FDA approved drugs:
(show top 50)
(show all 68)
| # |
|
Drug Name |
Active Ingredient(s) 19
|
Company |
Approval Date |
| 1 |
|
Abraxane
19
50
|
PACLITAXEL |
Celgene |
October 2012 |
Disease/s that Drug Treats:non-small cell lung cancer
Indications and Usage:
19
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:
19
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.
|
| 2 |
|
Afinitor
19
50
|
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:
19
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:
19
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.
|
| 3 |
|
Akynzeo
19
50
|
NETUPITANT AND PALONOSETRON (hydrochloride) |
Helsinn |
October 2014 |
Disease/s that Drug Treats:chemotherapy-induced nausea and vomiting
Indications and Usage:
19
AKYNZEO is a fixed combination of netupitant, a substance P/neurokinin 1(NK1) receptor antagonist, and palonosetron, a serotonin-3 (5-HT3) receptorantagonist indicated for the prevention of acute and delayed nausea andvomiting associated with initial and repeat courses of cancer chemotherapy,including, but not limited to, highly emetogenic chemotherapy. Oralpalonosetron prevents nausea and vomiting during the acute phase andnetupitant prevents nausea and vomiting during both the acute and delayedphase after cancer chemotherapy. (1)
DrugBank Targets:
16
1. Substance-P receptor;2. 5-hydroxytryptamine receptor 3A
Mechanism of Action:
19
Target: neurokinin 1 (NK1) receptors/ substance P mediated responses [netupitant] & 5-HT3 receptor [palonosetron]
Action: activator/ inhibitor & agonist
FDA: Netupitant is a selective antagonist of human substance P/neurokinin 1 (NK1) receptors.Palonosetron is a 5-HT3 receptor antagonist with a strong binding affinity for this receptor and little or noaffinity for other receptors. Cancer chemotherapy may be associated with a high incidence of nausea andvomiting, particularly when certain agents, such as cisplatin, are used. 5-HT3 receptors are located on thenerve terminals of the vagus in the periphery and centrally in the chemoreceptor trigger zone of the areapostrema. Chemotherapeutic agents produce nausea and vomiting by stimulating the release of serotoninfrom the enterochromaffin cells of the small intestine. Serotonin then activates 5-HT3 receptors located onvagal afferents to initiate the vomiting reflex. The development of acute emesis is known to depend onserotonin and its 5-HT3 receptors have been demonstrated to selectively stimulate the emetic response.Delayed emesis has been largely associated with the activation of tachykinin family neurokinin 1 (NK1)receptors (broadly distributed in the central and peripheral nervous systems) by substance P. As shown inin vitro and in vivo studies, netupitant inhibits substance P mediated responses.
|
| 4 |
|
Aloxi
19
50
|
PALONOSETRON (hydrochloride) |
MGI Pharma, Helsinn Healthcare |
August 2003 |
Disease/s that Drug Treats:Chemotherapy side effects
Indications and Usage:
19
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:
19
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.
|
| 5 |
|
Arzerra
19
50
|
OFATUMUMAB |
GlaxoSmithKline |
October 2009 |
Disease/s that Drug Treats:chronic lymphocytic leukemia
Indications and Usage:
19
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:
19
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.
|
| 6 |
|
Bexxar
19
50
|
TOSITUMOMAB; IODINE I 131 TOSITUMOMAB |
Corixa |
June 2003 |
Disease/s that Drug Treats:Non-Hodgkin's Lymphoma
Indications and Usage:
19
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:
19
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.
|
| 7 |
|
Degarelix
19
50
|
degarelix |
Ferring Pharmaceuticals |
December of 2008 |
Disease/s that Drug Treats:Prostate Cancer
Indications and Usage:
19
DrugBank Targets:
16
1. Gonadotropin-releasing hormone receptor
Mechanism of Action:
19
Target: Gonadotropin-releasing hormone (GnRH) receptor
Action: antagonist
FDA: -
|
| 8 |
|
Ellence
19
50
|
EPIRUBICIN HYDROCHLORIDE |
Pharmacia & Upjohn |
September 1999 |
Disease/s that Drug Treats:Component of adjuvant therapy in patients with evidence of axillary node tumor involvement for primary breast cancer
Indications and Usage:
19
ELLENCE Injection is an anthracycline topoisomerase II inhibitor indicatedas a component of adjuvant therapy in patients with evidence of axillary nodetumor involvement following resection of primary breast cancer (1).
DrugBank Targets:
16
1. Chromodomain-helicase-DNA-binding protein 1;2. DNA topoisomerase 2-alpha;3. DNA
Mechanism of Action:
19
Target: nucleic acid (DNA and RNA) and protein synthesis
Action: inhibitor
FDA: Epirubicin is an anthracycline cytotoxic agent. Although it is known that anthracyclines can interfere with a number of biochemical andbiological functions within eukaryotic cells, the precise mechanisms of epirubicinâs cytotoxic and/or antiproliferative properties have not beencompletely elucidated.Epirubicin forms a complex with DNA by intercalation of its planar rings between nucleotide base pairs, with consequent inhibition of nucleicacid (DNA and RNA) and protein synthesis.Such intercalation triggers DNA cleavage by topoisomerase II, resulting in cytocidal activity. Epirubicin also inhibits DNA helicase activity,preventing the enzymatic separation of double-stranded DNA and interfering with replication and transcription. Epirubicin is also involved inoxidation/reduction reactions by generating cytotoxic free radicals. The antiproliferative and cytotoxic activity of epirubicin is thought to resultfrom these or other possible mechanisms.Epirubicin is cytotoxic in vitro to a variety of established murine and human cell lines and primary cultures of human tumors. It is also activein vivo against a variety of murine tumors and human xenografts in athymic mice, including breast tumors.
|
| 9 |
|
Emend
19
50
|
APREPITANT FOSAPREPITANT DIMEGLUMINE |
Merck |
March 2003 |
Disease/s that Drug Treats:Chemotherapy-induced Nausea and Vomiting
Indications and Usage:
19
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:
19
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.
|
| 10 |
|
Evista
19
50
|
RALOXIFENE HYDROCHLORIDE |
Eli Lilly |
September 2007 |
Disease/s that Drug Treats:osteoporosis and reduction of breast cancer risk in postmenopausal women
Indications and Usage:
19
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:
19
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.
|
| 11 |
|
Faslodex
19
50
|
FULVESTRANT |
AstraZeneca |
April 2002 |
Disease/s that Drug Treats:Hormone receptor positive metastatic breast cancer
Indications and Usage:
19
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:
19
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.
|
| 12 |
|
Folotyn
19
50
|
PRALATREXATE |
Allos Therapeutics |
September 2009 |
Disease/s that Drug Treats:peripheral T-cell lymphoma
Indications and Usage:
19
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:
19
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.
|
| 13 |
|
Fusilev
19
|
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:
19
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:
19
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.
|
| 14 |
|
Gardasil
19
50
|
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:
19
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:
19
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.
|
| 15 |
|
Gazyva
19
50
|
OBINUTUZUMAB |
Genentech |
October of 2013 |
Disease/s that Drug Treats:previously untreated chronic lymphocytic leukemia
Indications and Usage:
19
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:
19
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.
|
| 16 |
|
Herceptin
19
50
|
TRASTUZUMAB |
Genentech |
October 1998 |
Disease/s that Drug Treats:Breast cancer/gastric cancer
Indications and Usage:
19
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:
19
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.
|
| 17 |
|
Hycamtin
19
50
|
TOPOTECAN HYDROCHLORIDE |
GlaxoSmithKline/ SmithKline Beecham |
October 2007/May 1996 |
Disease/s that Drug Treats:small cell lung cancer/ ovarian cancer
Indications and Usage:
19
HYCAMTIN for injection is a topoisomerase inhibitor indicated for: metastatic carcinoma of the ovary after disease progression on or afterinitial or subsequent chemotherapy. (1.1) small cell lung cancer platinum-sensitive disease in patients whoprogressed after first-line chemotherapy. (1.2) combination therapy with cisplatin for Stage IV-B, recurrent, orpersistent carcinoma of the cervix which is not amenable to curativetreatment. (1.3)
DrugBank Targets:
16
1. DNA topoisomerase 1;2. DNA topoisomerase I, mitochondrial;3. DNA
Mechanism of Action:
19
Target: topoisomerase I
Action: inhibitor
FDA: Topoisomerase I relieves torsional strain in DNA by inducing reversible single-strand breaks.Topotecan binds to the topoisomerase I-DNA complex and prevents re-ligation of these singlestrandbreaks. The cytotoxicity of topotecan is thought to be due to double-strand DNA damageproduced during DNA synthesis, when replication enzymes interact with the ternary complexformed by topotecan, topoisomerase I, and DNA. Mammalian cells cannot efficiently repairthese double-strand breaks.
|
| 18 |
|
Intron A
19
50
|
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:
19
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:
19
Target: intracellular oncogene expression, natural killer and cytotoxic T-cells, microphage, cytokine production
Action: stimulation, induction (unspecified effects on oncogene expression)
FDA: -
|
| 19 |
|
Iressa
19
50
|
GEFITINIB |
AstraZeneca |
May 2003 |
Disease/s that Drug Treats:Non-Small-Cell Lung Cancer
Indications and Usage:
19
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:
19
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.
|
| 20 |
|
Ixempra
19
50
|
IXABEPILONE |
Bristol-Myers Squibb |
October 2007 |
Disease/s that Drug Treats:Breast cancer
Indications and Usage:
19
IXEMPRA, a microtubule inhibitor, in combination with capecitabine isindicated for the treatment of metastatic or locally advanced breastcancer in patients after failure of an anthracycline and a taxane (1). IXEMPRA as monotherapy is indicated for the treatment of metastaticor locally advanced breast cancer in patients after failure of ananthracycline, a taxane, and capecitabine (1).
DrugBank Targets:
16
1. Tubulin beta-3 chain
Mechanism of Action:
19
Target: β-tubulin subunits on microtubules
Action: suppressor of dynamics
FDA: Ixabepilone is a semi-synthetic analog of epothilone B. Ixabepilone binds directlyto β-tubulin subunits on microtubules, leading to suppression of microtubule dynamics.Ixabepilone suppresses the dynamic instability of αβ-II and αβ-III microtubules.Ixabepilone possesses low in vitro susceptibility to multiple tumor resistance mechanisms including efflux transporters, such as MRP-1 and P-glycoprotein (P-gp). Ixabepiloneblocks cells in the mitotic phase of the cell division cycle, leading to cell death.
|
| 21 |
|
Kyprolis
19
50
|
CARFILZOMIB |
Onyx Pharmaceuticals |
July 2012 |
Disease/s that Drug Treats:multiple myeloma
Indications and Usage:
19
Kyprolis is a proteasome inhibitor that is indicated in combination with lenalidomide and dexamethasone for the treatment ofpatients with relapsed multiple myeloma who have received one to threeprior lines of therapy . (1, 14) as a single agent for the treatment of patients with multiple myeloma whohave received at least two prior therapies including bortezomib and animmunomodulatory agent and have demonstrated disease progression on orwithin 60 days of completion of the last therapy. Approval is based onresponse rate. Clinical benefit, such as improvement in survival orsymptoms, has not been verified. (1, 14)
DrugBank Targets:
16
1. Proteasome subunit beta type-5;2. Proteasome subunit beta type-8;3. Proteasome subunit beta type-1;4. Proteasome subunit beta type-9;5. Proteasome subunit beta type-2;6. Proteasome subunit beta type-10
Mechanism of Action:
19
Target: tetrapeptide epoxyketone proteasome
Action: inhibitor
FDA: Carfilzomib is a tetrapeptide epoxyketone proteasome inhibitor that irreversibly binds to theN-terminal threonine-containing active sites of the 20S proteasome, the proteolytic coreparticle within the 26S proteasome. Carfilzomib had antiproliferative and proapoptoticactivities in vitro in solid and hematologic tumor cells. In animals, carfilzomib inhibitedproteasome activity in blood and tissue and delayed tumor growth in models of multiplemyeloma, hematologic, and solid tumors.
|
| 22 |
|
Lazanda
19
|
FENTANYL CITRATE |
Archimedes |
June 2011 |
Disease/s that Drug Treats:breakthrough cancer pain
Indications and Usage:
19
Lazanda is an opioid agonist indicated for the management of breakthrough painin cancer patients 18 years of age and older who are already receiving and whoare tolerant to opioid therapy for their underlying persistent cancer pain. (1)Limitations of Use:Lazanda may be dispensed only to patients enrolled in the TIRF REMSAccess program.
