FDA approved drugs:
(show top 50)
(show all 204)
| # |
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Drug Name |
Active Ingredient(s) 18
|
Company |
Approval Date |
| 1 |
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Abraxane
18
49
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PACLITAXEL |
Celgene |
October 2012 |
Disease/s that Drug Treats:non-small cell lung cancer
Indications and Usage:
18
ABRAXANE is a microtubule inhibitor indicated for the treatment of: Metastatic breast cancer, after failure of combination chemotherapyfor metastatic disease or relapse within 6 months of adjuvantchemotherapy. Prior therapy should have included an anthracyclineunless clinically contraindicated. (1.1) Locally advanced or metastatic non-small cell lung cancer (NSCLC),as first-line treatment in combination with carboplatin, in patients whoare not candidates for curative surgery or radiation therapy. (1.2) Metastatic adenocarcinoma of the pancreas as first-line treatment, incombination with gemcitabine. (1.3), ABRAXANE is a microtubule inhibitor indicated for the treatment of: * Metastatic breast cancer, after failure of combination chemotherapy for metastatic disease or relapse within 6 months of adjuvant chemotherapy. Prior therapy should have included an anthracycline unless clinically contraindicated. (1.1) * Locally advanced or metastatic non-small cell lung cancer (NSCLC), as first-line treatment in combination with carboplatin, in patients who are not candidates for curative surgery or radiation therapy. (1.2) * Metastatic adenocarcinoma of the pancreas as first-line treatment, in combination with gemcitabine. (1.3)
DrugBank Targets:
16
1. Apoptosis regulator Bcl-2;;2. Tubulin beta-1 chain;;3. Nuclear receptor subfamily 1 group I member 2;;4. Microtubule-associated protein 4;;5. Microtubule-associated protein 2; ;6. Microtubule-associated protein tau, Apoptosis regulator Bcl-2|Tubulin beta-1 chain|Nuclear receptor subfamily 1 group I member 2|Microtubule-associated protein 4|Microtubule-associated protein 2|Microtubule-associated protein tau|
Mechanism of Action:
18
Target: microtubule , microtubule
Action: inhibitor
FDA: ABRAXANE is a microtubule inhibitor that promotes the assembly of microtubules from tubulin dimers and stabilizes microtubulesby preventing depolymerization. This stability results in the inhibition of the normal dynamic reorganization of the microtubulenetwork that is essential for vital interphase and mitotic cellular functions. Paclitaxel induces abnormal arrays or âbundlesâ ofmicrotubules throughout the cell cycle and multiple asters of microtubules during mitosis. , ABRAXANE is a microtubule inhibitor that promotes the assembly of microtubules from tubulin dimers and stabilizes microtubules by preventing depolymerization. This stability results in the inhibition of the normal dynamic reorganization of the microtubule network that is essential for vital interphase and mitotic cellular functions. Paclitaxel induces abnormal arrays or âbundlesâ of microtubules throughout the cell cycle and multiple asters of microtubules during mitosis.
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| 2 |
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Abstral
18
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FENTANYL (citrate) |
ProStrakan |
January 2011 |
Disease/s that Drug Treats:breakthrough cancer pain in opiod-tolerant patients
Indications and Usage:
18
ABSTRAL is an opioid agonist indicated for the management of breakthrough pain in cancer patients 18 years of age and older who are already receiving and who are tolerant to opioid therapy for their underlying persistent cancer pain. (1) Limitations of Use: ABSTRAL may be dispensed only to patients enrolled in the TIRF REMS Access program.
DrugBank Targets:
16
1. Mu-type opioid receptor ;2. Delta-type opioid receptor;3. Kappa-type opioid receptor
Mechanism of Action:
18
Target: µ-opioid receptor (possible mechanism of action)
Action: agonist
FDA: Fentanyl is a pure opioid agonist whose principal therapeutic action is analgesia. Other members of the classknown as opioid agonists include substances such as morphine, oxycodone, hydromorphone, codeine, andhydrocodone.
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| 3 |
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Actiq
18
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FENTANYL (citrate) |
Anesta Corporation |
November 1998 |
Disease/s that Drug Treats:cancer pain
Indications and Usage:
18
ACTIQ is an opioid agonist indicated for the management of breakthrough pain in cancer patients 16 years of age and older who are already receiving and who are tolerant to around-the-clock opioid therapy for their underlying persistent cancer pain. (1) Limitations of Use: ACTIQ may be dispensed only to patients enrolled in the TIRF REMS Access program. (1)
DrugBank Targets:
16
1. Mu-type opioid receptor ;2. Delta-type opioid receptor;3. Kappa-type opioid receptor
Mechanism of Action:
18
Target: -
Action: agonist
FDA: Fentanyl is a pure opioid agonist whose principal therapeutic action is analgesia. Other members of the class known as opioid agonists include substances such as morphine, oxycodone, hydromorphone, codeine, and hydrocodone.
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| 4 |
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Adcetris
18
49
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BRENTUXIMAB VEDOTIN |
Seattle Genetics |
August 2011 |
Disease/s that Drug Treats:Hodgkin lymphoma and anaplastic large cell lymphoma
Indications and Usage:
18
ADCETRIS is a CD30-directed antibody-drug conjugate indicated fortreatment of patients with: Hodgkin lymphoma after failure of autologous stem cell transplant(ASCT) or after failure of at least two prior multi-agent chemotherapyregimens in patients who are not ASCT candidates (1.1). Systemic anaplastic large cell lymphoma after failure of at least oneprior multi-agent chemotherapy regimen (1.2).Accelerated approval was granted for the above indications based onoverall response rate. An improvement in patient-reported outcomes orsurvival has not been established. Continued approval for these indicationsmay be contingent upon verification and description of clinical benefit inconfirmatory trials.
DrugBank Targets:
16
Tumor necrosis factor receptor superfamily member 8
Mechanism of Action:
18
Target: microtubule
Action: disruptor
FDA: Brentuximab vedotin is an ADC. The antibody is a chimeric IgG1 directed against CD30. Thesmall molecule, MMAE, is a microtubule disrupting agent. MMAE is covalently attached to theantibody via a linker. Nonclinical data suggest that the anticancer activity of ADCETRIS is dueto the binding of the ADC to CD30-expressing cells, followed by internalization of theADC-CD30 complex, and the release of MMAE via proteolytic cleavage. Binding of MMAE totubulin disrupts the microtubule network within the cell, subsequently inducing cell cycle arrestand apoptotic death of the cells.
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| 5 |
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Afinitor
18
49
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EVEROLIMUS |
Novartis |
March 2009 |
Disease/s that Drug Treats:renal cell carcinoma/ renal angiomyolipoma associated with tuberous sclerosis complex/ advanced pancreatic neuroendocrine tumors/ hormone receptor-positive, HER2-negative breast cancer
Indications and Usage:
18
AFINITOR is a kinase inhibitor indicated for the treatment of: postmenopausal women with advanced hormone receptor-positive, HER2- negative breast cancer (advanced HR+ BC) in combination with exemestane after failure of treatment with letrozole or anastrozole. (1.1) adults with progressive neuroendocrine tumors of pancreatic origin (PNET) that are unresectable, locally advanced or metastatic. AFINITOR is not indicated for the treatment of patients with functional carcinoid tumors. (1.2) adults with advanced renal cell carcinoma (RCC) after failure of treatment with sunitinib or sorafenib. (1.3) adults with renal angiomyolipoma and tuberous sclerosis complex (TSC), not requiring immediate surgery. The effectiveness of AFINITOR in the treatment of renal angiomyolipoma is based on an analysis of durable objective responses in patients treated for a median of 8.3 months. Further follow-up of patients is required to determine long-term outcomes. (1.4) AFINITOR and AFINITOR DISPERZ are kinase inhibitors indicated for the treatment of: pediatric and adult patients with tuberous sclerosis complex (TSC) who have subependymal giant cell astrocytoma (SEGA) that requires therapeutic intervention but cannot be curatively resected. The effectiveness is based on demonstration of durable objective response, as evidenced by reduction in SEGA tumor volume. Improvement in diseaserelated symptoms and overall survival in patients with SEGA and TSC has not been demonstrated. (1.5)
DrugBank Targets:
16
Serine/threonine-protein kinase mTOR
Mechanism of Action:
18
Target: mTOR
Action: inhibitor
FDA: Everolimus is an inhibitor of mammalian target of rapamycin (mTOR), a serine-threonine kinase, downstream of thePI3K/AKT pathway. The mTOR pathway is dysregulated in several human cancers. Everolimus binds to an intracellularprotein, FKBP-12, resulting in an inhibitory complex formation with mTOR complex 1 (mTORC1) and thus inhibition ofmTOR kinase activity. Everolimus reduced the activity of S6 ribosomal protein kinase (S6K1) and eukaryotic initiationfactor 4E-binding protein (4E-BP1), downstream effectors of mTOR, involved in protein synthesis. S6K1 is a substrate ofmTORC1 and phosphorylates the activation domain 1 of the estrogen receptor which results in ligand-independentactivation of the receptor. In addition, everolimus inhibited the expression of hypoxia-inducible factor (e.g., HIF-1) andreduced the expression of vascular endothelial growth factor (VEGF). Inhibition of mTOR by everolimus has been shownto reduce cell proliferation, angiogenesis, and glucose uptake in in vitro and/or in vivo studies.Constitutive activation of the PI3K/Akt/mTOR pathway can contribute to endocrine resistance in breast cancer. In vitrostudies show that estrogen-dependent and HER2+ breast cancer cells are sensitive to the inhibitory effects of everolimus,and that combination treatment with everolimus and Akt, HER2, or aromatase inhibitors enhances the anti-tumor activityof everolimus in a synergistic manner.Two regulators of mTORC1 signaling are the oncogene suppressors tuberin-sclerosis complexes 1 and 2 (TSC1, TSC2).Loss or inactivation of either TSC1 or TSC2 leads to activation of downstream signaling. In TSC, a genetic disorder,inactivating mutations in either the TSC1 or the TSC2 gene lead to hamartoma formation throughout the body.
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| 6 |
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Akynzeo
18
49
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NETUPITANT AND PALONOSETRON (hydrochloride) |
Helsinn |
October 2014 |
Disease/s that Drug Treats:chemotherapy-induced nausea and vomiting
Indications and Usage:
18
AKYNZEO is a fixed combination of netupitant, a substance P/neurokinin 1(NK1) receptor antagonist, and palonosetron, a serotonin-3 (5-HT3) receptorantagonist indicated for the prevention of acute and delayed nausea andvomiting associated with initial and repeat courses of cancer chemotherapy,including, but not limited to, highly emetogenic chemotherapy. Oralpalonosetron prevents nausea and vomiting during the acute phase andnetupitant prevents nausea and vomiting during both the acute and delayedphase after cancer chemotherapy. (1)
DrugBank Targets:
16
1. Substance-P receptor;2. 5-hydroxytryptamine receptor 3A
Mechanism of Action:
18
Target: neurokinin 1 (NK1) receptors/ substance P mediated responses [netupitant] & 5-HT3 receptor [palonosetron]
Action: activator/ inhibitor & agonist
FDA: Netupitant is a selective antagonist of human substance P/neurokinin 1 (NK1) receptors.Palonosetron is a 5-HT3 receptor antagonist with a strong binding affinity for this receptor and little or noaffinity for other receptors. Cancer chemotherapy may be associated with a high incidence of nausea andvomiting, particularly when certain agents, such as cisplatin, are used. 5-HT3 receptors are located on thenerve terminals of the vagus in the periphery and centrally in the chemoreceptor trigger zone of the areapostrema. Chemotherapeutic agents produce nausea and vomiting by stimulating the release of serotoninfrom the enterochromaffin cells of the small intestine. Serotonin then activates 5-HT3 receptors located onvagal afferents to initiate the vomiting reflex. The development of acute emesis is known to depend onserotonin and its 5-HT3 receptors have been demonstrated to selectively stimulate the emetic response.Delayed emesis has been largely associated with the activation of tachykinin family neurokinin 1 (NK1)receptors (broadly distributed in the central and peripheral nervous systems) by substance P. As shown inin vitro and in vivo studies, netupitant inhibits substance P mediated responses.
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| 7 |
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Alimta
18
49
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PEMETREXED (also Pemetrexed Disodium) |
Eli Lilly |
February 2004 |
Disease/s that Drug Treats:Mesothelioma
Indications and Usage:
18
ALIMTA® is a folate analog metabolic inhibitor indicated for: Locally Advanced or Metastatic Nonsquamous Non-Small CellLung Cancer: Initial treatment in combination with cisplatin. (1.1) Maintenance treatment of patients whose disease has notprogressed after four cycles of platinum-based first-linechemotherapy. (1.2) After prior chemotherapy as a single-agent. (1.3) Mesothelioma: in combination with cisplatin. (1.4)Limitations of Use: ALIMTA is not indicated for the treatment of patients withsquamous cell non-small cell lung cancer. (1.5)
DrugBank Targets:
16
1. Thymidylate synthase;2. Bifunctional purine biosynthesis protein PURH;3. Dihydrofolate reductase;4. Trifunctional purine biosynthetic protein adenosine-3
Mechanism of Action:
18
Target: folic acid/ thymidylate synthase, dihydrofolate reductase, and glycinamide ribonucleotide formyltransferase
Action: antagonist/ inhibitor
FDA: ALIMTA, pemetrexed for injection, is a folate analog metabolic inhibitor that exerts its action by disrupting folatedependentmetabolic processes essential for cell replication. In vitro studies have shown that pemetrexed inhibitsthymidylate synthase (TS), dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT),which are folate-dependent enzymes involved in the de novo biosynthesis of thymidine and purine nucleotides.Pemetrexed is taken into cells by membrane carriers such as the reduced folate carrier and membrane folate bindingprotein transport systems. Once in the cell, pemetrexed is converted to polyglutamate forms by the enzymefolylpolyglutamate synthetase. The polyglutamate forms are retained in cells and are inhibitors of TS and GARFT.Polyglutamation is a time- and concentration-dependent process that occurs in tumor cells and, is thought to occur to alesser extent, in normal tissues. Polyglutamated metabolites are thought to have an increased intracellular half-liferesulting in prolonged drug action in malignant cells.
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| 8 |
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Aloxi
18
49
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PALONOSETRON (hydrochloride) |
MGI Pharma, Helsinn Healthcare |
August 2003 |
Disease/s that Drug Treats:Chemotherapy side effects
Indications and Usage:
18
ALOXI is a serotonin-3 (5-HT3) receptor antagonist indicated in adults for: Moderately emetogenic cancer chemotherapy -- prevention ofacute and delayed nausea and vomiting associated with initial andrepeat courses (1.1) Highly emetogenic cancer chemotherapy -- prevention of acutenausea and vomiting associated with initial and repeat courses(1.1) Prevention of postoperative nausea and vomiting (PONV) for upto 24 hours following surgery. Efficacy beyond 24 hours has notbeen demonstrated (1.3)ALOXI is indicated in pediatric patients aged 1 month to less than 17 yearsfor: Prevention of acute nausea and vomiting associated with initialand repeat courses of emetogenic cancer chemotherapy, includinghighly emetogenic cancer chemotherapy (1.2)
DrugBank Targets:
16
5-hydroxytryptamine receptor 3A
Mechanism of Action:
18
Target: serotonin subtype 3 (5-HT3) receptor/ ion channels involved in ventricular polarization
Action: antagonist/ blocker
FDA: Palonosetron is a 5-HT3 receptor antagonist with a strong bindingaffinity for this receptor and little or no affinity for other receptors.Cancer chemotherapy may be associated with a high incidence ofnausea and vomiting, particularly when certain agents, such as cisplatin, areused. 5-HT3 receptors are located on the nerve terminals of the vagus in theperiphery and centrally in the chemoreceptor trigger zone of the areapostrema. It is thought that chemotherapeutic agents produce nausea andvomiting by releasing serotonin from the enterochromaffin cells of the smallintestine and that the released serotonin then activates 5-HT3 receptorslocated on vagal afferents to initiate the vomiting reflex.Postoperative nausea and vomiting is influenced by multiple patient,surgical and anesthesia related factors and is triggered by release of 5-HT ina cascade of neuronal events involving both the central nervous system andthe gastrointestinal tract. The 5-HT3 receptor has been demonstrated toselectively participate in the emetic response.
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| 9 |
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Aredia
18
49
|
PAMIDRONATE DISODIUM |
Chiron |
August 1996 |
Disease/s that Drug Treats:osteolytic bone metastases of breast cancer
Indications and Usage:
18
Hypercalcemia of MalignancyAredia, in conjunction with adequate hydration, is indicated for the treatment of moderate or severehypercalcemia associated with malignancy, with or without bone metastases. Patients who have eitherepidermoid or non-epidermoid tumors respond to treatment with Aredia. Vigorous saline hydration, anintegral part of hypercalcemia therapy, should be initiated promptly and an attempt should be made torestore the urine output to about 2 L/day throughout treatment. Mild or asymptomatic hypercalcemia maybe treated with conservative measures (i.e., saline hydration, with or without loop diuretics). Patientsshould be hydrated adequately throughout the treatment, but overhydration, especially in those patientswho have cardiac failure, must be avoided. Diuretic therapy should not be employed prior to correction ofhypovolemia. The safety and efficacy of Aredia in the treatment of hypercalcemia associated withhyperparathyroidism or with other non-tumor-related conditions has not been established.Pagetâs DiseaseAredia is indicated for the treatment of patients with moderate to severe Pagetâs disease of bone. Theeffectiveness of Aredia was demonstrated primarily in patients with serum alkaline phosphatase â¥3 timesthe upper limit of normal. Aredia therapy in patients with Pagetâs disease has been effective in reducingserum alkaline phosphatase and urinary hydroxyproline levels by â¥50% in at least 50% of patients, and byâ¥30% in at least 80% of patients. Aredia therapy has also been effective in reducing these biochemicalmarkers in patients with Pagetâs disease who failed to respond, or no longer responded to othertreatments.Osteolytic Bone Metastases of Breast Cancer and Osteolytic Lesions of MultipleMyelomaAredia is indicated, in conjunction with standard antineoplastic therapy, for the treatment of osteolyticbone metastases of breast cancer and osteolytic lesions of multiple myeloma. The Aredia treatment effectappeared to be smaller in the study of breast cancer patients receiving hormonal therapy than in the studyof those receiving chemotherapy, however, overall evidence of clinical benefit has been demonstrated(see CLINICAL PHARMACOLOGY, Osteolytic Bone Metastases of Breast Cancer and OsteolyticLesions of Multiple Myeloma, Clinical Trials section).
DrugBank Targets:
16
1. Farnesyl pyrophosphate synthase;2. Hydroxylapatite
Mechanism of Action:
18
Target: bone resorption; FPP synthase
Action: inhibitor
FDA: The principal pharmacologic action of Aredia is inhibition of bone resorption. Although the mechanism ofantiresorptive action is not completely understood, several factors are thought to contribute to this action.Aredia adsorbs to calcium phosphate (hydroxyapatite) crystals in bone and may directly block dissolutionof this mineral component of bone. In vitro studies also suggest that inhibition of osteoclast activitycontributes to inhibition of bone resorption. In animal studies, at doses recommended for the treatment ofhypercalcemia, Aredia inhibits bone resorption apparently without inhibiting bone formation andmineralization. Of relevance to the treatment of hypercalcemia of malignancy is the finding that Arediainhibits the accelerated bone resorption that results from osteoclast hyperactivity induced by varioustumors in animal studies.
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| 10 |
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Arimidex
18
49
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ANASTROZOLE |
AstraZeneca |
January 1996 |
Disease/s that Drug Treats:post menopausal breast cancer
Indications and Usage:
18
ARIMIDEX is an aromatase inhibitor indicated for: Adjuvant treatment of postmenopausal women withhormone receptor-positive early breast cancer (1.1) First-line treatment of postmenopausal women withhormone receptor-positive or hormone receptor unknownlocally advanced or metastatic breast cancer (1.2) Treatment of advanced breast cancer in postmenopausalwomen with disease progression following tamoxifentherapy. Patients with ER-negative disease and patientswho did not respond to previous tamoxifen therapy rarelyresponded to ARIMIDEX (1.3)
DrugBank Targets:
16
Cytochrome P450 19A1
Mechanism of Action:
18
Target: oral aromatase
Action: inhibitor
FDA: The growth of many cancers of the breast is stimulated or maintained by estrogens.In postmenopausal women, estrogens are mainly derived from the action of the aromataseenzyme, which converts adrenal androgens (primarily androstenedione and testosterone) toestrone and estradiol. The suppression of estrogen biosynthesis in peripheral tissues and inthe cancer tissue itself can therefore be achieved by specifically inhibiting the aromataseenzyme.Anastrozole is a selective non-steroidal aromatase inhibitor. It significantly lowers serumestradiol concentrations and has no detectable effect on formation of adrenal corticosteroidsor aldosterone.
