FDA approved drugs:
(show top 50)
(show all 211)
| # |
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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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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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| 4 |
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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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| 5 |
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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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| 6 |
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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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| 7 |
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Aredia
18
49
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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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| 8 |
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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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| 9 |
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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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| 10 |
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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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| 11 |
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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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| 12 |
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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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| 13 |
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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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| 14 |
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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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| 15 |
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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.
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| 16 |
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Bosulif
18
49
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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.
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| 17 |
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Bromfenac
18
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BROMFENAC SODIUM |
Duract, Wyeth-Ayerst Laboratories |
July 1997 |
Disease/s that Drug Treats:acute pain
Indications and Usage:
18
Bromfenac Ophthalmic Solutionis a nonsteroidal anti-inflamatory drug (NSAID) indicated for the treatment of postoperative inflammation and reduction of ocular pain in patients who have undergone cataract extraction (1).
DrugBank Targets:
16
1. Prostaglandin G/H synthase 2;2. Prostaglandin G/H synthase 1
Mechanism of Action:
18
Target: cyclooxygenas 1 and 2
Action: inhibitor
FDA: Bromfenac is a non-steroidal anti-inflamatory drug (NSAID) that has anti-inflammatory activity. The mechanism of its action is thought to be due to its ability to block prostaglandin synthesis bby inhibiting cyclooxygenase 1 and 2. Prostaglandins have been shown in many animal models to be mediators of certain kinds of intraocular inflammation. In studies performed in animal eyes, prostaglandins have been shown to produces disruption of the blood aqueous humor barrier, vasodilation, increased vascular permeability, leukocytosis, and increased intraocular pressure.
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| 18 |
|
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.
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| 19 |
|
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: -
|
| 20 |
|
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: -
|
| 21 |
|
Clolar
18
49
|
CLOFARABINE |
Genzyme |
December, 2004 |
Disease/s that Drug Treats:Lymphoblastic Leukemia
Indications and Usage:
18
Clolar (clofarabine) injection is a purine nucleoside metabolic inhibitorindicated for the treatment of pediatric patients 1 to 21 years old with relapsedor refractory acute lymphoblastic leukemia after at least two prior regimens.This indication is based upon response rate. There are no trials verifying animprovement in disease-related symptoms or increased survival with Clolar.(1)
DrugBank Targets:
16
1. DNA polymerase alpha catalytic subunit;2. Ribonucleoside-diphosphate reductase large subunit;3. DNA
Mechanism of Action:
18
Target: ribonucleotide reductase
Action: inhibitor
FDA: Clofarabine is sequentially metabolized intracellularly to the 5â-monophosphate metabolite bydeoxycytidine kinase and mono- and di-phospho-kinases to the active 5â-triphosphate metabolite.Clofarabine has affinity for the activating phosphorylating enzyme, deoxycytidine kinase, equalto or greater than that of the natural substrate, deoxycytidine. Clofarabine inhibits DNA synthesisby decreasing cellular deoxynucleotide triphosphate pools through an inhibitory action onribonucleotide reductase, and by terminating DNA chain elongation and inhibiting repair throughincorporation into the DNA chain by competitive inhibition of DNA polymerases. The affinity ofclofarabine triphosphate for these enzymes is similar to or greater than that of deoxyadenosinetriphosphate. In preclinical models, clofarabine has demonstrated the ability to inhibit DNArepair by incorporation into the DNA chain during the repair process. Clofarabine 5â-triphosphate also disrupts the integrity of mitochondrial membrane, leading to the release of thepro-apoptotic mitochondrial proteins, cytochrome C and apoptosis-inducing factor, leading toprogrammed cell death.Clofarabine is cytotoxic to rapidly proliferating and quiescent cancer cell types in vitro.
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| 22 |
|
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.
|
| 23 |
|
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.
|
| 24 |
|
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: -
|
| 25 |
|
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.
|
| 26 |
|
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).
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| 27 |
|
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.
|
| 28 |
|
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.
|
| 29 |
|
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.
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| 30 |
|
Erwinaze
18
49
|
asparaginase Erwinia chrysanthemi |
Eusa Pharma |
November of 2011 |
Disease/s that Drug Treats:acute lymphoblastic leukemia
Indications and Usage:
18
ERWINAZE (asparaginase Erwinia chrysanthemi) is an asparagine specificenzyme indicated as a component of a multi-agent chemotherapeutic regimenfor the treatment of patients with acute lymphoblastic leukemia (ALL) whohave developed hypersensitivity to E. coli-derived asparaginase. (1)
DrugBank Targets:
-
Mechanism of Action:
18
Target: deamidation of asparagine to aspartic acid and ammonia
Action: catalyzer
FDA: Asparaginase Erwinia chrysanthemi catalyzes the deamidation of asparagine to aspartic acid and ammonia, resultingin a reduction in circulating levels of asparagine. The mechanism of action of ERWINAZE is thought to be based onthe inability of leukemic cells to synthesize asparagine due to lack of asparagine synthetase activity, resulting incytotoxicity specific for leukemic cells that depend on an exogenous source of amino acid asparagine for theirprotein metabolism and survival.
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| 31 |
|
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: -
|
| 32 |
|
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.
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| 33 |
|
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.
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| 34 |
|
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.
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| 35 |
|
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.
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| 36 |
|
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.
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| 37 |
|
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.
|
| 38 |
|
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.
|
| 39 |
|
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.
|
| 40 |
|
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.
|
| 41 |
|
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.
|
| 42 |
|
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
|
| 43 |
|
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.
|
| 44 |
|
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.
|
| 45 |
|
Iclusig
18
49
|
PONATINIB HYDROCHLORIDE |
Ariad Pharmaceuticals |
December 2012 |
Disease/s that Drug Treats:chronic myeloid leukemia and Philadelphia chromosome positive acute lymphoblastic leukemia
Indications and Usage:
18
Iclusig is a kinase inhibitor indicated for the: Treatment of adult patients with T315I-positive chronic myeloidleukemia (chronic phase, accelerated phase, or blast phase) or T315IpositivePhiladelphia chromosome positive acute lymphoblasticleukemia (Ph+ ALL). Treatment of adult patients with chronic phase, accelerated phase, orblast phase chronic myeloid leukemia or Ph+ ALL for whom no othertyrosine kinase inhibitor (TKI) therapy is indicated. (1)These indications are based upon response rate. There are no trials verifying animprovement in disease-related symptoms or increased survival with Iclusig.
DrugBank Targets:
16
1. Tyrosine-protein kinase ABL1;2. Breakpoint cluster region protein;3. Mast/stem cell growth factor receptor Kit;4. Proto-oncogene tyrosine-protein kinase receptor Ret;5. Angiopoietin-1 receptor;6. Receptor-type tyrosine-protein kinase FLT3;7. Fibroblast growth factor receptor 1;8. Fibroblast growth factor receptor 2;9. Fibroblast growth factor receptor 3;10. Fibroblast growth factor receptor 4;11. Tyrosine-protein kinase Lck;12. Proto-oncogene tyrosine-protein kinase Src;13. Tyrosine-protein kinase Lyn;14. Vascular endothelial growth factor receptor 2;15. Platelet-derived growth factor receptor alpha
Mechanism of Action:
18
Target: tyrosine kinase activity of ABL and T315I mutant ABL
Action: inhibitor
FDA: Ponatinib is a kinase inhibitor. Ponatinib inhibited the in vitro tyrosine kinase activity of ABL and T315I mutant ABL withIC50 concentrations of 0.4 and 2.0 nM, respectively. Ponatinib inhibited the in vitro activity of additional kinases with IC50concentrations between 0.1 and 20 nM, including members of the VEGFR, PDGFR, FGFR, EPH receptors and SRCfamilies of kinases, and KIT, RET, TIE2, and FLT3. Ponatinib inhibited the in vitro viability of cells expressing native ormutant BCR-ABL, including T315I. In mice, treatment with ponatinib reduced the size of tumors expressing native orT315I mutant BCR-ABL when compared to controls.
|
| 46 |
|
Imbruvica
18
49
|
IBRUTINIB |
Pharmacyclics |
November of 2013/February 2014 |
Disease/s that Drug Treats:mantle cell lymphoma/chronic lymphocytic leukemia
Indications and Usage:
18
IMBRUVICA is a kinase inhibitor indicated for the treatment of patients with: Mantle cell lymphoma (MCL) who have received at least one priortherapy (1.1).Accelerated approval was granted for this indication based on overallresponse rate. Continued approval for this indication may be contingentupon verification of clinical benefit in confirmatory trials. Chronic lymphocytic leukemia (CLL) who have received at least oneprior therapy (1.2). Chronic lymphocytic leukemia with 17p deletion (1.3). Waldenströmâs macroglobulinemia (WM) (1.4).
DrugBank Targets:
16
1. Tyrosine-protein kinase BTK
Mechanism of Action:
18
Target: Bruton's tyrosine kinase (Btk)
Action: selective inhibitor
FDA: Ibrutinib is a small-molecule inhibitor of BTK. Ibrutinib forms a covalent bond with a cysteineresidue in the BTK active site, leading to inhibition of BTK enzymatic activity. BTK is asignaling molecule of the B-cell antigen receptor (BCR) and cytokine receptor pathways. BTKâsrole in signaling through the B-cell surface receptors results in activation of pathways necessaryfor B-cell trafficking, chemotaxis, and adhesion. Nonclinical studies show that ibrutinib inhibitsmalignant B-cell proliferation and survival in vivo as well as cell migration and substrateadhesion in vitro.
|
| 47 |
|
Inlyta
18
49
|
AXITINIB |
Pfizer |
January 2012 |
Disease/s that Drug Treats:advanced renal cell carcinoma
Indications and Usage:
18
INLYTA is a kinase inhibitor indicated for the treatment of advancedrenal cell carcinoma after failure of one prior systemic therapy. (1)
DrugBank Targets:
16
1. Vascular endothelial growth factor receptor 1;2. Vascular endothelial growth factor receptor 2;3. Vascular endothelial growth factor receptor 3
Mechanism of Action:
18
Target: receptor tyrosine kinases
Action: inhibitor
FDA: Axitinib has been shown to inhibit receptor tyrosine kinases including vascular endothelial growthfactor receptors (VEGFR)-1, VEGFR-2, and VEGFR-3 at therapeutic plasma concentrations. Thesereceptors are implicated in pathologic angiogenesis, tumor growth, and cancer progression. VEGFmediatedendothelial cell proliferation and survival were inhibited by axitinib in vitro and in mousemodels. Axitinib was shown to inhibit tumor growth and phosphorylation of VEGFR-2 in tumor xenograftmouse models.