DrugBank Targets:
16
1. Mu-type opioid receptor;2. Delta-type opioid receptor;3. Kappa-type opioid receptor
Mechanism of Action:
19
Target: opiod receptor
Action: agonist
FDA: Fentanyl is a pure opioid agonist whose principal therapeutic action is analgesia. Other members of the class known as opioidagonists include substances such as morphine, oxycodone, hydromorphone, codeine, and hydrocodone.
|
| 23 |
|
Lupron Depot
19
50
|
LEUPROLIDE ACETATE |
TAP Pharmaceuticals/ Abbott Laboratories |
July 1997/ January 1996 |
Disease/s that Drug Treats:prostate cancer
Indications and Usage:
19
LUPRON DEPOT is a gonadotropin releasing hormone (GnRH) agonistindicated for: palliative treatment of advanced prostatic cancer. (1)
DrugBank Targets:
16
1. Gonadotropin-releasing hormone receptor
Mechanism of Action:
19
Target: GnRH
Action: agonist
FDA: Leuprolide acetate, a GnRH agonist, acts as an inhibitor of gonadotropin secretion. Animalstudies indicate that following an initial stimulation, continuous administration of leuprolideacetate results in suppression of ovarian and testicular steroidogenesis. This effect was reversibleupon discontinuation of drug therapy.Administration of leuprolide acetate has resulted in inhibition of the growth of certain hormonedependent tumors (prostatic tumors in Noble and Dunning male rats and DMBA-inducedmammary tumors in female rats) as well as atrophy of the reproductive organs.
|
| 24 |
|
Lynparza
19
50
|
OLAPARIB |
AstraZeneca |
December 2014 |
Disease/s that Drug Treats:previously treated BRCA mutated advanced ovarian cancer
Indications and Usage:
19
Lynparza is a poly (ADP-ribose) polymerase (PARP) inhibitor indicated asmonotherapy in patients with deleterious or suspected deleterious germlineBRCA mutated (as detected by an FDA-approved test) advanced ovariancancer who have been treated with three or more prior lines of chemotherapy.(1.1)The indication is approved under accelerated approval based on objectiveresponse rate and duration of response. Continued approval for this indicationmay be contingent upon verification and description of clinical benefit inconfirmatory trials. (1 1, 14)
DrugBank Targets:
16
1. Poly [ADP-ribose] polymerase 1;2. Poly [ADP-ribose] polymerase 2;3. Poly [ADP-ribose] polymerase 3
Mechanism of Action:
19
Target: poly (ADP-ribose) polymerase (PARP)
Action: inhibitor
FDA: Lynparza is an inhibitor of poly (ADP-ribose) polymerase (PARP) enzymes, including PARP1, PARP2, and PARP3.PARP enzymes are involved in normal cellular homeostasis, such as DNA transcription, cell cycle regulation, and DNArepair. Olaparib has been shown to inhibit growth of select tumor cell lines in vitro and decrease tumor growth in mousexenograft models of human cancer both as monotherapy or following platinum-based chemotherapy. Increasedcytotoxicity and anti-tumor activity following treatment with olaparib were noted in cell lines and mouse tumor modelswith deficiencies in BRCA. In vitro studies have shown that olaparib-induced cytotoxicity may involve inhibition ofPARP enzymatic activity and increased formation of PARP-DNA complex, resulting in disruption of cellular homeostasisand cell death.
|
| 25 |
|
Nexavar
19
50
|
SORAFENIB TOSYLATE |
Bayer/Onyx |
December 2005 |
Disease/s that Drug Treats:Renal Cell Carcinoma
Indications and Usage:
19
NEXAVAR is a kinase inhibitor indicated for the treatment of Unresecta ble hepatocellular carcinoma (1.1) adjust thyroid repla cement therapy in patients with thyroid ca ncer. (5.12) Advanced renal cell carcinoma (1.2) Locally recurrent or meta static, progressive, differentiated thyroid carcinoma refractory to ra dioactive iodine treatment (1.3)
DrugBank Targets:
16
1. Serine/threonine-protein kinase B-raf;2. RAF proto-oncogene serine/threonine-protein kinase;3. Vascular endothelial growth factor receptor 3;4. Vascular endothelial growth factor receptor 2;5. Receptor-type tyrosine-protein kinase FLT3;6. Platelet-derived growth factor receptor beta;7. Mast/stem cell growth factor receptor Kit;8. Fibroblast growth factor receptor 1;9. Proto-oncogene tyrosine-protein kinase receptor Ret;10. Vascular endothelial growth factor receptor 1
Mechanism of Action:
19
Target: c-CRAF, BRAF and mutant BRAF, KIT, FLT- 3, RET, RET/PTC, VEGFR-1, VEGFR- 2, VEGFR- 3, and PDGFR-Ã
Action: inhibitor
FDA: Sorafenib is a kinase inhibitor that decreases tumor cell proliferation in vitro.Sorafenib was shown to inhibit multiple intracellular (c-CRAF, BRAF and mutant BRAF) and cell surfacekinases (KIT, FLT- 3, RET, RET/PTC, VEGFR-1, VEGFR- 2, VEGFR- 3, and PDGFR-Ã). Several of thesekinases are thought to be involved in tumor cell signaling, angiogenesis and apoptosis. Sorafenib inhibited tumorgrowth of HCC, RCC, and DTC human tumor xenografts in immunocompromised mice. Reductions in tumorangiogenesis were seen in models of HCC and RCC upon sorafenib treatment, and increases in tumor apoptosiswer e obser ved in models of HCC, RCC, and DTC.
|
| 26 |
|
Picato gel
19
|
INGENOL MEBUTATE |
LEO Pharma |
January 2012 |
Disease/s that Drug Treats:actinic keratosis
Indications and Usage:
19
Picato® gel is an inducer of cell death indicated for the topical treatment ofactinic keratosis. (1)
DrugBank Targets:
16
1. Protein kinase C delta type;2. Protein kinase C alpha type
Mechanism of Action:
19
Target: AK lesions
Action: inducer of apoptosis (otherwise, mechanism of action is unknown)
FDA: The mechanism of action by which Picato® gel induces cell death in treating AK lesions isunknown.
|
| 27 |
|
Plenaxis
19
|
ABARELIX |
Praecis Pharmaceuticals |
December 2003 |
Disease/s that Drug Treats:Prostate Cancer
Indications and Usage:
19
Plenaxis⢠is indicated for the palliative treatment of men with advanced symptomaticprostate cancer, in whom LHRH agonist therapy is not appropriate and who refusesurgical castration, and have one or more of the following: (1) risk of neurologicalcompromise due to metastases, (2) ureteral or bladder outlet obstruction due to localencroachment or metastatic disease, or (3) severe bone pain from skeletal metastasespersisting on narcotic analgesia.
DrugBank Targets:
16
1. Gonadotropin-releasing hormone receptor
Mechanism of Action:
19
Target: GnRH receptors in the pituitary gland
Action: competitive blocker
FDA: -
|
| 28 |
|
Provenge
19
50
|
sipuleucel-T |
Dendreon |
May 2010 |
Disease/s that Drug Treats:hormone refractory prostate cancer
Indications and Usage:
19
PROVENGE is an autologous cellularimmunotherapy indicated for the treatment ofasymptomatic or minimally symptomatic metastaticcastrate resistant (hormone refractory) prostatecancer. (1)
DrugBank Targets:
-
Mechanism of Action:
19
Target: PAP
Action: inducer of immune response against this antigen expressed in most prostate cancers
FDA: PROVENGE is classified as an autologous cellular immunotherapy. While the precisemechanism of action is unknown, PROVENGE is designed to induce an immune responsetargeted against PAP, an antigen expressed in most prostate cancers. During ex vivo culturewith PAP-GM-CSF, APCs take up and process the recombinant target antigen into smallpeptides that are then displayed on the APC surface.In Study 1, 237 out of the 512 patients randomized were evaluated for the development ofhumoral and T cell immune responses (proliferative and gamma-interferon (γIFN) ELISPOT)to the target antigens at Baseline, and at Weeks 6, 14, and 26. Antibody (IgM and IgG)responses against PAP-GM-CSF and PAP antigen alone were observed through thefollow-up period in the PROVENGE group. Neutralizing antibody responses to GM-CSFwere transient. T cell proliferative and γIFN ELISPOT responses to PAP-GM-CSF fusionprotein were observed in cells collected from peripheral blood of patients through thefollow-up period in the PROVENGE treatment group but not in controls. In some patients aresponse to PAP antigen alone was observed. No conclusions could be made regarding theclinical significance of the observed immune responses.
|
| 29 |
|
Rituxan
19
50
|
RITUXIMAB |
Biogen IDEC, Genentech |
November 1997 |
Disease/s that Drug Treats:non-hodgkin's lymphoma
Indications and Usage:
19
Rituxan® (rituximab) is a CD20-directed cytolytic antibody indicated for thetreatment of patients with: Non-Hodgkinâs Lymphoma (NHL) (1.1) Chronic Lymphocytic Leukemia (CLL) (1.2) Rheumatoid Arthritis (RA) in combination with methotrexate in adultpatients with moderately-to severely-active RA who have inadequateresponse to one or more TNF antagonist therapies (1.3) Granulomatosis with Polyangiitis (GPA) (Wegenerâs Granulomatosis) andMicroscopic Polyangiitis (MPA) in adult patients in combination withglucocorticoids (1.4)Limitations of Use: Rituxan is not recommended for use in patients withsevere, active infections (1.5).
DrugBank Targets:
16
1. Low affinity immunoglobulin gamma Fc region receptor III-B;2. Complement C1r subcomponent;3. Complement C1q subcomponent subunit A;4. Complement C1q subcomponent subunit B;5. Complement C1q subcomponent subunit C;6. Low affinity immunoglobulin gamma Fc region receptor III-A;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. B-lymphocyte antigen CD20
Mechanism of Action:
19
Target: CD20 antigen expressed on the surface ofpre-B and mature B-lymphocytes
Action: mediator of B-cell lysis through different possible types of cytotoxicity
FDA: Rituximab is a monoclonal antibody that targets the CD20 antigen expressed on the surface ofpre-B and mature B-lymphocytes. Upon binding to CD20, rituximab mediates B-cell lysis. Possiblemechanisms of cell lysis include complement dependent cytotoxicity (CDC) and antibody dependentcell mediated cytotoxicity (ADCC). The antibody induced apoptosis in the DHL 4 human B celllymphoma cell line.B cells are believed to play a role in the pathogenesis of rheumatoid arthritis (RA) and associatedchronic synovitis. In this setting, B cells may be acting at multiple sites in theautoimmune/inflammatory process, including through production of rheumatoid factor (RF) andother autoantibodies, antigen presentation, T-cell activation, and/or proinflammatory cytokineproduction.
|
| 30 |
|
Sancuso
19
|
GRANISETRON |
ProStrakan |
September 2008 |
Disease/s that Drug Treats:chemotherapy-induced nausea and vomiting
Indications and Usage:
19
Sancuso is a serotonin subtype 3 (5-HT3) receptor antagonist indicated for theprevention of nausea and vomiting in patients receiving moderately and/orhighly emetogenic chemotherapy for up to 5 consecutive days. (1)
DrugBank Targets:
16
1. 5-hydroxytryptamine receptor 3A
Mechanism of Action:
19
Target: 5-hydroxytryptamine3 (5-HT3) receptor
Action: agonist
FDA: Granisetron is a selective 5-hydroxytryptamine3 (5-HT3) receptor antagonist with little or no affinityfor other serotonin receptors, including 5-HT1, 5-HT1A, 5-HT1B/C, 5-HT2; for alpha1-, alpha2-, or betaadrenoreceptors;for dopamine-D2; or for histamine-H1; benzodiazepine; picrotoxin or opioidreceptors.Serotonin receptors of the 5-HT3 type are located peripherally on vagal nerve terminals and centrallyin the chemoreceptor trigger zone of the area postrema. During chemotherapy that inducesvomiting, mucosal enterochromaffin cells release serotonin, which stimulates 5-HT3 receptors. Thisevokes vagal afferent discharge, inducing vomiting. Animal studies demonstrate that, in binding to5-HT3 receptors, granisetron blocks serotonin stimulation and subsequent vomiting after emetogenicstimuli such as cisplatin. In the ferret animal model, a single granisetron injection preventedvomiting due to high-dose cisplatin or arrested vomiting within 5 to 30 seconds.
