kinase (CDK) inhibitor targets at cyclin D1/CDK4 and cyclin D3/CDK6 cell cycle pathway, with potential antineoplastic activity. Ribociclib specifically inhibits CDK4 and 6, thereby inhibiting retinoblastoma (Rb) protein phosphorylation. Inhibition of Rb phosphorylation prevents CDK-mediated G1-S phase transition, thereby arresting the cell cycle in the G1 phase, suppressing DNA synthesis and inhibiting cancer cell growth. Overexpression of CDK4/6, as seen in certain types of cancer, causes cell cycle deregulation.","Pharmacologic Substance"]
["C82689","Ribonuclease QBI-139","QBI-139|RNase QBI-139|Ribonuclease QBI-139","A nuclease of mammalian origin that cleaves the phosphodiester bond between nucleotides of ribonucleic acids with potential antineoplastic activity. Ribonuclease QBI-139 catalyzes the hydrolysis and degradation of RNA leading to the inhibition of protein synthesis and cell death.","Enzyme"]
["C78188","Ribosome-Inactivating Protein CY503","Ribosome-Inactivating Protein CY503","A recombinant protein that inactivates the ribosome with potential antineoplastic and immunomodulating activities. Ribosome-inactivating protein CY503 binds to the cell surface sialyltransferase CD75 and is internalized; intracellularly, CY503 cleaves an adenine-specific N-glycosidic bond on the 28S ribosomal subunit, which may result in tumor cell apoptosis. This agent has also been shown to activate natural killer (NK) cells, induce cytokine receptor expression, and stimulate the release of cytokines. CD75 is expressed on mature B-cells and subsets of T-cells and erythrocytes.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1865","Ribozyme RPI.4610","Angiozyme|Anti-Flt-1 Ribozyme|RPI.4610|RPI4610|Ribozyme RPI.4610","A nuclease-stabilized synthetic ribozyme (ribonucleic acid enzyme) with potential anti-angiogenesis activity. Ribozyme RPI.4610 specifically recognizes the mRNA for FLT1 (vascular endothelial growth factor receptor 1; VEGFR1), and hydrolyzes the mRNA, thereby preventing VEGFR1 proteins from being made. This may prevent VEGF-stimulated angiogenesis in cancerous tissue and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C111686","Rice Bran","Rice Bran","The nutrient-rich hard outer layer of the rice cereal grain, with potential chemopreventive, antioxidant, iron chelating, anticholesterol and anti-inflammatory activities. Rice bran is rich in fiber, such as beta-glucan, pectin and gum; it also comprises vitamins and minerals, such as iron, magnesium and phosphorus, and essential fatty acids. In addition, Rice bran contains various bioactive components, including ferulic acid, tricin, beta-sitosterol, gamma-oryzanol, phytic acid, and inositol hexaphosphate (IP6). The potential anticancer activity of rice bran may be due to the synergistic effects of these phytochemicals on their ability to induce apoptosis, inhibit cell proliferation, and alter cell cycle progression in cancer cells. Rice bran's bioactive components also protect against tissue damage by scavenging free radicals and blocking chronic inflammatory responses. In addition, they are able to modulate the gut microflora and carcinogen-metabolizing enzymes, thereby further exerting a chemopreventive effect.","Pharmacologic Substance"]
["C96431","Ricolinostat","2-(Diphenylamino)-N-(7-(hydroxyamino)-7-oxoheptyl)pyrimidine-5-carboxamide|ACY-1215|Histone Deacetylase 6 InhibitorACY-1215|RICOLINOSTAT|Ricolinostat","An orally bioavailable, specific inhibitor of histone deacetylase 6 (HDAC6) with potential antineoplastic activity. Ricolinostat selectively targets and binds to HDAC6, thereby disrupting the Hsp90 protein chaperone system through hyperacetylation of Hsp90 and preventing the subsequent aggresomal protein degradation. This leads to an accumulation of unfolded and misfolded ubiquitinated proteins and may eventually induce cancer cell apoptosis, and inhibition of cancer cell growth. HDAC6, a class II HDAC deacetylase located in the cytoplasm, appears to play a key role in the formation and activation of the aggresomes needed for degradation of misfolded proteins. Compared to non-selective HDAC inhibitor, ACY-1215 is able to reduce the toxic effects on normal, healthy cells.","Pharmacologic Substance"]
["C49061","Ridaforolimus","AP23573|Deforolimus|MK-8669|RIDAFOROLIMUS|Rapamycin, 42-(dimethylphosphinate)|Ridaforolimus|ridaforolimus","A small molecule and non-prodrug analogue of the lipophilic macrolide antibiotic rapamycin with potential antitumor activity. Ridaforolimus binds to and inhibits the mammalian target of rapamycin (mTOR), which may result in cell cycle arrest and, consequently, the inhibition of tumor cell growth and proliferation. Upregulated in some tumors, mTOR is a serine/threonine kinase involved in regulating cellular proliferation, motility, and survival that is located downstream of the PI3K/Akt signaling pathway.","Pharmacologic Substance"]
["C71355","Rigosertib Sodium","ON 01910.Na|Polo-like kinase 1 Inhibitor ON 01910.Na|RIGOSERTIB SODIUM|Rigosertib Sodium","A synthetic benzyl styryl sulfone analogue with potential antineoplastic activity. Polo-like kinase 1 inhibitor ON 01910.Na inhibits polo-like kinase1 (Plk1), inducing selective G2/M arrest followed by apoptosis in a variety of tumor cells while causing reversible cell arrest at the G1 and G2 stage without apoptosis in normal cells. This agent may exhibit synergistic antitumor activity in combination with other chemotherapeutic agents. Plk1, named after the polo gene of Drosophila melanogaster, is a serine/threonine protein kinase involved in regulating mitotic spindle function in a non-ATP competitive manner.","Pharmacologic Substance"]
["C38681","Rilimogene Galvacirepvec","PROSTVAC|Prostvac-V|Recombinant Vaccinia-PSA(L155)-TRICOM Vaccine|Recombinant Vaccinia-PSA(L155)/TRICOM Vaccine|Recombinant Vaccinia-PSA(L155)/TRICOM|Rilimogene Galvacirepvec|rVaccinia-PSA(L155)-TRICOM Vaccine|rVaccinia-Prostate-Specific Antigen/TRICOM Vaccine","A vaccine formulation consisting of recombinant vaccinia virus encoding prostate specific antigen (PSA) and recombinant vaccinia virus encoding three co-stimulatory molecule transgenes B7.1, ICAM-1, and LFA-3 (TRICOM). Vaccination with PSA in combination with TRICOM may enhance antigen presentation, resulting in the augmentation of a cytotoxic T cell (CTL) immune response against tumor cells expressing PSA.","Immunologic Factor|Pharmacologic Substance|Virus"]
["C67079","Rilotumumab","AMG 102|Anti-HGF Monoclonal Antibody AMG 102|Fully Human Anti-HGF Monoclonal Antibody AMG 102|RILOTUMUMAB|Rilotumumab|anti-HGF monoclonal antibody AMG 102","A fully human IgG2 monoclonal antibody directed against the human hepatocyte growth factor (HGF) with potential antineoplastic activity. Anti-HGF monoclonal antibody AMG 102 binds to and neutralizes HGF, preventing the binding of HGF to its receptor c-Met and so c-Met activation; inhibition of c-Met-mediated signal transduction may result in the induction of apoptosis in cells expressing c-Met. c-Met (HGF receptor or HGFR), a receptor tyrosine kinase overexpressed or mutated in a variety of epithelial cancer cell types, plays a key role in cancer cell growth, survival, angiogenesis, invasion, and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C69076","Rindopepimut","Anti-EGFRvIII Vaccine CDX-110|CDX-110|L-Cysteine, L-leucyl-L-alpha-glutamyl-L-alpha-glutamyl-L-lysyl-L-lysylglycyl-L-asparaginyl-L-tyrosyl-L-valyl-L-valyl-L-threonyl-L-alpha-aspartyl-L-histidyl-S-(1-((4-carboxycyclohexyl)methyl)-2,5-dioxo-3-pyrrolidinyl)-, complex with hemocyanin (Megathura crenulata)|PF-04948568|Rindopepimut","A cancer vaccine consisting of a human epidermal growth factor receptor variant III (EGFRvIIi)-specific peptide conjugated to the non-specific immunomodulator keyhole limpet hemocyanin (KLH) with potential antineoplastic activity. Vaccination with anti-EGFRvIII vaccine CDX-110 may elicit a cytotoxic T-lymphocyte (CTL) immune response against tumor cells expressing EGFRvIII. EGFRvIII, a functional variant of EGFR that is not expressed in normal tissues, was originally discovered in glioblastoma multiforme (GBM) and has also been found in various other cancers such as breast, ovarian, metastatic prostate, colorectal, and head and neck cancers. EGFRvIII contains an 83 amino acid deletion in its extracellular domain and has been shown to transform NIH/3T3 mouse embryonic fibroblast cells in vitro.","Immunologic Factor|Pharmacologic Substance"]
["C75294","Ritrosulfan","Lycurim|R-74|RITROSULFAN|Ritrosulfan","A sulfonate-based alkylation agent with potential antineoplastic activity. Ritrosulfan appears to alkylate DNA, thereby producing DNA crosslinks, resulting in cell cycle arrest.","Pharmacologic Substance"]
["C1702","Rituximab","ABP 798|BI 695500|C2B8 Monoclonal Antibody|CT-P10|Chimeric Anti-CD20 Antibody|IDEC-102|IDEC-C2B8 Monoclonal Antibody|IDEC-C2B8|MabThera|Monoclonal Antibody IDEC-C2B8|PF-05280586|RITUXIMAB|RTXM83|Rituxan|Rituximab Biosimilar ABP 798|Rituximab Biosimilar BI 695500|Rituximab Biosimilar CT-P10|Rituximab Biosimilar PF-05280586|Rituximab Biosimilar RTXM83|Rituximab Biosimilar SAIT101|Rituximab|rituximab","A recombinant chimeric murine/human antibody directed against the CD20 antigen, a hydrophobic transmembrane protein located on normal pre-B and mature B lymphocytes. Following binding, rituximab triggers a host cytotoxic immune response against CD20-positive cells. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C118947","RNA Electroporated CD19CAR-CD3zeta-4-1BB-expressing Autologous T-lymphocytes","RNA Anti-CD19 CAR T Cells|RNA Electroporated CD19CAR-CD3zeta-4-1BB-expressing Autologous T-lymphocytes","Autologous, genetically engineered T-lymphocytes that have been electroporated with an mRNA encoding for an anti-CD19 chimeric antigen receptor (CAR) consisting of an anti-CD19 single chain variable fragment (scFv) coupled to the co-stimulatory signaling domain of 4-1BB (CD137) and the zeta chain of the T-cell receptor CD3 complex (CD3-zeta), with potential immunomodulating and antineoplastic activities.  Upon transfusion, the RNA electroporated CD19CAR-CD3zeta-4-1BB-expressing autologous T-lymphocytes attach to cancer cells expressing CD19. This induces selective toxicity against CD19-expressing tumor cells and causes tumor cell lysis. The 4-1BB co-stimulatory molecule signaling domain enhances T-cell activation and signaling after recognition of CD19. CD19 antigen is a B-cell specific cell surface antigen, which is expressed in all B-cell lineage malignancies.","Pharmacologic Substance"]
["C114976","RNR Inhibitor COH29","COH29|N-(4-(3,4-dihydroxyphenyl)-5-phenylthiazol-2-yl)-3,4-dihydroxybenzamide|RNR Inhibitor COH29|Ribonucleotide Reductase Holoenzyme Inhibitor COH29","An orally available, aromatically substituted thiazole and inhibitor of the human ribonucleotide reductase (RNR), with potential antineoplastic activity. Upon oral administration, the RNR inhibitor COH29 binds to the ligand-binding pocket of the RNR M2 subunit (hRRM2) near the C-terminal tail. This blocks the interaction between the hRRM1 and hRRM2 subunits and interferes with the assembly of the active hRRM1/hRRM2 complex of RNR. Inhibition of RNR activity decreases the pool of deoxyribonucleotide triphosphates available for DNA synthesis. The resulting decrease in DNA synthesis causes cell cycle arrest and growth inhibition. In addition, this agent may inhibit the nuclear enzyme poly (ADP-ribose) polymerase (PARP) 1, which prevents the repair of damaged DNA, and causes both the accumulation of single and double strand DNA breaks and the induction of apoptosis. RNR, an enzyme that catalyzes the conversion of ribonucleoside diphosphate to deoxyribonucleoside diphosphate, is essential for de novo DNA synthesis and plays an important role in cell growth; it is overexpressed in many cancer cell types and is associated with increased drug resistance, cancer cell growth and metastasis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C64174","Ro 16-9100","Ro 16-9100|Ro-16-9100","A synthetic retinoid with differentiation inducing and potential antineoplastic activities. Like other retinoic acid agents, Ro 16-9100 binds to and activates retinoic acid receptors (RARs), thereby altering the expression of certain genes leading to cell differentiation and decreased cell proliferation in susceptible cells.","Pharmacologic Substance"]
["C71527","Robatumumab","Anti-IGF-1R Recombinant Monoclonal Antibody SCH 717454|Immunoglobulin G1, Anti-(Human Insulin-Like Growth Factor I Receptor) (Human Monoclonal SCH 717454 Heavy Chain), Disulfide with Human Monoclonal SCH 717454 Light Chain, Dimer|ROBATUMUMAB|Robatumumab|Sch717454","A recombinant, fully human monoclonal antibody directed against the insulin-like growth factor 1 receptor (IGF-1R) with potential antineoplastic activity. Anti-IGF-1R fully human monoclonal antibody SCH 717454 binds to membrane-bound IGF-1R, preventing binding of the ligand IGF-1 and the subsequent triggering of the PI3K/Akt signaling pathway; downregulation of this survival pathway may result in the induction of apoptosis and decreased cellular proliferation. The activation of IGF-1R, a tyrosine kinase and a member of the insulin receptor family, stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF-1R signaling has been highly implicated in tumorigenesis and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C97275","Rodorubicin","Cytorhodin S|HLB 817|RODORUBICIN|Rodorubicin","A synthetic tetraglycosidic anthracycline antibiotic with antineoplastic activity. Rodorubicin appears to intercalate DNA and causes cell death. Due to its severe cardiotoxic effects, this agent was never marketed.","Organic Chemical"]
["C1832","Rofecoxib","4-[4'-(Methylsulfonyl)phenyl]-3-phenyl-2(5H)-furanone|MK 966|ROFECOXIB|Rofecoxib|Vioxx|rofecoxib","A synthetic, nonsteroidal derivative of phenyl-furanone with antiinflammatory, antipyretic and analgesic properties and potential antineoplastic properties.  Rofecoxib binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in an inhibition of the conversion of arachidonic acid to prostaglandins.  COX-related metabolic pathways may represent key regulators of cell proliferation and neo-angiogenesis. Some epithelial tumor cell types overexpress pro-angiogenic COX-2. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C76890","Roflumilast","3-Cyclopropylmethoxy-N-(3,5-dichloropyridin-4-yl)-4-(difluoromethoxy)benzamide|B9302-107|BY217|BYK20869|Daliresp|ROFLUMILAST|Roflumilast","An orally available, long-acting inhibitor of phosphodiesterase (PDE) type 4 (PDE4), with anti-inflammatory and potential antineoplastic activities. Upon administration, roflumilast and its active metabolite roflumilast N-oxide selectively and competitively bind to and inhibit PDE4, which leads to an increase of both intracellular levels of cyclic-3',5'-adenosine monophosphate (cAMP) and cAMP-mediated signaling. cAMP prevents phosphorylation of spleen tyrosine kinase (SYK) and abrogates activation of the PI3K/AKT/mTOR signaling pathway, which may result in the induction of apoptosis. PDE4, a member of the PDE superfamily that hydrolyses cAMP and 3',5'-cyclic guanosine monophosphate (cGMP) to their inactive 5' monophosphates, is upregulated in a variety of cancers and may contribute to chemoresistance; it also plays a key role in inflammation, especially in inflammatory airway diseases.","Pharmacologic Substance"]
["C1427","Rogletimide","Pyridoglutethimide|ROGLETIMIDE|Rogletimide","An orally active aminoglutethimide derivative with potential antineoplastic activity. Rogletimide reversibly inhibits the activity of aromatase, a cytochrome P450 family enzyme found in many tissues and the key enzyme in the oxidative aromatization process of androgens to estrogens. In estrogen-dependent cancers, the inhibition of aromatase by this agent leads to a reduction in the synthesis of estrogen, thereby inhibiting estrogen-mediated signal transduction and consequently reducing tumor cell growth. In addition, rogletimide also inhibits enzymes that catalyzing conversion of cholesterol to corticosteroids.","Organic Chemical|Pharmacologic Substance"]
["C1544","Romidepsin","N-[(3S,4E)-3-Hydroxy-7-mercapto-1-oxo-4-heptenyl]-D-valyl-D-cysteinyl-(2Z)-2-amino-2-butenoyl-L-valine, (4->1) Lactone, Cyclic|Antibiotic FR 901228|Depsipeptide|FK228|FR901228|Istodax|L-Valine, N- (3-hydroxy-7-mercapto-1-oxo-4-heptenyl)valyl- cysteinyl-2, 3-didehydro-2-aminobutanoyl-,xi-lactone, cyclic (1-2)-disulfide|L-Valine, N-(3-Hydroxy-7-Mercapto-1-Oxo-4-Heptenyl)-D-Valyl-D-Cysteinyl-(Z)-2,3 -Didehydro-2-Aminobutanoyl-, xi-Lactone, Cyclic (1-2)-Disulfide, (S-(E))-|N-[(3S,4E)-3-Hydroxy-7-mercapto-1-oxo-4-heptenyl]-D-valyl-D-cysteinyl-(2Z)-2-amino-2-butenoyl-L-valine, (4-1) Lactone, Cyclic|ROMIDEPSIN|Romidepsin|depsipeptide|romidepsin","A bicyclic depsipeptide antibiotic isolated from the bacterium Chromobacterium violaceum with antineoplastic activity. After intracellular activation, romidepsin binds to and inhibits histone deacetylase (HDAC), resulting in alterations in gene expression and the induction of cell differentiation, cell cycle arrest, and apoptosis. This agent also inhibits hypoxia-induced angiogenesis and depletes several heat shock protein 90 (Hsp90)-dependent oncoproteins.","Amino Acid, Peptide, or Protein|Antibiotic"]
["C92579","Roniciclib","BAY1000394|RONICICLIB|Roniciclib","An orally bioavailable cyclin dependent kinase (CDK) inhibitor with potential antineoplastic activity. Roniciclib selectively binds to and inhibits the activity of CDK1/Cyclin B, CDK2/Cyclin E, CDK4/Cyclin D1, and CDK9/Cyclin T1, serine/threonine kinases that play key roles in the regulation of the cell cycle progression and cellular proliferation. Inhibition of these kinases leads to cell cycle arrest during the G1/S transition, thereby leading to an induction of apoptosis, and inhibition of tumor cell proliferation. CDKs are often dysregulated in cancerous cells.","Pharmacologic Substance"]
["C1519","Roquinimex","1,2-Dihydro-4-hydroxy-N,1-dimethyl-2-oxo-3-quinolinecarboxanilide|1,2-Dihydro-4-hydroxy-N,1-dimethyl-2-oxo-N-phenyl-3-quinolinecarboxamide|FCF 89|LS 2616|Linomide|N-Phenyl-N-methyl-1,2-dihydro-4-hydroxy-1-methyl-2-oxoquinoline-3-carboxamide|ROQUINIMEX|Roquinimex","A quinoline-3-carboxamide with potential antineoplastic activity.  Roquinimex inhibits endothelial cell proliferation, migration, and basement membrane invasion; reduces the secretion of the angiogenic factor tumor necrosis factor alpha by tumor-associated macrophages (TAMs); and inhibits angiogenesis.  This agent is also an immune modulator that appears to alter cytokine profiles and enhance the activity of T cells, natural killer cells, and macrophages. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C117237","ROR1 CAR-specific Autologous T-Lymphocytes","Autologous ROR1-CAR-T Cells|Chimeric Anti-ROR1 T-cell Receptor-expressing Autologous T-lymphocytes|ROR1 CAR-specific Autologous T-Lymphocytes|ROR1-CAR-T","A mixture of two T-lymphocyte preparations expressing a chimeric antigen receptor (CAR) consisting of an anti-receptor tyrosine kinase-like orphan receptor 1 (ROR1) single chain variable fragment (scFv) fused to either the co-stimulatory signaling domain cluster of differentiation 28 (CD28), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta) (ROR1CD28zeta), or the co-stimulatory signaling domain cluster of differentiation 137 (CD137; 4-1BB), and the zeta chain of the T-cell receptor (TCR)/CD3 complex (CD3-zeta) (ROR1CD137zeta), with potential immunomodulating and antineoplastic activities. Upon simultaneous administration of the two T-lymphocyte populations ROR1CD28zeta and ROR1CD137zeta , the ROR1 CAR-specific autologous T-lymphocytes are directed to tumor cells expressing ROR1, which may result in a selective toxicity against, and lysis of ROR1-expressing tumor cells. CD28, a T-cell surface-associated co-stimulatory molecule, is required for full T-cell activation, proliferation, and survival. The 4-1BB co-stimulatory molecule signaling domain enhances activation and signaling after recognition of ROR1. ROR1, also known as neurotrophic tyrosine kinase, receptor-related 1, is expressed during embryogenesis and by certain leukemias.","Cell|Pharmacologic Substance"]
["C77066","Rosabulin","3-[(4-Cyanophenyl)methyl]-N-(3-methyl-5-isothiazolyl)-alpha-oxo-1-indolizineacetamide|ROSABULIN|Rosabulin|STA-5312","A small molecule vascular disrupting agent, with potential antimitotic and antineoplastic activities. Rosabulin binds to tubulin in a similar manner as colchicine and inhibits microtubule assembly. This results in the disruption of the cytoskeleton of tumor endothelial cells, ultimately leading to cell cycle arrest and blockage of cell division. By destroying proliferating vascular cells, blood flow to the tumor is reduced and eventually leads to a decrease in tumor cell proliferation.","Pharmacologic Substance"]
["C2583","Rosiglitazone Maleate","(+/-)-5-[[4-[2-(Methyl-2-pyridinylamino)ethoxy]phenyl]methyl]-2,4-thiazolidinedione, ( Z )-2-Butenedioate (1:1)|Avandia|BRL49653|ROSIGLITAZONE MALEATE|Rosiglitazone Maleate|rosiglitazone maleate","The maleate salt of rosiglitazone, an orally-active thiazolidinedione with antidiabetic properties and potential antineoplastic activity.  Rosiglitazone activates peroxisome proliferator-activated receptor gamma (PPAR-gamma), a ligand-activated transcription factor, thereby inducing cell differentiation and inhibiting cell growth and angiogenesis.  This agent also modulates the transcription of insulin-responsive genes, inhibits macrophage and monocyte activation, and stimulates adipocyte differentiation.","Pharmacologic Substance"]
["C66523","Rosuvastatin","ROSUVASTATIN|Rosuvastatin","A statin with antilipidemic and potential antineoplastic activities. Rosuvastatin selectively and competitively binds to and inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a precursor of cholesterol. This leads to a decrease in hepatic cholesterol levels and increase in uptake of LDL cholesterol. In addition, rosuvastatin, like other statins, exhibits pro-apoptotic, growth inhibitory, and pro-differentiation activities in a variety of tumor cell types; these antineoplastic activities may be due, in part, to inhibition of the isoprenylation of Ras and Rho GTPases and related signaling cascades.","Pharmacologic Substance"]
["C1485","Rubitecan","9-NC|9-Nitro-20(S)-camptothecin|9-nitrocamptothecin|Camptogen|Nitrocamptothecin|Orathecin|RFS 2000|RUBITECAN|Rubitecan|nitrocamptothecin","A semisynthetic agent related to camptothecin with potent antitumor and antiviral properties.  Rubitecan binds to and inhibits the enzyme topoisomerase I and induces protein-linked DNA single-strand breaks, thereby blocking DNA and RNA synthesis in dividing cells; this agent also prevents repair of reversible single-strand DNA breaks. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C131178","Rucaparib Camsylate","8-Fluoro-2-(4-((methylamino)methyl)phenyl)-1,3,4,5-tetrahydro-6H-pyrrolo(4,3,2-ef)(2)benzazepin-6-one (7,7-dimethyl-2-oxobicyclo(2.2.1)heptan-1-yl)methanesulfonate (1:1)|8-Fluoro-2-{4-[(methylamino)methyl]phenyl}-1,3,4,5-tetrahydro-6H-azepino[5,4,3-cd]indol-6-one ((1S,4R)-7,7dimethyl-2-oxobicyclo[2.2.1]hept-1-yl)methanesulfonic Acid Salt|Bicyclo(2.2.1)heptane-1-methanesulfonic acid, 7,7-dimethyl-2-oxo-, (1S,4R)-, Compound with 8-Fluoro-1,3,4,5-tetrahydro-2-(4-((methylamino)methyl)phenyl)-6H-pyrrolo(4,3,2-ef)(2)benzazepin-6-one (1:1)|C0-338|RUCAPARIB CAMSYLATE|Rubrraca|Rucaparib Camsylate|Rucaparib Phosphate",null,"Organic Chemical|Pharmacologic Substance"]
["C78186","Rucaparib Phosphate","AG014699|PARP-1 inhibitor AG014699|PARP1 Inhibitor PF-01367338|PF-01367338|RUCAPARIB PHOSPHATE|Rucaparib Phosphate","A tricyclic indole poly(ADP-Ribose) polymerase (PARP1) inhibitor with potential chemosensitizing, radiosensitizing, and antineoplastic activities. Rucaparib selectively binds to PARP1 and inhibits PARP1-mediated DNA repair, thereby enhancing the accumulation of DNA strand breaks and promoting genomic instability and apoptosis. This may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapy and radiation therapy. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins and is activated by single-strand DNA (ssDNA) breaks.","Organic Chemical|Pharmacologic Substance"]
["C38686","Ruthenium Ru-106","Ru-106|Ruthenium Ru 106|Ruthenium Ru-106","A radioactive isotope of the rare element ruthenium, a member of the light platinum group. A radioactive plaque containing ruthenium 106 may be inserted into the eye to irradiate ophthalmic tumors. (NCI04)","Element, Ion, or Isotope"]
["C97948","Ruthenium-based Transferrin Targeting Agent NKP-1339","NKP-1339|Ruthenium-based Transferrin Targeting Agent NKP-1339","A ruthenium-containing cancer agent targeting transferrin with potential antineoplastic activity. Upon intravenous administration, NKP-1339 (Ru3+) binds to transferrin (Tf) and is taken up via Tf receptors (TfR), which are overexpressed on cancer cells. Once inside the cell, NKP-1339 is released from Tf and is reduced, within the acidic environment of the endosomes, to its active form NKP-119 (Ru2+). In turn, the active form induces a redox reaction, thereby leading to the formation of reactive oxygen species (ROS) which inhibits GRP78 and SOD, endoplasmic reticulum-stress modulating molecules as well as BAG4 and ERK, program cell death regulating molecules. This eventually induces caspase-dependent apoptosis.","Pharmacologic Substance"]
["C77888","Ruxolitinib","(3R)-3-cyclopentyl-3-(4-(7h-pyrrolo(2,3-d)pyrimidin-4-yl)pyrazol-1-yl)propanenitrile|INCB-18424|INCB18424|Oral JAK Inhibitor INCB18424|RUXOLITINIB|Ruxolitinib","An orally bioavailable Janus-associated kinase (JAK) inhibitor with potential antineoplastic and immunomodulating activities. Ruxolitinib specifically binds to and inhibits protein tyrosine kinases JAK 1 and 2, which may lead to a reduction in inflammation and an inhibition of cellular proliferation. The JAK-STAT (signal transducer and activator of transcription) pathway plays a key role in the signaling of many cytokines and growth factors and is involved in cellular proliferation, growth, hematopoiesis, and the immune response; JAK kinases may be upregulated in inflammatory diseases, myeloproliferative disorders, and various malignancies.","Organic Chemical|Pharmacologic Substance"]
["C97937","Ruxolitinib Phosphate","(3R)-3-cyclopentyl-3-(4-(7h-pyrrolo(2,3-d)pyrimidin-4-yl)pyrazol-1-yl)propanenitrile Phosphate (1:1)|1H-Pyrazole-1-propanenitrile, beta-cyclopentyl-4-(7H-pyrrolo(2,3-d)pyrimidin-4-yl)-,(betaR)-, phosphate (1:1)|INCB-18424 Phosphate|Jakafi|RUXOLITINIB PHOSPHATE|Ruxolitinib Phosphate","The phosphate salt form of ruxolitinib, an orally bioavailable Janus-associated kinase (JAK) inhibitor with potential antineoplastic and immunomodulating activities. Ruxolitinib specifically binds to and inhibits protein tyrosine kinases JAK 1 and 2, which may lead to a reduction in inflammation and an inhibition of cellular proliferation. The JAK-STAT (signal transducer and activator of transcription) pathway plays a key role in the signaling of many cytokines and growth factors and is involved in cellular proliferation, growth, hematopoiesis, and the immune response; JAK kinases may be upregulated in inflammatory diseases, myeloproliferative disorders, and various malignancies.","Organic Chemical|Pharmacologic Substance"]
["C106368","S1P Receptor Agonist KRP203","2-Amino-2-propanediol Hydrochloride|KRP-203|KRP203|S1P Receptor Agonist KRP203","The hydrochloride salt form of 2-amino-2 propanediol (KRP-203), a sphingosine 1-phosphate (S1P) receptor agonist, with potential immunosuppressive activity. Upon administration of S1P receptor agonist KRP203, this agent binds to S1P receptors on lymphocytes, which prevents binding of serum S1P to S1P receptors and leads to S1P receptor internalization. This reduces the number of circulating blood leukocytes and accelerates lymphocyte homing into peripheral lymph nodes, thereby preventing their infiltration into peripheral inflammatory sites. This agent also decreases the production of inflammatory cytokines by lymphocytes, such as interferon gamma (IFN-g), interleukin-12 (IL-12), and tumor necrosis factor (TNF).","Pharmacologic Substance"]
["C2671","S-3304","S-3304","An orally-agent agent with potential antineoplastic activity.  S-3304 inhibits matrix metalloproteinases (MMPs), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis. (NCI04)","Pharmacologic Substance"]
["C1706","Sabarubicin","(7S,9S)-7-{(4-O-(3-Amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)-2,6-dideoxy-alpha-L-lyxo-hexopyranosyl)oxy}-6,9,11-trihydroxy-9-(hydroxyacetyl)-7,8,9,10-tetrahydrotetracene-5,12-dione|BMS-195615|MEN-10755|SABARUBICIN|Sabarubicin","A disaccharide analogue of the anthracycline antineoplastic antibiotic doxorubicin.  Sabarubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.  This agent also induces apoptosis through a p53-independent mechanism.  Sabarubicin is less cardiotoxic than doxorubicin.","Antibiotic|Organic Chemical"]
["C102783","Sacituzumab Govitecan","IMMU-132|RS7-SN38|SACITUZUMAB GOVITECAN|Sacituzumab Govitecan|hRS7-SN38 Antibody Drug Conjugate","An antibody drug conjugate containing the humanized monoclonal antibody, hRS7, against tumor-associated calcium signal transducer 2 (TACSTD2 or TROP2) and linked to the active metabolite of irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), with potential antineoplastic activity. The antibody moiety of sacituzumab govitecan selectively binds to TROP2. After internalization and proteolytic cleavage, SN-38 selectively stabilizes topoisomerase I-DNA covalent complexes, resulting in DNA breaks that inhibit DNA replication and trigger apoptosis. TROP2, also known as epithelial glycoprotein-1 (EGP-1), is a transmembrane calcium signal transducer that is overexpressed by a variety of human epithelial carcinomas; this antigen is involved in the regulation of cell-cell adhesion and its expression is associated with increased cancer growth, aggressiveness and metastasis.","Pharmacologic Substance"]
["C63661","S-Adenosylmethionine","5'-[(3-Amino-3-carboxypropyl)methylsulfonio]-5'-deoxyadenosine Hydroxide, Inner Salt|Active Methionine|S-Adenosyl-l-methionine 1,4-Butanedisulfonate|S-Adenosyl-l-methionine|S-Adenosyl-methionine|S-Adenosylmethionine","A nutritional supplement that is synthesized from adenosine triphosphate (ATP) and the amino acid methionine by the endogenous essential enzyme methionine adenosyltransferase (MAT), with potential antineoplastic activity.  Upon administration, S-adenosylmethionine acts as a methyl donor for various transmethylation reactions. In cancer cells, this agent induces the methylation of tumor promoting genes, reverses DNA hypomethylation, and leads to the suppression of oncogene transcription. This induces apoptosis in and inhibits proliferation of susceptible tumor cells.","Amino Acid, Peptide, or Protein"]
["C1568","Safingol","(2S,3S)-2-Amino-1,3-Octadecanediol|Kynacyte|L-(-)-threo-Sphingnine|L-Threo-Dihydrosphingosine|L-threo-2-Amino-1,3-octadecanediol|L-threo-dihydrosphingosine|SAFINGOL|SPC-100270|Safingol|Sphinganine|safingol","A saturated derivative of sphingosine. As an inhibitor of protein kinase C (PKC), safingol competitively binds to the regulatory phorbol-binding domain of PKC, a kinase involved in tumorigenesis. This agent has been shown to act synergistically with other chemotherapeutic agents and may potentiate chemotherapy drug-induced apoptosis in vitro and in vivo.","Organic Chemical|Pharmacologic Substance"]
["C61072","Sagopilone","(1S,3S,7S,10R,11S,12S,16R)-7,11-dihydroxy-8,8,12,16-tetramethyl-3-(2-methyl-1,3-benzothiazol-5-yl)-10-(prop-2-enyl)-4,17-dioxabicyclo(14.1.0)heptadecane-5,9-dione|DE-03757|Epothilone ZK219477|SAGOPILONE|SH-Y03757A|Sagopilone|ZK-219477|ZK-EPO|ZK-Epothilone|epothilone ZK219477","A fully synthetic low-molecular-weight epothilone with potential antineoplastic activity. Sagopilone binds to tubulin and induces microtubule polymerization while stabilizing microtubules against depolymerization, which may result in the inhibition of cell division, the induction of G2/M arrest, and apoptosis. The agent is not a substrate for the P-glycoprotein (P-gp) efflux pump and so may exhibit activity in multidrug-resistant (MDR) tumors. The epothilone class of metabolites was originally isolated from the myxobacterium Solangium cellulosum.","Chemical Viewed Structurally|Pharmacologic Substance"]
["C71146","Salirasib","2-(((2E,6E)-3,7,11-Trimethyl-2,6,10-dodecatrienyl)sulfanyl)benzoic Acid|S-Farnesylthiosalicylic Acid|SALIRASIB|Salirasib","A salicylic acid derivative with potential antineoplastic activity. Salirasib dislodges all Ras isoforms from their membrane-anchoring sites, thereby preventing activation of RAS signaling cascades that mediated cell proliferation, differentiation, and senescence. RAS signaling is believed to be abnormally activated in one-third of human cancers, including cancers of the pancreas, colon, lung and breast.","Organic Chemical|Pharmacologic Substance"]
["C2556","Salmonella VNP20009","Auxotrophic Lipid A S. Typhimurium mutant|Live, Attenuated Salmonella Typhimurium|Salmonella VNP20009|VNP 20009|VNP20009","A genetically stable Salmonella typhimurium strain, attenuated by chromosomal deletion of the purI and msbB genes, with tumor-targeting activity. In rodent models, salmonella VNP20009 has been shown to selectively accumulate and grow in a variety of tumor types, inhibiting the growth of primary and metastatic tumors. This agent may be genetically engineered to contain transgenes that express therapeutic agents or cell surface tumor-associated antigen-specific antibodies, such as CEA-specific antibodies, which may improve its tumor targeting and therapeutic potential.","Pharmacologic Substance"]
["C97663","Sam68 Modulator CWP232291","CWP232291|Sam68 Modulator CWP232291","A small molecule and prodrug of CWP232204 targeting Src associated in mitosis, of 68 kDa (Sam68 or KHDRBS1), with potential antineoplastic activity. CWP232291 is converted in serum into its active form CWP232204 which binds to Sam68, thereby resulting in the induction of apoptosis in selective cancer cells. Due to the multimodular structure of Sam68, the apoptosis mediated by CWP232204-Sam68 interaction can attribute from 1) activation of transcription factor NF-kB induced by tumor necrosis factor alpha signaling, 2) alternative splicing of BCL-2 apoptosis gene, driving the balance towards pro-apoptotic as opposed to anti-apoptotic isoforms, 3) down-regulation of the anti-apoptotic protein survivin via Wnt signaling. Sam68, a KH domain RNA-binding protein belonging to the signal transduction and activation of RNA (STAR) family, plays a key role in various cellular processes including cell cycle progression and apoptosis; it is upregulated in many types of cancer cells and its expression is associated with increased cell proliferation and survival.","Pharmacologic Substance"]
["C64541","Sapacitabine","CS-682|CYC682|N-(1-(2-Cyano-2-deoxy-beta-D-arabinofuranosyl)-2-oxo-1,2-dihydropyrimidin-4-yl)-hexadecanamide|SAPACITABINE|Sapacitabine","An orally bioavailable pyrimidine analogue prodrug with potential antineoplastic activity. Sapacitabine is hydrolyzed by amidases to the deoxycytosine analogue CNDAC (2'-Cyano-2'-deoxyarabinofuranosylcytosine), which is then phosphorylated into the active triphosphate form. As an analogue of deoxycytidine triphosphate, CNDAC triphosphate incorporates into DNA strands during replication, resulting in single-stranded DNA breaks during polymerization due to beta-elimination during the fidelity checkpoint process; cell cycle arrest in the G2 phase and apoptosis ensue. The unmetabolized prodrug may exhibit antineoplastic activity as well.","Organic Chemical|Pharmacologic Substance"]
["C90548","Sapanisertib","INK-128|INK128|MLN-0128|MLN0128|SAPANISERTIB|Sapanisertib|TAK-228","An orally bioavailable inhibitor of raptor-mTOR (TOR complex 1 or TORC1) and rictor-mTOR (TOR complex 2 or TORC2) with potential antineoplastic activity. Sapanisertib binds to and inhibits both TORC1 and TORC2 complexes of mTOR, which may result in tumor cell apoptosis and a decrease in tumor cell proliferation. TORC1 and 2 are upregulated in some tumors and play an important role in the PI3K/Akt/mTOR signaling pathway, which is frequently dysregulated in human cancers.","Pharmacologic Substance"]
["C77887","Sapitinib","2-(4-((4-((3-chloro-2-fluorophenyl)amino)-7-methoxyquinazolin-6-yl)oxy)piperidin-1-yl)-n-methylacetamide|AZD8931|ErbB Kinase Inhibitor AZD8931|SAPITINIB|Sapitinib","An erbB receptor tyrosine kinase inhibitor with potential antineoplastic activity. erbB kinase inhibitor AZD8931 binds to and inhibits erbB tyrosine receptor kinases, which may result in the inhibition of cellular proliferation and angiogenesis in tumors expressing erbB. The erbB protein family, also called the epidermal growth factor receptor (EGFR) family, plays major roles in tumor cell proliferation and tumor vascularization.","Organic Chemical|Pharmacologic Substance"]
["C48378","Saracatinib","4-Quinazolinamine, N-(5-chloro-1,3-benzodioxol-4-yl)-7-[2-(4-methyl-1-piperazinyl)ethoxy]-5-[(tetrahydro-2H-pyran-4-yl)oxy]-|AZD0530|N-(5-Chloro-1,3-Benzodioxol-4-Yl)-7-(2-(4-Methylpiperazin-1-yl)Ethoxy)-5-((Oxan-4-yl)Oxy)Quinazolin-4-Amine|SARACATINIB|SRC Kinase Inhibitor AZD0530|Saracatinib","An orally available 5-, 7-substituted anilinoquinazoline with anti-invasive and anti-tumor activities. Saracatinib is a dual-specific inhibitor of Src and Abl, protein tyrosine kinases that are overexpressed in chronic myeloid leukemia cells. This agent binds to and inhibits these tyrosine kinases and affects cell motility, cell migration, adhesion, invasion, proliferation, differentiation, and survival. Specifically, Saracatinib inhibits Src kinase-mediated osteoclast bone resorption.","Pharmacologic Substance"]
["C95224","Saracatinib Difumarate","4-Quinazolinamine, N-(5-Chloro-1,3-Benzodioxol-4-yl)-7-(2-(4-Methyl-1-Piperazinyl)Ethoxy)-5-((Tetrahydro-2H-Pyran-4-yl)Oxy)-, (2e)-2-Butenedioate (1:2)|AZD-0530 Difumarate|AZD0530 Difumarate|N-(5-Chloro-1,3-Benzodioxol-4-yl)-7-(2-(4-Methylpiperazin-1-yl)Ethoxy)-5-(Tetrahydro-2H-Pyran-4-yloxy)Quinazolin-4-Amine Di((2e)-but-2-Enedioate)|SARACATINIB DIFUMARATE|Saracatinib Difumarate","The difumarate salt of saracatinib, an orally available 5-, 7-substituted anilinoquinazoline with anti-invasive and anti-tumor activities. Saracatinib is a dual-specific inhibitor of Src and Abl, protein tyrosine kinases that are overexpressed in chronic myeloid leukemia cells. This agent binds to and inhibits these tyrosine kinases and affects cell motility, cell migration, adhesion, invasion, proliferation, differentiation, and survival. Specifically, Saracatinib inhibits Src kinase-mediated osteoclast bone resorption.","Pharmacologic Substance"]
["C963","SarCNU","2-Chloroethyl-3-Sarcosinamide-1-Nitrosourea|SarCNU|sarCNU|sarcosinamide nitrosourea","An alkylating chloroethylnitrosourea with antineoplastic activity.  Selectively accumulating in some tumor cells, SarCNU forms covalent linkages with nucleophilic centers in DNA, causing depurination, base pair miscoding, strand scission, and DNA-DNA cross-linking, which may result in cytotoxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1673","Sardomozide","2-[4-(Aminoiminomethyl)-2,3-dihydro-1H-inden-1-ylidene]hydrazinecarboximidamide|Amidinoindan-1-one.2'-amidinohydrazone|CGP 48664|CGP-48664|SAM 486A|SARDOMOZIDE|Sardomozide","A methylglyoxal-bis(guanylhydrazone) (MGBG) derivative with potential antineoplastic and antiviral properties. Sardomozide selectively binds to and inhibits S-adenosylmethionine decarboxylase (SAMDC), an enzyme essential for the biosynthesis of polyamines, such as spermine and spermidine that bind to DNA and play critical roles in cell division, cell differentiation and membrane function. By inhibiting SAMDC, sardomozide reduces the intracellular polyamine concentration, thereby interfering with cell growth and differentiation. In addition, this agent also exhibits anti-HIV effect via suppressing expression of eukaryotic translation initiation factor 5A (eIF-5A), which is essential for retroviral replication.","Organic Chemical|Pharmacologic Substance"]
["C1492","Sargramostim","23-L-Leucinecolony-Stimulating Factor 2|DRG-0012|Leukine|Prokine|SARGRAMOSTIM|Sagramostim|Sargramostatin|Sargramostim|rhu GM-CFS|sargramostim","A recombinant therapeutic agent chemically identical to endogenous human GM-CSF except a leucine substitution in position 23.  Binding to specific cell surface receptors, sargramostim modulates the proliferation and differentiation of a variety of hematopoietic progenitor cells with some specificity towards stimulation of leukocyte production and may reverse treatment-induced neutropenias. This agent also promotes antigen presentation, up-regulates antibody-dependent cellular cytotoxicity (ADCC), and increases interleukin-2-mediated lymphokine-activated killer cell function; it may also augment host antitumoral immunity.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2445","Sargramostim Plasmid DNA Pancreatic Tumor Cell Vaccine","GM-CSF plasmid DNA pancreatic tumor cell vaccine|Sargramostim Plasmid DNA Pancreatic Tumor Cell Vaccine","A whole cell vaccine comprised of irradiated allogenic pancreatic tumor cells transfected with a plasmid DNA encoding human sargramostim (GM-CSF). Vaccination results in expression of GM-CSF, which induces proliferation and differentiation of hematopoietic lineage cells as well as stimulating macrophage and dendritic cell functions in antigen presentation and antitumor cell-mediated immunity. Furthermore, administration of this pancreatic tumor cell vaccine may elicit a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor growth.","Immunologic Factor|Pharmacologic Substance"]
["C2429","Sargramostim Plasmid DNA Sarcoma Vaccine","GM-CSF plasmid DNA sarcoma vaccine|Sargramostim Plasmid DNA Sarcoma Vaccine","An autologous sarcoma cell vaccine with potential immunostimulatory activity. Tumor cells harvested from a patient with sarcoma are transfected with a plasmid DNA encoding for human sargramostim (GM-CSF) using a particle-mediated gene transfer (PMGT) technique, which avoids the use of infectious components. Vaccination with an autologous sargramostim sarcoma vaccine produces high levels of GM-CSF, a cytokine that enhances antigen presentation by activated macrophages and increases the recognition of weakly immunogenic tumors by cytotoxic T-lymphocytes.","Immunologic Factor|Pharmacologic Substance"]
["C80063","Saridegib","FIN-5|IP9 Free Base|IPI-926 Free Base|IPI-926|SARIDEGIB|Saridegib|Smoothened Antagonist IPI-926","An orally bioavailable, cyclopamine-derived inhibitor of the Hedgehog (Hh) pathway with potential antineoplastic activity. Specifically, Saridegib binds to and inhibits the cell membrane-spanning G-protein coupled receptor SMO, which may result in the suppression of Hh pathway signaling and a decrease in tumor cell proliferation and survival. SMO is activated upon binding of Hh ligand to the cell surface receptor Patched (PTCH); inappropriate activation of Hh signaling and uncontrolled cellular proliferation may be associated with SMO mutations. The Hh signaling pathway plays an important role in proliferation of neuronal precursor cells in the developing cerebellum and other tissues.","Pharmacologic Substance"]
["C1493","Satraplatin","(OC-6-43)-bis(acetato)amminedichloro(cyclohexylamine)platinum|(OC-6-43)-bis(acetato-O)amminedichloro(cyclohexanamine)platinum|BMS-182751|BMY-45594|JM 216|JM-216|Orplatna|SATRAPLATIN|Satraplatin|platinum,bis(acetato-O)amminedichloro(cyclohexanamine)-,(OC-6-43)|satraplatin","An orally administered third generation platinum compound with potential antineoplastic activity. Satraplatin forms highly reactive, charged, platinum complexes which bind to nucleophilic groups in DNA, inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. These cross-links result in cell growth inhibition and apoptosis.","Inorganic Chemical|Pharmacologic Substance"]
["C52199","SB-743921","SB-743921","A synthetic small molecule with potential antineoplastic properties. SB-743921 selectively inhibits kinesin spindle protein (KSP), an important protein involved in the early stages of mitosis that is expressed in proliferating cells. Inhibition of KSP results in inhibition of mitotic spindle assembly and interrupts cell division, thereby causing cell cycle arrest and induction of apoptosis.","Pharmacologic Substance"]
["C48421","SB-AS15 Adjuvant","SB AS15|SB-AS15 Adjuvant","A vaccine adjuvant containing CpG 7909, monophosphoryl lipid, and QS-21 with potential antineoplastic and immunostimulatory activities. CpG 7909 is a synthetic 24-mer oligonucleotide containing 3 CpG motifs that selectively targets Toll-like receptor 9 (TLR9), thereby activating dendritic and B cells and stimulating cytotoxic T cell and antibody responses against tumor cells bearing tumor antigens. Monophosphoryl lipid is a detoxified derivative of lipid A, a component of Salmonella minnesota lipopolysaccharide (LPS); this agent may enhance humoral and cellular responses to various antigens. QS-21 is a purified, naturally occurring saponin derived from the South American tree Quillaja saponaria Molina and exhibits various immunostimulatory activities. Combinations of monophosphoryl lipid and QS-21 may be synergistic in inducing humoral and cellular immune responses. (NCI05)","Pharmacologic Substance"]
["C29418","SBIL-2","SBIL-2","An retroviral vector encoding human IL-2 with potential antineoplastic property. SBIL-2 (Surgery Branch IL-2) can be used to transfect tumor infiltrating lymphocytes, which can then be re-introduced back to cancer patients, thereby stimulate T cell activation and immunopotentiation responses.","Pharmacologic Substance"]
["C126100","Scopoletin","2H-1-Benzopyran-2-One, 7-Hydroxy-6-Methoxy- (9CI)|2H-1-Benzopyran-2-One, 7-Hydroxy-6-Methoxy-|6-Methoxyumbelliferone|6-Methylesculetin|6-O-Methylesculetin|7-Hydroxy-5-Methoxycoumarin|7-Hydroxy-6-Methoxychromen-2-One|7-Hydroxy-6-Methoxycoumarin|Chrysatropic Acid|Coumarin, 7-Hydroxy-6-Methoxy-|Escopoletin|Esculetin-6-Methyl Ether|Gelseminic Acid|Methylesculetin|Murrayetin|Scopoletin|Scopoletine|Scopoletol","A coumarin compound found in several plants including those in the genus Scopolia and the genus Brunfelsia, as well as chicory (Cichorium), redstem wormwood (Artemisia scoparia), stinging nettle (Urtica dioica), passion flower (Passiflora), noni (Morinda citrifolia fruit) and European black nightshade (Solanum nigrum) that is comprised of umbelliferone with a methoxy group substituent at position 6. Scopoletin is used to standardize and establish pharmacokinetic properties for products derived from the plants that produce it, such as noni extract. Although the mechanism(s) of action have not yet been established, this agent has potential antineoplastic, antidopaminergic, antioxidant, anti-inflammatory and anticholinesterase effects.","Organic Chemical"]
["C99379","SDF-1-targeted agent NOX-A12","NOX-A12|SDF-1-targeted agent NOX-A12","A 45-mer L-stereoisomer RNA oligonucleotide linked to a 40 kDa polyethyleneglycol that targets the small chemokine stromal cell-derived factor 1 (SDF-1 or CXCL12) with potential antineoplastic and hematopoietic stem cell-mobilization activities. SDF-1 targeted agent NOX-A12 specifically binds to SDF-1 thereby preventing the binding of SDF-1 to its receptors CXCR4 and CXCR7 blocking the subsequent receptor activation. This may prevent angiogenesis, tumor cell proliferation, invasion and metastasis and could sensitize tumor cells to chemotherapy. In addition, inhibition of SDF-1/CXCR4 interaction may induce mobilization of hematopoietic cells from the bone marrow into blood. The unique mirror-image configuration of this agent renders it resistant to hydrolysis and does not hybridize with native nucleic acids. Furthermore, this agent does not induce the innate immune response and has shown a favorable immunogenicity profile.","Organic Chemical|Pharmacologic Substance"]
["C1576","Sedoxantrone Trihydrochloride","2H-(1)Benzothiopyrano(4,3,2-cd)indazol-8-ol, 5-((2-aminoethyl)amino)-2-(2-(diethylamino)ethyl)-, Trihydrochloride|CI 958|CI-958|LEDOXANTRONE TRIHYDROCHLORIDE|Ledoxantrone Trihydrochloride|Sedoxantrone Trihydrochloride|sedoxantrone trihydrochloride","The trihydrochloride salt of the anthrapyrazole antineoplastic antibiotic sedoxantrone with potential antineoplastic activity. Sedoxantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis.","Organic Chemical|Pharmacologic Substance"]
["C111764","Selatinib Ditosilate","Selatinib Ditosilate","An orally bioavailable ditosilate salt form of selatinib, an analog of the quinazoline lapatinib and dual inhibitor of epidermal growth factor receptor (EGFR) and Human Epidermal Growth Factor Receptor 2 (ErbB-2 or HER-2), with potential antineoplastic activity. Upon administration, selatinib reversibly blocks phosphorylation of both EGFR and ErbB2, thereby suppressing tumor growth in EGFR/ErbB-2-overexpressing tumor cells. The tyrosine kinases EGFR and ErbB2 have been implicated in the growth of various tumor types.","Pharmacologic Substance"]
["C106235","Selective Estrogen Receptor Degrader ARN-810","ARN-810|GDC-0810|RO7056118|SERD ARN-810|Selective Estrogen Receptor Degrader ARN-810","An orally available, nonsteroidal selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon oral administration, SERD ARN-810 binds to the estrogen receptor and induces a conformational change that results in the degradation of the receptor. This may inhibit the growth and survival of ER-expressing cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C122834","Selective Estrogen Receptor Degrader AZD9496","(E)-3-(3,5-Difluoro-4-((1R,3R)-2-(2-fluoro-2-methylpropyl)-3-methyl-2,3,4,9-tetrahydro-1H-pyrido[3,4-b]indol-1-yl)phenyl)acrylic Acid|AZD 9496|AZD-9496|AZD9496|SERD AZD9496|Selective Estrogen Receptor Degrader AZD9496","An orally available selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon administration, SERD AZD9496 binds to the estrogen receptor (ER) and induces a conformational change that results in the degradation of the receptor. This prevents ER-mediated signaling and inhibits the growth and survival of ER-expressing cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C128280","Selective Estrogen Receptor Degrader LSZ102","LSZ 102|LSZ102|SERD LSZ 102|SERD LSZ102|Selective Estrogen Receptor Degrader LSZ102","An selective estrogen receptor (ER) degrader (SERD), with potential antineoplastic activity. Upon administration of LSZ102, this agent binds to the ER and induces the degradation of the receptor. This prevents ER activation and ER-mediated signaling, and inhibits the growth and survival of ER-expressing cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C120037","Selective Estrogen Receptor Degrader SRN-927","SERD SRN-927|SRN-927|Selective Estrogen Receptor Degrader SRN-927","An orally available, nonsteroidal selective estrogen receptor degrader (SERD), with potential antineoplastic activity. Upon oral administration, SERD SRN-927 specifically binds to the estrogen receptor (ER) and induces a conformational change that results in the degradation of the receptor. This prevents ER-mediated signaling and inhibits the growth and survival of ER-expressing cancer cells.","Pharmacologic Substance"]
["C120211","Selective Estrogen Receptor Degrader/Modulator RAD1901","RAD1901|SERD/SERM RAD1901|Selective Estrogen Receptor Degrader/Modulator RAD1901","An orally available, selective estrogen receptor degrader (SERD) and selective estrogen receptor modulator (SERM), with potential antineoplastic and estrogen-like activities. Upon oral administration of higher doses of RAD1901, this agent acts as a SERD, which binds to the estrogen receptor (ER) and induces a conformational change that results in the degradation of the receptor. This may inhibit the growth and survival of ER-expressing cancer cells. At lower doses of this agent, RAD1901 acts as a SERM and has estrogen-like effects in certain tissues, which can both reduce hot flashes and protect against bone loss. In addition, RAD1901 is able to cross the blood-brain barrier (BBB).","Pharmacologic Substance"]
["C62783","Seliciclib","CYC202|R-roscovitine|SELICICLIB|Seliciclib","An orally available small molecule and cyclin-dependent kinase (CDK) inhibitor with potential apoptotic and antineoplastic activity. CDKs, serine/threonine kinases that play an important role in cell cycle regulation, are overexpressed in various malignancies. Seliciclib primarily inhibits CDK 2, 7, and 9 by competing for the ATP binding sites on these kinases, leading to a disruption of cell cycle progression. In addition, this agent seems to interfere with CDK-mediated phosphorylation of the carboxy-terminal domain of RNA polymerase II, thereby inhibiting RNA polymerase II-dependent transcription. This may lead to the down-regulation of anti-apoptotic factors, such as myeloid cell leukemia sequence 1 (Mcl-1), a protein crucial for the survival of a range of tumor cell types. The down-regulation of anti-apoptotic factors may lead to an induction of apoptosis, thereby further contributing to seliciclib's antiproliferative effects.","Organic Chemical|Pharmacologic Substance"]
["C102546","Selinexor","CRM1 Nuclear Export Inhibitor KPT-330|KPT-330|SINE KPT-330|Selective Inhibitor of Nuclear Export KPT-330|Selinexor","An orally available, small molecule inhibitor of CRM1 (chromosome region maintenance 1 protein, exportin 1 or XPO1), with potential antineoplastic activity. Selinexor modifies the essential CRM1-cargo binding residue cysteine-528, thereby irreversibly inactivates CRM1-mediated nuclear export of cargo proteins such as tumor suppressor proteins (TSPs), including p53, p21, BRCA1/2, pRB, FOXO, and other growth regulatory proteins. As a result, this agent, via the approach of selective inhibition of nuclear export (SINE), restores endogenous tumor suppressing processes to selectively eliminate tumor cells while sparing normal cells. CRM1, the major export factor for proteins from the nucleus to the cytoplasm, is overexpressed in a variety of cancer cell types.","Pharmacologic Substance"]
["C66939","Selumetinib","ARRY-142886|AZD6244|MEK Inhibitor AZD6244|MEK inhibitor AZD6244|SELUMETINIB|Selumetinib","An orally active, small molecule with potential antineoplastic activity. Selumetinib is an ATP-independent inhibitor of mitogen-activated protein kinase kinase (MEK or MAPK/ERK kinase) 1 and 2. MEK 1 and 2 are dual specificity kinases that are essential mediators in the activation of the RAS/RAF/MEK/ERK pathway, are often upregulated in various cancer cells, and are drivers of diverse cellular responses, including proliferation. Inhibition of both MEK1 and 2 by selumetinib prevents the activation of MEK1/2 dependent effector proteins and transcription factors, thereby leading to an inhibition of cellular proliferation in various cancers.","Pharmacologic Substance"]
["C95225","Selumetinib Sulfate","1H-Benzimidazole-6-Carboxamide, 5-((4-Bromo-2-Chlorophenyl)Amino)-4-Fluoro-N-(2- Hydroxyethoxy)-1-Methyl-, Sulfate (1:1)|1h-Benzimidazole-6-Carboxamide,5-((4-Bromo-2-Chlorophenyl)Amino)-4-Fluoro-N-(2- Hydroxyethoxy)-1-Methyl-, Sulphate (1:1)|5-((4-Bromo-2-Chlorophenyl)amino)-4-Fluoro-N-(2-Hydroxyethoxy)-1-Methyl-1H- Benzimidazole-6-Carboxamide Sulfate|5-((4-Bromo-2-Chlorophenyl)amino)-4-Fluoro-N-(2-Hydroxyethoxy)-1-Methyl-1H- Benzimidazole-6-Carboxamide Sulphate|AZD-6244 Hydrogen Sulfate|AZD6244 Hydrogen Sulfate|AZD6244 Hydrogen Sulphate|SELUMETINIB SULFATE|Selumetinib Sulfate|Selumetinib Sulphate","The sulfate salt of selumetinib, an orally active, small molecule with potential antineoplastic activity. Selumetinib is an ATP-independent inhibitor of mitogen-activated protein kinase kinase (MEK or MAPK/ERK kinase) 1 and 2. MEK 1 and 2 are dual specificity kinases that are essential mediators in the activation of the RAS/RAF/MEK/ERK pathway, are often upregulated in various cancer cells, and are drivers of diverse cellular responses, including proliferation. Inhibition of both MEK1 and 2 by selumetinib prevents the activation of MEK1/2 dependent effector proteins and transcription factors, thereby leading to an inhibition of cellular proliferation in various cancers.","Pharmacologic Substance"]