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| 11 |
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Aromasin Tablets
18
49
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EXEMESTANE |
Pharmacia & Upjohn |
October 21. 1999 |
Disease/s that Drug Treats:advanced breast cancer in postmenopausal women whose disease has progressed following tamoxifen therapy
Indications and Usage:
18
AROMASIN is an aromatase inhibitor indicated for: Incidences of cardiac ischemic events (myocardial infarction, angina, adjuvant treatment of postmenopausal women with estrogen-receptor and myocardial ischemia) were AROMASIN 1.6%, tamoxifen 0.6%.positive early breast cancer who have received two to three years of Incidence of cardiac failure: AROMASIN 0.4%, tamoxifen 0.3% (6,tamoxifen and are switched to AROMASIN for completion of a total of 6.1).five consecutive years of adjuvant hormonal therapy (14.1). Advanced breast cancer: Most common adverse events were mild to treatment of advanced breast cancer in postmenopausal women whose moderate and included hot flushes (13% vs. 5%), nausea (9% vs. 5%),disease has progressed following tamoxifen therapy (14.2).
DrugBank Targets:
16
Cytochrome P450 19A1
Mechanism of Action:
18
Target: steroidal aromatase
Action: inactivator
FDA: Breast cancer cell growth may be estrogen-dependent. Aromatase is the principal enzyme that convertsandrogens to estrogens both in pre- and postmenopausal women. While the main source of estrogen (primarilyestradiol) is the ovary in premenopausal women, the principal source of circulating estrogens in postmenopausalwomen is from conversion of adrenal and ovarian androgens (androstenedione and testosterone) to estrogens(estrone and estradiol) by the aromatase enzyme in peripheral tissues. Estrogen deprivation through aromataseinhibition is an effective and selective treatment for some postmenopausal patients with hormone-dependent breastcancer.Exemestane is an irreversible, steroidal aromatase inactivator, structurally related to the natural substrateandrostenedione. It acts as a false substrate for the aromatase enzyme, and is processed to an intermediate that bindsirreversibly to the active site of the enzyme, causing its inactivation, an effect also known as âsuicide inhibition.âExemestane significantly lowers circulating estrogen concentrations in postmenopausal women, but has nodetectable effect on adrenal biosynthesis of corticosteroids or aldosterone. Exemestane has no effect on otherenzymes involved in the steroidogenic pathway up to a concentration at least 600 times higher than that inhibitingthe aromatase enzyme.
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| 12 |
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Arranon
18
49
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NELARABINE |
GlaxoSmithKline |
October 2005 |
Disease/s that Drug Treats:Lymphoblastic Leukemia
Indications and Usage:
18
ARRANON is a nucleoside metabolic inhibitor indicated for the treatment ofpatients with T-cell acute lymphoblastic leukemia and T-cell lymphoblasticlymphoma whose disease has not responded to or has relapsed followingtreatment with at least two chemotherapy regimens. This use is based on theinduction of complete responses. Randomized trials demonstrating increasedsurvival or other clinical benefit have not been conducted. (1)
Mechanism of Action:
18
Target: DNA synthesis
Action: disruptor --> apoptosis
FDA: Nelarabine is a pro-drug of the deoxyguanosine analogue 9-β-D-arabinofuranosylguanine266 (ara-G), a nucleoside metabolic inhibitor. Nelarabine is demethylated by adenosine deaminase267 (ADA) to ara-G, mono-phosphorylated by deoxyguanosine kinase and deoxycytidine kinase, and268 subsequently converted to the active 5â-triphosphate, ara-GTP. Accumulation of ara-GTP in269 leukemic blasts allows for incorporation into deoxyribonucleic acid (DNA), leading to inhibition270 of DNA synthesis and cell death. Other mechanisms may contribute to the cytotoxic and271 systemic toxicity of nelarabine.
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| 13 |
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Arzerra
18
49
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OFATUMUMAB |
GlaxoSmithKline |
October 2009 |
Disease/s that Drug Treats:chronic lymphocytic leukemia
Indications and Usage:
18
ARZERRA (ofatumumab) is a CD20-directed cytolytic monoclonal antibodyindicated: in combination with chlorambucil, for the treatment of previouslyuntreated patients with chronic lymphocytic leukemia (CLL) for whomfludarabine-based therapy is considered inappropriate. (1.1) for the treatment of patients with CLL refractory to fludarabine andalemtuzumab. (1.2)
DrugBank Targets:
16
no entry
Mechanism of Action:
18
Target: B-cell
Action: promotes lysis
FDA: Ofatumumab binds specifically to both the small and large extracellular loops of the CD20402 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B- to mature403 B-lymphocyte) and on B-cell CLL. The CD20 molecule is not shed from the cell surface and is404 not internalized following antibody binding.405406 The Fab domain of ofatumumab binds to the CD20 molecule and the Fc domain mediates407 immune effector functions to result in B-cell lysis in vitro. Data suggest that possible408 mechanisms of cell lysis include complement-dependent cytotoxicity and antibody-dependent,409 cell-mediated cytotoxicity.
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| 14 |
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Avastin
18
49
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BEVACIZUMAB |
Genentech |
July 2009 |
Disease/s that Drug Treats:renal cell carcinoma & Colorectal Cancer
Indications and Usage:
18
Avastin is a vascular endothelial growth factor-specific angiogenesisinhibitor indicated for the treatment of: Metastatic colorectal cancer, with intravenous 5-fluorouracil-basedchemotherapy for first- or second-line treatment. (1.1) Metastatic colorectal cancer, with fluoropyrimidine- irinotecan- orfluoropyrimidine-oxaliplatin-based chemotherapy for second-linetreatment in patients who have progressed on a first-line Avastincontainingregimen. (1.1) Non-squamous non-small cell lung cancer, with carboplatin and paclitaxelfor first line treatment of unresectable, locally advanced, recurrent ormetastatic disease. (1.2) Glioblastoma, as a single agent for adult patients with progressive diseasefollowing prior therapy. (1.3)-Effectiveness based on improvement in objective response rate. No dataavailable demonstrating improvement in disease-related symptoms orsurvival with Avastin. Metastatic renal cell carcinoma with interferon alfa (1.4) Cervical cancer, in combination with paclitaxel and cisplatin or paclitaxeland topotecan in persistent, recurrent, or metastatic disease. (1.5) Platinum-resistant recurrent epithelial ovarian, fallopian tube or primaryperitoneal cancer, in combination with paclitaxel, pegylated liposomaldoxorubicin or topotecan (1.6) Limitation of Use: Avastin is not indicated for adjuvant treatment of coloncancer. (1.1)
DrugBank Targets:
16
1. Vascular endothelial growth factor A;2. Low affinity immunoglobulin gamma Fc region receptor III-B;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Low affinity immunoglobulin gamma Fc region receptor III-A;8. High affinity immunoglobulin gamma Fc receptor I;9. Low affinity immunoglobulin gamma Fc region receptor II-a;10. Low affinity immunoglobulin gamma Fc region receptor II-b;11. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:
18
Target: VEGF
Action: inhibitor
FDA: Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR)697 on the surface of endothelial cells. The interaction of VEGF with its receptors leads to endothelial698 cell proliferation and new blood vessel formation in in vitro models of angiogenesis. Administration699 of bevacizumab to xenotransplant models of colon cancer in nude (athymic) mice caused reduction700 of microvascular growth and inhibition of metastatic disease progression
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| 15 |
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Beleodaq
18
49
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BELINOSTAT |
Spectrum Pharmaceuticals |
July 2014 |
Disease/s that Drug Treats:relapsed or refractory peripheral T-cell lymphoma
Indications and Usage:
18
Beleodaq is a histone deacetylase inhibitor indicated for the treatment ofpatients with relapsed or refractory peripheral T-cell lymphoma (PTCL). Thisindication is approved under accelerated approval based on tumor responserate and duration of response. An improvement in survival or disease-relatedsymptoms has not been established. Continued approval for this indicationmay be contingent upon verification and description of clinical benefit in theconfirmatory trial. (1)
DrugBank Targets:
16
no entry
Mechanism of Action:
18
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: Beleodaq is a histone deacetylase (HDAC) inhibitor. HDACs catalyze the removal of acetyl groups from thelysine residues of histones and some non-histone proteins. In vitro, belinostat caused the accumulation ofacetylated histones and other proteins, inducing cell cycle arrest and/or apoptosis of some transformed cells.Belinostat shows preferential cytotoxicity towards tumor cells compared to normal cells. Belinostat inhibitedthe enzymatic activity of histone deacetylases at nanomolar concentrations (<250 nM).
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| 16 |
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Bexxar
18
49
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TOSITUMOMAB; IODINE I 131 TOSITUMOMAB |
Corixa |
June 2003 |
Disease/s that Drug Treats:Non-Hodgkin's Lymphoma
Indications and Usage:
18
BEXXAR (tositumomab and Iodine I 131 tositumomab) is a CD20-directedradiotherapeutic antibody indicated for the treatment of patients with CD20-positive, relapsed or refractory, low-grade, follicular, or transformed nonHodgkin'slymphoma who have progressed during or after rituximab therapy,including patients with rituximab-refractory non-Hodgkin's lymphoma. (1.1)Determination of the effectiveness of the BEXXAR therapeutic regimen isbased on overall response rates in patients whose disease is refractory tochemotherapy and rituximab. The effects of the BEXXAR therapeuticregimen on survival are not known. (1.1)Important Limitation of Use BEXXAR therapeutic regimen is only indicated for a single course oftreatment and is not indicated for a first-line treatment. (1.2)
DrugBank Targets:
16
1. B-lymphocyte antigen CD20;2. Low affinity immunoglobulin gamma Fc region receptor III-B;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Low affinity immunoglobulin gamma Fc region receptor III-A;8. High affinity immunoglobulin gamma Fc receptor I;9. Low affinity immunoglobulin gamma Fc region receptor II-a;10.Low affinity immunoglobulin gamma Fc region receptor II-b;11. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:
18
Target: CD20
Action: cytotoxic antibody
FDA: Tositumomab binds specifically to an epitope within the extracellular domain of the586 CD20 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B lymphocytes587 to mature B lymphocytes) and on B-cell non-Hodgkin's lymphomas. The CD20 molecule is not588 shed from the cell surface and is not internalized following antibody binding. The BEXXAR589 therapeutic regimen induces cell death by emitting ionizing radiation to CD20-expressing590 lymphocytes or neighboring cells. In addition to cell death mediated by the radioisotope, other591 possible mechanisms of action include antibody-dependent cellular cytotoxicity, complement-592 dependent cytotoxicity, and CD20-mediated apoptosis.
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| 17 |
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Blincyto
18
49
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BLINATUMOMAB |
Amgen |
December 2014 |
Disease/s that Drug Treats:Philadelphia chromosome-negative relapsed /refractory B cell precursor acute lymphoblastic leukemia
Indications and Usage:
18
BLINCYTO is a bispecific CD19-directed CD3 T-cell engager indicated forthe treatment of Philadelphia chromosome-negative relapsed or refractory Bcellprecursor acute lymphoblastic leukemia (ALL). This indication isapproved under accelerated approval. Continued approval for this indicationmay be contingent upon verification of clinical benefit in subsequent trials. (1)
DrugBank Targets:
16
1. B-lymphocyte antigen CD19;2. T-cell surface glycoprotein CD3 delta chain
Mechanism of Action:
18
Target: CD19-directed CD3 T-cell
Action: engager
FDA: Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on thesurface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenousT cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant Bcells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell,upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatorycytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells.
|
| 18 |
|
Bosulif
18
49
|
BOSUTINIB MONOHYDRATE |
Pfizer |
September 2012 |
Disease/s that Drug Treats:Ph+ chronic myelogenous leukemia
Indications and Usage:
18
BOSULIF is a kinase inhibitor indicated for the treatment of adult patientswith chronic, accelerated, or blast phase Ph+ chronic myelogenous leukemia(CML) with resistance or intolerance to prior therapy. (1)
DrugBank Targets:
16
1. Breakpoint cluster region protein;2. Tyrosine-protein kinase ABL1;3. Tyrosine-protein kinase Lyn;4. Tyrosine-protein kinase HCK;5. Proto-oncogene tyrosine-protein kinase Src;6. Cyclin-dependent kinase 2;7. Dual specificity mitogen-activated protein kinase kinase 1;8. Dual specificity mitogen-activated protein kinase kinase 2;9. Mitogen-activated protein kinase kinase kinase 2;10. Calcium/calmodulin-dependent protein kinase type II subunit gamma
Mechanism of Action:
18
Target: tyrosine kinase/ Src-family kinases including Src, Lyn, and Hck
Action: inhibitor
FDA: Bosutinib is a tyrosine kinase inhibitor. Bosutinib inhibits the Bcr-Abl kinase that promotes CML; it is also aninhibitor of Src-family kinases including Src, Lyn, and Hck. Bosutinib inhibited 16 of 18 imatinib-resistant forms ofBcr-Abl expressed in murine myeloid cell lines. Bosutinib did not inhibit the T315I and V299L mutant cells. In mice,treatment with bosutinib reduced the size of CML tumors relative to controls and inhibited growth of murine myeloidtumors expressing several imatinib-resistant forms of Bcr-Abl.
|
| 19 |
|
Busulfex
18
49
|
BUSULFAN |
Orphan Medical |
February 1999 |
Disease/s that Drug Treats:leukemia
Indications and Usage:
18
BUSULFEX is an alkylating drug indicated for: Use in combination with cyclophosphamide as a conditioning regimenprior to allogeneic hematopoietic progenitor cell transplantation forchronic myelogenous leukemia (CML) (1)
Mechanism of Action:
18
Target: DNA
Action: alkylyzer
FDA: Busulfan is a bifunctional alkylating agent in which two labile methanesulfonate groups are attached to opposite ends of afour-carbon alkyl chain. In aqueous media, busulfan hydrolyzes to release the methanesulfonate groups. This producesreactive carbonium ions that can alkylate DNA. DNA damage is thought to be responsible for much of the cytotoxicity ofbusulfan.
|
| 20 |
|
Campath
18
49
|
ALEMTUZUMAB |
Berlex Laboratories |
May 2001 |
Disease/s that Drug Treats:Leukemia
Indications and Usage:
18
LEMTRADA is a CD52-directed cytolytic monoclonal antibody indicated dizziness, abdominal pain, flushing, and vomiting. (6.1) for the treatment of patients with relapsing forms of multiple sclerosis(MS).
DrugBank Targets:
16
1. CAMPATH-1 antigen;2. Low affinity immunoglobulin gamma Fc region receptor III-B;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Low affinity immunoglobulin gamma Fc region receptor III-A;8. High affinity immunoglobulin gamma Fc receptor I;9. Low affinity immunoglobulin gamma Fc region receptor II-a;10. Low affinity immunoglobulin gamma Fc region receptor II-b;11. Low affinity immunoglobulin gamma Fc region receptor II-c;;
Mechanism of Action:
18
Target: CD52 antigen
Action: after binding, induces cell lysis
FDA: The precise mechanism by which alemtuzumab exerts its therapeutic effects in multiple490 sclerosis is unknown but is presumed to involve binding to CD52, a cell surface antigen491 present on T and B lymphocytes, and on natural killer cells, monocytes, and492 macrophages. Following cell surface binding to T and B lymphocytes, alemtuzumab493 results in antibody-dependent cellular cytolysis and complement-mediated lysis.
|
| 21 |
|
Campostar
18
49
|
IRINOTECAN HYDROCHLORIDE |
Pharmacia & Upjohn |
June 1996 |
Disease/s that Drug Treats:metastatic colorectal cancer
Indications and Usage:
18
CAMPTOSAR is a topoisomerase inhibitor indicated for: First-line therapy in combination with 5-fluorouracil and leucovorin forpatients with metastatic carcinoma of the colon or rectum. (1) Patients with metastatic carcinoma of the colon or rectum whose diseasehas recurred or progressed following initial fluorouracil-based therapy. (1)
DrugBank Targets:
16
1. DNA topoisomerase I, mitochondrial;2. DNA topoisomerase 1
Mechanism of Action:
18
Target: topoisomerase I-DNA complex
Action: inhibitor of repairs to DNA
FDA: Irinotecan is a derivative of camptothecin. Camptothecins interact specifically with the enzymetopoisomerase I, which relieves torsional strain in DNA by inducing reversible single-strandbreaks. Irinotecan and its active metabolite SN-38 bind to the topoisomerase I-DNA complexand prevent religation of these single-strand breaks. Current research suggests that thecytotoxicity of irinotecan is due to double-strand DNA damage produced during DNA synthesiswhen replication enzymes interact with the ternary complex formed by topoisomerase I, DNA,and either irinotecan or SN-38. Mammalian cells cannot efficiently repair these double-strandbreaks.
|
| 22 |
|
CEA-Scan
18
|
|
Immunomedics |
April 1996 |
Disease/s that Drug Treats:colorectal cancer
Indications and Usage:
18
DrugBank Targets:
16
1. Carcinoembryonic antigen-related cell adhesion molecule 1
Mechanism of Action:
18
Target: carcinoembryonic antigen (""CEA"")
Action: marks
FDA: -
|
| 23 |
|
Cervarix
18
49
|
Human Papillomavirus Bivalent (Types 16 and 18) Vaccine, Recombinant |
GlaxoSmithKline |
October 2009 |
Disease/s that Drug Treats:prevention of cervical cancer and cervical intraepithelial neoplasia caused by HPV types 16 and 18
Indications and Usage:
18
DrugBank Targets:
-
Mechanism of Action:
18
Target: IgG neutralizing antibodies directed against HPV-L1 capsid proteins
Action: activates/ provokes production
FDA: -
|
| 24 |
|
Cometriq
18
49
|
CABOZANTINIB S-MALATE |
Exelixis |
November 2012 |
Disease/s that Drug Treats:thyroid cancer
Indications and Usage:
18
COMETRIQ is a kinase inhibitor indicated for the treatment ofpatients with progressive, metastatic medullary thyroid cancer(MTC). (1)
DrugBank Targets:
16
1. Hepatocyte growth factor receptor;2. Vascular endothelial growth factor receptor 2;3. Proto-oncogene tyrosine-protein kinase receptor Ret
Mechanism of Action:
18
Target: tyrosine kinase activity of RET, MET, VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, and TIE-2
Action: inhibitor
FDA: In vitro biochemical and/or cellular assays have shown that cabozantinib inhibits the tyrosinekinase activity of RET, MET, VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, and TIE-2.These receptor tyrosine kinases are involved in both normal cellular function and pathologicprocesses such as oncogenesis, metastasis, tumor angiogenesis, and maintenance of the tumormicroenvironment.
|
| 25 |
|
Cyramza
18
49
|
RAMUCIRUMAB |
Eli Lilly |
April 2014 |
Disease/s that Drug Treats:gastric cancer
Indications and Usage:
18
CYRAMZA® is a human vascular endothelial growth factor receptor 2antagonist indicated as a single agent or in combination with paclitaxel, for treatmentof advanced gastric or gastro-esophageal junctionadenocarcinoma, with disease progression on or after priorfluoropyrimidine- or platinum-containing chemotherapy. (1.1) in combination with docetaxel, for treatment of metastatic nonsmallcell lung cancer with disease progression on or afterplatinum-based chemotherapy. Patients with EGFR or ALKgenomic tumor aberrations should have disease progression onFDA-approved therapy for these aberrations prior to receivingCYRAMZA. (1.2) in combination with FOLFIRI, for the treatment of metastaticcolorectal cancer with disease progression on or after priortherapy with bevacizumab, oxaliplatin, and a fluoropyrimidine.(1.3)
DrugBank Targets:
-
Mechanism of Action:
18
Target: ligand-stimulated activation of VEGF Receptor 2
Action: inhibitor
FDA: Ramucirumab is a vascular endothelial growth factor receptor 2 antagonist that specifically binds VEGF Receptor2 and blocks binding of VEGFR ligands, VEGF-A, VEGF-C, and VEGF-D. As a result, ramucirumab inhibits ligandstimulatedactivation of VEGF Receptor 2, thereby inhibiting ligand-induced proliferation, and migration of humanendothelial cells. Ramucirumab inhibited angiogenesis in an in vivo animal model.
|
| 26 |
|
Degarelix
18
49
|
degarelix |
Ferring Pharmaceuticals |
December of 2008 |
Disease/s that Drug Treats:Prostate Cancer
Indications and Usage:
18
DrugBank Targets:
16
1. Gonadotropin-releasing hormone receptor
Mechanism of Action:
18
Target: Gonadotropin-releasing hormone (GnRH) receptor
Action: antagonist
FDA: -
|
| 27 |
|
Doxil
18
49
|
DOXORUBICIN HYDROCHLORIDE |
Alza |
June 1999 |
Disease/s that Drug Treats:ovarian cancer that is refractory to other first-line therapies
Indications and Usage:
18
DOXIL is an anthracycline topoisomerase II inhibitor indicated for: Ovarian cancer (1.1)After failure of platinum-based chemotherapy. AIDS-related Kaposiâs Sarcoma (1.2)After failure of prior systemic chemotherapy or intolerance to such therapy. Multiple Myeloma (1.3)In combination with bortezomib in patients who have not previouslyreceived bortezomib and have received at least one prior therapy.