|
| 31 |
|
Self-examination breast pad
19
|
|
Inventive Products |
on December 22, 1995 |
FDA Label: Self-examination breast pad
Disease/s that Drug Treats:breast self-examination
Indications and Usage:
19
DrugBank Targets:
-
Mechanism of Action:
19
Target: -
Action: -
FDA: -
|
| 32 |
|
Stivarga
19
50
|
REGORAFENIB |
Bayer/ Bayer HealthCare Pharmaceuticals |
February 2013/ September 2012 |
Disease/s that Drug Treats:gastrointestinal stromal tumor/ metastatic colorectal cancer
Indications and Usage:
19
Stivarga is a kinase inhibitor indicated for the treatment of patients with: Metastatic colorectal cancer (CRC) who have been previously treated withfluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, an antiVEGFtherapy, and, if KRAS wild type, an anti-EGFR therapy. (1.1) Locally advanced, unresectable or metastatic gastrointestinal stromal tumor(GIST) who have been previously treated with imatinib mesylate andsunitinib malate. (1.2)
DrugBank Targets:
16
1. Proto-oncogene tyrosine-protein kinase receptor Ret;2. Vascular endothelial growth factor receptor 1;3. Vascular endothelial growth factor receptor 2;4. Vascular endothelial growth factor receptor 3;5. Mast/stem cell growth factor receptor Kit;6. Platelet-derived growth factor receptor alpha;7. Platelet-derived growth factor receptor beta;8. Fibroblast growth factor receptor 1;9. Fibroblast growth factor receptor 2;10. Angiopoietin-1 receptor;11. Discoidin domain-containing receptor 2;12. High affinity nerve growth factor receptor;13. Ephrin type-A receptor 2;14. RAF proto-oncogene serine/threonine-protein kinase;15. Serine/threonine-protein kinase B-raf;16. Mitogen-activated protein kinase 11;17. Tyrosine-protein kinase FRK;18. Tyrosine-protein kinase ABL1
Mechanism of Action:
19
Target: RET, VEGFR1, VEGFR2, VEGFR3, KIT, PDGFR-alpha, PDGFR-beta, FGFR1, FGFR2,TIE2, DDR2, TrkA, Eph2A, RAF-1, BRAF, BRAFV600E , SAPK2, PTK5, and Abl kinases
Action: inhibitor
FDA: Regorafenib is a small molecule inhibitor of multiple membrane-bound and intracellular kinases involved in normalcellular functions and in pathologic processes such as oncogenesis, tumor angiogenesis, and maintenance of the tumormicroenvironment. In in vitro biochemical or cellular assays, regorafenib or its major human active metabolites M-2 andM-5 inhibited the activity of RET, VEGFR1, VEGFR2, VEGFR3, KIT, PDGFR-alpha, PDGFR-beta, FGFR1, FGFR2,TIE2, DDR2, TrkA, Eph2A, RAF-1, BRAF, BRAFV600E , SAPK2, PTK5, and Abl at concentrations of regorafenib thathave been achieved clinically. In in vivo models, regorafenib demonstrated anti-angiogenic activity in a rat tumor model,and inhibition of tumor growth as well as anti-metastatic activity in several mouse xenograft models including some forhuman colorectal carcinoma.
|
| 33 |
|
Synercid I.V.
19
|
DALFOPRISTIN; QUINUPRISTIN QUINUPRISTIN; DALFOPRISTIN |
Rhone Poulenc Rorer |
September 1999 |
Disease/s that Drug Treats:For serious or life-threatening infections associated w/ vancomycin-resistant Enterococcus faecium (VREF) bacteremia.
Indications and Usage:
19
Synercid is indicated in adults for the treatment of the following infections when caused bysusceptible strains of the designated microorganisms.Complicated skin and skin structure infections caused by Staphylococcus aureus (methicillinsusceptible) or Streptococcus pyogenes. (See CLINICAL STUDIES.)
DrugBank Targets:
16
16
1. Streptogramin A acetyltransferase| 1. 23S rRNA;2. 50S ribosomal protein L10;3. 50S ribosomal protein L22
Mechanism of Action:
19
Target: bacterial ribosome - protien synthesis
Action: inhibitor
FDA: The site of action of quinupristin and dalfopristin is the bacterial ribosome. Dalfopristin has beenshown to inhibit the early phase of protein synthesis while quinupristin inhibits the late phase ofprotein synthesis. Synercid is bactericidal against isolates of methicillin-susceptible andmethicillin-resistant staphylococci. The mode of action of Synercid differs from that of otherclasses of antibacterial agents such as Ã-lactams, aminoglycosides, glycopeptides, quinolones,macrolides, lincosamides and tetracyclines. Therefore, there is no cross resistance betweenSynercid and these agents when tested by the minimum inhibitory concentration (MIC) method.
|
| 34 |
|
Tarceva
19
50
|
ERLOTINIB HYDROCHLORIDE |
Genentech, OSI Pharmaceuticals |
November, 2004 |
Disease/s that Drug Treats:Non-small cell lung cancer
Indications and Usage:
19
TARCEVA is a kinase inhibitor indicated for: First-line treatment of patients with metastatic non-small cell lungcancer (NSCLC) whose tumors have epidermal growth factor receptor(EGFR) exon 19 deletions or exon 21 (L858R) substitution mutations asdetected by an FDA-approved test. (1.1) Maintenance treatment of patients with locally advanced or metastaticNSCLC whose disease has not progressed after four cycles of platinumbasedfirst-line chemotherapy. (1.1) Treatment of locally advanced or metastatic NSCLC after failure of atleast one prior chemotherapy regimen. (1.1) First-line treatment of patients with locally advanced, unresectable ormetastatic pancreatic cancer, in combination with gemcitabine. (1.2)
DrugBank Targets:
16
1. Epidermal growth factor receptor;2. Nuclear receptor subfamily 1 group I member 2
Mechanism of Action:
19
Target: Human Epidermal Growth Factor Receptor Type 1/Epidermal Growth Factor Receptor (HER1/EGFR) tyrosine kinase
Action: inhibitor
FDA: Epidermal growth factor receptor (EGFR) is expressed on the cell surface of both normal and cancer cells. In some tumor cells signalingthrough this receptor plays a role in tumor cell survival and proliferation irrespective of EGFR mutation status. Erlotinib reversiblyinhibits the kinase activity of EGFR, preventing autophosphorylation of tyrosine residues associated with the receptor and therebyinhibiting further downstream signaling. Erlotinib binding affinity for EGFR exon 19 deletion or exon 21 (L858R) mutations is higherthan its affinity for the wild type receptor. Erlotinib inhibition of other tyrosine kinase receptors has not been fully characterized.
|
| 35 |
|
Tasigna
19
50
|
NILOTINIB HYDROCHLORIDE MONOHYDRATE |
Novartis |
October 2007 |
Disease/s that Drug Treats:chronic myelogenous leukemia
Indications and Usage:
19
Tasigna is a kinase inhibitor indicated for:The treatment of newly diagnosed adult patients with Philadelphiachromosome positive chronic myeloid leukemia (Ph+ CML) in chronic phase.The treatment of chronic phase (CP) and accelerated phase (AP) Ph+ CML inadult patients resistant to or intolerant to prior therapy that included imatinib.(1.2)--------------
DrugBank Targets:
16
1. Tyrosine-protein kinase ABL1;2. Mast/stem cell growth factor receptor Kit
Mechanism of Action:
19
Target: Bcr-Abl kinase, c-kit and Platelet Derived Growth Factor (PDGF)
Action: inhibitor of signal transduction
FDA: Nilotinib is an inhibitor of the BCR-ABL kinase. Nilotinib binds to and stabilizes the inactive conformation ofthe kinase domain of ABL protein. In vitro, nilotinib inhibited BCR-ABL mediated proliferation of murineleukemic cell lines and human cell lines derived from patients with Ph+ CML. Under the conditions of theassays, nilotinib was able to overcome imatinib resistance resulting from BCR-ABL kinase mutations, in 32 outof 33 mutations tested. In vivo, nilotinib reduced the tumor size in a murine BCR-ABL xenograft model.Nilotinib inhibited the autophosphorylation of the following kinases at IC50 values as indicated: BCR-ABL (20to 60 nM), PDGFR (69 nM), c-KIT (210 nM), CSF-1R (125 to 250 nM), and DDR1 (3.7 nM).
|
| 36 |
|
Torisel
19
50
|
TEMSIROLIMUS |
Wyeth |
May 2007 |
Disease/s that Drug Treats:renal cell carcinoma
Indications and Usage:
19
TORISEL® is a kinase inhibitor indicated for the treatment of advanced renalcell carcinoma. (1)
DrugBank Targets:
16
1. Serine/threonine-protein kinase mTOR
Mechanism of Action:
19
Target: mTOR
Action: inhibitor
FDA: Temsirolimus is an inhibitor of mTOR (mammalian target of rapamycin). Temsirolimus binds toan intracellular protein (FKBP-12), and the protein-drug complex inhibits the activity of mTORthat controls cell division. Inhibition of mTOR activity resulted in a G1 growth arrest in treatedtumor cells. When mTOR was inhibited, its ability to phosphorylate p70S6k and S6 ribosomalprotein, which are downstream of mTOR in the PI3 kinase/AKT pathway was blocked. Inin vitro studies using renal cell carcinoma cell lines, temsirolimus inhibited the activity of mTORand resulted in reduced levels of the hypoxia-inducible factors HIF-1 and HIF-2 alpha, and thevascular endothelial growth factor.
|
| 37 |
|
Treanda
19
50
|
BENDAMUSTINE HYDROCHLORIDE |
Cephalon |
October 2008 |
Disease/s that Drug Treats:Chronic lymphocytic leukemia and B-cell non-Hodgkinâs lymphoma
Indications and Usage:
19
TREANDA is an alkylating drug indicated for treatment of patients with: Chronic lymphocytic leukemia (CLL). Efficacy relative to first linetherapies other than chlorambucil has not been established. (1.1) Indolent B-cell non-Hodgkin lymphoma (NHL) that has progressed duringor within six months of treatment with rituximab or a rituximab-containingregimen. (1.2)
DrugBank Targets:
-
Mechanism of Action:
19
Target: -
Action: -
FDA: Bendamustine is a bifunctional mechlorethamine derivative containing a purine-like benzimidazole ring.Mechlorethamine and its derivatives form electrophilic alkyl groups. These groups form covalent bonds with electronrichnucleophilic moieties, resulting in interstrand DNA crosslinks. The bifunctional covalent linkage can lead to celldeath via several pathways. Bendamustine is active against both quiescent and dividing cells. The exact mechanism ofaction of bendamustine remains unknown.
|
| 38 |
|
Trelstar Depot/ Trelstar LA
19
|
TRIPTORELIN PAMOATE |
Debio Rechereche Pharmaceutique, Target Research Associates/ Debiopharm |
June 2000/ June 2001 |
Disease/s that Drug Treats:advanced prostate cancer/ Prostate cancer
Indications and Usage:
19
TRELSTAR is a gonadotropin releasing hormone (GnRH) agonist indicated for the palliative treatmentof advanced prostate cancer. (1)
DrugBank Targets:
-
Mechanism of Action:
19
Target: gonadotropin releasing hormone (GnRH)
Action: agonist
FDA: Triptorelin is a synthetic decapeptide agonist analog of gonadotropin releasing hormone (GnRH).Comparative in vitro studies showed that triptorelin was 100-fold more active than native GnRH instimulating luteinizing hormone release from monolayers of dispersed rat pituitary cells in culture and20-fold more active than native GnRH in displacing 125I-GnRH from pituitary receptor sites. In animalstudies, triptorelin pamoate was found to have 13âfold higher luteinizing hormone-releasing activity and21-fold higher follicle-stimulating hormone-releasing activity compared to the native GnRH.
|
| 39 |
|
Valchlor
19
|
MECHLORETHAMINE HYDROCHLORIDE |
Ceptaris Therapeutics |
August 2013 |
Disease/s that Drug Treats:Stage IA/IB mycosisfungoides-type cutaneous T-cell lymphoma
Indications and Usage:
19
VALCHLOR is an alkylating drug indicated for the topical treatmentof Stage IA and IB mycosis fungoidesâtype cutaneous Tâcelllymphoma in patients who have received prior skinâdirected therapy(1). Â
DrugBank Targets:
16
1. DNA
Mechanism of Action:
19
Target: rapidly-proliferating cells
Action: inhibitor
FDA: Mechlorethamine, also known as nitrogen mustard, is an alkylating agent which inhibits rapidly proliferating cells.