["C1831","Semaxanib","H-Indol-2-one, 3-((3,5-dimethyl-1H-pyrrol-2-yl)methylene)-1,3-dihydro-|SEMAXANIB|SU 5416|SU5416|Semaxanib|Semoxind|Sugen 5416|semaxanib","A quinolone derivative with potential antineoplastic activity. Semaxanib reversibly inhibits ATP binding to the tyrosine kinase domain of vascular endothelial growth factor receptor 2 (VEGFR2), which may inhibit VEGF-stimulated endothelial cell migration and proliferation and reduce the tumor microvasculature. This agent also inhibits the phosphorylation of the stem cell factor receptor tyrosine kinase c-kit, often expressed in acute myelogenous leukemia cells.","Organic Chemical|Pharmacologic Substance"]
["C78447","Semuloparin","AVE-5026|AVE5026|SEMULOPARIN|Semuloparin|ULMW heparin AVE5026|Ultra-low-molecular-weight Heparin (2000-3000 MW; Phosphazene Depolymerization)|Ultralow-Molecular-Weight Heparin AVE5026","An ultralow-molecular-weight heparin (ULMWH) (Mw: 2000-3000 daltons)consisting of a polydisperse mixture of oligomeric heparin fragments with potential anticoagulant activity. Ultralow-molecular-weight heparin AVE5026 binds to and activates antithrombin III (ATIII), which may result in the inhibition of activated factor Xa and, to a much lesser extent, factor IIa (thrombin) and so the inhibition of fibrin formation. Compared to low-molecular-weight heparins (LMWHs), AVE5026 exhibits an even higher ratio of anti-Factor Xa to anti-Factor IIa activity (>30:1). Compared to unfractionated heparins, the use of LMWHs is associated with lower incidences of major bleeding, osteoporosis and heparin-induced thrombocytopenia. Like LMWHs, this agent may inhibit tumor growth by regulating angiogenesis and apoptosis. AVE5026 is prepared by partial depolymerization of unfractionated porcine mucosal heparin.","Organic Chemical|Pharmacologic Substance"]
["C827","Semustine","1-(2-Chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea|1-(2-Chloroethyl)-3-(Trans-4-Methylcyclohexane)-1-Nitrosourea|1-(2-Chloroethyl)-3-(trans-4-methylcyclohexane)-1-nitrosourea|1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea|Lomustine, Methyl|Lomustine, methyl|MCCNU|MeCCNU|Methyl CCNU|Methyl Lomustine|SEMUSTINE|Semustine|Urea, 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitroso-, trans- (8CI)|Urea, N-(2-chloroethyl)-N'-(4-methylcyclohexyl)-N-nitroso-, trans- (9CI)|methyl-CCNU|semustine|trans-Methyl-CCNU|urea, 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitroso-, trans- (8CI)|urea, N-(2-chloroethyl)-N'-(4-methylcyclohexyl)-N-nitroso-, trans- (9CI)","A methylated derivative of carmustine with antineoplastic activity. As an alkylating agent, semustine forms covalent linkages with nucleophilic centers in DNA, causing depurination, base-pair miscoding, strand scission, and DNA-DNA cross-linking, which may result in cytotoxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C62524","Seneca Valley Virus-001","NTX-010|SVV-001|Seneca Valley Virus-001|Seneca Valley virus-001","A replication-competent oncolytic picornavirus with potential antineoplastic activity. Administered systemically, Seneca Valley virus-001 specifically targets and infects tumor cells with neuroendocrine characteristics. Upon infection, this agent replicates intracellularly, resulting in tumor cell lysis and reduced tumor cell proliferation. The selective tropism of virus replication may involve receptor-mediated internalization.","Pharmacologic Substance|Virus"]
["C26669","Seocalcitol","(1R-(1alpha(1R*,2E,4E),3abeta,4E(1R*,3S*,5Z),7aalpha))-5-((1-(6-Ethyl-6-hydroxy-1-methyl-2,4-octadienyl)octahydro-7a-methyl-4H-inden-4-ylidene)ethylidene)-4-methylene-1,3-cyclohexanediol|1(S),3(R)-Dihydroxy-20(R)-(5'-ethyl-5'-hydroxyhepta-1'(E),3'(E)-dien-1'-yl)-9,10-secopregna-5(Z),7(E),10(19)-triene|EB1089|SEOCALCITOL|Seocalcitol|seocalcitol","A vitamin D3 analogue with potential antineoplastic activity. Seocalcitol binds to and activates the vitamin D receptor, a cytoplasmic polypeptide expressed in normal vitamin D responsive tissues, but also overexpressed in certain cancers including hepatocellular carcinoma and pancreatic cancer. Mediated through vitamin D receptor, this agent induces cancer cell differentiation, inhibits cancer cell growth and induces apoptosis. In addition, seocalcitol may also induce growth arrest and apoptosis independent of vitamin D receptor activation through mechanisms that are not fully elucidated.","Pharmacologic Substance"]
["C61091","Sepantronium Bromide","1H-Naphth(2,3-d)imidazolium, 4,9-dihydro-1-(2-methoxyethyl)-2-methyl-4,9-dioxo-3-(pyrazinylmethyl)-, Bromide|SEPANTRONIUM BROMIDE|Sepantronium Bromide|Survivin Inhibitor YM155|YM-155","A small-molecule proapoptotic agent with potential antineoplastic activity. Sepantronium bromide selectively inhibits survivin expression in tumor cells, resulting in inhibition of survivin antiapoptotic activity (via the extrinsic or intrinsic apoptotic pathways) and tumor cell apoptosis. Survivin, a member of the inhibitor of apoptosis (IAP) gene family, is expressed during embryonal development and is absent in most normal, terminally differentiated tissues; upregulated in a variety of human cancers, its expression in tumors is associated with a more aggressive phenotype, shorter survival times, and a decreased response to chemotherapy.","Chemical Viewed Functionally"]
["C120313","S-equol","(-)-Equol|(3S)-3,4-dihydro-3-(4-hydroxyphenyl)-2H-1-benzopyran-7-ol|2H-1-benzopyran-7-ol, 3,4-Dihydro-3-(4-hydroxyphenyl)-, (3S)-|EQUOL, (-)-|S-equol","An orally bioavailable, non-steroidal estrogen naturally produced by the metabolism of the isoflavonoid daidzein by human intestinal microflora, with potential chemoprotective and estrogen receptor (ER) modulating activities. S-equol preferentially binds to and activates the beta isoform of ER in certain target tissues, while having an antagonistic effect in other tissues. This modulates the expression of ER-responsive genes in a tissue-specific manner. This agent may increase bone mineral density, affect vasomotor symptoms, and may decrease the proliferation rate of susceptible cancer cells. In addition, this agent interferes with the activity of enzymes involved in steroid biosynthesis. S-equol inhibits dihydrotestosterone (DHT) production and may inhibit the proliferation of androgen-driven prostate cancer. S-equol is the biologically active enantiomer while R-equol is essentially inactive and has a weak affinity for alpha-ER.","Pharmacologic Substance"]
["C1763","Sergiolide","Sergeolide|Sergiolide","A quassinoid phytochemical isolated from Cedronia granatensis and other plant species with potential antineoplastic activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C78859","Seribantumab","MM-121|SAR 256212|SERIBANTUMAB|Seribantumab","A fully human monoclonal antibody directed against the human epidermal growth factor receptor ErbB3 (Her3) with potential antineoplastic activity. Seribantumab binds to and inhibits ErbB3 activation, which may result in inhibition of ErbB3-dependent PI3K/Akt signaling and so inhibition of cellular proliferation and differentiation. ErbB3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in solid tumors, including breast, lung, and colorectal tumors of epithelial origin; it has no active kinase domain itself but is activated through heterodimerization with other members of the EGFR receptor family that do.","Pharmacologic Substance"]
["C73985","Serine Protease Inhibitor WX-671","Serine Protease Inhibitor WX-671|WX-671","An orally bioavailable, 3-amidinophenylalanine-derived, second generation serine protease inhibitor prodrug targeting the human urokinase plasminogen activator (uPA) system with potential antineoplastic and antimetastatic activities. After oral administration, serine protease inhibitor WX-671 is converted to the active N alpha-(2,4,6-triisopropylphenylsulfonyl)-3-amidino-(L)-phenylalanine-4-ethoxycarbonylpiperazide (WX-UK1), which inhibits several serine proteases, particularly uPA; inhibition of uPA may result in the inhibition of tumor growth and metastasis. uPA is a serine protease involved in degradation of the extracellular matrix and tumor cell migration and proliferation.","Pharmacologic Substance"]
["C68963","Serine/Threonine Kinase Inhibitor XL418","Serine/Threonine Kinase Inhibitor XL418|XL418","A selective, orally active small molecule, targeting protein kinase B (PKB or AKT) and ribosomal protein S6 Kinase (p70S6K), with potential antineoplastic activity. XL418 inhibits the activities of PKB and p70S6K, both acting downstream of phosphoinosotide-3 kinase (PI3K). These kinases are often upregulated in a variety of cancers. Inhibition of PKB by this agent will induce apoptosis, while inhibition of p70S6K will result in the inhibition of translation within tumor cells.","Pharmacologic Substance"]
["C122403","Sevacizumab","Sevacizumab","A monoclonal antibody directed against the human vascular endothelial growth factor (VEGF), with potential antiangiogenic activity. Upon administration, sevacizumab specifically binds to and inhibits VEGF, thereby preventing its binding to VEGF receptors (VEGFRs). This prevents VEGF/VEGFR-mediated signaling and inhibits the proliferation of vascular endothelial cells and tumor cells. VEGF, overexpressed in a variety of cancer cells, is associated with increased invasiveness and decreased survival.","Immunologic Factor|Pharmacologic Substance"]
["C29424","Shared Anti-Idiotype-AB-S006","Murine Monoclonal Antibody To Human B Cell Lymphomas (Anti- Idiotypes) (S006)|Shared Anti-Idiotype AB-S006|Shared Anti-Idiotype-AB-S006","A murine monoclonal anti-idiotype antibody that targets human B-cell lymphomas with potential antineoplastic activity.  Shared Anti-Id-Ab-S006 binds to antigens on neoplastic B cells, resulting in tumor cell destruction by the reticuloendothelial system or cytotoxic T lymphocytes (CTL). (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C29432","Shared Anti-Idiotype-AB-S024A","Shared Anti-Idiotype-AB-S024A","A murine monoclonal anti-idiotype antibody with potential antineoplastic activity. Shared anti-id-Ab-S024A binds to tumor-associated antigens (TAAs) on the surface of neoplastic cells resulting in tumor cell destruction by the reticuloendothelial system or cytotoxic T lymphocytes (CTL).","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2318","Shark Cartilage","BeneFin (Lane Shark Cartilage Powder)|Cartilade|Shark Cartilage","A nutritional supplement gleaned from the exoskeleton of the shark. Shark cartilage inhibits metalloproteinases (MMPs) and possesses antiangiogenic and antimetastatic properties. (NCI04)","Pharmacologic Substance"]
["C1798","Shark Cartilage Extract AE-941","AE-941|Neovastat|Shark Cartilage Extract AE-941|[AElig]-941","A multifunctional antiangiogenic agent derived from shark cartilage with potential antineoplastic activity. Shark cartilage extract AE-941 competitively inhibits the binding of pro-angiogenic vascular endothelial growth factor (VEGF) to its cellular receptor, thereby inhibiting endothelial cell proliferation. This agent also inhibits matrix metalloproteinases (MMPs), stimulates tissue plasminogen activator (tPA), and activates caspase-mediated apoptotic pathways in endothelial cells.","Organic Chemical|Pharmacologic Substance"]
["C82692","Sheddase Inhibitor INCB007839","INCB007839|Sheddase Inhibitor INCB007839","An orally bioavailable inhibitor of the ADAM (A Disintegrin And Metalloprotease) family of multifunctional membrane-bound proteins with potential antineoplastic activity. Sheddase inhibitor INCB007839 represses the metalloproteinase \"\"sheddase\"\" activities of ADAM10 and ADAM17, which may result in the inhibition of tumor cell proliferation. The metalloproteinase domains of ADAMs cleave cell surface proteins at extracellular sites proximal to the cell membrane, releasing or \"\"shedding\"\" soluble protein etcodomains from the cell surface; the disintegrin domains of these multifunctional proteins interact with various components of the extracellular matrix (ECM). ADAM10 processes particular epithelial growth factor receptor (EGFR) ligands and appears to regulate Notch signaling through the cleavage of Notch and its related ligand delta-like ligand-1 (Dll-1). ADAM17 (also known as Tumor necrosis factor-Converting Enzyme or TACE) is involved in processing tumor necrosis factor (TNF) from its membrane bound precursor to its soluble circulating form and in processing ligands for the epidermal growth factor receptor (EGFR) family.","Pharmacologic Substance"]
["C88290","Short Chain Fatty Acid HQK-1004","HQK-1004|SCFA HQK-1004|Short Chain Fatty Acid HQK-1004","A short chain fatty acid (SCFA) with potential herpes simplex virus thymidine kinase gene (HSV-TK)-inducing activity. Upon administration, short chain fatty acid HQK-1004 may induce the expression of thymidine kinase (TK) by a silenced HSV-TK, which may activate a co-administered antiviral prodrug such as ganciclovir, resulting in the destruction of virally-infected cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C2690","Sho-Saiko-To","Keisho-To|Minor Bupleurum Formula|Sho-Saiko-To|Sho-saiko-to|TJ-9|Xiao Chai Hu Tang|Xiao-Chai-Hu-Tang","A botanical formulation with potential chemopreventive activities. Sho-Saiko-to, an herbal mixture, contains seven herbal extracts whose mechanism of action if not fully understood. There is evidence of antiproliferative effects against hepatocellular carcinoma in vitro. Other effects of this agent described in animal models include the prevention of liver injury and hepatocyte-regenerating activity. Antitumor effects associated with this herbal product may include induction of apoptosis, cell cycle arrest at the G0/G1 phase, and activation of an immune response, characterized by the release of cytokines as well as activation of effector cells, such as macrophages and natural killer cells.","Pharmacologic Substance"]
["C120207","Shu Yu Wan Formula","Pill of Chinese Yam|Shu Yu Wan Formula|Shu Yu Wan|Shuyu Wan","A traditional Chinese medicine comprising different herbs that may be used for a variety of medical purposes. Shu Yu Wan contains the following herbs: Da Zao (Fructus Jujubae), Shu Yu (Radix Dioscoreae Quinquelobae), Gan Cao (Radix Glycyrrhizae Uralensis), Shu Di Huang (Radix Rehmanniae Glutinosae Praeparata), Dang Gui (Radix Angelicae Sinensis), Shen Qu (Massa Medica Fermentata), Gui Zhi (Ramulus Cinnamomi Cassiae), Da Dou Juan (Semen Glycines Germinatum), E Jiao (Gelatinum Corii Asini), Ren Shen (Radix Ginseng), Bai Zhu (Rhizoma Atractylodis Macrocephalae), Fu Ling (Sclerotium Poriae Cocos), Chuan Xiong (Radix Ligustici Wallichii), Bai Shao Yao (Radix Paeoniae Lactiflorae), Mai Men Dong (Tuber Ophiopogonis Japonici), Chai Hu (Radix Bupleuri), Fang Feng (Radix Ledebouriellae Divaricatae), Jie Geng (Radix Platycodi Grandiflori), Xing Ren (Semen Pruni Armeniacae), Bai Lian (Radix Ampelopsis Japonicae) and Sheng Jiang (Rhizoma Zingiberis Officinalis Recens). This formula may be used to relieve chemotherapeutic side effects or cancer-related symptoms.","Pharmacologic Substance"]
["C69000","Sialyl Lewis-Keyhole Limpet Hemocyanin Conjugate Vaccine","Sialyl Lewis-Keyhole Limpet Hemocyanin Conjugate Vaccine","A vaccine consisting of the oligosaccharide antigen sialyl Lewis (CA19-9) conjugated to the nonspecific immunomodulator keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Upon administration, sialyl Lewis-keyhole limpet hemocyanin conjugate vaccine may induce production of IgG and IgM antibodies as well as trigger an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells expressing the sialyl Lewis antigen. Sialyl Lewis is a blood group antigen and a tumor-associated antigen associated with epithelial cancers such as breast cancer and various digestive cancers. Sialyl Lewis serves as a ligand for the cytokine-inducible cell adhesion molecule (CAM) E-selectin, an endothelial cell-specific type I transmembrane surface protein, thus facilitating hematogenous metastasis by mediating the adhesion of circulating cancer cells to vascular endothelium.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1226","Sialyl Tn Antigen","CD175s|STn Antigen|STn|Sialyl Tn Antigen|Sialyl-Tn Antigen|Sialyl-Tn","A tumor-associated core-region carbohydrate antigen of epithelial mucin, expressed in most colon carcinoma, mucinous carcinoma, pancreatic cancer, gastric, lung, breast, and ovarian carcinoma. Sialosyl-Tn (STn) antigen has been shown to be highly sensitive and a specific marker of colorectal cancer, associated with more aggressive diseases and poor prognosis. STn antigen and its immediate precursor, Tn antigen, are mucin type glycoprotein structures associated with the earliest steps of mucin O-linked glycosylation. When combined with a carrier molecule, keyhole limpet hemocyanin (KLH), this antigen may be co-administered with oral cyclophosphamide as an immune modulator.","Immunologic Factor|Organic Chemical"]
["C1690","Sialyl Tn-KLH Vaccine","STn-KLH Vaccine|Sialyl Tn-KLH Vaccine|Sialyl Tn-KLH|Theratope STn-KLH Vaccine|Theratope siayl-Tn-KLH vaccine|Theratope|sialyl Tn-KLH","A vaccine containing a pancarcinoma carbohydrate antigen conjugated with keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Sialylated Tn antigen (sTn) is a monosaccharide glycan usually O-linked to serine or threonine residues of mucins found on most epithelial cancers. Conjugation with KLH, a hapten carrier and an immunostimulant, improves host immune responses. Vaccination with sTn-KLH vaccine may produce antibodies and elicit a cytotoxic T lymphocyte (CTL) response against those tumor cells expressing sTn, resulting in decreased tumor growth.","Immunologic Factor|Pharmacologic Substance"]
["C95772","siG12D LODER","siG12D LODER","A proprietary, miniature biodegradable polymeric matrix containing small-interfering RNAs for the mutated KRAS oncogene, KRASG12D, (siG12D), with potential antitumor activity. Upon intratumoral injection, this siG12D is released locally, thereby preventing translation of KRAS proteins and potentially inhibiting growth of tumor cells overexpressing KRAS. KRAS, a member of the small GTPase superfamily, is mutated in over 90% of human pancreatic ductal adenocarcinomas (PDAC) and is associated with tumor cell proliferation and reduced survival.","Pharmacologic Substance"]
["C64618","Silatecan AR-67","7-Tert-butyldimethylsilyl-10-hydroxycamptothecin|7-t-butyldimethylsilyl-10-hydroxycamptothecin|AR-67|DB-67|Silatecan AR-67","A synthetic, highly lipophilic derivative of camptothecin, with potential antineoplastic and radiosensitizing activities. 7-tert-butyldimethylsilyl-10-hydroxycamptothecin binds to and stabilizes the topoisomerase I-DNA covalent complex. This inhibits the religation of topoisomerase I-mediated single-stranded DNA breaks and produces lethal double-stranded DNA breaks when encountered by the DNA replication machinery, thereby inhibiting DNA replication and inducing apoptosis. Camptothecin readily undergoes hydrolysis at physiological pH, changing its conformation from the active lactone structure to an inactive carboxylate form. Modifications on the E ring of camptothecin prevent binding of human serum albumin, which prefers the inactive carboxylate form, thereby enhancing the stability of the active lactone structure and resulting in prolonged agent activity. In addition, this agent sensitizes tumor cells toward radiation treatment.","Organic Chemical|Pharmacologic Substance"]
["C85460","Silmitasertib Sodium","5-((3-chlorophenyl)amino)-benzo(c)-2,6-naphthyridine-8-carboxylic Acid Sodium Salt|CK2 Inhibitor CX-4945|CX-4945|SILMITASERTIB SODIUM|Silmitasertib Sodium","The sodium salt of silmitasertib, an orally bioavailable small-molecule inhibitor of CK2 with potential antineoplastic activity. Silmitasertib selectively binds to and inhibits the enzyme casein kinase II (CK2), which may lead to an inhibition of cellular proliferation. CK2, a protein kinase often overexpressed in a variety of cancer cell types, appears to be correlated with malignant transformation, tumor growth and survival.","Pharmacologic Substance"]
["C61084","Siltuximab","Anti-IL-6 Chimeric Monoclonal Antibody|CNTO 328|CNTO-328|SILTUXIMAB|Siltuximab|Sylvant|anti-IL-6 chimeric monoclonal antibody|cCLB8","A chimeric, human-murine, monoclonal antibody targeting the pro-inflammatory cytokine interleukin 6 (IL-6), with antitumor and anti-inflammatory activities. Upon intravenous administration of siltuximab, this agent targets and binds to IL-6. This inhibits the binding of IL-6 to the IL-6 receptor (IL-6R), which results in the blockade of the IL-6/IL-6R-mediated signal transduction pathway. This inhibits cancer cell growth in tumors overexpressing IL-6.","Amino Acid, Peptide, or Protein"]
["C1227","Simalikalactone D","(+)-Simalikalactone D|Picras-3-ene-2,16-dione, 13,20-epoxy-1,11,12-trihydroxy-15-(2-methyl-1-oxobutoxy)-, (11beta)-|Simalikalactone D","A quassinoid phytochemical isolated from Simaba multiflora, Quassia africana and other plant species with potential antineoplastic activity.  This agent also has antimalarial and antiviral properties. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C129015","Simeprevir","HSDB 8227|N-(17-(2-(4-isopropylthiazole-2-yl)-7-methoxy-8-methylquinolin-4-yloxy)-13-methyl-2,14-dioxo-3,13-diazatricyclo(13.3.0.04,6)octadec-7-ene-4-carbonyl)(cyclopropyl)sulfonamide|Olysio|SIMEPREVIR|Simeprevir|TMC 435|TMC-435|TMC435","An orally bioavailable inhibitor of the hepatitis C virus (HCV) protease complex comprised of non-structural protein 3 and 4A (NS3/NS4A), with activity against HCV genotype 1. Upon administration, simeprevir reversibly binds to the active center and binding site of the HCV NS3/NS4A protease and prevents NS3/NS4A protease-mediated polyprotein maturation. This disrupts both the processing of viral proteins and the formation of the viral replication complex, which inhibits viral replication in HCV genotype 1-infected host cells. NS3, a serine protease, is essential for the proteolytic cleavage of multiple sites within the HCV polyprotein and plays a key role during HCV ribonucleic acid (RNA) replication. NS4A is an activating factor for NS3. HCV is a small, enveloped, single-stranded RNA virus belonging to the Flaviviridae family; HCV infection is associated with the development of hepatocellular carcinoma (HCC).","Pharmacologic Substance"]
["C91735","Simtuzumab","AB-0024|AB0024|GS 6624|GS-6624|SIMTUZUMAB|Simtuzumab","A humanized monoclonal antibody against lysyl oxidase-like 2 (LOXL2), with potential antineoplastic activity. Anti-LOXL2 monoclonal antibody GS 6624 targets and specifically binds to the scavenger receptor cysteine rich domain 4 (SRCR-4) on LOXL2, thereby preventing the crosslinking of collagen and inhibiting the recruitment and activation of fibroblasts. Inhibiting fibroblast activation and the subsequent production of growth factors and chemokines may lead to an inhibition of tumor cell proliferation. LOXL2, a member of the lysyl oxidase (LO) gene family, is an extracellular, copper-dependent enzyme overexpressed in a variety of tumor cell types, and contributes to tumor cell invasion and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C38685","Siplizumab","MEDI-507|Siplizumab|siplizumab","A humanized monoclonal immunoglobulin G1 antibody with potential antineoplastic activity. Siplizumab binds to CD2, a specific receptor found in T cells and NK cells, thereby triggering a host immune response that results in lysis of CD2+ cells, selective suppression of the immune system, and control of activated T cell growth.","Immunologic Factor|Pharmacologic Substance"]
["C1985","Sipuleucel-T","APC8015 Vaccine|APC8015|PA2024 (PAP/GM-CSF)-Loaded Dendritic Cell Vaccine|Provenge|SIPULEUCEL-T|Sipuleucel-T|sipuleucel-T","A cell-based vaccine composed of autologous antigen-presenting peripheral blood mononuclear cells (enriched for a dendritic cell fraction) that have been exposed to a recombinant protein consisting of granulocyte-macrophage colony-stimulating factor (GM-CSF) fused to prostatic-acid phosphatase (PAP), a protein expressed by prostate cancer cells.  Upon administration, the vaccine may stimulate an antitumor T-cell response against tumor cells expressing PAP. (NCI05)","Cell|Immunologic Factor"]
["C62536","siRNA-Expressing SV40","siRNA-Expressing SV40","A simian virus 40 (SV40)-based shuttle vector, encoding small interfering RNA (siRNA), with potential antineoplastic activity. The expression of siRNA in target tumor cells transfected with an siRNA-expressing SV40 vector may result in siRNA-mediated silencing of target oncogenes and, so, the inhibition of tumor cell growth and the induction of tumor cell death.","Pharmacologic Substance"]
["C116353","siRNA-transfected Peripheral Blood Mononuclear Cells APN401","APN401|siRNA-transfected PBMC APN401|siRNA-transfected Peripheral Blood Mononuclear Cells APN401","Autologous peripheral blood mononuclear cells (PBMCs) transfected ex vivo with small-interfering ribonucleic acid (siRNA) directed against the E3 ubiquitin ligase casitas B-lineage lymphoma-b gene (Cbl-b), with potential immunoactivating and antineoplastic activities. The Cbl-b gene is silenced ex vivo through the binding of Cbl-b siRNA to Cbl-b mRNA, which prevents the translation of the Cbl-b protein in T-lymphocytes. Upon infusion, the activated, Cbl-b-silenced T-lymphocytes are able to increase the production of cytokines, proliferate and activate the immune system, which leads to cancer cell eradication. Cbl-b, a negative regulator of the immune system, is mutated in a variety of cancer cell types. Its expression is inversely correlated with activation of T-lymphocytes and tumor cell eradication.","Cell|Pharmacologic Substance"]
["C117734","Sitravatinib","1,1-Cyclopropanedicarboxamide, N-(3-Fluoro-4-((2-(5-(((2-methoxyethyl)amino)methyl)-2-pyridinyl)thieno(3,2-b)pyridin-7-yl)oxy)phenyl)-N'-(4-fluorophenyl)-|MGCD516|SITRAVATINIB|Sitravatinib","An orally bioavailable, receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Upon administration, sitravatinib binds to and inhibits the activity of several RTKs including hepatocyte growth factor receptor (HGFR; c-Met; MET), tyrosine-protein kinase receptor UFO (AXL receptor tyrosine kinase; AXL), mast/stem cell growth factor receptor (SCFR; c-kit; KIT), the receptor tyrosine kinase MER, discoidin domain receptor 2 (DDR2), vascular endothelial growth factor receptor (VEGFR) types 1 (VEGFR-1; FLT1), 2 (VEGFR-2; KDR; Flk-1) and 3 (VEGFR-3), members of the platelet-derived growth factor receptor (PDGFR) family, RET (rearranged during transfection), tropomyosin-related kinases (TRK) and members of the ephrin (Eph) family of receptor tyrosine kinases. This may result in both the inhibition of signal transduction pathways mediated by these RTKs and the reduction of tumor cell proliferation in cancer cell types that overexpress these RTKs.","Pharmacologic Substance"]
["C61305","Sivifene","4,4'-Dihydroxybenzophenone 2,4-dinitrophenylhydrazone|A-007|Aryl Hydrazone A-007 Gel|SIVIFENE|Sivifene","The phenylhydrazone 4,4'-dihydroxybenzophenone-2,4-dinitrophenylhydrazone formulated as a topical agent with immunomodulating and potential antineoplastic activities. Applied topically as a gel, sivifene may stimulate a local immune response against human papillomavirus (HPV)-induced cervical intraepithelial neoplasia (CIN).","Pharmacologic Substance"]
["C824","Sizofiran","MC-Glucan|Poly(3-(O-beta-D-glucopyranosyl-(1-3)-O-(beta-D-glucopyranosyl-(1-6))-O-beta-D-glucopyranosyl-(1-3)-O-beta-D-glucopyranosyl)-1)|SIZOFIRAN|Schizophyllan|Schizophyllane|Sixofilan|Sizofiran|Sonifilan","A soluble beta-D-glucan produced by the Basidiomycetes fungus, Schizophyllum commune Fries, with potential immunomodulating and antitumor activities. Although sizofiran's exact mechanism of action has yet to be fully elucidated, this agent appears to stimulate the immune system by increasing cytokine production, activating macrophages and enhancing the activity of polymorphonuclear leukocytes (PML) and natural killer (NK) cells.","Organic Chemical|Pharmacologic Substance"]
["C38130","SL11093","SL11093","A synthetic compound of the polyamine class of chemicals with potential antineoplastic activity. Natural endogenous polyamines bind to DNA and are involved in a number of cellular processes such as cell division, differentiation, and membrane function. SL11093 displaces these polyamines from their DNA binding sites, resulting in cessation of cell growth and cell death. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C88274","Smac Mimetic GDC-0152","GDC-0152|IAP Antagonist GDC-0152|Smac Mimetic GDC-0152","A second mitochondrial activator of caspases (Smac) mimetic inhibitor of IAPs (Inhibitor of Apoptosis Proteins) with potential antineoplastic activity. Smac mimetic GDC-0152 binds to the Smac binding groove on IAPs, including the direct caspase inhibitor X chromosome-linked IAP (XIAP) and the cellular IAPs 1 and 2, which may inhibit their activities and promote the induction of apoptosis through apoptotic signaling pathways.  IAPs are overexpressed by many cancer cell types and suppress apoptosis by binding to and inhibiting active caspases-3, -7 and -9 via their baculoviral lAP repeat (BIR) domains. Smac, the endogenous IAP antagonist, relies on its N-terminal four amino-acid motif for binding to IAPs.","Pharmacologic Substance"]
["C103825","Smac Mimetic GDC-0917","GDC-0917|IAP Antagonist GDC-0917|SMAC/DIABLO Mimetic GDC-0917|Smac Mimetic GDC-0917","An orally available, monovalent mimetic of second mitochondrial-derived activator of caspases (Smac/DIABLO) and inhibitor of IAPs (Inhibitor of Apoptosis Proteins) with potential antineoplastic activity. Smac mimetic GDC-0917 binds to the Smac binding groove on IAPs, including the direct caspase inhibitor X chromosome-linked IAP (XIAP) and the cellular IAPs 1 and 2. This inhibits the activities of these IAPs and promotes the induction of apoptosis through apoptotic signaling pathways.  IAPs are overexpressed by many cancer cell types and suppress apoptosis by binding to and inhibiting active caspases-3, -7 and -9 via their baculoviral lAP repeat (BIR) domains.","Pharmacologic Substance"]
["C91079","Smac Mimetic LCL161","LCL161|Smac Mimetic LCL161","An orally bioavailable second mitochondrial-derived activator of caspases (SMAC) mimetic and inhibitor of IAP (Inhibitor of Apoptosis Protein) family of proteins, with potential antineoplastic activity. SMAC mimetic LCL161 binds to IAPs, such as X chromosome-linked IAP (XIAP) and cellular IAPs 1 and 2. Since IAPs shield cancer cells from the apoptosis process, this agent may restore and promote the induction of apoptosis through apoptotic signaling pathways in cancer cells. IAPs are overexpressed by many cancer cell types and suppress apoptosis by binding and inhibiting active caspases-3, -7 and -9, which play essential roles in apoptosis (programmed cell death), necrosis and inflammation.","Pharmacologic Substance"]
["C77861","Smoothened Antagonist BMS-833923","BMS-833923|Smoothened Antagonist BMS-833923|XL139","An orally bioavailable small molecule SMO (Smoothened) inhibitor with potential antineoplastic activity. SMO inhibitor BMS-833923 inhibits the sonic hedgehog (SHH) pathway protein SMO, which may result in a suppression of the SHH signaling pathway.  SMO is a G-protein coupled receptor that lies just downstream of the SHH ligand cell surface receptor Patched-1 in the SHH pathway; in the absence of ligand Patched-1 inhibits SMO and ligand binding to Patched-1 results in increased levels of SMO. The SHH signaling pathway plays an important role in cellular growth, differentiation and repair; constitutive activation of this pathway is associated with uncontrolled cellular proliferation and has been observed in a variety of cancers.","Organic Chemical|Pharmacologic Substance"]
["C88337","Smoothened Antagonist LDE225 Topical","LDE225|Smoothened Antagonist LDE225 Topical","A topical formulation of the small-molecule Smoothened (Smo) antagonist LDE225 with potential antineoplastic activity. Upon topical application, smoothened antagonist LDE225 selectively binds to the Hedgehog (Hh)-ligand cell surface receptor Smo, which may result in the suppression of the Hh signaling pathway and, so, the inhibition of tumor cells in which this pathway is abnormally activated. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair. Inappropriate activation of Hh pathway signaling and uncontrolled cellular proliferation, as is observed in a variety of cancers, may be associated with mutations in the Hh-ligand cell surface receptor Smo.","Pharmacologic Substance"]
["C91089","Smoothened Antagonist LEQ506","LEQ506|Smoothened Antagonist LEQ506","An orally bioavailable small-molecule Smoothened (Smo) antagonist with potential antineoplastic activity. Smoothened antagonist LEQ506 selectively binds to the Hedgehog (Hh)-ligand cell surface receptor Smo, which may result in the suppression of the Hh signaling pathway, thereby inhibiting tumor cell growth. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair. Dysregulated activation of Hh pathway signaling and uncontrolled cellular proliferation, as is observed in a variety of cancers, may be associated with mutations in the Hh-ligand cell surface receptor Smo.","Pharmacologic Substance"]
["C116874","Smoothened Antagonist TAK-441","6-Ethyl-N-[1-(hydroxyacetyl)piperidin-4-yl]-1-methyl-4-oxo-5-(2-oxo-2-phenylethyl)-3-(2,2,2-trifluoroethoxy)-4,5-dihydro-1H-pyrrolo[3,2-c]pyridine-2-carboxamide|Smoothened Antagonist TAK-441|TAK-441","An orally bioavailable pyrrolopyridine derivative and Smoothened (Smo) antagonist with potential antineoplastic activity. Smo antagonist TAK-441 selectively binds to and inhibits the activity Smo, which is a cell surface co-receptor for ligands in the Hedgehog (Hh) family. This may result in a suppression of Hh-mediated signaling pathways, thereby inhibiting the growth of tumor cells in which this pathway is aberrantly activated.  Smo is a G-protein coupled receptor that lies just downstream of the Hh cell surface receptor Patched-1 in the Hh pathway; in the absence of ligand, Patched-1 (Ptch1) inhibits Smo, and ligand binding to Ptch1 results in increased levels of Smo. The Hh-mediated signaling pathways play an important role in cellular growth and differentiation, and tissue repair; constitutive activation of this pathway is associated with uncontrolled cellular proliferation in a variety of cancers.","Organic Chemical|Pharmacologic Substance"]
["C71521","SN-38-Loaded Polymeric Micelles NK012","NK012|SN-38-Loaded Polymeric Micelles NK012","A formulation consisting of polymeric micelles loaded with the irinotecan metabolite SN-38 with potential antineoplastic activity. SN-38-loaded polymeric micelles NK012 is an SN-38-releasing nanodevice constructed by covalently attaching SN-38 to the block copolymer PEG-PGlu, followed by self-assembly of amphiphilic block copolymers in an aqueous milieu. SN-38 (7-ethyl-10-hydroxy-camptothecin), a biological active metabolite of the prodrug irinotecan (CPT-11), binds to and inhibits topoisomerase I by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks, inhibition of DNA replication, and apoptosis. SN-38 has been reported to exhibit up to 1,000-fold more cytotoxic activity against various cancer cells in vitro than irinotecan. This formulation increases the water-solubility of SN-38 and allows the delivery of higher doses of SN-38 than those achievable with SN-38 alone.","Pharmacologic Substance"]
["C98288","SNS01-T Nanoparticles","SNS01-T Nanoparticles|SNS01-T","A colloidal mixture of nanoparticles consisting of small interfering RNA (siRNA) targeting the native eukaryotic translation initiation factor 5A (eIF5A), plasmids expressing a pro-apoptotic mutant of elF5A under the control of a B-cell specific promoter (B29), and a synthetic cationic polymer polyethylenimine (PEI) as a delivery vehicle, with potential antineoplastic activity. Upon administration, the siRNA component of SNS01-T suppresses elF5A expression, thereby interfering with translation of eIF5A and reducing levels of hypusinated elF5A in cancer cells. In turn, this inhibits activation of the transcription factor NF-kB and induces apoptosis. In addition, the B-cell specific plasmid component expresses an arginine substituted form of eIF5A, eIF5AK50R, which can not be hypusinated, thus leads to a selective induction of apoptosis in B-cells. The native unhypusinated form of eIF5A is pro-apoptotic and can be modified at the lysine residue, by deoxyhypusine synthase (DHS) and subsequently deoxyhypusine hydroxylase (DHH), to the anti-apoptotic hypusinated form which is associated with tumor cell growth and survival. The delivery vehicle protects the siRNA and plasmid from degradation.","Pharmacologic Substance"]
["C66540","Sobuzoxane","1,2-Bis(4-isobutoxycarbonyloxymethyl-3,5-dioxo-piperazin-1-yl)ethane|MST-16|SOBUZOXANE|Sobuzoxane","The orally available active prodrug of ICRF-154, a bisdioxopiperazine derivative, with cardioprotective and antineoplastic activities. Like other ICRF compounds, sobuzoxane and its active metabolite ICRF-154 interfere with topoisomerase II activity prior to the formation of intermediate cleavable DNA-enzyme complexes during the catalytic cycle resulting in tumor cell growth inhibition. Furthermore, sobuzoxane chelates metal cations thereby limiting the formation of free radical-generating anthracycline-metal complexes and may prevent anthracycline-induced oxidative damage to cardiac and soft tissues.","Pharmacologic Substance"]
["C2208","Sodium Borocaptate","BSH|Borocaptate Sodium|Borocarpin|Sodium Borocaptate|sodium borocaptate","A boron-carrying compound. After parenteral administration, sodium borocaptate accumulates preferentially in tumor cells. When exposed to neutron irradiation, borocaptate absorbs neutrons and self-destructs releasing short-range alpha radiation and 'recoil' lithium in tumor cells, resulting in alpha radiation-induced tumor cell death. This highly selective, localized radiotargeting of tumor cells, known as boron neutron capture therapy (BNCT), spares adjacent normal tissues. (NCI04)","Inorganic Chemical|Pharmacologic Substance"]
["C2337","Sodium Butyrate","Butyrate sodium|Butyrate|Butyric Acid, Sodium Salt|SODIUM BUTYRATE|Sodium Butyrate|Sodium butanoate|Sodium butyrate|butyric acid, sodium salt|sodium butanoate","The sodium salt of butyrate with potential antineoplastic activity. Butyrate, a short chain fatty acid, competitively binds to the zinc sites of class I and II histone deacetylases (HDACs). This binding affects hyperacetylation of histones, resulting in a modified DNA conformation, which subsequently leads to the uncoiling or relaxing of chromatin. Enhanced accessibility of chromatin to transcription-regulatory complexes leads to increased transcriptional activation of various epigenetically suppressed genes. Butyrate, a HDAC inhibitor, induces cell cycle arrest in G1 or G2/M and also increases the expression of other genes and proteins involved in cellular differentiation and apoptotic signaling.","Organic Chemical|Pharmacologic Substance"]
["C73591","Sodium Dichloroacetate","CPC 211|Dichloroacetic Acid, Sodium Salt|SODIUM DICHLOROACETATE|Sodium Dichloroacetate","The sodium salt of dichloroacetic acid with potential antineoplastic activity. Dichloroacetate ion inhibits pyruvate dehydrogenase kinase, resulting in the inhibition of glycolysis and a decrease in lactate production. This agent may stimulate apoptosis in cancer cells by restoring normal mitochondrial-induced apoptotic signaling.","Pharmacologic Substance"]
["C91098","Sodium Metaarsenite","KML-001|SODIUM ARSENITE|Sodium Arsenite|Sodium Metaarsenite","A highly soluble, orally available trivalent arsenic-containing telomerase inhibitor with potential antitumor activity. Although the exact mechanism through which sodium metaarsenite exerts its effect has yet to be fully elucidated, this agent appears to target and bind to telomeric sequences, specifically TTAGGG repeats, leading to a shortening of telomeres, and subsequent induction of apoptosis and inhibition of tumor cell growth. In addition, sodium metaarsenite also leads to the translocation of the catalytic subunit of telomerase into the cytoplasm and inhibition of the activity of telomerase. Telomerase is active in most tumors cells and is responsible for the maintenance of telomere length and plays a key role in cellular proliferation, but is quiescent in normal, healthy cells. The susceptibility to sodium metaarsenite seems to be inversely correlated with initial length of telomeres.","Inorganic Chemical|Pharmacologic Substance"]
["C1440","Sodium Phenylbutyrate","4-Phenylbutyric Acid, Sodium Salt|Buphenyl|Phenylbutyrate Sodium|SODIUM PHENYLBUTYRATE|SPB11|Sodium 4-Phenylbutyrate|Sodium 4-phenylbutyrate|Sodium Phenylbutyrate|phenylbutyrate","The sodium salt of phenylbutyrate, a derivative of the short-chain fatty acid butyrate, with potential antineoplastic activity. Phenylbutyrate reversibly inhibits class I and II histone deacetylases (HDACs), which may result in a global increase in gene expression, decreased cellular proliferation, increased cell differentiation, and the induction of apoptosis in susceptible tumor cell populations.","Organic Chemical|Pharmacologic Substance"]
["C834","Sodium Salicylate","Benzoic acid, 2-hydroxy-, monosodium salt|SODIUM SALICYLATE|Salicylate, sodium|Sodium Salicylate|Sodium salicylate|sodium salicylate","The sodium salt of salicylic acid. As a nonsteroidal anti-inflammatory drug (NSAID), sodium salicylate irreversibly acetylates cyclooxygenases I and II, thereby inhibiting prostaglandin synthesis and associated inflammation and pain.  This agent may also activate mitogen-activated protein kinase (p38MAPK), thereby inducing apoptosis in cancer cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C87346","Sodium Selenite","Disodium Selenium Trioxide|SODIUM SELENITE|Selenious Acid Disodium Salt|Selenious Acid, Sodium Salt (1:2)|Sodium Selenite","An inorganic form of the trace element selenium with potential antineoplastic activity. Selenium, administered in the form of sodium selenite, is reduced to hydrogen selenide (H2Se) in the presence of glutathione (GSH) and subsequently generates superoxide radicals upon reaction with oxygen. This may inhibit the expression and activity of the transcription factor Sp1; in turn Sp1 down-regulates androgen receptor (AR) expression and blocks AR signaling. Eventually, selenium may induce apoptosis in prostate cancer cells and inhibit tumor cell proliferation.","Pharmacologic Substance"]
["C61083","Sodium Stibogluconate","Antimony Sodium Gluconate|Lenocta|Myostibin|Pentostam|SODIUM STIBOGLUCONATE|SSG|Sodium Stibogluconate|Solustibosan|Solustin|VQD001|sodium stibogluconate","Pentavalent antimony (Sb) in differential complex formation with gluconic acid with leishmanicidal and potential antineoplastic activities. The Sb moiety of sodium stibogluconate (SSG) may inhibit protein tyrosine phosphorylases (PTPases) by covalently modifying sulfhydryl groups in PTPase cysteine residues, resulting in specific inactivation of SH2 domain-containing tyrosine phosphatases-1 and -2 (SHP-1 and SHP-2), PTPases which negatively regulate interferon (IFN) signaling; enhancement of IFN-induced Stat1 tyrosine phosphorylation; and induction of cellular protein tyrosine phosphorylation. SSG in combination with IFN-alpha may synergize to overcome tumor cell resistance to IFN-alpha-mediated apoptosis.","Chemical Viewed Functionally|Organic Chemical|Pharmacologic Substance"]
["C77854","Solitomab","Anti-EpCAM BiTE|MT110|SOLITOMAB|Solitomab","A recombinant bispecific monoclonal antibody directed against both CD3 and epithelial cell adhesion molecule (EpCAM) with potential immunomodulating and antineoplastic activities. Solitomab attaches to both CD3-expressing T lymphocytes and EpCAM-expressing tumor cells, thereby selectively cross-linking tumor and T lymphocytes; this may result in the recruitment of cytotoxic T lymphocytes (CTL) to T lymphocyte/tumor cell aggregates and the CTL-mediated death of EpCAM-expressing tumor cells. CD3 is an antigen expressed on mature T cells; EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C78195","Sonepcizumab","Asonep|LT1009|Sonepcizumab","A humanized monoclonal antibody directed against sphingosine 1-phosphate (S1P) with potential antiangiogenic and antineoplastic activities. Upon administration, sonepcizumab binds S1P, which may result in the inhibition of tumor angiogenesis. S1P is the extracellular ligand for the G protein-coupled lysophospholipid receptor EDG-1 (endothelial differentiation gene-1).","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C82385","Sonidegib","(1,1'-Biphenyl)-3-carboxamide, N-(6-((2R,6S)-2,6-dimethyl-4-morpholinyl)-3-pyridinyl)-2- methyl-4'-(trifluoromethoxy)-, rel-|ERISMODEGIB|Erismodegib|LDE-225|LDE225|Odomzo|Smoothened Antagonist LDE225|Sonidegib","An orally bioavailable small-molecule smoothened (Smo) antagonist with potential antineoplastic activity. Sonidegib selectively binds to the hedgehog (Hh)-ligand cell surface receptor Smo, which may result in the suppression of the Hh signaling pathway and, so, the inhibition of tumor cells in which this pathway is abnormally activated. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair. Inappropriate activation of Hh pathway signaling and uncontrolled cellular proliferation, as is observed in a variety of cancers, may be associated with mutations in the Hh-ligand cell surface receptor Smo.","Pharmacologic Substance"]
["C61948","Sorafenib","BAY 43-9006|SORAFENIB|Sorafenib|sorafenib","A synthetic compound targeting growth signaling and angiogenesis. Sorafenib blocks the enzyme RAF kinase, a critical component of the RAF/MEK/ERK signaling pathway that controls cell division and proliferation; in addition, sorafenib inhibits the VEGFR-2/PDGFR-beta signaling cascade, thereby blocking tumor angiogenesis.","Pharmacologic Substance"]
["C2194","Sorafenib Tosylate","4-(4-(3-(4-Chloro-3-trifluoromethylphenyl)ureido)phenoxy)pyridine-2-carboxyllic Acid Methyamide-4-methylbenzenesulfonate Tosylate|BAY 43-9006 Tosylate|BAY 54-9085|Nexavar|SORAFENIB TOSYLATE|Sorafenib Tosylate|sorafenib tosylate|sorafenib","The tosylate salt of sorafenib, a synthetic compound targeting growth signaling and angiogenesis. Sorafenib blocks the enzyme RAF kinase, a critical component of the RAF/MEK/ERK signaling pathway that controls cell division and proliferation; in addition, sorafenib inhibits the VEGFR-2/PDGFR-beta signaling cascade, thereby blocking tumor angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C111681","Sorghum bicolor Supplement","Jobelyn|Sorghum bicolor Extract|Sorghum bicolor Supplement","An herbal-based nutritional supplement containing the leaf sheaths of the plant Sorghum bicolor, with potential antioxidant, anti-inflammatory, chemopreventive and immunomodulating activities. Sorghum bicolor supplement contains various phytochemicals, including phenolic acids and polyphenols such as proanthocyanidins. Sorghum bicolor supplement is particularly rich in 3-deoxyanthocyanins, such as luteolinidin and apigeninidin, and appears to induce apoptosis and inhibit cell proliferation in cancer cells through the stimulation of various apoptosis promoter genes and the downregulation of certain apoptosis inhibitor genes. In addition, due to the strong antioxidant nature of the phytochemicals, these compounds are able to scavenge free radicals and prevent tissue damage. Also, intake of this supplement modulates the immune system by both increasing the activity of natural killer (NK) cells and initiating the activation of macrophages.","Pharmacologic Substance"]
["C80630","Sotrastaurin","SOTRASTAURIN|Sotrastaurin","An orally available pan-protein kinase C (PKC) inhibitor with potential immunosuppressive and antineoplastic activities. Sotrastaurin inhibits both T- and B-cell activations via PKC theta and beta isozymes, respectively. Both PKCs are important in the activation of nuclear factor-kappaB (NF-kB). Inhibition of PKC beta in B-cells results in prevention of NF-kB-mediated signaling and down regulation of NF-kB target genes. This may eventually lead to an induction of G1 cell cycle arrest and tumor cell apoptosis in susceptible tumor cells. This agent may act synergistically with other chemotherapeutic agents. PKC, a family of serine/threonine protein kinases overexpressed in certain types of cancer cells, is involved in cell differentiation, mitogenesis, inflammation, and the activation and survival of lymphocytes.","Pharmacologic Substance"]
["C80631","Sotrastaurin Acetate","3-(1H-Indol-3-yl)-4-(2-(4-methylpiperazin-1-yl)quinazolin-4- yl)-1H-pyrrole-2,5-dione Acetate|AEB 071|AEB071|SOTRASTAURIN ACETATE|Sotrastaurin Acetate","The acetate salt form of sotrastaurin, an orally available pan-protein kinase C (PKC) inhibitor with potential immunosuppressive and antineoplastic activities. Sotrastaurin inhibits both T- and B-cell activations via PKC theta and beta isozymes, respectively. Both PKCs are important in the activation of nuclear factor-kappaB (NF-kB). Inhibition of PKC beta in B-cells results in prevention of NF-kB-mediated signaling and down regulation of NF-kB target genes. This may eventually lead to an induction of G1 cell cycle arrest and tumor cell apoptosis in susceptible tumor cells. This agent may act synergistically with other chemotherapeutic agents. PKC, a family of serine/threonine protein kinases overexpressed in certain types of cancer cells, is involved in cell differentiation, mitogenesis, inflammation, and the activation and survival of lymphocytes.","Pharmacologic Substance"]
["C65152","Soy Isoflavones","NovaSoy|SOY ISOFLAVONES|Solgen 40|Soy Isoflavone|Soy Isoflavones|Soybean Isoflavone Mixture","A dietary supplement isolated from soybeans containing phytoestrogen isoflavones. Although the mechanism of action is unclear, soy isoflavones mimic estrogen action mediated through estrogen receptors. In addition, this agent also modulates estrogen metabolism. As a result, soy isoflavones have been shown to reduce tumor cell proliferation and induce tumor cell apoptosis, as well as to be able to regulate hormone balance and reduce the risks of breast cancer, heart disease, and osteoporosis.","Pharmacologic Substance"]
["C1803","Soy Protein Isolate","SOY PROTEIN|Soy Protein Isolate|Soybean Protein Isolate","A dietary protein isolated from soybeans that contains isoflavone phytoestrogens.  Soy protein isolate has been shown to reduce tumor incidence and growth in some animal studies, possibly by modulating estrogen metabolism, reducing tumor cell proliferation, and inducing tumor cell apoptosis.  Soy protein isolate may also inhibit endothelial cell proliferation.  Isoflavone phytoestrogens display mild estrogen-like activities which may regulate hormone balance and reduce the risks of breast cancer, heart disease, and osteoporosis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2353","Sparfosate Sodium","CI-882|L-Aspartic Acid, N-(phosphonoacetyl)-, Disodium Salt|N-Phosphonacetyl-L-aspartate Disodium|PALA Disodium|SPARFOSATE SODIUM|Sparfosate Sodium","The disodium salt form of N-phosphonacetyl-L-aspartate (PALA), a pyrimidine antimetabolite with antineoplastic activity.  PALA inhibits pyrimidine biosynthesis and increases the extent to which fluorouracil is incorporated into RNA. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1398","Sparfosic Acid","L-Aspartic acid, N-(phosphonoacetyl)-|N-Phosphonacetyl-L-aspartate|N-phosphonacetyl-L-aspartate|PALA|Phosphonacetyl-L-aspartic Acid|SPARFOSIC ACID|Sparfosate|Sparfosic Acid","A stable transition state analogue for an aspartate transcarbamylase-catalyzed reaction with antineoplastic activity. Sparfosic acid is a stable transition analogue of the activated complex for the reaction catalyzed by aspartate transcarbamylase, the first step in the pyrimidine biosynthetic pathway. This agent inhibits de novo pyrimidine biosynthesis and increases the extent to which fluorouracil metabolites are incorporated into RNA.","Organic Chemical|Pharmacologic Substance"]
["C97037","Spebrutinib","2-Propenamide, N-(3-((5-fluoro-2-((4-(2-methoxyethoxy)phenyl)amino)-4-pyrimidinyl)amino)phenyl)-|AVL-292|Bruton's Tyrosine Kinase Inhibitor CC-292|CC-292|SPEBRUTINIB|Spebrutinib","An orally bioavailable, selective inhibitor of Bruton's agammaglobulinemia tyrosine kinase (BTK), with potential antineoplastic activity. Upon administration, spebrutinib targets and covalently binds to BTK, thereby preventing its activity. By irreversibly inhibiting BTK, administration of this agent may lead to an inhibition of B cell receptor (BCR) signaling and may inhibit cell proliferation of B-cell malignancies. BTK, a cytoplasmic tyrosine kinase and member of the Tec family of kinases, plays an important role in B lymphocyte development, activation, signaling, proliferation and survival.","Pharmacologic Substance"]
["C98278","Sphingosine Kinase-2 Inhibitor ABC294640","ABC294640|SK2 inhibitor ABC294640|Sphingosine Kinase-2 Inhibitor ABC294640","An orally available, aryladamantane compound and selective inhibitor of sphingosine kinase-2 (SK2) with potential antineoplastic activity. Upon administration, ABC294640 competitively binds to and inhibits SK2, thereby preventing the phosphorylation of the pro-apoptotic amino alcohol sphingosine to sphingosine 1-phosphate (S1P), the lipid mediator that is pro-survival and critical for immunomodulation. This may eventually lead to the induction of apoptosis and may result in an inhibition of cell proliferation in cancer cells overexpressing SK2. SK2 and its isoenzyme SK1 are overexpressed in numerous cancer cell types.","Pharmacologic Substance"]
["C1232","Spirogermanium","2-Aza-8-germaspiro[4.5]decane-2-propanamine, 8, 8-diethyl-N,N-dimethyl-, Dihydrochloride|2-Aza-8-germaspiro[4.5]decane-2-propanamine, 8, 8-diethyl-N,N-dimethyl-, dihydrochloride|2-[3-(Dimethyl-amino)propyl]-8,8-diethyl-2-aza-8-germaspiro[4,5]decane|8,8-Diethyl-N,N-dimethyl-3-aza-8-germaspiro[4,5]decane-2-propanamine|S 99 A|SPG|Spiro 32|Spiro-32|Spirogermanium Compound|Spirogermanium HCl|Spirogermanium Hydrochloride|Spirogermanium compound|Spirogermanium hydrochloride|Spirogermanium","A synthetic organometallic compound containing the element germanium with possible antineoplastic activity. Spirogermanium exhibits significant toxicity, particularly neurotoxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1233","Spiromustine","1,3-diazaspiro(4,5)decane-2,4-dione,3-(2-(bis-chloroethyl)amino)ethyl|SHM|Spirohydantoin Mustard|Spirohydantoin mustard|Spiromustine","A bifunctional nitrogen alkylating agent with antineoplastic activity and lipophilic properties. Containing a lipophilic hydantoin group that serves as a carrier to cross the blood brain barrier, spiromustine forms covalent linkages with nucleophilic centers in DNA, causing depurination, base-pair miscoding, strand scission, and DNA-DNA cross-linking, which may result in cytotoxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1234","Spiroplatin","Cis-1,1-diamino-methylcyclohexane sulfato-platinum|Platinum, (1,1-cyclohexanedimethanamine-n,n')(sulfato(2-)-O,O')-, (sp-4-2)-|SPIROPLATIN|Spiroplatin|TNO-6","A synthetic derivative of cyclohexane sulfatoplatinum with antineoplastic properties.  Spiroplatin induces DNA cross-links, thereby inhibiting DNA replication and RNA and protein synthesis. Similar to other platinum compounds, this agent has been shown to be mutagenic and carcinogenic. (NCI04)","Inorganic Chemical|Pharmacologic Substance"]
["C113162","Spleen Tyrosine Kinase Inhibitor TAK-659","Spleen Tyrosine Kinase Inhibitor TAK-659|Spleen Tyrosine Kinase Inhibitor TAK659|TAK-659|TAK659|syk Inhibitor TAK-659|syk Inhibitor TAK659|syk-Inhibitor TAK-659|syk-Inhibitor TAK659","An inhibitor of spleen tyrosine kinase (syk), with potential anti-inflammatory, immunomodulating, and antineoplastic activities. Spleen tyrosine kinase inhibitor TAK-659 may inhibit the activity of syk, which abrogates downstream B-cell receptor (BCR) signaling and leads to an inhibition of B-cell activation, chemotaxis, adhesion and proliferation. Syk, a BCR-associated non-receptor tyrosine kinase that mediates diverse cellular responses, including proliferation, differentiation, and phagocytosis, is expressed in hematopoietic tissues and is often overexpressed in hematopoietic malignancies.","Pharmacologic Substance"]
["C129546","Splicing Inhibitor H3B-8800","H3B 8800|H3B-8800|Splicing Factor Inhibitor H3B-8800|Splicing Inhibitor H3B-8800|Splicing Modulator H3B-8800","An orally bioavailable inhibitor of the splicing factor 3B subunit 1 (SF3B1), with potential antineoplastic activity. Upon administration, H3B-8800 binds to and blocks the activity of SF3B1, a core spliceosome protein that is mutated in various cancer cells. This modulates RNA splicing by preventing aberrant mRNA splicing by the spliceosome, blocks RNA mis-splicing, enhances proper RNA splicing and prevents the expression of certain tumor-associated genes. This leads to an induction of apoptosis and prevents tumor cell proliferation. In many cancer cells, core spliceosome proteins, including SF3B1, U2 small nuclear ribonucleoprotein auxiliary factor 1 (U2AF1), serine/arginine-rich splicing factor 2 (SRSF2) and U2 small nuclear ribonucleoprotein auxiliary factor subunit-related protein 2 (ZRSR2), are mutated and aberrantly activated leading to a dysregulation of mRNA splicing.","Pharmacologic Substance"]