DrugBank Targets:
16
1. DNA;2. DNA topoisomerase 2-alpha
Mechanism of Action:
18
Target: nucleic acidsynthesis
Action: inhibitor
FDA: The active ingredient of DOXIL is doxorubicin HCl. The mechanism of action ofdoxorubicin HCl is thought to be related to its ability to bind DNA and inhibit nucleic acidsynthesis. Cell structure studies have demonstrated rapid cell penetration and perinuclearReference ID: 373359617 chromatin binding, rapid inhibition of mitotic activity and nucleic acid synthesis, andinduction of mutagenesis and chromosomal aberrations.
|
| 28 |
|
Elitek
18
49
|
RASBURICASE |
sanofi-aventis |
October 2009 |
Disease/s that Drug Treats:management of plasma uric acid levels in adults with malignancies
Indications and Usage:
18
Elitek is a recombinant urate-oxidase indicated for initial management ofplasma uric acid levels in pediatric and adult patients with leukemia,lymphoma, and solid tumor malignancies who are receiving anti-cancertherapy expected to result in tumor lysis and subsequent elevation of plasmauric acid (1).Limitation of use: Elitek is indicated only for a single course of treatment (1).
DrugBank Targets:
16
1. Uric acid
Mechanism of Action:
18
Target: uric acid
Action: converter to alantoin
FDA: In humans, uric acid is the final step in the catabolic pathway of purines. Rasburicase catalyzesenzymatic oxidation of poorly soluble uric acid into an inactive and more soluble metabolite(allantoin).
|
| 29 |
|
Eloxatin
18
49
|
OXALIPLATIN |
Sanofi-aventis |
August 2002 |
Disease/s that Drug Treats:Metastatic colon or rectum carcinomas that have recurred or progressed within six months folowing first-line treatment
Indications and Usage:
18
ELOXATIN is a platinum-based drug used in combination with infusional 5-fluorouracil /leucovorin, which is indicated for: adjuvant treatment of stage III colon cancer in patients who haveundergone complete resection of the primary tumor. (1) treatment of advanced colorectal cancer. (1)
DrugBank Targets:
16
1. DNA
Mechanism of Action:
18
Target: DNA replication and transcription
Action: inhibitor
FDA: Oxaliplatin undergoes nonenzymatic conversion in physiologic solutions to active derivatives viadisplacement of the labile oxalate ligand. Several transient reactive species are formed, includingmonoaquo and diaquo DACH platinum, which covalently bind with macromolecules. Both interandintrastrand Pt-DNA crosslinks are formed. Crosslinks are formed between the N7 positions oftwo adjacent guanines (GG), adjacent adenine-guanines (AG), and guanines separated by anintervening nucleotide (GNG). These crosslinks inhibit DNA replication and transcription.Cytotoxicity is cell-cycle nonspecific.In vivo studies have shown antitumor activity of oxaliplatin against colon carcinoma. Incombination with 5-fluorouracil, oxaliplatin exhibits in vitro and in vivo antiproliferative activitygreater than either compound alone in several tumor models [HT29 (colon), GR (mammary), andL1210 (leukemia)].
|
| 30 |
|
Emend
18
49
|
APREPITANT FOSAPREPITANT DIMEGLUMINE |
Merck |
March 2003 |
Disease/s that Drug Treats:Chemotherapy-induced Nausea and Vomiting
Indications and Usage:
18
EMEND® is a substance P/neurokinin 1 (NK1) receptor antagonist,indicated: in combination with other antiemetic agents for the:o prevention of acute and delayed nausea and vomitingassociated with initial and repeat courses of highly emetogeniccancer chemotherapy (HEC) including high-dose cisplatin (1.1)o prevention of nausea and vomiting associated with initial andrepeat courses of moderately emetogenic cancer chemotherapy(MEC) (1.1) for the prevention of postoperative nausea and vomiting (PONV)(1.2)Limitations of Use (1.3) Not studied for the treatment of established nausea and vomiting. Chronic continuous administration is not recommended.
DrugBank Targets:
16
1. Substance-P receptor
Mechanism of Action:
18
Target: emesis induced by cytotoxic chemotherapeutic agents, such as cisplatin
Action: inhibitor
FDA: Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors.Aprepitant has little or no affinity for serotonin (5-HT3), dopamine, and corticosteroid receptors, the targetsof existing therapies for chemotherapy-induced nausea and vomiting (CINV) and postoperative nauseaand vomiting (PONV).Aprepitant has been shown in animal models to inhibit emesis induced by cytotoxicchemotherapeutic agents, such as cisplatin, via central actions. Animal and human Positron EmissionTomography (PET) studies with aprepitant have shown that it crosses the blood brain barrier and occupiesbrain NK1 receptors. Animal and human studies show that aprepitant augments the antiemetic activity ofthe 5-HT3-receptor antagonist ondansetron and the corticosteroid dexamethasone and inhibits both theacute and delayed phases of cisplatin-induced emesis.
|
| 31 |
|
Erbitux
18
49
|
CETUXIMAB |
Imclone, Bristol-Myers Squibb |
February 2004 |
Disease/s that Drug Treats:Colorectal Cancer
Indications and Usage:
18
Erbitux® is an epidermal growth factor receptor (EGFR) antagonist indicatedfor treatment of:Head and Neck Cancer Locally or regionally advanced squamous cell carcinoma of the headand neck in combination with radiation therapy. (1.1, 14.1) Recurrent locoregional disease or metastatic squamous cell carcinomaof the head and neck in combination with platinum-based therapy with5-FU. (1.1, 14.1) Recurrent or metastatic squamous cell carcinoma of the head and neckprogressing after platinum-based therapy. (1.1, 14.1)Colorectal CancerK-Ras wild-type, EGFR-expressing, metastatic colorectal cancer asdetermined by FDA-approved tests in combination with FOLFIRI for first-line treatment, in combination with irinotecan in patients who are refractory toirinotecan-based chemotherapy, as a single agent in patients who have failed oxaliplatin- andirinotecan-based chemotherapy or who are intolerant to irinotecan.(1.2, 5.7, 12.1, 14.2)Limitation of Use: Erbitux is not indicated for treatment of Ras-mutantcolorectal cancer. (5.7, 14.2)
DrugBank Targets:
16
1. Epidermal growth factor receptor;2. Low affinity immunoglobulin gamma Fc region receptor III-B;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Low affinity immunoglobulin gamma Fc region receptor III-A;8. Complement C1s subcomponent;9. High affinity immunoglobulin gamma Fc receptor I;10. Low affinity immunoglobulin gamma Fc region receptor II-a;11. Low affinity immunoglobulin gamma Fc region receptor II-b;12. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:
18
Target: binding of epidermal growth factor (EGF) and other ligands to epidermal growth factor receptor (EGFR, HER1, c-ErbB-1)
Action: inhibitor
FDA: The epidermal growth factor receptor (EGFR, HER1, c-ErbB-1) is a transmembraneglycoprotein that is a member of a subfamily of type I receptor tyrosine kinases including EGFR,HER2, HER3, and HER4. The EGFR is constitutively expressed in many normal epithelialtissues, including the skin and hair follicle. Expression of EGFR is also detected in many humancancers including those of the head and neck, colon, and rectum. Cetuximab binds specifically to the EGFR on both normal and tumor cells, and competitivelyinhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforminggrowth factor-alpha. In vitro assays and in vivo animal studies have shown that binding ofcetuximab to the EGFR blocks phosphorylation and activation of receptor-associated kinases,resulting in inhibition of cell growth, induction of apoptosis, and decreased matrixmetalloproteinase and vascular endothelial growth factor production. Signal transduction throughthe EGFR results in activation of wild-type Ras proteins, but in cells with activating Ras somaticmutations, the resulting mutant Ras proteins are continuously active regardless of EGFRregulation.In vitro, cetuximab can mediate antibody-dependent cellular cytotoxicity (ADCC) against certainhuman tumor types. In vitro assays and in vivo animal studies have shown that cetuximabinhibits the growth and survival of tumor cells that express the EGFR. No anti-tumor effects ofcetuximab were observed in human tumor xenografts lacking EGFR expression. The addition ofcetuximab to radiation therapy or irinotecan in human tumor xenograft models in mice resultedin an increase in anti-tumor effects compared to radiation therapy or chemotherapy alone.
|
| 32 |
|
Erivedge
18
49
|
VISMODEGIB |
Genentech |
January 2012 |
Disease/s that Drug Treats:basal cell carcinoma
Indications and Usage:
18
ERIVEDGE (vismodegib) capsule is a hedgehog pathway inhibitor indicatedfor the treatment of adults with metastatic basal cell carcinoma, or with locallyadvanced basal cell carcinoma that has recurred following surgery or who arenot candidates for surgery, and who are not candidates for radiation. (1)
DrugBank Targets:
16
1. Smoothened homolog
Mechanism of Action:
18
Target: hedgehog (Hh) signaling pathway
Action: innhibitor
FDA: Vismodegib is an inhibitor of the Hedgehog pathway. Vismodegib binds to and inhibitsSmoothened, a transmembrane protein involved in Hedgehog signal transduction.
|
| 33 |
|
Ethyol
18
|
AMIFOSTINE |
Alza |
December 8, 1995 |
Disease/s that Drug Treats:ovarian cancer
Indications and Usage:
18
ETHYOL (amifostine) is indicated to reduce the cumulative renal toxicity associated withrepeated administration of cisplatin in patients with advanced ovarian cancer.ETHYOL is indicated to reduce the incidence of moderate to severe xerostomia in patientsundergoing post-operative radiation treatment for head and neck cancer, where the radiationport includes a substantial portion of the parotid glands (see Clinical Studies).For the approved indications, the clinical data do not suggest that the effectiveness of cisplatin basedchemotherapy regimens or radiation therapy is altered by ETHYOL. There are at present only limiteddata on the effects of ETHYOL on the efficacy of chemotherapy or radiotherapy in other settings.ETHYOL should not be administered to patients in other settings where chemotherapy can produce asignificant survival benefit or cure, or in patients receiving definitive radiotherapy, except in thecontext of a clinical study (see WARNINGS).
DrugBank Targets:
16
1. Ectonucleotide pyrophosphatase/phosphodiesterase family member 1;2. Alkaline phosphatase, placental-like
Mechanism of Action:
18
Target: -
Action: -
FDA: -
|
| 34 |
|
Eulexin
18
|
FLUTAMIDE |
Schering-Plough |
June 1996 |
Disease/s that Drug Treats:prostate cancer
Indications and Usage:
18
EULEXIN capsules are indicated for use in combination with LHRH agonists for the management of locally confined Stage B2C and Stage D2 metastatic carcinoma of the prostate. Stage B2C Prostatic Carcinoma: Treatment with EUlEXIN an the goserelin acetate implant shouls start 8 weeks prior to initiating radiation therapy and continue during radiation therapy. Stage D2 Metastatic Carcinoma: To acheive benefit from treatment, EULEXIN Capsules should be initiated with the LHRH-agonist and continued until progression.
DrugBank Targets:
16
1. Androgen receptor;2. Aryl hydrocarbon receptor
Mechanism of Action:
18
Target: androgen uptake and/or nuclear binding of angrogen in target tissues
Action: inhibitor
FDA: In animal studies, flutamide demonstrates potent anti-angrogenic effects. It exerts an antiandrogenic action by inhibiting angrogen uptake and/or by inhibiting nuclear binding of androgen in target tissues or both. Prostatic carcinoma is known to be androgen-sensitive and responds to treatment that counteracts the effect of androgen and/or removes the source of androgen, eg. castration. Elevations of plasma testosterone and estraidiol levels have been noted following flutamide administration.
|
| 35 |
|
Evista
18
49
|
RALOXIFENE HYDROCHLORIDE |
Eli Lilly |
September 2007 |
Disease/s that Drug Treats:osteoporosis and reduction of breast cancer risk in postmenopausal women
Indications and Usage:
18
EVISTA is an estrogen agonist/antagonist indicated for Treatment and prevention of osteoporosis in postmenopausal women.(1.1)
DrugBank Targets:
16
1. Estrogen receptor;2. Estrogen receptor beta
Mechanism of Action:
18
Target: estrogenic pathways
Action: can be an activator or antooagonist
FDA: Decreases in estrogen levels after oophorectomy or menopause lead to increases in bone resorption andaccelerated bone loss. Bone is initially lost rapidly because the compensatory increase in bone formation isinadequate to offset resorptive losses. In addition to loss of estrogen, this imbalance between resorption andformation may be due to age-related impairment of osteoblasts or their precursors. In some women, these changeswill eventually lead to decreased bone mass, osteoporosis, and increased risk for fractures, particularly of the spine,hip, and wrist. Vertebral fractures are the most common type of osteoporotic fracture in postmenopausal women.The biological actions of raloxifene are largely mediated through binding to estrogen receptors. This bindingresults in activation of certain estrogenic pathways and blockade of others. Thus, raloxifene is an estrogenagonist/antagonist, commonly referred to as a selective estrogen receptor modulator (SERM).Raloxifene decreases resorption of bone and reduces biochemical markers of bone turnover to thepremenopausal range. These effects on bone are manifested as reductions in the serum and urine levels of boneturnover markers, decreases in bone resorption based on radiocalcium kinetics studies, increases in bone mineraldensity (BMD), and decreases in incidence of fractures.
|
| 36 |
|
Farydak
18
49
|
PANOBINOSTAT LACTATE |
Novartis |
February 2015 |
Disease/s that Drug Treats:Multiple myeloma
Indications and Usage:
18
FARYDAK, a histone deacetylase inhibitor, in combination with bortezomiband dexamethasone, is indicated for the treatment of patients with multiplemyeloma who have received at least 2 prior regimens, including bortezomiband an immunomodulatory agent. This indication is approved underaccelerated approval based on progression free survival. Continued approvalfor this indication may be contingent upon verification and description ofclinical benefit in confirmatory trials. (1)
DrugBank Targets:
-
Mechanism of Action:
18
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: FARYDAK is a histone deacetylase (HDAC) inhibitor that inhibits the enzymatic activity of HDACs atnanomolar concentrations. HDACs catalyze the removal of acetyl groups from the lysine residues of histonesand some non-histone proteins. Inhibition of HDAC activity results in increased acetylation of histone proteins,an epigenetic alteration that results in a relaxing of chromatin, leading to transcriptional activation. In vitro,Reference ID: 3699607 panobinostat caused the accumulation of acetylated histones and other proteins, inducing cell cycle arrest and/orapoptosis of some transformed cells. Increased levels of acetylated histones were observed in xenografts frommice that were treated with panobinostat. Panobinostat shows more cytotoxicity towards tumor cells comparedto normal cells.
|
| 37 |
|
Faslodex
18
49
|
FULVESTRANT |
AstraZeneca |
April 2002 |
Disease/s that Drug Treats:Hormone receptor positive metastatic breast cancer
Indications and Usage:
18
FASLODEX is an estrogen receptor antagonist indicated for the: Treatment of hormone receptor positive metastatic breast cancer inpostmenopausal women with disease progression followingantiestrogen therapy.
DrugBank Targets:
16
1. Estrogen receptor
Mechanism of Action:
18
Target: estrogen receptors on tumor cells
Action: antagonist
FDA: Many breast cancers have estrogen receptors (ER) and thegrowth of these tumors can be stimulated by estrogen.Fulvestrant is an estrogen receptor antagonist that binds to theestrogen receptor in a competitive manner with affinitycomparable to that of estradiol and downregulates the ERprotein in human breast cancer cells.In vitro studies demonstrated that fulvestrant is a reversibleinhibitor of the growth of tamoxifen-resistant, as well asestrogen-sensitive human breast cancer (MCF-7) cell lines. Inin vivo tumor studies, fulvestrant delayed the establishment oftumors from xenografts of human breast cancer MCF-7 cellsin nude mice. Fulvestrant inhibited the growth of establishedMCF-7 xenografts and of tamoxifen-resistant breast tumorxenografts.Fulvestrant showed no agonist-type effects in in vivouterotropic assays in immature or ovariectomized mice andrats. In in vivo studies in immature rats and ovariectomizedmonkeys, fulvestrant blocked the uterotrophic action ofestradiol. In postmenopausal women, the absence of changesin plasma concentrations of FSH and LH in response tofulvestrant treatment (250 mg monthly) suggests no peripheralsteroidal effects.
|
| 38 |
|
Femara
18
49
|
LETROZOLE |
Novartis |
January 2001 |
Disease/s that Drug Treats:Hormone receptor positive or hormone receptor unknown locally advanced or metastatic breast cancer
Indications and Usage:
18
Femara is an aromatase inhibitor indicated for: Adjuva nt treatment of postmenopausal women with hormone receptorpositive early brea st cancer (1.1) Extended adjuvant treatment of postmenopausal women with early brea stcancer who have received prior standard adju vant ta moxifen thera py (1.2) First a nd second-line treatment of postmenopausal women with hormonereceptor positive or unknown advanced breast cancer (1.3)
DrugBank Targets:
16
1. Cytochrome P450 19A1
Mechanism of Action:
18
Target: aromatase enzyme system
Action: inhibitor
FDA: The growth of some cancers of the breast is stimulated or maintained by estrogens. Treatment of breastcancer thought to be hormonally responsive (i.e., estrogen and/or progesterone receptor positive orreceptor unknown) has included a variety of efforts to decrease estrogen levels (ovariectomy,adrenalectomy, hypophysectomy) or inhibit estrogen effects (antiestrogens and progestational agents).These interventions lead to decreased tumor mass or delayed progression of tumor growth in somewomen.In postmenopausal women, estrogens are mainly derived from the action of the aromatase enzyme, whichconverts adrenal androgens (primarily androstenedione and testosterone) to estrone and estradiol. Thesuppression of estrogen biosynthesis in peripheral tissues and in the cancer tissue itself can therefore beachieved by specifically inhibiting the aromatase enzyme.Letrozole is a nonsteroidal competitive inhibitor of the aromatase enzyme system; it inhibits theconversion of androgens to estrogens. In adult nontumor- and tumor-bearing female animals, letrozole isas effective as ovariectomy in reducing uterine weight, elevating serum LH, and causing the regression ofestrogen-dependent tumors. In contrast to ovariectomy, treatment with letrozole does not lead to anincrease in serum FSH. Letrozole selectively inhibits gonadal steroidogenesis but has no significant effecton adrenal mineralocorticoid or glucocorticoid synthesis.Letrozole inhibits the aromatase enzyme by competitively binding to the heme of the cytochrome P450subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues. Treatment of womenwith letrozole significantly lowers serum estrone, estradiol and estrone sulfate and has not been shown tosignificantly affect adrenal corticosteroid synthesis, aldosterone synthesis, or synthesis of thyroidhormones.
|
| 39 |
|
Folotyn
18
49
|
PRALATREXATE |
Allos Therapeutics |
September 2009 |
Disease/s that Drug Treats:peripheral T-cell lymphoma
Indications and Usage:
18
FOLOTYN is a folate analog metabolic inhibitor indicated for the treatment ofpatients with relapsed or refractory peripheral T-cell lymphoma (PTCL). Thisindication is based on overall response rate. Clinical benefit such asimprovement in progression-free survival or overall survival has not beendemonstrated. (1)
DrugBank Targets:
16
1. Dihydrofolate reductase;2. Thymidylate synthase
Mechanism of Action:
18
Target: dihydrofolate reductase
Action: inhibitor
FDA: Pralatrexate is a folate analog metabolic inhibitor that competitively inhibits dihydrofolate reductase. It is also acompetitive inhibitor for polyglutamylation by the enzyme folylpolyglutamyl synthetase. This inhibition resultsin the depletion of thymidine and other biological molecules the synthesis of which depends on single carbontransfer.