|
| 40 |
|
Vandetanib
19
50
|
vandetanib |
AstraZeneca |
April 2011 |
Disease/s that Drug Treats:thyroid cancer
Indications and Usage:
19
DrugBank Targets:
16
1. Vascular endothelial growth factor A;2. Epidermal growth factor receptor;3. Protein-tyrosine kinase 6;4. Angiopoietin-1 receptor
Mechanism of Action:
19
Target: tyrosine kinases
Action: inhibitor
FDA: -
|
| 41 |
|
Xofigo
19
50
|
RADIUM RA-223 DICHLORIDE |
Bayer Healthcare Pharmaceuticals |
May 2013 |
Disease/s that Drug Treats:prostate cancer with bone metastases
Indications and Usage:
19
Xofigo is an alpha particle-emitting radioactive therapeutic agent indicated forthe treatment of patients with castration-resistant prostate cancer, symptomaticbone metastases and no known visceral metastatic disease. (1)
DrugBank Targets:
-
Mechanism of Action:
19
Target: bone mineral hydroxyapatite at areas of increased bone turnover
Action: forms complexes, destroys DNA
FDA: The active moiety of Xofigo is the alpha particle-emitting isotope radium-223 (as radium Ra 223 dichloride), whichmimics calcium and forms complexes with the bone mineral hydroxyapatite at areas of increased bone turnover, such asbone metastases (see Table 2). The high linear energy transfer of alpha emitters (80 keV/micrometer) leads to a highfrequency of double-strand DNA breaks in adjacent cells, resulting in an anti-tumor effect on bone metastases. The alphaparticle range from radium-223 dichloride is less than 100 micrometers (less than 10 cell diameters) which limits damageto the surrounding normal tissue.
|
| 42 |
|
Zoladex
19
50
|
GOSERELIN ACETATE |
AstraZeneca |
January 1996 |
Disease/s that Drug Treats:prostate cancer
Indications and Usage:
19
ZOLADEX is a Gonadotropin Releasing Hormone (GnRH) agonist indicatedfor: Use in combination with flutamide for the management of locally confinedcarcinoma of the prostate (1.1) Palliative treatment of advanced carcinoma of the prostate (1.2) The management of endometriosis (1.3) Use as an endometrial-thinning agent prior to endometrial ablation fordysfunctional uterine bleeding (1.4) Use in the palliative treatment of advanced breast cancer in pre- andperimenopausal women (1.5)
DrugBank Targets:
16
1. Lutropin-choriogonadotropic hormone receptor;2. Gonadotropin-releasing hormone receptor
Mechanism of Action:
19
Target: pituitary gonadotropinsecretion
Action: inhibitor
FDA: ZOLADEX is a synthetic decapeptide analogue of GnRH. ZOLADEX acts as an inhibitor of pituitary gonadotropinsecretion when administered in the biodegradable formulation. In animal and in vitro studies, administration of goserelinresulted in the regression or inhibition of growth of the hormonally sensitive dimethylbenzanthracene (DMBA)-inducedrat mammary tumor and Dunning R3327 prostate tumor.
|
| 43 |
|
Zuplenz
19
|
ONDANSETRON |
Strativa Pharmaceuticals |
July 2010 |
Disease/s that Drug Treats:post-operative, chemotherapy and radiotherapy induced nausea and vomiting
Indications and Usage:
19
ZUPLENZ is a 5-HT3 receptor antagonist indicated for: Prevention of nausea and vomiting associated with highly emetogenic cancerchemotherapy. (1.1) Prevention of nausea and vomiting associated with initial and repeat coursesof moderately emetogenic cancer chemotherapy. (1.2) Prevention of nausea and vomiting associated with radiotherapy in patientsreceiving total body irradiation, single high-dose fraction to abdomen, ordaily fractions to the abdomen. (1.3) Prevention of postoperative nausea and/or vomiting. (1.4)
DrugBank Targets:
16
1. 5-hydroxytryptamine receptor 3A;2. 5-hydroxytryptamine receptor 4;3. Mu-type opioid receptor;4. 5-hydroxytryptamine receptor 1A;5. 5-hydroxytryptamine receptor 1B
Mechanism of Action:
19
Target: 5-HT3 receptor
Action: selective antagonist
FDA: Ondansetron is a selective 5-HT3 receptor antagonist. While its mechanism of action has not been fully characterized, ondansetron isnot a dopamine-receptor antagonist. Serotonin receptors of the 5-HT3 type are present both peripherally on vagal nerve terminals andcentrally in the chemoreceptor trigger zone of the area postrema. It is not certain whether ondansetronâ s antiemetic action is mediatedcentrally, peripherally, or in both sites. However, cytotoxic chemotherapy appears to be associated with release of serotonin from theenterochromaffin cells of the small intestine. In humans, urinary 5-HIAA (5-hydroxyindoleacetic acid) excretion increases aftercisplatin administration in parallel with the onset of emesis. The released serotonin may stimulate the vagal afferents through the 5-HT3 receptors and initiate the vomiting reflex. In animals, the emetic response to cisplatin can be prevented by pretreatment with aninhibitor of serotonin synthesis, bilateral abdominal vagotomy and greater splanchnic nerve section, or pretreatment with a serotonin5-HT3 receptor antagonist.
|
| 44 |
|
Zykadia
19
50
|
CERITINIB |
Novartis |
April 2014 |
Disease/s that Drug Treats:ALK+ metastatic non-small cell lung cancer
Indications and Usage:
19
ZYKADIA is a kinase inhibitor indicated for the treatment of patients withanaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lungcancer (NSCLC) who have progressed on or are intolerant to crizotinib. 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 inconfirmatory trials. (1) , ZYKADIA is a kinase inhibitor indicated for the treatment of patients with anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer (NSCLC) who have progressed on or are intolerant to crizotinib. This indication is approved under accelerated approval based on tumor response rate and duration of response. An improvement in survival or disease-related symptoms has not been established. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. (1)
DrugBank Targets:
16
1. ALK tyrosine kinase receptor, ALK tyrosine kinase receptor
Mechanism of Action:
19
Target: ALK, insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1, anaplastic lymphoma kinase (ALK)
Action: kinase inhibitor, highly-selective inhibitor
FDA: Ceritinib is a kinase inhibitor. Targets of ceritinib inhibition identified in either biochemical or cellular assays at clinicallyrelevant concentrations include ALK, insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1.Among these, ceritinib is most active against ALK. Ceritinib inhibited autophosphorylation of ALK, ALK-mediatedphosphorylation of the downstream signaling protein STAT3, and proliferation of ALK-dependent cancer cells in in vitroand in vivo assays.Ceritinib inhibited the in vitro proliferation of cell lines expressing EML4-ALK and NPM-ALK fusion proteins anddemonstrated dose-dependent inhibition of EML4-ALK-positive NSCLC xenograft growth in mice and rats. Ceritinibexhibited dose-dependent anti-tumor activity in mice bearing EML4-ALK-positive NSCLC xenografts with demonstratedresistance to crizotinib, at concentrations within a clinically relevant range. , Ceritinib is a kinase inhibitor. Targets of ceritinib inhibition identified in either biochemical or cellular assays at clinically relevant concentrations include ALK, insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1. Among these, ceritinib is most active against ALK. Ceritinib inhibited autophosphorylation of ALK, ALK-mediated phosphorylation of the downstream signaling protein STAT3, and proliferation of ALK-dependent cancer cells in in vitro and in vivo assays. Ceritinib inhibited the in vitro proliferation of cell lines expressing EML4-ALK and NPM-ALK fusion proteins and demonstrated dose-dependent inhibition of EML4-ALK-positive NSCLC xenograft growth in mice and rats. Ceritinib exhibited dose-dependent anti-tumor activity in mice bearing EML4-ALK-positive NSCLC xenografts with demonstrated resistance to crizotinib, at concentrations within a clinically relevant range.
|
| 45 |
|
Aldurazyme
19
|
LARONIDASE |
Genzyme |
May 2003 |
Disease/s that Drug Treats:Mucopolysaccharidosis I
Indications and Usage:
19
ALDURAZYME is a hydrolytic lysosomal glycosaminoglycan (GAG)- specific enzyme indicated for patients with Hurler and Hurler-Scheie forms of Mucopolysaccharidosis I (MPS I) and for patients with the Scheie form who have moderate to severe symptoms. The risks and benefits of treating mildly affected patients with the Scheie form have not been established. ALDURAZYME has been shown to improve pulmonary function and walking capacity. ALDURAZYME has not been evaluated for effects on the central nervous system manifestations of the disorder (1).
DrugBank Targets:
16
Iduronic acid
Mechanism of Action:
19
Target: α-L-iduronidase
Action: replacement
FDA: Mucopolysaccharide storage disorders are caused by the deficiency of specific lysosomal enzymes required for the catabolism of glycosaminoglycans (GAG). Mucopolysaccharidosis I (MPS I) is characterized by the deficiency of ï¡-L-iduronidase, a lysosomal hydrolase which catalyzes the hydrolysis of terminal ï¡-L-iduronic acid residues of dermatan sulfate and heparan sulfate. Reduced or absent ï¡-L-iduronidase activity results in the accumulation of the GAG substrates, dermatan sulfate and heparan sulfate, throughout the body and leads to widespread cellular, tissue, and organ dysfunction. The rationale of ALDURAZYME therapy in MPS I is to provide exogenous enzyme for uptake into lysosomes and increase the catabolism of GAG. ALDURAZYME uptake by cells into lysosomes is most likely mediatedby the mannose-6-phosphate-terminated oligosaccharide chains of laronidase binding to specific mannose-6- phosphate receptors. Because many proteins in the blood are restricted from entry into the central nervous system (CNS) by the blood brain barrier, effects of intravenously administered ALDURAZYME on cells within the CNS cannot be inferred from activity in sites outside the CNS. The ability of ALDURAZYME to cross the blood brain barrier has not been evaluated in animal models or in clinical studies.
|
| 46 |
|
Allegra
19
|
FEXOFENADINE HYDROCHLORIDE |
Hoechst Marion Roussel |
July 1996 |
Disease/s that Drug Treats:seasonal allergic rhinitis
Indications and Usage:
19
Seasonal Allergic Rhinitis ALLEGRA is indicated for the relief of symptoms associated with seasonal allergic rhinitis in adults and children 6 years of age and older. Symptoms treated effectively were sneezing, rhinorrhea, itchy nose/palate/throat, itchy/watery/red eyes. Chronic Idiopathic Urticaria ALLEGRA is indicated for treatment of uncomplicated skin manifestations of chronic idiopathic urticaria in adults and children 6 years of age and older. It significantly reduces pruritus and the number of wheals.
DrugBank Targets:
16
Histamine H1 receptor
Mechanism of Action:
19
Target: -
Action: -
FDA: Fexofenadine hydrochloride is an antihistamine with selective peripheral H1-receptor antagonist activity. Both enantiomers of fexofenadine hydrochloride displayed approximately equipotent antihistaminic effects. Fexofenadine inhibited histamine release from peritoneal mast cells in rats. In laboratory animals, no anticholinergic, alpha1-adrenergic or beta-adrenergic-receptor blocking effects were observed. No sedative or other central nervous system effects were observed. Radiolabeled tissue distribution studies in rats indicated that fexofenadine does not cross the blood-brain barrier.
|
| 47 |
|
Avelox I.V.