["C2051","Spongistatin","Altohyrtin A|Spongistatin 1|Spongistatin","A highly cytotoxic macrocyclic lactone polyether with antitumor activity. Spongistatin, originally isolated from marine Spongia species, binds to the vinca domain of tubulin, thereby interferes with microtubule assembly and results in inhibition of mitosis. This agent does not affect the binding of colchicine to tubulin, but it was a potent inhibitor of the binding of vinblastine and GTP to tubulin.","Organic Chemical|Pharmacologic Substance"]
["C1482","Squalamine Lactate","3beta-N-1-(N-(3-(4-Aminobutyl))-1,3-diaminopropane)-7alpha,24-dihydroxy-5alpha-cholestane 24-sulfate|MSI-1256F|SQUALAMINE LACTATE|Squalamine Lactate|Squalamine|squalamine lactate","The lactate salt form of squalamine, an aminosterol isolated from tissues of the dogfish shark Squalus acanthias.  Possessing anti-angiogenic properties, squalamine inhibits the sodium-hydrogen exchanger NHE3, resulting in suppression of endothelial cell proliferation and migration.  This agent also has broad-spectrum antimicrobial properties. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C61435","SR31747A","SR31747A","A synthetic peripheral sigma receptor ligand with immunomodulatory and potential antitumor activities. Although the exact mechanism by which SR31747A exerts its antitumor effects has not been fully established, SR31747A binds to and inhibits the sigma1 receptor (SR31747A-binding protein-1 or SR-BP1), human sterol isomerase (emopamil-binding protein) and the sigma2 receptor, which may result in a reduction in tumor cell proliferation and tumor cell apoptosis. In addition, this agent inhibits the production of pro-inflammatory cytokines while increasing anti-inflammatory cytokines. Upregulated in various cancers, the sigma1 and sigma2 receptors and human sterol isomerase are proteins that are involved in the regulation of cell proliferation and survival.","Pharmacologic Substance"]
["C74077","Src Kinase Inhibitor KX2-391","KX01|KX2-391|Src Kinase Inhibitor KX2-391","An orally bioavailable small molecule Src kinase inhibitor with potential antineoplastic activity. Unlike other Src kinase inhibitors which bind to the ATP-binding site, Src kinase inhibitor KX2-391 specifically binds to the peptide substrate binding site of Src kinase; inhibition of kinase activity may result in the inhibition of primary tumor growth and the suppression of metastasis. Src tyrosine kinases are upregulated in many tumor cells and play important roles in tumor cell proliferation and metastasis.","Pharmacologic Substance"]
["C120210","Src Kinase Inhibitor KX2-391 Ointment","KX2 391 Ointment|KX2-391 Ointment|Src Kinase Inhibitor KX2-391 Ointment","An ointment containing an inhibitor for both Src tyrosine kinase and tubulin polymerization, with potential antineoplastic activity. Unlike other Src kinase inhibitors which bind to the ATP-binding site, Src kinase inhibitor KX2-391 binds to the peptide substrate binding site of Src kinase, upon topical application. This inhibits both downstream signaling and the proliferation of tumor cells overexpressing Src. Src tyrosine kinase, a non-receptor tyrosine kinase upregulated in many tumor cell types, plays an important role in tumor cell proliferation, motility, invasiveness and survival. KX2-391 also binds to tubulin heterodimers and inhibits microtubule polymerization, which disrupts microtubule formation and mitosis, leading to further inhibition of cell proliferation. In addition, KX2-391 inhibits T-cell migration.","Pharmacologic Substance"]
["C102976","Src/Abl Kinase Inhibitor AZD0424","AZD0424|Src/Abl Kinase Inhibitor AZD0424","An orally bioavailable small molecule tyrosine kinase inhibitor that targets both Abl and Src kinases with potential antineoplastic activity. Upon oral administration, AZD0424 selectively inhibits both Src and Abl kinase activity which may result in the inhibition of tumor growth in susceptible tumor cells. Src and Abl kinases are upregulated in certain tumor cells and play important roles in tumor cell proliferation and metastasis.","Pharmacologic Substance"]
["C120101","Src/tubulin Inhibitor KX02","KX02|KX2-361|Src/tubulin Inhibitor KX02","A lipophilic, orally available inhibitor of both Src kinase activity and tubulin polymerization, with potential antineoplastic activity. Upon oral administration, src/tubulin inhibitor KX02 binds to and inhibits the activity of Src kinase. This inhibits both downstream signaling and the proliferation of Src kinase-expressing tumor cells. KX02 also binds to tubulin heterodimers and inhibits microtubule polymerization, thereby disrupting microtubule formation, mitosis, and further proliferation. Src, a non-receptor tyrosine kinase, is overexpressed in a variety of tumor cell types and plays a key role in tumor cell proliferation, angiogenesis, migration, and metastasis.","Pharmacologic Substance"]
["C99460","SR-T100 Gel","SR-T100 Gel|SR-T100","A cutaneous gel preparation containing an extract from Solanum incanum with potential antineoplastic activity. SR-T100 gel contains high amounts of the steroidal alkaloid glycoside solamargine. Solamargine is able to upregulate expression of tumor necrosis factor receptors 1 (TNFR1) and 6 (TNFRSF6 or Fas), and their signaling adaptors TNFR1-associated death domain, and Fas-associated death domain. In addition, this agent is able to upregulate expression of apoptosis promoter Bax, and suppress the expression of the anti-apoptotic proteins Bcl-xL and Bcl-2. Altogether, this induces apoptosis in tumor cells and may lead to an inhibition of tumor cell proliferation.","Pharmacologic Substance"]
["C2609","SS1(dsFv)-PE38 Immunotoxin","Immunotoxin, SS1(dsFv)-PE38|SS1(dsFv) PE38|SS1(dsFv)-PE38 Immunotoxin|SS1P","A recombinant immunotoxin consisting of the single chain anti-mesothelin monoclonal antibody SS1(dsFv) linked to Pseudomonas exotoxin PE-38. The monoclonal antibody moiety of the agent binds to cells that express mesothelin, a cell surface glycoprotein which may be overexpressed in ovarian cancer, mesotheliomas, and some squamous cell carcinomas; after internalization, the exotoxin moiety inactivates eukaryotic translation elongation factor 2, thereby disrupting tumor cell protein synthesis. (NCI04)","Biologically Active Substance|Pharmacologic Substance"]
["C2589","St. John's Wort","Hypericum Perforatum Extract|ST. JOHN'S WORT|St John's Wort|St. John's Wort|St. John's wort|hypericum perforatum","An herbal extract prepared from the plant Hypericum perforatum (St. John's wort) with photodynamic, antineoplastic, and antidepressant activities. Hypericin, one of the active compounds found in Hypericum perforatum, is a photosensitizer that, when exposed to a particular wavelength and intensity of light, may induce tumor cell apoptosis. Another compound, hyperforin, induces caspase-dependent apoptosis in certain tumor cell lines. Hypericum perforatum preparations may also stimulate the activity of cytochrome P450 enzymes and P-glycoprotein drug transporters, resulting in increased metabolism and decreased efficacy of various chemotherapeutic agents and other drugs.","Pharmacologic Substance"]
["C1517","Stallimycin","DISTAMYCIN A|Distamycin 3|Distamycin A|Herperetin|STALLIMYCIN|Stallimycin","An oligopeptide antineoplastic antibiotic isolated from the bacterium Streptomyces distallicus.  Distamycin preferentially binds to adenine-thymine (A-T) rich sequences in the minor groove of DNA, thereby inhibiting DNA replication and RNA transcription.  In addition to antitumor effects, distamycin also possesses antiviral and antiprotozoal activities and is used as a chromosome dye. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C1083","Staphylococcal Enterotoxin A","SEA|Staphylococcal Enterotoxin A","A bacterial enterotoxin with potential immunostimulatory activity. Staphylococcal enterotoxin A (SEA), a gram positive bacterial superantigen (SAg), is a potent stimulator of T-cell activation. SEA superantigen binds directly to class II major histocompatibility complex (MHC) molecules and to the V beta region of the T-cell receptor (TCR), leading to an amplified T-cell response. In response to SEA, both CD4+ and CD8+ cells proliferate, secrete cytokines, and demonstrate enhanced cytotoxic activity against a broad range of antigens. Vaccination with the SEA protein, administered by direct transfection into tumor cells, may elicit a non-specific cytotoxic T-cell (CTL) response and result in decreased tumor cell growth.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1084","Staphylococcal Enterotoxin B","SEB|Staphylococcal Enterotoxin B","A bacterial enterotoxin with potential immunostimulatory activity. Staphylococcal enterotoxin B (SEB), a gram positive superantigen produced by Staphylococcus aureus, is a potent stimulator of T-cell activation. SEB binds directly to class II major histocompatibility complex (MHC) molecules and the V beta region of the T-cell receptor (TCR), leading to an amplified T-cell response. In response to SEB, both CD4+ and CD8+ cells proliferate, secrete cytokines and demonstrate enhanced cytotoxic activity against a broad range of antigens. Co-administration of SEB with interleukin-2 (IL-2) by direct injection into tumor cells, may induce clonal T-cell expansion and potentiate apoptosis of tumor cells, resulting in decreased tumor growth.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C116873","STAT Inhibitor OPB-111077","OPB-111077|STAT Inhibitor OPB-111077","An orally bioavailable inhibitor of one or more signal transducer and activator of transcription (STAT) protein(s), with potential antineoplastic activity. Upon oral administration, OPB-111077 binds to and inhibits the phosphorylation of STATs. This prevents binding of STATs to DNA sequences on a variety of STAT-responsive gene promoters, which may result in the inhibition of both STAT-mediated transcription and tumor cell proliferation. STATs are constitutively activated in a variety of cancers and play a key role in tumor cell proliferation.","Pharmacologic Substance"]
["C101368","STAT3 Antisense Oligonucleotide ISIS 481464","AZD9150|ISIS 481464|ISIS-STAT3rx|STAT3 Antisense Oligonucleotide ISIS 481464","An antisense oligonucleotide targeting signal transducer and activator of transcription 3 (STAT3) with potential antitumor activity. STAT3 antisense oligonucleotide ISIS 481464 binds to STAT3 mRNA, thereby inhibiting translation of the transcript. Suppression of STAT3 expression induces tumor cell apoptosis and decreases tumor cell growth. STAT3, a protein overexpressed in a variety of human cancers, plays a critical role in tumor cell growth and survival.","Pharmacologic Substance"]
["C78822","STAT3 Decoy Oligonucleotide","STAT3 Decoy ODN|STAT3 Decoy Oligonucleotide|STAT3 Decoy","A double-stranded 15-mer oligonucleotide, corresponding closely to the signal transducer and activator of transcription 3 (STAT3) response element within the c-fos promoter, with potential antineoplastic activity. STAT3 decoy oligonucleotide binds specifically to activated STAT3 and blocks binding of STAT3 to DNA sequences on a variety of STAT3-responsive promoters, which results in the inhibition of STAT3-mediated transcription and, potentially, the inhibition of tumor cell proliferation. STAT3 is constitutively activated in a variety of cancers including squamous cell carcinoma of the head and neck, contributing to the loss of cell growth control and neoplastic transformation.","Pharmacologic Substance"]
["C90588","STAT3 Inhibitor OPB-31121","OPB-31121|STAT3 Inhibitor OPB-31121","An orally bioavailable inhibitor of signal transducer and activator of transcription 3 (STAT3), with potential antineoplastic activity. OPB-31121 inhibits the phosphorylation of STAT3, which prevents binding of STAT3 to DNA sequences on a variety of STAT3-responsive promoters and may result in the inhibition of STAT3-mediated transcription and, potentially, the inhibition of tumor cell proliferation. STAT3 is constitutively activated in a variety of cancers, contributing to the loss of cell growth control and neoplastic transformation.","Pharmacologic Substance"]
["C95889","STAT3 Inhibitor OPB-51602","OPB-51602|STAT3 Inhibitor OPB-51602","An orally bioavailable inhibitor of signal transducer and activator of transcription 3 (STAT3), with potential antineoplastic activity. STAT3 inhibitor OPB-51602 inhibits the phosphorylation and thus the activation of STAT3 protein, impeding STAT3 protein from translocating from the cytoplasm to the nucleus and thereby blocking STAT3's regulation of gene expression through direct binding to the promoters of responsive genes. STAT3 regulates the cellular functions that lead to the cancer phenotype, and constitutive activation of STAT3 is observed in a wide range of human cancers, inducing uncontrolled proliferation and neoplastic transformation.","Pharmacologic Substance"]
["C1237","Staurosporine","(9alpha,10beta,11beta,13alpha)-(+)-2,3,10,11,12,13-Hexahydro-10-methoxy-9-methyl-11-(methylamino)-9,13-epoxy-1H-9H-diindolo[1,2,3-gh:3',2',1'-lm]pyrrolo[3,4-j][1,7]benzodiazonin-1-one|8,12-Epoxy-1H,8H-2,7b,12a-triazadibenzo(a,g)cyclonona(cde)trinden-1-one, 2,3,9,10,11,12-hexahydro-9-methoxy-8-methyl-10-(methylamino)-, (8alpha,9beta,10beta,12alpha)-(+)-|AM-2282|Antibiotic 230|Antibiotic AM 2282|CGP-39360|STAUROSPORINE|Staurosporine|staurosporine","A cell permeable alkaloid isolated from Streptomyces staurosporeus exhibiting anti-cancer activity.  Staurosporine is a potent, non-selective inhibitor of protein kinases, including protein kinase C.  This agent induces apoptosis by an undetermined mechanism. (NCI)","Organic Chemical"]
["C125902","STING-activating Cyclic Dinucleotide Agonist MIW815","ADU-S100|CDN Agonist ADU-S100|MIW815|STING-activating Cyclic Dinucleotide Agonist MIW815","A synthetic, cyclic dinucleotide (CDN) and agonist of stimulator of interferon genes protein (STING; transmembrane protein 173; TMEM173), with potential immunomodulating and antineoplastic activities. Upon intratumoral administration, the STING agonist MIW815 binds to STING and stimulates STING-mediated pathways. This activates the immune response through the activation of certain immune cells, including dendritic cells (DCs), which induces the expression of cytokines and chemokines, and leads to an antigen-specific T-cell mediated immune response against cancer cells. STING, a transmembrane protein that activates immune cells in the tumor microenvironment, plays a key role in the activation of the innate immune system.","Pharmacologic Substance"]
["C77873","Strawberry-Blackberry-Black Raspberry-Blueberry Mixture","Strawberry-Blackberry-Black Raspberry-Blueberry Mixture","A dietary supplement consisting of a mixture of strawberries, blackberries, black raspberries and blueberries with potential antineoplastic activity. Although the exact mechanism of action through which berries may exert their anti-tumor effect has yet to be elucidated, in vivo studies suggest that the ingestion of a mixture of berries seems to result in a reduction in tumor growth and tumor development. As berries are rich in phytonutrients, such as anthocyanins, flavonols, ellagitannins, galltannins, proanthocyanidins, and phenolic acids, the antineoplastic effects of strawberry-blackberry-black raspberry-blueberry berry mixture on cancer cells may be attributable to phytonutrient antioxidant and apoptotic activities. In addition, phytoestrogens in berries may be protective against estrogen-sensitive tumors.","Pharmacologic Substance"]
["C844","Streptonigrin","5-Amino-6-(7-amino-5,8-dihydro-6-methoxy-5,8-dioxo-2-quinolyl)-4-(2-hydroxy-3,4-dimethoxyphenyl)-3-methyl-2-pyridinecarboxylic Acid|5-Amino-6-(70-amino-5,8-dihydro-6-methoxy-5,8-dioxo-2-quinolyl)-4-(2-hydroxy-3,4-dimethoxyphenyl)-3-methylpicolinic Acid|BA-163|Bruneomycin|PC-501|Rufocromomycin|STN|STREPTONIGRIN|Streptonigrin","An aminoquinone antineoplastic antibiotic isolated from the bacterium Streptomyces flocculus.  Streptonigrin complexes with DNA and topoisomerase II, resulting in DNA cleavage and inhibition of DNA replication and RNA synthesis.  This agent also acts as a reverse transcriptase inhibitor and causes free radical-mediated cellular damage. (NCI04)","Antibiotic|Organic Chemical"]
["C845","Streptozocin","2-Deoxy-2-(3-methyl-3-nitrosoureido)-D-glucopyranose|2-deoxy-2-(3-methyl-3-nitrosoureido)-D-glucopyranose|2-deoxy-2-[[(methylnitrosamino)-carbonyl]amino]-D-glucopyranose|STREPTOZOCIN|STZ|Streptozocin|Streptozotocin|U 9889|U-9889|Zanosar|streptozocin","A methylnitrosourea antineoplastic antibiotic isolated from the bacterium Streptomyces achromogenes.  Streptozocin alkylates DNA, forming inter-strand DNA cross-links and inhibiting DNA synthesis.  Due to its glucose moiety, this agent is readily taken up by pancreatic beta cells, inducing diabetes mellitus at high concentrations.  Unlike other nitrosoureas, streptozocin causes little myelosuppression. (NCI04)","Antibiotic|Organic Chemical"]
["C1238","Strontium Chloride Sr-89","Metastron|STRONTIUM CHLORIDE SR-89|Strontium Chloride Sr-89|strontium chloride Sr 89","The chloride salt of a radioactive isotope of strontium. Strontium chloride Sr 89 is taken up and incorporated preferentially in metastatic lesions in bone where it emits cytotoxic beta radiation, resulting in an inhibition and/or reduction of tumor growth and so tumor-related bone pain. (NCI04)","Pharmacologic Substance"]
["C61507","SU014813","SU014813","An orally-active, tyrosine kinase receptor inhibitor with potential antitumor activity. SU014813 binds to and inhibits the phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor (PDGFR) alpha and beta, c-Kit and Fms-related tyrosine kinase 3 (Flt-3). This leads to an inhibition of cellular proliferation and angiogenesis and an induction of apoptosis.","Pharmacologic Substance"]
["C116066","Sulfatinib","HMPL-012|Sulfatinib","An orally bioavailable, small molecule inhibitor of vascular endothelial growth factor receptors (VEGFR) 1, 2, and 3, and the fibroblast growth factor receptor type 1 (FGFR1), with potential antineoplastic and anti-angiogenic activities. Upon oral administration, sulfatinib binds to and inhibits VEGFRs and FGFR1 thereby inhibiting VEGFR- and FGFR1-mediated signal transduction pathways. This leads to a reduction of angiogenesis and tumor cell proliferation in VEGFR/FGFR1-overexpressing tumor cells. Expression of VEGFRs and FGFR1 may be upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C850","Sulindac","(Z)-5-fluoro-2-methyl-1-[[4-(methylsulfinyl)phenyl]methylene]-1H-indene-3-acetic acid|Aflodac|Algocetil|Apo-Sulin|Arthrocine|Artribid|Citireuma|Clinoril|Clisundac|Imbaral|MK-231|Novo-Sundac|Reumofil|Reumyl|SULINDAC|Sudac|Sulindac Sulfoxide|Sulindac|Sulinol|Sulreuma|cis-5-fluoro-2-methyl-1-[p-(methylsulfinyl)benzylidene]indene-3-acetic acid|sulindac","A sulfinylindene derivative prodrug with potential antineoplastic activity. Converted in vivo to an active metabolite, sulindac, a nonsteroidal anti-inflammatory drug (NSAID), blocks cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway; this inhibition permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1432","Sulofenur","LY186641|SULOFENUR|Sulofenur","A diarylsulfonylurea with potential antineoplastic activity. Sulofenur's antineoplastic mechanism of action is unknown. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C71622","Sunitinib","1H-Pyrrole-3-carboxamide, N-(2-(diethylamino)ethyl)-5-((Z)-(5-fluoro-1,2-dihydro-2-oxo-3H-indol-3-ylidene)methyl)-2,4-dimethyl-|SUNITINIB|Sunitinib|sunitinib","An indolinone derivative and tyrosine kinase inhibitor with potential antineoplastic activity. Sunitinib blocks the tyrosine kinase activities of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor b (PDGFRb), and c-kit, thereby inhibiting angiogenesis and cell proliferation.  This agent also inhibits the phosphorylation of Fms-related tyrosine kinase 3 (FLT3), another receptor tyrosine kinase expressed by some leukemic cells.","Pharmacologic Substance"]
["C26673","Sunitinib Malate","Butanedioic acid, hydroxy-, (2S)-, compd. with N-(2-(diethylamino)ethyl)-5-((Z)-(5-fluoro-1,2-dihydro-2-oxo-3H-indol-3-ylidene)methyl)-2,4-dimethyl-1H-pyrrole-3-carboxamide (1:1)|SU011248|SU11248|SUNITINIB MALATE|Sunitinib Malate|Sutent|sunitinib malate|sunitinib","The orally bioavailable malate salt of an indolinone-based tyrosine kinase inhibitor with potential antineoplastic activity.  Sunitinib blocks the tyrosine kinase activities of vascular endothelial growth factor receptor 2 (VEGFR2), platelet-derived growth factor receptor b (PDGFRb), and c-kit, thereby inhibiting angiogenesis and cell proliferation.  This agent also inhibits the phosphorylation of Fms-related tyrosine kinase 3 (FLT3), another receptor tyrosine kinase expressed by some leukemic cells.","Pharmacologic Substance"]
["C107503","Superagonist Interleukin-15:Interleukin-15 Receptor alphaSu/Fc Fusion Complex ALT-803","ALT-803|IL-15N72D/IL-15Ra-Fc|IL-15N72D:IL-15RaSu/Fc Fusion Complex|Superagonist Interleukin-15:Interleukin-15 Receptor alphaSu/Fc Fusion Complex ALT-803","A fusion protein complex composed of a mutated form of the cytokine interleukin (IL)-15 (IL-15N72D) and a soluble, dimeric IL-15 receptor alpha (IL-15Ra) Fc fusion protein (IL-15Ra-Fc) (IL-15N72D/IL-15Ra-Fc), with potential antineoplastic activity. Upon administration, superagonist interleukin-15:interleukin-15 receptor alphaSu/Fc fusion complex ALT-803 binds to the IL-2/IL-15 receptor beta-common gamma chain (IL-2Rbetagamma) receptor on natural killer (NK) and CD8+ T lymphocytes, which activates and increases the levels of NK cells and memory CD8+(CD44high) T-cells. The memory T-cells enhance the secretion of the cytokine interferon-gamma (IFN-g), which further potentiates the immune response against tumor cells. This may increase tumor cell killing and decrease tumor cell proliferation. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. By coupling IL-15 to IL15Ra-Fc, this agent has a prolonged drug half-life and shows an increased ability to bind IL-2Rbetagamma, which enhances its immune stimulatory activity as compared to IL-15 alone.","Pharmacologic Substance"]
["C853","Suramin","SURAMIN|Suramin|suramin","A polysulphonated naphthylurea with potential antineoplastic activity.  Suramin blocks the binding of various growth factors, including insulin-like growth factor I (IGF-I), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and tumor growth factor-beta (TGF-beta), to their receptors, thereby inhibiting endothelial cell proliferation and migration.  This agent also inhibits vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (bFGF)-induced angiogenesis; retroviral reverse transcriptase; uncoupling of G-proteins from receptors; topoisomerases; cellular folate transport; and steroidogenesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1848","Suramin Sodium","309 F|8,8'-(Carbonylbis(imino-3,1-phenylenecarbonylimino(4-methyl-3,1-phenylene)carbonylimino))bis-1,3,5-naphthalenetrisulfonic Acid Hexasodium Salt|Antrypol|Bayer 205|Belganyl|CI-1003|Fourneau 309|Germanin|Metaret|Moranyl|Naganin|Naganinum|Naganol|Naphuride|SURAMIN SODIUM|Sodium Suramin|Sodium suramin|Suramin Hexasodium|Suramin Sodium|Suramin sodium","A sodium salt form of suramin, a polysulphonated naphthylurea with potential antineoplastic activity.  Suramin blocks the binding of various growth factors, including insulin-like growth factor I (IGF-I), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and tumor growth factor-beta (TGF-beta), to their receptors, thereby inhibiting endothelial cell proliferation and migration.  This agent also inhibits vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (bFGF)-induced angiogenesis; retroviral reverse transcriptase; uncoupling of G-proteins from receptors; topoisomerases; cellular folate transport; and steroidogenesis.","Organic Chemical|Pharmacologic Substance"]
["C37449","Survivin Antigen","Survivin Antigen","A tumor-associated antigen. Vaccination with survivin antigen may result in a cytotoxic T-cell response against survivin antigen-expressing tumor cells, resulting in decreased tumor cell proliferation and tumor cell death. Overexpressed in many tumors, endogenous survivin inhibits tumor cell apoptosis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C97951","Survivin Antigen Vaccine DPX-Survivac","DPX-Survivac|Survivin Antigen Vaccine DPX-Survivac","A lipid depot-based therapeutic cancer vaccine composed of survivin epitopes, a universal T Helper peptide and a polynucleotide adjuvant encapsulated in liposomes and then formulated in the hydrophobic carrier Montanide ISA51 VG, with potential immunopotentiating and antineoplastic activities. Upon injection of the survivin antigen vaccine DPX-Survivac, a depot is created at the injection site from which the antigens and adjuvant are released. This vaccine may elicit a long lasting cellular response against survivin-expressing cancers, resulting in a decrease in tumor cell proliferation and an induction of tumor cell death. Survivin, a member of the inhibitor of apoptosis (IAP) family expressed during embryonic development, is upregulated in a variety of human cancers while absent in most normal adult cells; its expression in tumors is associated with a more aggressive phenotype, decreased survival, and increased resistance to chemotherapy.","Immunologic Factor|Pharmacologic Substance"]
["C92578","Survivin mRNA Antagonist EZN-3042","EZN-3042|LNA-RNA Antagonist EZN-3042|Survivin mRNA Antagonist EZN-3042","A locked nucleic acid (LNA) antisense oligonucleotide targeting survivin mRNA, with potential antineoplastic activity. EZN-3042 hybridizes to survivin mRNA, thereby blocking translation of survivin protein and inhibiting survivin-induced anti-apoptotic activity and promoting tumor cell apoptosis in survivin-overexpressing tumor cells. Survivin, a member of the inhibitor of apoptosis (IAP) family expressed during embryonic development, is upregulated in a variety of human cancers while absent in most normal adult cells; its expression in tumors is associated with a more aggressive phenotype, decreased survival, and increased resistance to chemotherapy. LNAs contain a methylene bridge linking 2'-oxygen and 4'-carbon of ribose sugar rings, thereby increasing their stability and decreasing degradation.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C71741","Survivin Sur1M2 Peptide Vaccine","Survivin Sur1M2 Peptide Vaccine","A modified recombinant nonapeptide (LMLGEFLKL) derived from the anti-apoptosis protein survivin with potential immunopotentiating and antineoplastic activities. Upon administration, survivin Sur1M2 peptide vaccine may elicit humoral and cellular immune responses against survivin-expressing cancers, resulting in decreased tumor cell proliferation and tumor cell death. The survivin protein inhibits caspase activation and apoptosis; it is undetectable in normal adult tissues but is expressed by several human cancers including lung, colon, breast, pancreas, and prostate cancer as well as hematopoietic malignancies and skin cancers.","Immunologic Factor|Pharmacologic Substance"]
["C114285","Survivin/p53/HER2 Antigen-loaded Autologous Dendritic Cell Vaccine","Survivin/p53/HER2 Antigen-loaded Autologous DC Vaccine|Survivin/p53/HER2 Antigen-loaded Autologous Dendritic Cell Vaccine","An autologous dendritic cell (DC) vaccine loaded with tumor-associated antigens (TAAs) derived from survivin, p53 and human epidermal growth factor receptor 2 (HER2 or ERBB2), with immunostimulating and antineoplastic activities. Upon administration, this DC vaccine may elicit a potent cytotoxic T-cell (CTL) response against tumor cells expressing these TAAs, resulting in tumor cell death. Survivin, p53 and HER2 are essential in neoplastic growth, and are considered to be universal tumor antigens.","Pharmacologic Substance"]
["C116884","Sustained-release Lipid Inhaled Cisplatin","SLIT Cisplatin|SR Inhaled Lipid Cisplatin|Sustained-release Lipid Inhalation Targeting Cisplatin|Sustained-release Lipid Inhaled Cisplatin","A sustained-release formulation for inhalation in which the inorganic platinum (Pt) agent cisplatin is encapsulated in lipids, with potential antineoplastic activity. Upon inhalation of the sustained-release lipid inhalation targeting (SLIT) cisplatin into the lungs, this agent forms highly reactive, positively charged, Pt complexes, which covalently bind to nucleophilic groups in DNA, preferably at the N7 position of guanine bases. Pt complex binding introduces intrastrand and interstrand DNA cross-links, and DNA-Pt-protein cross-links. These cross-links result in apoptosis and cell growth inhibition of lung cancer cells. Encasement in liposomes prolongs cisplatin's efficacy when compared to intravenously administered cisplatin; inhalation of cisplatin improves its concentration at tumor sites in the lungs while minimizing its systemic toxicity.","Inorganic Chemical|Pharmacologic Substance"]
["C126642","Sustained-release Mitomycin C Hydrogel Formulation","MP77-08|Mitogel|RTGel with MMC|RTGel with Mitomycin C|SR Mitomycin C|Sustained-release Mitomycin C Gel Formulation|Sustained-release Mitomycin C Hydrogel Formulation","A sustained-release (SR) hydrogel polymer-based formulation containing the antineoplastic antibiotic mitomycin C (MMC), with potential antineoplastic activity. Upon local administration of the SR MMC hydrogel formulation to the upper urinary tract via a ureteral catheter, the gel solidifies and deposits MMC locally to prevent the excretion of this chemotherapeutic agent via urinary flow. In turn, MMC alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. Due to its reverse thermal-gelation properties, this gel is able to stay in a liquid state at cold temperatures and solidifies at body temperature. This allows for increased accumulation of MMC locally in the upper urinary tract which leads to increased efficacy compared to standard intravesical delivery of MMC for upper tract urothelial carcinoma (UTUC).","Antibiotic|Organic Chemical"]
["C95705","SVN53-67/M57-KLH Peptide Vaccine","SVN53-67/M57-KLH Peptide Vaccine","A peptide vaccine containing a 15-mer peptide (DLAQMFFCFKELEGW), with C to M alteration at amino acid position 57, derived from the anti-apoptosis protein survivin, and conjugated with keyhole limpet hemocyanin (KLH), with potential immunopotentiating and antineoplastic activities. Upon subcutaneous administration of SVN53-67/M57-KLH peptide vaccine, this peptide is able to bind both HMC class I and II molecules and may activate the immune system to mount a cytotoxic T-lymphocyte (CTL) as well as a T-helper cell response against survivin-expressing cancer cells. This may result in decreased tumor cell proliferation and ultimately tumor cell death. Survivin, a member of the inhibitor of apoptosis (IAP) family, expressed during embryonic development while absent in most normal adult cells, is upregulated in a variety of human cancers; its expression in tumors is associated with a more aggressive phenotype, decreased survival, and increased resistance to chemotherapy. KLH may enhance immune recognition and may promote an enhanced response. As SVN53-67 is weakly immunogenic in humans, the M57 alteration may lead to greater affinity towards HLA-A*0201 and thus an enhanced antitumor immune response.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C123912","Syk Inhibitor HMPL-523","HMPL-523|Spleen Tyrosine Kinase Inhibitor HMPL-523|Syk Inhibitor HMPL-523","An orally available inhibitor of spleen tyrosine kinase (Syk), with potential immunomodulating and antineoplastic activities. Upon oral administration of Syk inhibitor HMPL-523, this agent binds to and inhibits the activity of Syk. This inhibits B-cell receptor (BCR) signaling, which leads to the inhibition of B-cell activation, and prevents tumor cell activation, migration, adhesion and proliferation. Syk, a non-receptor cytoplasmic, BCR-associated tyrosine kinase, is expressed in hematopoietic tissues and is often overexpressed in hematopoietic malignancies; it plays a key role in B-cell receptor signaling.","Pharmacologic Substance"]
["C113173","Syk-JAK Inhibitor PRT062070","PRT062070|Syk-JAK Inhibitor PRT062070|Syk/JAK Inhibitor PRT062070","An orally bioavailable dual inhibitor of spleen tyrosine kinase (Syk) and Janus-associated kinases (JAK), with potential anti-inflammatory and antineoplastic activity. Upon oral administration, Syk-JAK inhibitor PRT062070 specifically binds to and inhibits the activity of Syk, JAK1, and JAK3 with preferential inhibition of JAK1 and JAK3-dependent cytokine-mediated signaling and functional responses. This negatively affects the downstream JAK-STAT (signal transducer and activator of transcription) pathway, and leads to both reduced inflammation in various animal models and enhanced antiproliferative activity towards non-Hodgkin's lymphoma (NHL) cell lines. Syk is a non-receptor cytoplasmic tyrosine kinase involved in signal transduction in cells of hematopoietic origin including B cells, macrophages, basophils and neutrophils. Abnormal function of Syk has been implicated in several hematopoietic malignancies including NHL and chronic lymphocytic leukemia (CLL). The JAK-STAT pathway plays a key role in the signaling of many cytokines and growth factors and is involved in cellular proliferation, growth, hematopoiesis, and the immune response; JAK kinases may be upregulated in inflammatory diseases, myeloproliferative disorders, and various malignancies.","Pharmacologic Substance"]
["C2650","Synchrotope TA2M Plasmid DNA Vaccine","Synchrotope TA2M Plasmid DNA Vaccine","A recombinant plasmid DNA vaccine encoding epitopes of tyrosinase with potential antineoplastic activity. Synchrotope TA2M vaccine contains a plasmid encoding 2 epitopes, amino acid sequences 207-216 and 1-17 of tyrosinase, a protein frequently expressed by melanoma cells. Vaccination with the TA2M plasmid DNA vaccine may induce the production of anti-tyrosinase antibodies as well as elicit a cytotoxic T-lymphocyte (CTL) response against tyrosinase-expressing tumor cells, resulting in decreased tumor growth.","Pharmacologic Substance"]
["C28549","Synchrovax SEM Plasmid DNA Vaccine","Synchrotope MA2M Plasmid DNA Vaccine|Synchrovax SEM Plasmid DNA Vaccine","A bivalent DNA vaccine encoding epitopes for both Melan-A (MART-1) and tyrosinase with potential antineoplastic activity. Synchrovax SEM plasmid DNA vaccine contains a plasmid pSEM that encodes 4 epitopes: Melan-A (26-35), Melan-A (31-96), tyrosinase (1-9), and tyrosinase (369-377). Both Melan-A and tyrosinase are tumor antigens associated with melanoma. Vaccination with this plasmid DNA vaccine may induce both humoral and cytotoxic lymphocyte (CTL) responses against cells expressing either or both of these antigens, resulting in decreased tumor growth.","Pharmacologic Substance"]
["C74079","Synthetic Brain Tumor Peptides-Pulsed Autologous Dendritic Cell Vaccine","Synthetic Brain Tumor Peptides-Pulsed Autologous Dendritic Cell Vaccine","A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with synthetic brain tumor peptides with potential immunostimulatory and antineoplastic activities. Upon administration, synthetic brain tumor peptides-pulsed autologous dendritic cell vaccine may stimulate anti-tumoral cytotoxic T lymphocyte (CTL)l and antibody responses against glioma tumor cells, resulting in glioma tumor cell lysis.","Pharmacologic Substance"]
["C61076","Synthetic Breast Cancer Peptides-Tetanus Toxoid-Montanide ISA-51 Vaccine","Synthetic Breast Cancer Peptides-Tetanus Toxoid-Montanide ISA-51 Vaccine","A cancer vaccine comprised of multiple synthetic breast cancer peptides and the adjuvant tetanus toxoid helper peptide emulsified in the adjuvant Montanide ISA-51 with immunopotentiation activity. Vaccination with this cancer vaccine may elicit a specific cytotoxic T-lymphocyte response against breast cancer cells. Synthetic breast cancer peptides may stimulate the immune response against cells that produce breast cancer markers such as erbB2 (HER2/neu) while tetanus toxoid helper peptide binds to class II MHC molecules as a nonspecific vaccine helper epitope, resulting in a long-term immunopotentiation by increasing the helper T-cell response. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.","Amino Acid, Peptide, or Protein"]
["C100099","Synthetic Breast Cancer Peptides-Tetanus Toxoid-Poly ICLC Vaccine","Synthetic Breast Cancer Peptides-Tetanus Toxoid-Poly ICLC Vaccine","A cancer vaccine comprised of nine class I major histocompatibility complex (MHC)-restricted breast cancer associated peptides, the tetanus toxoid helper peptide and the Toll-like receptor 3 (TLR3) agonist poly ICLC, with potential immunostimulatory and antineoplastic activities. The nine peptides derived from six cancer associated proteins are epidermal growth factor receptor 2 (HER2/neu), carcinoembryonic antigen (CEA) and four cancer/testis antigens (CTAs: MAGE-A1, -A3, -A10, and NY-ESO-1). Vaccination with this vaccine may elicit a specific cytotoxic T-lymphocyte (CTL) response against cells overexpressing these tumor associated antigens (TAAs). As a nonspecific T-helper epitope, tetanus toxoid helper peptide binds to class II MHC and results in long-term immunopotentiation by increasing the helper T-cell response. Poly ICLC, the double-stranded RNA molecules of polyinosinic-polycytidylic acid stabilized with poly L-lysine in carboxymethylcellulose, binds to TLR3 and induces the release of cytokines which may help boost the immune response against the TAAs.","Pharmacologic Substance"]
["C116332","Synthetic Glioblastoma Mutated Tumor-specific Peptides Vaccine Therapy APVAC2","APVAC2|Synthetic Glioblastoma Mutated Tumor-specific Peptides Vaccine Therapy APVAC2","A personalized peptide-based cancer vaccine comprised of one or two de novo synthesized patient-specific tumor-mutated peptides associated with glioblastoma (GB), with potential immunomodulating and antineoplastic activities. Vaccination with synthetic GB mutated tumor-specific peptides vaccine therapy APVAC2 stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the selected mutated tumor-associated peptides, which results in decreased GB growth. These peptides are specifically selected and synthesized based on the expression of the patient's own mutated tumor-associated antigens, which were detected during individual tumor genome sequencing.","Immunologic Factor|Pharmacologic Substance"]
["C116331","Synthetic Glioblastoma Tumor-associated Peptides Vaccine Therapy APVAC1","APVAC1|Synthetic Glioblastoma Tumor-associated Peptides Vaccine Therapy APVAC1","A personalized peptide-based cancer vaccine comprised of five to ten peptides associated with glioblastoma (GB), with potential immunomodulating and antineoplastic activities. Vaccination with synthetic GB tumor-associated peptides vaccine therapy APVAC1 stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the tumor associated peptides, and results in decreased GB growth. The peptides are derived from a glioma actively personalized vaccine consortium (GAPVAC) warehouse and are specifically selected based on the patient's expression of tumor-associated antigens.","Immunologic Factor|Pharmacologic Substance"]
["C120118","Synthetic hTERT DNA Vaccine INO-1400","INO-1400|Synthetic hTERT DNA Vaccine INO-1400","A DNA vaccine consisting of a plasmid encoding the full-length sequence of the tumor-associated antigen (TAA) human telomerase reverse transcriptase (hTERT), which is the catalytic subunit of human telomerase and synthesizes telomeric DNA at the chromosome ends, containing two immunogenic mutations, with potential immunostimulating and antineoplastic activities. Upon intradermal vaccination of the hTERT encoding DNA vaccine INO-1400 in combination with electroporation, hTERT protein is expressed and activates the immune system to mount a cytotoxic T-cell (CTL) response against telomerase-expressing tumor cells, which may result in tumor cell death. Telomerase prolongs the functional lifespan of cells via the restoration and maintenance of telomere length. Abnormally activated in tumorigenesis, telomerase is expressed in the majority of human cancer cells, but its expression is low or non-existent in normal cells.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C38726","Synthetic Human Papillomavirus 16 E6 Peptide","HPV-16 E6 Peptide|HPV-16 E6|Human Papillomavirus 16 E6 Peptide|Synthetic Human Papillomavirus 16 E6 Peptide","A synthetic peptide sequence of human papillomavirus (HPV) type 16 oncoprotein E6.  The E6 oncoprotein is implicated in the tumorigenesis of cervical carcinoma.  Vaccination with HPV 16 E6 peptide may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against cells expressing the E6 oncoprotein, resulting in tumor cell lysis.","Immunologic Factor"]
["C122400","Synthetic Hypericin","Synthetic Hypericin|Topical SGX301","A topical ointment formulation containing a synthetic form of hypericin, an anthraquinone derivative that is naturally found in the yellow flower of Hypericum perforatum (St. John's wort), with potential antineoplastic and photosensitizing activities. Upon topical administration of the ointment to the tumor site, hypericin becomes activated through the application of visible fluorescent light. During photoactivation, hypericin generates singlet oxygen, which induces DNA damage, necrosis and apoptosis, thereby inhibiting tumor cell growth. The use of visible light for activation avoids the risk of developing secondary malignancies, which are frequently associated with other photodynamic therapies that are dependent on ultraviolet A exposure.","Pharmacologic Substance"]
["C129652","Synthetic Long E6 Peptide-Toll-like Receptor Ligand Conjugate Vaccine ISA201","HPV E Six Peptide Conjugated to Amplivant|HPV16 peptides AMPLIVANT Vaccine|Hespecta|ISA201|PV E6 Peptides-Amplivant|PV16 E6 Peptide Conjugated to Amplivant|SLP HPV16 E6/Amplivant Vaccine ISA201|SLP-Amplivant ISA201|Synthetic Long E6 Peptide-Toll-like Receptor Ligand Conjugate Vaccine ISA201","A therapeutic peptide vaccine consisting of two highly immunogenic synthetic long peptides (SLPs), which are 25-35 amino acids in size, derived from the human papillomavirus (HPV) type 16 oncoprotein E6, and conjugated to a proprietary toll-like receptor 2 (TLR2) ligand (TLR2-L) immunoadjuvant, with potential immunostimulating and antitumor activities. Upon administration, the TLR2-L moiety of the synthetic long E6 peptides TLR ligand conjugate vaccine targets and binds to TLRs expressed on antigen-presenting cells (APCs), particularly dendritic cells (DCs). This increases the direct targeting of, binding to, uptake by, and processing of the SLPs into small pieces by the DCs. The processed viral epitopes are presented by DCs, which activate and stimulate the host immune system to mount specific cytotoxic T-lymphocyte (CTL) and helper T (Th) cell responses against HPV E6-expressing tumor cells. This results in the destruction of tumor cells and leads to decreased growth of HPV E6-expressing tumor cells. The E6 oncoprotein is implicated in tumorigenesis in a variety of cancers. The TLR2-L improves antigen processing and presentation by, and activation of APCs, thereby improving the immunostimulatory effect of the vaccine. The two peptides cover the most immunodominant regions of the HPV16 E6 oncogenic protein and contain both Th and CTL epitopes.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C111037","Synthetic Long E6/E7 Peptides Vaccine HPV-01","HPV-01|ISA101|SLP-HPV-01|Synthetic Long E6/E7 Peptides Vaccine HPV-01","A therapeutic peptide vaccine consisting of thirteen synthetic long peptides (SLPs), which are 25-35 amino acids in size, derived from the human papillomavirus (HPV) type 16 oncoproteins E6 and E7, with potential immunostimulating and antitumor activities. Upon administration, synthetic long E6/E7 peptides vaccine HPV-01 is taken up and degraded into small pieces by dendritic cells. The processed viral epitopes are presented by dendritic cells, which may stimulate the host immune system to mount both cytotoxic T-cell lymphocyte (CTL) and helper T cell responses against HPV E6/E7-expressing tumor cells. This results in the destruction of tumor cells and leads to decreased tumor growth. The E6 and E7 oncoproteins are implicated in the tumorigenesis in a variety of cancers. The SLPs allow for optimal presentation by antigen-presenting cells.","Immunologic Factor|Pharmacologic Substance"]
["C48639","Synthetic Melanoma-Associated Antigens Vaccine","Synthetic Melanoma-Associated Antigens Vaccine","A cancer vaccine containing synthetic epitope peptides derived from melanoma tumor-associated antigens (TAAs), including melanoma-melanocyte antigen gp100(280-288), melanoma-associated antigen tyrosinase(1-9), and melanoma-associated antigen melan-A(27-35). Upon administration, synthetic melanoma-associated antigens vaccine may stimulate a cytotoxic T-lymphocyte immune response against melanoma cells that express TAAs which share epitopes with the vaccine epitope peptides, resulting in tumor cell lysis.","Pharmacologic Substance"]
["C67098","Synthetic Peptides E-PRA And E-PSM Vaccine","Synthetic Peptides E-PRA And E-PSM Vaccine","A cancer vaccine consisting of E-PRA and E-PSM, two synthetic peptide analogs of PRAME (PReferential Antigen MElanoma) and PSMA (Prostate Specific Membrane Antigen), with potential immunostimulating activity. Upon direct administration into lymph nodes, synthetic peptides E-PRA and E-PSM vaccine may stimulate a cytotoxic T-lymphocyte (CTL) response against PRAME- and PSMA-expressing tumor cells. PRAME and PSMA are tumor-associated antigens upregulated and expressed on the cell surfaces of certain tumor cell types.","Pharmacologic Substance"]
["C106117","T1E28z CAR-expressing Autologous CD4-positive T Lymphocytes","4ab T1E28z Positive T-cells|T1E28z CAR-expressing Autologous CD4-positive T Lymphocytes","Autologous CD4 positive T-lymphocytes engineered to express the chimeric antigen receptor (CAR) T1E28z containing the ErbB ligand, T1E, fused to the hinge region, transmembrane domain and endodomain of CD28 and the CD3zeta endodomain, with potential immunomodulating and antineoplastic activities. T1E, a chimeric polypeptide containing the N-terminus of human transforming growth factor (TGF)-alpha fused to the C-terminus of epidermal growth factor (EGF), binds to ErbB1 homodimers and heterodimers as well as ErbB2/3 heterodimers, but not to ErbB2 or erbB3 alone. Upon intratumoral administration, the promiscuous ErbB ligand T1E of the T1E28z CAR-expressing autologous CD4-positive T lymphocytes binds to the specific ErbB homo- and heterodimers on tumor cells. This induces selective toxicity in ErbB-expressing tumor cells resulting in tumor cell lysis. ErbB1, ErbB2 and ErbB3, members of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, are frequently overexpressed in solid tumors and play key roles in tumor cell proliferation and tumor angiogenesis.","Pharmacologic Substance"]
["C26674","T900607","T900607","A pentafluorophenylsulfonamide compound with potential antineoplastic activity. T900607 inhibits tubulin polymerization by binding irreversibly to colchicine binding sites, resulting in cell cycle arrest and apoptosis. (NCI04)","Pharmacologic Substance"]
["C91727","Tabalumab","Anti-BAFF Monoclonal Antibody LY2127399|LY2127399|TABALUMAB|Tabalumab","A human IgG4 monoclonal antibody against B-cell activating factor (BAFF), with potential immunomodulating and antineoplastic activities. Tabalumab binds to and inhibits the activity of both soluble and cell surface-bound BAFF. This may reduce the activity, proliferation and survival of B-cells. A dysregulated expression of BAFF, a member of the tumor necrosis factor (TNF) family of proteins, is often seen in certain autoimmune diseases and certain cancers, and may promote B lymphocyte activation, proliferation and survival.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2202","Tacedinaline","4-(Acetylamino)-N-(2-aminophenyl)benzamide|Acetyldinaline|CI-994|GOE5549|N-acetyl Dinaline|N-acetyldinaline|PD 123654|TACEDINALINE|Tacedinaline","An orally bioavailable substituted benzamide derivative with potential antineoplastic activity. Tacedinaline inhibits histone deacetylation, which may result in histone hyperacetylation, followed by the induction of differentiation, the inhibition of cell proliferation, and apoptosis in susceptible tumor cell populations.","Organic Chemical|Pharmacologic Substance"]
["C48264","Talabostat","PT-100|TALABOSTAT|Talabostat|[(2R)-1-[(2S)-2-amino-3-methylbutanoyl]pyrrolidin-2-yl]boronic acid|talabostat","A small molecule with antineoplastic and hematopoiesis- stimulating activities. By cleaving N-terminal Xaa-Pro or Xaa-Ala residues, talabostat inhibits dipeptidyl peptidases, such as fibroblast activation protein (FAP), resulting in the stimulation of cytokine and chemokine production and specific T-cell immunity and T-cell dependent activity. This agent may also stimulate the production of colony stimulating factors, such as granulocyte colony stimulating factor (G-CSF), resulting in the stimulation of hematopoiesis. Dipeptidyl peptidases are involved in the activation of polypeptide hormones and chemokines.","Pharmacologic Substance"]
["C80682","Talabostat Mesylate","((2R)-1-((2S)-2-amino-3-methylbutanoyl)pyrrolidin-2-yl)boronic Acid Methanesulfonate|TALABOSTAT MESYLATE|Talabostat Mesylate|Val-boro-Pro|talabostat mesylate","The mesylate salt of an orally active small molecule with antineoplastic and hematopoiesis- stimulating activities. By cleaving N-terminal Xaa-Pro or Xaa-Ala residues, talabostat inhibits dipeptidyl peptidases, such as fibroblast activation protein (FAP), resulting in the stimulation of cytokine and chemokine production and specific T-cell immunity and T-cell dependent activity. This agent may also stimulate the production of colony stimulating factors, such as granulocyte colony stimulating factor (G-CSF), resulting in the stimulation of hematopoiesis. Dipeptidyl peptidases are involved in the activation of polypeptide hormones and chemokines.","Pharmacologic Substance"]
["C78460","Talactoferrin Alfa","Oral Recombinant Human Lactoferrin|Oral rhLF|TALACTOFERRIN ALFA|TLF|Talactoferrin Alfa|talactoferrin alfa|talactoferrin","An orally bioavailable recombinant human lactoferrin produced in the fungus Aspergillus niger with potential antineoplastic and immunomodulating activities. Upon oral administration, talactoferrin is transported into small intestinal Peyer's patches of the gut-associated lymphoreticular tissues (GALT), where it recruits circulating immature dendritic cells (DCs) bearing tumor antigens and induces their maturation. In the GALT, DC maturation in the presence of tumor antigens and lymphoid effector cells may induce systemic innate and adaptive immune responses mediated by anti-tumor natural killer (NK) cells, cytotoxic T lymphocytes, and natural killer T (NKT) cells; activation of tumor-draining lymph nodes, cellular infiltration of distant tumors, and tumor-cell death may follow. Raising the initial immune response in the GALT, distant from the primary tumor, may counter local tumor-mediated immunosuppression.","Organic Chemical|Pharmacologic Substance"]
["C103826","Taladegib","4-Fluoro-N-methyl-N-(1-(4-(1-methyl-1H-pyrazol-5-yl)phthalazin-1-yl)piperidin-4-yl)-2-(trifluoromethyl)benzamide|Benzamide, 4-Fluoro-N-methyl-N-(1-(4-(1-methyl-1H-pyrazol-5-yl)-1-phthalazinyl)-4-piperidinyl)-2-(trifluoromethyl)-|LY-2940680|LY2940680|TALADEGIB|Taladegib","An orally bioavailable small molecule antagonist of the Hedgehog (Hh)-ligand cell surface receptor smoothened (Smo) with potential antineoplastic activity. Taladegib inhibits signaling that is mediated by the Hh pathway protein Smo, which may result in a suppression of the Hh signaling pathway and may lead to the inhibition of the proliferation of tumor cells in which this pathway is abnormally activated. The Hh signaling pathway plays an important role in cellular growth, differentiation and repair; constitutive activation of this pathway is associated with uncontrolled cellular proliferation and has been observed in a variety of cancers.","Organic Chemical|Pharmacologic Substance"]
["C38139","Talampanel","(R)-(-)-1-(4-Aminophenyl)-3-acetyl-4-methyl-7,8-methylenedioxy-3,4-dihydro-5H-2,3-benzodiazepine|GYKI-53773|LY-300164|TALAMPANEL|Talampanel|talampanel","A synthetic derivative of dioxolo-benzodiazepine with anti-seizure activity.  Talampanel antagonizes the AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) subtype of glutamate excitatory amino acid receptors and may inhibit the growth of gliomas by interfering with neurotransmitters involved in brain tumor growth. This agent may also protect against traumatic brain injury.","Organic Chemical|Pharmacologic Substance"]
["C26675","Talaporfin Sodium","LS11|Laserphyrin|ME2906|Mono-L-aspartyl Chlorin e6|NPe6|TALAPORFIN SODIUM|Talaporfin Sodium|Taporfin Sodium|talaporfin sodium","An agent consisting of chlorin e6, derived from chlorophyll, and L-aspartic acid with photosensitizing activity.  After intratumoral activation by light emitting diodes, taporfin sodium forms an extended high energy conformational state that generates singlet oxygen, resulting in free radical-mediated cell death. (NCI04)","Pharmacologic Substance"]
["C95733","Talazoparib","BMN 673|BMN-673|Talazoparib","An orally bioavailable inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential antineoplastic activity. Talazoparib selectively binds to PARP and prevents PARP-mediated DNA repair of single strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks, promotes genomic instability and eventually leads to apoptosis. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by single-strand DNA breaks.","Pharmacologic Substance"]
["C61314","Talimogene Laherparepvec","ICP34.5-, ICP47-deleted Herpes Simplex Virus 1 (HSV-1) Incorporating the Human GM-CSF Gene|Imlygic|JS1 34.5-hGMCSF 47- pA-|OncoVEX GM-CSF|T-VEC|TALIMOGENE LAHERPAREPVEC|Talimogene Laherparepvec","An ICP34.5, ICP47-deleted, oncolytic herpes simplex type-1 virus (HSV-1) based on the JS1 strain, and encoding the immunostimulating factor human cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with potential immunostimulating and antineoplastic activities. Upon intratumoral injection, talimogene laherparepvec selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, GM-CSF attracts dendritic cells (DCs) and may stimulate a cytotoxic T cell response against tumor cells, which results in immune-mediated tumor cell death. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Additionally, deletion of ICP47 causes increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and oncolysis of tumor cells.","Pharmacologic Substance"]
["C1603","Tallimustine","FCE 24517|PNU-152241|TALLIMUSTINE|Tallimustine","A benzoyl mustard derivative of the antiviral agent distamycin A with potential antineoplastic activity. Tallimustine selectively binds to A-T rich regions in the minor groove of DNA and alkylates at the N3 position of adenine in a highly sequence-specific manner. This prevents DNA replication, inhibits cellular proliferation and triggers apoptosis. Moreover, unlike other clinical nitrogen mustards, tallimustine does not carry out guanine-N7 alkylation in the major groove of DNA, which may lead to a high selectivity of action.","Organic Chemical|Pharmacologic Substance"]
["C79841","Talmapimod","1H-indole-3-acetamide, 6-Chloro-5-[[(2R,5S)-4-[(4-fluorophenyl)methyl]-2,5-dimethyl-1- piperazinyl]carbonyl]-N,N,1-trimethyl-alpha-oxo-|2-[6-Chloro-5-[[(2R,5S)-4-(4-fluorobenzyl)-2,5-dimethylpiperazin-1-yl]carbonyl]-1- methyl-1H-indol-3-yl]-N,N-dimethyl-2-oxoacetamide|SCIO 469|TALMAPIMOD|Talmapimod","An orally bioavailable, small-molecule, p38 mitogen-activated protein kinase (MAPK) inhibitor with potential immunomodulating, anti-inflammatory, and antineoplastic activities. Talmapimod specifically binds to and inhibits the phosphorylation of p38 MAPK, which may result in the induction of tumor cell apoptosis, the inhibition of tumor cell proliferation, and the inhibition of tumor angiogenesis. This agent may also enhance proteasome inhibitor-induced apoptosis. p38 MAPK is a serine/threonine protein kinase involved in a MAPK signaling cascade that controls cellular responses to various environmental stresses, cytokines, and endotoxins.","Pharmacologic Substance"]