|
| 48 |
|
Intron A
18
49
|
INTERFERON ALFA-2B |
Schering-Plough |
December 1997/ December 1995/ March 1997 |
Disease/s that Drug Treats:non-Hodgkin's lymphoma/ malignant melanoma / Hepatitis C
Indications and Usage:
18
Hairy Cell Leukemia INTRON® A is indicated for the treatment of patients 18 years ofage or older with hairy cell leukemia.Malignant Melanoma INTRON A is indicated as adjuvant to surgical treatment inpatients 18 years of age or older with malignant melanoma who are free of disease butat high risk for systemic recurrence, within 56 days of surgery.Follicular Lymphoma INTRON A is indicated for the initial treatment of clinicallyaggressive (see Clinical Pharmacology) follicular Non-Hodgkinâs Lymphoma inconjunction with anthracycline-containing combination chemotherapy in patients 18years of age or older. Efficacy of INTRON A therapy in patients with low-grade, lowtumorburden follicular Non-Hodgkinâs Lymphoma has not been demonstrated.Condylomata Acuminata INTRON A is indicated for intralesional treatment of selectedpatients 18 years of age or older with condylomata acuminata involving externalsurfaces of the genital and perianal areas (see DOSAGE AND ADMINISTRATION).The use of this product in adolescents has not been studied.AIDS-Related Kaposi's Sarcoma INTRON A is indicated for the treatment of selectedpatients 18 years of age or older with AIDS-Related Kaposi's Sarcoma. The likelihoodof response to INTRON A therapy is greater in patients who are without systemic symptoms, who have limited lymphadenopathy and who have a relatively intact immunesystem as indicated by total CD4 count.Chronic Hepatitis C INTRON A is indicated for the treatment of chronic hepatitis C inpatients 18 years of age or older with compensated liver disease who have a history ofblood or blood-product exposure and/or are HCV antibody positive. Studies in thesepatients demonstrated that INTRON A therapy can produce clinically meaningful effectson this disease, manifested by normalization of serum alanine aminotransferase (ALT)and reduction in liver necrosis and degeneration.A liver biopsy should be performed to establish the diagnosis of chronic hepatitis.Patients should be tested for the presence of antibody to HCV. Patients with othercauses of chronic hepatitis, including autoimmune hepatitis, should be excluded. Priorto initiation of INTRON A therapy, the physician should establish that the patient hascompensated liver disease. The following patient entrance criteria for compensated liverdisease were used in the clinical studies and should be considered before INTRON Atreatment of patients with chronic hepatitis C: No history of hepatic encephalopathy, variceal bleeding, ascites, or otherclinical signs of decompensation Bilirubin Less than or equal to 2 mg/dL Albumin Stable and within normal limits Prothrombin Time Less than 3 seconds prolonged WBC Greater than or equal to 3000/mm3 Platelets Greater than or equal to 70,000/mm3Serum creatinine should be normal or near normal.Prior to initiation of INTRON A therapy, CBC and platelet counts should beevaluated in order to establish baselines for monitoring potential toxicity. These testsshould be repeated at Weeks 1 and 2 following initiation of INTRON A therapy, andmonthly thereafter. Serum ALT should be evaluated at approximately 3-month intervalsto assess response to treatment (see DOSAGE AND ADMINISTRATION).Patients with preexisting thyroid abnormalities may be treated if thyroidstimulatinghormone (TSH) levels can be maintained in the normal range by medication.TSH levels must be within normal limits upon initiation of INTRON A treatment and TSHtesting should be repeated at 3 and 6 months (see PRECAUTIONS, LaboratoryTests).INTRON A in combination with REBETOL® is indicated for the treatment ofchronic hepatitis C in patients 3 years of age and older with compensated liver diseasepreviously untreated with alpha interferon therapy and in patients 18 years of age andolder who have relapsed following alpha interferon therapy. See REBETOL prescribinginformation for additional information. Chronic Hepatitis B INTRON A is indicated for the treatment of chronic hepatitis B inpatients 1 year of age or older with compensated liver disease. Patients who have beenserum HBsAg positive for at least 6 months and have evidence of HBV replication(serum HBeAg positive) with elevated serum ALT are candidates for treatment. Studiesin these patients demonstrated that INTRON A therapy can produce virologic remissionof this disease (loss of serum HBeAg) and normalization of serum aminotransferases.INTRON A therapy resulted in the loss of serum HBsAg in some responding patients.Prior to initiation of INTRON A therapy, it is recommended that a liver biopsy beperformed to establish the presence of chronic hepatitis and the extent of liver damage.The physician should establish that the patient has compensated liver disease. Thefollowing patient entrance criteria for compensated liver disease were used in theclinical studies and should be considered before INTRON A treatment of patients withchronic hepatitis B: No history of hepatic encephalopathy, variceal bleeding, ascites, or othersigns of clinical decompensation Bilirubin Normal Albumin Stable and within normal limits Prothrombin Time Adults less than 3 seconds prolongedPediatrics less than or equal to 2 seconds prolonged WBC Greater than or equal to 4000/mm3 Platelets Adults greater than or equal to 100,000/mm3Pediatrics greater than or equal to 150,000/mm3Patients with causes of chronic hepatitis other than chronic hepatitis B or chronichepatitis C should not be treated with INTRON A. CBC and platelet counts should beevaluated prior to initiation of INTRON A therapy in order to establish baselines formonitoring potential toxicity. These tests should be repeated at treatment Weeks 1, 2,4, 8, 12, and 16. Liver function tests, including serum ALT, albumin, and bilirubin,should be evaluated at treatment Weeks 1, 2, 4, 8, 12, and 16. HBeAg, HBsAg, andALT should be evaluated at the end of therapy, as well as 3- and 6-months posttherapy,since patients may become virologic responders during the 6-month periodfollowing the end of treatment. In clinical studies in adults, 39% (15/38) of respondingpatients lost HBeAg 1 to 6 months following the end of INTRON A therapy. Ofresponding patients who lost HBsAg, 58% (7/12) did so 1 to 6 months post-treatment.A transient increase in ALT greater than or equal to 2 times baseline value (flare)can occur during INTRON A therapy for chronic hepatitis B. In clinical trials in adultsand pediatrics, this flare generally occurred 8 to 12 weeks after initiation of therapy andwas more frequent in responders (adults 63%, 24/38; pediatrics 59%, 10/17) than innonresponders (adults 27%, 13/48; pediatrics 35%, 19/55). However, in adults andpediatrics, elevations in bilirubin greater than or equal to 3 mg/dL (greater than or equalto 2 times ULN) occurred infrequently (adults 2%, 2/86; pediatrics 3%, 2/72) duringtherapy. When ALT flare occurs, in general, INTRON A therapy should be continued unless signs and symptoms of liver failure are observed. During ALT flare, clinicalsymptomatology and liver function tests including ALT, prothrombin time, alkalinephosphatase, albumin, and bilirubin, should be monitored at approximately 2-weekintervals (see WARNINGS).
DrugBank Targets:
16
1. Interferon alpha/beta receptor 2;2. Interferon alpha/beta receptor 1
Mechanism of Action:
18
Target: intracellular oncogene expression, natural killer and cytotoxic T-cells, microphage, cytokine production
Action: stimulation, induction (unspecified effects on oncogene expression)
FDA: -
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| 49 |
|
Iressa
18
49
|
GEFITINIB |
AstraZeneca |
May 2003 |
Disease/s that Drug Treats:Non-Small-Cell Lung Cancer
Indications and Usage:
18
IRESSA is indicated as monotherapy for the continued treatment of patients with locally advanced ormetastatic non-small cell lung cancer after failure of both platinum-based and docetaxelchemotherapies who are benefiting or have benefited from IRESSA.In light of positive survival data with other agents including another oral EGFR inhibitor, physiciansshould use other treatment options in advanced non-small cell lung cancer patient populations whohave received one or two prior chemotherapy regimens and are refractory or intolerant to their mostrecent regimen. The effectiveness of IRESSA was initially based on objective response rates (see CLINICALPHARMACOLOGY-Clinical Studies section). Subsequent studies intended to demonstrate anincrease in survival have been unsuccessful. Specifically, results from a large placebo-controlledrandomized trial in patients with advanced NSCLC who progressed while receiving or within 90 daysof the last dose of chemotherapy or were intolerant to the most recent prior chemotherapy regimen, didnot show an improvement in survival (see CLINICAL PHARMACOLOGY- Clinical Studiessection).Results from two large, controlled, randomized trials in first-line treatment of non-small cell lungcancer showed no benefit from adding IRESSA to doublet, platinum-based chemotherapy. , IRESSA is indicated as monotherapy for the continued treatment of patients with locally advanced or metastatic non-small cell lung cancer after failure of both platinum-based and docetaxel chemotherapies who are benefiting or have benefited from IRESSA. In light of positive survival data with other agents including another oral EGFR inhibitor, physicians should use other treatment options in advanced non-small cell lung cancer patient populations who have received one or two prior chemotherapy regimens and are refractory or intolerant to their most recent regimen. The effectiveness of IRESSA was initially based on objective response rates (see CLINICAL PHARMACOLOGY-Clinical Studies section). Subsequent studies intended to demonstrate an increase in survival have been unsuccessful. Specifically, results from a large placebo-controlled randomized trial in patients with advanced NSCLC who progressed while receiving or within 90 days of the last dose of chemotherapy or were intolerant to the most recent prior chemotherapy regimen, did not show an improvement in survival (see CLINICAL PHARMACOLOGY- Clinical Studies section). Results from two large, controlled, randomized trials in first-line treatment of non-small cell lung cancer showed no benefit from adding IRESSA to doublet, platinum-based chemotherapy.
DrugBank Targets:
16
1. Epidermal growth factor receptor, Epidermal growth factor receptor
Mechanism of Action:
18
Target: EGFR tyrosine kinase and other tyrosine kinases, EGFR tyrosine kinase
Action: inhibitor
FDA: The mechanism of the clinical antitumor action of gefitinib is not fully characterized. Gefitinibinhibits the intracellular phosphorylation of numerous tyrosine kinases associated with transmembranecell surface receptors, including the tyrosine kinases associated with the epidermal growth factorreceptor (EGFR-TK). EGFR is expressed on the cell surface of many normal cells and cancer cells.No clinical studies have been performed that demonstrate a correlation between EGFR receptorexpression and response to gefitinib., The mechanism of the clinical antitumor action of gefitinib is not fully characterized. Gefitinib inhibits the intracellular phosphorylation of numerous tyrosine kinases associated with transmembrane cell surface receptors, including the tyrosine kinases associated with the epidermal growth factor receptor (EGFR-TK). EGFR is expressed on the cell surface of many normal cells and cancer cells. No clinical studies have been performed that demonstrate a correlation between EGFR receptor expression and response to gefitinib.
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| 50 |
|
Istodax
18
49
|
ROMIDEPSIN |
Gloucester Pharmaceuticals |
November 2009 |
Disease/s that Drug Treats:cutaneous T-cell lymphoma
Indications and Usage:
18
ISTODAX is a histone deacetylase (HDAC) inhibitor indicated for: Treatment of cutaneous T-cell lymphoma (CTCL) in patients who havereceived at least one prior systemic therapy (1). Treatment of peripheral T-cell lymphoma (PTCL) in patients who havereceived at least one prior therapy (1).These indications are based on response rate. Clinical benefit such asimprovement in overall survival has not been demonstrated (1).
DrugBank Targets:
-
Mechanism of Action:
18
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: Romidepsin is a histone deacetylase (HDAC) inhibitor. HDACs catalyze the removal of acetyl groups from acetylated lysine residues in histones, resulting in themodulation of gene expression. HDACs also deacetylate non-histone proteins, such as transcription factors. In vitro, romidepsin causes the accumulation of acetylatedhistones, and induces cell cycle arrest and apoptosis of some cancer cell lines with IC50 values in the nanomolar range. The mechanism of the antineoplastic effect ofromidepsin observed in nonclinical and clinical studies has not been fully characterized.