19
|
MOXIFLOXACIN HYDROCHLORIDE |
Bayer |
November 2001 |
Disease/s that Drug Treats:Susceptible strains of sinusitis, bronchitis, pneumonia, skin structure infections
Indications and Usage:
19
AVELOX is a fluoroquinolone antibacterial indicated for treating infections in adults 18 years of age and older caused by designated susceptible bacteria, in the conditions listed below: * Acute Bacterial Sinusitis (1.1) * Acute Bacterial Exacerbation of Chronic Bronchitis (1.2) * Community Acquired Pneumonia (1.3) * Skin and Skin Structure Infections: Uncomplicated (1.4) and Complicated (1.5) * Complicated Intra-Abdominal Infections (1.6) * Plague (1.7) To reduce the development of drug-resistant bacteria and maintain the effectiveness of AVELOX and other antibacterial drugs. AVELOX should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. (1.8)
DrugBank Targets:
16
DNA gyrase subunit A|DNA topoisomerase 4 subunit A|DNA topoisomerase 2-alpha
Mechanism of Action:
19
Target: topoisomerase II (DNA gyrase) and topoisomerase IV
Action: inhibitpr
FDA: AVELOX is a member of the fluoroquinolone class of antibacterial agents [see Microbiology (12.4)]. The bactericidal action of moxifloxacin results from inhibition of the topoisomerase II (DNA gyrase) and topoisomerase IV required for bacterial DNA replication, transcription, repair, and recombination.
|
| 48 |
|
Biaxin XL
19
|
CLARITHROMYCIN |
Abbott Laboratories |
March 2000 |
Disease/s that Drug Treats:Acute Bacterial Exacerbation of Chronic Bronchitis (AECB) and Acute Maxillary Sinusitis
Indications and Usage:
19
BIAXIN Filmtab (clarithromycin tablets, USP) and BIAXIN Granules (clarithromycin for oral suspension, USP) are indicated for the treatment of mild to moderate infections caused by susceptible isolates of the designated bacteria in the conditions as listed below: Adults (BIAXIN Filmtab Tablets and Granules for Oral Suspension) Pharyngitis/Tonsillitis due to Streptococcus pyogenes (The usual drug of choice in the treatment and prevention of streptococcal infections and the prophylaxis of rheumatic fever is penicillin administered by either the intramuscular or the oral route. Clarithromycin is generally effective in the eradication of S. pyogenes from the nasopharynx; however, data establishing the efficacy of clarithromycin in the subsequent prevention of rheumatic fever are not available at present). Acute maxillary sinusitis due to Haemophilus influenzae, Moraxella catarrhalis, or Streptococcus pneumoniae. Acute bacterial exacerbation of chronic bronchitis due to Haemophilus influenzae, Haemophilus parainfluenzae, Moraxella catarrhalis, or Streptococcus pneumoniae. Community-Acquired Pneumonia due to Haemophilus influenzae, Mycoplasma pneumoniae, Streptococcus pneumoniae, or Chlamydophila pneumoniae (TWAR). Uncomplicated skin and skin structure infections due to Staphylococcus aureus, or Streptococcus pyogenes (Abscesses usually require surgical drainage). Disseminated mycobacterial infections due to Mycobacterium avium, or Mycobacterium intracellulare BIAXIN (clarithromycin) Filmtab tablets in combination with amoxicillin and PREVACID (lansoprazole) or PRILOSEC (omeprazole) Delayed-Release Capsules, as triple therapy, are indicated for the treatment of patients with Helicobacter pylori infection and duodenal ulcer disease (active or five-year history of duodenal ulcer) to eradicate H. pylori. BIAXIN Filmtab tablets in combination with PRILOSEC (omeprazole) capsules or TRITEC (ranitidine bismuth citrate) tablets are also indicated for the treatment of patients with an active duodenal ulcer associated with H. pylori infection. However, regimens which contain clarithromycin as the single antimicrobial agent are more likely to be associated with the development of clarithromycin resistance among patients who fail therapy. Clarithromycincontaining regimens should not be used in patients with known or suspected clarithromycin resistant isolates because the efficacy of treatment is reduced in this setting. In patients who fail therapy, susceptibility testing should be done if possible. If resistance to clarithromycin is demonstrated, a non-clarithromycin-containing therapy is recommended. (For Reference ID: 3836666 information on development of resistance see Microbiology section.) The eradication of H. pylori has been demonstrated to reduce the risk of duodenal ulcer recurrence. Children (BIAXIN Filmtab Tablets and Granules for Oral Suspension) Pharyngitis/Tonsillitis due to Streptococcus pyogenes. Community-Acquired Pneumonia due to Mycoplasma pneumoniae, Streptococcus pneumoniae, or Chlamydophila pneumoniae (TWAR) Acute maxillary sinusitis due to Haemophilus influenzae, Moraxella catarrhalis, or Streptococcus pneumoniae Acute otitis media due to Haemophilus influenzae, Moraxella catarrhalis, or Streptococcus pneumoniae NOTE: For information on otitis media, see CLINICAL STUDIES - Otitis Media. Uncomplicated skin and skin structure infections due to Staphylococcus aureus, or Streptococcus pyogenes (Abscesses usually require surgical drainage.) Disseminated mycobacterial infections due to Mycobacterium avium, or Mycobacterium intracellulare Adults (BIAXIN XL Filmtab Tablets) BIAXIN XL Filmtab (clarithromycin extended-release tablets) are indicated for the treatment of adults with mild to moderate infection caused by susceptible strains of the designated microorganisms in the conditions listed below: Acute maxillary sinusitis due to Haemophilus influenzae, Moraxella catarrhalis, or Streptococcus pneumoniae Acute bacterial exacerbation of chronic bronchitis due to Haemophilus influenzae, Haemophilus parainfluenzae, Moraxella catarrhalis, or Streptococcus pneumoniae Community-Acquired Pneumonia due to Haemophilus influenzae, Haemophilus parainfluenzae, Moraxella catarrhalis, Streptococcus pneumoniae, Chlamydophila pneumoniae (TWAR), or Mycoplasma pneumoniae THE EFFICACY AND SAFETY OF BIAXIN XL IN TREATING OTHER INFECTIONS FOR WHICH OTHER FORMULATIONS OF BIAXIN ARE APPROVED HAVE NOT BEEN ESTABLISHED. Prophylaxis BIAXIN Filmtab tablets and BIAXIN Granules for oral suspension are indicated for the prevention of disseminated Mycobacterium avium complex (MAC) disease in patients with advanced HIV infection. To reduce the development of drug-resistant bacteria and maintain the effectiveness of BIAXIN and other antibacterial drugs, BIAXIN should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. When culture and susceptibility information are available, they should be considered in selecting or modifying Reference ID: 3836666 antibacterial therapy. In the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.
DrugBank Targets:
16
50S ribosomal protein L10|Multidrug resistance protein 1|Potassium voltage-gated channel subfamily H member 2|Cytochrome P450 3A4|Solute carrier organic anion transporter family member 1B1|Solute carrier organic anion transporter family member 1B3
Mechanism of Action:
19
Target: -
Action: -
FDA: -
|
| 49 |
|
Cedax
19
|
CEFTIBUTEN DIHYDRATE |
Schering-Plough |
December 1995 |
Disease/s that Drug Treats:chronic bronchitis, infection of the middle ear, pharyngitis/tonsillitis
Indications and Usage:
19
CEDAX (ceftibuten) is indicated for the treatment of individuals with mild-to-moderate infections caused by susceptible strains of the designated microorganisms in the specific conditions listed below (see DOSAGE AND ADMINISTRATION and CLINICAL STUDIES sections). Acute Bacterial Exacerbations of Chronic Bronchitis due to Haemophilus influenzae (including β-lactamase-producing strains), Moraxella catarrhalis (including β-lactamaseproducing strains), or Streptococcus pneumoniae (penicillin-susceptible strains only). NOTE: In acute bacterial exacerbations of chronic bronchitis clinical trials where Moraxella catarrhalis was isolated from infected sputum at baseline, ceftibuten clinical efficacy was 22% less than control. Acute Bacterial Otitis Media due to Haemophilus influenzae (including β-lactamase-producing strains), Moraxella catarrhalis (including β-lactamase-producing strains), or Streptococcus pyogenes. NOTE: Although ceftibuten used empirically was equivalent to comparators in the treatment of clinically and/or microbiologically documented acute otitis media, the efficacy against Streptococcus pneumoniae was 23% less than control. Therefore, ceftibuten should be given empirically only when adequate antimicrobial coverage against Streptococcus pneumoniae has been previously administered. Pharyngitis and Tonsillitis due to Streptococcus pyogenes. NOTE: Only penicillin by the intramuscular route of administration has been shown to be effective in the prophylaxis of rheumatic fever. Ceftibuten is generally effective in the eradication of Streptococcus pyogenes from the oropharynx; however, data establishing the efficacy of the CEDAX product for the prophylaxis of subsequent rheumatic fever are not available.
DrugBank Targets:
16
Peptidoglycan synthase FtsI|Penicillin-binding protein 1A|Penicillin-binding protein 1B|Penicillin-binding protein 2
Mechanism of Action:
19
Target: -
Action: -
FDA: -
|
| 50 |
|
Cefazolin and Dextrose USP
19
|
CEFAZOLIN SODIUM |
B Braun Medical |
July 2000 |
Disease/s that Drug Treats:Various bacterial infections, septicemia, endocarditis, and perioperative prophylaxis
Indications and Usage:
19
Cefazolin for Injection USP and Dextrose Injection USP is a cephalosporin antibacterial indicated in the treatment of the following infections caused by susceptible isolates of the designated microorganisms: Respiratory tract infections (1.1); urinary tract infections (1.2); skin and skin structure infections (1.3); biliary tract infections (1.4); bone and joint infections (1.5); genital infections (1.6); septicemia (1.7); endocarditis (1.8) and perioperative prophylaxis (1.9).
DrugBank Targets:
16
Penicillin-binding protein 1A|Penicillin-binding protein 1B|Penicillin-binding protein 1C|Penicillin-binding protein 2
Mechanism of Action:
19
Target: -
Action: -
FDA: Cefazolin is an antibacterial drug [see Microbiology (12.4)]. Cefazolin is a bactericidal agent that acts by inhibition of bacterial cell wall synthesis.