["C29341","Talotrexin","N(alpha)-(4-Amino-4-deoxypteroyl)-N(delta)-hemiphthaloyl-L-ornithine|PT523|TALOTREXIN|Talopterin|Talotrexin|talotrexin","An antimetabolite analogue of aminopterin with potential antineoplastic activity. As a folate antagonist, talotrexin binds to and inhibits the function of dihydrofolate reductase, resulting in the inhibition of folate metabolism, DNA synthesis, and cell division. Hydrosoluble, talotrexin is actively transported into cells by the reduced folate carrier (RFC) and, therefore, is unlikely to be associated with P-glycoprotein-mediated multidrug resistance.","Pharmacologic Substance"]
["C80159","Talotrexin Ammonium","2-(((4S)-4-Carboxy-4-((4-(((2,4-diaminopteridin-6-yl)methyl)amino)benzoyl)amino)butyl)carbamoyl)benzoic Acid Monoammonium Salt|PT-523|PT523|TALOTREXIN AMMONIUM|Talotrexin Ammonium","An ammonium salt of tallotrexin, an analogue of aminopterin with potential antineoplastic activity. As a folate antagonist, talotrexin binds to and inhibits the function of dihydrofolate reductase, resulting in the inhibition of folate metabolism, DNA synthesis, and cell division. Hydrosoluble, talotrexin is actively transported into cells by the reduced folate carrier (RFC) and, therefore, is unlikely to be associated with P-glycoprotein-mediated multidrug resistance.","Pharmacologic Substance"]
["C75998","Taltobulin","HTI-286|SPA-110|TALTOBULIN|Taltobulin","An analogue of the naturally occurring tripeptide hemiasterlin, with potential antimitotic and antineoplastic activities. Taltobulin binds tubulin in a similar manner as colchicine and inhibits tubulin polymerization. This results in the disruption of the cytoskeleton, ultimately leading to cell cycle arrest in G2/M phase, blockage of cell division and apoptosis.","Pharmacologic Substance"]
["C71025","Tamibarotene","4-((5,6,7,8-Tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)carbamoyl)|Am-80|Am80|Benzoic Acid, 4-(((5,6,7,8-tetrahydro-5,5,8,8-Tetramethyl-2-naphthalenyl)amino)carbonyl)-|INNO-507|N-(5,6,7,8-Tetrahydro-5,5,8,8-tetramethyl-2-naphthyl)terephthalamic Acid|Retinobenzoic Acid|SY-1425|TAMIBAROTENE|TM-411|TOS-80T|Tamibarotene|Z-208","An orally active, synthetic retinoid, developed to overcome all-trans retinoic acid (ATRA) resistance, with potential antineoplastic activity. As a specific retinoic acid receptor (RAR) alpha/beta agonist, tamibarotene is approximately ten times more potent than ATRA in inducing cell differentiation and apoptosis in HL-60 (human promyelocytic leukemia) cell lines in vitro. Due to a lower affinity for cellular retinoic acid binding protein (CRABP), tamibarotene may show sustained plasma levels compared to ATRA. In addition, this agent may exhibit a lower toxicity profile than ATRA, in part, due to the lack of affinity for the RAR-gamma receptor, the major retinoic acid receptor in the dermal epithelium.","Organic Chemical|Pharmacologic Substance"]
["C62078","Tamoxifen","1-p-beta-dimethylamino-ethoxyphenyl-trans-1,2-diphenylbut-1-ene|TAMOXIFEN|Tamoxifen|tamoxifen","An antineoplastic nonsteroidal selective estrogen receptor modulator (SERM).  Tamoxifen competitively inhibits the binding of estradiol to estrogen receptors, thereby preventing the receptor from binding to the estrogen-response element on DNA.  The result is a reduction in DNA synthesis and cellular response to estrogen.  In addition, tamoxifen up-regulates the production of transforming growth factor B (TGFb), a factor that inhibits tumor cell growth, and down-regulates insulin-like growth factor 1 (IGF-1), a factor that stimulates breast cancer cell growth.","Organic Chemical|Pharmacologic Substance"]
["C855","Tamoxifen Citrate","(Z)-2-[4-(1,2-Diphenyl-1-butenyl)phenoxy]-N,N-dimethylethanamine 2-Hydroxy-1,2,3-propanetricarboxylate|(Z)-2-[4-(1,2-diphenyl-1-butenyl)phenoxy]-N,N-dimethylethanamine citrate|1-p-beta-dimethylamino-ethoxyphenyl-trans-1,2-diphenylbut-1-ene Citrate|Apo-Tamox|Clonoxifen|Dignotamoxi|Ebefen|Emblon|Estroxyn|Fentamox|Gen-Tamoxifen|Genox|ICI 46,474|ICI-46474|Jenoxifen|Kessar|Ledertam|Lesporene|Nolgen|Noltam|Nolvadex-D|Nolvadex|Nourytam|Novo-Tamoxifen|Novofen|Noxitem|Oestrifen|Oncotam|PMS-Tamoxifen|Soltamox|TAM|TAMOXIFEN CITRATE|Tamax|Tamaxin|Tamifen|Tamizam|Tamofen|Tamoxasta|Tamoxifen Citrate|Tamoxifen citrate|Tamoxifeni Citras|Zemide|tamoxifen citrate","The citrate salt of an antineoplastic nonsteroidal selective estrogen receptor modulator (SERM). Tamoxifen competitively inhibits the binding of estradiol to estrogen receptors, thereby preventing the receptor from binding to the estrogen-response element on DNA. The result is a reduction in DNA synthesis and cellular response to estrogen. In addition, tamoxifen up-regulates the production of transforming growth factor B (TGFb), a factor that inhibits tumor cell growth, and down-regulates insulin-like growth factor 1 (IGF-1), a factor that stimulates breast cancer cell growth. Tamoxifen also down-regulates protein kinase C (PKC) expression in a dose-dependant manner, inhibiting signal transduction and producing an antiproliferative effect in tumors such as malignant glioma and other cancers that overexpress PKC.","Organic Chemical|Pharmacologic Substance"]
["C48404","Tandutinib","1-Piperazinecarboxamide, 4-(6-Methoxy-7-(3-(1-piperidinyl)propoxy)-4-quinazolinyl)-N-(4-(1-methylethoxy)phenyl)-|CT53518|MLN 518|MLN518|TANDUTINIB|Tandutinib|tandutinib","A piperazinyl quinazoline receptor tyrosine kinase inhibitor with antineoplastic activity. Tandutinib inhibits the autophosphorylation of FLT3 (FMS-Like Tyrosine kinase-3), c-KIT and PDGF (platelet-derived growth factor) receptor tyrosine kinases, thereby inhibiting cellular proliferation and inducing apoptosis.","Pharmacologic Substance"]
["C37899","Tanespimycin","17-(Allylamino)-17-demethoxygeldanamycin|17-AAG|17-Allylamino-17-demethoxygeldanamycin|17-Demethoxy-17-(2-propenylamino)geldanamycin|17-N-allylamino-17-demethoxy geldanamycin|17-N-allylamino-17-demethoxygeldanamycin|Geldanamycin, 17-allylamino-17-demethoxy-|KOS-953|TANESPIMYCIN|Tanespimycin|tanespimycin","A benzoquinone antineoplastic antibiotic derived from the antineoplastic antibiotic geldanamycin.  Tanespimycin binds to and inhibits the cytosolic chaperone functions of heat shock protein 90 (HSP90).  HSP90 maintains the stability and functional shape of many oncogenic signaling proteins; the inhibition of HSP90 promotes the proteasomal degradation of oncogenic signaling proteins that may be overexpressed by tumor cells.","Antibiotic|Organic Chemical"]
["C102877","Tanibirumab","TTAC-0001|Tanibirumab","A fully human monoclonal antibody targeting the vascular endothelial growth factor receptor 2 (VEGFR2), with potential antiangiogenic activity. Upon administration, tanibirumab specifically binds to VEGFR2, thereby preventing the binding of its ligand VEGF. This may result in the inhibition of tumor angiogenesis and a decrease in tumor nutrient supply. VEGFR2 is a pro-angiogenic growth factor receptor tyrosine kinase expressed by endothelial cells, while VEGF is overexpressed in many tumors and is correlated to tumor progression.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C1705","Tanomastat","(S)-3-[(4'-Chloro-4-biphenylyl)carbonyl]-2-[(phenylthio)methyl]propionic acid|4-[4-(chlorophenyl)phenyl]-4-oxo-2S-(phenylthiomethyl) butanoic acid|BAY 12-9566|BAY-12-9566|TANOMASTAT|Tanomastat","A biphenyl matrix metalloproteinase (MMP) inhibitor (MMPI) with potential antineoplastic activity. Tanomastat inhibits MMP-2, MMP-3, and MMP-9, inhibiting extracellular matrix degradation and potentially inhibiting angiogenesis, tumor growth and invasion, and metastasis. MMPs consist of at least 18 zinc-containing endo-proteinases that are capable of degrading collagen and proteoglycan.","Organic Chemical|Pharmacologic Substance"]
["C26666","Tarenflurbil","(R)-2-Fluoro-alpha-methyl[1,1'-biphenyl]-4-acetic Acid|E-7869|Flurizan|MPC-7869|R-Flurbiprofen|R-flurbiprofen|TARENFLURBIL|Tarenflurbil","An orally active synthetic enantiomer of flurbiprofen.  Tarenflurbil activates c-Jun N terminal kinase, increases AP-1 binding to DNA, and downregulates cyclin D1 expression, resulting in arrest of tumor cells in the G1 phase of the cell cycle and apoptosis. This agent also affects the expression of nuclear factor kappa B, a rapid response transcription factor that stimulates the immune response to tumor cells. R-flurbiprofen does not inhibit the enzyme cyclo-oxygenase.","Organic Chemical|Pharmacologic Substance"]
["C95719","Tarextumab","MoAb OMP-59R5|OMP 59R5|OMP-59R5|TAREXTUMAB|Tarextumab","A monoclonal antibody directed against the Notch receptor with potential antineoplastic activity. Tarextumab binds to Notch on the cell surface, thereby inhibiting Notch-mediated signaling and gene transcription, which may impede tumor angiogenesis. Notch receptors are important for cell-cell communication, which involves gene regulation mechanisms that control multiple cell differentiation processes during embryonic and adult life. Dysregulated Notch signaling is implicated in many diseases including T-ALL (T-cell acute lymphoblastic leukemia), CADASIL (Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy), MS (Multiple Sclerosis), and many other disease states.","Immunologic Factor|Pharmacologic Substance"]
["C2246","Tariquidar","TARIQUIDAR|Tariquidar|XR9576|tariquidar","An anthranilamide derivative with multidrug resistance properties.  Tariquidar non-competitively binds to the p-glycoprotein transporter, thereby inhibiting transmembrane transport of anticancer drugs.  Inhibition of transmembrane transport may result in increased intracellular concentrations of an anticancer drug, thereby augmenting its cytotoxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C85462","TARP 27-35 Peptide Vaccine","TARP 27-35 Peptide Vaccine","A peptide-based cancer vaccine, containing amino acid residues 27 through 35 of T cell receptor gamma alternate reading frame protein (TARP), with potential immunostimulatory and antineoplastic activities. Upon administration, TARP 27-35 peptide vaccine may stimulate a host cytotoxic T-cell (CTL) response against TARP-expressing tumor cells, resulting in tumor cell cytotoxicity. The nuclear protein TARP is commonly expressed on prostate and breast cancer cells and is highly immunogenic.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C85463","TARP 29-37-9V Peptide Vaccine","TARP 29-37-9V Peptide Vaccine","A peptide-based cancer vaccine, consisting of amino acid residues 29 through 37 of T cell receptor gamma alternate reading frame protein (TARP) with a leucine-to-valine substitution at position 9, with potential immunostimulatory and antineoplastic activities. Upon administration, TARP 29-37-9V peptide vaccine may induce a cytotoxic T-lymphocyte (CTL) response against TARP-expressing tumor cells, which may result in decreased tumor cell proliferation. The leucine-to-valine substitution at position 9 of this peptide improves its immunogenicity. The nuclear protein TARP is commonly expressed on prostate and breast cancer cells and is highly immunogenic.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C61494","TAS-108","(7)-21-[4-[(diethylamino)methyl]-2-methoxyphenoxy]-7-methyl-19-norpregna-1,3,5(10)-trien-3-ol 2-hydroxy-1,2,3-propanetricarboxylate|SR 16234|SR16234|TAS-108","A synthetic, antiestrogenic steroidal compound with potential antitumor activity. TAS-108 binds to and inhibits estrogenic receptor alpha (ERa), mainly expressed in the mammary gland and uterus and upregulated in estrogen-dependent tumors. Blockage of ERa by TAS-108 prevents the binding and effects of estrogen and may lead to an inhibition of estrogen-dependent cancer cell proliferation. TAS-108 also is a partial agonist of the estrogenic receptor beta (ERb), expressed in many tissues including the central nervous system, urogenital tract, bone and cardiovascular system, thereby exerting a positive effect on these tissues. In addition, TAS-108 activates the co-repressor Silencing Mediator for Retinoid and Thyroid hormone receptor (SMRT), a protein that inhibits the activities of the estrogen receptors, which may contribute to the antitumor activity of TAS-108.","Organic Chemical|Pharmacologic Substance"]
["C116876","Taselisib","GDC-0032|TASELISIB|Taselisib","An orally bioavailable inhibitor of the class I phosphatidylinositol 3-kinase (PI3K) alpha isoform (PIK3CA), with potential antineoplastic activity. Taselisib selectively inhibits PIK3CA and its mutant forms in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PIK3CA-expressing tumor cells. By specifically targeting class I PI3K alpha, this agent may be more efficacious and less toxic than pan PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and causes increased tumor cell growth, survival, and resistance to both chemotherapy and radiotherapy. PIK3CA, which encodes the p110-alpha catalytic subunit of the class I PI3K, is mutated in a variety of cancer cell types and plays a key role in cancer cell growth and invasion.","Pharmacologic Substance"]
["C77067","Tasidotin","ILX651|TASIDOTIN|Tasidotin","A third generation, synthetic, water-soluble, pentapeptide analog of the marine depsipeptide dolastatin 15, with potential antimitotic and antineoplastic activities. Tasidotin and its metabolite, tasidotin C-carboxylate, suppress the dynamic instability behavior of the microtubules through a reduction of the shortening rate (disassembly); reduction of the switching frequency from growth to shortening; and by reducing microtubules growth time. This may eventually result in a reduction of cell growth.","Pharmacologic Substance"]
["C62794","Tasisulam","LY-573636|LY573636|N-(2,4-Dichlorobenzoyl)-5-bromothiophene-2-sulfonamide|TASISULAM|Tasisulam","An acyl-sulfonamide with potential antineoplastic activity. Selectively toxic towards tumor cells, tasisulam appears to induce tumor cell apoptosis by a mitochondrial-targeted mechanism involving the loss of mitochondrial membrane potential and induction of reactive oxygen species (ROS). In combination with an angiogenesis inhibitor, this agent may exhibit synergistic antiangiogenic activity.","Pharmacologic Substance"]
["C88304","Tasisulam Sodium","Benzamide, N-[(5-Bromo-2-thienyl)sulfonyl]-2,4-dichloro-, Sodium Salt|LY-573636.Na|LY573636-Sodium|TASISULAM SODIUM|Tasisulam Sodium","The sodium salt of an acyl-sulfonamide with potential antineoplastic activity. Selectively toxic towards tumor cells, tasisulam appears to induce tumor cell apoptosis by a mitochondrial-targeted mechanism involving the loss of mitochondrial membrane potential and induction of reactive oxygen species (ROS). In combination with an angiogenesis inhibitor, this agent may exhibit synergistic antiangiogenic activity.","Pharmacologic Substance"]
["C74080","Tasquinimod","ABR-215050|TASQ|TASQUINIMOD|Tasquinimod","A quinoline-3-carboxamide linomide analogue with antiangiogenic and potential antineoplastic activities. Tasquinimod has been shown to decrease blood vessel density but the exact mechanism of action is not known. This agent has also been shown to augment the antineoplastic effects of docetaxel and androgen ablation in a murine model of prostate cancer involving human prostate cancer xenografts.","Pharmacologic Substance"]
["C2639","Taurolidine","Bis(1,1-dioxoperhydro-1,2,4-thiadiazinyl-4)-methane|TAUROLIDINE|Taurolidine|Taurolin|taurolidine","A synthetic broad-spectrum antibiotic with antibacterial, anticoagulant and potential antiangiogenic activities. Taurolidine, derived from the amino acid taurine, binds to and neutralizes bacterial exotoxins and endotoxins, or lipopolysaccharides (LPS). Taurolidine binding to LPS prevents bacterial adherence to host epithelial cells, thereby prevents bacterial invasion of uninfected host cells. Although the mechanism underlying its antineoplastic activity has not been fully elucidated, it may be related to this agent's anti-adherence property. In addition, taurolidine also promotes apoptosis by inducing various apoptotic factors and suppresses the production of vascular endothelial growth factor (VEGF), a protein that plays an important role in angiogenesis.","Antibiotic"]
["C954","Tauromustine","1-(2-Chloroethyl)-3-(2-(dimethylaminosulfonyl)ethyl)-1-nitrosourea|LS-2667|TAUROMUSTINE|TCNU|Tauromustine","A water-soluble taurine-based nitrosourea with potential antineoplastic activity. Tauromustine alkylates DNA and causes DNA cross links independent of cell cycle, thereby resulting in disruption of DNA function and induction of apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C75290","Taurultam","TAURULTAM|Taurultam","A reversible metabolite of taurolidine and an amino acid taurine derivative, with antibacterial and antineoplastic activity. Taurultam, like its congener taurolidine, inhibits proliferation of microvascular endothelial cells, although to a lesser extent, by selectively inhibiting the adhesion of endothelial cells to laminin but not to collagen I and fibronectin.","Pharmacologic Substance"]
["C116871","Taxane Analogue MST-997","5Beta,20-epoxy-1,2alpa,4,7beta,10beta,13alpha-hexahydroxytax-11-en-9-one-4-acetate 2-benzoate Ester with (2R,3S)-N-Isopropoxycarbonyl-3-(2-thienyl) Isoserine|MST-997|TL-909|Taxane Analogue MST-997|Taxane-997","A semi-synthetic, orally bioavailable, third-generation taxane derivative and microtubule-stabilizing agent, with potential antineoplastic activity. Upon administration, taxane analogue MST-997 binds to tubulin, promotes microtubule assembly and stabilization, and prevents microtubule depolymerization. This results in G2/M arrest, apoptosis and the inhibition of cell proliferation in susceptible tumor cells. This agent is a poor substrate for P-glycoprotein-related drug resistance mechanisms; therefore, it may be useful for treating multi-drug resistant tumors. MST-997 is more potent than paclitaxel and docetaxel and overcomes paclitaxel and docetaxel resistance in certain tumor cell types.","Pharmacologic Substance"]
["C48424","Taxane Analogue TPI 287","TPI 287|Taxane Analogue TPI 287","A synthetic, third generation taxane with potential antineoplastic activity. TPI 287 binds to tubulin and stabilizes microtubules, resulting in inhibition of microtubule assembly/disassembly dynamics, cell cycle arrest at the G2/M phase, and apoptosis.","Pharmacologic Substance"]
["C84839","Taxol Analogue SID 530","SID 530|Taxol Analogue SID 530","An intravenous formulation containing docetaxel, a semi-synthetic, second-generation taxane derived from a compound found in the European yew tree, Taxus baccata, with potential antineoplastic activity. Taxol analogue SID 530 binds to and stabilizes tubulin, inhibiting microtubule disassembly, which results in cell-cycle arrest at the G2/M phase and cell death.","Pharmacologic Substance"]
["C29487","Tazarotene","6-[(3,4-dihydro-4,4-dimethyl-2H-1-benzothiopyran-6-yl)ethynyl]- 3-Pyridinecarboxylic Acid, Ethyl Ester|AGN-190168|Avage|Ethyl 6-(2-(4,4-Dimethylthiochroman-6-yl)ethynyl)nicotinate|TAZAROTENE|Tazarotene|Tazorac|tazarotene","A synthetic, topical retinoid.  Tazarotene induces the expression of tazarotene-induced gene 3 (TIG3), a tumor suppressor gene.  In psoriasis, tazarotene normalizes abnormal keratinocyte differentiation and reduces their hyperproliferation. (NCI04)","Pharmacologic Substance"]
["C107506","Tazemetostat","E7438|EPZ-6438|EPZ6438|N-((4,6-Dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-(ethyl(oxan-4-yl)amino)-4-methyl-4'-((morpholin-4-yl)methyl)(1,1'-biphenyl)-3-carboxamide|N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-(ethyl(tetrahydro-2H-pyran-4-yl)amino)-4-methyl-4'-(morpholinomethyl)-[1,1'-biphenyl]-3-carboxamide|TAZEMETOSTAT|Tazemetostat","An orally available, small molecule selective and S-adenosyl methionine (SAM) competitive inhibitor of histone methyl transferase EZH2, with potential antineoplastic activity. Upon oral administration, tazemetostat selectively inhibits the activity of both wild-type and mutated forms of EZH2. Inhibition of EZH2 specifically prevents the methylation of histone H3 lysine 27 (H3K27). This decrease in histone methylation alters gene expression patterns associated with cancer pathways and results in decreased tumor cell proliferation in EZH2 mutated cancer cells. EZH2, which belongs to the class of histone methyltransferases (HMTs), is overexpressed or mutated in a variety of cancer cells and plays a key role in tumor cell proliferation.","Organic Chemical|Pharmacologic Substance"]
["C29476","TBC-CEA-Contaminated W/ BVDV","TBC-CEA-Contaminated W/ BVDV","A cancer vaccine consisting of a recombinant vector encoding the tumor-associated carcinoembryonic antigen (CEA) that is contaminated with bovine viral diarrhea virus (BVDV). The carcinoembryonic antigen (CEA) is a prevalent tumor marker expressed by a number of different cancers such as colorectal, breast, lung and ovarian carcinomas; vaccination with vaccinia virus genetically engineered to express CEA may generate antitumoral T-cell responses. BVDV is an RNA pestivirus that may contaminate vaccines due to its presence in fetal calf serum used as a growth supplement in the tissue culture of mammalian cells used in vaccine production. (NCI04)","Pharmacologic Substance"]
["C91737","Technetium Tc-99m Glycopeptide","99mTc-GP|Technetium Tc-99m Glycopeptide","A technetium Tc 99m radiopharmaceutical of a glutamate-rich peptide (GP) conjugated, via carbodiimide linker, to the heparin-like polysaccharide chitosan (CH) in a 1:1 ratio, with potential tumor targeting property. Upon administration, 99m Tc-glycopeptide targets and is taken up by glutamate-specific transporters on tumor cells. Upon internalization, the Tc99m moiety can be visualized upon scanning. GP may potentially be used as a drug carrier for antineoplastic drug delivery to tumor cells.","Pharmacologic Substance"]
["C1605","Tecogalan Sodium","DS-4152|SP-PG|Sulfated Polysaccharide Tecogalan DS-4152|Tecogalan Sodium","A sulfated polysaccharide isolated from various Arthrobacter bacterial species.  Possessing potential antiangiogenic and antineoplastic properties, tecogalan binds to basic fibroblast growth factor (bFGF), thereby preventing bFGF from binding to its receptors.  Disruption of this receptor binding results in the inhibition of bFGF-stimulated endothelial cell growth, proliferation, and migration. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C513","Tegafur","5-Fluoro-1-(tetrahydro-2-furanyl)-2,4(1H,3H)-pyrimidinedione|5-Fluoro-1-(tetrahydro-2-furanyl)-2,4-(1H,3H)-pyrimidinedione|5-Fluoro-1-(tetrahydro-2-furyl)-uracil|Citofur|Coparogin|Exonal|FT-207|FT|Fental|Florafur|Fluorofur|Ftorafur|Ftoral|Ftoralon|Fulaid|Fulfeel|Furafluor|Furofutran|Futraful|Lamar|Lifril|MJF-12264|N1-(2'-Furanidyl)-5-fluorouracil|Neberk|Nitobanil|Riol|Sinoflurol|Sunfural|TEGAFUR|Tefsiel|Tegafur|Uracil, 5-fluoro-1-(tetrahydro-2-furyl)-|Utefos|WR-220066|tegafur","A congener of the antimetabolite fluorouracil with antineoplastic activity. Tegafur is a prodrug that is gradually converted to fluorouracil in the liver by the cytochrome P-450 enzyme. Subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells.  FdUMP inhibits DNA synthesis and cell division by inhibiting thymidylate synthase and reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C1833","Tegafur-gimeracil-oteracil Potassium","BMS 247616|BMS-247616|S-1|TS-1|Tegafur, mixture with Gimeracil and Potassium Oxonate|Tegafur-gimeracil-oteracil Potassium","An orally bioavailable fluoropyrimidine antagonist composed of tegafur combined with two modulators of 5-fluorouracil (5-FU) activity, gimeracil and potassium oxonate, in a molar ratio of 1:0.4:1. Tegafur is a prodrug of 5-fluorouracil, an antimetabolite that inhibits thymidylate synthase, DNA synthesis and cell division, and competes with uridine triphosphate, thus inhibiting RNA and protein synthesis. Gimeracil is a reversible inhibitor of dihydropyrimidine dehydrogenase (DPD), the liver enzyme responsible for rapid catabolism of 5-FU into inactive metabolites. Potassium oxonate preferentially localizes in the gut and inhibits the enzyme orotate phosphoribosyl-transferase (OPRT), thereby decreasing activation of 5-FU in the gut and activated 5-FU-related gastrointestinal toxicity.","Organic Chemical|Pharmacologic Substance"]
["C120099","Tegafur-Gimeracil-Oteracil Potassium-Leucovorin Calcium Oral Formulation","TAS-118|Tegafur-Gimeracil-Oteracil Potassium-Leucovorin Calcium Oral Formulation","An orally bioavailable granular formulation composed of the fluoropyrimidine antagonist tegafur combined with two modulators of 5-fluorouracil (5-FU) activity, gimeracil and oteracil potassium, and the folic acid derivative leucovorin calcium, with potential antineoplastic activity. Tegafur is a prodrug of 5-fluorouracil (5-FU), an antimetabolite that is further metabolized to 5-fluoro-2'-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). FdUMP inhibits thymidylate synthase, DNA synthesis and cell division; FUTP competes with uridine triphosphate (UTP), thus inhibiting RNA and protein synthesis. Gimeracil is a reversible inhibitor of dihydropyrimidine dehydrogenase (DPD), the liver enzyme responsible for rapid catabolism of 5-FU into inactive metabolites. Oteracil potassium preferentially localizes in the gut and inhibits the enzyme orotate phosphoribosyl-transferase (OPRT), which converts tegafur to 5-FU. This decreases the amount of 5-FU in the gut and prevents activated 5-FU-related gastrointestinal (GI) toxicity. Leucovorin calcium, an active metabolite of folic acid, counteracts the toxic effects of 5-FU, thereby 'rescuing' the patient while permitting the antitumor activity of 5-FU.","Organic Chemical|Pharmacologic Substance"]
["C9506","Tegafur-Uracil","Oral Fluorouracil-Uracil|Tegafur-Uracil|UFT|Uftoral|Uracil and Ftorafur|Uracil and Tegafur|Uracil and Tetrahydrofuranyl-5-Fluorouracil|Uracil/Tegafur (UFT)|tegafur-uracil","A formulated therapeutic oral agent consisting of a combination of the 5-fluorouracil (5-FU) congener prodrug tegafur (tetrahydrofuranyl-5-fluorouracil) and uracil (1:4). The high concentration of uracil reversibly inhibits the uracil-reducing enzyme dihydropyrimidine dehydrogenase (DPD), thereby inhibiting first-pass DPD-mediated hepatic metabolism of the uracil analogue 5-FU and permitting administration of 5-FU as the orally bioavailable prodrug tegafur. Tegafur is bioactivated to 5-FU by liver microsomal cytochrome P450 enzymes. 5-FU is subsequently converted into its active metabolites 5-fluoro-deoxyuridine-monophosphate (FdUMP) and 5-fluorouridine-triphosphate (FUTP) intracellularly; these metabolites inhibit the enzyme thymidylate synthase and intercalate into RNA, resulting in decreased thymidine synthesis, reduced DNA synthesis, disrupted RNA function, and tumor cell cytotoxicity.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C90746","Teglarinad","Pyridinium, 4-[[[[6-(4-chlorophenoxy)hexyl]amino](cyanoamino)methylene]amino]-1-(3-oxo-2,4,7,10,13,16-hexaoxaheptadec-1-yl)-|TEGLARINAD|Teglarinad","A water-soluble prodrug of a pyridyl cyanoguanidine compound and an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT) with potential antineoplastic activity. Teglarinad is rapidly converted in the bloodstream into an active compound through hydrolytic cleavage of the carbonate ester bond. The activated form inhibits NAMPT, thereby inhibiting nicotinamide adenine dinucleotide (NAD+) biosynthesis and induces a rapid decline in intracellular NAD+ followed by ATP reduction. As NAD+ is essential for tumor cell growth, inhibition of NAMPT induces tumor cell death. NAMPT is an essential enzyme in the synthesis of NAD+ and is upregulated in some cancers.","Organic Chemical|Pharmacologic Substance"]
["C68931","Teglarinad Chloride","CHS828 Prodrug|EB1627|GMX1777|Pyridinium, 4-[[[[6-(4-chlorophenoxy)hexyl]amino](cyanoamino) methylene]amino]-1-(3-oxo-2,4,7,10,13,16-hexaoxaheptadec-1-yl)-, chloride|TEGLARINAD CHLORIDE|Teglarinad Chloride","A water-soluble prodrug of a cyanoguanidine compound with potential antineoplastic activity. In vivo, teglarinad chloride is rapidly converted into active drug through hydrolytic cleavage of a carbonate ester bond. Although the exact mechanism of action has yet to be fully elucidated, the active drug appears to antagonize nuclear factor-kappa B (NF-kB) transcription, resulting in the induction of tumor cell apoptosis.","Pharmacologic Substance"]
["C104057","Telapristone","11Beta-(4-(dimethylamino)phenyl)-17-hydroxy-21-methoxy-19- norpregna-4,9-diene-3,20-dione|Telapristone","An orally available 21-substituted-19-nor-progestin and selective progesterone receptor modulator (SPRM), with potential anti-progesterone and antineoplastic activities. Upon oral administration, telapristone competitively binds to the progesterone receptor (PR) in progesterone-responsive tissue and inhibits PR-mediated gene expression. This interferes with progesterone activity in the reproductive system. As a result, this agent may suppress ovulation and inhibit proliferation of endometrial tissue. Also, this agent may prevent cell growth and induce apoptosis in estrogen receptor (ER) and PR-positive breast cancer cells through a reduction in progesterone levels, ER downregulation and a suppression of the expression of cyclin-dependent kinases (CDK) 2 and 4, ultimately leading to G1/S cell cycle arrest. Unlike some other SPRMs, this agent does not exert any estrogenic, androgenic, anti-estrogenic, and anti-androgenic activities.","Organic Chemical|Pharmacologic Substance"]
["C104055","Telapristone Acetate","(8S,11R,13S,14S,17R)-11-(4-(Dimethylamino)phenyl)-17-(2-methoxyacetyl)-13-methyl-3-oxo-2,3,6,7,8,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-17-yl Acetate|CDB-4124|Proellex|Progenta|Telapristone Acetate","The acetate form of the 21-substituted-19-nor-progestin telapristone, an orally available selective progesterone receptor modulator (SPRM), with potential anti-progesterone and antineoplastic activities. Upon oral administration, CDB-4124 competitively binds to the progesterone receptor (PR) in progesterone-responsive tissue and inhibits PR-mediated gene expression. This interferes with progesterone activity in the reproductive system. As a result, this agent may suppress ovulation and inhibit proliferation of endometrial tissue. Also, this agent may prevent cell growth and induce apoptosis in estrogen receptor (ER) and PR-positive breast cancer cells through a reduction in progesterone levels, ER downregulation and a suppression of the expression of cyclin-dependent kinases (CDK) 2 and 4, ultimately leading to G1/S cell cycle arrest. Unlike some other SPRMs, this agent does not exert any estrogenic, androgenic, anti-estrogenic, and anti-androgenic activities.","Organic Chemical|Pharmacologic Substance"]
["C87837","Telatinib Mesylate","17-Demethoxy-17-Allylaminogeldanamycin Mesylate|Telatinib Mesylate","The orally bioavailable mesylate salt of the 17-allylaminogeldanamycin (17-AAG) small-molecule inhibitor of several receptor protein tyrosine kinases with potential antiangiogenic and antineoplastic activities. Telatinib binds to and inhibits the vascular endothelial growth factor receptors (VEGFRs) type 2 and 3, platelet-derived growth factor receptor beta (PDGFRb) and c-Kit, which may result in the inhibition of angiogenesis and cellular proliferation in tumors in which these receptors are upregulated. These telatinib-inhibited receptor protein tyrosine kinases are overexpressed or mutated in many tumor cell types and may play key roles in tumor angiogenesis and tumor cell proliferation. 17-AAG is a synthetic analogue of the benzoquinone ansamycin antibiotic geldanamycin and has also been found to inhibit the molecular chaperone Hsp90.","Pharmacologic Substance"]
["C62756","Telomerase Peptide Vaccine GV1001","GV1001|PrimoVax|Telomerase Peptide Vaccine GV1001","A synthetic peptide vaccine, containing 16 amino acid residues (611-626) of the human telomerase reverse transcriptase catalytic subunit (hTERT), with potential antineoplastic activity. Telomerase, a reverse transcriptase normally repressed in healthy cells, is overexpressed in most cancer cells and plays a key role in cellular proliferation. Vaccination with the telomerase peptide GV1001 may activate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against telomerase-expressing cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2640","Telomerase: 540-548 Peptide Vaccine","Telomerase: 540-548 Peptide Vaccine|Telomerase:540-548 Peptide","A recombinant peptide consisting of the amino acid residues 540 to 548 of the human telomerase reverse transcriptase (hTERT). Telomerase expression has been directly linked to tumor development; its catalytic subunit is expressed in the majority of human cancer cells, but infrequently in normal cells.  Vaccination with telomerase:540-548 peptide may stimulate cytotoxic T cells to recognize and kill telomerase-expressing cells. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C119617","Telomerase-specific Type 5 Adenovirus OBP-301","OBP-301|Telomelysin|Telomerase-specific Type 5 Adenovirus OBP-301","A replication-competent oncolytic, telomerase-specific adenovirus serotype 5 (Ad5), with potential antineoplastic activity. OBP-301 contains the human telomerase reverse transcriptase (hTERT) gene promoter sequence that drives the expression of the E1A and E1B genes, and is linked to an internal ribosomal entry site (IRES). Upon administration, OBP-301 selectively infects and replicates in cancer cells that are expressing telomerase, which causes cell lysis. This adenovirus does not infect or replicate in normal, healthy cells. OBP-301 may also potentially be used as a chemosensitizer. hTERT, which encodes for the catalytic protein subunit of telomerase, is overexpressed in a variety of cancer cell types but not in normal, healthy cells. The insertion of an IRES further improves selectivity towards telomerase-expressing cancer cells.","Pharmacologic Substance"]
["C1520","Teloxantrone","Anthra(1,9-cd)pyrazol-6(2H)-one,7,10-dihydroxy-2-(2-((2-hydroxyethyl)amino)ethyl)-5-((2-(methylamino)ethyl)amino)-|CI-937|Moxantrazole|TELOXANTRONE|Teloxantrone","An anthrapyrazole antineoplastic antibiotic. Teloxantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair, as well as RNA and protein synthesis","Organic Chemical|Pharmacologic Substance"]
["C74544","Teloxantrone Hydrochloride","Anthra(1,9-cd)pyrazol-6(2H)-one,7,10-dihydroxy-2-(2-((2-hydroxyethyl)amino)ethyl)-5-((2-(methylamino)ethyl)amino) Dihydrochloride|CI-937|DUP 937|Moxantrazole Hydrochloride|TELOXANTRONE HYDROCHLORIDE|Teloxantrone Hydrochloride","The hydrochloride salt of an anthrapyrazole antineoplastic antibiotic. Teloxantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair, as well as RNA and protein synthesis","Organic Chemical|Pharmacologic Substance"]
["C63953","Temarotene","1,2,3,4-Tetrahydro-1,1,4,4-tetramethyl-6-[(1E)-1-methyl-2-phenylethenyl]naphthalene|Ro 15-0778|TEMAROTENE|TTNPB, Decarboxylated Analog|Temaroten|Temarotene","A synthetic bioactive retinoid with differentiation inducing and potential antineoplastic activities. Like other retinoic acid agents, temarotene binds to and activates retinoic acid receptors (RARs), thereby altering the expression of certain genes leading to cell differentiation and decreased cell proliferation in susceptible cells.","Pharmacologic Substance"]
["C1669","Temoporfin","5,10,15,20-Tetra-(m-hydroxyphenyl)chlorin|Foscan|TEMOPORFIN|Temoporfin|m-Tetrahydroxyphenyl-chlorin|mTHPC|meta-Tetrahydroxyphenyl Chlorin|meta-Tetrahydroxyphenylchlorin|temoporfin","A synthetic light-activated chlorin with photodynamic activity. Upon systemic administration, temoporfin distributes throughout the body and is taken up by tumor cells. Upon stimulation of temoporfin by non-thermal laser light (at 652 nm), and in the presence of oxygen, this agent produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to tumor cells. This may kill tumor cells and may reduce the tumor size.","Organic Chemical|Pharmacologic Substance"]
["C1244","Temozolomide","3,4-dihydro-3-methyl-4-oxoimidazo[5,1-d]-1,2,3,5-tetrazine-8-carboxamide|8-carbamoyl-3-methylimidazo[5,1-d]-1,2,3,5-tetrazin-4(3H)-one|CCRG-81045|Imidazo[5,1-d]-1,2,3,5-tetrazine-8-carboxamide, 3, 4-dihydro-3-methyl-4-oxo-|M & B 39831|M and B 39831|Methazolastone|RP-46161|SCH 52365|TEMOZOLOMIDE|Temcad|Temodal|Temodar|Temomedac|Temozolomide|imidazo[5,1-d]-1,2,3,5-tetrazine-8-carboxamide, 3, 4-dihydro-3-methyl-4-oxo-|temozolomide","A triazene analog of dacarbazine with antineoplastic activity.  As a cytotoxic alkylating agent, temozolomide is converted at physiologic pH to the short-lived active compound, monomethyl triazeno imidazole carboxamide (MTIC). The cytotoxicity of MTIC is due primarily to methylation of DNA at the O6 and N7 positions of guanine, resulting in inhibition of DNA replication. Unlike dacarbazine, which is metabolized to MITC only in the liver, temozolomide is metabolized to MITC at all sites. Temozolomide is administered orally and penetrates well into the central nervous system. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1844","Temsirolimus","42-(3-Hydroxy-2-(hydroxymethyl)-2-methylpropanoate)rapamycin|CCI-779 Rapamycin Analog|CCI-779|Cell Cycle Inhibitor 779|Rapamycin Analog CCI-779|Rapamycin Analog|TEMSIROLIMUS|Temsirolimus|Torisel|temsirolimus","An ester analog of rapamycin. Temsirolimus binds to and inhibits the mammalian target of rapamycin (mTOR), resulting in decreased expression of mRNAs necessary for cell cycle progression and arresting cells in the G1 phase of the cell cycle. mTOR is a serine/threonine kinase which plays a role in the PI3K/AKT pathway that is upregulated in some tumors.","Organic Chemical"]
["C64772","Tenifatecan","(4S)-4,11-diethyl-4-hydroxy-3,14-dioxo-3,4,12,14-tetrahydro-1H-pyrano[3',4':6,7]indolizino[1,2-b]quinolin- 9-yl (2R)-2,5,7,8-tetramethyl-2-[(4R,8R)-4,8,12-trimethyltridecyl]-3,4-dihydro-2H-1-benzopyran-6-yl Butanedioate|SN-2310|SN2310|TENIFATECAN|Tenifatecan|Tocopherol Succinate 7-Ethyl-10-Hydroxycamptothecin","A highly lipophilic preparation of 7-Ethyl-10-hydroxycamptothecin (SN-38) with potential antineoplastic activity. SN2310 is an oil-in-water emulsion of tocopherol covalently linked, via a succinate linker, to SN-38, a synthetic derivative of the cytotoxic alkaloid camptothecin. After succinate linker is hydrolyzed in vivo, the active moiety SN-38 is released and selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-stranded DNA breaks and inducing lethal double-stranded DNA breaks. This inhibits DNA replication and triggers programmed cell death. SN2310 emulsion provides longer circulation time and potentiates drug exposure as compared to the unconjugated SN-38.","Organic Chemical|Pharmacologic Substance"]
["C857","Teniposide","4'-Demethylepipodophyllotoxin 9-(4,6-O-2-Thenylidene-beta-D-glucopyranoside)|4'-Demethylepipodophyllotoxin-beta-D-thenylidine Glucoside|EPT|PTG|TENIPOSIDE|Teniposide|Thenylidene Lignan|VM 26|VM-26|Vehem|Vumon|[5R-[5Alpha,5a beta,8a alpha, 9beta(R*)]]-5,8,8a,9-tetrahydro-5-(4-hydroxy-3,5-dimethoxyphenyl)-9-[[4,6-O-(2-thienylmethylene)-beta-D-glucopyranosyl]oxy]furo[3',4':6,7]-naphtho[2,3-d]-1,3-dioxol-6(5aH)-one|teniposide","A semisynthetic derivative of podophyllotoxin with antineoplastic activity. Teniposide forms a ternary complex with the enzyme topoisomerase II and DNA, resulting in dose-dependent single- and double-stranded breaks in DNA, DNA: protein cross-links, inhibition of DNA strand religation, and cytotoxicity. This agent acts in the late S or early G phase of the cell cycle. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C88314","Tepotinib","Benzonitrile, 3-(1,6-Dihydro-1-((3-(5-((1-methyl-4-piperidinyl)methoxy)-2-pyrimidinyl)phenyl)methyl)-6-oxo-3-pyridazinyl)-|EMD 1214063|EMD-1214063|EMD1214063|TEPOTINIB|Tepotinib","An inhibitor of MET tyrosine kinase with potential antineoplastic activity. Tepotinib selectively binds to MET tyrosine kinase and disrupts MET signal transduction pathways, which may induce apoptosis in tumor cells overexpressing this kinase. The receptor tyrosine kinase MET (also known as hepatocyte growth factor receptor or HGFR), is the product of the proto-oncogene c-Met and is overexpressed or mutated in many tumor cell types; this protein plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C95797","Teprotumumab","Anti-IGF-1R Monoclonal Antibody R1507|Immunoglobulin G1, Anti-(Human Insulin-like Growth Factor I Receptor)(Human Monoclonal Heavy Chain), Disulfide with Human Monoclonal Light Chain, Dimer|R1507|RG1507|RO4858696-000|RV001|TEPROTUMUMAB|Teprotumumab","A recombinant, fully human monoclonal antibody directed against the insulin-like growth factor-1 receptor (IGF-1R) with potential antineoplastic activity. Teprotumumab binds to membrane-bound IGF-1R, preventing the binding of the natural ligand IGF-1 and the activation of PI3K/AKT signal transduction; downregulation of the PI3K/AKT survival pathway may result in the induction of apoptosis and decreased cellular proliferation. The activation of IGF-1R, a receptor tyrosine kinase of the insulin receptor superfamily, stimulates cell proliferation, enables oncogenic transformation, and suppresses apoptosis; IGF-1R signaling has been implicated in tumorigenesis and metastasis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C61441","Terameprocol","1,1'-(2,3-Dimethyl-1,4-butanediyl)bis(3,4-dimethoxybenzene)|EM-1421|M4N|TERAMEPROCOL|TMNDGA|Terameprocol|Tetra-O-methyl Nordihydroguaiaretic Acid|Tetra-O-methyl-NDGA|Tetramethoxynordihydroguaiaretic Acid|tetra-O-methyl NDGA|tetra-O-methyl nordihydroguaiaretic acid","A synthetic tetra-methylated derivative of nordihydroguaiaretic acid (NDGA) and transcriptional inhibitor with potential antiviral, antiangiogenic, and antineoplastic activities. Terameprocol competes with the transcription factor Sp1 for specific Sp1 DNA binding domains within gene promoter regions during DNA synthesis. In virally-infected cells, blocking of the Sp1 binding site suppresses Sp1-regulated viral promoter activity and gene expression, thereby inhibiting viral transcription and replication. In tumor cells, blockage of Sp1 binding sites by this agent interferes with the transcription of the Sp1-dependant genes cyclin-dependant kinase (Cdc2), survivin, and vascular endothelial growth factor (VEGF), which are overexpressed in a variety of cancers. By suppressing Sp1-regulated transcription of these genes, terameprocol may reduce tumor angiogenesis and tumor cell proliferation and induce tumor cell apoptosis.","Pharmacologic Substance"]
["C75292","Terfluranol","TERFLURANOL|Terfluranol","A trifluoroethyl derivative with antineoplastic agent.","Pharmacologic Substance"]
["C66985","Tergenpumatucel-L","Hyperacute Lung Cancer Vaccine|Tergenpumatucel-L","An allogeneic lung cancer vaccine with potential immunostimulating and antineoplastic activities. Derived from allogeneic lung tumor cells, tergenpumatucel-L is engineered to express the murine alpha-1,3-galactosyltransferase (GalT), an enzyme humans lack. GalT catalyzes the expression of foreign alpha-1,3-galactosyl (alpha-gal) carbohydrate epitopes in glycoproteins and in glycolipids on the cell membranes of the allogeneic lung tumor cells present in the vaccine, essentially producing a 'xenograft'. The hyperacute rejection involves pre-existing human anti-alpha-gal antibodies that bind the foreign alpha-gal epitopes expressed by the vaccine tumor cell xenograft, resulting in complement-mediated cytotoxicity (CMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) towards endogenous lung tumor cells with unmodified carbohydrate epitopes.","Cell|Pharmacologic Substance"]
["C2320","Teroxirone","Henkel's Compound|TEROXIRONE|Teroxirone|alpha-1,3,5-triglycidyl-s-triazinetrione|alpha-TGI|alpha-Triglycidyl Isocyanurate","A triazene triepoxide with antineoplastic activity. Teroxine alkylates and cross-links DNA, thereby inhibiting DNA replication. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C37451","Tesetaxel","DJ-927|TESETAXEL|Tesetaxel","A semi-synthetic, orally bioavailable taxane derivative with potential antineoplastic and antiangiogenic properties. Tesetaxel binds to and stabilizes tubulin, promoting microtubule assembly and thereby preventing microtubule depolymerization. This may lead to cell cycle arrest and an inhibition of cell proliferation. This agent may also inhibit pro-angiogenic factors such as vascular endothelial growth factor (VEGF). As it represents poor substrate for P-glycoprotein-related drug resistance mechanisms, this agent may be useful for treating multi-drug resistant tumors.","Pharmacologic Substance"]
["C62496","Tesevatinib","4-Quinazolinamine, N-(3,4-dichloro-2-fluorophenyl)-6-methoxy-7-(((3aalpha,5beta,6aalpha)-octahydro-2-methylcyclopenta(c)pyrrol-5-yl)methoxy)-|EXEL 7647|KD 019|KD019|TESEVATINIB|Tesevatinib|XL647","An orally bioavailable small-molecule receptor tyrosine kinase (RTK) inhibitor with potential antineoplastic activity. Tesevatinib binds to and inhibits several tyrosine receptor kinases that play major roles in tumor cell proliferation and tumor vascularization, including epidermal growth factor receptor (EGFR; ERBB1), epidermal growth factor receptor 2 (HER2; ERBB2), vascular endothelial growth factor receptor (VEGFR), and ephrin B4 (EphB4). This may result in the inhibition of tumor growth and angiogenesis, and tumor regression.","Pharmacologic Substance"]
["C129315","Tesidolumab","LFG-316|LFG316|NOV-4|TESIDOLUMAB|Tesidolumab","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the complement pathway protein C5, with complement pathway inhibitory activity and potential immunomodulating activity. Upon administration, tesidolumab targets and binds to C5, thereby preventing both C5 convertase-mediated cleavage of C5 and the formation of C5a and C5b. This inhibits C5-mediated signal transduction, the formation of the membrane attack complex (MAC) and the activation of the terminal complement pathway, and results in the prevention and/or inhibition of both complement-mediated inflammation and cell destruction. C5 plays a key role in the activation of the complement cascade.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2301","Testolactone","1,2,3,4,4a,4b,7,9,10,10a-Decahydro-2-hydroxy-2,4b-dimethyl-7-oxo-1-phenanthrenepropionic Acid Delta-Lactone|1-Dehydrotestololactone|13-Hydroxy-3-0x0-13,17-secoandrosta-1,4-dien-17-oic Acid Delta-Lactone|17Alpha-oxo-D-homo-1,4-androstadiene-3,17-dione|D-Homo-17a-oxaandrosta-1,4-diene-3,17-dione|Delta-1-Testololactone|Fludestrin|SQ 9538|SQ-9538|TESTOLACTONE|Teslac|Testolactone|Therapeutic Testolactone","A progesterone derivative with antineoplastic activity. Testolactone inhibits steroid aromatase, thereby preventing the formation of estrogen from adrenal androstenedione and reducing endogenous estrogen levels. (NCI04)","Hormone|Organic Chemical"]
["C2468","Tetanus Peptide Melanoma Vaccine","Tetanus Peptide Melanoma Vaccine","A vaccine consisting of peptides derived from melanoma-associated antigens and a modified T-cell epitope derived from tetanus toxoid. Vaccination with this agent may stimulate a host cytotoxic and helper T-cell response against tumor cells expressing melanoma-associated antigens, resulting in decreased tumor growth. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C2660","Tetanus Toxoid Vaccine","TT|Tetanus Toxoid Vaccine|Tetanus Toxoid|tetanus toxoid","A preparation of formaldehyde-deactivated toxin isolated from the bacterium Clostridium tetani. Tetanus toxoid is used for booster injection and can stimulate the production of antitoxin antibodies. This agent may be used as an adjuvant in cancer vaccines.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C866","Tetradecanoylphorbol Acetate","12-O-tetradecanoylphorbol-13-acetate|Lonomycin|PHORBOL 12-MYRISTATE 13-ACETATE DIESTER|PMA|Phorbol Myristate Acetate|TPA (Phorbol Ester)|TPA|Tetradecanoylphorbol Acetate|tetradecanoylphorbol acetate","A phorbol ester with potential antineoplastic effects.  Tetradecanoylphorbol acetate (TPA) induces maturation and differentiation of hematopoietic cell lines, including leukemic cells. This agent may induce gene expression and protein kinase C (PKC) activity.  In addition to potential antineoplastic effects, TPA may exhibit tumor promoting activity. (NCI04)","Organic Chemical"]
["C868","Tetrahydrouridine","2(1H)-pyrimidinone, tetrahydro-4-hydroxy-1-beta-D-ribofuranosyl-|THU|Tetrahydrouridine|tetrahydrouridine","A synthetic pyrimidine nucleoside analogue with biomodulating activity. Tetrahydrouridine increases the efficacy of the radiosensitizer cytochlor (5-chloro-2'-deoxycytidine) by inhibiting the enzyme deoxycytidine monophosphate (dCMP) deaminase and preventing the premature deamination of the cytochlor metabolite 5-chloro-2'-deoxycytidine monophosphate (CldCMP) to 5-chloro-2'-deoxyuridine monophosphate (CldUMP); in turn, this increases tumor concentrations of CldUMP which is then further anabolized and incorporated selectively into tumor DNA as CldU (5-chloro-2'-deoxyuridine). (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C88344","Tetraphenyl Chlorin Disulfonate","Amphinex|Disulfonated Tetraphenylchlorin|TPCS2a|Tetraphenyl Chlorin Disulfonate","A meso-tetraphenylchlorin substituted by two adjacent sulfonated groups with potential photosensitizing activity. Upon administration, tetraphenyl chlorin disulfonate incorporates into the cell's endosome and lysosome membranes. Subsequently, cytotoxic agents are administered and accumulate in endosomal and lysosomal compartments; upon local activation by light, tetraphenyl chlorin disulfonate produces reactive oxygen species (ROS), such as singlet oxygen, damaging endo/lysosomal membranes and accumulated cytotoxic agents are released into the tumor cell cytosol. This photochemical internalization (PCI) method can enhance the efficacy and selectivity of cytotoxic agents.","Pharmacologic Substance"]
["C122396","Tetravalent RNA-lipoplex Cancer Vaccine","Lipo-MERIT|Tetravalent RNA-lipoplex Cancer Vaccine","A RNA-lipoplex (RNA-LP)-based cancer vaccine containing four naked ribonucleic acid (RNA)-drug products (DPs) RBL001.1, RBL002.2, RBL003.1, and RBL004.1 encoding melanoma-associated antigens (MAAs) encapsulated in liposomes, with potential antineoplastic activity. Upon intravenous administration of the tetravalent RNA-lipoplex cancer vaccine, the liposomes protect the RNA from degradation in the bloodstream, travel to the spleen and are taken up by antigen-presenting cells (APCs); RNA is translocated to the cytoplasm and translated into the four tumor-associated proteins. The expressed proteins are processed and the human leukocyte antigen (HLA)-peptide complexes are presented to the immune system. This induces antigen-specific CD8+ and CD4+ T-cell responses against the four selected MAAs.","Immunologic Factor|Pharmacologic Substance"]
["C1539","Tezacitabine","2'-Deoxy-2'-(fluoromethylene)cytidine|FMdC|MDL 101,731|TEZACITABINE|Tezacitabine","A synthetic pyrimidine nucleoside analogue with potential antineoplastic activity. Phosphorylated by cellular kinases, tezacitabine is converted into its active diphosphate and triphosphate metabolites. Tezacitabine diphosphate binds to and irreversibly inhibits the activity of the enzyme ribonucleotide reductase (RNR), which may result in the inhibition of DNA synthesis in tumor cells and tumor cell apoptosis. Tezacitabine triphosphate acts as a substrate for DNA polymerase, further compromising DNA replication. This agent is relatively resistant to metabolic deactivation by cytidine deaminase. RNR catalyzes the conversion of ribonucleoside 5'-diphosphates to deoxyribonucleoside 5'-diphosphates necessary for DNA synthesis and is overexpressed in many tumor types.","Organic Chemical|Pharmacologic Substance"]
["C95916","Tezacitabine Anhydrous","2'-Deoxy-2'-(fluoromethylene)cytidine Anhydrous|FMdC Anhydrous|TEZACITABINE ANHYDROUS|Tezacitabine Anhydrous","The anhydrous form of tezacitabine, a synthetic pyrimidine nucleoside analogue with potential antineoplastic activity. Phosphorylated by cellular kinases, tezacitabine is converted into its active diphosphate and triphosphate metabolites. Tezacitabine diphosphate binds to and irreversibly inhibits the activity of the enzyme ribonucleotide reductase (RNR), which may result in the inhibition of DNA synthesis in tumor cells and eventually tumor cell apoptosis. Tezacitabine triphosphate acts as a substrate for DNA polymerase, thereby further inhibiting DNA replication. RNR catalyzes the conversion of ribonucleoside 5'-diphosphates to deoxyribonucleoside 5'-diphosphates, a necessary step for DNA synthesis, and is overexpressed in many tumor cell types.","Organic Chemical|Pharmacologic Substance"]
["C2529","TF(c)-KLH Conjugate Vaccine","TF (c)-KLH conjugate vaccine|TF(c)-KLH Conjugate Vaccine|TF(c)-KLH|vaccine, TF (c)-KLH conjugate|vaccine, TF(c)-KLH conjugate","A vaccine containing a clustered pancarcinoma carbohydrate antigen, Thomsen-Friedenreich (TF) antigen, conjugated with keyhole limpet hemocyanin (KLH) with potential antineoplastic activity. TF antigen is a disaccharide epitope (galactose-beta1-3-N-acetylgalactose), normally O-linked to serine or threonine of tumor-associated epithelial mucins. This vaccine contains the TF epitope cluster (c) that is synthesized by linking 3 copies of the TF epitope on a threonine backbone to achieve the essential immunogenic structure. KLH is a hapten carrier and serves as an immunostimulant to improve immune recognition. Vaccination with TF(c)-KLH peptide vaccine may produce antibodies and elicit a cytotoxic T lymphocyte (CTL) response against those tumor cells expressing TF antigen, resulting in decreased tumor growth.","Immunologic Factor|Pharmacologic Substance"]
["C29483","TGFa-PE38 Immunotoxin","Cervene|TGFa-PE38 Immunotoxin|TP-38 immunotoxin|TP-38","A recombinant, chimeric toxin composed of human transforming growth factor alpha (TGF-alpha) fused to a fragment of Pseudomonas exotoxin (PE38) without its cell-binding domain.  The TGF-alpha moiety of the agent attaches to tumor cells expressing the epithelial growth factor receptor (EGFR); the exotoxin induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C111992","TGFbDNRII-transduced Autologous Tumor Infiltrating Lymphocytes","TGFbDNRII-transduced Autologous TILs|TGFbDNRII-transduced Autologous Tumor Infiltrating Lymphocytes","A preparation of tumor infiltrating lymphocytes (TILs) that are transduced with a retroviral vector encoding a gene for a dominant-negative form of the transforming growth factor beta (TGFb) receptor, TGFbDNRII, with potential immunomodulating activity. Upon administration, the TGFbDNRII-transduced autologous TILs recognize and kill tumor cells. The expression of TGFbDNRII allows for the TILs to be resistant to TGF-b-mediated inhibition of T cell proliferation and activation, which allows optimal TIL activity. The immunosuppressant TGF-b is produced by tumor cells and plays a key role in the repression of the immune system.","Cell|Pharmacologic Substance"]
["C77859","TGF-beta-Resistant LMP-Specific Cytotoxic T-Lymphocytes","TGF-beta-Resistant LMP-Specific CTLs|TGF-beta-Resistant LMP-Specific Cytotoxic T-Lymphocytes","A preparation of transforming growth factor-beta (TGF-beta)-resistant cytotoxic T-lymphocytes (CTL) reactive to Epstein-Barr virus (EBV) latent membrane proteins 1 and 2 (LMP 1 and 2) with potential antineoplastic activity. T lymphocytes are transduced with a retroviral vector expressing the dominant-negative mutant type II TGF-beta receptor, which blocks signaling by all three TGF-beta isoforms. These TGF-beta-resistant T-lymphocytes are exposed ex-vivo to dendritic cells (DCs) transfected with a replication-deficient adenovirus encoding EBV LMP; subsequent exposure to LMP1- or LMP2-expressing lymphoblastoid cell lines is used to expand the CTL.  Administered to patients with EBV-positive tumors, TGF-beta-resistant LMP-specific CTL target LMP-positive cells, which may result in a specific CTL response, followed by cell lysis and inhibition of tumor cell proliferation. Tumor-expressed TGF-beta inhibits T lymphocyte activation and expansion.","Immunologic Factor|Pharmacologic Substance"]