|
| 40 |
|
Fusilev
18
|
LEVOLEUCOVORIN CALCIUM |
Spectrum Pharmaceuticals |
March of 2008 |
Disease/s that Drug Treats:rescue after high-dose methotrexate therapy in osteosarcoma and to reduce the toxicity of methotrexate
Indications and Usage:
18
Fusilev is a folate analog indicated for: Rescue after high-dose methotrexate therapy in osteosarcoma. Diminishing the toxicity and counteracting the effects of impairedmethotrexate elimination and of inadvertent overdosage of folic acidantagonists. Use in combination chemotherapy with 5-fluorouracil in the palliativetreatment of patients with advanced metastatic colorectal cancer.(1)Limitations of UseFusilev is not approved for pernicious anemia and megaloblastic anemias.Improper use may cause a hematologic remission while neurologicmanifestations continue to progress. (1.1)
DrugBank Targets:
16
1. Thymidylate synthase
Mechanism of Action:
18
Target: therapeutic and toxic effects of folic acidantagonists / therapeutic and toxic effects of fluoropyrimidines used in cancer therapy
Action: counteract/enhance
FDA: 12.1.1 Levoleucovorin effects during high-dose methotrexate therapyLevoleucovorin is the pharmacologically active isomer of 5-formyl tetrahydrofolic acid. Levoleucovorin does not requirereduction by the enzyme dihydrofolate reductase in order to participate in reactions utilizing folates as a source of âonecarbonâmoieties. Administration of levoleucovorin can counteract the therapeutic and toxic effects of folic acidantagonists such as methotrexate, which act by inhibiting dihydrofolate reductase.12.1.2 Levoleucovorin effects in combination with 5-fluorouracilLevoleucovorin can enhance the therapeutic and toxic effects of fluoropyrimidines used in cancer therapy such as5-fluorouracil. 5-fluorouracil is metabolized to 5-fluoro-2'-deoxyuridine-5'-monophosphate (FdUMP), which binds to andinhibits thymidylate synthase (an enzyme important in DNA repair and replication). Levoleucovorin is readily convertedto another reduced folate, 5,10-methylenetetrahydrofolate, which acts to stabilize the binding of FdUMP to thymidylatesynthase and thereby enhances the inhibition of this enzyme.
|
| 41 |
|
Gardasil
18
49
|
quadrivalent human papillomavirus (types 6, 11, 16, 18) recombinant vaccine |
Merck |
June 2006 |
Disease/s that Drug Treats:Cervical Cancer Caused by Human Papillomavirus
Indications and Usage:
18
GARDASIL is a vaccine indicated in girls and women 9 through 26years of age for the prevention of the following diseases caused byHuman Papillomavirus (HPV) types included in the vaccine: Cervical, vulvar, vaginal, and anal cancer caused by HPV types 16and 18 (1.1) Genital warts (condyloma acuminata) caused by HPV types 6 and11 (1.1)And the following precancerous or dysplastic lesions caused by HPVtypes 6, 11, 16, and 18: Cervical intraepithelial neoplasia (CIN) grade 2/3 and Cervicaladenocarcinoma in situ (AIS) (1.1) Cervical intraepithelial neoplasia (CIN) grade 1 (1.1) Vulvar intraepithelial neoplasia (VIN) grade 2 and grade 3 (1.1) Vaginal intraepithelial neoplasia (VaIN) grade 2 and grade 3 (1.1) Anal intraepithelial neoplasia (AIN) grades 1, 2, and 3 (1.1)GARDASIL is indicated in boys and men 9 through 26 years of age forthe prevention of the following diseases caused by HPV types includedin the vaccine: Anal cancer caused by HPV types 16 and 18 (1.2) Genital warts (condyloma acuminata) caused by HPV types 6 and11 (1.2)And the following precancerous or dysplastic lesions caused by HPVtypes 6, 11, 16, and 18: Anal intraepithelial neoplasia (AIN) grades 1, 2, and 3. (1.2)Limitations of GARDASIL Use and Effectiveness: GARDASIL does not eliminate the necessity for women tocontinue to undergo recommended cervical cancer screening.(1.3, 17) Recipients of GARDASIL should not discontinue anal cancerscreening if it has been recommended by a health care provider.(1.3, 17) GARDASIL has not been demonstrated to provide protectionagainst disease from vaccine and non-vaccine HPV types to whicha person has previously been exposed through sexual activity.(1.3, 14.4, 14.5) GARDASIL is not intended to be used for treatment of activeexternal genital lesions; cervical, vulvar, vaginal, and analcancers; CIN; VIN; VaIN, or AIN. (1.3) GARDASIL has not been demonstrated to protect againstdiseases due to HPV types not contained in the vaccine. (1.3,14.4, 14.5) Not all vulvar, vaginal, and anal cancers are caused by HPV, andGARDASIL protects only against those vulvar, vaginal, and analcancers caused by HPV 16 and 18. (1.3) GARDASIL does not protect against genital diseases not causedby HPV. (1.3) Vaccination with GARDASIL may not result in protection in allvaccine recipients. (1.3) GARDASIL has not been demonstrated to prevent HPV-relatedCIN 2/3 or worse in women older than 26 years of age. (14.7)
DrugBank Targets:
-
Mechanism of Action:
18
Target: humoral immune response
Action: inducer
FDA: HPV only infects human beings. Animal studies with analogous animal papillomaviruses suggest thatthe efficacy of L1 VLP vaccines may involve the development of humoral immune responses. Humanbeings develop a humoral immune response to the vaccine, although the exact mechanism of protectionis unknown.
|
| 42 |
|
Gazyva
18
49
|
OBINUTUZUMAB |
Genentech |
October of 2013 |
Disease/s that Drug Treats:previously untreated chronic lymphocytic leukemia
Indications and Usage:
18
GAZYVA (obinutuzumab) is a CD20-directed cytolytic antibody and isindicated, in combination with chlorambucil, for the treatment of patients withpreviously untreated chronic lymphocytic leukemia. (1, 14)
DrugBank Targets:
16
1. B-lymphocyte antigen CD20
Mechanism of Action:
18
Target: CD20 antigen expressed on the surface of pre B- and mature B-lymphocytes
Action: engager of immune cells and/or activator of intracellular death signaling pathways and/or activator of the complement cascade
FDA: Obinutuzumab is a monoclonal antibody that targets the CD20 antigen expressed on the surfaceof pre B- and mature B-lymphocytes. Upon binding to CD20, obinutuzumab mediates B-celllysis through (1) engagement of immune effector cells, (2) by directly activating intracellulardeath signaling pathways and/or (3) activation of the complement cascade. The immune effectorcell mechanisms include antibody-dependent cellular cytotoxicity and antibody-dependentcellular phagocytosis.
|
| 43 |
|
Gemzar
18
49
|
GEMCITABINE HYDROCHLORIDE |
Eli Lilly |
May 1996 |
Disease/s that Drug Treats:pancreatic cancer/Lung cancer
Indications and Usage:
18
Gemzar® is a nucleoside metabolic inhibitor indicated: in combination with carboplatin, for the treatment of advanced ovariancancer that has relapsed at least 6 months after completion of platinumbasedtherapy (1.1) in combination with paclitaxel, for first-line treatment of metastaticbreast cancer after failure of prior anthracycline-containing adjuvantchemotherapy, unless anthracyclines were clinically contraindicated(1.2) in combination with cisplatin for the treatment of non-small cell lungcancer (1.3) as a single agent for the treatment of pancreatic cancer (1.4)
DrugBank Targets:
16
1. DNA;2. Ribonucleoside-diphosphate reductase large subunit;3. Thymidylate synthase;4. UMP-CMP kinase
Mechanism of Action:
18
Target: ribonucleotide reductase
Action: inhibitor
FDA: Gemcitabine kills cells undergoing DNA synthesis and blocks the progression of cells through the G1/S-phase boundary.Gemcitabine is metabolized by nucleoside kinases to diphosphate (dFdCDP) and triphosphate (dFdCTP) nucleosides. Gemcitabinediphosphate inhibits ribonucleotide reductase, an enzyme responsible for catalyzing the reactions that generate deoxynucleosidetriphosphates for DNA synthesis, resulting in reductions in deoxynucleotide concentrations, including dCTP. Gemcitabinetriphosphate competes with dCTP for incorporation into DNA. The reduction in the intracellular concentration of dCTP by the actionof the diphosphate enhances the incorporation of gemcitabine triphosphate into DNA (self-potentiation). After the gemcitabinenucleotide is incorporated into DNA, only one additional nucleotide is added to the growing DNA strands, which eventually results inthe initiation of apoptotic cell death.
|
| 44 |
|
Gilotrif
18
49
|
AFATINIB DIMALEATE |
Boehringer Ingelheim |
July 2013 |
Disease/s that Drug Treats:metastatic non-small cell lung cancer with EGFR mutations
Indications and Usage:
18
GILOTRIF is a kinase inhibitor indicated for the first-line treatment ofpatients with metastatic non-small cell lung cancer (NSCLC) whose tumorshave epidermal growth factor receptor (EGFR) exon 19 deletions or exon 21(L858R) substitution mutations as detected by an FDA-approved test (1)Limitation of Use: Safety and efficacy of GILOTRIF have not beenestablished in patients whose tumors have other EGFR mutations (1)
DrugBank Targets:
16
1. Epidermal growth factor receptor;2. Receptor tyrosine-protein kinase erbB-2;3. Receptor tyrosine-protein kinase erbB-4
Mechanism of Action:
18
Target: tyrosine kinase autophosphorylation
Action: inhibitor
FDA: Afatinib covalently binds to the kinase domains of EGFR (ErbB1), HER2 (ErbB2), and HER4 (ErbB4) andirreversibly inhibits tyrosine kinase autophosphorylation, resulting in downregulation of ErbB signaling.Afatinib demonstrated inhibition of autophosphorylation and in vitro proliferation of cell lines expressing wildtypeEGFR or those expressing selected EGFR exon 19 deletion mutations or exon 21 L858R mutations,including some with a secondary T790M mutation, at afatinib concentrations achieved, at least transiently, inpatients. In addition, afatinib inhibited in vitro proliferation of cell lines overexpressing HER2.Treatment with afatinib resulted in inhibition of tumor growth in nude mice implanted with tumors eitheroverexpressing wild type EGFR or HER2 or in an EGFR L858R/T790M double mutant model.
|
| 45 |
|
Gleevec
18
49
|
IMATINIB MESYLATE |
Novartis |
May 2001 |
Disease/s that Drug Treats:chronic myeloid leukemia/Gastrointestinal stromal tumors (GISTs)
Indications and Usage:
18
Gleevec⢠(imatinib mesylate) is indicated for the treatment of newly diagnosed adultpatients with Philadelphia chromosome positive chronic myeloid leukemia (CML) in chronicphase. Follow-up is limited. Page 10Gleevec is also indicated for the treatment of patients with Philadelphia chromosomepositive chronic myeloid leukemia (CML) in blast crisis, accelerated phase, or in chronicphase after failure of interferon-alpha therapy. Gleevec is also indicated for the treatment ofpediatric patients with Ph+ chronic phase CML whose disease has recurred after stem celltransplant or who are resistant to interferon alpha therapy. There are no controlled trialsdemonstrating a clinical benefit, such as improvement in disease-related symptoms orincreased survival.Gleevec is also indicated for the treatment of patients with Kit (CD117) positiveunresectable and/or metastatic malignant gastrointestinal stromal tumors (GIST). (SeeCLINICAL STUDIES: Gastrointestinal Stromal Tumors.) The effectiveness of Gleevec inGIST is based on objective response rate (see CLINICAL STUDIES). There are no controlledtrials demonstrating a clinical benefit, such as improvement in disease-related symptoms orincreased survival.
DrugBank Targets:
16
1. BCR/ABL fusion protein isoform X9;2. Mast/stem cell growth factor receptor Kit;3. RET proto-oncogene;4. High affinity nerve growth factor receptor;5. Macrophage colony-stimulating factor 1 receptor;6. Platelet-derived growth factor receptor alpha;7. Epithelial discoidin domain-containing receptor 1;8. Tyrosine-protein kinase ABL1;9. Platelet-derived growth factor receptor beta
Mechanism of Action:
18
Target: protein-tyrosine kinase
Action: inhibitor
FDA: Imatinib mesylate is a protein-tyrosine kinase inhibitor that inhibits the Bcr-Abl tyrosinekinase, the constitutive abnormal tyrosine kinase created by the Philadelphia chromosomeabnormality in chronic myeloid leukemia (CML). It inhibits proliferation and inducesapoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphiachromosome positive chronic myeloid leukemia. In colony formation assays using ex vivoperipheral blood and bone marrow samples, imatinib shows inhibition of Bcr-Abl positivecolonies from CML patients.In vivo, it inhibits tumor growth of Bcr-Abl transfected murine myeloid cells as wellas Bcr-Abl positive leukemia lines derived from CML patients in blast crisis.Imatinib is also an inhibitor of the receptor tyrosine kinases for platelet-derivedgrowth factor (PDGF) and stem cell factor (SCF), c-kit, and inhibits PDGF- andSCF-mediated cellular events. In vitro, imatinib inhibits proliferation and induces apoptosis ingastrointestinal stromal tumor (GIST) cells, which express an activating c-kit mutation.
|
| 46 |
|
Gliadel Wafer
18
49
|
CARMUSTINE |
Rhone-Poulenc Rorer, Guilford Pharmaceuticals |
February 1997 |
Disease/s that Drug Treats:brain cancer
Indications and Usage:
18
GLIADELWaferisanalkylatingdrugindicatedforthetreatmentof: newly-diagnosedhigh-grade-malignantgliomaasanadjuncttosurgeryandradiation(1)and recurrentglioblastomamultiformeasanadjuncttosurgery(1)
DrugBank Targets:
16
1. Glutathione reductase, mitochondrial;2. DNA;3. RNA
Mechanism of Action:
18
Target: DNA and RNA
Action: alkylating agent
FDA: The activity of GLIADEL Wafer is due to release of cytotoxic concentrations of carmustine, aDNA and RNA alkylating agent, into the tumor resection cavity. On exposure to the aqueousenvironment of the resection cavity, the anhydride bonds in the copolymer are hydrolyzed,releasing carmustine, carboxyphenoxypropane, and sebacic acid into the surrounding braintissue.
|
| 47 |
|
Halaven
18
49
|
ERIBULIN MESYLATE |
Eisai |
November 2010 |
Disease/s that Drug Treats:metastatic breast cancer
Indications and Usage:
18
HALAVEN is a microtubule inhibitor indicated for the treatment ofpatients with metastatic breast cancer who have previously receivedat least two chemotherapeutic regimens for the treatment ofmetastatic disease. Prior therapy should have included ananthracycline and a taxane in either the adjuvant or metastaticsetting (1)
DrugBank Targets:
-
Mechanism of Action:
18
Target: microtubule dynamics
Action: inhibitor
FDA: Eribulin inhibits the growth phase of microtubules without affecting the shortening phase and sequesterstubulin into nonproductive aggregates. Eribulin exerts its effects via a tubulin-based antimitoticmechanism leading to G 2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic celldeath after prolonged mitotic blockage
|
| 48 |
|
Herceptin
18
49
|
TRASTUZUMAB |
Genentech |
October 1998 |
Disease/s that Drug Treats:Breast cancer/gastric cancer
Indications and Usage:
18
Herceptin is a HER2/neu receptor antagonist indicated for: the treatment of HER2 overexpressing breast cancer (1.1, 1.2). the treatment of HER2-overexpressing metastatic gastric orgastroesophageal junction adenocarcinoma (1.3)
DrugBank Targets:
16
1. Receptor tyrosine-protein kinase erbB-2;2. Epidermal growth factor receptor;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Complement C1s subcomponent;8. High affinity immunoglobulin gamma Fc receptor I;9. Low affinity immunoglobulin gamma Fc region receptor II-a;10. Low affinity immunoglobulin gamma Fc region receptor II-b;11. Low affinity immunoglobulin gamma Fc region receptor II-c;12. Low affinity immunoglobulin gamma Fc region receptor III-B;13. Low affinity immunoglobulin gamma Fc region receptor III-A
Mechanism of Action:
18
Target: human epidermal growth factor receptor 2 protein (HER2)
Action: binds with strong affinity for immune response
FDA: The HER2 (or c-erbB2) proto-oncogene encodes a transmembrane receptor protein of 185 kDa, which is structurally related to the epidermal growth factor receptor. Herceptin has been shown, in both in vitro assays and in animals, to inhibit the proliferation of human tumor cells that overexpress HER2. Herceptin is a mediator of antibody-dependent cellular cytotoxicity (ADCC). In vitro, Herceptin-mediated ADCC has been shown to be preferentially exerted on HER2 overexpressing cancer cells compared with cancer cells that do not overexpress HER2.
|
| 49 |
|
Hycamtin
18
49
|
TOPOTECAN HYDROCHLORIDE |
GlaxoSmithKline/ SmithKline Beecham |
October 2007/May 1996 |
Disease/s that Drug Treats:small cell lung cancer/ ovarian cancer
Indications and Usage:
18
HYCAMTIN for injection is a topoisomerase inhibitor indicated for: metastatic carcinoma of the ovary after disease progression on or afterinitial or subsequent chemotherapy. (1.1) small cell lung cancer platinum-sensitive disease in patients whoprogressed after first-line chemotherapy. (1.2) combination therapy with cisplatin for Stage IV-B, recurrent, orpersistent carcinoma of the cervix which is not amenable to curativetreatment. (1.3)
DrugBank Targets:
16
1. DNA topoisomerase 1;2. DNA topoisomerase I, mitochondrial;3. DNA
Mechanism of Action:
18
Target: topoisomerase I
Action: inhibitor
FDA: Topoisomerase I relieves torsional strain in DNA by inducing reversible single-strand breaks.Topotecan binds to the topoisomerase I-DNA complex and prevents re-ligation of these singlestrandbreaks. The cytotoxicity of topotecan is thought to be due to double-strand DNA damageproduced during DNA synthesis, when replication enzymes interact with the ternary complexformed by topotecan, topoisomerase I, and DNA. Mammalian cells cannot efficiently repairthese double-strand breaks.
|
| 50 |
|
Ibrance
18
49
|
PALBOCICLIB |
Pfizer |
February 2015 |
Disease/s that Drug Treats:ER-positive, HER2-negative breast cancer
Indications and Usage:
18
IBRANCE is a kinase inhibitor indicated in combination with letrozole for thetreatment of postmenopausal women with estrogen receptor (ER)-positive,human epidermal growth factor receptor 2 (HER2)-negative advanced breastcancer as initial endocrine-based therapy for their metastatic disease. Thisindication is approved under accelerated approval based on progression-freesurvival (PFS). Continued approval for this indication may be contingentupon verification and description of clinical benefit in a confirmatory trial. (1)
DrugBank Targets:
16
1. Cyclin-dependent kinase 4;2. Cyclin-dependent kinase 6
Mechanism of Action:
18
Target: cyclin-dependent kinase (CDK) 4 and 6
Action: inhibitor
FDA: Palbociclib is an inhibitor of cyclin-dependent kinase (CDK) 4 and 6. Cyclin D1 and CDK4/6 aredownstream of signaling pathways which lead to cellular proliferation. In vitro, palbociclib reducedcellular proliferation of estrogen receptor (ER)-positive breast cancer cell lines by blocking progressionof the cell from G1 into S phase of the cell cycle. Treatment of breast cancer cell lines with thecombination of palbociclib and antiestrogens leads to decreased retinoblastoma protein (Rb)phosphorylation resulting in reduced E2F expression and signaling and increased growth arrestcompared to treatment with each drug alone. In vitro treatment of ER-positive breast cancer cell lineswith the combination of palbociclib and antiestrogens leads to increased cell senescence, which wassustained for up to 6 days following drug removal. In vivo studies using a patient-derived ER-positivebreast cancer xenograft model demonstrated that the combination of palbociclib and letrozole increasedthe inhibition of Rb phosphorylation, downstream signaling and tumor growth compared to each drugalone.