|
Drugs for Lymphoma, Hodgkin, Classic (from DrugBank, HMDB, Dgidb, PharmGKB, IUPHAR, NovoSeek, BitterDB):
(show top 50)
(show all 581)
| # |
|
Name |
Status |
Phase |
Clinical Trials |
Cas Number |
PubChem Id |
| 1 |
|
Prednisolone phosphate |
Approved, Vet_approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
302-25-0 |
|
|
Synonyms:
Prednisolone 21-(dihydrogen phosphate)
Prednisolone 21-monophosphate
|
Prednisolone 21-phosphate
|
|
| 2 |
|
Prednisone |
Approved, Vet_approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
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
|
|
| 3 |
|
Vinblastine |
Approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
865-21-4 |
241903
13342
|
|
Synonyms:
(2a,2'b,3b,4a,5b)-VINCALEUKOBLASTINE
(2ALPHA,2'BETA,3BETA,4ALPHA,5BETA)-VINCALEUKOBLASTINE
(2xi,3beta,4'beta,19xi)-vincaleukoblastine
(2α,2'β,3β,4α,5β)-vincaleukoblastine
(3aR-(3aalpha,4beta,5beta,5abeta,9(3R*,5S*,7R*,9S*),10bR*,13aalpha))-methyl 4-(acetyloxy)-3a-ethyl-9-(5-ethyl-1,4,5,6,7,8,9,10-octahydro-5-hydroxy-9-(methoxycarbonyl)-2H-3,7-methanoazacycloundecino(5,4-b)indol-9-yl)-3a,4,5,5a,6,11,12,13a-octahydro-5-hydroxy-8-methoxy-6-methyl-1H-indolizino(8,1-cd)carbazole-5-carboxylate
143-67-9
1z2b
29060-LE
865-21-4
AC1L21JC
AC1L68D2
AC1MXZJ2
AC-20335
BIDD:PXR0201
Bio-0111
BRD-K01188359-065-02-5
BSPBio_001228
BSPBio_003594
C07201
C46H58N4O9
CCRIS 9002
Cell pharm brand OF vinblastine sulfate
Cellblastin
CHEBI:171516
CHEBI:27375
CHEMBL159
CHEMBL607706
CID13342
CID241903
CID3823887
CID6710780
D08675
DB00570
EG labo brand OF vinblastine sulfate
EINECS 212-734-0
Faulding brand OF vinblastine sulfate
Gastrozepin brand OF vinblastine sulfate
Gry brand OF vinblastine sulfate
Hexal brand OF vinblastine sulfate
HMS2090K05
HSDB 3263
KBio3_003033
Lemblastine
Lemery brand OF vinblastine sulfate
Lilly brand OF vinblastine sulfate
|
LS-1859
LS-187263
MolPort-002-518-262
MolPort-005-910-359
NCGC00022585-04
NCGC00181127-01
NChemBio.2007.10-comp22
nchembio873-comp22
NCI60_004200
NCI-C04842
NDC 0002-1452-01
Neuro_000020
Nincaluicolflastine
NSC 47842
Rozevin
SPBio_000680
Spectrum2_000890
Spectrum3_001994
STOCK1N-38480
Sulfate, vinblastine
UNII-5V9KLZ54CY
Velban
Velbe
Vinblastin
Vinblastin hexal
Vinblastina
Vinblastina (TN)
Vinblastina [Dcit]
Vinblastina [DCIT]
Vinblastina lilly
vinblastine
Vinblastine
Vinblastine (INN)
Vinblastine [INN:BAN]
Vinblastine sulfate
Vinblastine Sulfate
Vinblastinsulfat-gry
Vinblastinum
Vinblastinum [INN-Latin]
Vincaleucoblastin
Vincaleucoblastine
Vincaleukoblastine
Vincoblastine
VLB
VR-8
|
|
| 4 |
|
Methylprednisolone hemisuccinate |
Approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
2921-57-5 |
|
|
Synonyms:
Methylprednisolone hydrogen succinate
|
Methylprednisolone succinate
|
|
| 5 |
|
Prednisolone |
Approved, Vet_approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
50-24-8 |
5755
|
|
Synonyms:
(11b)-11,17,21-Trihydroxypregna-1,4-diene-3,20-dione
(11beta)-11,17,21-Trihydroxypregna-1,4-diene-3,20-dione
(11β)-11,17,21-trihydroxypregna-1,4-diene-3,20-dione
.DELTA.1-Cortisol
.DELTA.1-Dehydrocortisol
.DELTA.1-Dehydrohydrocortisone
.DELTA.1-Hydrocortisone
.delta.-Cortef
.delta.-Stab
1,2-Dehydrohydrocortisone
1,4-Pregnadiene-11b,17a,21-triol-3,20-dione
1,4-Pregnadiene-11beta,17alpha,21-triol-3,20-dione
1,4-pregnadiene-11β,17α,21-triol-3,20-dione
1,4-Pregnadiene-11β,17α,21-triol-3,20-dione
1,4-Pregnadiene-3,20-dione-11b,17a,21-triol
1,4-Pregnadiene-3,20-dione-11beta,17alpha,21-triol
1,4-pregnadiene-3,20-dione-11β,17α,21-triol
1,4-Pregnadiene-3,20-dione-11β,17α,21-triol
1-Dehydrocortisol
1-Dehydrohydrocortisone
3,20-dioxo-11b,17a,21-Trihydroxy-1,4-pregnadiene
3,20-dioxo-11beta,17alpha,21-Trihydroxy-1,4-pregnadiene
3,20-dioxo-11β,17α,21-trihydroxy-1,4-pregnadiene
46656_FLUKA
46656_RIEDEL
50-24-8
58201-11-9
8056-11-9
AC-1773
AC1L1L2E
Ak-Pred
Ak-Tate
Alphadrol
Articulose-50
Bio-0666
BPBio1_000164
BRD-K98039984-001-03-0
BRN 1354103
BSPBio_000148
Bubbli-Pred
C07369
CCRIS 980
CHEBI:8378
CHEMBL131
CID5755
Codelcortone
Co-Hydeltra
CO-Hydeltra
component of Ataraxoid
component of K-Predne-Dome
Cordrol
Cortalone
Cotogesic
Cotolone
CPD000718761
D00472
D011239
DB00860
Decaprednil
Decortin H
Delcortol
Delta F
delta(1)-Cortisol
delta(1)-Dehydrocortisol
Delta(1)-Dehydrocortisol
delta(1)-Dehydrohydrocortisone
Delta(1)-dehydrohydrocortisone
Delta(1)-Dehydrohydrocortisone
delta(1)-Hydrocortisone
Delta(1)-Hydrocortisone
delta(sup 1)-Cortisol
delta(sup 1)-Dehydrocortisol
delta(sup 1)-Dehydrohydrocortisone
delta(sup 1)-Hydrocortisone
Delta-Cortef
Delta-Cortef (TN)
Deltacortenol
Deltacortril
Deltacortril Enteric
delta-dehydrocortisol
delta-dehydrohydrocortisone
Delta-Ef-Cortelan
delta-hydrocortisone
Deltahydrocortisone
Deltasolone
Delta-stab
Delta-Stab
Deltisilone
Depo-Medrol
Derpo Pd
Derpo PD
Dexa-Cortidelt hostacortin H
Dexa-Cortidelt Hostacortin H
Di adreson F
Di Adreson F
Di-adreson F
Di-Adreson F
Di-adreson-F
DiAdresonF
Di-Adreson-F
Dicortol
Donisolone
Dydeltrone
Eazolin D
Econopred
Econopred Plus
EINECS 200-021-7
Erbacort
Erbasona
Estilsona
Fernisolone
Fernisolone P
Fernisolone-P
Flamasone
HMS1568H10
HMS2090J05
Hostacortin H
HSDB 3385
Hydeltra
Hydeltrasol
Hydeltra-Tba
Hydeltrone
|
Hydrodeltalone
Hydrodeltisone
Hydroretrocortin
Hydroretrocortine
Inflamase Forte
Inflamase Mild
I-Pred
K 1557
Key-Pred
Klismacort
Lentosone
Lite Pred
LMST02030179
LS-7669
Medrol
Medrol Acetate
Metacortandralone
Methylprednisolone acetate
Methylprednisolone Acetate
Meticortelone
Meti-Derm
Metreton
MLS001304083
MLS002154250
MLS002207037
MolPort-002-507-147
M-Predrol
NCGC00179649-01
Neo-Delta-Cortef
Nisolone
Nor-Pred T.B.A.
NSC 9120
NSC9120
NSC9900
Ocu-Pred
Ocu-Pred Forte
Ophtho-Tate
Orapred
P0152_SIGMA
P0637
P6004_SIGMA
Panafcortelone
Paracortol
Paracotol
Pediapred
Poly-Pred
PRDL
Precortalon
Precortancyl
Precortilon
Precortisyl
Pred Forte
Pred Mild
Predair
Predair A
Predair Forte
Predalone 50
Predalone T.B.A.
Predate
Predate Tba
Predate-50
Predcor-25
Predcor-50
Predcor-Tba
PRED-G
Predisolone sodium phosphate
Predisolone Sodium Phosphate
Predne-Dome
Prednelan
Prednicen
Predni-Dome
Predniliderm
Predniretard
Prednis
Prednisolona
Prednisolona [INN-Spanish]
prednisolone
Prednisolone
Prednisolone (anhydrous)
Prednisolone (JP15/USP/INN)
Prednisolone [INN:BAN:JAN]
Prednisolone acetate
Prednisolone Acetate
Prednisolone sodium phosphate
Prednisolone Sodium Phosphate
Prednisolone tebutate
Prednisolone Tebutate
Prednisolonum
Prednisolonum [INN-Latin]
Predonin
Predonine
Prelone
Prenolone
Prestwick_404
Prestwick0_000274
Prestwick1_000274
Prestwick2_000274
Prestwick3_000274
Rolisone
S1737_Selleck
SAM002264639
Scherisolon
SMR000718761
Solone
SPBio_002367
Steran
Sterane
Sterolone
Supercortisol
Ulacort
Ultra Pred
Ultracorten H
Ultracortene H
Ultracortene-H
Ultracortene-hydrogen
Ultracortene-Hydrogen
UNII-9PHQ9Y1OLM
ZINC03833821
δ(1)-dehydrocortisol
δ(1)-dehydrohydrocortisone
δ(1)-hydrocortisone
|
|
| 6 |
|
Methylprednisolone |
Approved, Vet_approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
83-43-2 |
6741
|
|
Synonyms:
(6a,11b)-11,17,21-Trihydroxy-6-methylpregna-1,4-diene-3,20-dione
(6alpha,11beta)-11,17,21-Trihydroxy-6-methylpregna-1,4-diene-3,20-dione
(6S,8S,9S,10R,11S,13S,14S,17R)-11,17-dihydroxy-17-(2-hydroxyacetyl)-6,10,13-trimethyl-7,8,9,11,12,14,15,16-octahydro-6H-cyclopenta[a]phenanthren-3-one
(6α,11β)-11,17,21-trihydroxy-6-methylpregna-1,4-diene-3,20-dione
.DELTA.1-6.alpha.-Methylhydrocortisone
11beta,17,21-Trihydroxy-6alpha-methylpregna-1,4-diene-3,20-dione
11-beta,17,21-Trihydroxy-6-alpha-methylpregna-1,4-diene-3,20-dione
11beta,17alpha,21-Trihydroxy-6alpha-methyl-1,4-pregnadiene-3,20-dione
11beta,17alpha,21-Trihydroxy-6alpha-methylpregna-1,4-diene-3,20-dione
121673-01-6
1-dehydro-6alpha-Methylhydrocortisone
1-Dehydro-6alpha-methylhydrocortisone
1-dehydro-6a-Methylhydrocortisone
1-dehydro-6α-methylhydrocortisone
4-08-00-03498 (Beilstein Handbook Reference)
46436_FLUKA
46436_RIEDEL
570-35-4
6 Methylprednisolone
6.alpha.-Methylprednisolone
6923-42-8
6alpha-Methyl-11beta,17alpha,21-trihydroxy-1,4-pregnadiene-3,20-dione
6alpha-methyl-11beta,17alpha,21-triol-1,4-pregnadiene-3,20-dione
6alpha-Methyl-11beta,17alpha,21-triol-1,4-pregnadiene-3,20-dione
6alpha-Methylprednisolone
6-alpha-Methylprednisolone
6a-Methyl-11b,17a,21-triol-1,4-pregnadiene-3,20-dione
6-Methylprednisolone
6α-methyl-11β,17α,21-triol-1,4-pregnadiene-3,20-dione
83-43-2
AC1L1N7A
Artisone-wyeth
Artisone-Wyeth
Besonia
Bio-0658
BPBio1_000174
BRD-K35240538-001-03-1
BRN 2340300
BSPBio_000158
CHEBI:6888
CHEMBL650
CID6741
CPD000058330
D00407