|
Drugs for Myeloma, Multiple (from DrugBank, HMDB, Dgidb, PharmGKB, IUPHAR, NovoSeek, BitterDB):
(show top 50)
(show all 714)
| # |
|
Name |
Status |
Phase |
Clinical Trials |
Cas Number |
PubChem Id |
| 1 |
|
Bortezomib |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Early Phase 1,Not Applicable |
|
179324-69-7 |
387447
93860
|
|
Synonyms:
[(1R)-3-methyl-1-({(2S)-3-phenyl-2-[(pyrazin-2-ylcarbonyl)amino]propanoyl}amino)butyl]boronic acid
[(1R)-3-methyl-1-[[(2S)-3-phenyl-2-(pyrazine-2-carbonylamino)propanoyl]amino]butyl]boronic acid
179324-69-7
341, PS
AC1L8TUW
bortezomib
Bortezomib
Bortezomib (JAN/USAN/INN)
CHEBI:287372
CHEBI:41143
CHEMBL325041
CID387447
D03150
DB07475
DPBA
FT-0082488
I14-3268
LDP 341
LDP341
LDP-341
|
LPD 341
LPD-341
MLN341
MolPort-003-845-298
N-[(1R)-1-(dihydroxyboranyl)-3-methylbutyl]-Nalpha-(pyrazin-2-ylcarbonyl)-L-phenylalaninamide
N-[(1R)-1-(DIHYDROXYBORYL)-3-methylbutyl]-N-(pyrazin-2-ylcarbonyl)-L-phenylalaninamide
N-[(1R)-1-(DIHYDROXYBORYL)-3-METHYLBUTYL]-N-(PYRAZIN-2-YLCARBONYL)-L-PHENYLALANINAMIDE
NCI60_029010
NSC681239
NSC-681239
PROSCRIPT BORONIC ACID
PS 341
PS-341
Pyz-Phe-boroLeu
S1013_Selleck
SBB071337
Velcade
Velcade (TN)
Velcade, MG-341, PS-341, Bortezomib
|
|
| 2 |
|
Doxorubicin |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
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
|
|
| 3 |
|
Dexamethasone acetate |
Approved, Investigational, Vet_approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
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
|
|
| 4 |
|
Dexamethasone |
Approved, Investigational, Vet_approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
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
|
|
| 5 |
|
Zoledronic acid |
Approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
118072-93-8 |
68740
|
|
Synonyms:
(1-Hydroxy-2-(1H-imidazol-1-yl)ethylidene)bisphosphonate
(1-hydroxy-2-(1H-imidazol-1-yl)ethylidene)bisphosphonic acid
(1-Hydroxy-2-(1H-imidazol-1-yl)ethylidene)bisphosphonic acid
(1-hydroxy-2-imidazol-1-yl-1-phosphonoethyl)phosphonic acid
(1-Hydroxy-2-imidazol-1-ylethylidene)diphosphonate
(1-hydroxy-2-imidazol-1-ylethylidene)diphosphonic acid
(1-Hydroxy-2-imidazol-1-ylethylidene)diphosphonic acid
(1-hydroxy-2-imidazol-1-yl-phosphonoethyl)phosphonic acid monohydrate
[1-hydroxy-2-(1H-imidazol-1-yl)ethane-1,1-diyl]bis(phosphonic acid)
118072-93-8
2-(imidazol-1-yl)-1-hydroxyethane-1,1-diphosphonic acid
2-(imidazol-1-yl)-1-hydroxyethylidene-1,1-bisphosphonic acid
2-(Imidazol-1-yl)-1-hydroxyethylidene-1,1-bisphosphonic acid
AC-1092
AC1L2ACJ
AC1Q6RN3
Aclasta
AKOS005145739
Anhydrous Zoledronic Acid
BIDD:GT0292
BIDD:PXR0134
Bio-0112
Bisphosphonate 3
C088658
CGP 42446
CGP 42'446
CGP 42446A
CGP-42446
CGP-42'446
CHEBI:46557
CHEMBL924
CID68740
|
D08689
DB00399
FT-0082657
HMS2089O09
I06-0710
KS-1132
LS-181815
MolPort-002-885-874
MolPort-003-850-890
NCGC00159521-02
NCGC00159521-03
Novartis brand of zoledronic acid
Novartis brand OF zoledronic acid
NSC721517
Reclast
Reclast (TN)
S00092
S1314_Selleck
UNII-70HZ18PH24
Zol
ZOL
Zoledronate
Zoledronic acid
Zoledronic acid (INN)
Zoledronic acid [USAN:INN]
Zoledronic Acid Anhydrous
Zoledronic Acid, Anhydrous
Zometa
Zometa (Novartis)
Zometa (TN)
Zometa Concentrate
Zometa, Zomera, Aclasta and Reclast, Zoledronic Acid
|
|
| 6 |
|
Cyclophosphamide |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
6055-19-2, 50-18-0 |
2907
|
|
Synonyms:
(-)-Cyclophosphamide
(+-)-Cyclophosphamide
(RS)-Cyclophosphamide
1-(bis(2-chloroethyl)amino)-1-oxo-2-aza-5-oxaphosphoridine
1-Bis(2-chloroethyl)amino-1-oxo-2-aza-5-oxaphosphoridin
2-[Bis(2-chloroethylamino)]-tetrahydro-2H-1,3,2-oxazaphosphorine-2-oxide
4-Hydroxy-cyclophosphan-mamophosphatide
50-18-0
60007-95-6
6055-19-2 (monohydrate)
75526-90-8
AC1L1EQQ
AI3-26198
Anhydrous cyclophosphamide
Anhydrous, cyclophosphamide
ASTA
Asta B 518
ASTA B518
B 518
B-518
bis(2-Chloroethyl)phosphami de cyclic propanolamide
bis(2-Chloroethyl)phosphamide cyclic propanolamide ester
Bis(2-chloroethyl)phosphoramide cyclic propanolamide ester
BRN 0011744
BSPBio_002099
C 0768
C07888
C7H15Cl2N2O2P
CB 4564
CB-4564
CCRIS 188
CHEBI:4027
CHEMBL32520
CHEMBL88
Ciclofosfamida
Ciclofosfamida [INN-Spanish]
Ciclofosfamide
Ciclophosphamide
Ciclophosphamide [INN]
CID2907
Clafen
Claphene
CP
CPA
CTX
CY
Cycloblastin
Cyclophosphamid
cyclophosphamide
Cyclophosphamide
Cyclophosphamide (anhydrous form)
Cyclophosphamide (anhydrous)
Cyclophosphamide (INN)
Cyclophosphamide (TN)
Cyclophosphamide anhydrous
Cyclophosphamide monohydrate
Cyclophosphamide Monohydrate
Cyclophosphamide Sterile
Cyclophosphamide, (+-)-Isomer
Cyclophosphamide, (R)-isomer
Cyclophosphamide, (S)-isomer
Cyclophosphamides
Cyclophosphamidum
Cyclophosphamidum [INN-Latin]
Cyclophosphan
Cyclophosphane
Cyclophosphanum
Cyclophosphoramide
Cyclostin
Cyklofosfamid
Cyklofosfamid [Czech]
Cytophosphan
Cytophosphane
Cytoxan
Cytoxan (TN)
|
Cytoxan Lyoph
D,L-Cyclophosphamide
D07760
DB00531
DivK1c_000246
EINECS 200-015-4
Endoxan
Endoxan R
Endoxana
Endoxanal
Endoxan-Asta
Endoxane
Enduxan
EU-0100238
Genoxal
Hexadrin
HMS2090A12
HSDB 3047
IDI1_000246
KBio1_000246
KBio2_001338
KBio2_003906
KBio2_006474
KBio3_001319
KBioGR_000888
KBioSS_001338
Ledoxina
Lopac0_000238
Lopac-C-0768
LS-1302
LS-99787
Lyophilized Cytoxan
Mitoxan
MolPort-001-783-420
Monohydrate, cyclophosphamide
N,N-Bis(2-chloroethyl)-1,3,2-oxazaphosphinan-2-amine 2-oxide
N,N-Bis(2-chloroethyl)tetrahydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide
NCGC00015209-01
NCGC00015209-03
NCGC00015209-06
NCGC00091741-02
NCGC00091741-03
NCI60_002097
NCI-C04900
Neosar
NINDS_000246
NSC 26271
NSC26271
NSC-26271
NSC273033
NSC273034
Occupation, cyclophosphamide exposure
Procytox
RCRA waste no. U058
Rcra waste number U058
Rcra Waste Number U058
Revimmune
S1217_Selleck
Semdoxan
Sendoxan
Senduxan
SK 20501
SPBio_001071
Spectrum_000858
Spectrum2_001146
Spectrum3_000370
Spectrum4_000304
Spectrum5_000795
STK177249
STOCK2S-91217
UNII-6UXW23996M
WLN: T6MPOTJ BO BN2G2G
Zyklophosphamid
Zyklophosphamid [German]
|
|
| 7 |
|
Epirubicin |
Approved |
Phase 4,Phase 3,Phase 2 |
|
56420-45-2 |
41867
|
|
Synonyms:
(1S,3S)-3,5,12-trihydroxy-3-(hydroxyacetyl)-10-(methyloxy)-6,11-dioxo-1,2,3,4,6,11-hexahydrotetracen-1-yl 3-amino-2,3,6-trideoxy-alpha-L-arabino-hexopyranoside
(1S,3S)-3,5,12-trihydroxy-3-(hydroxyacetyl)-10-methoxy-6,11-dioxo-1,2,3,4,6,11-hexahydrotetracen-1-yl 3-amino-2,3,6-trideoxy-alpha-L-arabino-hexopyranoside
(7S,9R)-7-[(2S,4S,5R,6S)-4-Amino-5-hydroxy-6-methyl-oxan-2-yl]oxy-6,9,11-trihydroxy-9-(2-hydroxyacetyl)-4-methoxy-8,10-dihydro-7H-tetracene-5,12-dione
(7S,9S)-7-[(2R,4S,5R,6S)-4-amino-5-hydroxy-6-methyloxan-2-yl]oxy-6,9,11-trihydroxy-9-(2-hydroxyacetyl)-4-methoxy-8,10-dihydro-7H-tetracene-5,12-dione
10-((3-amino-2,3,6-trideoxy-beta-L-arabino-hexopyranosyl)oxy)-7,8,9,10-tetrahydro-6,8,11-trihydroxy-8-(hydroxyacetyl)-1-methoxy-(8S-cis)-5,12-naphthacenedione
4' Epi adriamycin
4' Epi doxorubicin
4' Epi DXR
4' Epiadriamycin
4' Epidoxorubicin
4'-Epiadriamycin
4'-Epi-adriamycin
4'-epidoxorubicin
4'-epi-Doxorubicin
4'-Epidoxorubicin
4'-Epi-doxorubicin
4-Epidoxorubicin
4'-epi-DX
4'-Epi-DXR
56390-09-1
56390-09-1 (hydrochloride)
56420-45-2
57918-25-9
AC1L26NP
AC1Q6JIV
BRN 1445813
C11230
C27H29NO11
CCRIS 2261
Cell pharm brand OF epirubicin
CHEBI:47898
CHEMBL417
CID41867
D07901
DB00445
Ellence
EPI cell
Epiadriamycin
EPIcell
EPI-cell
Epidoxorubicin
Epi-Dx
Epi-DX
Epilem
Epirubicin
|
Epirubicin (INN)
Epirubicin [INN:BAN]
Epirubicin hydrochloride
Epirubicina
Epirubicina [INN-Spanish]
Epirubicina [Spanish]
Epirubicine
Epirubicine [French]
Epirubicine [INN-French]
Epirubicinum
Epirubicinum [INN-Latin]
Epirubicinum [Latin]
Farmorubicin
Farmorubicin (TN)
Farmorubicina
Farmorubicine
HSDB 6962
Hydrochloride, epirubicin
IMI 28
IMI28
IMI-28
Kenfarma brand OF epirubicin hydrochloride
Lemery brand OF epirubicin hydrochloride
LS-187190
LS-93992
MLS000759412
NChemBio.2007.10-comp15
NSC 256942
NSC256942
NSC-256942
Pfizer brand OF epirubicin hydrochloride
Pharmorubicin
Pharmorubicin Pfs
Pidorubicin
Pidorubicina
Pidorubicina [INN-Spanish]
Pidorubicine
Pidorubicine [INN-French]
Pidorubicinum
Pidorubicinum [INN-Latin]
Ridorubicin
SMR000466308
Triferric doxorubicin
UNII-3Z8479ZZ5X
WP 697
|
|
| 8 |
|
Melphalan |
Approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
148-82-3 |
4053
460612
|
|
Synonyms:
(2s)-2-amino-3-(4-[bis(2-chloroethyl)amino]phenyl)propanoic acid
(2S)-2-amino-3-[4-[bis(2-chloroethyl)amino]phenyl]propanoic acid
148-82-3
3-(p-(Bis(2-chloroethyl)amino)phenyl)alanine
3-(p-(Bis(2-chloroethyl)amino)phenyl)-L-alanine
3-(P-(Bis(2-chloroethyl)amino)phenyl)-L-alanine
3025 c.b
3025 C.B.
3223-07-2
3-p-(Di(2-chloroethyl)amino)-phenyl-L-alanine
3-P-(Di(2-chloroethyl)amino)-phenyl-L-alanine
4-(Bis(2-chloroethyl)amino)-L-phenylalanine
4-(Bis(2-chloroethyl)amino)phenylalanine
4-[Bis(2-chloroethyl)amino]-L-phenylalanine
4-[Bis-(2-chloroethyl)amino]-L-phenylalanine
4-14-00-01689 (Beilstein Handbook Reference)
AC1LA2OE
Alanine Nitrogen Mustard
Alkeran
ALKERAN (TN)
AmbotzHAA1563
At-290
AY3360000
BIDD:GT0044
BRD-K87827419-001-02-8
BRN 2816456
BSPBio_002407
C13H18Cl2N2O2
CB 3025
CB-3025
CCRIS 374
CHEBI:165415
CHEBI:28876
CHEMBL852
CID460612
D00369
DivK1c_000653
EINECS 205-726-3
HMS2090B09
HMS2091B16
HMS502A15
HSDB 3234
IDI1_000653
KBio1_000653
KBio2_000877
KBio2_003445
KBio2_006013
KBio3_001627
KBioGR_001284
KBioSS_000877
L-3-(p-(Bis(2-chloroethyl)amino)phenyl)alanine
L-3-(P-(Bis(2-chloroethyl)amino)phenyl)alanine
L-3-(para-(Bis(2-chloroethyl)amino)phenyl)alanine
Levofalan
Levofolan
Levopholan
L-PAM
L-Phenylalanine mustard
LS-15868
LS-865
L-Sarcolysin
L-Sarcolysine
L-Sarkolysin
M2011_SIGMA
|
Medphalan
Melfalan
Melfalano
Melfalano [INN-Spanish]
melphalan
Melphalan (JP15/USP/INN)
MELPHALAN (SEE ALSO TRANSGENIC MODEL EVALUATION (MELPHALAN))
Melphalan [USAN:INN:BAN:JAN]
Melphalanum
Melphalanum [INN-Latin]
Mephalan
Merphalan
MLS001333666
MLS002153368
MolPort-003-665-535
Mustard, phenylalanine
NCGC00090757-01
NCGC00090757-02
NCGC00090757-03
NCI-C04853
NINDS_000653
NIOSH/AY3360000
NSC 241286
NSC 8806
NSC241286
NSC8806
NSC-8806
P-Bis(b-chloroethyl)aminophenylalanine
p-Bis(beta-chloroethyl)aminophenylalanine
P-Bis(beta-chloroethyl)aminophenylalanine
P-Bis(β-chloroethyl)aminophenylalanine
p-Di-(2-chloroethyl)amino-L-phenylalanine
P-Di-(2-chloroethyl)amino-L-phenylalanine
Phenylalanine mustard
phenylalanine nitrogen mu stard
Phenylalanine nitrogen mustard
p-L-Sarcolysin
P-L-Sarcolysin
p-L-sarcolysine
p-N,N-bis(2-chloroethyl)amino-L-phenylalanine
P-N,N-Bis(2-chloroethyl)amino-L-phenylalanine
p-N-Bis(2-chloroethyl)amino-L-phenylalanine
P-N-Bis(2-chloroethyl)amino-L-phenylalanine
p-N-di(chloroethyl)aminophenylala nine
p-N-Di(chloroethyl)aminophenylalanine
Prestwick_1006
RCRA waste no. U150
Rcra waste number U150
Sarcolysine
Sarkolysin
SK-15673
SMP2_000174
SMR000058720
SPBio_000287
Spectrum_000397
SPECTRUM1500382
Spectrum2_000074
Spectrum3_000684
Spectrum4_000882
Spectrum5_001601
TL8001065
TRANSGENIC LEP (MELPHALAN) (SEE ALSO MELPHALAN)
TRANSGENIC MODEL EVALUATION (MELPHALAN)
UNII-Q41OR9510P
|
|
| 9 |
|
Prednisone |
Approved, Vet_approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
53-03-2 |
5865
|
|
Synonyms:
(1S,2R,10S,11S,14R,15S)-14-hydroxy-14-(2-hydroxyacetyl)-2,15-dimethyltetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadeca-3,6-diene-5,17-dione
(8S,9S,10R,13S,14S,17R)-17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-6,7,8,9,12,14,15,16-octahydrocyclopenta[a]phenanthrene-3,11-dione
(8xi,9xi,14xi)-17,21-dihydroxypregna-1,4-diene-3,11,20-trione
.delta. E
.delta.(sup1)-Cortisone
.delta.1-Cortisone
.delta.1-Dehydrocortisone
.delta.-Cortelan
.delta.-Cortisone
.delta.-Cortone
.delta.-E
.delta.sone
1,2-Dehydrocortisone
1,4-Pregnadiene-17.alpha.,21-diol-3,11,20-trione
1,4-Pregnadiene-17a,21-diol-3,11,20-trione
1,4-Pregnadiene-17alpha,21-diol-3,11,20-trione
1,4-Pregnadiene-17-alpha,21-diol-3,11,20-trione
1,4-Pregnadiene-17α,21-diol-3,11,20-trione
17,21-Dihydroxypregna-1,4-diene-3,11,20-trione
17alpha,21-Dihydroxy-1,4-pregnadiene-3,11,20-trione
1-Cortisone
1-Dehydrocortisone
53-03-2
68-59-7
81552_FLUKA
AC-11112
AC1L1LB2
AC1Q29EZ
Acis brand OF prednisone
ACon0_000082
ACon1_000297
Adasone
AI3-52939
Ancortone
apo-Prednisone
Apo-prednisone
Apo-Prednisone
Apotex brand OF prednisone
Aventis brand OF prednisone
Betapar
Bicortone
Bio-0649
BPBio1_000323
BRD-K85883481-001-04-2
BSPBio_000293
C07370
C21H26O5
Cartancyl
CCRIS 2646
CHEBI:8382
CHEMBL635
CID5865
Colisone
Cortan
Cortancyl
Cortidelt
Cotone
CPD001227202
Cutason
Dacorten
Dacortin
DB00635
Decortancyl
Decortin
Decortisyl
Dehydrocortisone
Dekortin
Delcortin
Dellacort
Dellacort A
delta cortelan
Delta Cortelan
Delta E
Delta E.