|
Drugs for Endometrial Stromal Sarcoma (from DrugBank, HMDB, Dgidb, PharmGKB, IUPHAR, NovoSeek, BitterDB):
(show top 50)
(show all 77)
| # |
|
Name |
Status |
Phase |
Clinical Trials |
Cas Number |
PubChem Id |
| 1 |
|
Lenograstim |
Approved, Investigational |
Phase 3 |
|
135968-09-1 |
|
|
Synonyms:
G-CSF (CHO cell derived)
Glycosylated recombinant G-CSF
Glycosylated recombinant granulocyte colony stimulating factor
Granulocyte colony stimulating factor 3 (CHO cell derived)
|
Granulocyte colony-stimulating factor lenograstim
Lenograstim (genetical recombination)
Lenograstim rDNA
|
|
| 2 |
|
Ifosfamide |
Approved |
Phase 3 |
|
3778-73-2 |
3690
|
|
Synonyms:
(+-)-Ifosfamid
(+-)-Ifosphamide
(+-)-Tetrahydro-N,3-bis(2-chloroethyl)-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide
(D,L)-Ifosfamide
(R,S)-Ifosphamide
(R,S)-N,3-Bis(2-chloroethyl)tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide
{3-(2-Chloroethyl)-2-[(2-chloroethyl)amino]perhydro-2H-1,
1,3,2-Oxazaphosphorine, 3-(2-chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-, 2-oxide
1,3,2-Oxazaphosphorine, 3-(2-chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-, 2-oxide
2,3-(N,N(sup 1)-Bis(2-chloroethyl)diamido)-1,3,2-oxazaphosphoridinoxyd
2,3-N,N(sup 1)-Bis(2-chloroethyl)diamido-1,3,2-oxazaphosphoridinoxyd
2H-1,3,2-Oxazaphosphorin-2-amine, N,3-bis( 2-chloroethyl)tetrahydro-, 2-oxide
2H-1,3,2-Oxazaphosphorin-2-amine, N,3-bis(2-chloroethyl)tetrahydro-, 2-oxide
2H-1,3,2-Oxazaphosphorine, 3-(2-chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-, 2-oxide
2H-1,3,2-Oxazaphosphorine, 3-(2-chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-, 2-oxide (8CI)
2H-1,3,2-Oxazaphosphorine, 3-(2-chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-, 2-oxide
3-(2-Chloroethyl)-2-((2-chloroethyl)amino)perhydro-2H-1,3,2-oxazaphosphorine oxide
3-(2-Chloroethyl)-2-((2-chloroethyl)amino)tetrahydro-2H-1,3,2-oxazaphosphorine 2-oxide
3-(2-Chloroethyl)-2-[(2-chloroethyl)amino]perhydro-2H-1,3,2-oxazaphosphorine oxide
3-(2-Chloroethyl)-2-[(2-chloroethyl)amino]perhydro-2H-1,3,2-oxazaphosphorineoxide
3-(2-Chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-2H-1,3,2-oxazaphosphorine 2- oxide
3-(2-Chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-2H-1,3,2-oxazaphosphorine 2-oxide
3,} 2-oxazaphosphorine oxide
36341-88-5
3778-73-2
84711-20-6
A 4942
AB00513932
AC1L1GHW
AC-2113
Ambap3778-73-2
Asta Z 4942
ASTA Z 4942
BPBio1_000865
BRN 0611835
BSPBio_000785
C07047
CAS-3778-73-2
CCRIS 352
CHEBI:5864
CHEMBL1024
CID3690
Cyfos
D00343
D007069
DB01181
EINECS 223-237-3
HMS1570H07
HMS2090M12
HMS2093N07
Holoxan
Holoxan 1000
HSDB 7023
I06-0494
Ifex
IFEX (TN)
Ifosfamid
Ifosfamida
Ifosfamida [INN-Spanish]
ifosfamide
Ifosfamide (JAN/USP/INN)
Ifosfamide [USAN:INN:BAN:JAN]
Ifosfamide sterile
|
Ifosfamide Sterile
Ifosfamidum
Ifosfamidum [INN-Latin]
Ifosphamide
Ifsofamide
Iphosphamid
Iphosphamid(e)
Iphosphamide
I-phosphamide
I-Phosphamide
iso Endoxan
Iso Endoxan
iso-Endoxan
Isoendoxan
Iso-Endoxan
Isofosfamide
Isophosphamide
isosfamide
Isosfamide
LS-102
LS-99799
Mitoxana
Mitoxana, Ifex, Ifosfamide
MJF 9325
MJF-9325
MLS002154021
MolPort-003-666-704
N-(2-Chloraethyl)-N'-(2-chloraethyl)-N',O-propylen-phosphorsaureester-diamid
N-(2-Chloraethyl)-N'-(2-chloraethyl)-N',O-propylen-phosphorsaureester-diamid [German]
N-(2-Chloroethyl)-N'-(2-chloroethyl)-N',O-propylen ephosphoric acid diamide
N-(2-Chloroethyl)-N'-(2-chloroethyl)-N',O-propylene phosphoric acid ester diamide
N-(2-Chloroethyl)-N'-(2-chloroethyl)-N',O-propylenephosphoric acid diamide
N-(2-Chloroethyl)-N'-(2-chloroethyl)-N',O-propylenephosphoric acid ester diamide
N-(2-Chloroethyl)-N-(3-(2-chloroethyl)-2-oxido-1,3,2-oxazaphosphinan-2-yl)amine
N,3-Bis(2-chloroethyl)-1,3,2-oxazaphosphinan-2-amine 2-oxide
N,3-Bis(2-chloroethyl)tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide
N,N-Bis(beta-chloroethyl)-amino-N',O-propylene-phosphoric acid ester diamide
Naxamide
NCGC00016639-01
NCGC00179435-01
NCI60_000233
NCI-C01638
NPFAPI-04
NSC 109,724
NSC 109724
NSC109,724
NSC-109,724
NSC109724
NSC-109724
Prestwick0_000833
Prestwick1_000833
Prestwick2_000833
Prestwick3_000833
S1302_Selleck
SMR001233348
SPBio_002706
STL058690
UNII-UM20QQM95Y
WLN: T6NPOTJ AM2G BO B2G
Z 4942
Z4942
Z-4942
|
|
| 3 |
|
Doxorubicin |
Approved, Investigational |
Phase 3,Phase 2 |
|
23214-92-8 |
31703
|
|
Synonyms:
(1S,3S)-3-Glycoloyl-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1,2,3,4,6,11-hexahydrotetracen-1-yl 3-amino-2,3,6-trideoxy-a-L-lyxo-hexopyranoside
(1S,3S)-3-Glycoloyl-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1,2,3,4,6,11-hexahydrotetracen-1-yl 3-amino-2,3,6-trideoxy-alpha-L-lyxo-hexopyranoside
(1S,3S)-3-Glycoloyl-3,5,12-trihydroxy-10-methoxy-6,11-dioxo-1,2,3,4,6,11-hexahydrotetracen-1-yl 3-amino-2,3,6-trideoxy-α-L-lyxo-hexopyranoside
(8S-cis)-10-((3-amino-2,3,6-Trideoxy-a-L-lyxo-hexopyranosyl)oxy)-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-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
(8S-cis)-10-((3-amino-2,3,6-Trideoxy-α-L-lyxo-hexopyranosyl)oxy)-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-5,12-naphthacenedione
111266-55-8
14-hydroxydaunomycin
14-Hydroxydaunomycin
14-hydroxydaunorubicine
14-Hydroxydaunorubicine
23214-92-8
23257-17-2
24385-08-8
25311-50-6
25316-40-9
25316-40-9 (hydrochloride)
29042-30-6
AC1L1M5T
AC1Q29OJ
adiblastine (hydrochloride salt)
ADM
ADR
adr iablatina (hydrochloride salt)
Adriablastin
Adriablastine
adriablastine (hydrochloride salt)
adriablatina (hydrochloride salt)
Adriacin (hydrochloride salt)
Adriamycin
Adriamycin PFS
Adriamycin PFS (hydrochloride salt)
Adriamycin RDF
Adriamycin RDF (hydrochloride salt)
Adriamycin semiquinone
Adriamycin Semiquinone
Adriblas tina
Adriblastin
Adriblastina
Adriblastina (hydrochloride salt)
Adriblastina (TN)
Adriblastine
adriblatina (hydrochloride salt)
Adrimedac
Aerosolized Doxorubicin
Baxter brand OF doxorubicin hydrochloride
Bedford brand OF doxorubicin hydrochloride
BPBio1_000502
BRD-K92093830-003-04-3
Bristol-myers squibb brand OF doxorubicin hydrochloride
BSPBio_000456
BSPBio_001031
C01661
C27H29NO11
Caelyx
CCRIS 739
Cell pharm brand OF doxorubicin hydrochloride
CHEBI:28748
CHEMBL179
CID31703
Columbia brand OF doxorubicin hydrochloride
Conjugate of doxorubicin with humanized monoclonal antibody LL1 against CD74
Conjugate of doxorubicin with monoclonal antibody P4/D10 against GP120
D03899
DB00997
DM2
Doxil
Doxo
doxo Cell
doxo-Cell
Doxolem
doxorubicin
Doxorubicin
Doxorubicin (USAN/INN)
Doxorubicin [USAN:INN:BAN]
Doxorubicin citrate
Doxorubicin HCl
|
Doxorubicin hexal
Doxorubicin hydrochloride
Doxorubicin Hydrochloride
Doxorubicin hydrochloride (hydrochloride salt)
Doxorubicin NC
Doxorubicina
Doxorubicina [INN-Spanish]
Doxorubicina ferrer farm
Doxorubicina funk
Doxorubicina tedec
Doxorubicine
Doxorubicine [INN-French]
Doxorubicine baxter
Doxorubicin-hLL1
Doxorubicin-hLL1 conjugate
Doxorubicin-P4/D10
Doxorubicin-P4/D10 conjugate
Doxorubicinum
Doxorubicinum [INN-Latin]
Doxotec
DOX-SL
EINECS 245-495-6
Elan brand OF doxorubicin hydrochloride
Farmablastina (hydrochloride salt)
Farmiblastina
Ferrer brand OF doxorubicin hydrochloride
FI 106
Hexal brand OF doxorubicin hydrochloride
HMS2089H06
HSDB 3070
Hydrochloride, doxorubicin
Hydroxydaunomycin hydrochlor ide (hydrochloride salt)
Hydroxydaunomycin hydrochloride (hydrochloride salt)
Hydroxydaunorubicin
Hydroxydaunorubicin hydrochloride (hydrochloride salt)
JT9100000
Kenfarma brand OF doxorubicin hydrochloride
Lemery brand OF doxorubicin hydrochloride
LMPK13050001
LS-1029
LS-165655
Medac brand OF doxorubicin hydrochloride
MLS000759533
Myocet
NChemBio.2007.10-comp13
nchembio809-comp5
NCI-C01514
NDC 38242-874
Neocorp brand OF doxorubicin hydrochloride
NIOSH/JT9100000
NSC 123127
Onkodox
Onkoworks brand OF doxorubicin hydrochloride
Pfizer brand OF doxorubicin hydrochloride
Prasfarma brand OF doxorubicin hydrochloride
Prestwick0_000438
Prestwick1_000438
Prestwick2_000438
Prestwick3_000438
Probes1_000151
Probes2_000129
RDF Rubex
Resmycin
Ribodoxo
Ribosepharm brand OF doxorubicin hydrochloride
Rubex
Rubex (hydrochloride salt)
SMP1_000106
SPBio_002395
Tedec meiji brand OF doxorubicin hydrochloride
ThermoDox
TLC D-99
Triferric doxorubicin
UNII-80168379AG
Urokit doxo cell
Urokit doxo-cell
|
|
| 4 |
|
Mechlorethamine |
Approved, Investigational |
Phase 3 |
|
51-75-2 |
4033
|
|
Synonyms:
.Beta.,.beta.'-Dichlorodiethyl-N-methylamine
1, 5-Dichloro-3-methyl-3-azapentane hydrochloride
126-85-2 (N-oxide)
2,2'-Dichlorodiethyl-methylamine
2,2'-Dichloro-N-me
2,2'-dichloro-N-methyldiethylamine
2,2'-dichloro-N-Methyldiethylamine
2,2'-Dichloro-N-methyldiethylamine
2-Chloro-N-(2-chloroethyl)-N-methylethanamine
302-70-5 (N-oxide, hydrochloride)
51-75-2
55-86-7 (HYDROCHLORIDE)
AC1L1H9H
Antimit
b,Beta'-dichlorodiethyl-N-methylamine
beta,beta'-Dichlorodiethyl-N-methylamine
beta,Beta'-dichlorodiethyl-N-methylamine
Bis(2-chloroethyl)methylamine
Bis(b-chloroethyl)methylamine
Bis(beta-chloroethyl) methylamine
Bis(beta-chloroethyl)methylamine
Bis(β-chloroethyl)methylamine
BRN 0605323
BSPBio_001947
C07115
C5H11Cl2N
Carolysine
Caryolysin
Caryolysine
CCRIS 447
CHEBI:28925
CHEMBL427
Chloramine (the nitrogen mustard)
Chlorethazine
Chlormethine
Chlormethine (INN)
Chlormethine [INN:BAN]
Chlormethinum [INN-Latin]
CID4033
Cloramin
Clormetina
Clormetina [INN-Spanish]
D07671
DB00888
Di(2-chloroethyl)methylamine
Dichlor amine
Dichloren
DivK1c_000759
EINECS 200-120-5
Embechine
Embichin
ENT-25294
HMS1920J15
HMS2091B04
HMS502F21
HN2
HN-2
HSDB 5083
Hydrochloride N-oxide, mechlorethamine
Hydrochloride, mechlorethamine
I14-8708
IBS-L0033631
IDI1_000759
KBio1_000759
KBio2_001369
KBio2_003937
KBio2_006505
KBio3_001447
KBioGR_001448
KBioSS_001369
LS-7559
MBA
Me chloroethamine
Mebichloramine
mechlorethamine
|
Mechlorethamine
Mechlorethamine hydrochloride
Mechlorethamine hydrochloride N oxide
Mechlorethamine hydrochloride N-oxide
Mechlorethamine N oxide
Mechlorethamine N-oxide
Mechlorethamine oxide
Mechlorethanamine
Mechloroethamine
Mecloretamina
Mecloretamina [Italian]
Merck brand OF mechlorethamine hydrochloride
Merck frosst brand OF mechlorethamine hydrochloride
Methylbis(2-chloroethyl)amine
Methylbis(b-chloroethyl)amine
Methylbis(beta-chloroethyl)amine
Methylbis(β-chloroethyl)amine
Methylchlorethamine
Methyldi(2-chloroethyl)amine
Mitomen
Mitoxine (*Hydrochloride*)
MolPort-001-785-592
Mustargen
Mustine
Mustine note
Mutagen
N,N-Bis(2-chloroethyl)methylamine
N,N-Bis(2-chloroethyl)-N-methylamine
N,N-Di(chloroethyl)methylamine
NCGC00091835-02
NCGC00091835-03
NCGC00091835-04
NCGC00091835-05
NCI60_041682
NINDS_000759
Nitol (*Hydrochloride*)
Nitrogen mustard
Nitrogen mustard (HN-2)
Nitrogen mustard N oxide
Nitrogen mustard N-oxide
Nitrogranulogen
Nitromin
N-Lost
N-Methyl lost
N-Methyl-2,2'-dichlorodiethylamine
N-methyl-bis(2-chloroethyl)amine
N-Methyl-bis(2-chloroethyl)amine
N-Methyl-bis(b-chloroethyl)amine
N-Methyl-bis(beta-chloroethyl)amine
N-Methyl-bis(β-chloroethyl)amine
N-Methyl-bis-chloraethylamin
N-Methyl-bis-chloraethylamin [German]
N-Methyl-lost
N-Methyl-lost [German]
N-Oxide, mechlorethamine hydrochloride
N-Oxide, nitrogen mustard
NSC 762
NSC762
NSC-762
SPBio_000496
Spectrum_000889
SPECTRUM1500375
Spectrum2_000448
Spectrum3_000484
Spectrum4_000924
Spectrum5_001702
Stickstofflost (*Hydrochloride*)
Stickstofflost (ebewe)
T 1024
T-1024
thyldiethylamine
TL 146
UNII-50D9XSG0VR
β,beta'-dichlorodiethyl-N-methylamine
β,β'-dichlorodiethyl-N-methylamine
|
|
| 5 |
|
Histamine |
Approved, Investigational |
Phase 3 |
|
51-45-6, 75614-87-8 |
774
|
|
Synonyms:
.beta.-Imidazolyl-4-ethylamine
[3H]histamine
1avn
1H-Imidazole-4-ethanamine
1H-Imidazole-5-ethanamine
1qft
2-(1H-imidazol-4-yl)ethan-1-amine
2-(1H-Imidazol-4-yl)ethanamine
2-(1H-Imidazol-4-yl)ethylamine
2-(1H-imidazol-5-yl)ethanamine
2-(1H-Imidazol-5-yl)ethanamine
2-(1H-Imidazol-5-yl)ethylamine
2-(3H-Imidazol-4-yl)-ethylamine
2-(4-Imidazolyl)ethanamine
2-(4-imidazolyl)ethylamine
2-(4-Imidazolyl)ethylamine
2-[4-Imidazolyl]ethylamine
2-Imidazol-4-ylethylamine
2-Imidazol-4-yl-ethylamine
4-(2-Aminoethyl)-1H-imidazole
4-(2-Aminoethyl)imidazole
4-imidazoleethylamine
4-Imidazoleethylamine
51-45-6
53290_FLUKA
5-imidazoleethylamine
5-Imidazoleethylamine
64422-25-9
924364-91-0
AC-13185
AC1L19ZT
AC1Q54BV
AC1Q54BW
AKOS000274386
ALBB-005968
BCBcMAP01_000250
beta-aminoethylglyoxaline
beta-Aminoethylglyoxaline
beta-aminoethylimidazole
beta-Aminoethylimidazole
beta-aminothethylglyoxaline
beta-Aminothethylglyoxaline
beta-Imidazolyl-4-ethylamine
b-Imidazolyl-4-ethylamine
Bio1_000487
Bio1_000976
Bio1_001465
Bio2_000389
Bio2_000869
bmse000744
BSPBio_001117
BSPBio_002124
C00388
CCRIS 6535
Ceplene
CHEBI:18295
CHEMBL90
CID774
D08040
Dihydrochloride, histamine
DivK1c_000308
EINECS 200-100-6
Eramin
Ergamine
Ergotidine
F411C768-A159-4FC0-A195-291A08BB03AA
Free histamine
H7125_SIGMA
histamine
Histamine (DCF)
|
Histamine [USAN]
Histamine Base
Histamine dihydrochloride
Histamine hydrochloride
Histamine, Free Base
Histaminum
Histaminum (TN)
HMS1362G19
HMS1792G19
HMS1990G19
HSDB 3338
HSM
Hydrochloride, histamine
IDI1_000308
IDI1_002144
Imidazole-4-ethylamine
Istamina
Istamina [Italian]
KBio1_000308
KBio2_000457
KBio2_001325
KBio2_003025
KBio2_003893
KBio2_005593
KBio2_006461
KBio3_000853
KBio3_000854
KBio3_001344
KBioGR_000457
KBioGR_001580
KBioSS_000457
KBioSS_001325
L000292
L-Histamin base
L-histamine
L-Histamine
Lopac0_000595
Lopac-H-7250
LS-75835
MLS000069447
MolPort-001-785-597
MolPort-002-042-264
NCGC00015513-01
NCGC00015513-08
NCGC00093371-02
NCGC00093371-03
NCGC00093371-04
NCGC00093371-05
nchembio.87-comp54
nchembio714-comp1
NINDS_000308
NSC 33792
NSC33792
Peremin
SDCCGMLS-0066601.P001
SMP1_000151
SMR000059091
SPBio_000729
Spectrum_000845
Spectrum2_000665
Spectrum3_000452
Spectrum4_000960
Spectrum5_000796
ST073926
STK346752
STOCK5S-55669
Theramine
UNII-820484N8I3
WLN: T5M CNJ D2Z
ZERO/004089
|
|
| 6 |
|
Cyproheptadine |
Approved |
Phase 3 |
|
129-03-3 |
2913
|
|
Synonyms:
129-03-3
1-methyl-4-(5-dibenzo(a,e)cycloheptatrienylidene)piperidine
1-Methyl-4-(5-dibenzo(a,e)cycloheptatrienylidene)piperidine
1-Methyl-4-(5H-dibenzo(a,d)cycloheptenylidene)piperidine
1-Methyl-4-(5H-dibenzo(a,D)cycloheptenylidene)piperidine
4-(5-dibenzo(a,D)Cyclohepten-5-ylidine)-1-methylpiperidine
4-(5-Dibenzo(a,d)cyclohepten-5-ylidine)-1-methylpiperidine
4-(5-Dibenzo(a,D)cyclohepten-5-ylidine)-1-methylpiperidine
4-(5H-Dibenzo(a,d)cyclohepten-5-ylidene)-1-methylpiperidene
4-(5H-dibenzo(a,D)Cyclohepten-5-ylidene)-1-methylpiperidine
4-(5H-Dibenzo(a,d)cyclohepten-5-ylidene)-1-methylpiperidine
4-(5H-Dibenzo(a,D)cyclohepten-5-ylidene)-1-methylpiperidine
4-(5H-dibenzo[a,d][7]annulen-5-ylidene)-1-methylpiperidine