D008775
DB00959
delta(1)-6alpha-Methylhydrocortisone
Delta(1)-6alpha-Methylhydrocortisone
delta(1)-6a-Methylhydrocortisone
delta(sup 1)-6-alpha-Methylhydrocortisone
Depo-Medrol (acetate)
Dopomedrol
EINECS 201-476-4
Esametone
Firmacort
HMS1568H20
HMS2090B13
HSDB 3127
Lemod
LMST02030178
LS-118498
M0639_SIGMA
M1665
Medesone
Medixon
Medlone 21
Medrate
Medric acid
|
Medrol
Medrol (TN)
Medrol adt pak
Medrol Adt Pak
Medrol dosepak
Medrol Dosepak
Medrol, Solu-Medrol, Medrone, Methylprednisolone
Medrone
MEPRDL
Mesopren
Metastab
Methyleneprednisolone
Methylprednisolon
methylprednisolone
Methylprednisolone
Methylprednisolone (JP15/USP/INN)
Methylprednisolone [USAN:INN:BAN:JAN]
Methylprednisolone, 6-alpha
Methylprednisolonum
Methylprednisolonum [INN-Latin]
methylprenisolone
Metilbetasone
Metilprednisolona
Metilprednisolona [INN-Spanish]
Metilprednisolone
Metilprednisolone [Dcit]
Metilprednisolone [DCIT]
Metipred
Metrisone
Metrocort
Metysolon
MLS000028541
MLS001148159
MLS002207191
Moderin
MolPort-002-528-554
NCGC00022735-03
NCI60_001657
Nirypan
Noretona
NSC19987
NSC-19987
Predni N Tablinen
Prednol- L
Pregna-1,4-diene-3,20-dione, 11beta,17,21-trihydroxy-6alpha-methyl- (8CI)
Prestwick_622
Prestwick0_000279
Prestwick1_000279
Prestwick2_000279
Prestwick3_000279
Promacortine
Reactenol
S1733_Selleck
SAM002589984
Sieropresol
SMR000058330
Solomet
SPBio_002377
Summicort
Suprametil
U 7532
UNII-X4W7ZR7023
Urbason
Urbasone
Wyacort
ZINC03875560
δ(1)-6a-methylhydrocortisone
δ(1)-6α-methylhydrocortisone
|
|
| 7 |
|
Cyclophosphamide |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
50-18-0, 6055-19-2 |
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
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]
|
|
| 8 |
|
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
(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
(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
|
|
| 9 |
|
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
Lenograstim (genetical recombination)
Lenograstim rDNA
|
|
| 10 |
|
Dacarbazine |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
4342-03-4 |
5351166
|
|
Synonyms:
(5E)-5-(dimethylaminohydrazinylidene)imidazole-4-carboxamide
(5Z)-5-(dimethylaminohydrazinylidene)imidazole-4-carboxamide
(Dimethyltriazeno)imidazolecarboxamide
37626-23-6
4-(3,3-dimethyl-1-triazeno)imidazole-5-carboxamide
4-(3,3-Dimethyl-1-triazeno)imidazole-5-carboxamide
4-(3,3-Dimethyltriazeno)imidazole-5-carboxamide
4(5)-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide
4-(5)-(3,3-dimethyl-1-triazeno)imidazole-5(4)-carboxamide
4(5)-(3,3-Dimethyl-1-triazeno)imidazole-5(4)-carboxamide
4-(5)-(3,3-Dimethyl-1-triazeno)imidazole-5(4)-carboxamide
4-(Dimethyltriazeno)imidazole-5-c arboxamide
4-(dimethyltriazeno)imidazole-5-carboxamide
4-(dimethyltriazeno)Imidazole-5-carboxamide
4-(Dimethyltriazeno)imidazole-5-carboxamide
4-(or 5)-(3,3-Dimethyl-1-triazeno)imidazole-5(or 4)-carboxamide
4-(or 5)-(3,3-Dimethyl-1-triazeno)imidazole-5(or 4)-carboxamide
4-[(1E)-3,3-Dimethyltriaz-1-en-1-yl]-1H-imidazole-5-carboxamide
4-[3,3-dimethyltriaz-1-en-1-yl]-1H-imidazole-5-carboxamide
4342-03-4
5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide
5-(3,3-Dimethyl-1-triazeno)imidazole-4-carboxamide
5-(3,3-Dimethyl-1-triazenyl)-1H-imidazole-4-carboxamide
5-(3,3-Dimethyl-1-triazenyl)imidazole-4-carboxamide
5-(3,3-Dimethyltri azeno)imidazole-4-carboxamide
5-(3,3-dimethyltriaz-1-en-1-yl)-1H-imidazole-4-carboxamide
5-(3,3-Dimethyltriazeno)-imidazole-4-carbamide
5-(3,3-dimethyltriazeno)imidazole-4-carboxamide
5-(3,3-dimethyltriazeno)Imidazole-4-carboxamide
5-(3,3-Dimethyltriazeno)imidazole-4-carboxamide
5-(dimethylaminohydrazinylidene)imidazole-4-carboxamide
5-(Dimethyltriazeno)-4-imidazolecarboxamide
5-(dimethyltriazeno)imidazole-4-carboxamide
5-(dimethyltriazeno)Imidazole-4-carboxamide
5-(Dimethyltriazeno)imidazole-4-carboxamide
5-(Dimethyltriazeno)imidazole-4-carboximide
5(or 4)-(dimethyltriazeno)imidazol e-4(or 5)-carboxamide
5(or 4)-(dimethyltriazeno)imidazole-4(or 5)-carboxamide
5-[3,3-Dimethyl-1-triazenyl]imidazole-4-carboxamide
94361-71-4
AC1NQXVV
AC1NS01W
AC1NS4BN
AI3-52825
Biocarbazin
Biocarbazine
Biocarbazine R
BPBio1_000428
BRD-K35520305-001-07-8
BSPBio_000388
BSPBio_002091
C6H10N6O
Carboxamide, Dimethyl Imidazole
CAS-891986
CCRIS 190
CHEBI:4305
CHEMBL476
CID5281007
CID5351166
CID5353562
D00288
D003606
D2390_SIGMA
D3634
Dacarbazin
Dacarbazina
dacarbazine
Dacarbazine
Dacarbazine (JAN/USP/INN)
Dacarbazine [USAN:INN:BAN:JAN]
Dacarbazino
Dacarbazino [INN-Spanish]
Dacarbazinum
Dacarbazinum [INN-Latin]
Dacatic
DB00851
Decarbazine
Deticene
|
DIC
Dimethyl Imidazole Carboxamide
Dimethyl Triazeno Imidazole Carboxamide
Dimethyltriazenoimidazolecarboxamide
Di-methyl-triazenoimidazolecarboxamide
Di-me-triazenoimidazolecarboxamide
DivK1c_000326
DTCI
DTIC
DTIC Dome
DTIC, DTIC-Dome, Dacarbazine
Dtic-dome
Dtic-Dome
DTICDome
DTIC-Dome
Dtic-Dome (TN)
DTIE
EINECS 224-396-1
HE1150000
HMS1569D10
HMS2090A20
HMS2091I20
HMS501A08
HSDB 3219
I06-2280
I14-1659
ICDMT
ICDT
IDI1_000326
Imidazole carboxamide
Imidazole Carboxamide
Imidazole Carboxamide, Dimethyl
KBio1_000326
KBio2_001364
KBio2_003932
KBio2_006500
KBio3_001311
KBioGR_000896
KBioSS_001364
LS-119
MLS001332543
MLS001332544
MolPort-003-666-153
MolPort-003-846-120
MolPort-006-709-420
NCGC00016986-01
NCGC00091861-01
NCGC00091861-02
NCGC00091861-03
NCGC00091861-04
NCI60_004053
NCI-C04717
NCIMech_000261
NINDS_000326
NIOSH/HE1150000
NPFAPI-05
NSC 45388
NSC45388
NSC-45388
Prestwick_904
Prestwick0_000574
Prestwick1_000574
Prestwick2_000574
Prestwick3_000574
S1221_Selleck
SMP2_000251
SMR000857131
SPBio_001075
SPBio_002607
Spectrum_000884
SPECTRUM1500218
Spectrum2_001148
Spectrum3_000366
Spectrum4_000308
Spectrum5_000823
ST51014976
UNII-7GR28W0FJI
WLN: T5M CNJ DVZ ENUNN1&1
|
|
| 11 |
|
Sargramostim |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
123774-72-1, 83869-56-1 |
|
|
Synonyms:
123774-72-1
D05803
Leukine
Leukine (TN)
Recombinant human granulocyte-macrophage colony stimulating factor
rGM-CSF
|
rHu GM-CSF
Sargramostim
Sargramostim (genetical recombination)
Sargramostim (genetical recombination) (JAN)
Sargramostim (USAN/INN)
|
|
| 12 |
|
Bleomycin |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
11056-06-7 |
5360373
|
|
Synonyms:
(betaR)-N(alpha)-{[6-amino-2-((1S)-3-amino-1-{[(2S)-2,3-diamino-3-oxopropyl]amino}-3-oxopropyl)-5-methylpyrimidin-4-yl]carbonyl}-beta-{2-O-[3-O-(aminocarbonyl)-alpha-D-mannopyranosyl]-alpha-L-gulopyranosyloxy}-N-[(1R,2S,3S)-5-({(1S,2R)-1-[({2-[4-({[3-(dimethylsulfonio)propyl]amino}carbonyl)-2,4'-bi-1,3-thiazol-2'-yl]ethyl}amino)carbonyl]-2-hydroxypropyl}amino)-3-hydroxy-4-methyl-5-oxopentan-2-yl]-L-histidinamide
11056-06-7
11116-31-7
1400-95-9
3-[[2-[2-[2-[[(2S,3R)-2-[[(2S,3S,4R)-4-[[(2S)-2-[[6-amino-2-[(1S)-3-amino-1-[[(2S)-2,3-diamino-3-oxopropyl]amino]-3-oxopropyl]-5-methylpyrimidine-4-carbonyl]amino]-3-[(2R,3S,4S,5S,6S)-3-[(2R,3S,4S,5R,6R)-4-carbamoyloxy-3,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-4,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxy-2-methylpentanoyl]amino]-3-hydroxybutanoyl]amino]ethyl]-1,3-thiazol-4-yl]-1,3-thiazole-4-carbonyl]amino]propyl-dimethylsulfanium
3-[[2-[2-[2-[[(2S,3R)-2-[[(2S,3S,4R)-4-[[(2S,3R)-2-[[6-amino-2-[(1S)-3-amino-1-[[(2S)-2,3-diamino-3-oxopropyl]amino]-3-oxopropyl]-5-methylpyrimidine-4-carbonyl]amino]-3-[(2R,3S,4S,5S,6S)-3-[(2R,3S,4S,5R,6R)-4-carbamoyloxy-3,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-4,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxy-2-methylpentanoyl]amino]-3-hydroxybutanoyl]amino]ethyl]-1,3-thiazol-4-yl]-1,3-thiazole-4-carbonyl]amino]propyl-dimethylsulfanium
3-[[2-[2-[2-[[(2S,3R)-2-[[(2S,3S,4R)-4-[[(2S,3R)-2-[[6-amino-2-[(1S)-3-amino-1-[[(2S)-2,3-diamino-3-oxopropyl]amino]-3-oxopropyl]-5-methylpyrimidine-4-carbonyl]amino]-3-[3-[4-carbamoyloxy-3,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-4,5-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3-(1H-imidazol-5-yl)propanoyl]amino]-3-hydroxy-2-methylpentanoyl]amino]-3-hydroxybutanoyl]amino]ethyl]-1,3-thiazol-4-yl]-1,3-thiazole-4-carbonyl]amino]propyl-dimethylsulfanium
37208-04-1
37293-16-6
37353-43-8
9041-93-4
9041-93-4 (sulfate (salt))
AC1L9UFF
AC1NSEJD
AC1NUTOQ
Almirall brand OF bleomycin sulfate
Bellon brand OF bleomycin sulfate
Bellon, bléomycine
Blanoxan
Blenoxane
Bleo
bleo Cell
bleo-Cell
BLEOcell
Bleocin
Bleogin
Bleolem
Bleomicin
Bleomicina
Bleomicina [INN-Spanish]
bleomycin
Bleomycin
Bleomycin a(2)
Bleomycin A(2)
bleomycin a2
Bleomycin a2
Bleomycin A2
Bleomycin A2 & Bleomycin B2.