["C869","Thalicarpine","4H-Dibenzo[de,g]quinoline, 5,6,6a, 7-tetrahydro-9-[4,5-dimethoxy-2-[(1,2,3,4-tetrahydro-6, 7-dimethoxy-2-methyl-1-isoquinolinyl)methyl]phenoxy]-1,2, 10-trimethoxy-6-methyl-|4H-Dibenzo[de,g]quinoline, 5,6,6a, 7-tetrahydro-9-[4,5-dimethoxy-2-[(1,2,3,4-tetrahydro-6, 7-dimethoxy-2-methyl-1-isoquinolinyl)methyl]phenoxy]-1,2,10-trimethoxy-6-methyl-|4H-Dibenzo[de,g]quinoline, 9-[4, 5-dimethoxy-2-[(1,2,3,4-tetrahydro-6, 7-dimethoxy-2-methyl-1-isoquinolinyl)methyl]phenoxy]-5,6,6a, 7-tetrahydro-1,2,10-trimethoxy-6-methyl-, [S-(R*,R*)]- (9CI)|4H-dibenzo[de,g]quinoline, 9-[4, 5-dimethoxy-2-[(1,2,3,4-tetrahydro-6, 7-dimethoxy-2-methyl-1-isoquinolinyl)methyl]phenoxy]-5,6,6a,7-tetrahydro-1,2,10-trimethoxy-6-methyl-, [S-(R*,R*)]- (9CI)|6a-Alpha-aporphine, 9-[[4, 5-dimethoxy-alpha-(1beta,2,3,4-tetrahydro-6, 7-dimethoxy-2-methyl-1-isoquinolyl)-o-tolyl]oxy]-1,2, 10-trimethoxy- (8CI)|6a-Alpha-aporphine, 9-[[4,5-dimethoxy-alpha-((S)-1,2,3, 4-tetrahydro-6,7-dimethoxy-2-methyl-1-isoquinolyl)-o-tolyl]oxy]-1, 2,10-trimethoxy-|6a.alpha.-Aporphine, 9-[[4, 5-dimethoxy-.alpha.-(1.beta.,2,3,4-tetrahydro-6, 7-dimethoxy-2-methyl-1-isoquinolyl)-o-tolyl]oxy]-1,2, 10-trimethoxy- (8CI)|6a.alpha.-Aporphine, 9-[[4,5-dimethoxy-.alpha.-((S)-1,2,3, 4-tetrahydro-6,7-dimethoxy-2-methyl-1-isoquinolyl)-o-tolyl]oxy]-1, 2,10-trimethoxy-|THALICARPINE|Taliblastine|Thaliblastine|Thalicarpin|Thalicarpine|[S-(R*,R*)]-9-[4,5-dimethoxy-2-[(1,2,3,4-tetrahydro-6,7-dimethoxy-2-methyl-1-isoquinolinyl)-methyl]phenoxy]-5,6,6a,7-tetrahydro-1,2,10-trimethoxy-6-methyl-4H-dibenzo[de,g]quinoline","A natural aporphine benzylisoquinoline vinca alkaloid with antineoplastic activity. Thalicarpine binds to and inhibits p-glycoprotein, the multidrug resistance efflux pump. Thalicarpine also induces single-strand breaks in DNA and arrests cancer cells at the G2/M and G1 phase of the cell cycle. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C870","Thalidomide","(+)-Thalidomide|(-)-Thalidomide|.alpha.-Phthalimidoglutarimide|2, 6-Dioxo-3-phthalimidopiperidine|2,6-Dioxo-3-phthalimidopiperidine|2-(2,6-Dioxo-3-piperidinyl)-1H-isoindole-1,3(2H)-dione|3-Phthalimidoglutarimide|Alpha-Phthalimidoglutarimide|Contergan|Distaval|Kevadon|N-(2,6-Dioxo-3-piperidyl)phthalimide|N-Phthaloylglutamimide|N-Phthalylglutamic Acid Imide|N-Phthalylglutamic acid imide|Neurosedyn|Pantosediv|Phthalimide, N-(2, 6-dioxo-3-piperidyl)-, (+)-|Phthalimide, N-(2, 6-dioxo-3-piperidyl)-, (-)-|Sedalis|Sedoval K-17|Softenon|Synovir|THALIDOMIDE|Talimol|Thalidomide|Thalomid|thalidomide","A synthetic derivative of glutamic acid (alpha-phthalimido-glutarimide) with teratogenic, immunomodulatory, anti-inflammatory and anti-angiogenic properties.  Thalidomide acts primarily by inhibiting both the production of tumor necrosis factor alpha (TNF-alpha) in stimulated peripheral monocytes and the activities of interleukins and interferons.  This agent also inhibits polymorphonuclear chemotaxis and monocyte phagocytosis.  In addition, thalidomide inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), thereby inhibiting angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C2385","Theramide","DTP-DPP|N-acetylglucsamnmyl-N-acetylmuramyl-L-Al-D-isoglu-L-Ala-dipalmitoxy propylamide|Theramide","A lipophilic disaccharide derivative of muramyl dipeptide (MDP) with strong immunostimulating activity and used as a vaccine adjuvant. MDP, a component of bacterial cell wall, is the minimum chemical structure required for macrophage activation. Due to MDP's toxicity and short duration of action, theramide was developed with improved stability, and can be administered without a liposome carrier. Theramide stimulates macrophage activity, which in turn potentiates other immune responses, including the release of proinflammatory interleukins and tumor necrosis factor alpha (TNF alpha). The release of these cytokines further augments the activation of cellular and humoral immune system.","Organic Chemical|Pharmacologic Substance"]
["C68962","Therapeutic Angiotensin-(1-7)","Ang 1-7|Angiotensin 1-7|Therapeutic Angiotensin-(1-7)|therapeutic angiotensin-(1-7)","A synthetic heptapeptide identical to endogenous angiotensin-(1-7) with vasodilator and antiproliferative activities. Therapeutic angiotensin 1-7 may inhibit cyclooxygenase 2 (COX-2) and the production of proinflammatory prostaglandins and may activate the angiotensin-(1-7) receptor Mas, resulting in diminished tumor cell proliferation. Activation of the angiotensin-(1-7) receptor Mas, a G-protein coupled, seven transmembrane protein, may down-regulate the phosphorylation and activation of Erk1 and Erk2 in the Erk1/Erk2 MAPK signaling pathway. In the renin-angiotensin system, the vasodilating activity of angiotensin- (1-7), hydrolysed from angiotensin II by the type I transmembrane metallopeptidase and carboxypeptidase angiotensin converting enzyme 2 (ACE2) in vivo, counteracts the vasoconstricting activity of angiotensin II.","Pharmacologic Substance"]
["C2594","Therapeutic Autologous Dendritic Cells","Therapeutic Autologous Dendritic Cells","A population of a type of antigen-presenting cell (APC), the dendritic cell (DC), harvested from a patient and grown in vitro in the presence of tumor-associated antigens (TAAs) derived from the patient's tumor (a technique known as 'pulsing') and then injected back into the patient; autologous DCs so manipulated may stimulate a specific cell-mediated antitumoral cytotoxicity. DCs derived from a patient may also be fused with the patient's tumor cells in vitro to combine sustained tumor antigen expression with the antigen-presenting and immunostimulatory capacities of DCs; when injected back into the patient, these autologous DC-tumor cell hybrids (fusion cells) may stimulate an active antitumoral immune response.","Cell|Pharmacologic Substance"]
["C91077","Therapeutic Breast/Ovarian/Prostate Peptide Cancer Vaccine DPX-0907","DPX-0907|Therapeutic Breast/Ovarian/Prostate Peptide Cancer Vaccine DPX-0907","A lipid-based multi-peptide cancer vaccine targeted against multiple cancers with immunopotentiating activity. Therapeutic breast/ovarian/prostate peptide cancer vaccine DPX-0907 is a lyophilized liposomal proprietary preparation comprised of 7 tumor-specific HLA-A2-restricted epitopes (TAAs): Topoisomerase II alpha, B-cell receptor-associated protein 31 (CDM protein), TNF-alpha-converting enzyme (TACE/ADAM17), Abelson homolog 2 (Abl2), gamma catenin (Junction plakoglobin), epithelial discoidin domain receptor 1 (EDDR1) and integrin beta 8 subunit. Upon vaccination, the lyophilized antigen/adjuvant/liposome complex is re-suspended in Montanide 1SA51 VG to create a depot effect, thereby presenting the TAAs to the immune system for a prolonged period of time. This may stimulate a potent cytotoxic T-lymphocyte (CTL) immune response against cancer cells that express these 7 TAAs and share epitopes with the vaccine epitope peptides, resulting in tumor cell lysis. The 7 TAAs are overexpressed on the surface of breast/ovarian and prostate cancer cells and play an important role in tumor cell growth and survival.","Pharmacologic Substance"]
["C123819","Therapeutic Dendritic Cells/Cytokine-induced Killer Cells","DC-CIK|Therapeutic Dendritic Cells/Cytokine-induced Killer Cells","A preparation of autologous dendritic cells (DC) mixed with cytokine-induced killer (CIK) cells (DC-CIK), with potential immunopotentiating and antineoplastic activities. DCs were obtained ex vivo by incubation of peripheral blood lymphocytes (PBLs) with granulocyte-macrophage colony-stimulating factor stimulating factor (GM-CSF or CSF2), tumor necrosis factor (TNF), and interleukin (IL)-24 and were sensitized with tumor-associated antigens (TAAs). Cytokine-induced killer (CIK) cells are immune effector cells with both T-cell and natural killer (NK) cell like phenotype. CIKs are non-major histocompatibility complex (MHC)-restricted, NK-like T-lymphocytes, which express both CD3, a T-cell surface marker, and CD56, a natural killer cell surface marker, and have been generated ex vivo by incubation of peripheral blood lymphocytes (PBLs) with anti-CD3 monoclonal antibody, IL-2, IL-1 alpha, and interferon gamma (IFN-gamma) and then expanded. Upon co-culture of DCs and CIKs, and administration of DC-CIK cells into the patient, the DCs are able to stimulate the immune response to exert a specific anti-tumor immune response, while the CIK cells exert direct oncolytic activity.","Cell|Pharmacologic Substance"]
["C124644","Therapeutic gamma delta T-lymphocytes","Therapeutic gamma delta T-lymphocytes|gammadelta T Cells|gd T Cells","A subset of therapeutic autologous T-lymphocytes that express a T-cell receptor (TCR) composed of one gamma chain and one delta chain, with potential immunomodulating and antineoplastic activities. Upon administration of the therapeutic gamma delta T-lymphocytes, these cells secrete interferon-gamma (IFN-g), and exert direct killing of tumor cells. In addition, these cells activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against tumor cells. Gamma delta T-lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect.","Cell|Pharmacologic Substance"]
["C2701","Therapeutic Immune Globulin","BayGam|Gamimune N|Gamma Globulin|Gammagard S/D|Gammar-P|IgIV|Immune Globulin IV|Immune Globulin Intravenous|Immune Globulin|Iveegam EN|Panglobulin|Polygam S/D|Sandoglobulin|Therapeutic Immune Globulin|Therapeutic Immunoglobulin|Venoglobulin-I|Venoglobulin-S|WinRho SDF","A preparation of plasma proteins derived from the pooled plasma of adult donors. Largely comprised of IgG antibodies, therapeutic immune globulin provides passive immunization by increasing the recipient's serum levels of circulating antibodies. IgG antibodies have multiple functions, including binding to and neutralizing bacterial toxins; opsonization of pathogens; activation of complement; and suppression of pathogenic cytokines and phagocytes through binding to CD5, interleukin-1a (IL-1a), interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and T-cell receptors. Therapeutic immune globulin may diminish pathogenic mechanisms in some autoimmune diseases by binding to and inhibiting the activity of autoantibodies. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C28699","Therapeutic Tumor Infiltrating Lymphocytes","Therapeutic Tumor Infiltrating Lymphocytes|Tumor Infiltrating Lymphocytes","A preparation of cells, consisting of autologous tumor infiltrating lymphocytes, that are manipulated in vitro and, upon administration in vivo, re-infiltrate the tumor to initiate tumor cell lysis. In vitro, therapeutic tumor-infiltrating lymphocytes (TILs) are isolated from tumor tissue and cultured with lymphokines such as interleukin-2; the therapeutic TILs are then infused into the patient, where, after re-infiltration of the tumor, they may induce lysis of tumor cells and tumor regression.  The use of therapeutic TILs is considered a form of adoptive immunotherapy.","Pharmacologic Substance"]
["C92589","Thiarabine","4-thio-araC|Thiarabine","A analog of antimetabolite cytarabine (ara-C), with potential antineoplastic activity. Upon administration, thiarabine (T-araC) is phosphorylated to the triphosphate form T-araCTP and competes with cytidine for incorporation into DNA. This results in an inhibition of DNA replication and RNA synthesis, chain termination and may eventually decrease tumor cell proliferation. Compared to ara-C, T-araC appears to have a longer half-life and has a higher efficacy.","Pharmacologic Substance"]
["C75295","Thiodiglycol","Bis(2-hydroxyethyl)sulfide|THIODIGLYCOL|Thiodiethylene Glycol|Thiodiglycol|beta-Hydroxyethyl Sulfide","A hydrolysis product of mustard gas, an alkylating agent, with antineoplastic activity.","Pharmacologic Substance"]
["C876","Thioguanine","2-Amino 6MP|2-Amino-1,7-dihydro-6H-purine-6-thione|2-Amino-6-mercaptopurine|2-Amino-6-purinethiol|2-Aminopurin-6-thiol|2-Aminopurine-6(1H)-thione|2-Aminopurine-6-thiol|2-Mercapto-6-aminopurine|6 Mercaptoguanine|6 Thioguanine|6-Amino-2-mercaptopurine|6-Mercapto-2-aminopurine|6-Mercaptoguanine|6-TG|6-Thioguanine|6H-Purine-6-thione, 2-amino-1,7-dihydro- (9CI)|BW 5071|Lanvis|THIOGUANINE|Tabloid|Thioguanine|Tioguanin|Tioguanine|WR-1141|Wellcome U3B|X 27|thioguanine","A synthetic guanosine analogue antimetabolite. Phosphorylated by hypoxanthine-guanine phosphoribosyltransferase, thioguanine incorporates into DNA and RNA, resulting in inhibition of DNA and RNA syntheses and cell death. This agent also inhibits glutamine-5-phosphoribosylpyrophosphate amidotransferase, thereby inhibiting purine synthesis. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C61970","Thioguanine Anhydrous","THIOGUANINE ANHYDROUS|Thioguanine Anhydrous","The anhydrous salt form of thioguanine, a synthetic guanosine analogue antimetabolite, with antineoplastic activity. Thioguanine is phosphorylated by hypoxanthine-guanine phosphoribosyltransferase to 6-thioguanylic acid (TGMP) and upon conversion to thioguanosine diphosphate (TGDP) and thioguanosine triphosphate (TGTP), this agent is incorporated into DNA and RNA, resulting in inhibition of DNA and RNA synthesis and cell death. This agent also inhibits glutamine-5-phosphoribosylpyrophosphate amidotransferase, thereby inhibiting purine ribonulceotide synthesis.","Pharmacologic Substance"]
["C877","Thioinosine","6-Mercaptopurine ribonucleoside|6-Mercaptopurine riboside|6-mercaptopurine ribonucleoside|6-mercaptopurine riboside|Mercaptopurine Riboside|THIOINOSINE|Thioinosine|inosine, 6-thio|ribosyl-6-mercaptopurine","A sulfhydryl analog of inosine and an antimetabolite with potential antineoplastic and immunosuppressive properties. Thioinosine interferes with de novo purine synthesis and perturbs the pool of nucleotides necessary for DNA replication. As a result, this agent inhibits DNA synthesis, blocks cellular proliferation and induces apoptosis.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C74082","Thioredoxin-1 Inhibitor PX-12","1-Methylpropyl 2-Imidazolyl Disulfide|PX-12|Thioredoxin-1 Inhibitor PX-12","An orally bioavailable small molecule with potential antineoplastic activity. Thioredoxin-1 inhibitor PX-12 irreversibly binds to thioredoxin-1 (Trx-1) and inhibits its activity, which may result in growth inhibition and the induction of apoptosis. Overexpressed in many cancer cell types, the low molecular weight redox protein Trx-1 regulates transcription factor activity and inhibits apoptosis, promoting cell growth and survival; it also interacts with growth factors extracellularly to stimulate cell growth.","Pharmacologic Substance"]
["C875","Thiotepa","1,1',1\"-phosphinothioylidynetrisaziridine|1,1',1''-Phosphinothioyldynetrisaziridine|1,1',1''-Phosphinothioylidynetrisaziridine|Girostan|N,N', N''-Triethylenethiophosphoramide|N,N',N''-triethylenethiophosphoramide|Oncotiotepa|STEPA|TESPA|THIOTEPA|TIO TEF|TSPA|Tepadina|Tespamin|Tespamine|Thio-Tepa|Thiofosfamide|Thiofozil|Thiophosphamide|Thiophosphoramide|Thioplex|Thiotef|Thiotepa|Tifosyl|Tio-tef|Triethylene Thiophosphoramide|Triethylene thiophosphoramide|Triethylenethiophosphoramide|Tris(1-aziridinyl)phosphine sulfide|WR 45312|thiotepa|triethylenethiophosphoramide|tris(1-aziridinyl)phosphine sulfide","A polyfunctional, organophosphorus alkylating agent and a stable derivative of N,N',N''-triethylenephosphoramide (TEPA), with antineoplastic activity. Upon administration, thiotepa is converted into highly reactive ethylenimine groups, which covalently bind to nucleophilic groups in DNA and demonstrate a preference for the N7 position of guanine bases. This induces crosslinking of alkylated guanine bases in double-stranded DNA, interferes with both DNA replication and cell division, and results in both the induction of apoptosis and the inhibition of cell growth.","Organic Chemical|Pharmacologic Substance"]
["C102881","Thioureidobutyronitrile","Kevetrin|Thioureidobutyronitrile","A water-soluble, small molecule and activator of the tumor suppressor protein p53, with potential antineoplastic activity. Upon intravenous administration, thioureidobutyronitrile activates p53 which in turn induces the expressions of p21 and PUMA (p53 up-regulated modulator of apoptosis), thereby inhibiting cancer cell growth and causing tumor cell apoptosis. Thioureidobutyronitrile may be effective in drug-resistant cancers with mutated p53. p53 tumor suppressor, a transcription factor regulating the expression of many stress response genes and mediating various anti-proliferative processes, is often mutated in cancer cells.","Pharmacologic Substance"]
["C88275","THL-P","THL-P","A proprietary, oral Chinese medicinal herb preparation with potential antioxidant, immunomodulating, and antineoplastic activities. THL-P (Tien-Hsien Liquid-P) contains fourteen Chinese medicinal herbs including: Cordyceps sinensis, Oldenlandia diffusa, Indigo pulverata levis, Polyporus umbellatus, Radix astragali, Panax ginseng, Solanum nigrum L., Pogostemon cablin, Atractylodis macrocephalae rhizoma, Trichosanthes radix, Clematis radix, Margarite, Ligustrum lucidum Ait and Glycyrrhiza radix. Administered as an oral liquid, THL-P may modulate the activity of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs), macrophages and polymorphonuclear leukocytes, and enhance the secretion of interleukins (ILs) and interferon-gamma (IFN-gamma). This agent may also induce G2/M cell cycle arrest and downregulate several important oncogenic signaling pathways.","Pharmacologic Substance"]
["C2528","Thomsen-Friedenreich Antigen","Antigen, Thomsen-Friedenreich|TF(c)|Thomsen-Friedenreich Antigen","A type 1 core O-glycan with potential immunotherapeutic property. Thomsen-Friedenreich (TF) antigen, a galactose disaccharide, is normally O-linked to serine or threonine residue of mucins (MUC1), a transmembrane glycoprotein overexpressed on epithelial cell surface of a variety of tumor cells. The expression of this antigen is associated with tumor cell adhesion, tissue invasion and aggressiveness. When administered in a vaccine formulation, TF antigen may stimulate a cytotoxic T cell response against tumors expressing TF epitope, which may result in a reduction in tumor size.","Immunologic Factor|Organic Chemical"]
["C128288","Threonine Tyrosine Kinase Inhibitor CFI-402257","CFI-402257|MSP1 Inhibitor CFI-402257|N-cyclopropyl-4-(7-((((1s,3s)-3-hydroxy-3-methylcyclobutyl)methyl)amino)-5-(pyridin-2-yloxy)pyrazolo[1,5-a]pyridin-3-yl)-2-methylbenzamide|TTK Inhibitor CFI-402257|Threonine Tyrosine Kinase Inhibitor CFI-402257","An orally bioavailable, selective inhibitor of the dual specificity protein kinase TTK (monopolar spindle 1 kinase, Mps1), with potential antineoplastic activity. Upon administration, the Mps1 inhibitor CFI-402257 selectively binds to and inhibits the activity of Mps1. This inactivates the spindle assembly checkpoint (SAC) and accelerates mitosis, which results in chromosomal misalignment and missegregation, and mitotic checkpoint complex destabilization. This induces cell death in Mps1-overexpressing cancer cells. Mps1, a tyrosine and serine/threonine kinase expressed in proliferating normal tissues, is essential for proper SAC functioning and chromosome alignment. Overexpressed in various human tumors, Mps1 plays a key role in uncontrolled tumor cell growth.","Pharmacologic Substance"]
["C116720","Thymidylate Synthase Inhibitor DFP-11207","DFP-11207|TS Inhibitor DFP-11207|Thymidylate Synthase Inhibitor DFP-11207","An orally available thymidylate synthase (TS) inhibitor with potential antineoplastic activity. Upon oral administration, DFP-11207 binds to and inhibits TS. This reduces thymine nucleotide synthesis, inhibits DNA synthesis and cell division, causes DNA damage and leads to tumor cell apoptosis. TS catalyzes the conversion of deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP).","Pharmacologic Substance"]
["C1294","Thymopentin","Immunox|Mepentil|N-(N-(N-(N(2)-L-Arginyl-L-Lysyl)-L-alpha-Aspartyl)-L-Valyl)-L-Tyrosine|N-[N-[N-(N{2}-L-Arginyl-L-lysyl)-L-alpha-aspartyl]-L-valyl]-L-tyrosine|ORF-15244|Sintomodulina|THYMOPENTIN|Thymopentin|Timunox","A synthetic pentapeptide which is the active site of the naturally occurring hormone thymopoietin with immunomodulating properties. Thymopentin enhances the production of thymic T cells and may help restore immunocompetence in immunosuppressed subjects. This agent also augments the effects of ionizing radiation by arresting cancer cells in the G2/M phase of the cell cycle. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1254","Tiazofurin","2-.beta.-D-Ribofuranosyl-4-thiazolecarboxamide|2-.beta.-D-Ribofuranosylthiazole-4-carboxamide|2-Beta-D-ribofuranosyl-4-thiazolecarboxamide|2-Beta-D-ribofuranosylthiazole-4-carboxamide|4-Thiazolecarboxamide, 2-.beta.-D-ribofuranosyl- (9CI)|4-Thiazolecarboxamide, 2-Beta-D-ribofuranosyl- (9CI)|Riboxamide|TCAR|TIAZOFURIN|Tiazofurin|tiazofurin","A synthetic nucleoside analogue with antineoplastic activity. Tiazofurin (TR) is anabolized intracellularly to an analogue of NAD, tiazole-4-carboxamide adenine dinucleotide (TAD), a potent inhibitor of IMP dehydrogenase (IMPDH); IMPDH is the rate-limiting enzyme for de novo purine synthesis. Inhibition of IMPDH results in reduced levels of guanylates, resulting in the inhibition tumor cell growth in vitro and in vivo. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C78474","Tigapotide","PCK3145|Prostate-Secretory Protein-94-Derived Peptide PCK3145|TIGAPOTIDE|Tigapotide","A synthetic 15-mer peptide corresponding to amino acids 31-45 of the 94-amino acid isoform of human prostate secretory protein (PSP-94) with potential anti-metastasis and anti-angiogenesis activities. PSP-94-derived peptide PCK3145 may inhibit the secretion of the metastasis-related protein matrix metalloproteinase-9 (MMP-9) and its potential binding to its cell surface receptor CD44; may interfere with the vascular endothelial growth factor (VEGF) signaling pathway, resulting in an anti-angiogenesis effect; and may reduce the levels of parathyroid hormone-related protein (PTHrP), decreasing plasma calcium levels. PSP-94, one of three predominant proteins found in seminal fluid, may be down-regulated in prostate cancer, representing a potential survival mechanism for prostate cancer cells. MMP-9 is implicated in the invasion and metastasis of cancer. PTHrP may be expressed by various tumor cell types, resulting in the hypercalcemia of malignancy.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C62482","Tigatuzumab","Anti-DR5 MoAb|Anti-TRAIL-R2 MoAb|CS-1008|TIGATUZUMAB|Tigatuzumab|anti-[Homo sapiens TNFRSF10B (Tumor Necrosis Factor Receptor Superfamily Member 10B, DR5, TRAIL-R2, CD262)] Humanized Monoclonal TRA-8","A humanized agonistic monoclonal antibody directed against human tumor necrosis factor-related apoptosis-inducing ligand receptor 2 (TRAIL-R2) with potential antitumor activity. Mimicking the natural receptor ligand TRAIL, tigatuzumab binds to TRAIL-R2, activating signal transduction pathways that may result in tumor cell apoptosis and a reduction in tumor growth. A member of the tumor necrosis factor (TNF) receptor family, TRAIL-R2, also known as DR5 (death receptor 5), is expressed on the surfaces of many types of malignant cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C101787","TIL 1383I T Cell Receptor-Transduced Autologous T Cells","TIL 1383I T Cell Receptor-Transduced Autologous T Cells|TIL 1383I TCR Transduced Autologous T Cells","Autologous peripheral blood lymphocytes-derived T cells transduced with a retroviral encoding TIL 1383I, a T cell receptor (TCR) specific for melanoma antigen tyrosinase, with potential immunostimulating and antineoplastic activity. After transduction, expansion in culture, and reintroduction into the patient, TIL 1383I TCR-transduced autologous T cells bind to tumor cells expressing tyrosinase, which may induce cytokine expression, activation and proliferation of T-cells, and a specific cytotoxic T-lymphocyte (CTL) response against tyrosinase-expressing tumor cells. TIL 1383I TCR originated from a melanoma patient's CD4+ tumor-infiltrating lymphocytes and is reactive against a class I MHC (HLA-A2)-restricted epitope (368-376) of tyrosinase.","Cell|Pharmacologic Substance"]
["C1178","Tilarginine","N-Methylarginine|N5-(Methylamidino)-L-ornithine|NG-Monomethyl-L-Arginine|NG-monomethyl-L-arginine|NMA|TILARGININE|Targinine|Tilarginine|omega-N-Monomethylarginine","An amino acid derivative with potential antineoplastic activity. NG-monomethyl-L-arginine inhibits the enzyme nitric oxide synthase, resulting in a diminution of nitrous oxide production. This agent may inhibit tumor angiogenesis. (NCI04)","Amino Acid, Peptide, or Protein|Organic Chemical|Pharmacologic Substance"]
["C2354","Timonacic","4-Thiazolidine Carboxylic Acid|4-Thiazolidinecarboxylic Acid|ATC|Detoxepa|Hepalidine|Heparegen|TIMONACIC|Thiaproline|Thiazolidine Carboxylic Acid|Thiazolidine-4-carboxylic Acid|Thiazolidine-4-carboxylic acid|Thiazolidinecarboxylic Acid|Thioproline|Tiazolidin|Timonacic","A cyclic sulfur amino acid derivative with potential antineoplastic and antioxidant activities. Acting on cellular membranes of malignant cells through an unknown mechanism, timonacic may induce malignant cells to revert back to an untransformed state. This agent may also restore contact inhibition, a phenomenon characterized by the paracrine inhibition of mitosis following the formation of a critical cell mass, presumably the result of cell-to-cell signal transfer. Timonacic may also produce antioxidant effects secondary to its release of cysteine and restoration of glutathione concentrations.","Organic Chemical|Pharmacologic Substance"]
["C1255","Tin Ethyl Etiopurpurin","DRG-0268|SnET2|Tin Ethyl Etiopurpurin|Tin, (ethyl tetramethyl-20-phorbinecarboxylato(2-)-N23,N24,N25,N26)-, (SP-4-2)-|tin ethyl etiopurpurin","A synthetic purpurin with photosensitizing activity.  Tin ethyl etiopurpurin preferentially accumulates in tumor cells due to an increased rate of metabolism. Upon exposure to a light source, this agent absorbs light, forming an extended high energy conformational state that produces high quantum yields of singlet oxygen with local cytotoxic effects. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C60810","Tinzaparin Sodium","Enzyme Depolymerized Heparin (MW 6500)|Inno-hep|Innohep|LNH-1|Logiparin|TINZAPARIN SODIUM|Tinzaparin Sodium Injection|Tinzaparin Sodium|Tinzaparin|tinzaparin sodium","The sodium salt of a low molecular weight heparin (LMWH), obtained by controlled enzymatic depolymerization of heparin from porcine intestinal mucosa, with antithrombotic properties.  Tinzaparin is a potent inhibitor of several activated coagulation factors, especially Factors Xa and IIa (thrombin); its primary activity is mediated through the plasma protease inhibitor antithrombin. In addition, this agent may inhibit angiogenesis through: 1) competitive binding of the heparin-binding sites on endothelial cells for the proangiogenic cytokines vascular endothelial growth factor (VEGF) and beta-fibroblast growth factor (beta-FGF) and 2) increasing the release of tissue factor pathway inhibitor (TFPI), a negative regulator of angiogenesis.","Organic Chemical|Pharmacologic Substance"]
["C74001","Tiomolibdate Diammonium","ATTM|Ammonium Molybdenum Sulfide|Ammonium Tetrathiomolybdate|Coprexa|Diammonium Tetrathiomolybdate|Molybdate(2-), Tetrathioxo-, Ammonium (1:2), (T-4)-|Molybdate(2-), Tetrathioxo-, Diammonium, (T-4)-|TIOMOLIBDATE DIAMMONIUM|Tiomolibdate Diammonium|ammonium tetrathiomolybdate","An ammonium salt with potential antiangiogenic and antitumor activities. Tetrathiomolybdate has been found to deplete systemic copper reserves through an unknown mechanism. This agent has been shown to inhibit the activities of cuproenzymes, including superoxide dismutase 1 (SOD1) and cytochrome c oxidase (COX), which may contribute to its antiangiogenic and antitumor effects.","Pharmacologic Substance"]
["C1703","Tipifarnib","(+)-6-[Amino(4-chlorophenyl)(1-methyl-1H-imidazol-5-yl)methyl]-4-(3-chlorophenyl)-1-methyl-2(1H)-quinolinone|R115777|TIPIFARNIB|Tipifarnib|Zarnestra|tipifarnib","A nonpeptidomimetic quinolinone with potential antineoplastic activity. Tipifarnib binds to and inhibits the enzyme farnesyl protein transferase, an enzyme involved in protein processing (farnesylation) for signal transduction.  By inhibiting the farnesylation of proteins, this agent prevents the activation of Ras oncogenes, inhibits cell growth, induces apoptosis, and inhibits angiogenesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1464","Tirapazamine","3-Amino-1,2,4-benzotriazine-1,4-dioxide|SR 4233|SR4233|TIRAPAZAMINE|Tirapazamine|Tirazone|WIN 59075|tirapazamine","A benzotriazine di-N-oxide with potential antineoplastic activity.  Tirapazamine is selectively activated by multiple reductases to form free radicals in hypoxic cells, thereby inducing single-and double-strand breaks in DNA, base damage, and cell death.  This agent also sensitizes hypoxic cells to ionizing radiation and inhibits the repair of radiation-induced DNA strand breaks via inhibition of topoisomerase II. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C62437","Tivantinib","(3R,4R)-3-(5,6-Dihydro-4H-pyrrolo(3,2,1-ij)quinolin-1-yl)-4-(1H-indol-3-yl)pyrrolidine-2,5-dione|ARQ 197|ARQ-197|TIVANTINIB|Tivantinib|c-Met Inhibitor ARQ 197","An orally bioavailable small molecule inhibitor of c-Met with potential antineoplastic activity. c-Met inhibitor ARQ 197 binds to the c-Met protein and disrupts c-Met signal transduction pathways, which may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. c-Met protein, the product of the proto-oncogene c-Met, is a receptor tyrosine kinase also known as hepatocyte growth factor receptor (HGFR); this protein is overexpressed or mutated in many tumor cell types and plays key roles in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis.","Pharmacologic Substance"]
["C85444","Tivozanib","AV-951|TIVOZANIB|Tivozanib|Urea, N-[2-chloro-4-[(6,7-dimethoxy-4-quinolinyl)oxy]phenyl]-N'-(5-methyl-3-isoxazolyl)-","An orally bioavailable inhibitor of vascular endothelial growth factor receptors (VEGFRs) 1, 2 and 3 with potential antiangiogenic and antineoplastic activities.  Tivozanib binds to and inhibits VEGFRs 1, 2 and 3, which may result in the inhibition of endothelial cell migration and proliferation, inhibition of tumor angiogenesis and tumor cell death. VEGFR tyrosine kinases, frequently overexpressed by a variety of tumor cell types, play a key role in angiogenesis.","Pharmacologic Substance"]
["C2102","TLC ELL-12","1-0-Octadecyl-2-O-methyl-Sn-3-glycero-phosphocholine Liposome|ELL-12|TLC ELL-12","A liposomal formulation of the ether lipid 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphocholine with potential antineoplastic activity.  TLC ELL-12 induces tumor cell apoptosis via mitochondria- and caspase-mediated mechanisms.  Liposomal encapsulation reduces the free agent's hemolytic toxicity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C124653","TLR 7/8 Agonist MEDI9197","3M 052|3M-052|MEDI 9197|MEDI9197|TLR 7/8 Agonist MEDI9197|TLR7/TLR8 Dual Agonist MEDI9197|Toll-like Receptor 7/8 Agonist MEDI9197","A toll-like receptor type 7 and 8 (TLR7/8) agonist with potential immunostimulating and antitumor activities. Upon intratumoral administration, TLR7/8 agonist MEDI9197 binds to and activates TLR7 and 8, thereby stimulating antigen-presenting cells (APCs), including dendritic cells (DCs). Activation of DCs results in the production of proinflammatory cytokines, and the activation of cytotoxic T-lymphocyte (CTL) and B-lymphocyte immune responses. This may cause tumor cell lysis. TLR7 and 8, members of the TLR family, play fundamental roles in the activation of the immune system.","Organic Chemical|Pharmacologic Substance"]
["C77884","TLR Agonist CADI-05","CADI-05|TLR Agonist CADI-05|Toll-like Receptor Agonist CADI-05","A poly-Toll-like receptor (TLR) agonist polyantigenic vaccine containing heat killed Mycobacterium indicus pranii (Mycobacterium w or Mw) with potential immunostimulating and antineoplastic activities. Upon administration, poly-TLR agonist polyantigenic vaccine activates a number of TLRs, which may result in macrophage and plasmacytoid dendritic cell (pDC) stimulation; secretion of interferon alpha; production of pro-inflammatory cytokines; upregulation of co-stimulatory molecules, enhanced T and B-cell stimulatory responses; T cell proliferation, and a Th1 immune response. TLRs are transmembrane receptors that recognize structurally conserved microbial molecules such as bacterial cell-surface lipopolysaccharides (LPS), lipoproteins, lipopeptides, lipoarabinomannan and flagellin, among others; immune responses stimulated by TLR activation may result in antineoplastic effects.","Organic Chemical|Pharmacologic Substance"]
["C61104","TLR7 Agonist 852A","852A|TLR7 Agonist 852A","A synthetic imidazoquinoline Toll-like receptor 7 (TLR7) agonist with immunostimulating and potential antitumor activities. TLR7 agonist 852A binds to and activates TLR7, thereby stimulating plasmacytoid dendritic cells (pDC) through the TLR7-MyD88-dependent signaling pathway. Activation of pDC results in secretion of interferon alpha, the production of proimflammatory cytokines, the upregulation of co-stimulatory molecules, and enhanced T and B-cell stimulatory responses.","Organic Chemical|Pharmacologic Substance"]
["C114975","TLR7/8/9 Antagonist IMO-8400","IMO-8400|Oligonucleotide IMO-8400|TLR7/8/9 Antagonist IMO-8400","An oligonucleotide targeted to the mRNA of MYD88 L265P, a mutant form of the linker protein MYD88, with potential antitumor activity. Anti-MYD88 oligonucleotide IMO-8400 binds to and inhibits the translation of mutated MYD88 L265P mRNA. This prevents overactivation of signaling pathways mediated by toll-like receptors (TLRs) 7, 8, and 9, nuclear factor-kappa B (NF-kB) activity, Janus-associated kinases-signal transducer and activator of transcription (JAK-STAT) signaling and the production of various cytokines. Together, this leads to an induction of apoptosis and an inhibition of tumor cell proliferation in MYD88 L265P-expressing tumor cells. MYD88, a key adaptor protein in the TLR signaling pathway, is mutated in a variety of B-cell lymphomas, including Waldenstrom's macroglobulinemia (WM) and activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL).","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C80521","TLR8 Agonist VTX-2337","TLR8 Agonist VTX-2337|Toll-like Receptor 8 Agonist VTX-2337|VTX-2337","A small-molecule Toll-like receptor 8 (TLR8) agonist with potential immunostimulating and antineoplastic activities. TLR8 agonist VTX-2337 binds to TLR8, present in cutaneous dendritic cells, monocytes/macrophages, and mast cells, which may result in the activation of the central transcription factor nuclear factor-B, the secretion of proinflammatory cytokines and other mediators, and a Th1-weighted antitumoral cellular immune response. Primarily localized to endosomal membranes intracellularly, TLR8, like other TLRs, recognizes pathogen-associated molecular patterns (PAMPs) and plays a key role in the innate immune system.","Organic Chemical|Pharmacologic Substance"]
["C94207","TLR9 Agonist MGN1703","MGN1703|TLR9 Agonist MGN1703","A synthetic oligonucleotide based on a proprietary double stem-loop immunomodulator design with potential immunostimulating activity. TLR9 agonist MGN1703 binds to and activates intracellular Toll-like receptor 9 (TLR9) in monocytes/macrophages, plasmacytoidal and myeloid dendritic cells (DCs), and natural killer (NK) cells, initiating immune signaling pathways and inducing T-helper 1 cell (Th1) production leading to the production of memory T cells and a Th1-mediated immune response. By activating the immune system, MGN1703 may attack tumor associated antigen (TAAs). TLR9 is a member of the TLR family, which plays a fundamental role in pathogen recognition and activation of innate immunity.","Immunologic Factor|Pharmacologic Substance"]
["C82353","TLR-Directed Cationic Lipid-DNA Complex JVRS-100","JVRS-100|TLR-Directed Cationic Lipid-DNA Complex JVRS-100|Toll-Like Receptor-Directed Cationic Lipid-DNA Complex JVRS-100","A cationic lipid DNA complex (CLDC) consisting of DOTIM/cholesterol liposomes and plasmid DNA, containing immunostimulatory CpG and non-CpG motifs, with potential immunostimulating and antineoplastic activities. Upon systemic administration, TLR-directed cationic lipid-DNA complex JVRS-100 enters dendritic cells (DCs) and macrophages; immunostimulatory DNA binds to and activates Toll-like receptors (TLRs), which may result in the generation of anti-tumor natural killer (NK) cell and T-cell responses by the innate immune system. In addition, as a vaccine adjuvant, this agent may induce a strong cytotoxic T-lymphocyte (CTL) response to co-administered antigen.","Cell|Pharmacologic Substance"]
["C2474","Tn(c)-KLH Conjugate Vaccine","Tn(c)-KLH Conjugate Vaccine|Tn(c)-KLH","A vaccine containing a clustered pancarcinoma carbohydrate antigen conjugated with keyhole limpet hemocyanin (KLH) with potential antineoplastic activity. Alpha-N-acetylgalactosamine (Tn) is a monosaccharide usually O-linked to serine or threonine residues of mucins found on most epithelial cancers with the highest expression on prostate cancer. This vaccine contains the Tn epitope cluster (c) that is synthesized by linking 3 copies of the Tn epitope on a threonine backbone to achieve the essential immunogenic structure. KLH is a hapten carrier and serves as an immunostimulant to improve immune recognition. Vaccination with Tn(c)-KLH vaccine may produce antibodies and elicit a cytotoxic T lymphocyte (CTL) response against those tumor cells expressing Tn antigen, resulting in decreased tumor growth.","Immunologic Factor|Pharmacologic Substance"]
["C29482","TNF Transduced TIL","TNF Gene Transduced TIL|TNF Transduced TIL","A preparation of autologous tumor-infiltrating lymphocytes (TILs) that have been transduced with a retroviral vector encoding the gene for tumor necrosis factor (TNF), a cytokine with anti-angiogenic and cytotoxic activity.  Following genetic modification, the lymphocytes are returned to the patient, infiltrate the tumor site, and deliver TNF directly to the tumor site, thereby exerting a specific antitumor effect, and avoiding TNF-related systemic toxicity. (NCI04)","Cell|Pharmacologic Substance"]
["C84217","Tocilizumab","Actemra|Immunoglobulin G1, Anti-(Human Interleukin 6 Receptor) (Human-Mouse Monoclonal MRA Heavy Chain), Disulfide with Human-Mouse Monoclonal MRA Kappa-Chain, Dimer|MRA|R-1569|RoActemra|TOCILIZUMAB|Tocilizumab","A recombinant, humanized IgG1 monoclonal antibody directed against the interleukin-6 receptor (IL-6R) with immunosuppressant activity. Tocilizumab targets and binds to both the soluble form of IL-6R (sIL-6R) and the membrane-bound form (mIL-6R), thereby blocking the binding of IL-6 to its receptor. This prevents IL-6-mediated signaling. Il-6, a pro-inflammatory cytokine that plays an important role in the regulation of the immune response, is overproduced in autoimmune disorders and certain types of cancers.","Pharmacologic Substance"]
["C2571","Tocladesine","8-Chloro Cyclic AMP|8-Chloroadenosine Cyclic 3':5'-Monophosphate|8-Cl-cAMP|Adenazole|TOCLADESINE|Tocladesine|tocladesine","An antimetabolite and a chlorine derivative of the intracellular secondary messenger, cyclic adenosine 3,5-monophosphate (cAMP), with potential antineoplastic activity. Tocladesine appears to be converted to 8-chloro-adenosine by phosphodiesterases and subsequently phosphorylated to 8-chloro-ATP, which functions as a purine analogue and competes with ATP in transcription. In addition, generation of 8-chloro-ATP depletes endogenous ATP pool that is essential for many biological reactions in intracellular energy transfer. As a result, this agent causes RNA synthesis inhibition, blocks cellular proliferation, and induces apoptosis.","Pharmacologic Substance"]
["C68318","Tocotrienol","TOCOTRIENOL|Tocotrienol","Any of the four forms, alpha, beta, gamma and delta, of a member of the vitamin E family, with potential hypocholesterolemic, antithrombotic, antioxidant, immunomodulating and antineoplastic activities. Tocotrienol inhibits the activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, thereby lowering cholesterol levels. In addition, tocotrienol acts through multiple signal transduction pathways to induce cell cycle arrest and caspase-mediated apoptosis, and to decrease tumor cell proliferation. In addition, this agent may inhibit angiogenesis through the blockage of vascular endothelial growth factor receptor (VEGFR) and the subsequent inhibition of tumor cell-induced vessel formation. Also, this agent prevents free radical formation and inhibits lipid peroxidation, thereby preventing DNA cell damage. Tocotrienol farnesyl isoprenoid side chains contain 3 double bonds, which are absent in tocopherols, likely contribute to its anti-cancer activities.","Organic Chemical"]
["C101518","Tocotrienol-rich Fraction","TRF|Tocotrienol-rich Fraction","An orally available nutritional supplement containing high amounts of the vitamin E family member tocotrienol with antioxidant, hypolipidemic and potential immunomodulating and antiproliferative activity. Upon oral administration, tocotrienol-rich fraction (TRF) accumulates in tumor cells and induces cell cycle arrest, programmed cell death, and inhibits tumor cell proliferation. In addition, this agent suppresses 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity and inhibits angiogenesis. Rice bran oil, palm oil and annatto seed oil are common sources of TRF.","Pharmacologic Substance"]
["C125080","Toll-like Receptor 9 Agonist IMO-2125","IMO 2125|IMO-2125|TLR9 Agonist IMO-2125|Toll-like Receptor 9 Agonist IMO-2125","A proprietary synthetic oligonucleotide-based agonist of toll-like receptor 9 (TLR9), with potential immunostimulating activity. Upon administration, TLR9 agonist IMO-2125 binds to and activates TLR9 expressed by plasmacytoid dendritic cells (pDCs) and B-cells. This initiates immune signaling pathways, activates B-cells and pDCs, and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. TLR9 is a member of the TLR family, which plays a fundamental role in pathogen recognition and activation of innate immunity.","Pharmacologic Substance"]
["C75293","Tolnidamine","1b Indozadole|TOLNIDAMINE|Tolnidamine","An indazole carboxylic acid derivative with antispermatogenic and potential antineoplastic activity. As a male contraceptive, tolnidamine may irreversibly inhibit sperm production. This agent is less nephrotoxic than ionidamide, but it is just as effective in antispermatogenic action to ionidamide.","Pharmacologic Substance"]
["C88300","Tomato-Soy Juice","Tomato-Soy Juice","A juice containing tomato extract and soy protein with potential chemopreventive and antiproliferative activities. Tomato-soy juice contains phytochemicals, including flavonoids, such as the soy isoflavone genistein, and carotenoids, including lycopene. These phytochemicals may exhibit antioxidative activity, antitumor activity by modulating certain tumor-associated signal transduction pathways, and apoptosis-inducing activity.","Pharmacologic Substance"]
["C78477","Topical Betulinic Acid","Topical ALS-357|Topical Betulinic Acid","A topical formulation of a pentacyclic lupane-type triterpene derivative of betulin (isolated from the bark of Betula alba, the common white birch) with antiinflammatory, anti-HIV and antineoplastic activities. Betulinic acid induces apoptosis through induction of changes in mitochondrial membrane potential, production of reactive oxygen species, and opening of mitochondrial permeability transition pores, resulting in the release of mitochondrial factors involved in apoptosis, activation of caspases, and DNA fragmentation. Although originally thought to exhibit specific cytotoxicity against melanoma cells, this agent has been found to be cytotoxic against non-melanoma tumor cell types including neuroectodermal and brain tumor cells.","Organic Chemical|Pharmacologic Substance"]
["C125194","Topical Fluorouracil","Actino-Hermal|Arumel|Carac|Cytosafe|Efudex|Efurix|Fiverocil|Fluoroplex|Flurox|Timazin|Tolak|Topical Fluorouracil",": A topical formulation containing the antimetabolite 5-fluorouracil (5-FU), with antineoplastic activity. Upon topical administration, 5-FU is converted into the active metabolite 5-fluoroxyuridine monophosphate (F-UMP), which competes with uracil during RNA synthesis and inhibits RNA processing. Conversion of 5-FU into another active metabolite, 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate (F-dUMP), inhibits thymidylate synthase; this results in the depletion of thymidine triphosphate (TTP), one of the four nucleotide triphosphates used in DNA synthesis, and thus inhibits DNA synthesis. Altogether, this prevents the proliferation of tumor cells locally.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C74085","Topical Gemcitabine Hydrochloride","Topical Gemcitabine Hydrochloride","A topical preparation of gemcitabine hydrochloride with antineoplastic activity. Gemcitabine, an analogue of the antimetabolite nucleoside deoxycytidine, is converted intracellularly to the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis; dFdCTP is incorporated into DNA, resulting in DNA strand termination and apoptosis.","Pharmacologic Substance"]
["C125002","Topical Trichloroacetic Acid","Topical TCA|Topical Trichloroacetic Acid","A topical solution containing the caustic agent trichloroacetic acid (TCA), with potential keratolytic, anti-viral and antineoplastic activities. Upon topical application to the affected area, TCA causes tissue necrosis through coagulation of proteins, leads to the destruction of human papilloma virus (HPV)-associated warts and inhibits HPV-driven proliferation of cancer cells.","Pharmacologic Substance"]
["C75124","Topixantrone","BBR 3576|Indazolo(4,3-gh)isoquinolin-6(2H)-one, 5-((2-(dimethylamino)ethyl)amino)-2-(2-((2-hydroxyethyl)amino)ethyl)-|TOPIXANTRONE|Topixantrone","A 9-aza-anthrapyrazole antineoplastic antibiotic. Topixantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair as well as RNA and protein synthesis. Compared to other DNA intercalators, this agent shows minimal cardiotoxicity.","Pharmacologic Substance"]
["C84851","Topoisomerase I Inhibitor Genz-644282","Genz-644282|Topoisomerase I Inhibitor Genz-644282","A non-camptothecin inhibitor of topoisomerase I with potential antineoplastic activity. Topoisomerase I inhibitor Genz-644282 binds to and inhibits the enzyme topoisomerase I, which may result in the inhibition of repair of single-strand DNA breaks, DNA replication, and tumor cell growth in susceptible tumor cell populations.","Pharmacologic Substance"]
["C90594","Topoisomerase I Inhibitor LMP400","LMP400|Topoisomerase I Inhibitor LMP400","An indenoisoquinoline and non-camptothecin inhibitor of topoisomerase I (Top I) with potential antineoplastic activity. Topoisomerase I inhibitor LMP400 binds to the topoisomerase I-DNA covalent cleavage complexes, and inhibits repair of single-strand DNA breaks, DNA replication, and tumor cell growth in susceptible tumor cell populations. Compared to camptothecins, indenoisoquinolines are chemically stable, produce stable Top I-DNA cleavage complexes, induce unique DNA cleavage sites and appear more resistant to multidrug efflux pumps.","Pharmacologic Substance"]
["C90595","Topoisomerase I Inhibitor LMP776","LMP776|Topoisomerase I Inhibitor LMP776","An indenoisoquinoline and non-camptothecin inhibitor of topoisomerase I (Top I) with potential antineoplastic activity. Topoisomerase I inhibitor LMP776 binds to the topoisomerase I-DNA covalent cleavage complexes, and inhibits repair of single-strand DNA breaks, DNA replication, and tumor cell growth in susceptible tumor cell populations. Compared to camptothecins, indenoisoquinolines are chemically stable, produce stable Top I-DNA cleavage complexes, induce unique DNA cleavage sites and appear more resistant to multidrug efflux pumps.","Pharmacologic Substance"]
["C1413","Topotecan","(s)-10-[(dimethylamino)methyl]-4-ethyl-4,9-dihydroxy-1H-pyrano[3',4':6,7]indolizino[1,2-b]-quinoline-3,14(4H,12H)-dione|9-[(dimethylamino)methyl]-10-hydroxy-(20S)-camptothecin|Hycamptamine|TOPOTECAN|Topotecan Lactone|Topotecan|topotecan","A semisynthetic derivative of camptothecin, a cytotoxic, quinoline-based alkaloid extracted from the Asian tree Camptotheca acuminata. Topotecan inhibits topoisomerase I activity by stabilizing the topoisomerase I-DNA covalent complexes during S phase of cell cycle, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery.","Organic Chemical|Pharmacologic Substance"]
["C2828","Topotecan Hydrochloride","(S)-10-[(dimethylamino)methyl]-4-ethyl-4,9-dihydroxy-1H-pyrano[3',4':6,7] indolizino[1,2-b] quinoline-3,14-(4H,12H)-dione Monohydrochloride|Hycamptamine|Hycamtin|SKF S-104864-A|TOPOTECAN HYDROCHLORIDE|Topotecan HCl|Topotecan Hydrochloride|Topotecan hydrochloride|topotecan hydrochloride (oral)|topotecan hydrochloride","The hydrochloride salt of a semisynthetic derivative of camptothecin with antineoplastic activity. During the S phase of the cell cycle, topotecan selectively stabilizes topoisomerase I-DNA covalent complexes, inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when complexes are encountered by the DNA replication machinery. Camptothecin is a cytotoxic quinoline-based alkaloid extracted from the Asian tree Camptotheca acuminata.","Organic Chemical|Pharmacologic Substance"]
["C80065","Topotecan Hydrochloride Liposomes","Brakiva|Topotecan Hydrochloride Liposomes","The hydrochloride salt of a semisynthetic derivative of camptothecin mixed with sphingomyelin/cholesterol and sonicated to form small unilamellar vesicles containing topotecan, with potential antineoplastic activity. Topotecan hydrochloride liposomes mediates efficient drug delivery of topotecan into the cytosol from the endosome compartment. During the S phase of the cell cycle, topotecan selectively stabilizes topoisomerase I-DNA covalent complexes, inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when complexes are encountered by the DNA replication machinery.","Pharmacologic Substance"]
["C64779","Topsalysin","PORxin 302|PRX 302|PSA-PAH1|Pore-forming Protein (Synthetic Proaerolysin) Fusion Protein with Prostate-specific Antigen (Human)|TOPSALYSIN|Topsalysin","A targeted prodrug consisting of a recombinant modified form of the Aeromonas protoxin, proaerolysin (PA), bearing a prostate-specific protease cleavage site, with potential antineoplastic activity. When injected directly into the prostate, topsalysin is hydrolyzed to the active toxin aerolysin by the serine protease prostate specific antigen (PSA), a protein overexpressed by prostate cancers and prostate cells in hyperplastic prostatic tissue. Aerolysin molecules then oligomerize to form ring-like heptamers that are incorporated into the lipid bilayers of cell membranes, forming large membrane channels and resulting in the leakage of cellular contents and lysis of PSA-expressing prostate cells.","Pharmacologic Substance"]
["C101795","TORC1/2 Kinase Inhibitor DS-3078a","DS-3078a|TORC1/2 Kinase Inhibitor DS-3078a","An orally bioavailable inhibitor of raptor-mTOR protein complex (TORC1) and rictor-mTOR protein complex (TORC2) with potential antineoplastic activity. TORC1/2 inhibitor DS-3078a binds to and inhibits both TORC1 and TORC2, which may result in tumor cell apoptosis and a decrease in tumor cell proliferation. TORC1 and 2 are upregulated in some tumors and play an important role in the PI3K/Akt/mTOR signaling pathway, which is frequently dysregulated in human cancers.","Pharmacologic Substance"]
["C1256","Toremifene","(Z)-2-[4-(4-Chloro-1,2-diphenyl-1-butenyl)phenoxy]-N,N-dimethylethanamine|(Z)-4-Chloro-1,2-diphenyl-1[4-[2-(N,N-dimethylamino)ethoxy]phenyl]-1-butene|Farestone|TOREMIFENE|Toremifene|toremifene","A nonsteroidal triphenylethylene antiestrogen.  Chemically related to tamoxifen, toremifene is a selective estrogen receptor modulator (SERM).  This agent binds competitively to estrogen receptors, thereby interfering with estrogen activity.  Toremifene also has intrinsic estrogenic properties, which are manifested according to tissue type or species. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1756","Toremifene Citrate","(Z)-2-[4-(4-Chloro-1,2-diphenyl-1-butenyl)phenoxy]-N,N-dimethylethanamine 2-Hydroxy-1,2,3-propanetricarboxylate (1:1)|2-(p-[(Z)-4-chloro-1,2-diphenyl-1-butenyl]-phenoxy)- N,N-dimethylethylamine citrate (1:1)|Acapodene|FC-1157a|Fareston|GTx-006|TOREMIFENE CITRATE|Toremifene Citrate|Toremifene citrate","The citrate salt of a nonsteroidal triphenylethylene antiestrogen.  Chemically related to tamoxifen, toremifene is a selective estrogen receptor modulator (SERM).  This agent binds competitively to estrogen receptors, thereby interfering with estrogen activity.  Toremifene also has intrinsic estrogenic properties, which is manifested depending on the tissue or species. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C70650","Tosedostat","Aminopeptidase inhibitor CHR-2797|CHR-2797|Cyclopentyl (2S)-2-{(2R)-2-[(1S)-1-hydroxy-2-(hydroxyamino)-2-oxoethyl]-4- methylpentanamido}-2-phenylacetate|TOSEDOSTAT|Tosedostat","A proprietary orally bioavailable inhibitor of the M1 family of aminopeptidases with potential antineoplastic activity. Aminopeptidase inhibitor CHR-2797 is converted intracellularly into a poorly membrane-permeable active metabolite (CHR-79888) which inhibits the M1 family of aminopeptidases, particularly puromycin-sensitive aminopeptidase (PuSA), and leukotriene A4 (LTA4) hydrolase; inhibition of these aminopeptidases in tumor cells may result in amino acid deprivation, inhibition of protein synthesis due to a decrease in the intracellular free amino acid pool, an increase in the level of the proapoptotic protein Noxa, and cell death. Noxa is a member of the BH3 (Bcl-2 homology 3)-only subgroup of the proapoptotic Bcl-2 (B-cell CLL/lymphoma 2) protein family.","Pharmacologic Substance"]
["C2543","Tositumomab","Anti-CD20 Antibody|MoAb Anti-B1|Monoclonal Antibody Anti-B1|TOSITUMOMAB|Tositumomab|anti-B1|tositumomab","A murine IgG2 monoclonal antibody directed against the CD20 antigen, found on the surface of B-cells.  Tositumomab binds to the CD20 surface membrane antigen, resulting in apoptosis, and may stimulate antitumoral cell-mediated and/or antibody-dependent cytotoxicity. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C116913","Total Tumor RNA-loaded Dendritic Cell Vaccine","TTRNA-loaded DC Vaccine|Total Tumor RNA-loaded Dendritic Cell Vaccine","A cancer vaccine containing autologous dendritic cells (DCs) that are loaded with total tumor RNA (TTRNA) from a specific tumor, with potential immunostimulatory and antineoplastic activities. Upon administration, TTRNA-loaded DC vaccine may elicit a highly specific cytotoxic T-cell (CTL) response against the tumor-associated antigens (TAAs) encoded by the TTRNA.","Immunologic Factor|Pharmacologic Substance"]
["C61319","Tozasertib Lactate","Aurora Kinase Inhibitor MK-0457|L-001281814|MK-0457|Propanoic acid, 2-hydroxy-, (2S)-, compd. with N-(4-((4-(4-methyl-1-piperazinyl)-6-((5-methyl-1H-pyrazol-3-yl)amino)-2-pyrimidinyl)thio)phenyl)cyclopropanecarboxamide|TOZASERTIB LACTATE|Tozasertib Lactate|VX-680","The lactate salt of tozasertib, a synthetic, small-molecule Aurora kinase inhibitor with potential antitumor activity. Tozasertib binds to and inhibits Aurora kinases (AKs), thereby inducing apoptosis in tumor cells in which AKs are overexpressed. AKs, a family of serine-threonine kinases, are essential for mitotic progression, spindle formation, centrosome maturation, chromosomal segregation, and cytokinesis.","Pharmacologic Substance"]
["C2374","TP40 Immunotoxin","TP40 Immunotoxin|TP40|Transforming Growth Factor-Alpha-Pseudomonas Exotoxin-40","A chimeric fusion protein containing human transforming growth factor alpha (TGF-a) covalently linked to a truncated form of the bacterial toxin Pseudomonas exotoxin A, PE40, with potential antitumor activity. PE40 lacks the cell-binding domain, but retains domains II and III that are involved in membrane translocation and inhibition of protein synthesis in eukaryotic cells. TGF-a moiety of the TP40 immunotoxin binds to and activates epidermal growth factor receptor (EGFR), a tyrosine kinase receptor overexpressed on certain cancer cells. After internalization, the endotoxin moiety of the immunotoxin-receptor complex causes protein synthesis inhibition via modifying translation elongation factor 2 (EF-2), thereby impedes tumor cell growth and proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1691","Trabectedin","ET-743|Ecteinascidin 743|Ecteinascidin|Spiro(6,16-(epithiopropanoxymethano)-7,13-imino-12H-1,3-dioxolo(7,8)isoquino(3,2,-b)(3)benzazocine-20,1'(2'H)-isoquinolin)-19-one, 3',4',6,6a,7,13,14,16-Octahydro-5-(acetyloxy)-6',8,14-trihydroxy-7',9-dimethoxy-4,10,23-trimethyl-, (6R-(6-alpha,6a-beta,7-beta,13-beta,14-beta,16-alpha,20R*))-|TRABECTEDIN|Trabectedin|Yondelis|ecteinascidin 743|trabectedin","A tetrahydroisoquinoline alkaloid isolated from the marine tunicate Ecteinascidia turbinata with potential antineoplastic activity. Binding to the minor groove of DNA, trabectedin interferes with the transcription-coupled nucleotide excision repair machinery to induce lethal DNA strand breaks and blocks the cell cycle in the G2 phase.","Organic Chemical|Pharmacologic Substance"]