delta(sup 1)-Cortisone
delta(sup 1)-Dehydrocortisone
delta-1-Cortisone
delta-1-Dehydrocortisone
Delta-cortelan
Delta-Cortelan
Deltacortene
delta-Cortisone
Deltacortisone
Delta-cortisone
delta-Cortone
Deltacortone
Delta-cortone
Delta-dome
Delta-Dome
Deltasone
Deltasone, Liquid Pred, Orasone, Adasone, Deltacortisone,Prednisone
Deltison
Deltisona
Deltisone
Deltra
Diadreson
Di-Adreson
Diba brand OF prednisone
Econosone
EINECS 200-160-3
Encorton
Encortone
Enkortolon
Enkorton
Fawns and mcallan brand OF prednisone
Fernisone
Ferring brand OF prednisone
Fiasone
GALENpharma brand OF prednisone
Halsey drug brand OF prednisone
Hexal brand OF prednisone
HMS1568O15
HMS2090J13
|
Hoechst brand OF prednisone
Hostacortin
HSDB 3168
ICN brand OF prednisone
Incocortyl
In-Sone
Juvason
Kortancyl
Lichtenstein brand OF prednisone
Liquid pred
Liquid Pred
Lisacort
LMST02030180
Lodotra
LS-1325
MEGxm0_000443
Me-Korti
Merck brand OF prednisone
Merz brand OF prednisone
Metacortandracin
Meticorten
Meticorten (Veterinary)
Metrevet (Veterinary)
Mibe brand OF prednisone
MLS001061265
MLS001304073
MLS001335907
MLS001335908
MLS002154191
MLS002207083
MolPort-001-740-041
NCGC00090766-01
NCGC00090766-02
NCGC00090766-03
NCI60_000008
NCI-C04897
Nisona
Nizon
Novoprednisone
NSC 10023
NSC10023
Nurison
Orasone
Origen Prednisone
P1276
P6254_SIGMA
Panafcort
Panasol
Paracort
Parmenison
Pehacort
Pharmacia brand OF prednisone
PRD
Precort
Predeltin
Predni tablinen
Prednicen-M
Prednicorm
Prednicort
Prednicot
Prednidib
Prednilonga
Predniment
Prednison
Prednison acsis
Prednison galen
Prednison hexal
Prednisona
Prednisona [INN-Spanish]
Prednisone
Prednisone [INN:BAN]
Prednisone Intensol
Prednisonum
Prednisonum [INN-Latin]
Prednitone
Prednizon
Prednovister
Presone
Prestwick_405
Prestwick0_000077
Prestwick1_000077
Prestwick2_000077
Prestwick3_000077
Pronison
Pronisone
Rectodelt
Retrocortine
S1622_Selleck
SAM002264641
Schering-plough brand OF prednisone
Seatrace brand OF prednisone
Servisone
SK-Prednisone
SMR000718760
SMR001227202
Solvay brand OF prednisone
Sone
SPBio_002214
Sterapred
Supercortil
Trommsdorff brand OF prednisone
U 6020
Ultracorten
Ultracortene
UNII-VB0R961HZT
Winpred
WLN: L E5 B666 CV OV AHTTT&J A1 E1 FV1Q FQ
Wojtab
Zenadrid
Zenadrid (veterinary)
Zenadrid [veterinary]
ZINC03875357
|
|
| 10 |
|
Lenograstim |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
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
|
|
| 11 |
|
Lenalidomide |
Approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
191732-72-6 |
216326
|
|
Synonyms:
191732-72-6
1-oxo-2-(2,6-Dioxopiperidin-3-yl)-4-aminoisoindoline
3-(4-Amino-1-oxo-1,3-dihydro-2H-isoindol-2-yl)piperidine-2,6-dione
3-(4-amino-1-Oxoisoindolin-2-yl)piperidine-2,6-dione
3-(4-Amino-1-oxoisoindolin-2-yl)piperidine-2,6-dione
3-(7-amino-3-oxo-1H-isoindol-2-yl)piperidine-2,6-dione
3-(7-Amino-3-oxo-1H-isoindol-2-yl)-piperidine-2,6-dione
346670-73-3
443912-14-9
AC1L50II
AC-914
AKOS005146276
ALBB-015321
Bio-0168
C467567
CC 5013
CC5013
CC-5013
CC-5013, Revlimid, Lenalidomide
CDC 501
CDC-501
CDC-5013
Celgene brand of lenalidomide
Celgene brand OF lenalidomide
CHEMBL848
CID216326
D04687
|
DB00480
EC-000.2340
ENMD-0997
I06-0831
IMid-1
IMID-1
IMiD3
IMiD3 cpd
IMiD3 CPD
IMID-5013
lenalidomide
Lenalidomide
Lenalidomide (USAN/INN)
Lenalidomide [USAN]
LS-184040
MolPort-003-848-370
NCGC00167491-01
NSC747972
Revamid
Revimid
Revlimid
Revlimid (Celgene)
Revlimid (TN)
S1029_Selleck
STK639603
Thalidomide analog CC-5013
UNII-F0P408N6V4
|
|
| 12 |
|
Fludarabine |
Approved |
Phase 4,Phase 2,Phase 3,Phase 1,Not Applicable,Early Phase 1 |
|
75607-67-9, 21679-14-1 |
30751
|
|
Synonyms:
(2R,3S,4S,5R)-2-(6-amino-2-fluoro-9H-purin-9-yl)-5-(hydroxymethyl)oxolane-3,4-diol
(2R,3S,4S,5R)-2-(6-amino-2-fluoropurin-9-yl)-5-(hydroxymethyl)oxolane-3,4-diol
21679-14-1
2-F-ara-A
2-F-ARAA
2F-Ara-AMP
2-fluoro ARA-A
2-Fluoro Ara-A
2-Fluoro-9-beta-D-arabinofuranosyladenine
2-Fluoroadenine arabinoside 5'-monophosphate
2-Fluoroadenine arabinoside 5'-monophosphoric acid
2-fluoro-ARA AMP
9 beta-D-Arabinofuranosyl-2-fluoroadenine monophosphate
9-b-Arabinofuranosyl-2-fluoroadenine-5'-phosphate
9-b-Arabinofuranosyl-2-fluoroadenine-5'-phosphoric acid
9-b-D-Arabinofuranosyl-2-fluoroadenine 5'-(dihydrogen phosphate)
9-b-D-Arabinofuranosyl-2-fluoroadenine 5'-(dihydrogen phosphoric acid)
9-b-D-Arabinofuranosyl-2-fluoroadenine 5'-monophosphate
9-b-D-Arabinofuranosyl-2-fluoroadenine 5'-monophosphoric acid
9-beta-Arabinofuranosyl-2-fluoroadenine-5'-phosphate
9-beta-Arabinofuranosyl-2-fluoroadenine-5'-phosphoric acid
9-beta-D-arabinofuranosyl-2-fluoro-9H-purin-6-amine
9-beta-D-Arabinofuranosyl-2-fluoroadenine
9-beta-D-Arabinofuranosyl-2-fluoroadenine 5'-(dihydrogen phosphate)
9-beta-D-Arabinofuranosyl-2-fluoroadenine 5'-(dihydrogen phosphoric acid)
9-beta-D-Arabinofuranosyl-2-fluoroadenine 5'-monophosphate
9-beta-D-Arabinofuranosyl-2-fluoroadenine 5'-monophosphoric acid
9H-Purin-6-amine, 9-beta-D-arabinofuranosyl-2-fluoro- (9CI)
9-β-arabinofuranosyl-2-fluoroadenine-5'-phosphate
9-β-arabinofuranosyl-2-fluoroadenine-5'-phosphoric acid
9-β-D-arabinofuranosyl-2-fluoroadenine 5'-(dihydrogen phosphate)
9-β-D-arabinofuranosyl-2-fluoroadenine 5'-(dihydrogen phosphoric acid)
9-β-D-arabinofuranosyl-2-fluoroadenine 5'-monophosphate
9-β-D-arabinofuranosyl-2-fluoroadenine 5'-monophosphoric acid
AC1LCW8I
AC1Q51CF
Beneflur
C10H12FN5O4
CCRIS 3382
CHEMBL1568
CID657237
|
CPD000058874
D07966
EINECS 244-525-5
FAMP
FaraA
F-Ara-A
FaraAMP
F-Ara-AMP
Fludara
Fludara, Fludarabine
Fludarabina
Fludarabina [Spanish]
Fludarabine
Fludarabine (INN)
Fludarabine [INN]
Fludarabine 5'-monophosphate
Fludarabine 5'-monophosphoric acid
Fludarabine monophosphate
Fludarabine monophosphoric acid
Fludarabine phosphate
Fludarabinum
Fludarabinum [Latin]
Fludura
fluoro-Ara-AMP
Fluradosa
Fluradosa (TN)
FT-0082766
HSDB 6964
I14-4978
LS-15061
MLS000028687
NSC 118218
NSC 118218H
NSC-118218
S1491_Selleck
SAM002548956
SMR000058874
SQ Fludarabine
UNII-1X9VK9O1SC
UNII-P2K93U8740
ZINC04216238
|
|
| 13 |
|
Busulfan |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
55-98-1 |
2478
|
|
Synonyms:
1, {4-Bis[methanesulfonoxy]butane}
1, 4-Dimethanesulfonoxybutane
1, 4-Dimethylsulfonoxybutane
1,4-Bis(methanesulfonoxy)butane
1,4-Bis(methanesulfonyloxy)butane
1,4-Bis(methanesulphonoxy)butane
1,4-Bis[methanesulfonoxy]butane
1,4-Butanedi yl dimethanesulfonate
1,4-Butanediol dimethanesulfonate
1,4-BUTANEDIOL DIMETHANESULFONATE
1,4-Butanediol dimethanesulfonic acid
1,4-Butanediol dimethanesulphonate
1,4-Butanediol dimethanesulphonic acid
1,4-Butanediol dimethylsulfonate
1,4-Butanediol, dimethanesulfonate
1,4-Butanediol, dimethanesulphonate
1,4-Butanediyl dimethanesulfonate
1,4-Di(methylsulfonoxy)butane
1,4-Dimesyloxybutane
1,4-Dimethane sulfonyl oxybutane
1,4-Dimethanesulfonoxybutane
1,4-Dimethanesulfonoxylbutane
1,4-Dimethanesulfonyloxybutane
1,4-Dimethanesulphonoxybutane
1,4-Dimethanesulphonyloxybutane
1,4-Dimethylsulfonoxybutane
1,4-Dimethylsulfonyloxybutane
2041 C. B
2041 C. B.
2041 C.B
2041 C.B.
4-((Methylsulfonyl)oxy)butyl methanesulfonate
4-methylsulfonyloxybutyl methanesulfonate
55-98-1
AC-198
AC1L1DRQ
AC1Q4GRQ
acid, tetramethylene ester
AI3-25012
AKOS003614975
alkylating agent: crosslinks guanine residues
Ambap55-98-1
AN 33501
B1022
B2635_FLUKA
B2635_SIGMA
Bisulfex
Bisulphex
BRN 1791786
BSPBio_001920
Busilvex
busulfan
Busulfan
BUSULFAN (1,4-BUTANEDIOL, DIMETHANESULFONATE)
Busulfan (JP15/USP/INN)
Busulfan [INN:JAN]
Busulfan glaxosmithkline brand
Busulfan GlaxoSmithKline Brand
Busulfan orphan brand
Busulfan Orphan Brand
Busulfan wellcome
Busulfan Wellcome
Busulfan wellcome brand
Busulfan Wellcome Brand
Busulfano
Busulfano [INN-Spanish]
Busulfanum
Busulfanum [INN-Latin]
Busulfex
Busulphan
Busulphane
Busulphano
Busulphanum
butane-1,4-diyl dimethanesulfonate
Butanedioldimethanesulfonate
Buzulfan
C.B. 2041
C6H14O6S2
CB 2041
CCRIS 418
CHEBI:28901
CHEMBL820
CID2478
Citosulfan
CPD000058613
D002066
D00248
DB01008
DivK1c_000847
EINECS 200-250-2
FT-0083567
G.T. 41
glaxo Wellcome brand OF busulfan
Glaxo Wellcome Brand of Busulfan
GlaxoSmithKline brand OF busulfan
GlaxoSmithKline Brand of Busulfan
Glyzophrol
|
GT 2041
GT 41
HMS1920I07
HMS2091O09
HMS502K09
HSDB 7605
I09-1371
IDI1_000847
InChI=1/C6H14O6S2/c1-13(7,8)11-5-3-4-6-12-14(2,9)10/h3-6H2,1-2H3
KBio1_000847
KBio2_000512
KBio2_003080
KBio2_005648
KBio3_001420
KBioGR_000698
KBioSS_000512
Leucosulfan
Leucosulphan
LS-1358
Mablin
Methanesulfonic
Methanesulfonic acid, tetram ethylene ester
Methanesulfonic acid, tetramethylene ester
Mielevcin
Mielosan
Mielucin
Milecitan
Mileran
Misulban
Mitosan
Mitostan
MLS001076666
MolPort-001-783-406
Myeleukon
Myeloleukon
Myelosan
Myelosanum
Mylecytan
Myleran
Myléran
MYLERAN (TN)
Myleran tablets
Myleran Tablets
Myleran, Busulfex, Busulfan
Mylerlan
n-Butane-1,3-di(methylsulfonate)
N-Butane-1,3-di(methylsulfonate)
NCGC00090905-01
NCGC00090905-02
NCGC00090905-03
NCGC00090905-04
NCGC00090905-05
NCGC00090905-06
NCGC00090905-07
NCI60_041640
NCI-C01592
NCIMech_000192
NINDS_000847
NSC 750
NSC750
NSC-750
NSC-750sulphabutin
Orphan brand OF busulfan
Orphan Brand of Busulfan
Prestwick_989
S1692_Selleck
SAM002554887
SMR000058613
SPBio_000253
Spectrum_000092
SPECTRUM1500152
Spectrum2_000067
Spectrum3_000320
Spectrum4_000259
Spectrum5_000928
ST50825921
Sulfabutin
Sulfabutin (VAN)
Sulphabutin
Tetramethylene {bis[methanesulfonate]}
Tetramethylene bis(methanesulfonate)
Tetramethylene bis(methanesulfonic acid)
Tetramethylene bis(methanesulphonate)
Tetramethylene bis(methanesulphonic acid)
Tetramethylene bis[methanesulfonate]
Tetramethylene dimethane sulfonate
Tetramethylene Dimethane Sulfonate
Tetramethylenester kyseliny methansulfonove
Tetramethylenester Kyseliny Methansulfonove
Tetramethylenester kyseliny methansulfonove [Czech]
UNII-G1LN9045DK
Wellcome brand OF busulfan
Wellcome Brand of Busulfan
Wellcome, busulfan
Wellcome, Busulfan
WLN: WS1&O4OSW1
X 149
|
|
| 14 |
|
Vidarabine |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
24356-66-9 |
32326
21704
|
|
Synonyms:
(+)-Cyclaradine
.beta.-Adenosine
.beta.-D-Adenosine
1odi
2-(6-amino-PURIN-9-yl)-5-hydroxymethyl-tetrahydro-furan-3,4-diol
2-(6-AMINO-purin-9-yl)-5-hydroxymethyl-tetrahydro-furan-3,4-diol
2946-52-3
2fqy
2gl0
30143-02-3
3080-29-3
3228-71-5
4005-33-8
46946-45-6
46969-16-8
524-69-6
5536-17-4
58-61-7
9 beta Arabinofuranosyladenine
9 beta D Arabinofuranosyladenine
9-Arabinosyladenine
9-b-D-Arabinofuranosyl-9H-purin-6-amine
9-b-D-Arabinofuranosyladenine
9-beta-Arabinofuranosyladenine
9-beta-D-Arabinofuranosyl-9H-purin-6-amine
9-beta-D-arabinofuranosyl-adenine
9-beta-D-Arabinofuranosyladenine
9-beta-D-Arabinofuranosyl-adenine
9-β-D-arabinofuranosyl-9H-purin-6-amine
9-β-D-arabinofuranosyladenine
A 9251
a, alpha-Ara
a, Ara
a, beta-Ara
A0152
A4036_SIGMA
A4676_SIGMA
A5762_SIGMA
A9251_SIGMA
AC1L18OL
AC1L1U8O
AC1L2IWM
AC1L2SCM
AC1O4WIN
AC1O8PY7
AC1Q1ID3
AC1Q4Y1Z
AC1Q52XU
Adenine arabinoside
Adenine nucleoside
Adenine riboside
Adenine xyloside
adenine-D-ribose
Adenocard
Adenocard (TN)
Adenocard, Adenosine
Adenocor
Adenoscan
Adenoscan (TN)
Adenosin
Adenosin [German]
adenosine
Adenosine (JAN/USP)
Adenosine [USAN:BAN]
Adenosine arabinose
ADENOSINE, U.S.P.
Adenosine-8-14C
Adensoine
Ade-Rib
ADN
AI3-52413
AI3-52821
alpha Ara a
alpha D Arabinofuranosyladenine
alpha-Ara a
alpha-Ara A
alpha-D-Arabinofuranosyladenine
Ambap5536-17-4
AR-1H6029
Ara a
Ara A
Ara-a
Ara-A
ARA-A NSC 247519
Araadenosine
Ara-ATP
Arabinofuranosyladenine
Arabinoside adenine
Arabinoside, adenine
Arabinosyl adenine
Arabinosyladenine
Arabinosyl-adenine
Arasena-A
Armes
Armes (TN)
BB_NC-0565
beta Ara a
beta-Adenosine
beta-Ara a
beta-Ara A
beta-D-Adenosine
Bio1_000437
Bio1_000926
Bio1_001415
bmse000061
Boniton
BPBio1_000898
BRN 0624881
BSPBio_000816
BSPBio_001796
BSPBio_002000
C00212
CAS-5536-17-4
Caswell No. 010B
CCRIS 2557
CCRIS 3383
CHEBI:136932
CHEBI:16335
CHEBI:45327
CHEMBL1090
CHEMBL20247
CHEMBL477
CI 673
CI-673
CID102198
CID191
CID21704
CID60961
CID6420052
CID6713976
CPD000471872
D000241
D00045
D06298
DB00640
DivK1c_000191
EINECS 200-389-9
EINECS 217-911-6
|
EINECS 226-893-9
EU-0100123
FT-0082881
HMS1570I18
HMS1920A13
HMS1921K05
HMS2090F06
HMS2091G13
HMS2092C16
HMS500J13
HSDB 6514
I01-1121
IDI1_000191
KBio1_000191
KBio2_002418
KBio2_004986
KBio2_007554
KBio3_001296
KBio3_001500
KBioGR_001224
KBioSS_002424
L000094
Lopac0_000123
LS-15059
LS-15085
MEDR-640
MLS000069638
MLS000699527
MLS001066352
MLS001333133
MLS001333134
MLS002153227
MLS002153992
MolPort-001-785-903
MolPort-001-838-229
MolPort-003-666-308
Monarch brand OF vidarabine
Myocol
NCGC00016656-01
NCGC00023673-03
NCGC00023673-04
NCGC00023673-05
NCGC00023673-06
NCGC00023673-07
NCGC00094579-01
NCGC00094579-02
NCGC00094579-03
NCGC00094579-04
NCGC00178869-01
NCGC00179417-01
nchembio.143-comp9
nchembio.186-comp109
nchembio.64-comp4
nchembio706-5
NCI60_003823
NCI60_037192
NCIOpen2_003303
NCIOpen2_005376
NINDS_000191
NSC 247519
NSC 404241
NSC 627048
NSC 7359
NSC 7652
NSC247519
NSC404241
NSC-404241
NSC627048
NSC70422
NSC7359
NSC7652
NSC80832
NSC87676
NSC91041
Nucleocardyl
Pallacor
Parke davis brand OF vidarabine
PDSP1_001036
PDSP2_001020
Polyadenosine
Polyriboadenosine
Prestwick_983
Prestwick0_000768
Prestwick1_000768
Prestwick2_000768
Prestwick3_000768
RAB
S1647_Selleck
S1784_Selleck
SAM002564191
Sandesin
SMP1_000312
SMR000058216
SMR000225041
SMR000471872
SMR001233326
SPBio_001194
SPBio_001491
SPBio_002755
Spectrum_001894
SPECTRUM1500107
SPECTRUM1500609
Spectrum2_001257
Spectrum2_001336
Spectrum3_000288
Spectrum3_000580
Spectrum4_000782
Spectrum5_001429
Spongoadenosine
SR 96225
SR-96225
STK361815
SUN-Y4001
TL8003749
UNII-3XQD2MEW34
UNII-K72T3FS567
USAF CB-10
V0098
Vidarabin
Vidarabina
Vidarabina [DCIT]
Vidarabine
Vidarabine (JAN)
Vidarabine anhydrous
Vidarabinum
Vira a
Vira ATM
Vira-a
ViraA
Vira-A
Vira-A, Vidarabine
VIRDARABINE
XA
Xylosyl A
Xylosyladenine
ZINC00970363
ZINC02169830
|
|
| 15 |
|
Apixaban |
Approved |
Phase 4,Phase 3,Phase 2 |
|
503612-47-3 |
10182969
|
|
Synonyms:
1-(4-Methoxyphenyl)-7-oxo-6-[4-(2-oxopiperidin-1-yl)phenyl]-4,5,6,7-tetrahyd
2p16
503612-47-3
AKOS005146204
Apixaban
apixabán
Apixaban (JAN/USAN/INN)
apixabanum
BMS 562247-01
BMS-562247
BMS-562247-01
|
BMS-562247-01, Apixaban
CHEBI:49620
CHEMBL231779
CID10182969
D03213
DB07828
Eliquis
GG2
ro-1H-pyrazolo[3,4-c]pyridine-3-carboxylic acid amide
S1593_Selleck
UNII-3Z9Y7UWC1J
|
|
| 16 |
|
Iron |
Approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
7439-89-6 |
23925
|
|
Synonyms:
02583_FLUKA
12310_ALDRICH
12310_RIEDEL
129048-51-7
14067-02-8
161135-39-3
190454-13-8
195161-83-2
199281-22-6
209309_ALDRICH
209309_SIAL
255637_ALDRICH
266213_ALDRICH
266256_ALDRICH
267945_ALDRICH
267953_ALDRICH
26Fe
338141_ALDRICH
356808_ALDRICH
356824_ALDRICH
356832_ALDRICH
39344-71-3
3ZhP
413054_ALDRICH
443783-52-6
44890_ALDRICH
44890_FLUKA
675141-17-0
70884-35-4
73135-38-3
7439-89-6
8011-79-8
8053-60-9
AC1L2N38
Ancor B
Ancor en 80/150
armco Iron
Armco iron
Atomel 28
Atomel 300M200
Atomel 500M
Atomel 95
Atomiron 44MR
Atomiron 5M
Atomiron AFP 25
Atomiron AFP 5
ATW 230
ATW 432
C00023
C3518_SIAL
C3518_SIGMA
Carbonyl iron
CCRIS 1580
CHEBI:18248
CID23925
Copy Powder CS 105-175
D007501
DB01592
Diseases (animal), iron overload
Diseases, iron overload
DSP 1000
DSP 128B
DSP 135
DSP 135C
DSP 138
Ed-In-Sol
EF 1000
EF 250
EFV 200/300
EFV 250
EFV 250/400
EINECS 231-096-4
Eisen
Electrolytic iron
F 60 (metal)
Fe
FE
FE (II) ion
Fe(2+)
Fe(II)
Fe1+
|
Fe-40
fer
Feronate
Ferretts
Ferro-Caps
Ferro-Time
Ferrous ion
ferrous iron
Ferrousal
Ferrovac e
Ferrovac E
Ferrum
Ferrum metallicum
FT 3 (element)
GS 6
Hematite
Hemocyte
HF 2 (element)
hierro
Hierro
HL (iron)
Hoeganaes ATW 230