4-(5H-Dibenzo[a,d]cyclohepten-5-ylidene)-1-methylpiperidine
41354-29-4
4-dibenzo[a,D]Cyclohepten-5-ylidene-1-methyl-piperidine
4-Dibenzo[a,D]cyclohepten-5-ylidene-1-methyl-piperidine
5-(1-methylpiperidylidene-4)-5H-dibenzo(a,d)cyclopheptene
5-(1-Methylpiperidylidene-4)-5H-dibenzo(a,d)cyclopheptene
5-(1-Methylpiperidylidene-4)-5H-dibenzo(a,D)cyclopheptene
5-20-08-00500 (Beilstein Handbook Reference)
AC1L1ER8
AKOS004119847
Antergan
Axoprol
BIDD:GT0324
Biomol-NT_000131
BPBio1_000096
BPBio1_000155
BRD-K28143534-001-01-4
BRD-K28143534-003-03-6
BRN 1685976
BSPBio_000086
C06935
CAS-969-33-5
CCRIS 5232
CHEBI:4046
CHEMBL516
CID2913
Ciproheptadina
Ciproheptadina [INN-Spanish]
Ciprovit
Ciprovit (TN)
Cypoheptadine
Cyproheptadiene
Cyproheptadin
Cyproheptadine
|
CYPROHEPTADINE
Cyproheptadine (INN)
Cyproheptadine [INN:BAN]
Cyproheptadine Hcl
Cyproheptadinum
Cyproheptadinum [INN-Latin]
D07765
DB00434
Dibenzosuberonone/Cyproheptadine
Dihexazin
Dronactin
EINECS 204-928-9
Eiproheptadine
Glutodina
HMS2090P20
HSDB 3048
L001016
Lopac0_000246
Lopac-C-6022
LS-114933
MK 141
MolPort-002-507-777
NCGC00015252-01
NCGC00015252-02
NCGC00015252-03
NCGC00015252-09
NCGC00024293-02
NCGC00024293-04
NCGC00024293-05
nchembio.559-comp10
Oprea1_498140
PDSP1_001229
PDSP2_001213
Periactin
Periactine
Periactinol
Peritol
Prestwick0_000103
Prestwick1_000103
Prestwick2_000103
Prestwick3_000103
SPBio_002025
STK802098
Tocris-0996
UNII-2YHB6175DO
Viternum
|
|
| 7 |
|
Doxil |
Approved June 1999 |
Phase 3,Phase 2 |
|
|
31703
|
|
Synonyms:
|
|
LipoDox
liposomal doxorubicin
Pegylated Liposomal Doxorubicin Hydrochloride
|
|
| 8 |
|
Antineoplastic Agents, Alkylating |
|
Phase 3,Phase 2 |
|
|
|
| 9 |
|
Alkylating Agents |
|
Phase 3,Phase 2 |
|
|
|
| 10 |
|
Isophosphamide mustard |
|
Phase 3 |
|
|
0
|
|
Synonyms:
Ifosfamide mustard
Ifosforamide mustard
IPAM
Iphosphoramide mustard
Isophosphamide mustard
Isophosphoramide mustard
|
N,N'-di-(2-chloroethyl)phosphorodiamidic acid
NN'-Bis-(2-chloroethyl)phosphate
NN'-Bis-(2-chloroethyl)phosphoric acid
Palifosfamide-tris
zio-201Isophosphamide mustard
|
|
| 11 |
|
Anti-Bacterial Agents |
|
Phase 3,Phase 2 |
|
|
|
| 12 |
|
Topoisomerase Inhibitors |
|
Phase 3,Phase 2 |
|
|
|
| 13 |
|
Antibiotics, Antitubercular |
|
Phase 3,Phase 2 |
|
|
|
| 14 |
|
Gastrointestinal Agents |
|
Phase 3,Phase 2 |
|
|
|
| 15 |
|
Serotonin Agents |
|
Phase 3 |
|
|
|
| 16 |
|
Anti-Allergic Agents |
|
Phase 3 |
|
|
|
| 17 |
|
Serotonin Antagonists |
|
Phase 3 |
|
|
|
| 18 |
|
Histamine H1 Antagonists |
|
Phase 3 |
|
|
|
| 19 |
|
Histamine Phosphate |
|
Phase 3 |
|
51-74-1 |
65513
|
|
Synonyms:
1H-Imidazole-4-ethanamine, phosphate (1:2)
2-Imidazol-4-ylethylamine orthophosphoric acid (1:2)
4-(2-Aminoethyl)imidazole bis(dihydrogen phosphate)
4-(2-Aminoethyl)imidazole di-acid phosphate
4-2(2-Aminoethyl)Imidazole-Di-Acid Phosphate
51-74-1
53623-99-7
74-56-6
AC1L23E4
CID65513
D04445
DB00667
EINECS 200-118-4
|
H0147
Histamine acid phosphate
Histamine biphosphate
Histamine dihydrogen phosphate
Histamine diphosphate
Histamine phosphate (1:2)
Histamine phosphate (TN)
Histamine phosphate (USP)
Histamine phosphate [USP]
Histamine positive
LS-78569
UNII-QWB37T4WZZ
|
|
| 20 |
|
Antipruritics |
|
Phase 3 |
|
|
|
| 21 |
|
Neurotransmitter Agents |
|
Phase 3 |
|
|
|
| 22 |
|
Dermatologic Agents |
|
Phase 3 |
|
|
|
| 23 |
|
Histamine Antagonists |
|
Phase 3 |
|
|
|
| 24 |
|
Serotonin |
Investigational, Nutraceutical |
Phase 3 |
|
50-67-9 |
5202
|
|
Synonyms:
3-(2-Aminoethyl)-1H-indol-5-ol
3-(2-Aminoethyl)indol-5-ol
3-(b-Aminoethyl)-5-hydroxyindole
5 Hydroxytryptamine
5-HT
5-HTA
5-Hydroxy-3-(b-aminoethyl)indole
5-Hydroxyltryptamine
5-Hydroxytriptamine
5-Hydroxytryptamine
5-Hydroxy-tryptamine
Antemovis
|
DS Substance
Enteramin
Enteramine
Hippophaine
Hydroxytryptamine
Serotonine
sérotonine
thrombocytin
Thrombocytin
thrombotonin
Thrombotonin
|
|
| 25 |
|
Dacarbazine |
Approved, Investigational |
Phase 2 |
|
4342-03-4 |
5351166
|
|
Synonyms:
(5E)-5-(dimethylaminohydrazinylidene)imidazole-4-carboxamide
(5Z)-5-(dimethylaminohydrazinylidene)imidazole-4-carboxamide
(Dimethyltriazeno)imidazolecarboxamide
37626-23-6
4-(3,3-dimethyl-1-triazeno)imidazole-5-carboxamide
4-(3,3-Dimethyl-1-triazeno)imidazole-5-carboxamide
4-(3,3-Dimethyltriazeno)imidazole-5-carboxamide
4(5)-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide
4-(5)-(3,3-dimethyl-1-triazeno)imidazole-5(4)-carboxamide
4(5)-(3,3-Dimethyl-1-triazeno)imidazole-5(4)-carboxamide
4-(5)-(3,3-Dimethyl-1-triazeno)imidazole-5(4)-carboxamide
4-(Dimethyltriazeno)imidazole-5-c arboxamide
4-(dimethyltriazeno)imidazole-5-carboxamide
4-(dimethyltriazeno)Imidazole-5-carboxamide
4-(Dimethyltriazeno)imidazole-5-carboxamide
4-(or 5)-(3,3-Dimethyl-1-triazeno)imidazole-5(or 4)-carboxamide
4-(or 5)-(3,3-Dimethyl-1-triazeno)imidazole-5(or 4)-carboxamide
4-[(1E)-3,3-Dimethyltriaz-1-en-1-yl]-1H-imidazole-5-carboxamide
4-[3,3-dimethyltriaz-1-en-1-yl]-1H-imidazole-5-carboxamide
4342-03-4
5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide
5-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide
5-(3,3-Dimethyl-1-triazenyl)-1H-imidazole-4-carboxamide
5-(3,3-Dimethyl-1-triazenyl)imidazole-4-carboxamide
5-(3,3-Dimethyltri azeno)imidazole-4-carboxamide
5-(3,3-dimethyltriaz-1-en-1-yl)-1H-imidazole-4-carboxamide
5-(3,3-Dimethyltriazeno)-imidazole-4-carbamide
5-(3,3-dimethyltriazeno)imidazole-4-carboxamide
5-(3,3-dimethyltriazeno)Imidazole-4-carboxamide
5-(3,3-Dimethyltriazeno)imidazole-4-carboxamide
5-(dimethylaminohydrazinylidene)imidazole-4-carboxamide
5-(Dimethyltriazeno)-4-imidazolecarboxamide
5-(dimethyltriazeno)imidazole-4-carboxamide
5-(dimethyltriazeno)Imidazole-4-carboxamide
5-(Dimethyltriazeno)imidazole-4-carboxamide
5-(Dimethyltriazeno)imidazole-4-carboximide
5(or 4)-(dimethyltriazeno)imidazol e-4(or 5)-carboxamide
5(or 4)-(dimethyltriazeno)imidazole-4(or 5)-carboxamide
5-[3,3-Dimethyl-1-triazenyl]imidazole-4-carboxamide
94361-71-4
AC1NQXVV
AC1NS01W
AC1NS4BN
AI3-52825
Biocarbazin
Biocarbazine
Biocarbazine R
BPBio1_000428
BRD-K35520305-001-07-8
BSPBio_000388
BSPBio_002091
C6H10N6O
Carboxamide, Dimethyl Imidazole
CAS-891986
CCRIS 190
CHEBI:4305
CHEMBL476
CID5281007
CID5351166
CID5353562
D00288
D003606
D2390_SIGMA
D3634
Dacarbazin
Dacarbazina
dacarbazine
Dacarbazine
Dacarbazine (JAN/USP/INN)
Dacarbazine [USAN:INN:BAN:JAN]
Dacarbazino
Dacarbazino [INN-Spanish]
Dacarbazinum
Dacarbazinum [INN-Latin]
Dacatic
DB00851
Decarbazine
Deticene
|
DIC
Dimethyl Imidazole Carboxamide
Dimethyl Triazeno Imidazole Carboxamide
Dimethyltriazenoimidazolecarboxamide
Di-methyl-triazenoimidazolecarboxamide
Di-me-triazenoimidazolecarboxamide
DivK1c_000326
DTCI
DTIC
DTIC Dome
DTIC, DTIC-Dome, Dacarbazine
Dtic-dome
Dtic-Dome
DTICDome
DTIC-Dome
Dtic-Dome (TN)
DTIE
EINECS 224-396-1
HE1150000
HMS1569D10
HMS2090A20
HMS2091I20
HMS501A08
HSDB 3219
I06-2280
I14-1659
ICDMT
ICDT
IDI1_000326
Imidazole carboxamide
Imidazole Carboxamide
Imidazole Carboxamide, Dimethyl
KBio1_000326
KBio2_001364
KBio2_003932
KBio2_006500
KBio3_001311
KBioGR_000896
KBioSS_001364
LS-119
MLS001332543
MLS001332544
MolPort-003-666-153
MolPort-003-846-120
MolPort-006-709-420
NCGC00016986-01
NCGC00091861-01
NCGC00091861-02
NCGC00091861-03
NCGC00091861-04
NCI60_004053
NCI-C04717
NCIMech_000261
NINDS_000326
NIOSH/HE1150000
NPFAPI-05
NSC 45388
NSC45388
NSC-45388
Prestwick_904
Prestwick0_000574
Prestwick1_000574
Prestwick2_000574
Prestwick3_000574
S1221_Selleck
SMP2_000251
SMR000857131
SPBio_001075
SPBio_002607
Spectrum_000884
SPECTRUM1500218
Spectrum2_001148
Spectrum3_000366
Spectrum4_000308
Spectrum5_000823
ST51014976
UNII-7GR28W0FJI
WLN: T5M CNJ DVZ ENUNN1&1
|
|
| 26 |
|
Temozolomide |
Approved, Investigational |
Phase 2 |
|
85622-93-1 |
5394
|
|
Synonyms:
3,4-dihydro-3-methyl-4-oxoimidazo(5,1-d)-1,2,3,5-tetrazine-8-carboxamide
3,4-dihydro-3-Methyl-4-oxoimidazo(5,1-D)-1,2,3,5-tetrazine-8-carboxamide
3,4-Dihydro-3-methyl-4-oxoimidazo(5,1-d)-1,2,3,5-tetrazine-8-carboxamide
3,4-dihydro-3-methyl-4-oxoimidazo(5,1-d)-as-tetrazine-8-carboxamide
3,4-dihydro-3-Methyl-4-oxoimidazo(5,1-D)-as-tetrazine-8-carboxamide
3,4-Dihydro-3-methyl-4-oxoimidazo(5,1-d)-as-tetrazine-8-carboxamide
3-methyl-4-oxo-3,4-dihydroimidazo(5,1-d)(1,2,3,5)tetrazine-8-carboxamide
3-Methyl-4-oxo-3,4-dihydroimidazo(5,1-d)(1,2,3,5)tetrazine-8-carboxamide
3-Methyl-4-oxo-3,4-dihydroimidazo(5,1-D)(1,2,3,5)tetrazine-8-carboxamide
3-Methyl-4-oxo-3,4-dihydroimidazo[5,1-d][1,2,3,5]tetraazine-8-carboxamide
3-methyl-4-oxo-3,4-dihydroimidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide
3-methyl-4-oxoimidazo[5,1-d][1,2,3,5]tetrazine-8-carboxamide
85622-93-1
8-carbamoyl-3-methylimidazo(5,1-d)-1,2,3,5-tetrazin-4(3H)-one
8-Carbamoyl-3-methylimidazo(5,1-d)-1,2,3,5-tetrazin-4(3H)-one
8-Carbamoyl-3-methylimidazo(5,1-D)-1,2,3,5-tetrazin-4(3H)-one
AC1L1K9B
AC-758
BIDD:GT0204
Bio-0147
BRN 5547136
C047246
C6H6N6O2
CCRG 81045
CCRG-81045
CCRIS 8996
CHEBI:153686
CHEMBL810
CID5394
CPD000466338
D06067
DB00853
Essex brand of temozolomide
HMS2051O12
HMS2090B08
I06-0149
I14-1943
LS-80558
M B 39831
m & b 39831
M & B 39831
m And b 39831
|
m And b-39831
M&B 39831
M&B-39831
M-39831
MB 39831
Methazolastone
MLS000759447
MLS001424028
MLS002701861
NCGC00167429-01
NCGC00167429-02
NCI60_003316
NSC 362856
NSC362856
NSC-362856
SAM001246636
Sch 52365
SCH 52365
Sch-52365
Schering brand of temozolomide
Schering-Plough brand of temozolomide
SMR000466338
STK623541
Temodal
Temodal (TN)
Temodar
Temozolamide
Temozolodida
Temozolodida [Spanish]
Temozolomid
Temozolomida
temozolomide
Témozolomide
Temozolomide (JAN/USAN/INN)
Temozolomide [INN:BAN]
Temozolomidum
Temozolomidum [Latin]
TL8005593
TMZ
TMZ-Bioshuttle
UNII-YF1K15M17Y
ZINC01482184
|
|
| 27 |
|
Hydrocortisone acetate |
Approved, Vet_approved |
Phase 2 |
|
50-03-3 |
|
|
Synonyms:
21-O-acetylcortisol
Cortisol 21-acetate
|
Hydrocortisone 21-acetate
|
|
| 28 |
|
Hydrocortisone |
Approved, Vet_approved |
Phase 2 |
|
50-23-7 |
5754
|
|
Synonyms:
(11b)-11,17,21-Trihydroxypregn-4-ene-3,20-dione
(11beta)-11,17,21-Trihydroxypregn-4-ene-3,20-dione
(11β)-11,17,21-trihydroxypregn-4-ene-3,20-dione
[3H]cortisol
11 Epicortisol
11a-Hydroxycorticosterone
11alpha-Hydroxycorticosterone
11b,17,21-Trihydroxyprogesterone
11b,17a,21-Trihydroxy-4-pregnene-3,20-dione
11beta,17,21-Trihydroxyprogesterone
11beta,17alpha,21-Trihydroxy-4-pregnene-3,20-dione
11beta-hydrocortisone
11beta-Hydrocortisone
11-beta-Hydrocortisone
11beta-Hydroxycortisone
11-beta-Hydroxycortisone
11b-Hydrocortisone
11b-Hydroxycortisone
11-Epicortisol
11-Hydrocortisone
11β,17α,21-trihydroxy-4-pregnene-3,20-dione
11β-hydrocortisone
17a-Hydroxycorticosterone
17alpha-Hydroxycorticosterone
17-Hydroxycorticosterone
2v95
4-Pregnen-11b,17a,21-triol-3,20-dione
4-Pregnen-11beta,17alpha,21-triol-3,20-dione
4-pregnen-11β,17α,21-triol-3,20-dione
4-Pregnen-11β,17α,21-triol-3,20-dione
4-Pregnene-11alpha,21-triol 3,20-dione
4-Pregnene-11b,17a,21-triol-3,20-dione
50-23-7
8056-08-4
80562-38-5
8063-42-1
AC-12902
AC1L1L2B
ACETASOL HC
ACETIC ACID W/ HYDROCORTISONE
Acticort
Acticort (TN)
Aeroseb HC
Aeroseb-HC
AI3-25006
AKOS001582651
Alacort
Ala-cort
Ala-Cort
Ala-scalp
Ala-Scalp
Algicirtis
Alphaderm
Amberin
Anflam
Anti-inflammatory hormone
Anucort
Anucort-HC
Anusol HC
Anusol HC (TN)
Anusol-HC
Aquacort
Aquanil HC
B48448A1-24BA-47CA-8D9E-43E5BC949386
Balneol-hc
Balneol-HC
Barseb HC
Basan-corti
Basan-Corti
Beta-hc
Beta-HC
b-HC
Bio-0648
BPBio1_000544
BRD-K93568044-001-03-1
BSPBio_000494
C00735
C21H30O5
CaldeCORT spray
CaldeCORT Spray
CCRIS 5854
Cetacort
CHEBI:17650
CHEMBL389621
Chronocort
CID5754
Clear aid
Cleiton
Cobadex
Colocort
Colocort (TN)
component of Lubricort
component of Neo-Cort-Dome
component of Otalgine
Compound F
Compound F (kendall)
Corhydron
Cor-oticin
COR-OTICIN
Cortanal
Cor-tar-quin
Cort-dome
Cort-Dome
Cortef
Cortef (TN)
Cortenema
Cortesal
Corticreme
Cortifair
Cortifan
Cortifoam
Cortiment
Cortisol
Cortisol alcohol
Cortisol, Hydrocortisone
Cortisolonum
Cortisporin
Cortisporin otico
Cortisporin Otico
Cortispray
Cortizol
Cortolotion
Cortonema
Cortoxide
Cort-quin
Cortril
CORTRIL
CPD000653523
Cremesone
Cremicort-H
Cutisol
Cyclodextrin-encapsulated hydrocortisone
D00088
DB00741
DB07886
Delacort
Dermacort
Derm-aid
Derm-Aid
Dermaspray
Dermil
Dermocortal
Dermolate
Dihydrocostisone
Dioderm
Dome-cort
Domolene-HC
Drotic
DuoCort
Ef corlin
Efcorbin
Efcortelan
Efcortelin
EINECS 200-020-1
Eldecort
Eldercort
Epicort
Epicortisol
Epiderm H
Esiderm H
EU-0100594
Evacort
Ficortril
Fiocortril
Flexicort
Foille insetti
Foille Insetti
Genacort
Genacort (lotion)
Glycort
gyno-Cortisone
Gyno-Cortisone
H 4001
H0135_SIGMA
H0396_SIGMA
H0888_SIGMA
H3160_SIGMA
|
H4001_SIGMA
H6909_SIGMA
HC
HC #1
HC #4
HC (HYDROCORTISONE)
H-Cort
Heb cort
Heb Cort
Heb-cort
Heb-Cort
Hi-cor
Hidalone
hidro-Colisona
Hidro-Colisona
Hidrocortisona
Hidrocortisona [INN-Spanish]
HMS1569I16
HMS2090M04
HSDB 3339
Hycort
Hycortol
Hycortole
Hydracort
Hydrasson
hydro-Adreson
Hydro-Adreson
hydro-Colisona
Hydro-Colisona
Hydrocort
Hydrocortal
Hydrocorticosterone
hydrocortisone
Hydrocortisone
Hydrocortisone (JP15/USP/INN)
Hydrocortisone [INN:BAN:JAN]
Hydrocortisone acetate
Hydrocortisone alcohol
HYDROCORTISONE AND ACETIC ACID
Hydrocortisone base
Hydrocortisone butyrate
Hydrocortisone free alcohol
Hydrocortisone in absorbase
HYDROCORTISONE IN ABSORBASE
Hydrocortisone sodium phosphate
Hydrocortisone solution
Hydrocortisone valerate
Hydrocortisone, (11 alpha)-isomer
Hydrocortisone, (9 beta,10 alpha,11 alpha)-isomer
Hydrocortisone-Water Soluble
Hydrocortisonum
Hydrocortisonum [INN-Latin]
Hydrocortistab
Hydrocortisyl
Hydrocortone
HYDROCORTONE
hydro-RX
Hydro-RX
Hydroskin
Hydroxycortisone
Hysone
Hytisone
Hytone
Hytone (TN)
Hytone lotion
Idrocortisone
Idrocortisone [DCIT]
Incortin-H
Incortin-hydrogen
Kendall's compound F
Komed HC
Kyypakkaus
Lacticare HC
Lacticare-HC
Lactisona
LMST02030001
Locoid
Lopac0_000594
LS-7439
Lubricort
Maintasone
Medicort
Meusicort
Micort-HC
Mildison
Milliderm
MLS000069609
MLS001148103
MLS002207135
MLS002222189
MolPort-001-794-637
NCGC00022848-06
NCGC00022848-07
NCGC00022848-09
NCGC00022848-12
NCI60_000118
neo-Cort-dome
neo-Cortef
Neo-Cortef
Neosporin-H ear
Neosporin-H Ear
Nogenic HC
NSC 10483
NSC10483
NSC-10483
Nutracort
Nystaform-HC
Ophthocort
Optef
ORLEX HC
Otalgine
Otic-neo-cort-dome
Otobiotic
Otocort
Otosone-F
Pediotic suspension
Pediotic Suspension
Penecort
Permicort
Plenadren
Polcort H
Preparation H hydrocortisone cream
Preparation H Hydrocortisone Cream
Prepcort
Prestwick_265
Prestwick0_000447
Prestwick1_000447
Prestwick2_000447
Prestwick3_000447
Prevex HC
Proctocort
Proctofoam
Proctozone HC
Protocort
Racet
Rectasol-HC
Rectoid
Reichstein's substance m
Reichstein's substance M