["C80066","Trabedersen","AP 12009|Trabedersen","A transforming growth factor (TGF)-beta2 specific phosphorothioate antisense oligodeoxynucleotide with the sequence 5'-CGGCATGTCTATTTTGTA-3', with potential antineoplastic activity. Trebedersen binds to TGF-beta2 mRNA causing inhibition of protein translation, thereby decreasing TGF-beta2 protein levels; decreasing intratumoral TGF-beta2 levels may result in the inhibition of tumor cell growth and migration, and tumor angiogenesis. TGF-beta2, a cytokine often over-expressed in various malignancies, may play an important role in promoting the growth, progression, and migration of tumor cells.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C77908","Trametinib","GSK1120212|JTP-74057|MEK Inhibitor GSK1120212|Mekinist|N-(3-{3-cyclopropyl-5-[(2-fluoro-4-iodophenyl)amino]-6,8-dimethyl-2,4,7-trioxo-3,4,6,7-tetrahydropyrido[4,3-d]pyrimidin-1(2H)-yl}phenyl)acetamide|TRAMETINIB|Trametinib","An orally bioavailable inhibitor of mitogen-activated protein kinase kinase (MEK MAPK/ERK kinase) with potential antineoplastic activity. Trametinib specifically binds to and inhibits MEK 1 and 2, resulting in an inhibition of growth factor-mediated cell signaling and cellular proliferation in various cancers. MEK 1 and 2, dual specificity threonine/tyrosine kinases often upregulated in various cancer cell types, play a key role in the activation of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth.","Organic Chemical|Pharmacologic Substance"]
["C82695","Trans Sodium Crocetinate","TSC|Trans Sodium Crocetinate","The sodium salt of the trans-isomer of the carotenoid crocetin with potential antihypoxic and radiosensitizing activities. Trans sodium crocetinate (TSC) increases the diffusion rate of oxygen in aqueous solutions such as from plasma to body tissue. The agent has been shown to increase available oxygen during hypoxic and ischemic conditions that may occur in hemorrhage, vascular and neurological disorders, and in the tumor microenvionment.","Pharmacologic Substance"]
["C120308","Transdermal 17beta-Estradiol Gel BHR-200","BHR-200|Transdermal 17beta-Estradiol Gel BHR-200","A proprietary, transdermal, hydroalcoholic gel formulation containing 17beta-estradiol, with potential antineoplastic activity. Upon topical administration, 17beta-estradiol exerts its antineoplastic effect(s) through as of yet not fully elucidated mechanism(s) of action(s). This formulation may induce feedback inhibition via the hypothalamic-pituitary-gonadal axis feedback loop, block the secretion of luteinizing hormone (LH) and prevent the release of testosterone from Leydig cells in the testes, thus suppressing testosterone secretion. In addition, 17beta-estradiol inhibits enzymes involved in steroidogenesis, thereby further inhibiting androgen production. Since testosterone is required to sustain prostate growth, reducing testosterone levels may inhibit hormone-dependent prostate cancer cell proliferation. In addition, 17beta-estradiol prevents bone loss, and suppresses andropause symptoms, such as hot flashes, which appear during androgen-deprivation therapy (ADT) where the standard of care is the use of gonadotrophin releasing hormone (GnRH) analogs. Compared to oral estrogens, the topical gel formulation lowers the risk of cardiovascular side effects.","Pharmacologic Substance"]
["C114103","Transdermal 4-Hydroxytestosterone","Transdermal 4-Hydroxytestosterone|Transdermal 4-OHT|Transdermal CR1447","A transdermal formulation containing 4-hydroxytestosterone (4-OHT), a steroidal aromatase inhibitor (AI) and androgen receptor (AR) antagonist, with potential antineoplastic activity. 4-OHT is largely converted into 4-hydroxyandrostenedione (4-OHA) and irreversibly binds to and inhibits aromatase, thereby blocking the conversion of androstenedione to estrone, and testosterone to estradiol. This may inhibit tumor cell proliferation in estrogen-dependent tumor cells. In addition, 4-OHT binds to the AR and may inhibit AR-mediated tumor cell growth. Aromatase, a cytochrome P-450 enzyme, is overexpressed in a variety of cancer cells; it plays a key role in estrogen biosynthesis. Compared to oral 4-OHT, the transdermal formulation allows for continuous release of 4-OHT into the bloodstream and prevents first pass metabolism by the liver.","Organic Chemical|Pharmacologic Substance"]
["C78450","Transferrin Receptor-Targeted Anti-RRM2 siRNA CALAA-01","CALAA-01|Transferrin Receptor-Targeted Anti-RRM2 siRNA CALAA-01","A proprietary transferrin receptor-targeted nanoparticle preparation of a non-chemically modified small-interfering RNA (siRNA) directed against the M2 subunit of ribonucleotide reductase (RRM2) with potential antineoplastic activity. Upon administration, transferrin receptor-targeted anti-RRM2 siRNA CALAA-01 binds to transferrin receptors (TfRs), releasing anti-RRM2 siRNA after endocytosis; anti-RRM2 siRNA silences the expression of RRM2 via the RNAi pathway, impeding the assembly of the holoenzyme ribonucleotide reductase (RR) which catalyzes the production of deoxyribonucleotides. As a result, inhibition of cellular proliferation may occur in cells expressing TfR, a cell surface protein overexpressed on various cancer cell types.","Pharmacologic Substance"]
["C29474","Transferrin Receptor-Targeted Liposomal p53 cDNA","SGT-53|Synerlip p53|Transferrin Receptor-Targeted Liposomal p53 cDNA","A cationic liposomal, tumor-targeting p53 (TP53) gene delivery system with potential anti-tumor activity. Transferrin receptor-targeted liposomal p53 cDNA contains plasmid DNA encoding the tumor suppressor protein p53 packaged in membrane-like liposome capsules that are complexed with anti-transferrin receptor single-chain antibody (TfRscFv). Upon systemic administration, the anti-TfRscFv selectively binds to tumor cells expressing transferrin receptors. The p53 plasmid is delivered into the nucleus and as a result, p53 protein is produced in tumor cells that have altered p53 function. This results in the restoration of normal cell growth control mechanisms as well as normal response mechanisms to DNA damage.","Pharmacologic Substance"]
["C26676","Transferrin-CRM107","HN-66000|Transferrin-CRM107|transferrin-CRM107","A synthetic targeted protein toxin which consists of human transferrin (Tf) conjugated to a diphtheria toxin that contains a point mutation (CRM107). After binding to the transferrin receptor expressed on the tumor cell surface, transferrin-CRM107 is internalized, where the diphtheria toxin moiety exerts its cytotoxic effect intracellularly by inhibiting protein synthesis through ADP-ribosylation of elongation factor. (NCI04)","Pharmacologic Substance"]
["C38720","Transgenic Lymphocyte Immunization Vaccine","TLI Vaccine|Transgenic Lymphocyte Immunization Vaccine","A vaccine consisting of a preparation of allogeneic lymphocytes that encode a gene for telomerase.  In transgenic lymphocyte immunization, the transgenic cells are infused into the patient, where they serve as antigen- presenting cells (APCs) with the dual function of antigen synthesis and presentation.  Vaccination produces an immune response targeting cancer cells expressing telomerase. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C61980","Tranylcypromine Sulfate","(+-)-Trans-2-Phenylcyclopropylamine Sulfate (2:1)|1-Amino-2-phenylcyclopropane Sulfate|Parnate|TRANYLCYPROMINE SULFATE|Tranylcypromine Sulfate","The sulfate salt form of tranylcypromine, an orally bioavailable, nonselective, irreversible, non-hydrazine inhibitor of both monoamine oxidase (MAO) and lysine-specific demethylase 1 (LSD1/BHC110), with antidepressant and anxiolytic activities, and potential antineoplastic activities. Upon oral administration, tranylcypromine exerts its antidepressant and anxiolytic effects through the inhibition of MAO, an enzyme that catalyzes the breakdown of the monoamine neurotransmitters serotonin, norepinephrine, epinephrine and dopamine. This increases the concentrations and activity of these neurotransmitters. Tranylcypromine exerts its antineoplastic effect through the inhibition of LSD1. Inhibition of LSD1 prevents the transcription of LSD1 target genes. LSD1, a flavin-dependent monoamine oxidoreductase and a histone demethylase, is upregulated in a variety of cancers and plays a key role in tumor cell proliferation, migration, and invasion.","Pharmacologic Substance"]
["C1665","Trapoxin","Cyclo((S)-gamma-oxo-L-alpha-aminooxiraneoctanoyl-L-phenylalanyl-L-phenylalanyl-D-2-piperidinecarbonyl)|Cyclo((S)-phenylalanyl-(S)-phenylalanyl-(R)-pipecolinyl-(2S,9S)-2-amino-8-oxo-9,10-epoxydecanoyl)|Cyclo(L-phenylalanyl-L-phenylalanyl-D-pipecolinyl-L-2-amino-8-oxo -9,10-epoxy - decanoyl)|Trapoxin A|Trapoxin","An epoxide-containing cyclotetrapeptide with antitumor activity.  It is an irreversible inhibitor of histone deacetylase.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1647","Trastuzumab","ABP 980|Anti-ERB-2|Anti-HER2/c-erbB2 Monoclonal Antibody|Anti-c-ERB-2|Anti-c-erbB2 Monoclonal Antibody|Anti-erbB-2|Anti-erbB2 Monoclonal Antibody|Anti-p185-HER2|HER2 Monoclonal Antibody|Herceptin Biosimilar PF-05280014|Herceptin Trastuzumab Biosimilar PF-05280014|Herceptin|Immunoglobulin G 1 (Human-Mouse Monoclonal RhuMab HER2gamma1-Chain Antihuman p185(Sup c-erbB2) Receptor), Disulfide with Human-Mouse Monoclonal RhuMab HER2 Light Chain, Dimer|MoAb HER2|Monoclonal Antibody HER2|Monoclonal Antibody c-erb-2|PF-05280014|RO0452317|TRASTUZUMAB|Trastuzumab Biosimilar ABP 980|Trastuzumab Biosimilar PF-05280014|Trastuzumab|c-erb-2 Monoclonal Antibody|rhuMAb HER2|trastuzumab","A recombinant humanized monoclonal antibody directed against the human epidermal growth factor receptor 2 (HER2). After binding to HER2 on the tumor cell surface, trastuzumab induces an antibody-dependent cell-mediated cytotoxicity against tumor cells that overexpress HER2. HER2 is overexpressed by many adenocarcinomas, particularly breast adenocarcinomas. (NCI04)","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C82492","Trastuzumab Emtansine","Ado Trastuzumab Emtansine|Immunoglobulin G1, Anti-(Human p185neu Receptor) (Human-Mouse Monoclonal RhuMab HER2 Gamma1-Chain), Disulfide with Human-Mouse Monoclonal RhuMab HER2 Light Chain, Dimer, Tetraamide with N2'-(3-((1-((4-carboxycyclohexyl)methyl)-2,5-dioxo-3-pyrrolidinyl)thio)-1-oxopropyl)-N2'-deacetylMaytansine|Kadcyla|PRO132365|RO5304020|T-DM1|TRASTUZUMAB EMTANSINE|Trastuzumab Emtansine|Trastuzumab-DM1|Trastuzumab-MCC-DM1 Antibody-Drug Conjugate|Trastuzumab-MCC-DM1 Immunoconjugate|Trastuzumab-MCC-DM1","An antibody-drug conjugate (ADC) consisting of the recombinant anti-epidermal growth factor receptor 2 (HER2) monoclonal antibody trastuzumab conjugated to the maytansinoid DM1 via a nonreducible thioether linkage (MCC) with potential antineoplastic activity. The trastuzumab moiety of this ADC binds to HER2 on tumor cell surfaces; upon internalization, the DM1 moiety is released and binds to tubulin, thereby disrupting microtubule assembly/disassembly dynamics and inhibiting cell division and the proliferation of cancer cells that overexpress HER2. Linkage of antibody and drug through a nonreducible linker has been reported to contribute to the improved efficacy and reduced toxicity of this ADC compared to similar ADCs constructed with reducible linkers.","Immunologic Factor|Pharmacologic Substance"]
["C118674","Trastuzumab VC-seco-DUBA","ADC SYD985|Antibody-drug Conjugate SYD985|SYD985|Trastuzumab VC-seco-DUBA|Trastuzumab-drug Conjugate SYD985","An antibody-drug conjugate (ADC) composed of the recombinant humanized anti-epidermal growth factor receptor 2 (HER2) monoclonal antibody trastuzumab linked, via a cleavable linker, to the duocarmycin prodrug, seco-duocarmycin-hydroxybenzamide-azaindole (seco-DUBA), with potential antineoplastic activity. Upon administration of trastuzumab vc-seco-DUBA, the trastuzumab moiety binds to HER2 on the tumor cell surface, which triggers the endocytosis of this agent. The linker is then cleaved inside the tumor cell by proteases at the dipeptide valine-citrulline (vc), and releases the active moiety, duocarmycin. Duocarmycin binds to the minor groove of DNA, alkylates adenine at the N3 position, and induces cell death. In addition, trastuzumab induces antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells that overexpress HER2. HER2 is overexpressed by many carcinomas and is associated with a poor prognosis.","Pharmacologic Substance"]
["C91711","Trebananib","AMG 386|Angiopoietin 1/2-Neutralizing Peptibody AMG 386|TREBANANIB|Trebananib","An angiopoietin (Ang) 1 and 2 neutralizing peptibody, with potential antiangiogenic activity. AMG 386 targets and binds to Ang1 and Ang2, thereby preventing the interaction of the angiopoietins with their target tie2 receptors. This may inhibit angiogenesis and may eventually lead to an inhibition of tumor cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1257","Treosulfan","(S-(R*,R*))-1,2,3,4-butanetetrol,1,4-dimethanesulfonate|1,2,3, 4-Butanetetrol, 1,4-dimethanesulfonate, [R-(R*,S*)]-|Dihydroxybusulfan|L-Threitol 1,4-dimethanesulfonate|Ovastat|TREOSULFAN|Treosulfan|Treosulphan|Tresulfon|treosulfan","The prodrug of a bifunctional sulfonate alkylating agent with myeloablative, immunosuppressive, and antineoplastic activities. Under physiological conditions, treosulfan converts nonenzymatically to L-diepoxybutane via a monoepoxide intermediate. The monoepoxide intermediate and L-diepoxybutane alkylate DNA at guanine residues and produce DNA interstrand crosslinks, resulting in DNA fragmentation and apoptosis. In escalated doses, this agent also exhibits myeloablative and immunosuppressive activities.","Organic Chemical|Pharmacologic Substance"]
["C81554","Tretazicar","CB1954|TRETAZICAR|Tretazicar","A prodrug of a bifunctional alkylating, dinitrobenzamide derivative with antineoplastic activity. Tretazicar can be activated by the human enzyme quinone oxidoreductase 2 (NQO2) in the presence of the cosubstrate caricotamide, an analogue of the natural cosubstrate dihydronicotinamide riboside (NRH), which acts as an electron donor. The resulting active, but short-lived metabolite, dinitrobenzamide, leads to DNA replication inhibition and the induction of apoptosis in NQO2 expressing cancer cells. Due to the lack of the natural cosubstrate NRH, NQO2 expression is normally latent but is upregulated in certain types of tumor cells.","Pharmacologic Substance"]
["C900","Tretinoin","(All-E)-3,7-Dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)-2,4,6,8-nonatetraenoic Acid|2,4,6,8-Nonatetraenoic acid, 3, 7-dimethyl-9-(2,6,6-trimethyl-1-cyclohexen-1-yl)-, (all-E)-|ATRA|Aberel|Airol|Aknoten|All-trans Retinoic Acid|All-trans Vitamin A Acid|Avita|Cordes Vas|Dermairol|Epi-Aberel|Eudyna|Renova|Retin-A MICRO|Retin-A-Micro|Retin-A|Retinoic Acid|Retisol-A|Ro 5488|Stieva-A Forte|Stieva-A|TRETINOIN|Trans Retinoic Acid|Trans Vitamin A Acid|Tretinoin|Tretinoinum|Vesanoid|Vitamin A Acid|Vitamin A acid, all-trans-|Vitamin A acid|Vitinoin|all trans-Retinoic acid|all-trans retinoic acid|all-trans-Retinoic acid|all-trans-Vitamin A acid|beta-Retinoic Acid|retinoic acid|trans-Retinoic Acid|trans-Retinoic acid|tretinoin|vitamin A acid","A naturally-occurring acid of retinol. Tretinoin binds to and activates retinoic acid receptors (RARs), thereby inducing changes in gene expression that lead to cell differentiation, decreased cell proliferation, and inhibition of tumorigenesis.  This agent also inhibits telomerase, resulting in telomere shortening and eventual apoptosis of some tumor cell types.  The oral form of tretinoin has teratogenic and embryotoxic properties.","Organic Chemical|Pharmacologic Substance"]
["C2398","Tretinoin Liposome","AR-623|All-trans-retinoic acid liposomal|Atragen|Liposomal all-trans-retinoic acid|Liposomal tretinoin|Tretinoin Liposomal|Tretinoin Liposome|TretinoinLF","An intravenous formulation of tretinoin (vitamin A acid or all-trans retinoic acid) encased in liposomes. Tretinoin is a naturally occurring retinoic acid agent that binds to and activates retinoic acid receptors (RAR), effecting changes in gene expression that lead to cell differentiation, decreased cell proliferation, and inhibition of carcinogenesis.  This agent also inhibits telomerase, leading to telomere shortening and eventual apoptosis of certain tumor cell types. Liposome encapsulation extends the half-life of intravenously administered tretinoin.","Organic Chemical|Pharmacologic Substance"]
["C2242","Triapine","3-AP|3-Aminopyridine-2-carboxaldehyde Thiosemicarbazone|3-Apct|3-aminopyridine-2-carboxaldehyde thiosemicarbazone|OCX-191|Triapine","A synthetic heterocyclic carboxaldehyde thiosemicarbazone with potential antineoplastic activity. Triapine inhibits the enzyme ribonucleotide reductase, resulting in the inhibition of the conversion of ribonucleoside diphosphates to deoxyribonucleotides necessary for DNA synthesis. This agent has been shown to inhibit tumor growth in vitro. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C95208","Triazene Derivative TriN2755","TriN2755|Triazene Derivative TriN2755","A synthetic triazene derivative with antineoplastic activity. Upon metabolic activation via N-demethylation, TriN2755 is converted into highly reactive carbocations that can alkylate DNA and other macromolecules, thereby resulting in DNA cross links, inhibiting DNA replication and repair, and subsequently inducing apoptosis. This agent has high hydrophilicity and photostability and shows a favorable toxicity profile over the other triazenes.","Organic Chemical|Pharmacologic Substance"]
["C1258","Triazinate","BAF|Baker's Antifol soluble|Baker's Antifol|Baker's Antifolate|Bakers Antifol|Bakers Antifolate|Benzenesulfonyl fluoride, 3-chloro-4-[4-[2-chloro-4-(4, 6-diamino-2,2-dimethyl-1,3,5-triazin-1(2H)-yl)phenyl]butyl]-, monoethanesulfonate (9CI)|Ethanesulfonic Acid Compound|Ethanesulfonic acid, compd. with 3-chloro-4-[4-[2-chloro-4-(4, 6-diamino-2, 2-dimethyl-s-triazin-1(2H)-yl)phenyl]butyl]benzenesulfonyl fluoride (1:1) (8CI)|Ethanesulfonic acid, compd. with 3-chloro-4-[4-[2-chloro-4-(4,6-diamino-2, 2-dimethyl-s-triazin-1(2H)-yl)phenyl]butyl]benzenesulfonyl fluoride|Ethanesulfonic acid, compd. with 3-chloro-4-[4-[2-chloro-4-(4,6-diamino-2,2-dimethyl-1,3, 5-triazin-1(2H)-yl)phenyl]butyl]benzenesulfonyl fluoride (1:1) (9CI)|Soluble Baker's Antifol|TRIAZINATE|TZT|Triazinate|alpha-(2-chloro-4-(4,6-diamino-2,2-dimethyl-s-trizin-1(2H)-yl)phenoxy)-N,N-dimethyl-m-toluamide ethanesulfonic acid|benzenesulfonyl fluoride, 3-chloro-4-[4-[2-chloro-4-(4, 6-diamino-2,2-dimethyl-1,3,5-triazin-1(2H)-yl)phenyl]butyl]-, monoethanesulfonate (9CI)|ethanesulfonic acid compound with 3-((2-chloro-4-(4,6-diamino-2,2-dimethyl-1,3,5-triazin-1(2H)-yl)phenoxy)methyl)-N,N-dimethylben zamide (1:1)|ethanesulfonic acid, compd. with 3-chloro-4-[4-[2-chloro-4-(4, 6-diamino-2, 2-dimethyl-s-triazin-1(2H)-yl)phenyl]butyl]benzenesulfonyl fluoride (1:1)(8CI)|ethanesulfonic acid, compd. with 3-chloro-4-[4-[2-chloro-4-(4,6-diamino-2, 2-dimethyl-s-triazin-1(2H)-yl)phenyl]butyl]benzenesulfonyl fluoride|ethanesulfonic acid, compd. with 3-chloro-4-[4-[2-chloro-4-(4,6-diamino-2,2-dimethyl-1,3, 5-triazin-1(2H)-yl)phenyl]butyl]benzenesulfonyl fluoride (1:1)(9CI)","A synthetic dihydrotriazine derivative with antineoplastic properties.  As an antifolate agent related to methotrexate (MTX), triazinate inhibits the enzyme dihydrofolate reductase (DHFR), resulting in decreased tetrahydrofolate production and interference with thymidylate synthesis.  Unlike MTX, this agent is not converted to polyglutamate forms. Triazinate also inhibits the transport of folates and may be selectively toxic to MTX-resistant tumor cells. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C903","Triaziquone","TRIAZIQUONE|Triaziquone","An aziridinylbenzoquinone-based alkylating agent with potential antineoplastic activity. The alkylating group in triaziquone becomes activated upon reduction of quinone to the hydroquinone form. This eventually results in the alkylation and crosslinking of DNA, thereby inhibiting DNA replication followed by an induction of apoptosis. In addition, reactive oxygen species may form during redox cycling which may contribute to this agent's cytotoxic activity.","Organic Chemical|Pharmacologic Substance"]
["C1260","Tributyrin","1,2,3-Propanetriyl Butanoate|1,2,3-Tributyrylglycerol|Butanoic Acid 1,2,3-Propanetriyl Ester|Butanoic Acid, 1,2,3-Propanetriyl Ester|Butyryl Triglyceride|Glyceryl Tributyrate|Glyceryl tributyrate|TB|TRIBUTYRIN|Tributyrin|tributyrin","A triglyceride prodrug of butyric acid with potential antineoplastic activity. Butyrate, the active metabolite of tributyrin, inhibits histone deacetylase, resulting in increased differentiation, decreased proliferation, cell cycle arrest, and apoptosis in some tumor cell lines. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1262","Triciribine Phosphate","1, 5-Dihydro-5-methyl-1-(5-O-phosphono-.beta.-D-ribofuranosyl)-1,4,5, 6,8-pentaazaacenaphthylen-3-amine|1, 5-dihydro-5-methyl-1-(5-O-phosphono-beta-D-ribofuranosyl)-1,4,5, 6,8-pentaazaacenaphthylen-3-amine|1,4, 5,6,8-Pentaazaacenaphthylen-3-amine, 1, 5-dihydro-5-methyl-1-(5-O-phosphono-.beta.-D-ribofuranosyl)- (9CI)|1,4, 5,6,8-pentaazaacenaphthylen-3-amine, 1, 5-dihydro-5-methyl-1-(5-O-phosphono-beta-D-ribofuranosyl)- (9CI)|1,4,5,6, 8-Pentaazaacenaphthalen-3-amine, 1, 5-dihydro-5-methyl-1-(5-O-phosphono-.beta.-D-ribofuranosyl)-|1,4,5,6, 8-pentaazaacenaphthalen-3-amine, 1, 5-dihydro-5-methyl-1-(5-O-phosphono-beta-D-ribofuranosyl)|3-Amino-1, 5-dihydro-5-methyl-1-.beta.-D-ribofuranosyl-1,4,5,6, 8-pentaazaacenaphthylene 5'-(dihydrogen phosphate)|3-amino-1, 5-dihydro-5-methyl-1-beta-D-ribofuranosyl-1,4,5,6, 8-pentaazaacenaphthylene 5'-(dihydrogen phosphate)|TCN|TRICIRIBINE PHOSPHATE|Triciribine Phosphate|Triciribine|Tricyclic Nucleoside 5'-Phosphate|Tricycloside Phosphate","The phosphate salt of the synthetic, cell-permeable tricyclic nucleoside triciribine with potential antineoplastic activity. Triciribine inhibits the phosphorylation, activation, and signalling of Akt-1, -2, and -3, which may result in the inhibition of Akt-expressing tumor cell proliferation. Akts are anti-apoptotic serine/threonine-specific protein kinases that phosphorylate and inactivate components of the apoptotic machinery, including Bcl-xL/Bcl-2-associated death promoter (BAD) and caspase 9.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C61987","Trientine Hydrochloride","N,N-bis (2-aminoethyl)-1,2-ethanediamine Dihydrochloride|Syprine|TRIENTINE HYDROCHLORIDE|Trientine Hydrochloride","The hydrochloride salt form of a metal chelating agent with potential anti-angiogenic activity. Trientine chelates excess copper (Cu) ions in the body; the excess copper is subsequently removed from the body through the kidneys. As Cu is an essential cofactor for cuproenzymes, such as superoxide dismutase 1 (SOD1), depletion of copper may inhibit the activation of signal transduction pathways required for cellular proliferation and angiogenesis. In addition, trientine may inhibit copper-induced secretion of interleukin-8 (IL-8).","Pharmacologic Substance"]
["C29858","Triethylenemelamine","TEM|TRIETHYLENEMELAMINE|Triethylene Melamine|Triethylenemelamine","A trisaziridine alkylating agent with antineoplastic and carcinogenic properties.  Used to induce cancer in experimental animal models, triethylenemelamine ethylates DNA, resulting in inhibition of DNA replication, unscheduled DNA synthesis, chromosomal aberrations, and sister chromatid exchanges.  This agent also exhibits reproductive toxicities. (NCI04)","Pharmacologic Substance"]
["C905","Trifluridine","2'-Deoxy-5-trifluoromethyluridine|F3TdR|TRIFLURIDINE|Triflorothymidine|Trifluridine","A fluorinated thymidine analog with potential antineoplastic activity. Trifluridine is incorporated into DNA and inhibits thymidylate synthase, resulting in inhibition of DNA synthesis, inhibition of protein synthesis, and apoptosis. This agent also exhibits antiviral activity. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C102554","Trifluridine/Tipiracil Hydrochloride Combination Agent TAS-102","Lonsurf|TAS-102|Trifluridine/Tipiracil Hydrochloride Combination Agent TAS-102|Trifluridine/Tipiracil","An orally bioavailable combination agent composed of the cytotoxic pyrimidine analog trifluridine (5-trifluoro-2'-deoxythymidine or TFT) and a thymidine phosphorylase inhibitor (TPI) tipiracil hydrochloride, in a molar ratio of 1.0:0.5 (TFT:TPI), with potential antineoplastic activity. After oral administration of TAS-102, TFT is phosphorylated to the active monophosphate form TF-TMP, which binds covalently to the active site of thymidylate synthase, thereby reducing the nucleotide pool levels required for DNA replication. Furthermore, the triphosphate form TF-TTP can be incorporated into DNA, which induces DNA fragmentation and leads to the inhibition of tumor growth. TPI exhibits a dual effect: 1) an anti-angiogenic effect mediated through the inhibition of thymidine phosphorylase, which plays important role in nucleotide metabolism and a variety of development processes, including angiogenesis, 2) increased bioavailability of the normally short-lived antimetabolite TFT by preventing its degradation into the inactive form trifluorothymine (TF-Thy). The synergistic effect of the components in TAS-10 may demonstrate antitumor activity in 5-FU-resistant cancer cells.","Pharmacologic Substance"]
["C29485","Trimelamol","BRN 4261541|Methanol, ((s-triazine-2,4,6-triyl)trimethyltrinitrilo)tri-|Trimelamol|Trimethyloltrimethylmelamine","A synthetic derivative of trimethylmelamine with antineoplastic properties.  An analogue of siderophores (microbial iron chelators), trimelamol induces the formation of a reactive iminium species which may crosslink DNA. (NCI04)","Pharmacologic Substance"]
["C1264","Trimethylcolchicinic Acid","Colchicinic Acid, Trimethyl-|Desacetyl Colchicine D-tartrate|Desacetylcholchiceine|N-Deacetylcolchiceine|SKF 284|TMCA|TRIMETHYLCOLCHICINIC ACID|Trimethylcolchicinic Acid Methyl Ether d-tartrate|Trimethylcolchicinic Acid|Trimethylcolchicinic acid","A colchicine analog with potential antineoplastic activity.  Trimethylcolchicinic acid binds to tubulin, inhibiting its polymerization into microtubules and preventing cell division. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1314","Trimetrexate","2,4-Quinazolinediamine, 5-methyl-6-[[(3,4,5-trimethoxyphenyl)amino]methyl]-|5-Methyl-6-[[(3,4,5-trimethoxyphenyl)amino]methyl]-2,4-quinazolinediamine|CI-898|TMQ|TRIMETREXATE|Trimetrexate|Trimexate","A methotrexate derivative with potential antineoplastic activity.  Trimetrexate inhibits the enzyme dihydrofolate reductase, thereby preventing the synthesis of purine nucleotides and thymidylate, with subsequent inhibition of DNA and RNA synthesis.  Trimetrexate also exhibits antiviral activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1265","Trimetrexate Glucuronate","2,4-Diamino-5-methyl-6-[(3,4,5-trimethoxyanilino)methyl]quinazoline mono-D-glucuronate|Neutrexin|TRIMETREXATE GLUCURONATE|Trimetrexate Glucuronate|trimetrexate glucuronate","A lipid soluble methotrexate derivative with potential antineoplastic activity.  Trimetrexate glucuronate inhibits the enzyme dihydrofolate reductase, thereby preventing the synthesis of purine nucleotides and thymidylate, with subsequent inhibition of DNA and RNA synthesis.  Trimetrexate glucuronate also exhibits antiviral activity. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1266","Trioxifene","(3,4-Dihydro-2-(4-methoxyphenyl)-1-naphthalenyl)(4-(2-(1-pyrrolidinyl)ethoxy)phenyl) Methanone|TRIOXIFENE|Trioxifene","A nonsteroidal selective estrogen receptor modulator (SERM) with potential antineoplastic activity.  Trioxifene competes with estradiol in binding to estrogen receptor alpha (ER alpha), thereby inhibiting ER alpha-mediated signal transduction and gene expression. In addition, trioxifene exerts intrinsic estrogenic activity depending on the tissue. Clinical development of trioxifene has not been preceded due to its side effect profile and lack of increased efficacy over tamoxifen.","Organic Chemical|Pharmacologic Substance"]
["C111762","Triptolide Analog","Minnelide|Triptolide Analog","A water soluble analog of the diterpenoid triepoxide triptolide isolated from the Chinese herb Tripterygium wilfordii Hook.f., with potential antineoplastic activity. Upon intravenous administration, the triptolide analog inhibits heat shock protein 70 (HSP70) and prevents HSP70-mediated inhibition of apoptosis. This leads to both the induction of apoptosis and a reduction of cancer cell growth. HSP70, a molecular chaperone upregulated in various cancer cells, plays a key role in the inhibition of caspase-dependent and -independent apoptosis.","Pharmacologic Substance"]
["C1267","Triptorelin","6-D-Tryptophan-LH-RH|6-D-Tryptophanluteinizing Hormone-releasing Factor|AY-25650|CL-118,532|Decapeptyl|Detryptoreline|TRIPTORELIN|Triptorelin|triptorelin","A synthetic decapeptide agonist analog of luteinizing hormone releasing hormone (LHRH).  Possessing greater potency than endogenous LHRH, triptorelin reversibly represses gonadotropin secretion. After chronic, continuous administration, this agent effects sustained decreases in LH and FSH production and testicular and ovarian steroidogenesis. Serum testosterone concentrations may fall to levels typically observed in surgically castrated men. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1758","Tritylcysteine","3-Tritylthio-L-Alanine|S-Trityl-L-Cysteine|S-Trityl-L-cysteine|Tritylcysteine","A derivative of cysteine with antimitotic activity and potential antineoplastic activity. (NCI04)","Amino Acid, Peptide, or Protein"]
["C99132","Tri-virus/GD2-specific Allogeneic Cytotoxic T-lymphocytes","Tri-virus/GD2-specific Allogeneic Cytotoxic T-lymphocytes","Allogeneic tri-viral specific, Epstein-Barr virus (EBV), cytomegalovirus (CMV) and adenovirus (Ad), cytotoxic T-lymphocytes (tV-CTLs) expressing a chimeric antigen receptor (CAR) specific for disialoganglioside GD2 with potential antineoplastic activity. Tri-virus/GD2-specific allogeneic CTLs are produced by transducing tV-CTLs with a GD2-specific CAR retroviral vector. Upon administration, after an allogeneic hematopoietic stem cell transplant, these CTLs may be selective towards EBV, CMV, and Ad-infected cells and GD2-expressing tumor cells. The human glycosphingolipid GD2 is a tumor associated antigen overexpressed on the surface of all tumors of neuroectodermal origin.","Cell|Pharmacologic Substance"]
["C80491","TRK Inhibitor AZD6918","AZD6918|TRK Inhibitor AZD6918","An orally available liquid suspension containing the tropomyosin receptor kinase (Trk) inhibitor AZD6918 with potential antineoplastic activity. AZD6918 binds to Trk, thereby preventing neurotrophin-Trk interaction and Trk activation, and may eventually result in cell cycle arrest and apoptosis of tumor cells that express Trk. Trk, a receptor tyrosine kinase activated by neurotrophins, is mutated in a variety of cancer cell types and plays an important role in tumor cell growth and survival.","Pharmacologic Substance"]
["C115977","Trk Inhibitor LOXO-101","LOXO-101|Trk Inhibitor LOXO-101","An orally available, tropomyosin receptor kinase (Trk) inhibitor, with potential antineoplastic activity. Upon administration, LOXO-101 binds to Trk, thereby preventing neurotrophin-Trk interaction and Trk activation, which results in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress Trk. Trk, a receptor tyrosine kinase activated by neurotrophins, is mutated in a variety of cancer cell types and plays an important role in tumor cell growth and survival.","Pharmacologic Substance"]
["C123882","Trodusquemine","(24R)-3beta-((3-((4-((3-aminopropyl)amino)butyl)amino)propyl)amino)-7alpha-hydroxy-5alpha-cholestan-24-yl Hydrogen Sulfate|Cholestane-7,24-diol, 3-((3-((4-((3-aminopropyl)amino)butyl)amino)propyl)amino)-, 24-(Hydrogen Sulfate), (3beta,5alpha,7alpha,24R)-|MSI-1436|MSI-1436C|TRODUSQUEMINE|Trodusquemine","A naturally-occurring cholestane and non-competitive, allosteric inhibitor of protein tyrosine phosphatase 1B (PTP1B), with potential hypoglycemic, anti-diabetic, anti-obesity, and antineoplastic activities. Upon administration, trodusquemine selectively targets and inhibits PTP1B, thereby preventing PTP1B-mediated signaling. This prevents the dephosphorylation of the insulin receptor, which improves insulin signaling and insulin sensitivity, and decreases blood glucose levels. In susceptible cancer cells, inhibition of PTP1B causes a reduction of tumor cell proliferation. In addition, as trodusquemine can cross the blood-brain barrier (BBB), it centrally suppresses appetite and causes weight loss. PTP1B, a tyrosine phosphatase, is elevated in certain cancer cells; it is specifically upregulated in human epidermal growth factor receptor 2 (HER2)-driven cancers where it promotes cell growth, and is correlated with a poor prognosis and increased metastatic potential. In diabetes, PTP1B upregulation plays a major role in insulin resistance.","Pharmacologic Substance"]
["C1268","Trofosfamide","2-[bis(2-chloroethyl)amino]-3-(2-chloroethyl)tetrahydro-2H-1,3,2-oxaphosphorine 2-oxide|2H-1,3,2-Oxazaphosphorin-2-amine, N,N, 3-tris(2-chloroethyl)tetrahydro-, 2-oxide, (+)-|2H-1,3,2-Oxazaphosphorin-2-amine, N,N, 3-tris(2-chloroethyl)tetrahydro-, 2-oxide, (-)-|A-4828|Genoxal Trofosfamida|Ixoten|N,N,3-tris(2-chloroethyl)tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide|N,N,N'-tris(2-chloroethyl)-N',O-propylene phosphoric acid ester diamide|TROFOSFAMIDE|Trilophosphamide|Trofosfamid|Trofosfamide|Trophosphamide|Z 4828|Z-4828","An orally bioavailable oxazaphosphorine prodrug with antineoplastic activity. Trofosfamide (TFF) is metabolized predominantly to the cyclophosphamide analogue ifosfamide (IFO), which is then metabolized by liver cytochrome P450s to the active isophosphoramide mustard (IPM). IPM alkylates DNA to form DNA-DNA cross-links, which may result in inhibition of DNA, RNA and protein synthesis, and ultimately lead to tumor cell apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C1522","Troglitazone","5-((4-((3,4-dihydro-6-hydroxy-2,5,7,8-tetramethyl-2H-1-benzopyran-2-yl)methoxy)phenyl)methyl)-2,4-Thiazolidinedione|5-[4-[(6-Hydroxy-2,5,7,8-tetramethylchroman-2-yl)methoxy]benzyl]-2,4-thiazolidinedione|CI-991|CS-045|Prelay|Rezulin|Romozin|TROGLITAZONE|Troglitazone","An orally-active thiazolidinedione with antidiabetic and hepatotoxic properties and potential antineoplastic activity.  Troglitazone activates peroxisome proliferator-activated receptor gamma (PPAR-gamma), a ligand-activated transcription factor, thereby inducing cell differentiation and inhibiting cell growth and angiogenesis.  This agent also modulates the transcription of insulin-responsive genes, inhibits macrophage and monocyte activation, and stimulates adipocyte differentiation. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C99161","Tropomyosin Receptor Kinase Inhibitor AZD7451","AZD7451|TRK Inhibitor AZD7451|Tropomyosin Receptor Kinase Inhibitor AZD7451","A tropomyosin receptor kinase (TRK) inhibitor with potential antineoplastic activity. AZD7451 binds to TRK, thereby preventing the neurotrophin-TRK interaction and subsequent TRK activation. This may eventually result in an inhibition of tumor cell proliferation in TRK-expressing tumor cells. TRK, a receptor tyrosine kinase activated by neurotrophins, is mutated in a variety of cancer cell types and plays an important role in tumor cell growth, invasion and survival.","Pharmacologic Substance"]
["C1438","Troxacitabine","2(1H)-Pyrimidinone, 4-amino-1-((2S,4S)-2-(hydroxymethyl)-1,3-dioxolan-4-yl)-|BCH-4556|L-Oddc|TROXACITABINE|Troxacitabine|Troxatyl|troxacitabine","A dioxolane derivative and a novel L-configuration deoxycytidine analogue with potent antineoplastic activity. When incorporated into growing chain during DNA replication, troxacitabine stops DNA polymerization due to its unnatural L-configuration, in contrast to the normal nucleotides with D-configuration. As a result, this agent terminates DNA synthesis upon incorporated into DNA molecules, and consequently interrupts tumor cell proliferation.","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C99114","TRP2 mRNA-electroporated Autologous Langerhans-type Dendritic Cell Vaccine","TRP2 mRNA-electroporated Autologous Langerhans-type Dendritic Cell Vaccine","A cancer cell vaccine composed of autologous human Langerhans-type dendritic cells (also known as Langerhans cells or LCs) that are electroporated with mRNA encoding full-length murine tyrosinase-related peptide 2 (TRP2), with potential antineoplastic and immunomodulating activities. Upon vaccination, the TRP2 mRNA-electroporated autologous Langerhans-type dendritic cell vaccine may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against TRP2-expressing tumor cells. TRP2, a tautomerase involved in the synthesis of melanin, is only expressed in melanomas, melanocytes, and the retina. The LCs are differentiated from CD34 positive hematopoietic progenitor cells.","Pharmacologic Substance"]
["C101525","TRPV6 Calcium Channel Inhibitor SOR-C13","SOR-C13|TRPV6 Calcium Channel Inhibitor SOR-C13","An inhibitor of transient receptor potential cation channel vanilloid family member 6 (TRPV6, CaT1 or CATL) with potential antineoplastic activity. TRPV6 calcium channel inhibitor SOR-C13 binds to TRPV6 and prevents the influx of calcium ions into TRPV6-expressing tumor cells. This inhibits the activation of nuclear factor of activated T-cell (NFAT) transcription complex which may result in an inhibition of calcium-dependent cancer cell proliferation and an induction of apoptosis in tumor cells overexpressing TRPV6. The TRPV6 ion channel plays a key role in calcium homeostasis and is highly selective for calcium compared to other cations; it is overexpressed in a variety of tumors and initiates tumor cell growth, proliferation and metastases.","Pharmacologic Substance"]
["C82384","TSP-1 Mimetic Fusion Protein CVX-045","CVX-045|TSP-1 Mimetic Fusion Protein CVX-045|Thrombospondin-1 Mimetic Fusion Protein CVX-045","A fusion protein containing two thrombospondin (TSP-1)-derived nonamer peptides covalently attached, via a proprietary diketone linker, to a proprietary humanized catalytic monoclonal aldolase monoclonal antibody with potential antiangiogenic and antineoplastic activities.  The TSP-1 mimetic peptide moieties of TSP-1 mimetic fusion protein CVX-045 bind to TSP-1 receptors, such as CD36, and inhibit tumor angiogenesis, which may result in the inhibition of tumor cell proliferation. The proprietary humanized catalytic monoclonal aldolase monoclonal antibody contains reactive lysine residues in its binding sites, which react covalently with compounds having a diketone function; the TSP-1 mimetic peptide moieties are then covalently attached to the diketone linkers via a proprietary spacer.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C61566","TTI-237","TTI 237|TTI-237","A small synthetic molecule of triazolopyrimidine derivative with potential antitumor activity. With a novel mechanism of action distinct from the action of other vinca alkaloid compounds, TTI-237 specifically binds to tubulin at the vinca site, and promotes the polymerization of tubulin into microtubules. TTI-237 stabilizes tubulin and inhibits microtubule disassembly. This results in cell cycle arrest at the G2/M phase, and leading to cell death.","Organic Chemical|Pharmacologic Substance"]
["C911","Tubercidin","4-Amino-7-.beta.-D-ribofuranosyl-7H-pyrrolo[2, 3-d]pyrimidine|4-Amino-7.beta.-D-ribofuranosyl-7H-pyrrolo(2, 3-d)pyrimidine|4-amino-7-beta-D-ribofuranosyl-7H-pyrrolo[2,3-d]pyrimidine|7-Deazaadenosine|7-beta-D-ribofuranosyl-7H-pyrrolo[2,3-d]pyrimidin-4-amine|7-deazaadenosine|7H-Pyrrolo(2,3-d)pyrimidine, 4-amino-7.beta.-D-ribofuranosyl-|7H-Pyrrolo[2,3-d]pyrimidine, 4-amino-7-.beta.-D-ribofuranosyl-|TUBERCIDIN|Tubercidin|U 10071|U-10071","An antibiotic and adenosine analog isolated from the bacterium Streptomyces tubercidicus with potential antineoplastic activity.  Tubercidin is incorporated into DNA and inhibits polymerases, thereby inhibiting DNA replication and RNA and protein synthesis.  This agent also exhibits antifungal and antiviral activities. (NCI04)","Antibiotic|Nucleic Acid, Nucleoside, or Nucleotide"]
["C78842","Tubulin Inhibitor ALB 109564(a)","12'-methylthiovinblastine dihydrochloride|ALB 109564(a)|Tubulin Inhibitor ALB 109564(a)","A semi-synthetic derivative of the vinka alkaloid vinblastine with potential antineoplastic activity. Tubulin inhibitor ALB 109564(a) binds to tubulin monomers and inhibits microtubule formation, resulting in disruption of mitotic spindle assembly and arrest of tumor cells in the G2/M phase of the cell cycle.","Pharmacologic Substance"]
["C101264","Tubulin Polymerization Inhibitor CKD-516","(S)-N-(4-(3-(1H-1,2,4-Triazol-1-yl)-4-(3,4,5-trimethoxybenzoyl)phenyl)thiazol-2-yl)-2-amino-3-methylbutanamide Hydrochloride|CKD-516|Tubulin Polymerization Inhibitor CKD-516","A benzophenone derivative and water soluble valine prodrug of the tubulin binding agent S516, with potential tubulin-inhibiting, vascular-disrupting and antineoplastic activity. Upon administration, tubulin polymerization inhibitor CKD-516 is converted into its active metabolite S-516 that binds to tubulin and prevents its polymerization in tumor blood vessel endothelial cells and tumor cells. This blocks the formation of the mitotic spindle and leads to cell cycle arrest at the G2/M phase. As a result, this agent disrupts the tumor vasculature and tumor blood flow, deprives tumor cells of nutrients and induces tumor cell apoptosis. In addition, this agent has a direct cytotoxic effect on tumor cells by inhibiting tubulin polymerization.","Pharmacologic Substance"]
["C71525","Tubulin-Binding Agent SSR97225","Tubulin-Binding Agent SSR97225","An antimitotic tubulin-binding agent with potential antineoplastic activity. Tubulin-binding agent SSR97225 binds to tubulin, arresting the cell cycle at the G2/M checkpoint and preventing mitosis.","Pharmacologic Substance"]
["C2630","Tucotuzumab Celmoleukin","EMD 273066|EMD-273066|KSA-IL-2|KSA-Interleukin-2 Fusion Protein|KSA-interleukin-2|TUCOTUZUMAB CELMOLEUKIN|Tucotuzumab Celmoleukin|huKS-IL2 Fusion Protein","A recombinant fusion protein comprised of a human monoclonal antibody directed against the epithelial cell adhesion molecule (EpCAM or KS) linked to an active interleukin-2 (IL2) molecule with potential antineoplastic activity. Tucotuzumab Celmoleukin recognizes and binds to EpCAM, a cell surface epithelial protein that is expressed on a wide variety of cancer cells, thereby concentrating IL2 in EpCAM-expressing tumor tissue. Subsequently, the localized IL2 moiety of the fusion protein may stimulate a cytotoxic T-cell antitumor immune response.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2817","Tumor Cell Vaccine plus BCG","Tumor Cell Vaccine plus BCG","A mixture of allogeneic or autologous tumor cells and bacillus Calmette-Guerin (BCG) in a liquid vehicle with potential antineoplastic activity.  Vaccination of the host with tumor cell vaccine plus BCG may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against similar host tumor cells, resulting in decreased tumor growth. The BCG component serves as an adjuvant, a nonspecific stimulator of the immune response. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C107681","Tumor Cell-derived Dribbles Vaccine","Tumor Cell-derived Dribbles Vaccine|Tumor-derived DRiPs-containing Blebs Vaccine","An autophagosome-enriched cancer vaccine composed of short lived proteins (SLiPs) and defective ribosomal products (DRiPs) derived from tumor cells, with potential immunostimulating and antineoplastic activities. The Dribbles are DriPs- and SLiPs-filled autophagosomes that are made by treating cancer cells with both a proteasome inhibitor, to prevent protein degradation, and an autophagy inducer, which causes the accumulation of DriPs, SLiPs, and their immunogenic fragments. Upon administration of a Dribbles vaccine, the proteins or antigen fragments in Dribbles may stimulate the immune system to mount cytotoxic T-lymphocyte (CTL) and helper T-lymphocyte responses against the cancer-associated antigens (TAAs).","Immunologic Factor|Pharmacologic Substance"]
["C29478","Tumor Infiltrating Lymphocytes-N2-Transduced","Tumor Infiltrating Lymphocytes-N2-Transduced","A preparation of lymphocytes harvested from a patient and genetically modified ex vivo for use in gene therapy for the patient's cancer.  Ex vivo, the lymphocytes are transduced with the N2 retroviral vector, which is modified to express a gene whose protein product either kills tumor cells or elicits specific anti-tumor immunity. Genetically modified lymphocytes are infused back into the patient from whom they were harvested, locate to the tumor site, and express the candidate protein that kills tumor cells or stimulates host anti-tumor immunity. (NCI04)","Cell|Pharmacologic Substance"]
["C124055","Tumor Peptide-loaded Myeloid Dendritic Cells","Tumor Peptide-loaded Myeloid Dendritic Cells|Tumor Peptide-loaded myDC Vaccine","A cell-based cancer vaccine composed of myeloid dendritic cells (myDCs) pulsed with tumor peptides with potential immunostimulatory and antineoplastic activities. Upon administration, the tumor peptide-loaded myDCs stimulate a specific cytotoxic T-lymphocyte (CTL) response against the tumor cells, resulting in tumor cell lysis.","Cell|Pharmacologic Substance"]
["C103193","Tumor-Cells Apoptosis Factor Hormone-Peptide","Nerofe|Tumor-Cells Apoptosis Factor Hormone-Peptide","A synthetic 14-amino acid peptide derived from a novel human peptide hormone, Tumor-Cells Apoptosis Factor (TCApF), with potential antineoplastic activity. Upon intravenous administration, tumor-cells apoptosis factor hormone-peptide binds to the T1/ST2 receptor (IL1RL1) and activates both caspase 8 and Bcl-2 mediated apoptosis, in addition to the activation of p38 MAPK and JNK signaling cascades in tumor cells. Furthermore, this agent inhibits angiogenesis by suppressing the expressions of vascular endothelial growth factor A (VEGFA) and fms-related tyrosine kinase 1 (VEGFR1).  Tumor-cells apoptosis factor hormone-peptide also modulates immune system responses via increasing the expressions of interleukin-10 and anti-angiogenic interleukin. T1/ST2 receptor, a member of the toll/interleukin-1 receptor superfamily, is overexpressed in certain cancer cells.","Pharmacologic Substance"]
["C128892","Type-1 Polarized Dendritic Cell-induced Antigen-specific Autologous Cytotoxic T Lymphocytes","Autologous DC1-CTL|DC1-induced Antigen-specific Autologous CTLs|Type-1 Polarized DC-induced Antigen-specific Autologous CTLs|Type-1 Polarized Dendritic Cell-induced Antigen-specific Autologous Cytotoxic T Lymphocytes","A preparation of autologous cytotoxic T-lymphocytes (CTL), specifically reactive to melanoma-associated antigen 3 (MAGE-3), MAGE-4, survivin, human epidermal growth factor receptor 2 (HER2; ERBB2) and cyclooxygenase-2 (COX-2), with potential immunomodulating activity. Peripheral blood mononuclear cells (PBMCs) are collected from the patient. Subsequently, autologous dendritic cells (DCs) are separated, treated with a certain combination of cytokines to produce polarized type-1 DCs (DC1), and then are loaded with MAGE-3/MAGE-4/survivin/HER2/COX-2 CTL epitope peptides. In turn, autologous CTLs are collected, exposed ex vivo to the antigen-loaded DC1s and subsequently expanded in vitro. Upon re-infusion of the DC1-induced MAGE-3/MAGE-4/survivin/HER2/COX-2-specific autologous CTLs, the CTLs target and lyse tumor cells expressing the tumor-associated antigens (TAAs). Exposure to DC1s generates more potent CTLs and thus induces a more potent CTL response against TAA-expressing tumor cells. The targeted TAAs play key roles in cellular proliferation and are overexpressed by a variety of cancer cell types.","Cell|Pharmacologic Substance"]
["C77856","Tyroserleutide","CMS 024|Tyroserleutide|YSL","A tripeptide consisting of tyrosine, serine, and leucine with potential antineoplastic activity. Although the mechanism of its antitumor activity has yet to be fully elucidated, tyroserleutide appears to inhibit the expression of ICAM-1 (CD54), a cell adhesion factor of the immunoglobulin (Ig) superfamily that plays an important role in the invasion, adhesion, and metastasis of tumor cells. In addition, this agent may influence the Ca2+/calmodulin pathway, inhibiting phosphatidylinositol 3 kinase (PI3K); PI3K is upregulated in tumor cells and is involved in cellular proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2401","Tyrosinase Peptide","Tyrosinase Peptide|Tyrosinase Peptides|tyrosinase peptide","One of a number of recombinant peptides consisting of amino acid residues of the enzyme tyrosinase, a protein frequently expressed by melanoma cells.  Vaccination with tyrosinase peptide may stimulate cytotoxic T lymphocyte response against tyrosinase-expressing tumor cells, resulting in decreased tumor growth. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48630","Tyrosinase:146-156 Peptide","Tyrosinase:146-156 Peptide","A synthetic peptide consisting of amino acid residues 146 through 156 of the enzyme tyrosinase, a protein frequently expressed by melanoma cells, with antitumor activity. Vaccination with tyrosinase:146-156 peptide may stimulate cytotoxic T lymphocyte response against tyrosinase-expressing tumor cells, resulting in decreased tumor growth and cell lysis.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C2384","Tyrosinase-KLH","Tyrosinase-KLH","A peptide vaccine containing a tyrosinase epitope conjugated with keyhole lymphocyte hemocyanin (KLH) with potential antineoplastic activity. Tyrosinase, one of the melanoma differentiation antigens, is the rate-limiting enzyme for melanin synthesis. This tyrosine epitope is conjugated with KLH, which serves as an immunostimulant and a hapten carrier, to enhance immune recognition. Vaccination with tyrosinase-KLH peptide vaccine may produce anti-tyrosinase antibodies as well as elicit a cytotoxic T lymphocyte (CTL) response against cells expressing tyrosinase antigen, resulting in decreased tumor growth.","Pharmacologic Substance"]
["C70981","Tyrosine Kinase Inhibitor OSI-930","OSI-930|Tyrosine Kinase Inhibitor OSI-930","A selective thiophene-derived tyrosine kinase inhibitor with potential antineoplastic activity. Tyrosine kinase inhibitor OSI-930 inhibits stem cell factor receptor (c-Kit) and the vascular endothelial growth factor receptor 2 (VEGFR2), which may result in the inhibition of both tumor cell proliferation and tumor angiogenesis. Both c-Kit and VEGFR2 are overexpressed in a variety of cancers.","Pharmacologic Substance"]
["C1725","Tyrosine Kinase Inhibitor SU5402","3-[(3-(2-carboxyethyl)-4-methylpyrrol-2-yl)methylene]-2-indolinone|SU 5402|Tyrosine Kinase Inhibitor SU5402","An indolinone-based small molecule selective tyrosine kinase inhibitor with potential antineoplastic activity. SU5402 blocks the activities of vascular endothelial growth factor receptors (VEGFR) and fibroblast growth factor 1 (FGFR1) via competing with ATP for the specific binding site within the catalytic domain of these receptors. This agent was shown to inhibit cell growth, decrease cell viability in dose-dependent manner, and induce apoptosis.","Organic Chemical|Pharmacologic Substance"]
["C68929","Tyrosine Kinase Inhibitor XL228","Tyrosine Kinase Inhibitor XL228|XL228","A synthetic molecule that targets multiple tyrosine kinases with potential antineoplastic activity. Tyrosine kinase inhibitor XL228 binds to and inhibits the activities of multiple tyrosine kinases, such as the insulin-like growth factor 1 receptor (IGF1R), Src tyrosine kinase, and Bcr-Abl tyrosine kinase. Blockade of these kinases may result in the inhibition of tumor angiogenesis, cell proliferation, and metastasis. In addition, this agent may be a potent inhibitor of the T315I mutant form of the Abl protein, which is associated with the resistance of chronic myelogenous leukemia (CML) to other tyrosine kinase inhibitors. IGF1R and Src tyrosine kinases are upregulated in many tumor cells and play important roles in tumor cell proliferation and metastasis. Bcr-Abl translocation leads to constitutive activation of ABL kinase and is commonly associated with Philadelphia-positive acute lymphocytic leukemia (ALL).","Pharmacologic Substance"]
["C113788","UAE Inhibitor TAK-243","AOB87172|MLN7243|TAK-243|UAE Inhibitor TAK-243","A small molecule inhibitor of ubiquitin-activating enzyme (UAE), with potential antineoplastic activity. UAE inhibitor TAK-243 binds to and inhibits UAE, which prevents both protein ubiquitination and subsequent protein degradation by the proteasome. This results in an excess of proteins in the cells and may lead to endoplasmic reticulum (ER) stress-mediated apoptosis. This inhibits tumor cell proliferation and survival. UAE, also called ubiquitin E1 enzyme (UBA1; E1), is more active in cancer cells than in normal, healthy cells.","Pharmacologic Substance"]
["C1015","Ubenimex","Bestatin|L-Leucine, N-(3-amino-2-hydroxy-1-oxo-4-phenylbutyl)-, [S-(R*,S*)]-|N-[(2S,3R)-4-phenyl-3-amino-2-hydroxybutyryl]-L-leucine|NK 421|UBENIMEX|Ubenimex|[(2S,3R)-3-amino-2-hydroxy-4-phenylbutanoyl]-L-leucine|[S-(R*,S*)]-N-(3-amino-2-hydroxy-1-oxo-4-phenylbutyl)-L-leucine","A microbial metabolite and dipeptide with potential immunomodulatory and antitumor activities. Ubenimex competitively inhibits many aminopeptidases, including B, N and leucine aminopeptidases. Aminopeptidases has been implicated in the process of cell adhesion and invasion of tumor cells. Therefore, inhibiting aminopeptidases may partially attribute to the antitumor effect of ubenimex. This agent also activates T lymphocyte, macrophage and bone marrow stem cell as well as stimulates release of interleukin-1 and -2, thus further enhances its antitumor activity.","Amino Acid, Peptide, or Protein|Antibiotic"]
["C91078","Ublituximab","LFB-R603|TG-1101|TG-20|TGTX-1101|Ublituximab","A chimeric recombinant IgG1 monoclonal antibody directed against human CD20 with potential antineoplastic activity. Ublituximab specifically binds to the B cell-specific cell surface antigen CD20, thereby potentially inducing a B cell-directed complement dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC) against CD20-expressing B cells, leading to B cell apoptosis. CD20 is a non-glycosylated cell surface phosphoprotein that is exclusively expressed on B cells during most stages of B cell development and is often overexpressed in B-cell malignancies. Ublituximab has a specific glycosylation profile, with a low fucose content, that may enhance its ADCC response against malignant B cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C102851","Ulinastatin","UTI|Ulinastatin|Urinary Trypsin Inhibitor","A multivalent Kunitz-type serine protease inhibitor derived from human urine, with potential protective, anti-fibrinolytic and anticoagulant activities. Upon administration, ulinastatin (or urinary trypsinogen inhibitor) inhibits the activities of a variety of enzymes, including trypsin, chymotrypsin, thrombin, kallikrein, plasmin, elastase, cathepsin, lipase, hyaluronidase, factors IXa, Xa, XIa, and XlIa, and polymorphonuclear leukocyte elastase. In addition, ulinastatin inhibits the excessive release of proinflammatory mediators, such as tumor necrosis factor-alpha, interleukin-6 and -8, and chemokines. Altogether, this agent may improve the microcirculation, perfusion and function of tissues and may protect organ injury.","Pharmacologic Substance"]
["C104744","Ulixertinib","1H-Pyrrole-2-carboxamide, 4-(5-chloro-2-((1-methylethyl)amino)-4-pyridinyl)-N-((1S)-1-(3-chlorophenyl)-2-hydroxyethyl)-|BVD-523|ULIXERTINIB|Ulixertinib|VRT752271","An orally available inhibitor of extracellular signal-regulated kinase (ERK) 1 and 2, with potential antineoplastic activity. Upon oral administration, BVD-523 inhibits both ERK 1 and 2, thereby preventing the activation of ERK-mediated signal transduction pathways. This results in the inhibition of ERK-dependent tumor cell proliferation and survival. The mitogen-activated protein kinase (MAPK)/ERK pathway is often upregulated in a variety of tumor cell types and plays a key role in tumor cell proliferation, differentiation and survival.","Pharmacologic Substance"]