Hoeganaes EH
HQ (metal)
HS (iron)
HS 4849
HSDB 604
Infed
IRMM524A_FLUKA
IRMM524B_FLUKA
IRON
Iron (Fe)
Iron (Fe1+)
Iron ion (Fe+)
Iron ion(1+)
Iron ion(2+)
Iron monocation
Iron powder
Iron standard for AAS
Iron(1+)
Iron(1+) ion
Iron(III) nitrate solution
Iron, carbonyl
Iron, electrolytic
Iron, elemental
Iron, ion (Fe1+)
Iron, ion (Fe1+) (8CI,9CI)
Iron, reduced
Limonite
LOHA
LS-3196
Magnetite
Malleable iron
Metopirone
Metyrapone
MolPort-003-925-001
NC 100
PZh1M1
PZh-1M3
PZh-2
PZh2M
PZH2m
PZh2M1
PZh2M2
PZh3
PZh3M
PZh4M
PZhO
PZHO
Reduced iron
Remko
Siderol
Suy-b 2
SUY-B 2
Taconite
UNII-E1UOL152H7
Venofer
Vitedyn-Slo
Wrought iron
Yieronia
|
|
| 17 |
|
Daratumumab |
Approved |
Phase 4,Phase 2,Phase 3,Phase 1 |
|
945721-28-8 |
|
|
Synonyms:
|
| 18 |
|
Mesna |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1 |
|
3375-50-6 |
598
|
|
Synonyms:
1-THIOETHANEsulfonate
1-THIOETHANEsulfonIC ACID
1-THIOETHANEsulphonate
1-THIOETHANEsulphonic acid
2 Mercaptoethanesulfonate
2-Mercaptoethane
2-Mercaptoethanesulfonate
2-mercaptoethanesulfonic acid
2-Mercaptoethanesulfonic acid
2-Mercaptoethanesulphonate
2-Mercaptoethanesulphonate, sodium
2-mercaptoethanesulphonic acid
2-Mercaptoethanesulphonic acid
2-mercaptoethylsulfonate
2-Mercaptoethylsulfonate
2-Mercaptoethylsulfonic acid
2-Mercaptoethylsulphonate
2-Mercaptoethylsulphonic acid
2-sulfanylethylsulfonate
2-Sulfanylethylsulfonate
2-Sulfanylethylsulfonic acid
2-Sulphanylethylsulphonate
2-Sulphanylethylsulphonic acid
ASTA D 7093
ASTA medica brand OF mesna
ASTAD 7093
ASTA-D 7093
beta-Mercaptoethanesulfonate
beta-Mercaptoethanesulfonic acid
beta-Mercaptoethanesulphonate
beta-Mercaptoethanesulphonic acid
b-Mercaptoethanesulfonate
b-Mercaptoethanesulfonic acid
b-Mercaptoethanesulphonate
b-Mercaptoethanesulphonic acid
|
Bristol myers squibb brand OF mesna
Bristol-myers squibb brand OF mesna
Cell pharm brand OF mesna
Coenzima m
Coenzima M
Coenzym m
Coenzym M
Coenzyme m
CoM
HS-CoM
Kendrick brand OF mesna
MESNA cell
Mesna kendrick brand
Mesna sanfer brand
MESNA-cell
Mesnex
Mesnum
Mistabron
Mistabronco
Mitexan
Mucofluid
reduced coenzyme M
Reduced coenzyme m
reduced CoM
Reduced com
Sanfer brand OF mesna
Sodium 2-mercaptoethanesulphonate
UCB brand OF mesna
Uromitexan
Ziken
β-mercaptoethanesulfonate
β-mercaptoethanesulfonic acid
β-mercaptoethanesulphonate
β-mercaptoethanesulphonic acid
|
|
| 19 |
|
Phentolamine |
Approved |
Phase 4 |
|
50-60-2 |
5775
|
|
Synonyms:
2-((N-(m-Hydroxyphenyl)-p-toluidino)methyl)-2-imidazoline
2-(m-Hydroxy-N-p-tolylanilinomethyl)-2-imidazoline
2-(N-(m-Hydroxyphenyl)-p-toluidinomethyl)imidazoline
2-(N-(m-Hydroxyphenyl)-P-toluidinomethyl)imidazoline
2-(N'-p-Tolyl-N'-m-hydroxyphenylaminomethyl)-2-imidazoline
3-[(4,5-dihydro-1H-imidazol-2-ylmethyl)(4-methylphenyl)amino]phenol
3-[N-(4,5-dihydro-1H-imidazol-2-ylmethyl)-4-methylanilino]phenol
50-60-2
5-25-09-00365 (Beilstein Handbook Reference)
65-28-1 (mesylate (salt))
73-05-2 (mono-hydrochloride)
AC1L1L3Z
AC1Q2KIW
AKOS004119917
Alliance brand OF phentolamine mesylate
BCBcMAP01_000014
BPBio1_000307
BRD-K90333595-001-02-8
BRD-K90333595-003-04-0
BRN 0272944
BSPBio_000279
BSPBio_001435
BSPBio_002496
C 7337
C 7337 Ciba
C17H19N3O
CAS-73-05-2
CHEBI:120131
CHEMBL597
CID5775
D08362
DB00692
Dibasin
DivK1c_000807
EINECS 200-053-1
Fentolamin
Fentolamina
Fentolamina [INN-Spanish]
HMS1791H17
HMS1989H17
HMS2089E03
HSDB 3382
IDI1_000807
KBio1_000807
KBio2_000477
KBio2_003045
KBio2_005613
KBio3_001716
KBioGR_001338
KBioSS_000477
L001116
Lopac0_000982
LS-104396
Mesilate, phentolamine
Mesylate, phentolamine
Methanesulfonate, phentolamine
MLS000040874
|
MLS001201741
MolPort-001-783-569
mono-Hydrochloride, phentolamine
NCGC00016311-01
NCGC00016311-02
NCGC00016311-03
NCGC00016311-15
NCGC00021804-06
NCGC00021804-07
NCGC00021804-08
NCGC00021804-09
NCGC00021804-10
nchembio705-6
NINDS_000807
Novartis brand OF phentolamine mesylate
Paladin brand OF phentolamine mesylate
Phenotolamine
Phentalamine
Phentolamin
phentolamine
Phentolamine
Phentolamine (INN)
Phentolamine [INN:BAN]
Phentolamine mesilate
Phentolamine mesylate
Phentolamine mesylate [USAN]
Phentolamine mesylic acid
Phentolamine methanesulfonate
Phentolamine mono hydrochloride
Phentolamine mono-hydrochloride
Phentolamine, methyl sulfonate
Phentolaminum
Phentolaminum [INN-Latin]
Prestwick0_000230
Prestwick1_000230
Prestwick2_000230
Prestwick3_000230
Regitin
Regitina
Regitine
Regitipe
Regityn
Rogitine
Schering-plough brand OF phentolamine mesylate
SMP1_000236
SMR000058051
SPBio_002200
Spectrum_000077
Spectrum3_000788
Spectrum4_000899
Spectrum5_001704
STK802099
STOCK4S-00358
UNII-Z468598HBV
Vesomax
Z-Max
|
|
| 20 |
|
Thiotepa |
Approved, Investigational |
Phase 4,Phase 2,Phase 1,Not Applicable |
|
52-24-4 |
5453
|
|
Synonyms:
Girostan
Tepadina
Tespa
Tespamin
thio Tepa
|
Thiophosphamide
Thioplex
thio-Tepa
Triethylenethiophosphoramide
Tris(1-aziridinyl)phosphine sulfide
|
|
| 21 |
|
Ixazomib |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1 |
|
1072833-77-2 |
|
| 22 |
|
Ofloxacin |
Approved |
Phase 4,Phase 3,Phase 2 |
|
82419-36-1 |
4583
|
|
Synonyms:
( -)-9-Fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido(1,2,3-de)(1,4)benzoxazin-6-carbonsaeure
(+-)-9-Fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido(1,2,3-de)-1,4-benzoxazine-6-carboxylic acid
(+/-)-9-Fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperaz inyl)-7-oxo-7H-pyrido(1,2,3-de)-1,4-benzoxazine-6-carboxylic acid
(+/-)-9-Fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7- -oxo-7H-pyrido(1,2,3-de)- -1,4-benzoxazine-6-carboxylic acid
(+/-)-9-Fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido[1,2,3-de]-1,4-benzoxazine-6-carboxylic acid
(+/-)-Floxin
118120-51-7 (hydrochloride)
33703_FLUKA
33703_RIEDEL
82419-36-1
83380-47-6
85344-55-4
8-fluoro-3-Methyl-9-(4-methyl-piperazin-1-yl)-6-oxo-2,3-dihydro-6H-1-oxa-3a-aza-phenalene-5-carboxylate
8-fluoro-3-Methyl-9-(4-methyl-piperazin-1-yl)-6-oxo-2,3-dihydro-6H-1-oxa-3a-aza-phenalene-5-carboxylic acid
8-Fluoro-3-methyl-9-(4-methyl-piperazin-1-yl)-6-oxo-2,3-dihydro-6H-1-oxa-3a-aza-phenalene-5-carboxylic acid
9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid
AB00513820
AC1L1IHM
AC-7616
AKOS001033517
Bactocin
BB_SC-1252
BPBio1_000345
BRD-A24228527-001-05-9
BRN 3657947
BSPBio_000313
BSPBio_003117
C07321
C18H20FN3O4
CCRIS 5233
CHEBI:7731
CHEMBL4
CID4583
CPD000058192
D00453
Danoflox
DB01165
DEXTROFLOXACINE
DivK1c_000721
DL 8280
DL-8280
DL-8280, HOE-280, Exocin, Flobacin, Floxin, Floxil, Monoflocet, Ofloxacin
Effexin
EU-0100904
Exocin
Exocine
Flobacin
Flodemex
Flotavid
Flovid
Floxal
Floxil
Floxin
Floxin (TN)
FLOXIN IN DEXTROSE 5%
FLOXIN IN DEXTROSE 5% IN PLASTIC CONTAINER
Floxin otic
Floxstat
Fugacin
HMS1568P15
HMS1921H12
HMS2090F07
HMS2092B10
HMS502E03
Hoe 280
HOE 280
Hoe-280
I06-0112
I06-0380
IDI1_000721
Inoflox
KBio1_000721
KBio2_001666
KBio2_004234
KBio2_006802
KBio3_002617
KBioGR_000667
KBioSS_001666
Kinflocin
Kinoxacin
Liflox
Lopac0_000904
Loxinter
LS-133259
Marfloxacin
Medofloxine
Mergexin
MLS000028749
MLS001074203
MolPort-000-422-241
MolPort-000-873-068
NCGC00015772-02
NCGC00015772-10
|
NCGC00094219-01
NCGC00094219-02
NCGC00094219-03
NCGC00094219-04
NCGC00094219-05
NCGC00094219-06
NCGC00178284-01
NCGC00178284-02
NINDS_000721
Novecin
NSC727071
Nufafloqo
O 8757
O8757_SIGMA
Obide
Occidal
Ocuflox
Ofcin
Oflin
Oflocee
Oflocet
Oflocin
Oflodal
Oflodex
Oflodura
Oflox
O-Flox
ofloxacin
Ofloxacin (JP15/USP/INN)
Ofloxacin [USAN:BAN:INN:JAN]
Ofloxacin hydrochloride
Ofloxacin Otic
Ofloxacin, (S)-Isomer
Ofloxacina
Ofloxacina [DCIT]
Ofloxacine
Ofloxacine [French]
Ofloxacino
Ofloxacino [Spanish]
Ofloxacinum
Ofloxacinum [Latin]
Ofloxin
OFLX
Ofus
OFX
Onexacin
Operan
Oprea1_242882
ORF 18489
ORF-28489
Orocin
Otonil
Oxaldin
Pharflox
Praxin
Prestwick0_000237
Prestwick1_000237
Prestwick2_000237
Prestwick3_000237
PT 01
Puiritol
Qinolon
Qipro
Quinolon
Quotavil
Rilox
Ru-43280
S1463_Selleck
SAM002264629
Sinflo
SMR000058192
SPBio_001387
SPBio_002234
Spectrum_001186
SPECTRUM1502044
Spectrum2_001464
Spectrum3_001499
Spectrum4_000324
Spectrum5_001063
STK256723
Tabrin
Taravid
Tariflox
Tarivid
Telbit
Tructum
UNII-A4P49JAZ9H
Uro Tarivid
Viotisone
Visiren
WP-0405
XED
Zanocin
|
|
| 23 |
|
Levofloxacin |
Approved, Investigational |
Phase 4,Phase 3,Phase 2 |
|
100986-85-4 |
149096
|
|
Synonyms:
(−
(-)-(S)-9-Fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido(1,2,3-de)-1,4-benzoxazine-6-carboxylic acid
(-)-(S)-9-fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7Hpyrido[1,2,3-de]-1,4-benzoxazine-6-carboxylic acid hemihydrate
(-)-(S)-9-fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyridol[1,2,3-de]-1,4-benzoxazine-6-carboxylic acid hemihydrate
(-)-Ofloxacin
(3S)-(-)-9-fluoro-3-Methyl-10-(4-methyl-1-piperazinyl)-7-oxo-2,3-dihydro-7H-pyrido[1,2,3-de][1,4]benzoxazine-6-carboxylate
(3S)-(-)-9-fluoro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-2,3-dihydro-7H-pyrido[1,2,3-de][1,4]benzoxazine-6-carboxylic acid
(3S)-(-)-9-fluoro-3-Methyl-10-(4-methyl-1-piperazinyl)-7-oxo-2,3-dihydro-7H-pyrido[1,2,3-de][1,4]benzoxazine-6-carboxylic acid
(3S)-9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid
(R)-9-Fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido(1,2,3-de)-1,4-benzoxazine-6-carboxylic acid
(R)-isomer
(S)-(-)-9-fluoro-3-Methyl-10-(4-methyl-1-piperazinyl)-7-oxo-2,3-dihydro-7H-pyrido[1,2,3-de][1,4]benzooxazine-6-carboxylate
(S)-(-)-9-fluoro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-2,3-dihydro-7H-pyrido[1,2,3-de][1,4]benzooxazine-6-carboxylic acid