Remederm HC
S1696_Selleck
SAM002264617
Sanatison
Scalp-Cort
Scalpicin capilar
Scalpicin Capilar
Schericur
Scheroson F
Sigmacort
Signef
SMP1_000156
SMR000059022
SMR000653523
SPBio_002433
Stie-cort
Stiefcorcil
Synacort
Systral hydrocort
Systral Hydrocort
Tarcortin
Terra-cortril
Texacort
Texacort lotion 25
Timocort
Topicort
Transderma H
Traumaide
U-cort
Uniderm
UNII-WI4X0X7BPJ
UPCMLD-DP133
UPCMLD-DP133:001
Vioform-hydrocortisone
VoSol HC
Vytone
Zenoxone
β-HC
|
|
| 29 |
|
Dexamethasone acetate |
Approved, Investigational, Vet_approved |
Phase 2 |
|
1177-87-3 |
|
|
Synonyms:
16alpha-Methyl-9alpha-fluoroprednisolone 21-acetate
9alpha-Fluoro-16alpha-methylprednisolone acetate
Dexamethasone 21-acetate
|
Dexamethasone acetate anhydrous
Dexamethasone acetate, anhydrous
Dexamethasoni acetas
|
|
| 30 |
|
Dexamethasone |
Approved, Investigational, Vet_approved |
Phase 2 |
|
50-02-2 |
5743
|
|
Synonyms:
(3H)-Dexamethasone
.delta.(sup 1)-9-.alpha.-Fluoro-16-.alpha.-methylcortisol
.gamma.corten
137098-19-2
16.alpha.-Methyl-9.alpha.-fluoro-1-dehydrocortisol
16.alpha.-Methyl-9.alpha.-fluoroprednisolone
16alpha -Methyl-9alpha -fluoro-1-dehydrocortisol
16alpha -Methyl-9alpha -fluoroprednisolone
16alpha-Methyl-9alpha-fluoro-1-dehydrocortisol
16-alpha-Methyl-9-alpha-fluoro-1-dehydrocortisol
16alpha-Methyl-9alpha-fluoro-delta(sup 1)-hydrocortisone
16-alpha-Methyl-9-alpha-fluoro-delta(sup 1)-hydrocortisone
16-alpha-Methyl-9-alpha-fluoro-delta1-hydrocortisone
16alpha-Methyl-9alpha-fluoroprednisolone
16-alpha-Methyl-9-alpha-fluoroprednisolone
16a-Methyl-9a-fluoro-1-dehydrocortisol
16α-methyl-9α-fluoro-1-dehydrocortisol
16α-Methyl-9α-fluoro-1-dehydrocortisol
1-Dehydro-16.alpha.-methyl-9.alpha.-fluorohydrocortisone
1-dehydro-16alpha -Methyl-9alpha -fluorohydrocortisone
1-dehydro-16alpha-Methyl-9alpha-fluorohydrocortisone
1-Dehydro-16alpha-methyl-9alpha-fluorohydrocortisone
1-dehydro-16a-Methyl-9a-fluorohydrocortisone
1-dehydro-16α-methyl-9α-fluorohydrocortisone
1-Dehydro-16α-methyl-9α-fluorohydrocortisone
23495-06-9
31375_FLUKA
46165_FLUKA
46165_RIEDEL
50-02-2
8054-59-9
9.alpha.-Fluoro-16.alpha.-methylprednisolone
906422-84-2
9a-fluoro-16a-Methylprednisolone
9a-fluoro-16BETA-METHYLPREDNISOLONE
9A-FLUORO-16BETA-METHYLPREDNISOLONE
9alpha -fluoro-16alpha -Methylprednisolone
9alpha-fluoro-16alpha-Methylprednisolone
9alpha-fluoro-16alpha-Methyl-prednisolone
9-alpha-fluoro-16-alpha-Methylprednisolone
9alpha-Fluoro-16alpha-methylprednisolone
9-alpha-Fluoro-16-alpha-methylprednisolone
9-fluoro-11,17,21-Trihydroxy-16-methylpregna-1,4-diene-3,20-dione
9-fluoro-11alpha -Methylpregna-1,4-diene-3,20-dione
9-fluoro-16-Methylprednisolone
9α-fluoro-16α-methylprednisolone
9α-Fluoro-16α-methylprednisolone
AC-11056
AC1L1L1H
AC1Q29DM
Adexone
Aeroseb-D
Aeroseb-dex
Aeroseb-Dex
AI3-50934
Ak dex OPH otic soln 0.1%
Alcon brand OF dexamethasone
Alcon Brand of Dexamethasone
alpha -fluoro-16-alpha -Methylcortisol
Anaflogistico
Aphtasolon
Aphthasolone
apo-Dexamethasone
Auxiron
Azimycin (veterinary)
Azium
Azium (veterinary)
Azium (Veterinary)
BIDD:ER0494
BIDD:PXR0060
Bisu Ds
Bisu DS
BRD-K38775274-001-02-3
BRD-K38775274-001-06-4
BSPBio_000995
C15643
C22H29FO5
Calonat
CCRIS 7067
CHEBI:41879
CHEMBL384467
CID5743
Corson
Corsone
Cortisumman
CPD001227192
CPD-10549
D00292
D003907
D1756_SIGMA
D4902_SIGMA
D6645_SIGMA
D8893_SIGMA
D9184_SIGMA
DB01234
Decacort
Decacortin
Decaderm
Decadron
Decadron (TN)
Decadron Tablets, Elixir
Decadron, Dexamethasone
Decadron-La
Decadron-LA
Decagel
Decaject
Decaject l.a.
Decaject L.A.
Decaject-l.a.
Decaject-L.A.
Decalix
Decameth
Decasone
Decaspray
Dectancyl
Dekacort
delta(sup 1)-9-alpha-Fluoro-16-alpha-methylcortisol
delta1-9alpha-Fluoro-16alpha-methylcortisol
Delta1-9alpha-fluoro-16alpha-Methylcortisol
Deltafluorene
Dergramin
Deronil
Desadrene
Desametasone
Desametasone [Dcit]
Desametasone [DCIT]
Desamethasone
Desameton
Deseronil
DEX
Dexa
DEXA
Dexa mamallet
Dexa Mamallet
Dexacen-4
Dexacidin
Dexacort
Dexacortal
Dexa-cortidelt
Dexa-Cortidelt
Dexacortin
Dexa-cortisyl
Dexa-Cortisyl
Dexadeltone
Dexafarma
Dexair
Dexalona
Dexaltin
Dexa-Mamallet
Dexametasona
Dexametasona [INN-Spanish]
Dexametasone
Dexameth
Dexamethansone
dexamethasone
Dexamethasone
Dexamethasone (JP15/USP/INN)
|
Dexamethasone [INN:BAN:JAN]
Dexamethasone acetate
Dexamethasone Acetate
Dexamethasone alcohol
Dexamethasone Alcohol
Dexamethasone base
Dexamethasone Base
Dexamethasone intensol
Dexamethasone Intensol
Dexamethasone sodium phosphate
Dexamethasone Sodium Phosphate
Dexamethasone-omega
Dexamethasonum
Dexamethasonum [INN-Latin]
Dexamethazone
Dexamonozon
Dexapolcort
Dexapos
Dexaprol
Dexa-scheroson
Dexa-Scheroson
Dexa-sine
Dexa-Sine
Dexason
Dexasone
Dexasone 0.5MG
Dexasone 0.75MG
Dexasone 4MG
Dexasporin
Dex-ide
Dex-Ide
Dexinolon
Dexinoral
Dexone
Dexone 0.5
DEXONE 0.5
Dexone 0.75
DEXONE 0.75
Dexone 1.5
DEXONE 1.5
Dexone 4
DEXONE 4
Dexonium
Dexpak
Dextelan
Dezone
Dinormon
DXM
Dxms
DXMS
ECR brand OF dexamethasone
ECR Brand of Dexamethasone
EINECS 200-003-9
Fluormethylprednisolone
Fluormone
Fluorocort
Fortecortin
Foy brand OF dexamethasone
Foy Brand of Dexamethasone
FT-0080377
Gammacorten
Hexadecadrol
Hexadrol
Hexadrol elixir
Hexadrol Elixir
Hexadrol Tablets
Hl-dex
Hl-Dex
HL-Dex
HMS1792A17
HMS1990A17
HMS2089N13
HSDB 3053
I06-1196
ICN brand OF dexamethasone
ICN Brand of Dexamethasone
IontoDex
isopto-Dex
Isopto-Dex
Lokalison F
Loverine
LS-7300
Luxazone
Maxidex
Maxidex ont 0.1%
Maxidex sus 0.1%
Maxitrol
Mediamethasone
Merck brand OF dexamethasone
Merck Brand of Dexamethasone
Merz brand 1 OF dexamethasone
Merz Brand 1 of Dexamethasone
Merz brand 2 OF dexamethasone
Merz Brand 2 of Dexamethasone
Methylfluorprednisolone
Mexidex
Millicorten
MK 125
MLS001055412
MLS001332507
MLS001332508
MolMap_000018
MolPort-003-846-433
Mymethasone
Naquasone (veterinary)
NCGC00091019-01
NCGC00091019-02
NCGC00091019-03
NCGC00091019-04
NCGC00091019-05
nchembio809-comp2
NCI60_003067
Neomycin and polymyxin b sulfates and dexamethasone
Neomycin and polymyxin b sulphates and dexamethasone
NSC 34521
NSC34521
Ocu-trol
Ocu-Trol
Oradexon
OTO-104
Pet derm III
Pet Derm Iii
Pet Derm III
Pet-Derm Iii
PHL-Dexamethasone
PMS Dexamethasone elixir 0.5mg/5ML
PMS-Dexamethasone
Policort
Posurdex
Prednisolon F
Prednisolone F
Prodex
S1322_Selleck
SAM002548948
Sandoz dexamethasone
SGCUT00126
Sk-Dexamethasone
SK-Dexamethasone
SMP1_000092
SMR000857119
SMR001227192
Spectrum5_002019
Spoloven
ST50307091
Sunia sol D
Sunia Sol D
Superprednol
TL8003317
to_000038
Tobradex
Tobramycin and dexamethasone
Tresaderm (veterinary)
Turbinaire
UNII-7S5I7G3JQL
Visumetazone
WLN: L E5 B666 OV KU MUTJ A1 BF CQ E1 FV1Q FQ G1
ZINC03875332
|
|
| 31 |
|
Mifepristone |
Approved, Investigational |
Phase 2 |
|
84371-65-3 |
55245
|
|
Synonyms:
(11beta,17beta)-11-(4-(Dimethylamino)phenyl)-17-hydroxy-17-(1-propynyl)estra-4,9-dien-3-one
(11beta,17beta)-11-(4-(Dimethylamino)phenyl)-17-hydroxy-17-(1-propynyl)-estra-4,9-dien-3-one
(11beta,17beta)-11-(4-(Dimethylamino)-phenyl)-17-hydroxy-17-(1-propynyl)estra-4,9-dien-3-one
(11beta,17beta)-11-[4-(dimethylamino)phenyl]-17-hydroxy-17-prop-1-yn-1-ylestra-4,9-dien-3-one
(2E)-N-hydroxy-3-[4-({(2-hydroxyethyl)[2-(1H-indol-3-yl)ethyl]amino}methyl)phenyl]prop-2-enamide
(8S,11R,13S,14S,17S)-11-(4-dimethylaminophenyl)-17-hydroxy-13-methyl-17-prop-1-ynyl-1,2,6,7,8,11,12,14,15,16-decahydrocyclopenta[a]phenanthren-3-one
(E)-N-hydroxy-3-[4-[[2-hydroxyethyl-[2-(1H-indol-3-yl)ethyl]amino]methyl]phenyl]prop-2-enamide
11-(4-dimethylamino-PHENYL)-17-hydroxy-13-methyl-17-prop-1-ynyl-1,2,6,7,8,11,12,13,14,15,16,17-dodec ahydro-cyclopenta[a]phenanthren-3-one
11-(4-DIMETHYLAMINO-phenyl)-17-hydroxy-13-methyl-17-prop-1-ynyl-1,2,6,7,8,11,12,13,14,15,16,17-dodec ahydro-cyclopenta[a]phenanthren-3-one
11-(4-DIMETHYLAMINO-PHENYL)-17-HYDROXY-13-METHYL-17-PROP-1-YNYL-1,2,6,7,8,11,12,13,14,15,16,17-DODEC AHYDRO-CYCLOPENTA[A]PHENANTHREN-3-ONE
11beta-(4-(Dimethylamino)phenyl)-17beta-hydroxy-17-(1-propynyl)estra-4,9-dien-3-on
11beta-(4-(Dimethylamino)phenyl)-17-hydroxy-21-methyl-19-nor-17alpha-pregna-4,9-dien-20-m-3-on
11beta-(4-(N,N-Dimethylamino)phenyl)-17alpha-(prop-1-ynyl)-delta4,9-estradiene-17beta-ol-3-one
11beta-(4-Dimethyl-?amino)-?phenyl-17beta-hydroxy-17-(1-propynyl)-?estra-4,9-dien-3-one
11beta-(p-(Dimethylamino)phenyl)-17beta-hydroxy-17-(1-propynyl)estra-4,9-dien-3-one
122742-25-0
17-beta-Hydroxy-11-beta-(4-dimethylaminophenyl-1)-17-alpha-(prop-1-ynyl)oestra-4,9-dien-3-one
404951-53-7
83203-42-3
84371-65-3
AC1L1IOO
AC1O62SB
Ambap84371-65-3
BIDD:PXR0123
BPBio1_000262
BRD-K37270826-001-04-5
BRN 5779404
BSPBio_000238
C07652
C-1073
C29H35NO2
CHEBI:50692
CHEMBL157
CHEMBL356066
CI-1073
CID55245
CID6445533
Contragest brand OF mifepristone
Contragest Brand of Mifepristone
Corlux
CPD000058481
D00585
D015735
Dacinostat
danco Brand OF mifepristone
Danco Brand of Mifepristone
DB00834
EC-000.2469
EU-0100801
Exelgyn brand OF mifepristone
Exelgyn Brand of Mifepristone
FT-0082666
HMS1568L20
HMS2052L05
HMS2090L22
HSCI1_000369
HSDB 6841
I14-11726
LAQ-824
Lopac0_000801
LS-192513
LS-64723
M 8046
M8046_SIGMA
|
Mifegyne
Mifégyne
Mifeprex
Mifeprex (TN)
Mifepriston
Mifepristona
Mifepristona [Spanish]
mifepristone
Mifépristone
Mifepristone (USAN/INN)
Mifepristone [USAN:INN:BAN]
Mifepristone contragest brand
Mifepristone Contragest Brand
Mifepristone danco brand
Mifepristone Danco Brand
Mifepristone exelgyn brand
Mifepristone Exelgyn Brand
Mifepristonum
Mifepristonum [Latin]
MLS000069785
MLS001074115
MolPort-003-849-222
NCGC00025179-05
NCGC00025179-08
NCGC00179632-01
nchembio.313-comp12
NVP-LAQ 824
NVP-LAQ824
NVP-LAQ824, Dacinostat, LAQ824
Pictovir
Pictovir (TM)
Prestwick_570
Prestwick0_000299
Prestwick1_000299
Prestwick2_000299
Prestwick3_000299
R 38486
R38486
R-38486
RU 38486
RU 486
RU 486-6
RU38486
RU-38486
RU486
RU-486
RU-486, MIFEPRISTONE
RU-486, RU-38486, Mifegyne, Mifeprex, Mifepristone
S1095_Selleck
S1611_Selleck
SAM001246881
SMR000058481
SPBio_002457
Spectrum5_002045
TL8005515
UNII-320T6RNW1F
UNII-V10P524501
VGX-410
VGX-410C
VX-410
ZINC03831128
ZK 98296
ZK98296
ZK-98296
|
|
| 32 |
|
Sunitinib |
Approved, Investigational |
Phase 2 |
|
557795-19-4, 341031-54-7 |
5329102
|
|
Synonyms:
(2S)-2-hydroxybutanedioic acid
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-, (2S)-hydroxybutanedioate (1:1)
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-, (2S)-hydroxybutanedioate (1:1)
326914-13-0
341031-54-7
5-(5-FLUORO-2-OXO-1,2-DIHYDRO-INDOL-3-YLIDENEMETHYL)-2,4-DIMETHYL-1H-PYRROLE-3-CARBOXYLIC ACID (2-DIETHYLAMINO-ETHYL)-AMIDE
5-(5-fluoro-2-oxo-1,2-Dihydroindolylidenemethyl)-2,4-dimethyl-1H-pyrrole-3-carboxylic acid (2-diethylaminoethyl)amide
557795-19-4
AC1NS62J
AC1O5CMQ
AKOS005145765
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)
CHEBI:38940
CHEBI:550864
CHEMBL1567
CHEMBL535
CID5329102
CID6456015
D06402
D08552
DB01268
DB07417
EN002687
FT-0083555
FT-0083556
I01-1229
K00588a
KS-5022
LS-186078
LS-187023
LS-187648
MolPort-003-986-763
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 (2S)-hydroxybutanedioate
N-(2-diethylaminoethyl)-5-[(Z)-(5-fluoro-2-oxo-1H-indol-3-ylidene)methyl]-2,4-dimethyl-1H-pyrrole-3-carboxamide
N-[2-(diethylamino)ethyl]-5-[(Z)-(5-fluoro-2-oxo-1,2-dihydro-3H-indol-3-ylidene)methyl]-2,4-dimethyl-1H-pyrrole-3-carboxamide
NCGC00164631-01
|
NSC736511
NSC750690
PDGF TK antagonist
PHA-290940AD
PNU-290940AD
S1042_Selleck
ST51053712
SU 011248
SU 11248
SU010398
SU-010398
Su-011248
SU011248
SU011248 L-malate salt
SU-011248 L-malate salt
SU11248
SU-11248
SU-11248 L-malate salt
SU-11248J
SU-12662
Sunitanib
sunitinib
Sunitinib
Sunitinib (free base)
Sunitinib (INN)
Sunitinib malate
Sunitinib malate (JAN/USAN)
Sunitinib malate [USAN]
sunitinibum
Sunitinibum
Sutent
Sutent (TN)
Sutent, SU-11248
TL8002546
UNII-LVX8N1UT73
UNII-V99T50803M
|
|
| 33 |
|
Trabectedin |
Approved, Investigational |
Phase 2 |
|
114899-77-3 |
108150
|
|
Synonyms:
Ect 743
Ecteinascidin
Ecteinascidin 743
ET743
|
ET-743
NSC 684766
Yondelis
|
|
| 34 |
|
Paclitaxel |
Approved, Vet_approved |
Phase 2 |
|
33069-62-4 |
36314
|
|
Synonyms:
(2AR-(2aalpha,4b,4abeta,6b,9a(a r*,betas*),11a,12a,12balpha))-b-(benzoylamino)-a-hydroxybenzenepropanoate 6,12b-bis(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,11-dihydroxy-4a,8,13,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca(3,4)benz(1,2-b)oxet-9-yl ester
(2AR-(2aalpha,4b,4abeta,6b,9a(a r*,betas*),11a,12a,12balpha))-b-(benzoylamino)-a-hydroxybenzenepropanoic acid 6,12b-bis(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,11-dihydroxy-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(alpha r*,betas*),11alpha,12alpha,12balpha))-beta-(benzoylamino)-alpha-hydroxybenzenepropanoate 6,12b-bis(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,11-dihydroxy-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(alpha r*,betas*),11alpha,12alpha,12balpha))-beta-(benzoylamino)-alpha-hydroxybenzenepropanoic acid 6,12b-bis(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,11-dihydroxy-4a,8,13,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca(3,4)benz(1,2-b)oxet-9-yl ester
(2AR-(2aalpha,4β,4abeta,6β,9α(α r*,betas*),11α,12α,12balpha))-β-(benzoylamino)-α-hydroxybenzenepropanoate 6,12b-bis(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,11-dihydroxy-4a,8,13,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca(3,4)benz(1,2-b)oxet-9-yl ester
(2AR-(2aalpha,4β,4abeta,6β,9α(α r*,betas*),11α,12α,12balpha))-β-(benzoylamino)-α-hydroxybenzenepropanoic acid 6,12b-bis(acetyloxy)-12-(benzoyloxy)-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-4,11-dihydroxy-4a,8,13,13-tetramethyl-5-oxo-7,11-methano-1H-cyclodeca(3,4)benz(1,2-b)oxet-9-yl ester
12-benzoate, 9-ester with (2R,3S)-N-benzoyl-3-phenylisoserine
157069-30-2
33069-62-4
5b,20-Epoxy-1,2-a,4,7b,10b,13a-hexahydroxytax-11-en-9-one 4,10-diacetate 2-benzoate 13-ester with (2R,3S)-N-benzoyl-3-phenylisoserine
5b,20-Epoxy-1,2-a,4,7b,10b,13a-hexahydroxytax-11-en-9-one 4,10-diacetic acid 2-benzoic acid 13-ester with (2R,3S)-N-benzoyl-3-phenylisoserine
5beta,20-Epoxy-1,2-alpha,4,7beta,10beta,13alpha-hexahydroxytax-11-en-9-one 4,10-diacetate 2-benzoate 13-ester with (2R,3S)-N-benzoyl-3-phenylisoserine
5beta,20-Epoxy-1,2-alpha,4,7beta,10beta,13alpha-hexahydroxytax-11-en-9-one 4,10-diacetic acid 2-benzoic acid 13-ester with (2R,3S)-N-benzoyl-3-phenylisoserine
5β,20-epoxy-1,2-α,4,7β,10β,13α-hexahydroxytax-11-en-9-one 4,10-diacetate 2-benzoate 13-ester with (2R,3S)-N-benzoyl-3-phenylisoserine
5β,20-epoxy-1,2-α,4,7β,10β,13α-hexahydroxytax-11-en-9-one 4,10-diacetic acid 2-benzoic acid 13-ester with (2R,3S)-N-benzoyl-3-phenylisoserine
7 Epi taxol
7,11-Methano-1H-cyclodeca[3,4]benz[1,2-b]oxete, benzenepropanoic acid deriv.