["C95755","Ulocuplumab","BMS 936564|MDX-1338|Ulocuplumab","An orally bioavailable monoclonal antibody against CXC Chemokine Receptor 4 (CXCR4) with potential antineoplastic activity. Ulocuplumab binds to the chemokine receptor CXCR4, preventing the binding of stromal derived factor-1 (SDF-1) to the CXCR4 receptor and subsequent receptor activation, which may result in decreased tumor cell proliferation and migration. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types.","Pharmacologic Substance"]
["C118949","Umbilical Cord Blood-derived Natural Killer Cells","Cord Blood NK Cells|Umbilical Cord Blood-derived NK Cells|Umbilical Cord Blood-derived Natural Killer Cells","A population of allogeneic, cytokine-differentiated, highly lytic natural killer (NK) cells derived from CD34+ cells isolated from human umbilical cord blood (UCB) with potential cytotoxic activity. CD34+ hematopoietic stem cells (HSC) are isolated from human UCB mononuclear cells, differentiated into mature, highly lytic, CD3- CD56+ NK cells, by a specific combination of cytokines that includes stem cell factor (SCF), fms-related tyrosine kinase 3 ligand (Flt3-L), interleukin-15 (IL-15) and insulin-like growth factor-1 (IGF-1), and expanded ex vivo. Upon administration, the UCB-derived NK cells may lyse cancer cells.","Cell|Pharmacologic Substance"]
["C113799","Uncaria tomentosa Extract","Cat's Claw Herbal Extract|Uncaria tomentosa Extract","An extract of Uncaria tomentosa (U. tomentosa), also called Cat's claw, a native Amazonian plant belonging to the Rubiaceae species, with potential anti-inflammatory, immunomodulating, antioxidant and antineoplastic activities. Although the exact mechanism(s) by which U. tomentosa extract exerts its effect(s) has yet to be fully elucidated, this extract may inhibit the proliferation of certain types of cancer cells. This extract may modulate inflammatory and immune responses through the stimulation of T- and B-lymphocytes and certain cytokines, including interleukin (IL)-1, IL-6 and tumor necrosis factor-alpha (TNF-a). Components in U. tomentosa may both induce repair of chemically-induced DNA damage and scavenge free radicals, which may protect against reactive oxygen species (ROS)-mediated cellular damage. In addition, this extract stimulates myelopoiesis, which may prevent chemotherapy-induced neutropenia.","Pharmacologic Substance"]
["C91083","Uracil Ointment","Uracil Ointment","A 0.1% topical formulation of uracil used potentially to lower the incidence of hand-foot syndrome (HFS) (or palmar-plantar erythrodysesthesia) during 5-fluorouracil (5-FU) or 5-FU prodrug capecitabine chemotherapy. Upon local administration of uracil ointment to the skin, uracil competes with capecitabine or 5-FU as substrates for the activating enzyme thymidine phosphorylase and the metabolizing enzyme dihydropyrimidine dehydrogenase. This may prevent the production of 5-FU as well as the breakdown of 5-FU into the toxic metabolites locally. As the 5-FU metabolites are responsible for the presentation of HFS, inhibiting their formation may prevent this adverse effect. By applying a high concentration of uracil locally, the skin toxicities of 5-FU may be countered while preserving the systemic anti-cancer activity of the 5FU.","Pharmacologic Substance"]
["C62449","Urelumab","Anti-4-1BB Monoclonal Antibody|Anti-CD137 Monoclonal Antibody|BMS-663513|Immunoglobulin G4, Anti-(Human Receptor 4-1BB) (Human Gamma-Chain), Disulfide with Human Kappa-Chain, Dimer|URELUMAB|Urelumab","A fully human agonistic monoclonal antibody targeting the CD137 receptor with potential immunostimulatory and antineoplastic activities. Anti-CD137 monoclonal antibody specifically binds to and activates CD137-expressing immune cells, stimulating an immune response, in particular a cytotoxic T cell response, against tumor cells. CD137 is a member of the tumor necrosis factor (TNF)/nerve growth factor (NGF) family of receptors and is expressed by activated T- and B-lymphocytes and monocytes; its ligand has been found to play an important role in the regulation of immune responses.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C74087","URLC10 Peptide Vaccine","URLC10 Peptide Vaccine","A cancer vaccine containing URLC10 (up-regulated lung cancer 10) epitopes with potential immunostimulatory and antineoplastic activities. Upon administration, URL peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against URLC10-expressing tumor cells. Up-regulated in lung and esophageal cancers, the function of URLC10 is unknown.","Pharmacologic Substance"]
["C95212","URLC10-CDCA1-KOC1 Multipeptide Vaccine","URLC10-CDCA1-KOC1 Multipeptide Vaccine","A cancer vaccine containing multiple peptide epitopes with potential immunostimulatory and antitumor activities. Peptide epitopes in this vaccine are derived from, URLC10 (up-regulated lung cancer 10), CDCA1 (cell division cycle-associated protein 1), KOC1 (IGF II mRNA Binding Protein 3). Upon administration, URLC10-CDCA1-KOC1 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing URLC10, CDCA1, KCO1 peptides, resulting in cell lysis and decreased tumor growth.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C74088","URLC10-TTK-KOC1-VEGFR1-VEGFR2 Multipeptide Vaccine","URLC10-TTK-KOC1-VEGFR1-VEGFR2 Multipeptide Vaccine","A cancer vaccine containing five peptide epitopes with potential immunostimulatory and antitumor activity. Peptide epitopes in this vaccine are derived from: URLC10 (up-regulated lung cancer 10), TTK (TTK protein kinase), KOC1 (IGF II mRNA Binding Protein 3) and VEGFRs (vascular endothelial growth factor receptors) 1 and 2. Upon administration, URLC10-TTK-KOC1-VEGFR1-VEGFR2 multipeptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against tumor cells expressing URLC10, TTK, KCO1, VEGFR 1 and 2 peptides, resulting in cell lysis and decreased tumor growth.","Pharmacologic Substance"]
["C91709","Urokinase-Derived Peptide A6","A6|Urokinase-Derived Peptide A6|uPA-derived Peptide A6|urokinase plasminogen activator (uPA)-derived peptide A6","An octapeptide (amino acids 136-143) derived from the proteolytic enzyme urokinase plasminogen activator (uPA), with potential antineoplastic activity. A6 is derived from the nonreceptor-binding domain and connecting region of urokinase. Administration of A6 inhibits the interaction of uPA with its receptor uPAR, and may inhibit endothelial cell motility and tumor cell invasion. uPA and uPAR promote extracellular matrix degradation and growth factor activation and correlate positively with angiogenesis, cancer cell invasion and metastasis.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C121215","USP14/UCHL5 Inhibitor VLX1570","USP14/UCHL5 Inhibitor VLX1570|VLX1570","An inhibitor of the 19S proteasome-specific deubiquitylating enzymes (DUBs) USP14 and UCHL5, with apoptosis-inducing and antineoplastic activities. Upon administration, VLX1570 specifically binds to both USP14 and UCHL5, thereby blocking their deubiquitylating activity. This blocks the ubiquitin proteasome degradation pathway, prevents the degradation of defective proteins, and leads to an accumulation of poly-ubiquitylated proteins. This induces the unfolded protein response (UPR) and results in both the induction of tumor cell apoptosis and the inhibition of tumor cell growth. USP14 and UCHL5, overexpressed in various tumor cell types, play a key role in the correct folding and deubiquitination of proteins.","Pharmacologic Substance"]
["C104747","UV1 Telomerase Peptide Vaccine","UV1 Telomerase Peptide Vaccine|UV1/hTERT Peptide Vaccine","A synthetic, peptide cancer vaccine directed against the human telomerase reverse transcriptase catalytic subunit (hTERT) with potential immunomodulating activity. Vaccination with the UV1 telomerase peptide may stimulate cytotoxic T-cells to recognize and kill telomerase-expressing cells. Telomerase, a reverse transcriptase normally repressed in healthy cells, is overexpressed in most cancer cells and plays a key role in cellular proliferation.","Immunologic Factor|Pharmacologic Substance"]
["C61069","V930 Vaccine","V930 Vaccine","A novel cancer vaccine designed to treat HER-2- and/or CEA-expressing cancers.","Chemical Viewed Functionally"]
["C2542","Vaccine-Sensitized Draining Lymph Node Cells","VDLN Cells|Vaccine-Sensitized Draining Lymph Node Cells","Cells isolated from lymph nodes from patients, and activated in vitro to generate tumor-specific effector T cells.  Lymph nodes in the lymphatics draining tumors often contain T cells that are immunologically sensitized but functionally deficient. Vaccine-sensitized draining lymph node cells are prepared by isolating these lymphocytes in vitro and stimulating them with cytokines to differentiate into mature effector cells.  Vaccine-draining lymph node cells may also be produced by pharmacological activation of lymph node-derived lymphocytes with drugs such as ionomycin or with bacterial toxin; these activated lymphocytes may be expanded in culture with cytokines such as interleukin-2 prior to infusion into the patient. (NCI04)","Cell|Pharmacologic Substance"]
["C74089","Vaccinia Virus DD-CDSR","Vaccinia Virus (vvDD-CDSR)|Vaccinia Virus DD-CDSR|vvDD-CDSR","A highly tumor-selective vaccinia virus (vv) with an engineered double deletion (DD) of the thymidine kinase (tk) and vaccinia growth factor genes and additions of both a cytosine deaminase (CD) gene and a somatostatin receptor (SR) gene with potential oncolytic viral activity. The tk and vaccinia growth factor gene deletions in intratumorally administered vaccinia virus (vvDD-CDSR) help to restrict its replication and cytolytic activity to tumor cells with large nucleotide pools and tumor cells with activation of the EGFR-Ras pathway. Addition of the CD gene to the viral genome allows control of oncolytic viral infection through the administration of the prodrug 5-fluorocytosine (5-FC), converted by CD to the antimetabolite 5-fluorouracil (5-FU) in cells infected with this agent. Addition of the SR gene allows anatomical localization of vaccinia virus (vvDD-CDSR) through the use of octreotide scintigraphy.","Pharmacologic Substance"]
["C2674","Vaccinia-GM-CSF Vaccine","Recombinant Vaccinia-GM-CSF|Vaccinia-GM-CSF Vaccine|rV GM-CSF","A recombinant vaccinia virus that encodes granulocyte-macrophage colony stimulating factor (GM-CSF). By activating T-cells and macrophages, vaccination with recombinant vaccinia GM-CSF may enhance the host immune system response to poorly immunogenic tumors, resulting in decreased tumor growth. (NCI04)","Pharmacologic Substance"]
["C2531","Vaccinia-Tyrosinase Vaccine","Recombinant Vaccinia-Tyrosinase Vaccine|Recombinant Vaccinia-Tyrosinase|VACTYROS|Vaccinia-Tyrosinase Vaccine|rV-TYR Vaccine|rV-TYR","A vaccine consisting of recombinant vaccinia virus, based on the modified vaccinia virus Ankara (MVA) that encodes the melanoma-associated antigen tyrosinase. Vaccination with vaccinia-tyrosinase may stimulate the host immune system to mount a cytotoxic T-cell response against tumor cells expressing tyrosinase. Tyrosinase is a melanoma-specific differentiation agent that catalyzes the synthesis of the melanin precursor L-3,4-dihydroxyphenylalanine (L-DOPA).","Immunologic Factor|Pharmacologic Substance|Virus"]
["C102748","Vaccinium myrtillus/Macleaya cordata/Echinacea angustifolia Extract Granules","Samital Granules|V. myrtillus/M. cordata/E. angustfolia Extract Granules|Vaccinium myrtillus/Macleaya cordata/Echinacea angustifolia Extract Granules","A proprietary suspension formulation prepared from granules of standardized extracts from the fruits of Vaccinium myrtillus, the aerial parts of Macleaya cordata and the roots of Echinacea angustifolia, with potential anti-mucositis, anti-inflammatory, and analgesic activities. The main active ingredients of this formulation include anthocyanosides and procyanidins, benzophenanthridinic alkaloids, and alkylamides from V. myrtillus, M. cordata and E. angustifolia extracts, respectively. Upon administration in the mucosal cavity, the anthocyanosides scavenge free radicals, form a protective barrier on the mucosa, and protect the integrity of the capillary vessels; the benzophenanthridine alkaloids prevent the production of pro-inflammatory cytokines by inhibiting NF-kB and may halt the growth of microorganisms; the alkylamides inhibit cyclooxygenase and 5-lipoxygenase thereby blocking productions of prostaglandin and leukotriene. Furthermore, alkylamides modulate the expression of tumor necrosis factor alpha and other cytokines involved in inflammation processes through cannabinoid type 2 receptors and as cannabinomimetics they may also exert analgesic activity.","Pharmacologic Substance"]
["C111039","Vadastuximab Talirine","SGN-CD33A|VADASTUXIMAB TALIRINE|Vadastuximab Talirine","An immunoconjugate consisting of a humanized monoclonal antibody that is engineered to contain cysteine residues that are conjugated to the synthetic, DNA cross-linking, pyrrolobenzodiazepine dimer SGD-1882, via the protease-cleavable linker maleimidocaproyl-valine-alanine dipeptide, with potential antineoplastic activity. The monoclonal antibody portion of vadastuximab talirine specifically binds to the cell surface antigen CD33. This causes the internalization of SGN-CD33A, and the release of the cytotoxic moiety SGD-1882. SGD-1882 binds to and crosslinks DNA, which results in both cell cycle arrest and the induction of apoptosis in CD33-expressing tumor cells. CD33, a transmembrane receptor, is expressed on myeloid leukemia cells.","Pharmacologic Substance"]
["C2504","Vadimezan","5,6-Dimethylxanthenone-4-Acetic Acid|5,6-MexXAA|ASA404|DMXAA|Dimethyloxoxanthene Acetic Acid|Dimethylxanthenone Acetic Acid|VADIMEZAN|Vadimezan|dimethylxanthenone acetic acid","A fused tricyclic analogue of flavone acetic acid with potential antineoplastic activity. Vadimezan induces the cytokines tumor necrosis alpha (TNF-alpha), serotonin and nitric oxide, resulting in hemorrhagic necrosis and a decrease in angiogenesis.  This agent also stimulates the anti-tumor activity of tumor-associated macrophages.","Organic Chemical|Pharmacologic Substance"]
["C29536","Valproic Acid","2-Propylpentanoic Acid|2-Propylvaleric Acid|Depakene|Di-n-propylacetic Acid|Stavzor|VALPROIC ACID|Valproate|Valproic Acid|valproic acid","A synthetic derivative of propylpentanoic acid with antiepileptic properties and potential antineoplastic and antiangiogenesis activities.  In epilepsy, valproic acid appears to act by increasing the concentration of gamma-aminobutyric acid (GABA) in the brain. This agent's antitumor and antiangiogenesis activities may be related to the inhibition of histone deacetylases and nitric oxide synthase, which results in the inhibition of nitric oxide synthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1340","Valrubicin","AD 32|AD-32|N-Trifluoroacetyladriamycin-14-valerate|VALRUBICIN|Valrubicin|Valstar|Valtaxin|valrubicin","A semisynthetic derivative of the antineoplastic anthracycline antibiotic doxorubicin. With a mechanism of action that appears to differ from doxorubicin, valrubicin is converted intracytoplasmically into N-trifluoroacetyladriamycin, which interacts with topoisomerase II, stabilizing the complex between the enzyme and DNA; consequently, DNA replication and repair and RNA and protein synthesis are inhibited and the cell cycle is arrested in the G2 phase. In addition, this agent accumulates in the cell cytoplasm where it inhibits protein kinase C (PKC). Valrubicin is less cardiotoxic than doxorubicin when administered systemically; applied topically, this agent shows excellent tissue penetration. Structurally, the trifluoro-acetyl moiety on the amino group of the glycoside and the valerate moiety appear to result in a lipophilicity that is greater than of doxorubicin, resulting in increased intracytoplasmic concentrations.","Antibiotic|Organic Chemical"]
["C1405","Valspodar","6-[(2S,4R,6E)-4-Methyl-2-(methylamino)-3-oxo-6-octenoic Acid]cyclosporin D|Amdray|Cyclo((2S,4R,6E)-4-methyl-2-(methylamino)-3-oxo-6-octenoyl)-L-valyl-N-methylglycyl-N-methyl-L-leucyl-L-valyl-N-methyl-L-leucyl-L-alanyl-D-alanyl-N-me|PSC 833|PSC-833|SZD PSC 833|VALSPODAR|Valspodar","An analogue of cyclosporin-A. Valspodar inhibits p-glycoprotein, the multidrug resistance efflux pump, thereby restoring the retention and activity of some drugs in some drug-resistant tumor cells. This agent also induces caspase-mediated apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2737","Vandetanib","AZD6474|Caprelsa|VANDETANIB|Vandetanib|ZD-6474|ZD6474|Zactima|vandetanib","An orally bioavailable 4-anilinoquinazoline. Vandetanib selectively inhibits the tyrosine kinase activity of vascular endothelial growth factor receptor 2 (VEGFR2), thereby blocking VEGF-stimulated endothelial cell proliferation and migration and reducing tumor vessel permeability. This agent also blocks the tyrosine kinase activity of epidermal growth factor receptor (EGFR), a receptor tyrosine kinase that mediates tumor cell proliferation and migration and angiogenesis.","Pharmacologic Substance"]
["C116748","Vandortuzumab Vedotin","DSTP3086S|MSTP2109A|RG7450|Thio-anti-STEAP1-MC-vc-PAB-MMAE|Vandortuzumab Vedotin","An antibody-drug conjugate (ADC) composed of a humanized monoclonal antibody directed against the six transmembrane epithelial antigen of the prostate 1 (STEAP1), and conjugated, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule disrupting agent, with potential antineoplastic activity. Upon administration of vandortuzumab vedotin, the monoclonal antibody moiety of vandortuzumab vedotin binds to STEAP1-expressing tumor cells and is internalized, thereby delivering MMAE intracellularly. Proteolytic cleavage releases MMAE, which then binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. STEAP1, a tumor-associated antigen (TAA), is overexpressed in a variety of cancer cell types.","Pharmacologic Substance"]
["C96799","Vantictumab","OMP-18R5|Vantictumab","A monoclonal antibody directed against the Wnt signaling pathway with potential antineoplastic activity. Upon administration, vantictumab binds to certain receptors in the Wnt signaling pathway thereby preventing the activation of the Wnt signaling pathway. This may result in an inhibition of cancer stem cell (CSC) activity and a subsequent inhibition of cancer cell proliferation. The Wnt signaling pathway is dysregulated in many cancer cell types and appears to play a major role in CSC regulation and activity; CSC are tumor initiating cells that are able to self-renew and are responsible for tumor growth and resistance.","Immunologic Factor|Pharmacologic Substance"]
["C1429","Vapreotide","BMY-41606|Docrised|RC-160|VAPREOTIDE|Vapreotide|vapreotide","A synthetic cyclic octapeptide analogue of somatostatin with direct and indirect antitumor effects. Vapreotide binds to somatostatin receptors (SSTR), specifically SSTR-2 and to SSTR-5 with a lesser affinity, in the similar behaviors as other octapeptide somatostatin analogues. Like octreotide, this agent has direct and indirect antitumor effects via inhibiting the release of growth hormone and other peptides that regulate release of insulin, gastrointestinal hormones. Furthermore, vapreotide may also be useful for inducing hemostasis in cases of acute hemorrhage of the upper gastrointestinal tract.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C99127","Varlilumab","CDX 1127|CDX-1127|Immunoglobulin G1, Anti-(Human CD Antigen CD27) (Human Monoclonal CDX-1127 Clone 1f5 Heavy Chain), Disulfide with Human Monoclonal CDX-1127 Clone 1f5 Kappa-chain, Dimer|VARLILUMAB|Varlilumab","A human agonistic monoclonal antibody (MoAb) specific for CD27, with potential immunostimulating and antineoplastic activity. Upon administration of varlilumab, this MoAb binds to CD27 and may potentiate the immune response by increasing the cytotoxic T-lymphocyte (CTL) response against CD27-expressing tumor cells. This may lead to growth inhibition of CD27-expressing tumor cells. In addition, this agent may increase the proliferation and activation of antigen-specific T lymphocytes upon co-administration of TAA-containing vaccines, such as dendritic cell vaccines. CD27, a co-stimulatory molecule and member of the tumor necrosis factor family overexpressed in certain tumor cell types, is constitutively expressed on mature T-lymphocytes, memory B cells and natural killer cells and plays an important role in NK cell mediated cytolytic activity and T and B lymphocyte proliferation and activation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C62530","Varlitinib","ARRY-334543|VARLITINIB|Varlitinib","An orally bioavailable inhibitor of the epidermal growth factor receptor family with potential antineoplastic activity. Varlitinib selectively and reversibly binds to both EGFR (ErbB-1) and Her-2/neu (ErbB-2) and prevents their phosphorylation and activation, which may result in inhibition of the associated signal transduction pathways, inhibition of cellular proliferation and cell death. EGFR and Her-2 play important roles in cell proliferation and differentiation and are upregulated in various human tumor cell types. Due to the dual inhibition of both EGFR and Her-2, this agent may be therapeutically more effective than agents that inhibit EGFR or Her-2 alone.","Pharmacologic Substance"]
["C95226","Varlitinib Tosylate","4,6-Quinazolinediamine, N(Sup 4)-(3-Chloro-4-(2-Thiazolylmethoxy)Phenyl)-N(Sup 6)-((4r)-4,5-Dihydro-4-Methyl-2-Oxazolyl)-, 4-Methylbenzenesulphonate (1:2)|4-N-(3-Chloro-4-(Thiazol-2-Ylmethoxy)Phenyl)-6-N-((4r)-4-Methyl-4,5-Dihydrooxazol-2- Yl)Quinazoline-4,6-Diamine Bis(4-Methylbenzenesulphonate)|AR00334543 Ditosilate|AR00334543 Ditosylate|ARRY-334543 Ditosylate|ARRY-543 Ditosilate|ARRY-543 Ditosylate|VARLITINIB TOSYLATE|Varlitinib Tosylate","The tosylate salt form of varlitinib, an orally bioavailable inhibitor of the epidermal growth factor receptor family with potential antineoplastic activity. Varlitinib selectively and reversibly binds to both EGFR (ErbB-1) and Her-2/neu (ErbB-2) and prevents their phosphorylation and activation, which may result in inhibition of the associated signal transduction pathways, inhibition of cellular proliferation and cell death. EGFR and Her-2 play important roles in cell proliferation and differentiation and are upregulated in various human tumor cell types. Due to the dual inhibition of both EGFR and Her-2, this agent may be therapeutically more effective than agents that inhibit EGFR or Her-2 alone.","Pharmacologic Substance"]
["C88338","Vascular Disrupting Agent BNC105P","BNC105P|Vascular Disrupting Agent BNC105P","A benzofuran-based vascular disrupting agent (VDA) prodrug with potential anti-vascular and antineoplastic activities. Upon administration vascular disrupting agent BNC105P, the disodium phosphate ester of BNC105, is rapidly converted to BNC105; in activated endothelial cells, BNC105 binds to tubulin and inhibits its polymerization, which may result in a blockage of mitotic spindle formation, cell cycle arrest, and disruption of the tumor vasculature. Hypoxic conditions ensue, depriving tumor cells of nutrients and resulting in tumor cell apoptosis. In addition to its VDA activity, this agent has a direct cytotoxic effect on tumor cells by inhibiting tubulin polymerization. BNC105 is not a substrate for the multidrug-resistance P-glycoprotein (Pgp) transporter.","Pharmacologic Substance"]
["C2736","Vascular Disrupting Agent ZD6126","ANG453|N-[(5S)-6,7-Dihydro-9,10,11-trimethoxy-3-(phosphonooxy)-5H-dibenzo[a,c]cyclohepten-5-yl]acetamide|N-acetylcochinol-O-phosphate|Vascular Disrupting Agent ZD6126|ZD-6126|ZD6126|ZM-445526","A water-soluble phosphate prodrug of N-acetylcolchinol with potential antiangiogenesis and antineoplastic activities. ZD-6126 is converted in vivo into N-acetylcolchinol. N-acetylcolchinol binds to and destabilizes the tubulin cytoskeleton of endothelial cells in tumor blood vessels, which may result in tumor endothelial cell apoptosis, the selective occlusion of tumor blood vessels, cessation of tumor blood flow, and tumor necrosis.","Pharmacologic Substance"]
["C1868","Vatalanib","CGP 79787|CGP-79787|N-(4-Chlorophenyl)-4-(4-pyridinylmethyl)-1-phthalazinamine|PTK787/ZK 222584|VATALANIB|Vatalanib|ZK-232934|vatalanib","An orally bioavailable anilinophthalazine with potential antineoplastic activity.  Vatalanib binds to and inhibits the protein kinase domain of vascular endothelial growth factor receptors 1 and 2; both receptor tyrosine kinases are involved in angiogenesis.  This agent also binds to and inhibits related receptor tyrosine kinases, including platelet-derived growth factor (PDGF) receptor, c-Kit, and c-Fms.","Organic Chemical|Pharmacologic Substance"]
["C74945","Vatalanib Succinate","1-[4-Chloroanilino]-4-[4-pyridylmethyl]phthalazine Succinate|Butanedioic Acid, Compd. with N-(4-Chlorophenyl)-4-(4-pyridinylmethyl)-1-phthalazinamine (1:1)|CGP 79787D|PTK 787|PTK-787|PTK787|VATALANIB SUCCINATE|Vatalanib Succinate|ZK 222584","The succinate salt of vatalanib, an anilinophthalazine derivative, with antineoplastic activity.  Vatalanib binds to and inhibits the protein kinase domain of vascular endothelial growth factor receptors 1 and 2; both receptor tyrosine kinases are involved in angiogenesis.  This agent also binds to and inhibits related receptor tyrosine kinases, including platelet-derived growth factor (PDGF) receptor, c-Kit, and c-Fms.","Organic Chemical|Pharmacologic Substance"]
["C70971","Vector-peptide Conjugated Paclitaxel","Taxol-Angiopep Conjugate|Vector-peptide Conjugated Paclitaxel","A proprietary conjugate of paclitaxel with antineoplastic activity. Similar to the free drug, the paclitaxel moiety in vector-peptide conjugated paclitaxel binds to and stabilizes tubulin molecules, promoting assembly of microtubules and inhibiting tubulin disassembly which results in the inhibition of cell division. The Kunitz domain-derived vector-peptide carries the conjugated paclitaxel through the blood brain barrier (BBB), bypassing the transmembrane p-glycoprotein (P-gp) efflux pump, which may result in higher concentrations of paclitaxel in the brain parenchyma.","Pharmacologic Substance"]
["C95798","Vedolizumab","Entyvio|Immunoglobulin G1, Anti-(Human Integrin LPAM-1 (Lymphocyte Peyer's Patch Adhesion Molecule 1)) (Human-Mus musculus Heavy Chain), Disulfide with Human-Mus musculus kappa-chain, Dimer|Immunoglobulin G1, anti-(human integrin LPAM-1 (lymphocyte Peyer's patch adhesion molecule 1)) (human-Mus musculus heavy chain), disulfide with human-Mus musculus kappa-chain, dimer|LDP 02|LDP-02|LDP02|MLN0002|MLN02|VEDOLIZUMAB|Vedolizumab","A recombinant humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the human lymphocyte Peyer's patch adhesion molecule 1 (LPAM-1; alpha4beta7; a4b7), with immunomodulating, anti-inflammatory, and potential antineoplastic activities. Upon administration, vedolizumab selectively binds to integrin a4b7 and prevents the binding of a4b7, expressed on the surface of a subset of T-lymphocytes, to its natural ligand, mucosal addressin cell adhesion molecule-1 (MAdCAM-1), which is mainly expressed on the surface of gut endothelial cells. This prevents a4b7-mediated signaling, adhesion of lymphocytes to the endothelium and the migration of T-lymphocytes across the endothelium into inflamed gastrointestinal (GI) tissue. By preventing this infiltration to the affected area, inflammation is reduced. The human lymphocyte a4b7 integrin, plays a key role in gastrointestinal (GI) inflammation; it is overexpressed in certain types of cancer cells. The alpha4beta7/MAdCAM-1 signaling pathway plays a critical role in the homing of T-lymphocytes to intestinal tissue.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C91100","VEGF Inhibitor PTC299","PTC299|VEGF Inhibitor PTC299","An orally bioavailable, small molecule inhibitor of vascular endothelial growth factor (VEGF) synthesis with potential antiangiogenesis and antineoplastic activities. VEGF inhibitor PTC299 targets post-transcriptionally by selectively binding the 5'- and 3'-untranslated regions (UTR) of VEGF messenger RNA (mRNA), thereby preventing translation of VEGF. This inhibits VEGF protein production and decreases its levels in the tumor and bloodstream. In turn, this may result in the inhibition of migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and eventually the induction of tumor cell death. VEGFs are upregulated in a variety of tumor cell types and play key roles during angiogenesis. In addition, PTC299 may enhance the antitumor activity of other chemotherapeutic agents.","Pharmacologic Substance"]
["C117236","VEGF/HGF-targeting DARPin MP0250","Bispecific VEGF/HGF-targeting Darpin|MP0250|VEGF/HGF-targeting DARPin MP0250","A designed ankyrin repeat proteins (DARPin)-based agent targeting vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF), with potential antiangiogenic and antineoplastic activities. Compared to antibodies, DARPins are small in size, have favorable pharmacokinetics and allow for both high affinity binding and efficacy. Upon administration, the VEGF/HGF-targeting DARPin MP0250 binds to and inhibits both HGF and VEGF. This prevents HGF- and VEGF-mediated signaling, and inhibits the growth of HGF/VEGF-overexpressing tumor cells. This agent also prevents osteolysis, due to the inhibitory effect on HGF signaling. HGF and VEGF are overexpressed in a variety of cancer cell types and are associated with increased cell proliferation, migration and adhesion.","Pharmacologic Substance"]
["C88267","VEGFR Inhibitor KRN951","KRN951|N-{2-Chloro-4-[(6,7-dimethoxy-4-quinolyl)oxy]phenyl}-N'-(5-methyl-3-isoxazolyl) Urea Hydrochloride Monohydrate|VEGFR Inhibitor KRN951","An orally bioavailable quinoline-urea derivative inhibitor of vascular endothelial growth factor receptors (VEGFRs) 1 and 2 with potential antiangiogenesis and antineoplastic activities. VEGFR inhibitor KRN951 inhibits VEGF-induced phosphorylation of VEGFRs 1 and 2, which may result in inhibition of migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and tumor cell death. Expression of VEGFRs may be upregulated in a variety of tumor cell types.","Pharmacologic Substance"]
["C118628","VEGFR/FGFR Inhibitor ODM-203","ODM 203|ODM-203|VEGFR/FGFR Inhibitor ODM-203","An orally available inhibitor of the human vascular endothelial growth factor receptors (VEGFRs) and fibroblast growth factor receptors (FGFRs), with potential antiangiogenic and antineoplastic activities. VEGFR/FGFR inhibitor ODM-203 inhibits both VEGFRs and FGFRs, which may result in the inhibition of VEGFR- and FGFR-mediated signaling. This leads to an inhibition of angiogenesis and cell proliferation in tumor cells overexpressing VEGFR and/or FGFR. Both VEGFRs and FGFRs belong to the superfamily of receptor tyrosine kinases and are upregulated in various tumor cell types.","Pharmacologic Substance"]
["C95896","VEGFR/PDGFR Dual Kinase Inhibitor X-82","CM082|VEGFR/PDGFR Dual Kinase Inhibitor X-82|X-82","An orally available small molecule dual inhibitor targeting human vascular endothelial growth factor receptors (VEGFRs) and platelet-derived growth factor receptors (PDGFRs) with antiangiogenic and antineoplastic activities. VEGFR/PDGFR dual kinase inhibitor X-82 inhibits all isoforms of VEGFR and PDGFR, which may result in the inhibition of tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. Both VEGFRs and PDGFRs are receptor tyrosine kinases that may be upregulated in various tumor cell types. VEGFR/PDGFR dual kinase inhibitor X-82 has been shown to reduce tissue toxicity by 95 percent compared with first-generation kinase inhibitors.","Pharmacologic Substance"]
["C79794","VEGFR/PDGFR Tyrosine Kinase Inhibitor TAK-593","TAK-593|VEGFR/PDGFR Tyrosine Kinase Inhibitor TAK-593","An oral formulation containing a small-molecule receptor tyrosine kinase inhibitor of both vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) with potential antineoplastic activity. TAK-593 selectively binds to and inhibits VEGFR and PDGFR, which may result in the inhibition of angiogenesis and tumor cell proliferation.","Pharmacologic Substance"]
["C77895","VEGFR1-1084 Peptide Vaccine","VEGFR1-1084 Peptide Vaccine","A peptide vaccine containing an HLA-A*2402-restricted epitope of vascular endothelial growth factor receptor 1 (VEGFR1 or Flt-1) with potential immunostimulating, antiangiogenic, and antineoplastic activities. Upon vaccination, VEGFR1-1084 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against VEGFR1-expressing endothelial cells of the tumor microvasculature, which may inhibit tumor angiogenesis and tumor cell proliferation. VEGFR1, a receptor tyrosine kinase, may be overexpressed on endothelial cells of the tumor microvasculature and is associated with tumor cell proliferation, invasion and tumor angiogenesis. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenicity.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C99378","VEGFR-2 DNA Vaccine VXM01","VEGFR-2 DNA Vaccine VXM01|VXM01","An orally available DNA cancer vaccine containing an attenuated strain of the bacterium Salmonella typhimurium encoding murine vascular endothelial growth factor receptor 2 (VEGFR-2) (VXM01), with potential immunomodulating, anti-angiogenic and antineoplastic activity. Upon oral administration and successful transduction, VEGFR-2 DNA vaccine VXM01 expresses VEGFR-2 in addition to inducing the expression of T-cell activation markers, such as CD25, interleukin-2, the early T-cell activation antigen CD69 and the lymphocyte function-associated antigen LFA-2. The immune response targets the fast growing VEGFR-2 expressing endothelial cells found in the tumor vasculature, thereby blocking angiogenesis which may ultimately inhibit tumor cell proliferation. VEGFR-2 is a receptor tyrosine kinase overexpressed on proliferating endothelial cells in the tumor vasculature.","Immunologic Factor|Pharmacologic Substance"]
["C97950","VEGFR2 Tyrosine Kinase Inhibitor PF-00337210","PF-00337210|VEGFR2 Tyrosine Kinase Inhibitor PF-00337210","An orally available ATP-competitive inhibitor of the vascular endothelial growth factor receptor type 2 (VEGFR2), with potential anti-angiogenesis and antineoplastic activities. Upon administration, the VEGFR2 tyrosine kinase inhibitor PF-00337210 selectively binds to VEGFR2 and prevents its phosphorylation which may result in an inhibition of migration, proliferation and survival of endothelial cells, microvessel formation, the inhibition of tumor cell proliferation, and may eventually cause tumor cell death. VEGFR2, a receptor tyrosine kinase, is frequently overexpressed by a variety of tumor types.","Pharmacologic Substance"]
["C74090","VEGFR2-169 Peptide Vaccine","VEGFR2-169 Peptide Vaccine","A peptide vaccine containing an HLA-A*2402-restricted epitope of vascular endothelial growth factor receptor (VEGFR) 2 with potential immunostimulatory and antineoplastic activities. Upon administration, VEGFR2-169 peptide vaccine may stimulate a cytotoxic T lymphocyte (CTL) response against VEGFR2-expressing tumor cells. VEGFR2, a receptor tyrosine kinase, is overexpressed by a variety of tumor types; overexpression is associated with tumor cell proliferation and tumor angiogenesis. HLA-A*2402 is an MHC class I molecule that presents antigenic peptides to CD8+ T cells; epitope design restricted to epitopes that bind most efficiently to HLA-A*2402 may improve antigenic peptide immunogenicity.","Pharmacologic Substance"]
["C60768","Veliparib","2-((R)-2-Methylpyrrolidin-2-yl)-1H-benzimidazole-4-carboxamide|ABT-888|PARP-1 inhibitor ABT-888|VELIPARIB|Veliparib|veliparib","A poly(ADP-ribose) polymerase (PARP) -1 and -2 inhibitor with chemosensitizing and antitumor activities. With no antiproliferative effects as a single agent at therapeutic concentrations, ABT-888 inhibits PARPs, thereby inhibiting DNA repair and potentiating the cytotoxicity of DNA-damaging agents. PARP nuclear enzymes are activated by DNA single or double strand breaks, resulting in the poly(ADP-ribosyl)ation of other nuclear DNA binding proteins involved in DNA repair; poly(ADP-ribosyl)ation contributes to efficient DNA repair and to survival of proliferating cells exposed to mild genotoxic stresses as induced by as oxidants, alkylating agents or ionizing radiation.","Pharmacologic Substance"]
["C48406","Veltuzumab","Anti-CD20 Monoclonal Antibody hA20|HCD20|IMMU-106|MoAb hA20|Monoclonal Antibody hA20|VELTUZUMAB|Veltuzumab|hA20|veltuzumab","A humanized monoclonal antibody directed against the CD20 antigen with potential antineoplastic activity. Following binding, veltuzumab triggers complement-dependent cell lysis (CDCL) and antibody-dependent cell-mediated cytotoxicity (ADCC) in cells that overexpress CD20. CD20 antigen is a hydrophobic transmembrane protein located on pre-B and mature B lymphocytes.","Amino Acid, Peptide, or Protein|Immunologic Factor|Pharmacologic Substance"]
["C64768","Vemurafenib","1-propanesulfonamide, n-(3-((5-(4-chlorophenyl)-1h-pyrrolo(2,3-b)pyridin-3-yl)carbonyl)-2,4-difluorophenyl)-|BRAF (V600E) kinase inhibitor RO5185426|BRAF(V600E) Kinase Inhibitor RO5185426|PLX-4032|PLX4032|RG 7204|RG7204|RO 5185426|VEMURAFENIB|Vemurafenib|Zelboraf","An orally bioavailable, ATP-competitive, small-molecule inhibitor of BRAF(V600E) kinase with potential antineoplastic activity. Vemurafenib selectively binds to the ATP-binding site of BRAF(V600E) kinase and inhibits its activity, which may result in an inhibition of an over-activated MAPK signaling pathway downstream in BRAF(V600E) kinase-expressing tumor cells and a reduction in tumor cell proliferation. Approximately 90% of BRAF gene mutations involve a valine-to-glutamic acid mutation at residue 600 (V600E); the oncogene protein product, BRAF(V600E) kinase, exhibits a markedly elevated activity that over-activates the MAPK signaling pathway. The BRAF(V600E) gene mutation has been found to occur in approximately 60% of melanomas, and in about 8% of all solid tumors, including melanoma, colorectal, thyroid and other cancers.","Organic Chemical|Pharmacologic Substance"]
["C103147","Venetoclax","4-(4-((2-(4-Chlorophenyl)-4,4-dimethylcyclohex-1-en-1-yl)methyl)piperazin-1-yl)-N-((3-nitro-4-((tetrahydro-2H-pyran-4-ylmethyl)amino)phenyl)sulfonyl)-2-(1H-pyrrolo(2,3-b)pyridin-5-yloxy)benzamide|ABT-0199|ABT-199|ABT199|GDC-0199|RG7601|VENETOCLAX|Venclexta|Venetoclax","An orally bioavailable, selective small molecule inhibitor of the anti-apoptotic protein Bcl-2, with potential antineoplastic activity. Venetoclax mimics BH3-only proteins, the native ligands of Bcl-2 and apoptosis activators, by binding to the hydrophobic groove of Bcl-2 proteins thereby repressing Bcl-2 activity and restoring apoptotic processes in tumor cells. Bcl-2 protein is overexpressed in some cancers and plays an important role in the regulation of apoptosis; its expression is associated with increased drug resistance and tumor cell survival. Compared to the Bcl-2 inhibitor navitoclax, this agent does not inhibit bcl-XL and does not cause bcl-XL-mediated thrombocytopenia.","Pharmacologic Substance"]
["C928","Verapamil","VERAPAMIL|Verapamil|alpha-[3-[[2-(3,4-Dimethoxyphenyl)ethyl]methylamino]propyl]-3,4-dimethoxy-alpha-(1-methylethyl)benzeneacetonitrile","A phenylalkylamine calcium channel blocking agent. Verapamil inhibits the transmembrane influx of extracellular calcium ions into myocardial and vascular smooth muscle cells, causing dilatation of the main coronary and systemic arteries and decreasing myocardial contractility.  This agent also inhibits the drug efflux pump P-glycoprotein which is overexpressed in some multi-drug resistant tumors and may improve the efficacy of some antineoplastic agents. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C2811","Verpasep Caltespen","BCG65-E7|Bovine HSP fusion with E7 of HPV16|HPV 16 E7/HSP65 Vaccine|HPV E7 Peptide Epitope Vaccine|HspE7 Therapeutic Vaccine|HspE7|SGN-00101|VERPASEP CALTESPEN|Verpasep Caltespen","A recombinant chimeric protein composed of the heat shock protein 65 (Hsp65) from Mycobacterium bovis, and the human papilloma viral (HPV) protein E7.  Hsp65, similar to other members of its family of proteins, elicits a strong immune response and may be used to design vaccines against a number of different cancers.  E7 protein is involved in carcinogenesis of anal and cervical tumors, and represents a tumor antigen that may be specifically targeted by lymphocytes. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C96747","Verubulin","4-quinazolinamine, N-(4-methoxyphenyl)-N,2-dimethyl-|MX-128495|N-(4-methoxyphenyl)-N,2-dimethylquinazolin-4-amine|VERUBULIN|Verubulin","A quinazoline derivative with potential antineoplastic activities. Verubulin binds to and inhibits tubulin polymerization and interrupts microtubule formation, resulting in disruption of mitotic spindle assembly, cell cycle arrest in the G2/M phase, and cell death. This agent is not a substrate for several subtypes of multidrug resistance ABC transporters, and may be useful for treating multidrug resistant tumors. In addition, as a vascular disrupting agent, verubulin disrupts tumor microvasculature specifically, which may result in acute ischemia and massive tumor cell death. In addition, verubulin is able to cross the blood-brain barrier and accumulate in the brain.","Organic Chemical|Pharmacologic Substance"]
["C64782","Verubulin Hydrochloride","Azixa|MPC-6827|Microtubule Inhibitor MPC-6827|N-(4-methoxyphenyl)-n,2-dimethylquinazolin-4-amine Hydrochloride|VERUBULIN HYDROCHLORIDE|Verubulin Hydrochloride","The hydrochloride salt form of verubulin, a quinazoline derivative with potential dual antineoplastic activities. Verubulin binds to and inhibits tubulin polymerization and interrupts microtubule formation, resulting in disruption of mitotic spindle assembly, cell cycle arrest in the G2/M phase, and cell death. This agent is not a substrate for several subtypes of multidrug resistance ABC transporters, such as P-glycoprotein, multidrug resistance-associated protein 1 (MRP1), and breast cancer resistance protein 1 (BCRP1); therefore, it may be useful for treating multidrug resistant (MDR) tumors that express these transporters. In addition, as a vascular disrupting agent (VDA), verubulin appears to disrupt tumor microvasculature specifically, which may result in acute ischemia and massive tumor cell death.","Organic Chemical|Pharmacologic Substance"]
["C61073","Viagenpumatucel-L","Gp96-Ig Fusion Protein-Expressing Non-Small Cell Lung Cancer Cell Vaccine|HS-110|HS110|Viagenpumatucel-L","A proprietary, allogeneic tumor cell vaccine expressing a recombinant secretory form of the heat shock protein gp96 fusion (gp96-Ig) with potential antineoplastic activity. Upon administration of viagenpumatucel-L, the irradiated live tumor cells continuously secrete gp96-Ig along with its chaperoned tumor associated antigens (TAAs) into the blood stream, thereby activating antigen presenting cells, natural killer cells and priming potent cytotoxic T lymphocytes (CTLs) to respond against TAAs on the endogenous tumor cells. Furthermore, this vaccine may induce long-lived memory T cells that could fight recurring cancer cells. gp96-Ig is constructed by replacing the KDEL retention sequence of gp96, normally an endoplasmatic reticulum-resident chaperone peptide, with the Fc portion of mouse and human IgG1.","Immunologic Factor|Pharmacologic Substance"]
["C930","Vinblastine","VINBLASTINE|VLB|Vinblastine|Vincaleucoblastine|vinblastine","A natural alkaloid isolated from the plant Vinca rosea Linn. Vinblastine binds to tubulin and inhibits microtubule formation, resulting in disruption of mitotic spindle assembly and arrest of tumor cells in the M phase of the cell cycle. This agent may also interfere with amino acid, cyclic AMP, and glutathione metabolism; calmodulin-dependent Ca++ -transport ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C931","Vinblastine Sulfate","29060 LE|29060-LE|Exal|VINBLASTINE SULFATE|VINCALEUKOBLASTINE|Velban|Velbe|Velsar|Vinblastine Sulfate|vinblastine sulfate","The sulfate salt of vinblastine, a natural alkaloid isolated from the plant Catharanthus roseus (Madagascar periwinkle) with antineoplastic properties.  Vinblastine disrupts microtubule formation and function during mitosis and interferes with glutamic acid metabolism. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C933","Vincristine","22-Oxovincaleukoblastine|LEUROCRISTINE|Leurocristine|VCR|VINCRISTINE|Vincristine|Vincrystine|vincristine","A natural alkaloid isolated from the plant Vinca rosea Linn. Vincristine binds irreversibly to microtubules and spindle proteins in S phase of the cell cycle and interferes with the formation of the mitotic spindle, thereby arresting tumor cells in metaphase. This agent also depolymerizes microtubules and may also interfere with amino acid, cyclic AMP, and glutathione metabolism; calmodulin-dependent Ca++ -transport ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1739","Vincristine Sulfate","Kyocristine|Leurocristine Sulfate|Leurocristine sulfate|Leurocristine, sulfate|Oncovin|VINCRISTINE SULFATE|Vincasar|Vincosid|Vincrex|Vincristine Sulfate|Vincristine, sulfate|vincristine sulfate","The sulfate salt of a natural alkaloid isolated from the plant Catharanthus roseus (Vinca rosea L.) with antimitotic and antineoplastic activities. Vincristine binds irreversibly to microtubules and spindle proteins in S phase of the cell cycle and interferes with the formation of the mitotic spindle, thereby arresting tumor cells in metaphase. This agent also depolymerizes microtubules and may also interfere with amino acid, cyclic AMP, and glutathione metabolism; calmodulin-dependent Ca(2+)-activated ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis.","Organic Chemical|Pharmacologic Substance"]
["C2702","Vincristine Sulfate Liposome","Marqibo|Vincristine Sulfate Liposome","A sphingomyelin/cholesterol liposomal formulation of vincristine sulfate with potential antineoplastic activity. Vincristine, a vinca alkaloid isolated from the plant Vinca rosea, irreversibly binds to and stabilizes tubulin, thereby interrupting microtubule assembly/disassembly dynamics, thereby preventing the formation of the mitotic spindle and leading to cell cycle arrest in metaphase. Liposomal encapsulation prolongs bioavailability of vincristine, increases its delivery to tumor tissues and reduces its toxicity profile. Compared to standard liposomal delivery, sphingosomal drug delivery further increases circulation time of serum drug and enhances drug accumulation at tumor sites, thereby leading to a further increase in efficacy.","Organic Chemical|Pharmacologic Substance"]
["C934","Vindesine","3-(Aminocarbonyl)-O4-deacetyl-3-de-(methoxycarbonyl)vincaleukoblastine|Compound 112531|DAVA|DVA|Deacetyl Vinblastine Carboxamide|Deacetylvinblastine Carboxamide|Desacetylvinblastine Amide|Lilly CT-3231|VDS|VINDESINE|Vindesine|vindesine","A synthetic derivative of vinblastine, a naturally occurring vinca alkaloid. Vindesine binds to and stabilizes tubulin, thereby interrupting tubulin polymerization and preventing the formation of the mitotic spindle and cell division; treated cells are unable to undergo mitosis and are arrested in metaphase. This agent also disrupts macromolecular synthesis. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C1274","Vinepidine","4'-Deoxyepivincristine|VINEPIDINE|Vinepidine","A vinca alkaloid compound and semi-synthetic vincristine derivative with antineoplastic activity. Vinepidine binds to and stabilizes tubulin, thereby preventing tubulin polymerization and depolymerization, which result in microtubule assembly and disassembly, respectively. Treated cells are unable to complete mitosis process and are arrested in the metaphase, thereby leading to an inhibition of cell growth.","Organic Chemical|Pharmacologic Substance"]
["C61564","Vinflunine","4'-Deoxy-20',20'-difluoro-C'-norvincaleukoblastine|VINFLUNINE|Vinflunine|vinflunine","A bi-fluorinated derivative of the semi-synthetic vinca alkaloid vinorelbine with antitubulin, antineoplastic, and antiangiogenic activities. Vinflunine inhibits tubulin assembly without any stablization of assembled microtubules at concentrations comparable to those of other vinca alkaloids such as vincristine, vinblastine and vinorelbine; this effect on microtubule dynamics results in cell cycle arrest in mitosis and apoptosis. Compared to other vinca alkaloids, this agent binds weakly to the vinca-binding site, indicating that vinflunine may exhibit reduced neurotoxicity.","Organic Chemical|Pharmacologic Substance"]
["C76266","Vinflunine Ditartrate","Javlor|VINFLUNINE DITARTRATE|Vinflunine Ditartrate","The ditartrate salt of vinflunine, a bi-fluorinated derivative of the semisynthetic vinca alkaloid vinorelbine with potential antimitotic and antineoplastic activities. Vinflunine binds to tubulin and inhibits tubulin assembly and disrupts microtubule assembly dynamics. This results in cell cycle arrest in mitosis and an induction of apoptosis.","Pharmacologic Substance"]
["C2378","Vinfosiltine","S12363|VINFOSILTINE|Vincaleukoblastine, O4-Deacetyl-3-de(methoxycarbonyl)-3-(((1-(diethoxyphosphinyl)-2-methylpropyl)amin)carbonyl)-,(3(S))-,Sulfate(Salt)|Vinfosiltine","An aminophosphonate derivative of a vinca alkaloid with potential antineoplastic activity. Vinfosiltine exerts its antineoplastic action just like its parent compound, vinblastine, by immobilizing tubulin molecules, thereby interrupting microtubule assembly/disassembly dynamics. As a result, vinfosiltine prevents mitotic spindle formation and leads to cell cycle arrest in metaphase.","Organic Chemical|Pharmacologic Substance"]
["C1275","Vinorelbine","3',4'-Didehydro-4'-deoxy-C'-norvincaleukoblastine|5'-Nor-Anhydrovinblastine|Dihydroxydeoxynorvinkaleukoblastine|VINORELBINE|Vinorelbine|nor-5'-Anhydrovinblastine|vinorelbine","A semisynthetic vinca alkaloid. Vinorelbine binds to tubulin and prevents formation of the mitotic spindle, resulting in the arrest of tumor cell growth in metaphase. This agent may also interfere with amino acid, cyclic AMP. and glutathione metabolism; calmodulin-dependent Ca++ -transport ATPase activity; cellular respiration; and nucleic acid and lipid biosynthesis.","Organic Chemical|Pharmacologic Substance"]
["C1395","Vinorelbine Tartrate","Biovelbin|Eunades|KW-2307|NVB|Navelbine Ditartrate|Navelbine ditartrate|Navelbine|VINORELBINE TARTRATE|Vinorelbine Ditartrate|Vinorelbine Tartrate|vinorelbine tartrate","The ditartrate salt of a semisynthetic vinca alkaloid derived from the leaves of the periwinkle plant (Vinca rosea) with antineoplastic properties.  Vinorelbine binds to tubulin, thereby inhibiting tubulin polymerization into microtubules and spindle formation and resulting in apoptosis of susceptible cancer cells. Inhibition of mitotic microtubules correlates with antitumor activity, whereas inhibition of axonal microtubules seems to correlate with vinorelbine's neurotoxicity. Compared to related vinca alkaloids, vinorelbine is more selective against mitotic than axonal microtubules in vitro, which may account for its decreased neurotoxicity.  This agent is also a radiation-sensitizing agent. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C66943","Vinorelbine Tartrate Emulsion","ANX-530|Vinorelbine Tartrate Emulsion|Vinorelbine Tartrate Injectable Emulsion","An emulsion containing the tartrate salt of the semisynthetic vinca alkaloid vinorelbine with antineoplastic activity. Vinorelbine binds to tubulin, inhibiting tubulin polymerization into microtubules; cell division is prevented, the cell cycle is arrested metaphase and cell death ensues. In this formulation vinorelbine is emulsified in a homogeneous suspension of nanoparticles, which protects the venous endothelium from coming into direct contact with the active ingredient, potentially reducing vinorelbine-associated venous toxicity at the venous injection site.","Pharmacologic Substance"]
["C85457","Vinorelbine Tartrate Oral","Navelbine|Vinorelbine Tartrate Oral","An orally bioavailable tartrate salt of vinorelbine, a semisynthetic vinca alkaloid with potential antineoplastic activity. Vinorelbine binds to tubulin, thereby inhibiting tubulin polymerization into microtubules and spindle formation and resulting in apoptosis of susceptible cancer cells. Inhibition of mitotic microtubules correlates with antitumor activity, whereas inhibition of axonal microtubules seems to correlate with vinorelbine's neurotoxicity. Compared to related vinca alkaloids, vinorelbine is more selective against mitotic than axonal microtubules in vitro, which may account for its decreased neurotoxicity. This agent is also a radiation-sensitizing agent.","Pharmacologic Substance"]
["C62525","Vintafolide","EC145|Folate-Vinca Alkaloid Conjugate EC145|VINTAFOLIDE|Vintafolide","A water-soluble, folate-receptor-targeted conjugate of folate and the vinca alkaloid desacetylvinblastine monohydrazide (DAVLBH) with potential antineoplastic activity. The folate moiety of vintafolide binds to folic acid receptors on the tumor cell surface and the agent is internalized via folate receptor-mediated endocytosis, delivering the tubulin-binding DAVLBH moiety directly into the tumor cell; DAVLBH binding to tubulin results in the disruption of microtubule assembly-disassembly dynamics, cell cycle arrest, and tumor cell apoptosis. Folic acid receptors are frequently upregulated on the surfaces of many tumor cell types. DAVLBH is a derivative of the natural product vinblastine.","Organic Chemical|Pharmacologic Substance"]
["C1276","Vinzolidine","2H-3,7-Methanoazacycloundecino(5,4-b)indole-9-carboxylic acid, 9-((2-beta,3-beta,4-beta,5-alpha,12-beta,19-alpha)-4-(acetyloxy)-3'-(2-chloroethyl)-6,7-didehydro-16-methoxy-1-methyl-2',4'-dioxospiro(aspidospermidine-3,5'-oxazolidin)-15-yl)-5-ethyl-1,4,5,6,7,8,9,10-octahydro-5-hydroxy-, methyl ester, (3R-(3R*,5S*,7R*,9S*))-|VINZOLIDINE|Vinzolidine","An orally active semisynthetic vinca alkaloid with potential antineoplastic activity. Like other vinca alkaloid compounds, vinzolidine binds to and stabilizes tubulin molecules, thereby interfering with microtubule assembly/disassembly dynamics. As a result, vinzolidine prevents mitotic spindle formation and leads to cell cycle arrest in metaphase.","Organic Chemical|Pharmacologic Substance"]
["C87288","Vinzolidine Sulfate","2h-3,7-Methanoazacycloundecino(5,4-Beta)Indole-9-Carboxylic Acid, 9-((2Beta,3Beta,4Beta,5Alpha,12Beta,19Alpha)-4-(Acetyloxy)-3'-(2-Chloroethyl)-6,7-Didehydro-16-Methoxy-1-Methyl-2',4'-Dioxospiro(Aspidospermidine-3,5'-Oxazolidin)-15-Yl)-5-Ethy|LY104208|Methyl (3R,5S,7R,9S)-9-[3'-(2-Chloroethyl)-6,7-Didehydro-4Beta-Hydroxy-16-Methoxy-1-Methyl-2',4'-Dioxo-2Beta,3Beta,5Alpha,12Beta,19Alpha-Spiro(Aspidospermidine-3,5'-Oxazolidin]-15-yl)-5-Ethyl-1,4,5,6,7,8,9,10-Octahydro-5-Hydroxy-2H-3,7-Methano|VINZOLIDINE SULFATE|Vinzolidine Sulfate","The sulfate salt of vinzolidine, an orally active semisynthetic vinca alkaloid with potential antineoplastic activity. Like other vinca alkaloid compounds, vinzolidine binds to and stabilizes tubulin molecules, thereby interfering with microtubule assembly/disassembly dynamics. As a result, vinzolidine prevents mitotic spindle formation and leads to cell cycle arrest in metaphase.","Pharmacologic Substance"]
["C26677","Virulizin","Virulizin","A natural biological response modifier (BRM) isolated from bovine reticuloendothelial tissue. Viruzlin may enhance cell-mediated immune response to tumor cells by direct macrophage activation. (NCI04)","Pharmacologic Substance"]
["C74038","Vismodegib","2-chloro-N-[4-chloro-3-(pyridin-2-yl)phenyl]-4-(methylsulfonyl)benzamide|Erivedge|GDC-0449|Hedgehog Antagonist GDC-0449|VISMODEGIB|Vismodegib","An orally bioavailable small molecule with potential antineoplastic activity. Hedgehog antagonist GDC-0449 targets the Hedgehog signaling pathway, blocking the activities of the Hedgehog-ligand cell surface receptors PTCH and/or SMO and suppressing Hedgehog signaling. The Hedgehog signaling pathway plays an important role in tissue growth and repair; aberrant constitutive activation of Hedgehog pathway signaling and uncontrolled cellular proliferation may be associated with mutations in the Hedgehog-ligand cell surface receptors PTCH and SMO.","Pharmacologic Substance"]
["C88329","Vistusertib","AZD 2014|AZD-2014|AZD2014|Benzamide, 3-(2,4-Bis((3S)-3-methyl-4-morpholinyl)pyrido(2,3-d)pyrimidin-7-yl)-N-methyl-|VISTUSERTIB|Vistusertib","An orally bioavailable inhibitor of the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. Vistusertib inhibits the activity of mTOR, which may result in the induction of tumor cell apoptosis and a decrease in tumor cell proliferation. mTOR, a serine/threonine kinase that is upregulated in a variety of tumors, plays an important role downstream in the PI3K/Akt/mTOR signaling pathway.","Pharmacologic Substance"]