(S)-(-)-9-fluoro-3-Methyl-10-(4-methyl-1-piperazinyl)-7-oxo-2,3-dihydro-7H-pyrido[1,2,3-de][1,4]benzooxazine-6-carboxylic acid
(S)-(-)-Ofloxacin
(S)-9-fluoro-2,3-dihydro-3-Methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido(1,2,3-de)-1,4-benzoxazine-6-carboxylate
(S)-9-fluoro-2,3-dihydro-3-Methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido(1,2,3-de)-1,4-benzoxazine-6-carboxylic acid
(S)-9-Fluoro-2,3-dihydro-3-methyl-10-(4-methyl-1-piperazinyl)-7-oxo-7H-pyrido(1,2,3-de)-1,4-benzoxazine-6-carboxylic acid
(S)-Ofloxacin
)-Ofloxacin
100986-85-4
100986-86-5
28266_FLUKA
28266_SIGMA
AC1L3YF8
AC-7593
Aeroquin
Ambap100986-85-4
Anhydrous, levofloxacin
BRD-K09471561-001-06-7
BSPBio_002689
C07660
C18H20FN3O4
C18H20FN3O4.H2O
CCRIS 4073
CCRIS 4074
CHEMBL33
CID149096
CPD000466387
Cravit
Cravit (TN)
Cravit Ophthalmic
D08120
DB01137
d-Levofloxacin
DR 3354
DR3355
DR-3355
DR-3355: L-isomer of ofloxacin
Elequine
Floxacin
Floxel
Floxin
HMS1922J07
HMS2051G04
HMS2090O10
HMS2093E18
HR 355
HR-355
Iquix
KBio2_002199
|
KBio2_004767
KBio2_007335
KBio3_001909
KBioGR_001605
KBioSS_002199
L0193
Leroxacin
Lesacin
Levaquin
LEVAQUIN IN DEXTROSE 5% IN PLASTIC CONTAINER
LEVOFLOXACIN
Levofloxacin (INN)
Levofloxacin [USAN:INN:JAN]
Levofloxacin anhydrous
Levofloxacin hydrate
Levofloxacin tablet, suspension or intravenous
Levofloxacine
Levofloxacine [INN-French]
Levofloxacino
Levofloxacino [INN-Spanish]
Levofloxacinum
Levofloxacinum [INN-Latin]
Levokacin
Levox
Levoxacin
LFX
L-Ofloxacin
LS-133260
LS-171761
LVX
MLS000759524
MLS001165709
MLS001423977
MolPort-002-885-835
Mosardal
MP-376
NCGC00178529-01
Nofaxin
Ofloxacin
Ofloxacin S-(-)-form
Ofloxacin, (S)-isomer
Oftaquix
Quixin
Reskuin
R-Ofloxacin
RWJ 25213-097
RWJ-25213
S-(-)-Ofloxacin
S1940_Selleck
SAM001246758
SMR000466387
SPBio_001891
Spectrum_001719
SPECTRUM1504260
Spectrum2_001676
Spectrum3_000995
Spectrum4_001123
Spectrum5_001438
Tavanic
Volequin
|
|
| 24 |
|
Liraglutide |
Approved |
Phase 4 |
|
204656-20-2 |
44147092
|
|
Synonyms:
204656-20-2
Arg34Lys26-(N-ε-(γ-Glu(N-α-hexadecanoyl)))-GLP-1[7-37]
C439759
Liraglutida
Liraglutida [INN-Spanish]
Liraglutide
Liraglutide (genetical recombination)
Liraglutide (rDNA origin)
Liraglutide [USAN:INN]
Liraglutide recombinant
Liraglutidum
Liraglutidum [INN-Latin]
|
N26-(Hexadecanoyl-gamma-glutamyle)-(34-arginine)GLP-1-(7-37)-peptide
N26-(Hexadecanoyl-gamma-glutamyle)-(34-arginine)glucagon-like-peptide-1-(7-37)-peptide
N²⁶-(hexadecanoyl-gamma-glutamyle)-[34-arginine]GLP-1-(7-37)-peptide
N²⁶-(N-Hexadecanoyl-L-gamma-glutamyl)-[34-L-arginine]glucagon-like peptide 1-(7-37)-peptide
nn 2211
NN 2211
nn2211
NN2211
NN-2211
UNII-839I73S42A
victoza
Victoza
|
|
| 25 |
|
Serine |
Approved, Nutraceutical |
Phase 4,Phase 3,Phase 2,Phase 1 |
|
56-45-1 |
5951
|
|
Synonyms:
(-)-Serine
(2S)-2-amino-3-Hydroxypropanoate
(2S)-2-amino-3-Hydroxypropanoic acid
(S)-(-)-Serine
(S)-2-amino-3-Hydroxypropanoate
(S)-2-amino-3-Hydroxy-propanoate
(S)-2-amino-3-Hydroxypropanoic acid
(S)-2-amino-3-Hydroxy-propanoic acid
(S)-2-Amino-3-hydroxypropanoic acid
(S)-a-amino-b-Hydroxypropionate
(S)-a-amino-b-Hydroxypropionic acid
(S)-alpha-amino-beta-Hydroxypropionate
(S)-alpha-amino-beta-Hydroxypropionic acid
(S)-b-amino-3-Hydroxypropionate
(S)-b-amino-3-Hydroxypropionic acid
(S)-beta-amino-3-Hydroxypropionate
(S)-beta-amino-3-Hydroxypropionic acid
(S)-Serine
(S)-α-amino-β-hydroxypropionate
(S)-α-amino-β-hydroxypropionic acid
2-amino-3-Hydroxypropanoate
2-amino-3-Hydroxypropanoic acid
3-Hydroxy-L-alanine
|
alpha-Amino-beta-hydroxypropionic acid
beta-Hydroxyalanine
beta-Hydroxy-L-alanine
b-Hydroxyalanine
b-Hydroxy-L-alanine
L Serine
L-(-)-Serine
L-2-amino-3-Hydroxypropionate
L-2-amino-3-Hydroxypropionic acid
L-3-Hydroxy-2-aminopropionate
L-3-Hydroxy-2-aminopropionic acid
L-3-Hydroxy-alanine
L-Ser
L-Serin
L-Serine
S
Ser
Serina
SERINE
Serinum
β-hydroxyalanine
β-hydroxy-L-alanine
|
|
| 26 |
|
Glycine |
Approved, Nutraceutical, Vet_approved |
Phase 4,Phase 3,Phase 2,Phase 1 |
|
56-40-6 |
750
|
|
Synonyms:
(1-13c)glycinato
(15N)Glycine
15527_RIEDEL
15527_SIAL
15743-44-9 (mono-potassium salt)
17829-66-2 (cobalt salt)
18875-39-3
2,2-dialkylglycines
2311-65-1
25718-94-9
29728-27-6 (monoammonium salt)
2-Aminoacetate
2-Aminoacetic acid
32817-15-5 (copper salt)
33226_RIEDEL
33226_SIAL
33242-26-1 (calcium salt)
35947-07-0 (calcium salt (2:1))
410225_SIAL
50046_FLUKA
50046_SIGMA
513-29-1 (sulfate (3:1))
52955-63-2
56-40-6
57678-19-0
6000-43-7 (hydrochloride)
6000-44-8 (mono-hydrochloride salt)
63183-41-5 (hydrochloride hydrogen carbonate)
71295-98-2 (phosphate (1:1))
7490-95-1 (hydrochloride (2:1)
7490-95-1 (hydrochloride (2:1))
7575-55-5
848646-45-7
87867-94-5
AB1002628
AB-131/40217813
AC1L19XW
AC1Q28JW
AC1Q53O0
Acid, aminoacetic
Acide aminoacetique
Acide aminoacetique [INN-French]
Acido aminoacetico
Acido aminoacetico [INN-Spanish]
Acidum aminoaceticum
Acidum aminoaceticum [INN-Latin]
Aciport
AI3-04085
AKOS000119626
amino-Acetate
Aminoacetate
aminoacetic acid
amino-Acetic acid
Aminoacetic acid
AMINOACETIC ACID 1.5% IN PLASTIC CONTAINER
Aminoazijnzuur
Aminoessigsaeure
Aminoessigsäure
Aminoethanoate
Aminoethanoic acid
Amitone
an alpha amino acid ester
AR-1A0345
AR-1A0532
B72BA06C-60E9-4A83-A24A-A2D7F465BB65
Biomol-NT_000195
bmse000089
BPBio1_001222
C00037
Calcium salt glycine
CCRIS 5915
CHEBI:15428
CHEBI:15705
CHEBI:16228
CHEMBL773
CID750
Cobalt salt glycine
Copper salt glycine
Corilin
CPD-8569
D00011
DB00145
EINECS 200-272-2
FEMA No. 3287
FT-0083159
G
G0099
G0317
G5417_SIGMA
|
G5523_SIGMA
G7126_SIGMA
G7403_SIGMA
G8790_SIGMA
G8898_SIGMA
Glicina
Glicina [INN-Spanish]
Glicoamin
gly
Gly
GLY (IUPAC abbrev)
Glycin
glycine
Glycine (JP15/USP)
Glycine [INN]
GLYCINE 1.5% IN PLASTIC CONTAINER
Glycine carbonate (1:1), monosodium salt
Glycine carbonate (2:1), monolithium salt
Glycine carbonate (2:1), monopotassium salt
Glycine carbonate (2:1), monosodium salt
Glycine hydrochloride
Glycine hydrochloride (2:1)
Glycine iron sulphate (1:1)
Glycine phosphate
Glycine phosphate (1:1)
Glycine sulfate (3:1)
GLYCINE, ACS
Glycine, calcium salt
Glycine, calcium salt (2:1)
Glycine, cobalt salt
Glycine, copper salt
Glycine, homopolymer (VAN)
Glycine, labeled with carbon-14
Glycine, monoammonium salt
Glycine, monopotasssium salt
Glycine, monosodium salt
Glycine, non-medical
Glycine, sodium hydrogen carbonate
Glycine-UL-14C hydrochloride
Glycinum
Glycinum [INN-Latin]
Glycocoll
Glycolixir
Glycosthene
Glykokoll
Glyzin
Gyn-hydralin
H2N-CH2-COOH
Hampshire glycine
Hgly
H-Gly-OH
HSDB 495
Hydrochloride, glycine
InChI=1/C2H5NO2/c3-1-2(4)5/h1,3H2,(H,4,5
KST-1A2919
KST-1A8102
L001246
L-alpha-amino acids
Leimzucker
L-Glycine
LS-218
MolPort-000-871-607
Monoammonium salt glycine
Monopotasssium salt glycine
Monosodium salt glycine
NCGC00024503-01
NCGC00024503-02
nchem.554-comp2
nchembio.121-comp9
nchembio.145-comp33
nchembio.198-comp12
NChemBio.2007.13-comp1
nchembio.265-comp9
nchembio.266-comp30
NSC 25936
NSC25936
P8791_SIGMA
Padil
Phosphate, glycine
polyglycine
Polyglycine II
S04-0135
Salt glycine, monoammonium
Salt glycine, monosodium
Sucre de gelatine
Tocris-0219
UNII-TE7660XO1C
W328707_ALDRICH
WLN: Z1VQ
|
|
| 27 |
|
Pirarubicin |
Investigational |
Phase 4 |
|
72496-41-4 |
|
|
Synonyms:
Adriamycin, tetrahydropyranyl
Theprubicin
|
|
|
| 28 |
|
Doxil |
Approved June 1999 |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
31703
|
|
Synonyms:
|
|
LipoDox
liposomal doxorubicin
Pegylated Liposomal Doxorubicin Hydrochloride
|
|
| 29 |
|
Angiogenesis Inhibitors |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 30 |
|
Angiogenesis Modulating Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 31 |
|
Peripheral Nervous System Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 32 |
|
Anti-Bacterial Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 33 |
|
Anti-Inflammatory Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 34 |
|
HIV Protease Inhibitors |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 35 |
|
Hormones |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 36 |
|
protease inhibitors |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
|
Synonyms:
|
| 37 |
|
Anti-Infective Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 38 |
|
Autonomic Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 39 |
|
BB 1101 |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 40 |
|
Immunosuppressive Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 41 |
|
Topoisomerase Inhibitors |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 42 |
|
Antineoplastic Agents, Hormonal |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 43 |
|
Hormone Antagonists |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 44 |
|
Immunologic Factors |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 45 |
|
Antibiotics, Antitubercular |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 46 |
|
Antiemetics |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 47 |
|
Gastrointestinal Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 48 |
|
glucocorticoids |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 49 |
|
Hormones, Hormone Substitutes, and Hormone Antagonists |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 50 |
|
Bone Density Conservation Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
Interventional clinical trials:
(show top 50)
(show all 2629)
| # |
Name |
Status |
NCT ID |
Phase |
Drugs |
| 1 |
Efficacy Study of PAD and TAD in Newly Diagnosed Multiple Myeloma |
Unknown status |
NCT01249690
|
Phase 4 |
Bortezomib,Pirarubicin,Dexamethasone;Thalidomide,Pirarubicin,Dexamethasone |