7,11-Methano-5H-cyclodeca[3,4]benz[1,2-b]oxete,benzenepropanoic acid deriv.
7-epi-Paclitaxel
7-Epipaclitaxel
7-Epi-paclitaxel
7-epi-Taxol
7-Epitaxol
7-Epi-taxol
AB00513812
ABI 007
abi-007
ABI007
ABI-007
Abraxane
Abraxane (TN)
Abraxane I.V. Suspension
Abraxis BioScience brand of albumin-bound paclitaxel
AC1L1IOG
AC1L1VJI
AC1L9AVF
AC-675
ACon1_002231
albumin-bound paclitaxel
Ambotz33069-62-4
ANX-513
Anzatax
Asotax
BIDD:PXR0046
Bio-0076
Bio1_000362
Bio1_000851
Bio1_001340
Bio2_000416
Bio2_000896
BMS 181339-01
BMS-181339
BMS-181339-01
BPBio1_000320
BRD-A23723433-001-01-2
BRD-A28746609-001-04-0
BRD-K62008436-001-03-1
Bris taxol
Bristaxol
BSPBio_000290
BSPBio_001152
BSPBio_002614
C07394
C466458
C47H51NO14
Capxol
CCRIS 8143
CHEBI:103439
CHEBI:45863
CHEMBL100910
CHEMBL418410
CHEMBL48
CID36314
CID441276
CID4666
CID6713921
CID6915727
cMAP_000068
CPD-8718
D00491
DB01229
DHP-107
DHP-208
DivK1c_000441
DRG-0190
DTS-301
Ebetaxel
EmPAC
Epitaxol
EU-0101201
Genaxol
Genetaxyl
Genexol
Genexol-PM
HMS1362J13
HMS1568O12
HMS1792J13
HMS1922K08
HMS1990J13
HMS2090D07
HMS2093K15
HMS501G03
HSDB 6839
I06-0014
IDI1_000441
IDI1_002171
Intaxel
KBio1_000441
KBio2_000492
KBio2_002016
KBio2_002509
KBio2_003060
KBio2_004584
KBio2_005077
KBio2_005628
KBio2_007152
KBio2_007645
|
KBio3_000903
KBio3_000904
KBio3_001834
KBio3_002987
KBioGR_000492
KBioGR_001893
KBioGR_002509
KBioSS_000492
KBioSS_002016
KBioSS_002517
LipoPac
LMPR0104390001
Lopac0_001201
LS-31070
MBT 0206
MEGxp0_001940
Micellar Paclitaxel
Mitotax
MLS000863266
MLS001077297
MLS002154218
MLS002172439
MLS002695976
MolPort-001-742-627
MolPort-003-665-783
MolPort-003-932-365
MPI-5018
nab-paclitaxel
Nanotaxel
NCGC00024995-02
NCGC00024995-03
NCGC00024995-04
NCGC00024995-05
NCGC00024995-06
NCGC00024995-07
NCGC00164367-01
NCGC00164367-02
NCGC00164367-03
nchembio.188-comp1
nchembio.2007.34-comp9
nchembio.215-comp9
nchembio853-comp6
NCI60_000601
Neuro_000060
NINDS_000441
NK 105
Nova-12005
NP-010981
NSC 125973
NSC125973
NSC-125973
NSC358882
OAS-PAC-100
OncoGel
Onxal
Onxol
Onxol, Taxol, Nov-Onxol, Paclitaxel
P1632
Paclical
Pacligel
paclitaxel
Paclitaxel
Paclitaxel (JAN/USP)
Paclitaxel (JAN/USP/INN)
Paclitaxel (Taxol)
Paclitaxel [USAN:INN:BAN]
Paclitaxel, (4 alpha)-isomer
Paxceed
Paxene
Paxoral
Plaxicel
Praxel
Prestwick0_000155
Prestwick1_000155
Prestwick2_000155
Prestwick3_000155
Probes2_000350
QW 8184
S1150_Selleck
S-8184 Paclitaxel Injectable Emulsion
SDCCGMLS-0066823.P001
SDP-013
SMP1_000228
SMR000394086
SMR000857385
SPBio_000943
SPBio_002229
Spectrum_001536
SPECTRUM1503908
Spectrum2_000872
Spectrum3_001057
Spectrum4_001197
Spectrum5_001491
ST50306996
T 7402
T1912_SIGMA
T7191_SIGMA
T7402_SIGMA
TA1
TaxAlbin
Taxol
TAXOL
TAXOL (TN)
Taxol a
Taxol A
Taxol Konzentrat
TAXOL, 10-EPI,
Taxol, bris
Taxol.RTM. (Registered Trademark)
TXL
UNII-P88XT4IS4D
UPCMLD-DP108:001
UPCMLD-DP108:002
Vascular Wrap
weekly paclitaxel
Xorane
Yewtaxan
|
|
| 35 |
|
Nivolumab |
Approved |
Phase 2 |
|
946414-94-4 |
|
|
Synonyms:
|
| 36 |
|
Letrozole |
Approved, Investigational |
Phase 2 |
|
112809-51-5 |
3902
|
|
Synonyms:
1-[bis(4-cyanophenyl)methyl]-1,2,4-triazole
1-[Bis-(4-cyanophenyl)methyl]-1,2,4-triazole
112809-51-5
4,4'-((1h-1,2,4-triazol-1-yl)methylene)dibenzonitrile
4,4'-(1H-1,2,4-triazol-1-ylmethanediyl)dibenzonitrile
4,4'-(1h-1,2,4-triazol-1-ylmethylene) bis-benzonitrile
4,4'-(1H-1,2,4-triazol-1-yl-methylene)-bis(benzonitrile)
4,4'-(1H-1,2,4-Triazol-1-yl-methylene)-bis(benzonitrile)
4,4'-(1h-1,2,4-triazol-1-ylmethylene)bisbenzonitrile
4,4'-(1h-1,2,4-triazol-1-ylmethylene)bis-benzonitrile
4,4'-(1H-1,2,4-triazol-1-ylmethylene)bis-Benzonitrile Letrozole
4,4'-(1H-1,2,4-Triazol-1-ylmethylene)dibenzonitrile
4-[(4-cyanophenyl)-(1,2,4-triazol-1-yl)methyl]benzonitrile
AB00514009
AC-1193
AC1L1GYT
AKOS005145822
BIDD:GT0015
BIDD:PXR0130
Bio-0057
BPBio1_001331
BRD-K88789588-001-03-2
BSPBio_001209
C067431
C08163
C17H11N5
CAS-112809-51-5
CCRIS 8822
CGS 20267
CGS 20267, Femara, Piroxicam, Letrozole
CGS-20267
CHEBI:6413
CHEMBL1444
CID3902
CPD000466343
D00964
DB01006
|
FEM-345
Femara
Fémara
Femara (TN)
Femera
HMS1571M11
HMS2051E08
HMS2089L22
HSDB 7461
I06-0022
Letoval
Letrozol
letrozole
Letrozole (JAN/USP/INN)
Letrozole [USAN:INN]
LS-38788
MLS000759455
MLS001424038
MLS002584991
MolPort-003-848-373
NCGC00016973-01
NCGC00016973-02
Novartis brand OF letrozole
Novartis Brand of Letrozole
NSC719345
Prestwick0_001025
Prestwick1_001025
Prestwick2_001025
Prestwick3_001025
S1235_Selleck
SAM001246649
SMR000466343
SPBio_003070
TL8000371
UNII-7LKK855W8I
ZINC03778874
|
|
| 37 |
|
Exemestane |
Approved, Investigational |
Phase 2 |
|
107868-30-4 |
60198
|
|
Synonyms:
(8R,9S,10R,13S,14S)-10,13-dimethyl-6-methylidene-7,8,9,11,12,14,15,16-octahydrocyclopenta[a]phenanthrene-3,17-dione
107868-30-4
6-Methylenandrosta-1,4-diene-3,17-dione
6-Methyleneandrosta-1,4-diene-3,17-dione
6-methylideneandrosta-1,4-diene-3,17-dione
AC1L1SRB
AC1Q6AAZ
AC-2171
Ambap107868-30-4
Aromasil
Aromasin
Aromasin (TN)
Aromasin, Exemestane
Aromasine
C056516
C08162
CHEBI:4953
CHEMBL1200374
CID60198
CPD000466314
Curator_000009
D00963
DB00990
Examestane
EXE
Exemestance
exemestane
|
Exemestane
EXEMESTANE
Exemestane (JAN/USP/INN)
Exemestane [USAN:INN:BAN]
Exemestano
Exemestano [INN-Spanish]
Exemestanum
Exemestanum [INN-Latin]
Fce 24304
FCE-24304
HMS2051J04
HSDB 7463
LS-19329
MLS000759419
MLS001424062
MolPort-003-847-343
Nikidess
NSC713563
Pfizer brand of exemestane
PNU-155971
S1196_Selleck
S1196_Sellek
SAM001246574
SMR000466314
UNII-NY22HMQ4BX
ZINC03973334
|
|
| 38 |
|
Anastrozole |
Approved, Investigational |
Phase 2 |
|
120511-73-1 |
2187
|
|
Synonyms:
.alpha.,alpha.,.alpha.',.alpha.'-tetramethyl-5(1H-1,2,4-triazol-1-ylmethyl)-m-benzenediacetonitrile
1,3-benzenediacetonitrile, a, a, a', a'-tetramethyl-5-(1H-1,2,4-triazol-1-ylmethyl)
120511-73-1
2,2'-(5-(1H-1,2,4-triazol-1-ylmethyl)-1,3-phenylene)bis(2-methylpropionitrile)
2,2'-(5-(1H-1,2,4-Triazol-1-ylmethyl)-1,3-phenylene)bis(2-methylpropionitrile)
2,2'-[5-(1H-1,2,4-triazol-1-ylmethyl)-1,3-phenylene]bis(2-methylpropanenitrile)
2,2'-[5-(1H-1,2,4-triazol-1-ylmethyl)benzene-1,3-diyl]bis(2-methylpropanenitrile)
2-[3-(2-cyanopropan-2-yl)-5-(1,2,4-triazol-1-ylmethyl)phenyl]-2-methylpropanenitrile
a,a,Alpha',alpha'-tetramethyl-5-(1H-1,2,4-triazol-1-ylmethyl)-m-benzenediacetonitrile
AC1L1D49
AC-4234
alpha,alpha,alpha',alpha'-Tetramethyl-5-(1H-1,2,4-triazol-1-ylmethyl)-m-benzenediacetonitrile
alpha,alpha,Alpha',alpha'-tetramethyl-5-(1H-1,2,4-triazol-1-ylmethyl)-m-benzenediacetonitrile
anastrazole
Anastrazole
Anastrole
Anastrozol
anastrozole
Anastrozole (JAN/USAN/INN)
Anastrozole [USAN:INN:BAN]
Arimidex
Arimidex (TN)
Arimidex (Zeneca)
Arimidex, Anastrozole
Asiolex
Astra brand of anastrozole
Astra brand OF anastrozole
AstraZeneca brand of anastrozole
AstraZeneca brand OF anastrozole
C08159
C090450
C17H19N5
|
CHEBI:2704
CHEMBL1399
CID2187
CPD000466301
D00960
DB01217
HMS2052M11
HMS2089N10
HSDB 7462
I06-0021
ICI D1033
ICI-D 1033
ICI-D1033
LS-29563
MLS000759396
MLS001424217
MolPort-005-933-078
NCGC00164619-01
NSC719344
S1188_Selleck
SAM001246525
SBB066057
SMR000466301
UNII-2Z07MYW1AZ
ZD 1033
ZD1033
ZD-1033
Zeneca brand of anastrozole
Zeneca brand OF anastrozole
Zeneca ZD 1033
ZINC00000941
α,α,alpha',alpha'-tetramethyl-5-(1H-1,2,4-triazol-1-ylmethyl)-m-benzenediacetonitrile
|
|
| 39 |
|
Saracatinib |
Investigational |
Phase 2 |
|
379231-04-6 |
|
|
Synonyms:
|
| 40 |
|
Trebananib |
Investigational |
Phase 2 |
|
894356-79-7 |
|
|
Synonyms:
|
| 41 |
|
Antineoplastic Agents, Hormonal |
|
Phase 2 |
|
|
|
| 42 |
|
Cortisol succinate |
|
Phase 2 |
|
|
|
| 43 |
|
protease inhibitors |
|
Phase 2 |
|
|
|
|
Synonyms:
|
| 44 |
|
BB 1101 |
|
Phase 2 |
|
|
|
| 45 |
|
Hormones, Hormone Substitutes, and Hormone Antagonists |
|
Phase 2 |
|
|
|
| 46 |
|
Hormone Antagonists |
|
Phase 2 |
|
|
|
| 47 |
|
Hormones |
|
Phase 2 |
|
|
|
| 48 |
|
glucocorticoids |
|
Phase 2 |
|
|
|
| 49 |
|
Autonomic Agents |
|
Phase 2 |
|
|
|
| 50 |
|
Antiemetics |
|
Phase 2 |
|
|
|
Interventional clinical trials:
(show all 22)
| # |
Name |
Status |
NCT ID |
Phase |
Drugs |
| 1 |
Radiation Therapy or No Further Treatment Following Surgery in Treating Patients With Cancer of the Uterus |
Completed |
NCT00002459
|
Phase 3 |
|
| 2 |
Surgery With or Without Combination Chemotherapy in Treating Patients With Lung Metastases From Soft Tissue Sarcoma |
Completed |
NCT00002764
|
Phase 3 |
doxorubicin hydrochloride;ifosfamide |
| 3 |
Surgery With or Without Chemotherapy in Treating Patients With Soft Tissue Sarcoma |
Completed |
NCT00002641
|
Phase 3 |
doxorubicin hydrochloride;ifosfamide;isolated perfusion |
| 4 |
Cyproheptadine in Preventing Weight Loss in Children Receiving Chemotherapy for Cancer |
Terminated |
NCT01132547
|
Phase 3 |
cyproheptadine hydrochloride |
| 5 |
Temozolomide in Treating Patients With Advanced Soft Tissue Sarcoma |
Unknown status |
NCT00003718
|
Phase 2 |
temozolomide |
| 6 |
Medical Safety Follow-up Study for Patients Who Received More Than 28 Days of Total Exposure to BGG492 |
Completed |
NCT02150213
|
Phase 2 |
BGG492 |
| 7 |
Mifepristone for Patients With Endometrial Cancer and LGESS |
Completed |
NCT00505739
|
Phase 2 |
Mifepristone |
| 8 |
Chemotherapy in Treating Patients With Sarcoma of the Uterus |
Completed |
NCT00005643
|
Phase 2 |
pegylated liposomal doxorubicin hydrochloride |
| 9 |
AZD0530 in Treating Patients With Recurrent Locally Advanced or Metastatic Soft Tissue Sarcoma |
Completed |
NCT00659360
|
Phase 2 |
saracatinib |
| 10 |
BI 2536 in Treating Patients With Recurrent or Metastatic Solid Tumors |
Completed |
NCT00526149
|
Phase 2 |
BI 2536 |
| 11 |
Sunitinib in Treating Patients With Metastatic, Locally Advanced, or Locally Recurrent Sarcomas |
Completed |
NCT00474994
|
Phase 2 |
sunitinib malate |
| 12 |
Ecteinascidin 743 in Treating Patients With Advanced Soft Tissue Sarcoma |
Completed |
NCT00003939
|
Phase 2 |
trabectedin |
| 13 |
STI571 in Treating Patients With Recurrent or Refractory Soft Tissue Sarcoma |
Completed |
NCT00006357
|
Phase 1, Phase 2 |
imatinib mesylate |
| 14 |
Combination Chemotherapy in Treating Patients With Endometrial Cancer, Fallopian Tube Cancer, or Sarcoma of the Female Reproductive Tract |
Completed |
NCT00003334
|
Phase 2 |
paclitaxel;pegylated liposomal doxorubicin hydrochloride |
| 15 |
Perifosine in Treating Patients With Metastatic or Locally Advanced Soft Tissue Sarcoma |
Completed |
NCT00053794
|
Phase 2 |
perifosine |
| 16 |
Thalidomide in Treating Patients With Gynecologic Sarcomas |
Completed |
NCT00006005
|
Phase 2 |
thalidomide |
| 17 |
Trebananib in Treating Patients With Persistent or Recurrent Endometrial Cancer |
Completed |
NCT01210222
|
Phase 2 |
|
| 18 |
Phase II Study of Imatinib Mesylate in Patients With Life Threatening Malignant Rare Diseases |
Completed |
NCT00154388
|
Phase 2 |
Imatinib mesylate |
| 19 |
A Study of Nivolumab in Selected Uterine Cancer Patients |
Recruiting |
NCT03241745
|
Phase 2 |
Nivolumab |
| 20 |
Evaluation of Clinical Impact of Interruption VS Maintenance of AI in Patients With Locally Advanced/ Metastatic Low Grade Endometrial Stromal Sarcoma (LGESS) |
Not yet recruiting |
NCT03624244
|
Phase 2 |
Aromatase Inhibitors |
| 21 |
A Phase II of Nivolumab Plus Ipilimumab in Non-resectable Sarcoma and Endometrial Carcinoma |
Not yet recruiting |
NCT02982486
|
Phase 2 |
Ipilimumab;Nivolumab |
| 22 |
Collecting Tumor Samples From Patients With Gynecological Tumors |
Completed |
NCT00897442
|
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|