["C942","Vitamin E Compound","2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)chroman-6-ol|3,4-Dihydro-2,5,7,8-tetramethyl-2-(4,8,12-trimethyltridecyl)-2H-1-benzopyran-6-ol|5,7,8-Trimethyltocol|E Vitamin|Vitamin E Compound|Vitamin E|vitamin E","A natural fat-soluble antioxidant with potential chemopreventive activity. Also known as tocopherol, vitamin E ameliorates free-radical damage to biological membranes, protecting polyunsaturated fatty acids (PUFA) within membrane phospholipids and within circulating lipoproteins. Peroxyl radicals react 1000-fold faster with vitamin E than with PUFA.  In the case of oxygen free radical-mediated tumorigenesis, vitamin E may be chemopreventive. (NCI04)","Pharmacologic Substance|Vitamin"]
["C2432","Vitespen","Autologous gp96 Heat Shock Protein Peptide Complex Vaccine|HSP gp96-Peptide Complex|HSPPC-96|Heat Shock Protein Peptide Complex-96|Oncophage|Recombinant Human Tumor Rejection Antigen 1|VITESPEN|Vitespen|gp96 HSP-Peptide Complex|gp96 HSP-peptide complex|gp96 Heat Shock Protein-Peptide Complex|gp96 heat shock protein-peptide complex vaccine|vitespen","An autologous cancer vaccine derived from tumor-specific gp96 heat shock proteins.  Heat shock proteins chaperone peptides through the endoplasmic reticulum, are key regulators of dendritic cell maturation, migration and antigen processing, and are involved in T-cell activation. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C126422","VLP-encapsulated TLR9 Agonist CMP-001","ARB-1598|CMP-001|CYT 003|CYT-003|VLP-encapsulated TLR9 Agonist CMP-001","An agent composed of an unmethylated CpG motif-rich G10 oligonucleotide, which is an agonist of toll-like receptor 9 (TLR9), encapsulated in noninfectious virus-like particles (VLPs), with potential immunostimulating and antineoplastic activities. Upon administration of CMP-001, the VLPs are specifically taken up by and release the oligonucleotide into antigen-presenting cells (APCs), including dendritic cells (DCs). In turn, the oligonucleotide binds to and activates intracellular TLR9. This stimulates immune signaling pathways, induces the innate immune system and may promote the immune system to attack tumor cells. VLPs stimulate the immune system. TLR9, a member of the TLR family, plays a key role in both pathogen recognition and the activation of innate immunity.","Pharmacologic Substance"]
["C91734","Vocimagene Amiretrorepvec","DNA (Synthetic Toca 511-encoding Retroviral Vector AC3-yCD2(V))|Toca 511|VOCIMAGENE AMIRETROREPVEC|Vocimagene Amiretrorepvec","A replication competent retroviral vector, derived from the Moloney murine leukemia virus (MoMLV), encoding a modified form of the yeast suicide gene cytosine deaminase (CD) (Toca 511) used as an antineoplastic adjuvant. Upon transcranial injection, vocimagene amiretrorepvec preferentially enters and transfects tumor cells, and expresses cytosine deaminase, an enzyme that catalyzes the intracellular conversion of the prodrug flucytosine (5-FC) into the antineoplastic agent 5-fluorouracil (5-FU). After administration of 5-FC, the tumor can be eradicated upon activation of 5-FU.","Pharmacologic Substance|Virus"]
["C79844","Volasertib","BI 6727|BI-6727|Benzamide, N-(Trans-4-(4-(Cyclopropylmethyl)-1-Piperazinyl)Cyclohexyl)-4-(((7r)-7-Ethyl-5,6,7,8-Tetrahydro-5-Methyl-8-(1-Methylethyl)-6-Oxo-2-Pteridinyl)Amino)-3-Methoxy-|Polo-like Kinase 1 Inhibitor BI 6727|VOLASERTIB|Volasertib","A dihydropteridinone Polo-like kinase 1 (Plk1) inhibitor with potential antineoplastic activity. Volasertib selectively inhibits Plk1, inducing selective G2/M arrest followed by apoptosis in a variety of tumor cells while causing reversible cell arrest at the G1 and G2 stage without apoptosis in normal cells. Plk1, named after the polo gene of Drosophila melanogaster, is a serine/threonine protein kinase involved in regulating mitotic spindle function in a non-ATP competitive manner.","Pharmacologic Substance"]
["C104732","Volitinib","AZD6094|HMPL-504|SAVOLITINIB|Volitinib","An orally bioavailable inhibitor of the c-Met receptor tyrosine kinase with potential antineoplastic activity. Volitinib selectively binds to and inhibits the activation of c-Met in an ATP-competitive manner, and disrupts c-Met signal transduction pathways. This may result in cell growth inhibition in tumors that overexpress the c-Met protein. C-Met encodes the hepatocyte growth factor receptor tyrosine kinase and plays an important role in tumor cell proliferation, survival, invasion, and metastasis, and tumor angiogenesis; this protein is overexpressed or mutated in a variety of cancers.","Pharmacologic Substance"]
["C48426","Volociximab","Anti-alpha5-beta1 Integrin|M200|VOLOCIXIMAB|Volociximab|anti-a5-beta1 Integrin|volociximab","A chimeric monoclonal antibody with potential antineoplastic activity. Volociximab binds to and inhibits the activity of alpha(5)beta(1) integrin, thereby inhibiting endothelial cell-cell interactions, endothelial cell-matrix interactions, and angiogenesis. (NCI05)","Pharmacologic Substance"]
["C2492","Von Hippel-Lindau Peptide Vaccine","VHL Peptides|VHL peptide vaccine|Von Hippel-Lindau Peptide Vaccine","A cancer vaccine composed of peptides derived from a tumor-associated protein encoded by a mutated Von Hippel-Lindau (VHL) oncogene.  VHL peptide vaccine may stimulate a cytotoxic T cell response against tumor cells expressing the VHL tumor-associated protein. (NCI04)","Immunologic Factor|Pharmacologic Substance"]
["C1796","Vorinostat","L-001079038|MSK-390|N-Hydroxy-N'-phenyloctanediamide|SAHA|Suberanilohydroxamic Acid|Suberoylanilide Hydroxamic Acid|VORINOSTAT|Vorinostat|Zolinza|suberoylanilide hydroxamic acid|vorinostat","A synthetic hydroxamic acid derivative with antineoplastic activity. Vorinostat, a second generation polar-planar compound, binds to the catalytic domain of the histone deacetylases (HDACs). This allows the hydroxamic moiety to chelate zinc ion located in the catalytic pockets of HDAC, thereby inhibiting deacetylation and leading to an accumulation of both hyperacetylated histones and transcription factors. Hyperacetylation of histone proteins results in the upregulation of the cyclin-dependant kinase p21, followed by G1 arrest. Hyperacetylation of non-histone proteins such as tumor suppressor p53, alpha tubulin, and heat-shock protein 90 produces additional anti-proliferative effects. This agent also induces apoptosis and sensitizes tumor cells to cell death processes. Vorinostat crosses the blood-brain barrier.","Organic Chemical|Pharmacologic Substance"]
["C88315","Vorsetuzumab-mafodotin","Anti-CD70 MoAb SGN70-MMAF Conjugate|SGN-75|Vorsetuzumab-mafodotin","An antibody-drug conjugate (ADC) consisting of a humanized monoclonal antibody, directed against the extracellular domain of the human CD70 molecule, conjugated to the auristatin analogue monomethyl auristatin phenylalanine (MMAF), with potential antineoplastic activity. The anti-CD70 antibody moiety of vorsetuzumab-mafodotin selectively binds to the extracellular domain of CD70 on tumor cell surfaces. Upon internalization, the MMAF moiety is released, binds to tubulin and inhibits its polymerization, which may result in G2/M phase arrest, tumor cell apoptosis and inhibition of cellular proliferation in tumor cells that overexpress CD70. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C95148","Vosaroxin","1,4-Dihydro-7-(3-methoxy-4-methylamino-1-pyrrolidinyl)-4-oxo-1-(2-thiazolyl)-1,8-naphthyridine-3-carboxylic acid|AG-7352|SNS-595|SPC 595|VOSAROXIN|Voreloxin|Vosaroxin","A small molecule and a naphthyridine analogue with antineoplastic activity. Vosaroxin intercalates into DNA in a site-specific manner and blocks the re-ligation process carried out by topoisomerase II during DNA replication. As a result, inhibition of DNA replication, RNA and protein synthesis occurs, followed by cell cycle arrest at G2 phase and induced p53-independent apoptosis. This agent shows a favorable toxicity profile in several aspects: it does not generate reactive oxygen species, as do anthracyclines, hence reducing the risk of cardiotoxicity; it is not a P-glycoprotein (P-gp) substrate, and thereby evades the common mechanism for multidrug resistance; and it has limited distribution to normal tissues and a more chemically stable molecular structure.","Pharmacologic Substance"]
["C71704","Voxtalisib","SAR-245409|SAR245409|VOXTALISIB|Voxtalisib|XL-765|XL765","An orally bioavailable small molecule targeting the phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinases in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. Voxtalisib inhibits both PI3K kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in susceptible tumor cell populations. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion in response to nutrient and energy deprivation. Accordingly, this agent maybe more potent compared to an agent that inhibits either PI3K kinase or mTOR kinase alone.","Pharmacologic Substance"]
["C91725","WEE1 Inhibitor AZD1775","2-Allyl-1-(6-(2-hydroxypropan-2-yl)pyridin-2-yl)-6-((4-(4-methylpiperazin-1-yl)phenyl)amino)-1H-pyrazolo[3,4-d]pyrimidin-3(2H)-one|AZD-1775|AZD1775|MK-1775|MK1775|WEE1 Inhibitor AZD1775","A small molecule inhibitor of the tyrosine kinase WEE1 with potential antineoplastic sensitizing activity. AZD1775 selectively targets and inhibits WEE1, a tyrosine kinase that phosphorylates cyclin-dependent kinase 1 (CDK1, CDC2) to inactivate the CDC2/cyclin B complex. Inhibition of WEE1 activity prevents the phosphorylation of CDC2 and impairs the G2 DNA damage checkpoint. This may lead to apoptosis upon treatment with DNA damaging chemotherapeutic agents. Unlike normal cells, most p53 deficient or mutated human cancers lack the G1 checkpoint as p53 is the key regulator of the G1 checkpoint and these cells rely on the G2 checkpoint for DNA repair to damaged cells. Annulment of the G2 checkpoint may therefore make p53 deficient tumor cells more vulnerable to antineoplastic agents and enhance their cytotoxic effect.","Pharmacologic Substance"]
["C78490","White Button Mushroom Extract","WBM Extract|White Button Mushroom Extract","A heat-stable extract of white button mushrooms (Agaricus bisporus) with potential chemopreventive and immunomodulating activities. Phytochemicals, such as polysaccharides and especially beta-D-glucans found in the white button mushroom extract, bind to and inhibit the activity of aromatase, an enzyme responsible for the conversion of androgens to estrogens and which is often upregulated in breast cancer cells. The consequent decrease in estrogen production may result in the suppression of estrogen-dependent cellular proliferation. In addition, this extract may promote dendritic cell (DC) maturation, increase interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) production, and may enhance natural killer (NK) cell activity, thus amplifying both innate and T cell-mediated immune responses against cancer cells.","Organic Chemical|Pharmacologic Substance"]
["C126649","White Carrot","White Carrot","A vegetable, also known as Arracacha, with potential chemoprevenitve, anti-oxidant and protective activities. White carrot contains a variety of nutrients, including minerals and vitamins. Polyacetylenes, including falcarinol, falcarindiol and falcarindiol-3-acetate are mainly responsible for its potential anti-cancer activity.","Food"]
["C60774","Wild-type Reovirus","Reolysin|Wild-type Reovirus","A serotype 3 Dearing strain (T3D) of reovirus (Respiratory Enteric Orphan VIRUS). Reovirus, a dsRNA virus, is able to replicate specifically in cancer cells bearing an activated Ras pathway. In contrast to normal cells, two-thirds of human cancer cells are Ras-activated, and are deficient in their ability to trigger the antiviral response mediated by the host cellular protein, double-stranded RNA-dependent protein kinase (PKR). In Ras-activated cancer cells, reovirus is able to freely replicate and subsequently cause apoptosis in the tumor cells. Cell lysis frees progeny viral particles to infect surrounding cancer cells. This cycle of infection, replication and cell death is believed to be repeated until no more Ras-activated tumor cells are available. Because the reovirus kills Ras-activated cancer cells, this is a potential therapeutic for malignant glioma, pancreatic, colon and some lung cancers.","Pharmacologic Substance"]
["C113435","Wnt-5a Mimic Hexapeptide Foxy-5","Foxy-5|Wnt-5a Mimic Hexapeptide Foxy-5","A formylated, six amino acid, Wnt5a-derived peptide and wnt-5a mimetic with potential anti-metastatic activity. Upon intravenous administration, Wnt-5a mimic hexapeptide foxy-5 binds to and activates the wnt-5a receptors, Frizzled-2 and -5, which activates wnt-5a-mediated signaling. Increased wnt-5a signaling may inhibit endothelial tumor cell migration and invasion. This may decrease metastasis of susceptible tumor cells. However, foxy-5 does not affect tumor cell proliferation or apoptosis. Foxy-5 lacks a heparan sulfate-binding domain and contains a formyl group on its NH2-terminal methionine residue which decreases in vivo degradation. Decreased expression of wnt-5a protein is associated with increased motility of certain tumor cell types.","Pharmacologic Substance"]
["C28501","Wobe-Mugos E","Wobe-Mugos E","An enzymatic preparation containing proteolytic enzymes papain, trypsin and chymotrypsin with potential anti-inflammatory and anticarcinogenic activities. Papain can be extracted from the fruit of the papaya plant. Trypsin and chymotrypsin are serine proteases produced and secreted by the pancreas. Although its exact mechanisms has yet to be fully illustrated, Wobe-Mugos E appears to have the ability to modulate the immune system by degrading cytokines, and cytokine receptors and clearing circulating immune protein complexes, as well as disrupting adhesion molecules. This agent has been shown to reduce chemotherapy-induced toxicity, inhibit tumor cell proliferation and prolong survival rates.","Pharmacologic Substance"]
["C104738","WT1 124-138 Peptide Vaccine","WT1 124-138 Peptide Vaccine","A synthetic peptide vaccine consisting of a HLA-DR15-restricted human Wilms' Tumor protein-1 (WT1) peptide comprised of amino acids 124 through 138, a HLA class II-restricted WT1 peptide, with potential immunomodulating and antitumor activities. Vaccination with WT1 124-138 peptide may stimulate a CD4-positive helper T-lymphocyte-mediated immune response against WT1 expressing cells. Activated helper T-cells stimulate dendritic cells, and activate the proliferation of other T-lymphoctes and B-lymphocytes. This causes tumor cell lysis and inhibition of cancer cell proliferation in WT1-overexpressing tumor cells. WT1, a zinc finger DNA-binding protein, is overexpressed in most types of leukemia and in a variety of solid cancers.","Pharmacologic Substance"]
["C61442","WT1 126-134 Peptide Vaccine","WT1 126-134 Peptide Vaccine","A synthetic peptide vaccine consisting of the amino acids 126 through 134 of the human Wilms' Tumor protein-1 (WT1) with potential antitumor activity. WT1, a tumor associated antigen, is overexpressed in most types of leukemia and in a variety of solid cancers. Vaccination with WT1 126-134 peptide vaccine may induce a WT1-specific cytotoxic T-lymphocyte (CTL) response against WT1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation.","Pharmacologic Substance"]
["C104734","WT1 235-243 Peptide Vaccine","WT1 235-243 Peptide Vaccine","A synthetic peptide vaccine consisting of a HLA-A24-restricted human Wilms' Tumor protein-1 (WT1) peptide comprised of amino acids 235 through 243, a MHC class I-restricted peptide, with potential immunomodulating and antitumor activities. Vaccination with WT1 235-243 peptide may induce a WT1-specific cytotoxic T-lymphocyte (CTL) response against WT1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation. WT1, a zinc finger DNA-binding protein, is overexpressed in most types of leukemia and in a variety of solid cancers.","Pharmacologic Substance"]
["C104737","WT1 247-261 Peptide Vaccine","WT1 247-261 Peptide Vaccine","A synthetic peptide vaccine consisting of a HLA-DRw53-restricted human Wilms' Tumor protein-1 (WT1) peptide comprised of amino acids 247 through 261, a HLA class II-restricted WT1 peptide, with potential immunomodulating and antitumor activities. Vaccination with WT1 247-261 peptide may stimulate a CD4-positive helper T-lymphocyte-mediated immune response against WT1 expressing cells. Activated helper T-cells stimulate dendritic cells, and activate the proliferation of other T-lymphoctes and B-lymphocytes. This causes tumor cell lysis and inhibition of cancer cell proliferation in WT1-overexpressing tumor cells. WT1, a zinc finger DNA-binding protein, is overexpressed in most types of leukemia and in a variety of solid cancers.","Pharmacologic Substance"]
["C64635","WT1 Analog Peptide Vaccine","WT-1 vax|WT1 Analog Peptide Vaccine","A peptide vaccine comprised of an epitope of human Wilms tumor 1 (WT-1) with potential antineoplastic activity. WT-1, a transcription factor, is overexpressed in most types of leukemia and in some solid cancers. Vaccination with the WT-1 analog peptide vaccine may induce a cytotoxic T-lymphocyte (CTL) response against WT-1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C88260","WT1 mRNA-Electroporated Autologous Dendritic Cell Vaccine","WT1 mRNA-Electroporated Autologous Dendritic Cell Vaccine|Wilms Tumor 1 mRNA-Electroporated Autologous Dendritic Cell Vaccine","A cancer vaccine containing autologous dendritic cells electroporated with full-length mRNA encoding Wilms' tumor 1 (WT1) antigen with potential immunostimulatory and antineoplastic activities. Upon administration, WT1 mRNA-electroporated autologous dendritic cell vaccine may elicit a cytotoxic T-cell (CTL) response against tumor cells expressing WT1. Wt1 is frequently overexpressed in a variety of tumor cell types and often correlates with disease progression and poor prognosis.","Cell|Pharmacologic Substance"]
["C106257","WT1 Peptide Vaccine OCV-501","OCV-501|WT1 Peptide Vaccine OCV-501","A peptide cancer vaccine comprised of a peptide derived from Wilms tumor gene 1 (WT1) protein, with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration, WT1 peptide vaccine OCV-501 may stimulate a CD4-positive helper T-lymphocyte-mediated immune response against WT1 expressing cells. WT1 protein, a zinc finger DNA-binding protein, is overexpressed in leukemic cells and in some solid tumors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C102751","WT1 Peptide Vaccine WT2725","WT1 Peptide Vaccine WT2725|WT2725","A peptide cancer vaccine comprised of a peptide derived from Wilms tumor gene 1 (WT1) protein, with potential immunomodulating and antineoplastic activities. Upon administration, WT2725 may induce a specific cytotoxic T-lymphocyte (CTL) response against WT1-overexpressing tumor cells. WT1 protein, a zinc finger DNA-binding protein, is overexpressed in leukemic cells and in a vast number of non-hematological solid tumors.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C121957","WT1 Protein-derived Peptide Vaccine DSP-7888","DSP-7888|WT1 Protein-derived Peptide Vaccine DSP-7888","A peptide cancer vaccine comprised of peptides derived from the Wilms tumor gene 1 (WT1) protein, with potential immunomodulating and antineoplastic activities. Upon administration, WT1 protein-derived peptide vaccine DSP-7888 may induce a specific cytotoxic T-lymphocyte (CTL) response against WT1-overexpressing tumor cells. In addition, DSP-7888 induces a helper T-lymphocyte-mediated immune response against WT1 expressing tumor cells. WT1 protein, a zinc finger DNA-binding protein and transcription factor, is overexpressed in leukemic cells and in many non-hematological solid tumors.","Immunologic Factor|Pharmacologic Substance"]
["C78865","WT1-A10/AS01B Immunotherapeutic GSK2130579A","GSK2130579A|WT1-A10/AS01B Immunotherapeutic GSK2130579A","An immunotherapeutic consisting of the recombinant fusion protein WT1-A10 combined with the adjuvant ASO1B with potential immunostimulating and antineoplastic activities.  Upon administration, WT1-A10/AS01B immunotherapeutic GSK2130579AWT1 may induce a WT1-specific cytotoxic T-lymphocyte (CTL) response against WT1-expressing tumor cells, resulting in cell lysis and the inhibition of cellular proliferation. The tumor-associated antigen WT1 (Wilms tumor protein-1) is overexpressed in most types of leukemia and in a variety of solid cancers. WT1-A10 is a 292 amino acid recombinant fusion protein consisting of a 12-mer truncated tat sequence (leader sequence) and amino acids number 2-281 of the WT1 sequence; ASO1B consists of a combination of the adjuvants monophosporyl lipd A (MPL) and Q21.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C74091","WT1-Sensitized Allogeneic T-Lymphocytes","WT1-Sensitized Allogeneic T-Lymphocytes","A population of allogeneic T-cells sensitized with Wilms tumor 1 (WT1) antigen with potential immunostimulatory and antineoplastic activities. Upon administration, WT1-sensitized T cells may bind to and lyse WT1-expressing tumor cells. WT1 antigen, a zinc finger DNA-binding protein acting as a transcriptional activator or repressor depending on the cellular or chromosomal context, is overexpressed in leukemic cells and in a vast number of nonhematological solid tumors.","Pharmacologic Substance"]
["C121950","Xanthohumol","3'-[3,3-Dimethyl allyl]-2',4',4-trihydroxy-6'-methoxychalcone|Xanthohumol","A prenylated flavonoid derived from the female flowers of the hops plant (Humulus lupulus L), with potential chemopreventive and antineoplastic activities. Upon administration, xanthohumol scavenges reactive oxygen species (ROS), thereby preventing DNA damage due to oxidative stress. In addition, xanthohumol is able to increase the expression of phase II cytoprotective enzymes, thereby inactivating carcinogens. This agent exerts anti-inflammatory activity, through the inhibition of inflammation-inducing enzymes, inhibits DNA synthesis, and induces apoptosis of susceptible cancer cells. Xanthohumol also decreases the expression of C-X-C chemokine receptor 4 (CXCR4), thereby preventing cancer cell invasion.","Pharmacologic Substance"]
["C103823","XBP1-US/XBP1-SP/CD138/CS1 Multipeptide Vaccine PVX-410","PVX-410|XBP1-US/XBP1-SP/CD138/CS1 Multipeptide Vaccine PVX-410","A cancer vaccine containing immunogenic, HLA-A2-specific epitopes derived from X-box-binding protein 1-unspliced (XBP1-US), XBP1-spliced (SP), syndecan-1 (CD138), and CS1 (CD2 subset 1, CRACC, SLAMF7, CD319) with potential immunomodulating and antineoplastic activities. Upon subcutaneous administration, XBP1-US/XBP1-SP/CD138/CS1 multipeptide vaccine PVX-410 may stimulate the immune system to induce a cytotoxic T-lymphocyte response against the four myeloma-specific antigens.  The tumor associated antigens (TAAs) XBP1-US, XBP1-SP, CD138 and CS1, are overexpressed on the surface of multiple myeloma (MM) cells.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C68839","Xenogeneic Tyrosinase DNA Vaccine","Xenogeneic Tyrosinase DNA Vaccine","A plasmid DNA vaccine, encoding an epitope of mouse tyrosinase, with potential antineoplastic activity. Administered via intramuscular electroporation, vaccination with xenogeneic tyrosinase DNA vaccine may induce both humoral and cytotoxic lymphocyte (CTL) immune responses against melanoma cells that express tyrosinase, resulting in decreased tumor growth.","Pharmacologic Substance"]
["C123913","XIAP/cIAP1 Antagonist ASTX660","ASTX 660|ASTX660|XIAP/cIAP1 Antagonist ASTX660","An orally bioavailable, non-peptidomimetic antagonist of both X chromosome-linked inhibitor of apoptosis protein (XIAP) and cellular IAP 1 (cIAP1), with potential antineoplastic and pro-apoptotic activities. Upon administration, XIAP/cIAP1 antagonist ASTX660 selectively binds to and inhibits the activity of XIAP and cIAP1. This restores and promotes the induction of apoptotic signaling pathways in cancer cells, and inactivates the nuclear factor-kappa B (NF-kB)-mediated survival pathway. XIAP and cIAP1 are overexpressed by many cancer cell types and suppress apoptosis by inhibiting the activity of certain caspases; they promote both cancer cell survival and chemotherapy resistance.","Pharmacologic Substance"]
["C49090","XL820","XL820","An orally bioavailable, small molecule receptor tyrosine kinase inhibitor with potential antineoplastic activity. XL820 binds to and inhibits the receptor tyrosine kinases for vascular endothelial growth factor (VEGF), c-kit, and platelet-derived growth factor (PDGF). In tumor models of breast carcinomas, gliomas, and leukemia, this agent exhibits dose-dependent growth inhibition and has been shown to cause tumor regression.","Pharmacologic Substance"]
["C125193","XPO1 Inhibitor KPT-8602","Exportin 1 Inhibitor KPT-8602|KPT-8602|Selective Inhibitor of Nuclear Export KPT-8602|XPO1 Inhibitor KPT-8602|XPO1-inhibiting SINE Compound KPT-8602","An orally bioavailable inhibitor of exportin-1 (XPO1; chromosome region maintenance 1 protein homolog; CRM1), with potential antineoplastic activity. Upon administration, XPO1 inhibitor KPT-8602 binds to the XPO1 cargo binding site, which prevents the XPO1-mediated nuclear export of cargo proteins such as tumor suppressor proteins (TSPs), including p53, p73, BRCA1/2, pRB, FOXO, and other growth regulatory proteins and leads to their selective accumulation in the nuclei of tumor cells. As a selective inhibitor of nuclear export (SINE), KPT-8602 restores the nuclear localization and function of tumor suppressing proteins which leads to the induction of apoptosis in tumor cells. XPO1, the major export factor that transports proteins from the nucleus to the cytoplasm, is overexpressed in a variety of cancer cell types while minimally expressed in normal, healthy cells. The export of tumor suppressor proteins into the cytoplasm prevents them from initiating apoptosis and leads to uncontrolled tumor cell proliferation.","Pharmacologic Substance"]
["C128246","XPO1 Inhibitor SL-801","CBS 9106|SL 801|SL-801|XPO1 Inhibitor SL-801","An orally bioavailable inhibitor of the nuclear export protein exportin-1 (XPO1; chromosome region maintenance 1 protein homolog; CRM1), with potential antineoplastic and pro-apoptotic activities. Upon administration, XPO1 inhibitor SL-801 reversibly binds to the cargo binding site of XPO1, and prevents the XPO1-mediated nuclear export of cargo proteins, including tumor suppressor proteins (TSPs), such as p53, FOXO, p21, and p27, and leads to their selective accumulation in the nuclei of tumor cells. As a selective inhibitor of nuclear export (SINE), SL-801 restores the nuclear localization and function of TSPs, which leads to the induction of apoptosis in tumor cells. XPO1, the major export factor that transports proteins and RNA from the nucleus to the cytoplasm, is overexpressed in a variety of cancer cell types while minimally expressed in normal, healthy cells. The dysregulated export of TSPs into the cytoplasm prevents TSP-initiated apoptosis. XPO1 overexpression leads to uncontrolled tumor cell proliferation and is associated with poor prognosis.","Pharmacologic Substance"]
["C2597","Y 90 Monoclonal Antibody CC49","Y 90 Monoclonal Antibody CC49|Yttrium Y 90 Monoclonal Antibody CC49","A radioimmunoconjugate of the humanized monoclonal antibody (MoAb) CC49 labeled with Yttrium 90 (Y-90). MoAb CC49 recognizes the pancarcinoma tumor-associated glycoprotein (TAG)-72 with high affinity. Y-90 MoAb CC49 delivers beta particles emitting Y-90 radionuclide directly to tumor cells that express TAG-72, thereby this agent may be used in radioimmunotherapeutic treatment of cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2541","Y 90 Monoclonal Antibody HMFG1","MOAB HMFG1, yttrium Y 90|Y 90 MoAb HMFG1|Y 90 Monoclonal Antibody HMFG1|Yttrium Y 90 Monoclonal Antibody HMFG1|monoclonal antibody HMFG1, yttrium Y 90|yttrium Y 90 MOAB HMFG1","A radioimmunoconjugate of humanized monoclonal antibody (MoAb) HMFG1 labeled with Yttrium 90 (Y-90). MoAb MFG1 was raised against Human Milk Fat Globules and reacts with an epitope (PDTR) in the protein core of MUC1 mucins, which are up-regulated in human breast and other carcinomas.Y-90 MoAb HMFG1 delivers beta particle emitting Y-90 radionuclide directly to tumor cells that express MUC1, thereby this agent may be used in radioimmunotherapy of cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2247","Y 90 Monoclonal Antibody Lym-1","MOAB Lym-1, yttrium Y 90|Y 90 MoAb Lym-1|Y 90 Monoclonal Antibody Lym-1|Yttrium Y 90 Monoclonal Antibody Lym-1|monoclonal antibody Lym-1, yttrium Y 90|yttrium Y 90 MOAB Lym-1","A radioimmunoconjugate of a murine monoclonal antibody, MoAb Lym-1, labeled with yttrium 90 (Y-90). MoAb Lym-1 recognizes an epitope of the histocompatibility antigen HLA-DR, which is over-expressed on most B-cell lymphomas. Y-90 MoAb Lym-1 delivers Y-90 radionuclide directly to tumor cells that express HLA-DR antigen, thereby this agent may be used in radioimmunotherapy of cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2532","Y 90 Monoclonal Antibody m170","MOAB m170, yttrium Y 90|Y 90 MoAb m170|Y 90 Monoclonal Antibody m170|Yttrium Y 90 Monoclonal Antibody m170|monoclonal antibody m170, yttrium Y 90|yttrium Y 90 MOAB m170","A radioimmunoconjugate of m170 monoclonal antibody (MoAb) conjugated with isotope yttrium 90. MoAb m170 is a murine MoAb that recognizes MUC-1 antigen present on the surface of many adenocarcinomas. This radioimmunoconjugate emits beta particles that cause cytotoxicity in tumor cells and has both imaging and therapeutic uses.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2248","Y 90 Monoclonal Antibody M195","MOAB M195, yttrium Y 90|Y 90 MoAb M195|Y 90 Monoclonal Antibody M195|Yttrium Y 90 Monoclonal Antibody M195|monoclonal antibody M195, yttrium Y 90","A radioimmunoconjugate of humanized M195 monoclonal antibody (MoAb) conjugated with isotope yttrium 90. MoAb M195 is reactive with the cell surface antigen CD33, a glycoprotein found on myeloid leukemia blasts and early hematopoietic progenitor cells but not on normal stem cells. This radioimmunoconjugate emits beta particles that causes cytotoxicity in tumor cells and has both imaging and therapeutic uses.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C111897","Yangzheng Xiaoji Extract","DME25|YZXJ Extract|Yangzheng Xiaoji Extract","A traditional Chinese medicine (TCM)-based formulation containing the Yangzheng Xiaoji (YZXJ) extract, consisting of various components, with potential antineoplastic and anti-angiogenic activities. Some of the main components in Yangzheng Xiaoji are Radix Astragali, Fructus Ligustri Lucidi, Radix Ginseng, Ganoderma, Rhizoma Curcumac, Fried Rhizoma Atractylodis, Macrocephalae and Herba Hedyotidis. Although the exact mechanism(s) through which Yangzheng Xiaoji exerts its effects have yet to be fully elucidated, this agent, upon administration, inhibits the activation of various signaling protein kinases, such as focal adhesion kinase (FAK) and paxillin. This prevents signal transduction pathways that are upregulated in cancer, prevents the adhesion and migration of tumor cells and inhibits tumor cell growth.","Pharmacologic Substance"]
["C26678","YM598","Potassium (E)-N-[6-methoxy-5-(2-methoxyphenoxy)-2-(pyrimidin-2-yl)pyrimidin-4-yl]-2-phenylenthene Sulfonamidate|YM598","An orally active synthetic substituted phenylethenesulfonamide. As a selective endothelin A receptor antagonist, YM598 inhibits endothelin-mediated mechanisms involved in tumor cell growth and progression, angiogenesis, and metastasis. (NCI04)","Pharmacologic Substance"]
["C74093","Yttrium Y 90 Anti-CD45 Monoclonal Antibody AHN-12","Y 90 AHN-12|Yttrium Y 90 Anti-CD45 Monoclonal Antibody AHN-12","A radioimmunoconjugate comprised of the monoclonal antibody AHN-12 conjugated to the radioisotope yttrium 90 with potential radioimmunotherapeutic activity. Yttrium Y 90 monoclonal antibody AHN-12 binds to the tyrosine phosphatase CD45, expressed on the surface of normal and malignant hematopoietic cells. After binding and internalization by CD45-expressing tumor cells, this agent may deliver a cytotoxic dose of beta radiation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C95698","Yttrium Y 90 Anti-CD45 Monoclonal Antibody BC8","90Y Anti-CD45 MoAb BC8|Yttrium Y 90 Anti-CD45 Monoclonal Antibody BC8","A radioimmunoconjugate containing the murine IgG1 anti-CD45 monoclonal antibody (MoAb) BC8 labeled with yttrium 90 (Y90), with potential immunotherapeutic activity. Yttrium Y 90 anti-CD45 monoclonal antibody BC8 binds to CD45 antigen, a receptor protein-tyrosine phosphatase expressed on the surface of both normal and malignant hematopoietic cells. After binding and internalization by CD45-expressing tumor cells, this agent may deliver a cytotoxic dose of beta radiation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C122405","Yttrium Y 90 Anti-CDH3 Monoclonal Antibody FF-21101","FF-21101(90Y)|Yttrium Y 90 Anti-CDH3 Monoclonal Antibody FF-21101","A radioimmunoconjugate consisting of a chimeric monoclonal antibody targeting human cadherin-3 (CDH3) and labeled, via the macrocyclic chelator 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA), with the beta-emitting radioisotope yttrium Y 90, with potential antineoplastic activities. Upon administration, the antibody moiety of yttrium Y 90 anti-CDH3 monoclonal antibody FF-21101 binds to CDH3 expressed on tumor cells, thereby specifically delivering cytotoxic beta radiation to CDH3-expressing tumor cells. CDH3, also known as P-cadherin, is a tumor-associated antigen (TAA) and member of the cadherin family; it is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77885","Yttrium Y 90 Anti-CEA Monoclonal Antibody cT84.66","Yttrium Y 90 Anti-CEA Monoclonal Antibody cT84.66|Yttrium Y 90 DOTA Anti-CEA Monoclonal Antibody cT84.66|cT84.66","A radioimmunoconjugate comprised of a chimeric monoclonal antibody against human carcinoembryonic antigen (CEA) conjugated with the radioisotope yttrium 90 (Y-90) via the chelator tetra-azacyclododecanetetra-acetic acid (DOTA) with potential antineoplastic activity. The antibody moiety of yttrium Y90 DOTA anti-CEA monoclonal antibody cT84.66 binds to cells expressing the CEA antigen. Upon cellular internalization, this agent selectively delivers a cytotoxic dose of beta radiation. CEA, a tumor associated antigen, is overexpressed in many cancer types, including gastrointestinal, breast, non-small cell lung, and thyroid cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C99167","Yttrium Y 90 Basiliximab","90Y Basiliximab|Yttrium Y 90 Basiliximab","A radioimmunoconjugate composed of basiliximab, a chimeric, mouse-human monoclonal antibody directed against the alpha subunit of interleukin-2 receptor (IL-2R alpha, CD25 or Tac antigen), and labeled with yttrium y 90, with potential antineoplastic activity. The basiliximab moiety of yttrium Y 90 basiliximab selectively binds to IL-2R alpha expressed on the surface of activated T-lymphocytes, thereby preventing IL-2 binding and blocking the IL-2-mediated activation of lymphocytes. The yttrium y 90 moiety selectively delivers a cytotoxic dose of beta radiation to lymphocytes that express the IL-2 receptor. This may prevent T cell-mediated activation of the immune system against a certain transplant and may prevent transplant rejection.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C114495","Yttrium Y 90 Colloid","90Y Colloid|Yttrium Y 90 Colloid","An injectable, colloidal formulation of the radioisotope yttrium Y 90, with potential antineoplastic activity. When injected into the tumor, the yttrium Y 90 colloid selectively delivers a cytotoxic dose of beta-emitting yttrium Y 90 to the tumor site, which may result in both tumor cell death and tumor regression.","Pharmacologic Substance"]
["C2600","Yttrium Y 90 Daclizumab","Y90 Daclizumab|Y90 MOAB Anti-Tac|Yttrium Y 90 Daclizumab","A synthetic radioimmunoconjugate comprised of a humanized anti-interleukin-2 (IL-2) antibody linked to the radioisotope Yttrium 90 with potential antineoplastic activity.  Daclizumab binds with high affinity to the Tac (also called CD25) subunit of the IL-2 receptor complex and inhibits the binding of IL-2, thereby blocking the IL-2-mediated activation of lymphocytes.  As Yttrium Y 90 daclizumab, daclizumab delivers radiation specifically to lymphocytes that express the IL-2 receptor. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C77853","Yttrium Y 90 DOTA Anti-CEA Monoclonal Antibody M5A","M5A|Yttrium Y 90 DOTA Anti-CEA Monoclonal Antibody M5A|yttrium Y 90 DOTA anti-CEA monoclonal antibody M5A","A radioimmunoconjugate consisting of a monoclonal antibody directed against the human carcinoembryonic antigen (CEA) conjugated with the radioisotope yttrium 90 (Y-90) via the chelator tetra-azacyclododecanetetra-acetic acid (DOTA) with potential antineoplastic activity. The antibody moiety of yttrium Y 90 DOTA anti-CEA monoclonal antibody M5A binds to cells expressing the CEA antigen. Upon cellular internalization, this agent selectively delivers a cytotoxic dose of beta radiation. CEA, a tumor associated antigen, is overexpressed in many cancer types, including gastrointestinal, breast, non-small cell lung, and thyroid cancers.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2614","Yttrium Y 90 Monoclonal Antibody B3","90 Y-B3|MOAB B3, Yttrium Y 90|Y 90 Monoclonal Antibody B3|Y90-B3|Yttrium Y 90 Monoclonal Antibody B3","A radioimmunoconjugate of monoclonal antibody (MoAb) B3 conjugated with isotope yttrium 90. MoAb B3 is a murine MoAb that recognizes a Lewis Y carbohydrate antigen present on the surface of many carcinomas. This radioimmunoconjugate emits beta particles that causes cytotoxicity in tumor cells and has both diagnostic and therapeutic uses.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2607","Yttrium Y 90 Monoclonal Antibody BrE-3","MOAB BrE-3, Yttrium Y 90|Yttrium Y 90 Monoclonal Antibody BrE-3","A radioimmunotherapeutic agent consisting of a monoclonal antibody (BrE-3) directed against the tumor-associated antigen epithelial glycoprotein mucin chelated to the radioisotope yttrium-90.  Yttrium Y 90 monoclonal antibody BrE-3 binds to tumor cells expressing epithelial glycoprotein mucin, selectively delivering a cytotoxic dose of beta radiation. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C38678","Yttrium Y 90 Monoclonal Antibody Hu3S193","Y90 MOAB Hu3S193|Yttrium Y 90 Monoclonal Antibody Hu3S193","A radioimmunotherapeutic agent consisting of a humanized murine monoclonal antibody (hu3S193) directed against the tumor-associated Lewis Y epithelial antigen chelated to the radioisotope yttrium-90.  Yttrium Y 90 monoclonal antibody Hu3S193 binds to Lewis Y epithelial antigen-expressing tumor cells, selectively delivering a cytotoxic dose of beta radiation. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2249","Yttrium Y 90 Monoclonal Antibody MN-14","MOAB MN-14, yttrium Y 90|Y 90 MoAb MN-14|Y 90 Monoclonal Antibody MN-14|Yttrium 90 Monoclonal Antibody MN-14|Yttrium Y 90 Monoclonal Antibody MN-14|monoclonal antibody MN-14, yttrium Y 90|yttrium Y 90 MOAB MN-14","A radioimmunotherapeutic monoclonal antibody (MN-14) directed against tumor-associated carcinoembryonic antigen (CEA) and chelated to the radioisotope yttrium-90 (Y 90). Yttrium 90 monoclonal antibody MN-14 binds to tumor cell expressing CEA, delivering a cytotoxic dose of beta radiation. (NCI04)","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1808","Yttrium Y 90-DOTA-Biotin","90Y-DOTA-Biotin|90Y-DOTA-biotin|Yttrium Y 90-DOTA-Biotin|yttrium Y 90 DOTA-biotin","A radioconjugate of biotin and yttrium Y 90 (Y-90) linked through the bifunctional macrocyclic chelating agent tetra-azacyclododecanetetra-acetic acid (DOTA) with radioimmunotherapy property. Biotin is a water-soluble B-complex vitamin, present in minute amounts in every living cell, while its level in cancerous tissue is higher than that of normal tissue. Y 90-DOTA-Biotin could be used in 3-step pre-targeting radioimmunotherapy that employs a tumor targeting antibody conjugated with streptavidin, the natural ligand of biotin.","Pharmacologic Substance"]
["C119738","Yttrium Y 90-DOTA-di-HSG Peptide IMP-288","90-Y-IMP-288|90Y-IMP288|Yttrium Y 90-DOTA-di-HSG Peptide IMP-288","A radiolabeled divalent histamine-succinyl-glycine (HSG) hapten-peptide linked with the macrocyclic chelator 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) to the beta-emitting radionuclide yttrium 90 (Y-90), with radioimmunotherapeutic activity. After pre-treating and targeting tumor cells with a bi-specific monoclonal antibody (BiMoAB) directed against both a tumor-associated antigen (TAA) and the HSG hapten-peptide, the HSG portion of the administered yttrium Y 90-DOTA-di-HSG peptide IMP-288 binds to the anti-HSG sequence on the BiMoAB. In turn, Y-90 delivers a cytotoxic dose of beta radiation to tumor cells expressing the specific TAA.","Pharmacologic Substance"]
["C99168","Yttrium Y 90-labeled Anti-FZD10 Monoclonal Antibody OTSA101","OTSA101-DTPA-90Y|Yttrium Y 90-labeled Anti-FZD10 Monoclonal Antibody OTSA101","A radioimmunoconjugate composed of a humanized monoclonal antibody (MoAb) OTSA101 against FZD10 and labeled with yttrium y 90, with potential antineoplastic activity. The MoAb moiety of yttrium Y 90-labeled anti-FZD10 monoclonal antibody OTSA101 binds to FZD10, thereby delivering a cytotoxic dose of beta radiation to FZD10 positive tumor cells. FZD10 (also called CD350), a member of the Frizzled family of G protein-coupled receptors that is involved in the Wnt/beta-catenin/TCF signaling pathway, is overexpressed in a variety of cancer cell types but undetectable in normal, healthy human tissues except for the placenta.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48429","Yttrium Y-90 Clivatuzumab Tetraxetan","90Y-hPAM4|IMMU-107|YTTRIUM Y-90 CLIVATUZUMAB TETRAXETAN|Yttrium Y 90 Clivatuzumab Tetraxetan|Yttrium Y 90 DOTA Monoclonal Antibody HuPAM4|Yttrium Y-90 Clivatuzumab Tetraxetan|hPAM4-Cide|hPAM4-DOTA|yttrium Y 90 DOTA monoclonal antibody HuPAM4","A radioimmunoconjugate comprised of the humanized monoclonal antibody clivatuzumab, directed against the pancreatic cancer antigen MUC1, that is conjugated to the chelating agent tetraxetan and radiolabeled with the beta-emitting radioisotope Yttrium Y 90. Yttrium Y 90 clivatuzumab tetraxetan binds to tumor cells expressing MUC1 antigen, thereby selectively delivering a cytotoxic dose of beta radiation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2582","Yttrium Y-90 Epratuzumab Tetraxetan","Monoclonal antibody LL2, yttrium Y 90|Y 90 Humanized Monoclonal Antibody LL2|Y 90 MoAb LL2|Y 90 monoclonal antibody LL2|Y90 Humanized Epratuzumab Tetraxetan|YTTRIUM Y-90 EPRATUZUMAB TETRAXETAN|Yttrium Y 90 Humanized Epratuzumab Tetraxetan|Yttrium Y 90 Humanized Monoclonal Antibody LL2|Yttrium Y-90 Epratuzumab Tetraxetan|yttrium Y 90 MOAB LL2","A radioimmunotherapeutic humanized murine monoclonal antibody (LL2) directed against the CD22 pan-B-cell antigen and chelated to the radioisotope yttrium-90 (Y 90). Y 90 humanized monoclonal antibody LL2 binds to tumor cells expressing CD22, delivering a cytotoxic dose of beta radiation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C1812","Yttrium Y-90 Ibritumomab Tiuxetan","IDEC-Y2B8 monoclonal antibody|IDEC-Y2B8|Y 90 Ibritumomab Tiuxetan|Y 90 Zevalin|Y 90 ibritumomab tiuxetan|YTTRIUM Y-90 IBRITUMOMAB TIUXETAN|Yttrium Y 90 Ibritumomab Tiuxetan|Yttrium Y-90 Ibritumomab Tiuxetan|yttrium Y90 ibritumomab tiuxetan","A radioimmunotherapeutic agent consisting of a murine monoclonal anti-CD20 antibody (ibritumomab) linked by the chelator tiuxetan to the radioisotope yttrium-90 (Y 90).  Yttrium Y 90 ibritumomab tiuxetan binds to and specifically delivers beta radiation to CD20-expressing tumor cells, thereby minimizing the systemic effects of radiation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C48428","Yttrium Y-90 Tacatuzumab Tetraxetan","AFP-Cide|Y-90 hAFP-31|YTTRIUM Y-90 TACATUZUMAB TETRAXETAN|Yttrium Y 90 DOTA Monoclonal Antibody HuAFP31|Yttrium Y 90 Tacatuzumab Tetraxetan|Yttrium Y-90 Tacatuzumab Tetraxetan|yttrium Y 90 DOTA monoclonal antibody HuAFP31","A radioimmunoconjugate comprised of the humanized monoclonal antibody tacatuzumab, directed against alpha fetoprotein, that is conjugated to the chelating agent tetraxetan and radiolabeled with the beta-emitting radioisotope Yttrium Y 90. Yttrium Y 90 tacatuzumab tetraxetan binds to tumor cells expressing alpha fetoprotein, thereby selectively delivering a cytotoxic dose of beta radiation.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C61329","Z-360","Z-360","A selective, orally available, 1,5-benzodiazepine-derivative gastrin/cholecystokinin 2 (CCK-2) receptor antagonist with potential antineoplastic activity. Z-360 binds to the gastrin/CCK-2 receptor, thereby preventing receptor activation by gastrin, a peptide hormone frequently associated with the proliferation of gastrointestinal and pancreatic tumor cells.","Pharmacologic Substance"]
["C430","Zalcitabine","2',3'-Dideoxycytidine|Dideoxycytidine|Hivid|ZALCITABINE|Zalcitabine|ddC","A synthetic dideoxynucleoside. After intracellular phosphorylation to its active metabolite, zalcitabine preferentially inhibits the gamma form of DNA polymerase present in tumor cell mitochondria, resulting in the inhibition of tumor cell mitochondrial DNA replication and tumor cell death. (NCI04)","Nucleic Acid, Nucleoside, or Nucleotide|Pharmacologic Substance"]
["C64620","Zalutumumab","HuMax-EGFr, 2F8|Zalutumumab","A fully human IgG1 monoclonal antibody against epidermal growth factor receptor (EGFR) with potential antineoplastic activity. EGFR is a cell surface receptor tyrosine kinase, overexpressed on many cancer cells. Zalutumumab selectively binds to and blocks binding of EGF and transforming growth factor-alpha (TGF-a) to the EGFR receptor, thereby interfering with cellular signaling, leading to cell growth inhibition and apoptosis in tumor cells. In addition, zalutumumab also triggers cell lysis mediated through antibody dependent cellular cytotoxicity (ADCC) in EGFR-expressing cells.","Amino Acid, Peptide, or Protein|Immunologic Factor"]
["C91701","Zanolimumab","Anti-CD4 Monoclonal Antibody HuMax|HuMax-CD4|ZANOLIMUMAB|Zanolimumab","A human IgG1k monoclonal antibody against the CD4 receptor on T-lymphocytes, with potential antineoplastic and immunosuppressing activities. Zanolimumab targets and binds to the CD4 receptor on certain T-cells thereby preventing the interaction between the CD4 receptor and the major histocompatibility complex class II molecule. This prevents activation of CD4 positive T cells. In addition, zanolimumab is able to induce an antibody-dependent cellular cytotoxicity (ADCC) response against CD4-expressing tumor cells. CD4, a receptor located on a subset of T-lymphocytes, is upregulated in T-cell lymphomas.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C37455","Zebularine","1-beta-D-Ribofuranosyl-2(1H)-pyrimidinone|2-Pyrimidone-1-beta-D-riboside|Pyrimidin-2-one beta-Ribofuranoside|Zebularine","A synthetic cytidine analogue and a cytidine deaminase inhibitor with anticancer activity. Following metabolic activation by phosphorylation and incorporation into DNA, zebularine inhibits DNA methyltransferase through covalent complex formation between the enzyme and zebularine-substituted DNA, hence resulting in non-specific, genome-wide induction of demethylation including the removal of aberrant methylation of promoter regions of genes critical for normal cellular functions.","Pharmacologic Substance"]
["C95713","Z-Endoxifen Hydrochloride","4-Hydroxy-N-Desmethyltamoxifen Hydrochloride|Z-Endoxifen HCl|Z-Endoxifen Hydrochloride","The hydrochloride salt and the z (cis-) stereoisomer of endoxifen with potential antineoplastic activity. Endoxifen, the active metabolite of tamoxifen, competitively inhibits the binding of estradiol to estrogen receptors, thereby preventing the receptor from binding to the estrogen-response element on DNA and thus reducing DNA synthesis. Unlike tamoxifen, however, which relies on CYP2D6 activity for its conversion to the active metabolite endoxifen, the direct administration of endoxifen bypasses the CYP2D6 route. As CYP2D6 activity can vary widely among individuals due to genetic CYP2D6 polymorphisms, endoxifen is therefore theoretically more potent and more uniform in its bioavailability across patient populations.","Pharmacologic Substance"]
["C48430","Zibotentan","3-Pyridinesulfonamide, N-(3-methoxy-5-methylpyrazinyl)-2-(4-(1,3,4-oxadiazol-2-yl)phenyl)-|N-(3-methoxy-5-methylpyrazin-2-yl)-2-[4-(1,3,4-oxadiazol-2-yl)phenyl]pridine-3- sulfonamide|ZD-4054|ZD4054|ZIBOTENTAN|Zibotentan","An orally available selective antagonist of the endothelin-A (ET-A) receptor with potential antineoplastic activity. Zibotentan binds selectively to the ET-A receptor, thereby inhibiting endothelin-mediated mechanisms that promote tumor cell proliferation.","Pharmacologic Substance"]
["C129588","Zinc Finger Nuclease ZFN-603","ZFN ZFN-603|ZFN-603|ZFN603|Zinc Finger Nuclease ZFN-603","A zinc finger nuclease (ZFN) targeting the human papillomavirus (HPV) type 16 (HPV16) oncoprotein E7, with potential antineoplastic activity. Upon transfection of ZFN-603 into HPV16-positive cells, ZFN-603 targets, binds to and cleaves the HPV16 E7 oncogene in HPV16-infected cells. By cleaving the HPV16 E7 DNA, the E7 oncoprotein is not expressed. This results in an inhibition of E7-mediated signaling, an induction of apoptosis, and inhibition of tumor cell proliferation in HPV16-expressing cells. In addition, preventing E7 expression induces the expression of tumor suppressor genes, thereby further preventing HPV-induced cancer cell formation and proliferation. E7 plays a key role in promoting both viral infection and carcinogenesis. ZFN, an engineered endonuclease in which a DNA-binding zinc finger protein is fused to a DNA-cleavable domain, cleaves specific DNA sites.","Pharmacologic Substance"]
["C129589","Zinc Finger Nuclease ZFN-758","ZFN ZFN-758|ZFN-758|ZFN758|Zinc Finger Nuclease ZFN-758","A zinc finger nuclease (ZFN) targeting the human papillomavirus (HPV) type 18 (HPV18) oncoprotein E7, with potential antineoplastic activity. Upon transfection of ZFN-758 into HPV18-positive cells, ZFN-758 targets, binds to and cleaves the HPV18 E7 oncogene in HPV18-infected cells. By cleaving the HPV18 E7 DNA, the E7 oncoprotein is not expressed. This results in an inhibition of E7-mediated signaling, an induction of apoptosis, and an inhibition of tumor cell proliferation in HPV18-expressing cells. In addition, preventing E7 expression induces the expression of tumor suppressor genes, thereby further preventing HPV-induced cancer cell formation and proliferation. E7 plays a key role in promoting both viral infection and carcinogenesis. ZFN, an engineered endonuclease in which a DNA-binding zinc finger protein is fused to a DNA-cleavable domain, cleaves specific DNA sites.","Pharmacologic Substance"]
["C682","Zinostatin","A 8544527G1|Holoneocarzinostatin|NCS|Neocarzinostatin|Vinostatin|ZINOSTATIN|Zinostatin","An enediyne antineoplastic antibiotic hybrid containing an aminoglycoside chromophore.  Zinostatin is isolated from the bacterium Streptomyces carzinostaticus.  The aminoglycoside component of zinostatin intercalates into DNA and the benzene diradical intermediate of the enediyne core binds to the minor groove of DNA, resulting in single- and double-strand breaks in DNA and apoptosis. (NCI04)","Amino Acid, Peptide, or Protein|Antibiotic"]
["C104010","Zirconium Zr 89-labeled RO5479599","89Zr-RO5479599|89Zr-labeled RO5479599|Zirconium Zr 89-labeled RO5479599","A radioimmunoconjugate containing a glycoengineered, humanized monoclonal antibody directed against the human epidermal growth factor receptor HER3 (ErbB3) and labeled with the radioisotope zirconium Zr 89, with radioisotopic activity and potential use as an imaging agent as well as potential antineoplastic activity. Upon administration, the RO5479599 moiety of zirconium Zn 89-labeled RO5479599 binds to the extracellular domain of HER3 and inhibits HER3 dimerization, thereby preventing EGFR-dependent signaling. In addition, RO5479599 elicits enhanced antibody-dependent cellular cytotoxicity (ADCC). Upon binding, the radioisotope moiety may be detected using positron emission tomography (PET), thereby allowing the imaging and quantification of HER3-expressing tumor cells. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors; it has no active kinase domain but is activated through heterodimerization with other members of the EGFR receptor family, such as HER2.","Amino Acid, Peptide, or Protein|Pharmacologic Substance"]
["C2682","Ziv-Aflibercept","AFLIBERCEPT|AVE0005|Aflibercept|Eylea|VEGF Trap R1R2|VEGF Trap|VEGF-Trap|Vascular Endothelial Growth Factor Trap|Zaltrap|Ziv-Aflibercept|aflibercept|vascular endothelial growth factor trap","A recombinant protein comprised of epitopes of the extracellular domains of human vascular endothelial growth factor receptors (VEGFR) fused to the constant region (Fc) of human IgG1 with potential antiangiogenic activity. Afilbercept, functioning as a soluble decoy receptor, binds to pro-angiogenic vascular endothelial growth factors (VEGFs), thereby preventing VEGFs from binding to their endogenous receptors. Disruption of the binding of VEGFs to their cellular receptors may result in the inhibition of tumor angiogenesis, metastasis, and ultimately tumor regression.","Immunologic Factor"]
["C74025","Zoptarelin Doxorubicin","AEZS-108|AN-152|Doxorubicin-GNRH Agonist Conjugate AEZS-108|ZEN-008|Zoptarelin Doxorubicin","A peptide agonist of the gonadotropin releasing hormone-1 receptor (GnRH-1R) that is conjugated to the anthracycline antibiotic doxorubicin with potential antineoplastic activity. Zoptarelin doxorubicin binds to GnRH-1Rs, which may be highly expressed on endometrial and ovarian tumor cell membrane surfaces, and is internalized. Once inside the cell, the doxorubicin moiety of this agent intercalates into DNA and inhibits the topoisomerase II activity, which may result in the inhibition of tumor cell DNA replication and tumor cell proliferation.","Pharmacologic Substance"]
["C91365","Zorubicin","(2S-cis)-Benzoic Acid[1-[4-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-1,2,3,4,6,11-hexahydro-2,5,12-trihydroxy-7-methoxy-6,11-dioxo-2-naphthacenyl]ethylidene]hydrazide|Benzoic Acid Hydrazide 3-Hydrazone with Daunorubicin|Benzoylhydrazone Daunorubicin|Daunomycin Benzoylhydrazone|Rubidazon|Rubidazone|ZORUBICIN|Zorubicin","A benzoylhydrazone derivative of the anthracycline antineoplastic antibiotic daunorubicin. Zorubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair as well as RNA and protein synthesis.","Antibiotic|Organic Chemical"]
["C1458","Zorubicin Hydrochloride","(2S-cis)-Benzoic Acid[1-[4-[(3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranosyl)oxy]-1,2,3,4,6,11-hexahydro-2,5,12-trihydroxy-7-methoxy-6,11-dioxo-3-naphthacenyl]ethylidene]hydrazide|Benzoyl Hydrazone Daunorubicin|Daunorubicin Benzoylhydrazone Hydrochloride|RP 22,050 Hydrochloride|RP 22050|Rubidazone|ZORUBICIN HYDROCHLORIDE|Zorubicin Hydrochloride|Zorubicin hydrochloride","A benzoyl-hydrazone derivative of the anthracycline antineoplastic antibiotic daunorubicin.  Zorubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. (NCI04)","Antibiotic|Organic Chemical"]
["C28322","Zuclomiphene Citrate","Cis-Clomiphene Citrate|Cisclomiphene Citrate|Clomiphene citrate, cis-|ZUCLOMIPHENE CITRATE|Zuclomiphene Citrate|cis-Clomiphene citrate","The cis isomer of clomiphene which exhibits weak estrogen agonist activity evaluated for antineoplastic activity against breast cancer. (NCI04)","Organic Chemical|Pharmacologic Substance"]
["C64631","ZYC300","ZYC300","A formulation of a plasmid DNA encoding an inactivated form of the carcinogen activator cytochrome P450 1B1 (CYP1B1) encapsulated in biodegradable poly-DL-lactide-coglycolide microparticles with potential antineoplastic activity. CYP1B1, an extrahepatic monooxygenase of the cytochrome P450 family, is overexpressed in many cancers with only restricted expression in normal tissues. Vaccination with ZYC300 may stimulate the immune system to elicit a cytotoxic T lymphocyte (CTL) response against the tumor associated antigen CYP1B1, thereby causing lysis of tumor cells expressing CYP1B1.","Gene or Genome|Pharmacologic Substance"]