| 2 |
Stage I Multiple Myeloma Treatment |
Unknown status |
NCT00733538
|
Phase 4 |
zometa |
| 3 |
A Study of PAD Versus Velcade, Cyclophosphamide and Dexamethasone (VCD) Treatment in Subjects With Multiple Myeloma |
Unknown status |
NCT01868828
|
Phase 4 |
PAD;VCD |
| 4 |
Treatment With a Scheme With Low Doses of Bortezomib / Melphalan / Prednisone (MPV) in Patients With Multiple Myeloma |
Unknown status |
NCT02773550
|
Phase 4 |
Bortezomib;Melphalan;Prednisone |
| 5 |
Lenalidomide and Dexamethasone With/Without Stem Cell Transplant in Patients With Multiple Myeloma |
Completed |
NCT01731886
|
Phase 4 |
Lenalidomide;Dexamethasone |
| 6 |
A Pharmacokinetic Study of Bortezomib in Taiwanese Participants With Multiple Myeloma |
Completed |
NCT02268890
|
Phase 4 |
Bortezomib |
| 7 |
A Multiple Myeloma Trial in Patients With Bone Metastases |
Completed |
NCT00104104
|
Phase 4 |
zoledronic acid |
| 8 |
Bortezomib/Adriamycine/Melfalan/Prednisone (VAMP)/Thalidomide/Cyclophosphamide/Dexamethasone (TaCyDex) or Bortezomib/Melfalan/Prednisone (V-MP)/TaCyDex) in Refractary or Relapsed Multiple Myeloma |
Completed |
NCT00652041
|
Phase 4 |
Bortezomib;Thalidomide;Bortezomib |
| 9 |
Zoledronic Acid Treatment (Every 4 or 12 Weeks) to Prevent Skeletal Complications in Advanced Multiple Myeloma Patients |
Completed |
NCT00622505
|
Phase 4 |
zoledronic acid |
| 10 |
Evaluation of VELCADE Given as Retreatment to Multiple Myeloma Patients for Efficacy, Safety and Tolerability |
Completed |
NCT00257114
|
Phase 4 |
bortezomib |
| 11 |
Treatment With Zoledronic Acid in Patients With Breast Cancer, Multiple Myeloma, and Prostate Cancer With Cancer Related Bone Lesions |
Completed |
NCT00029224
|
Phase 4 |
zoledronic acid |
| 12 |
REmoval of Free Light Chains. A COmpaRison of Three Different dialyzERs |
Completed |
NCT02950389
|
Phase 4 |
|
| 13 |
PROMPT - Palifermin in Reduction of Oral Mucositis in PBSC Transplantation |
Completed |
NCT00352703
|
Phase 4 |
Kepivance (Palifermin) |
| 14 |
Effect of Epoetin Alfa on Hemoglobin, Symptom Distress, and Quality of Life in Patients Receiving Chemotherapy |
Completed |
NCT00524407
|
Phase 4 |
Epoetin alfa |
| 15 |
Long Term Efficacy and Safety of Zoledronic Acid Treatment in Patients With Bone Metastases |
Completed |
NCT00434447
|
Phase 4 |
Zoledronic acid |
| 16 |
FREE Study - Fracture Reduction Evaluation |
Completed |
NCT00211211
|
Phase 4 |
|
| 17 |
Bone Marrow Transplantation in Treating Patients With Hematologic Cancer |
Completed |
NCT00003398
|
Phase 4 |
cyclophosphamide;thiotepa |
| 18 |
Busulfan Safety/Efficacy as Conditioning Prior to Hematopoietic Cell Transplantation (HCT) |
Completed |
NCT00361140
|
Phase 4 |
Busulfan;Fludarabine |
| 19 |
A Study to Evaluate the Efficacy and Safety of Ixazomib in Combination With Lenalidomide and Dexamethasone in Patients With Relapsed and/or Refractory Multiple Myeloma Initially Treated With an Injection of Proteasome Inhibitor-Based Therapy |
Recruiting |
NCT03416374
|
Phase 4 |
Ixazomib;Bortezomib;Carfilzomib;Lenalidomide;Dexamethasone |
| 20 |
Prolonged Protection From Bone Disease in Multiple Myeloma |
Recruiting |
NCT02286830
|
Phase 4 |
Zoledronic acid |
| 21 |
An Effectiveness and Safety Study of Ixazomib in Combination With Lenalidomide and Dexamethasone (IRD) in Participants With Multiple Myeloma (MM) Previously Receiving a Bortezomib-based Induction Regimen (US MM-6) |
Recruiting |
NCT03173092
|
Phase 4 |
Ixazomib;Lenalidomide;Dexamethasone |
| 22 |
PDD vs PAD to Treat Initially Diagnosed MM |
Recruiting |
NCT02577783
|
Phase 4 |
Chemotherapy with PDD regimen;Chemotherapy with PAD regimen |
| 23 |
Zoledronic Acid in Patients With Multiple Myeloma and Asymptomatic Biochemical Relapse |
Active, not recruiting |
NCT01087008
|
Phase 4 |
zoledronic acid |
| 24 |
Modified Bortezomib-based Combination Therapy for Multiple Myeloma |
Active, not recruiting |
NCT02559154
|
Phase 4 |
Bortezomib;Dexamethasone;Doxorubicin;Cyclophosphamide;Mitoxsnteone;Thalidomide |
| 25 |
Apixaban for Primary Prevention of Venous Thromboembolism in Patients With Multiple Myeloma |
Active, not recruiting |
NCT02958969
|
Phase 4 |
Apixaban;Placebo Oral Tablet |
| 26 |
Pneumococcal Vaccination of Multiple Myeloma Patients on Novel Agents |
Enrolling by invitation |
NCT03619252
|
Phase 4 |
Standard Antibacterial Prophylaxis |
| 27 |
A Study of DARZALEX (Daratumumab) In Indian Participants With Relapsed and Refractory Multiple Myeloma, Whose Prior Therapy Included a Proteasome Inhibitor and an Immunomodulatory Agent |
Not yet recruiting |
NCT03768960
|
Phase 4 |
Daratumumab |
| 28 |
Stem Cell Harvesting Using GCSF Plus Plerxiafor, in First -Line, for Heavily Pre- Treated Pediatric Oncology Patients. |
Not yet recruiting |
NCT02006225
|
Phase 4 |
Plerixafor |
| 29 |
Antigen-Lipid-Driven Monoclonal Gammopathies Targeting Epicardial Fat |
Not yet recruiting |
NCT02920190
|
Phase 4 |
Liraglutide |
| 30 |
Ferric Carboxymaltose for Treatment of Anaemia of Cancer in Subjects With Multiple Myeloma Receiving Chemotherapy |
Terminated |
NCT01100879
|
Phase 4 |
Ferric carboxymaltose |
| 31 |
A Study to Assess the Hematopoyetic Response of Anemic Patients With Hematologic Malignancies Treated With Erythropoietin B |
Terminated |
NCT02608060
|
Phase 4 |
Epoetin Beta |
| 32 |
Evaluation of Vertebral Compression Fracture Fixation With RF Kyphoplasty in Patients With Multiple Myeloma |
Withdrawn |
NCT01410929
|
Phase 4 |
|
| 33 |
Open-label Study, to Evaluate the Safety and Tolerability of Zoledronic Acid in Patients With Bone Lesions Secondary to Multiple Myeloma. |
Withdrawn |
NCT00242528
|
Phase 4 |
Zoledronic acid |
| 34 |
Combination Chemotherapy With or Without Cyclophosphamide and Prednisone in Treating Older Patients With Multiple Myeloma |
Unknown status |
NCT00002653
|
Phase 3 |
carmustine;cyclophosphamide;doxorubicin hydrochloride;melphalan;prednisone |
| 35 |
Chemotherapy With or Without Wobe-Mugos E in Treating Patients With Stage II or Stage III Multiple Myeloma |
Unknown status |
NCT00014339
|
Phase 3 |
Wobe-Mugos E;melphalan;prednisone |
| 36 |
CyBorD vs. PAD in the Treatment of Newly Diagnosed Multiple Myeloma |
Unknown status |
NCT02362165
|
Phase 3 |
Cyclophosphamide;Bortezomib;Dexamethasone;Doxorubicin |
| 37 |
Combination Chemotherapy With or Without Thalidomide in Treating Patients With Multiple Myeloma |
Unknown status |
NCT00028886
|
Phase 3 |
cyclophosphamide;dexamethasone;doxorubicin hydrochloride;melphalan;thalidomide;vincristine sulfate |
| 38 |
Combination Chemotherapy and Interferon Alfa With or Without Bone Marrow or Peripheral Stem Cell Transplantation in Treating Patients With Myeloma |
Unknown status |
NCT00002599
|
Phase 3 |
carmustine;cyclophosphamide;doxorubicin hydrochloride;melphalan;methylprednisolone;prednisone;vincristine sulfate |
| 39 |
High-Dose Melphalan and a Second Stem Cell Transplant or Low-Dose Cyclophosphamide in Treating Patients With Relapsed Multiple Myeloma After Chemotherapy |
Unknown status |
NCT00747877
|
Phase 3 |
cyclophosphamide;melphalan |
| 40 |
Chemotherapy Plus Steroid Therapy in Treating Patients With Multiple Myeloma |
Unknown status |
NCT00003603
|
Phase 3 |
cyclophosphamide;dexamethasone;idarubicin;lomustine;melphalan;prednisolone |
| 41 |
MMVAR - Velcade: Study of Velcade for the Treatment of Myeloma Patients After Autologous Transplantation |
Unknown status |
NCT00256776
|
Phase 3 |
Velcade (Bortezomib);Thalidomide;Dexamethasone |
| 42 |
Evaluation of the Use of Apixaban in Prevnetion of Thromboembolic Disease in Patients With Myeloma Trated With iMiDs |
Unknown status |
NCT02066454
|
Phase 3 |
Apixaban |
| 43 |
Autologous Bone Marrow Transplantation (BMT) Compared With Allogeneic BMT in Multiple Myeloma |
Unknown status |
NCT00998270
|
Phase 2, Phase 3 |
|
| 44 |
Efficacy and Safety of Aprepitant in Subjects With Multiple Myeloma During and After High-dose Chemotherapy |
Unknown status |
NCT00571168
|
Phase 3 |
Emend;Placebo |
| 45 |
VELCADE-Thalidomide-Dexamethasone (VTD) vs Thalidomide-Dexamethasone (TD) Incorporated Into Double Autotransplantation for Untreated Multiple Myeloma (MM) |
Unknown status |
NCT01134484
|
Phase 3 |
Velcade;Thalidomide;Dexamethasone |
| 46 |
Evaluation of Bortezomib Induced Peripheral Neuropathy of Multiple Myeloma (MM) Patients |
Unknown status |
NCT00872352
|
Phase 3 |
|
| 47 |
Comparable Investigation of One Fraction Radiotherapy and Multifraction Radiotherapy in Patients With Multiple Myeloma. |
Unknown status |
NCT02024815
|
Phase 3 |
|
| 48 |
Iberoamerican Protocol With Thalidomide in Patients With Symptomatic Newly Diagnosed Multiple Myeloma Over 65 Years |
Unknown status |
NCT01532856
|
Phase 3 |
Thalidomide, Cyclophosphamide, Dexamethasone;Thalidomide, Dexamethasone;Thalidomide, Melphalan, Prednisone |
| 49 |
Study in Myeloma Patients Newly Diagnosed Treated as an Induction With Velcade-Dex or Velcade (Bortezomib) Thalidomide Dexamethasone (VTD) |
Unknown status |
NCT00910897
|
Phase 3 |
Velcade-Dexamethasone;Velcade-Thalidomide-Dexamethasone |
| 50 |
Hematopoietic Stem Cell Transplantation in Myeloma |
Unknown status |
NCT00415987
|
Phase 2, Phase 3 |
|
Inferred drug relations via
UMLS
73
/
NDF-RT
51
:
Cell-based therapeutics:
Data from LifeMap, the Embryonic Development and Stem Cells Database
Stem-cell-based therapeutic approaches for Myeloma, Multiple:
Embryonic/Adult Cultured Cells Related to Myeloma, Multiple:
Cochrane evidence based reviews: multiple myeloma
|
Rare neurological diseases