Bleomycin b(2)
Bleomycin B(2)
Bleomycin b2
Bleomycin B2
Bleomycin sulfate
|
Bleomycin sulphate
Bleomycine
Bleomycine [INN-French]
Bléomycine bellon
Bleomycins
Bleomycinum
Bleomycinum [INN-Latin]
Bleomycinum mack
BLM
Bristol myers squibb brand OF bleomycin sulfate
Bristol-myers squibb brand OF bleomycin sulfate
Bull brand OF bleomycin sulfate
C06854
C55H85N17O21S3
C55H86N17O21S3
CCRIS 2754
Cell pharm brand OF bleomycin sulfate
CHEBI:3139
CHEMBL403664
CID456190
CID5360373
CID5460769
DB00290
EINECS 234-356-5
HSDB 3208
Lemery brand OF bleomycin sulfate
LMPK14000006
LS-44860
LS-524
Lundbeck brand OF bleomycin sulfate
Mack brand OF bleomycin sulfate
Mack, bleomycinum
N(1)-[3-(dimethylsulfonio)propyl]bleomycinamide
N1-(3-(Dimethylsulfonio)propyl)bleomycinamide
NDC 0015-3010
NSC 125066
Pingyangmyvin A2
STOCK1N-74760
Sulfate, bleomycin
UNII-13M89UEA7W
UNII-40S1VHN69B
Zhengguangmycin A2
Zhengguangmycin A2 [Chinese]
|
|
| 13 |
|
Epirubicin |
Approved |
Phase 4,Phase 3,Phase 2,Not Applicable |
|
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
|
|
| 14 |
|
Vincristine |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
2068-78-2, 57-22-7 |
5978
|
|
Synonyms:
22-Oxovincaleukoblastin
22-Oxovincaleukoblastine
28379-27-3
57-22-7
AC1L1LJC
C07204
C46H56N4O10
CCRIS 5763
Cellcristin
CHEBI:28445
CID5978
Citomid
D08679
DB00541
EINECS 200-318-1
Farmistin
HMS2090E19
HSDB 3199
Indole alkaloid
LCR
Leurocristine
Lilly 37231 (1:1 sulfate salt)
Liposomal Vincristine
LS-228
Marqibo
NCGC00163700-01
NCI60_026703
NCI-C04864
NSC-67574
Onco TCS
Oncovin
Oncovin (1:1 sulfate salt)
Oncovine
Onkocristin
|
PFS, Vincasar
Sulfate, vincristine
Tecnocris
Tecnocris (TN)
UNII-5J49Q6B70F
VCR
VIN
Vincaleukoblastine, 22-oxo- 22-Oxovincaleukoblastine
Vincasar
Vincasar (1:1 sulfate salt)
Vincasar PFS
Vincrex
Vincrex (1:1 sulfate salt)
Vincristin
Vincristin bristol
Vincristin medac
Vincristina
Vincristina [DCIT]
vincristine
Vincristine
Vincristine (INN)
Vincristine [INN:BAN]
Vincristine sulfate
Vincristine Sulfate
Vincristine Sulfate PFS
Vincristinum
Vincristinum [INN-Latin]
Vincrisul
Vincrstine
Vincrystine
Vinkristin
Vintec
Z-D-Val-lys(Z)-OH
Z-D-Val-Lys(Z)-OH
|
|
| 15 |
|
Etoposide |
Approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
33419-42-0 |
36462
|
|
Synonyms:
(−)-etoposide
(-)-Etoposide
121471-01-0
136598-18-0
201594-04-9
33419-42-0
35317-32-9
4'-Demethylepipodophyllotoxin 9-(4,6-O-(R)-ethylidene-b-D-glucopyranoside)
4'-Demethylepipodophyllotoxin 9-(4,6-O-(R)-ethylidene-beta-D-glucopyranoside)
4'-Demethylepipodophyllotoxin 9-(4,6-O-(R)-ethylidene-β-D-glucopyranoside)
4'-Demethylepipodophyllotoxin 9-(4,6-O-ethylidene-beta-D-glucopyranoside)
4'-Demethyl-epipodophyllotoxin 9-[4,6-O-(R)-ethylidene-beta-D-glucopyranoside
4-Demethylepipodophyllotoxin b-D-ethylideneglucoside
4-Demethylepipodophyllotoxin beta-D-ethylideneglucoside
4'-Demethylepipodophyllotoxin ethylidene-.beta.-D-glucoside
4-demethylepipodophyllotoxin β-D-ethylideneglucoside
4-Demethylepipodophyllotoxin β-D-ethylideneglucoside
4-Demethylepipodophyllotoxin-.beta.-D-ethylideneglucoside
4'-O-Demethyl-1-O-(4,6-O-ethylidene-beta-D-glucopyranosyl)epipodophyllotoxin
51854-34-3
76576-58-4
9-((4,6-O-Ethylidine-b-D-glucopyranosyl)oxy)-5,8,8a,9-tetrahydro-5-(4-hydroxy-3,4-dimethyloxyphenyl)furo(3',4'':6,7)naptho-(2,3-D)-1,3-dioxol-6(5ah)-one
9-((4,6-O-Ethylidine-beta-D-glucopyranosyl)oxy)-5,8,8a,9-tetrahydro-5-(4-hydroxy-3,4-dimethyloxyphenyl)furo(3',4'':6,7)naptho-(2,3-d)-1,3-dioxol-6(5aH)-one
9-((4,6-O-Ethylidine-beta-D-glucopyranosyl)oxy)-5,8,8a,9-tetrahydro-5-(4-hydroxy-3,4-dimethyloxyphenyl)furo(3',4'':6,7)naptho-(2,3-D)-1,3-dioxol-6(5ah)-one
9-((4,6-O-Ethylidine-β-D-glucopyranosyl)oxy)-5,8,8a,9-tetrahydro-5-(4-hydroxy-3,4-dimethyloxyphenyl)furo(3',4'':6,7)naptho-(2,3-D)-1,3-dioxol-6(5ah)-one
AB00438905
AC1L1FN8
AC1L1VT3
AC1L6246
AC1NR4OG
AC1O4WGG
AC1O7M1N
AC1Q47JJ
alpha-D-Glucopyranosyl isomer etoposide
Ambap33419-42-0
Baxter brand OF etoposide
Baxter oncology brand OF etoposide
Bio1_000489
Bio1_000978
Bio1_001467
BPBio1_000673
BRD-K37798499-001-02-5
Bristol myers brand OF etoposide
Bristol myers squibb brand OF etoposide
Bristol-myers brand OF etoposide
Bristol-myers squibb brand OF etoposide
BSPBio_000611
C01576
CCRIS 2392
Celltop
CHEBI:4911
CHEBI:588795
CHEMBL44657
CID11758093
CID284997
CID3310
CID36462
CID5284558
CID6419930
CID6610299
CPD000112002
D00125
DB00773
DEMETHY-EPIPODOPHYLLOTOXIN,ETHYLIDENE GLUCOSIDE,
Demethyl epipodophyllotoxin ethylidine glucoside
Demethyl Epipodophyllotoxin Ethylidine Glucoside
Demethyl-epiodophyllotoxin ethylidene glucoside
Demethylepipodophyllotoxin-beta-D-ethylideneglucoside
E0675
E1383_SIGMA
EINECS 251-509-1
Epipodophyllotoxin VP-16213
Epipodophyllotoxin, 4'-demethyl-, 4,6-O-ethylidene-.beta.-D-glucopyranoside
Epipodophyllotoxin, 4'-demethyl-, 4,6-O-ethylidene-beta-D-glucopyranoside
Epipodophyllotoxin, 4'-demethyl-, 4,6-O-ethylidene-beta-D-glucopyranoside (8CI)
Epipodophyllotoxin, 4'-demethyl-, 9-(4,6-O-ethylidene-.beta.-D-glucopyranoside)
Epipodophyllotoxin, 4'-demethyl-, 9-(4,6-O-ethylidene-beta-D-glucopyranoside)
Eposide
Eposin
Eposin, Vepesid, VP-16, Toposar, Etoposide
eto GRY
eto-GRY
Etomedac
ETOP
Etopol
Etopophos
Etopophos (phosphate salt)
Etopos
|
etoposide
Etoposide
Etoposide (JP15/USP/INN)
Etoposide (VP16)
Etoposide [USAN:INN:BAN:JAN]
Etoposide pierre fabre
Etoposide teva
Etoposide, (5a alpha)-isomer
Etoposide, (5a alpha,9 alpha)-isomer
Etoposide, (5S)-isomer
Etoposide, alpha D glucopyranosyl isomer
Etoposide, alpha-D-glucopyranosyl isomer
Etoposido
Etoposido [INN-Spanish]
etoposido Ferrer farma
Etoposidum
Etoposidum [INN-Latin]
Etosid
Exitop
Ferrer brand OF etoposide
Gry brand OF etoposide
HMS1569O13
HMS2052N05
HMS2089F14
HSDB 6517
I06-0248
KBioSS_002410
Lastet
Lemery brand OF etoposide
LS-1214
Medac brand OF etoposide
MLS000049957
MLS001074951
MLS001424283
MLS002153463
MLS002207239
MLS002222184
MolPort-003-983-431
MolPort-004-905-001
MolPort-004-955-161
NCGC00025056-02
NChemBio.2007.10-comp19
nchembio.573-comp8
nchembio873-comp2
NK 171
Novartis brand OF etoposide
NSC 141540
NSC141540
NSC-141540
Onkoposid
Onkoworks brand OF etoposide
Pharmachemie brand OF etoposide
Pierre fabre brand OF etoposide
Prasfarma brand OF etoposide
Prestwick_211
Prestwick0_000396
Prestwick1_000396
Prestwick2_000396
Prestwick3_000396
Riboposid
Ribosepharm brand OF etoposide
S1225_Selleck
SAM001246880
Sanfer brand OF etoposide
SMR000112002
SPBio_002532
ST056353
Tedec meiji brand OF etoposide
Teva brand OF etoposide
Toposar
trans-Etoposide
UNII-6PLQ3CP4P3
Vepesid
VePesid
VePESID (TN)
Vepesid J
Vepeside
Vépéside sandoz
Vépéside-sandoz
VP 16
VP 16 (pharmaceutical)
VP 16213
VP 16-213
VP-16
VP-16-213
ZINC03830818
ZINC03938684
Zuyeyidal
|
|
| 16 |
|
rituximab |
Approved |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
174722-31-7 |
10201696
|
|
Synonyms:
AntiCD20
IDEC-102
IDEC-C2B8
Ig gamma-1 chain C region
Mabthera
|
MabThera
Rituxan
rituximab
rituximab-abbs
|
|
| 17 |
|
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
Thiotepa
Triethylenethiophosphoramide
Tris(1-aziridinyl)phosphine sulfide
|
|
| 18 |
|
Prednisolone hemisuccinate |
Experimental |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
2920-86-7 |
|
|
Synonyms:
(+)-prednisolone hemisuccinate
Prednisolonbisuccinat
Prednisolone 21-hemisuccinate
Prednisolone 21-succinate
|
Prednisolone bisuccinate
Prednisolone hydrogen succinate
Prednisolone succinate
|
|
| 19 |
|
Doxil |
Approved June 1999 |
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
31703
|
|
Synonyms:
|
|
LipoDox
liposomal doxorubicin
Pegylated Liposomal Doxorubicin Hydrochloride
|
|
| 20 |
|
Antineoplastic Agents, Hormonal |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 21 |
|
Antimitotic Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 22 |
|
Antineoplastic Agents, Alkylating |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 23 |
|
Hormones |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 24 |
|
Antirheumatic Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 25 |
|
Hormones, Hormone Substitutes, and Hormone Antagonists |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 26 |
|
Immunologic Factors |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 27 |
|
Alkylating Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 28 |
|
Methylprednisolone Acetate |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 29 |
|
Antiemetics |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 30 |
|
glucocorticoids |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 31 |
|
Immunosuppressive Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 32 |
|
Peripheral Nervous System Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 33 |
|
Anti-Inflammatory Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 34 |
|
Gastrointestinal Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 35 |
|
Protective Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 36 |
|
Neuroprotective Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 37 |
|
Autonomic Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 38 |
|
Hormone Antagonists |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 39 |
|
Prednisolone acetate |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 40 |
|
Antineoplastic Agents, Phytogenic |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 41 |
|
Anti-Bacterial Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 42 |
|
Antibiotics, Antitubercular |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 43 |
|
Topoisomerase Inhibitors |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 44 |
|
Antilymphocyte Serum |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 45 |
|
Antibodies |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 46 |
|
Antibodies, Monoclonal |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 47 |
|
Immunoglobulins |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 48 |
|
Etoposide phosphate |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 49 |
|
Mitogens |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 50 |
|
Cytarabine |
Approved, Experimental, Investigational |
Phase 3,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
147-94-4, 65-46-3 |
6253
|
|
Synonyms:
(beta-D-Arabinofuranosyl)cytosine
1-.beta.-D-arabinofuranosyl-cytosine
147-94-4
1-Arabinofuranosylcytosine
1-b-D-Arabinofuranosylcytosine
1beta -Arabinofuranasylcytosine
1-beta -D-Arabinofaranosylcytosine
1-beta -D-Arabinofuranosyl-4-amino-2(1H)pyrimidinone
1beta -D-Arabinofuranosylcytosine
1-beta -D-Arabinofuranosylcytosine
1beta -D-Arabinosylcytosine
1beta-Arabinofuranasylcytosine
1-beta-D-Arabinofaranosylcytosine
1-beta-D-Arabinofuranosyl-4-amino-2(1H)pyrimidinone
1beta-D-Arabinofuranosylcytosine
1-beta-D-Arabinofuranosylcytosine
1-beta-D-Arabinofuranosyl-cytosine
1-beta-D-Arabinofuranosylcytosine, cytosine arabinoside
1-beta-D-Arabinofuranosylcytosine, Cytosine Arabinoside
1beta-D-Arabinosylcytosine
1-beta-D-Arabinosylcytosine
1-beta-D-Arabinosyl-cytosine
1-beta-D-Ribofuranosylcytosine
1-β-D-arabinofuranosylcytosine
1β-D-ribofuranosylcytosine
2(1H)-Pyrimidinone, 4-amino-1- -D-arabinofuranosyl- [CAS]
2(1H)-Pyrimidinone, 4-amino-1- -D-arabinofuranosyl
30399_FLUKA
4-amino-1-[(2R,3S,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidin-2-one
4-amino-1-Arabinofuranosyl-2-oxo-1,2-dihydropyrimidin
4-Amino-1-arabinofuranosyl-2-oxo-1,2-dihydropyrimidin
4-Amino-1-arabinofuranosyl-2-oxo-1,2-dihydropyrimidin [Czech]
4-amino-1-Arabinofuranosyl-2-oxo-1,2-dihydropyrimidine
4-Amino-1-arabinofuranosyl-2-oxo-1,2-dihydropyrimidine
4-amino-1-b-D-Arabinofuranosyl-2(1H)-pyrimidinone
4-amino-1-b-D-Arabinofuranosyl-2-(1H)-pyrimidinone
4-Amino-1-b-D-arabinofuranosyl-2-(1H)-pyrimidinone
4-Amino-1-beta-D-arabinofuranosyl-2(1H)-pyrimidinon
4-Amino-1-beta-D-arabinofuranosyl-2(1H)-pyrimidinon [Czech]
4-amino-1-beta-D-Arabinofuranosyl-2(1H)-pyrimidinone
4-Amino-1-beta-D-arabinofuranosyl-2(1H)-pyrimidinone
4-amino-1-beta-D-arabinofuranosylpyrimidin-2(1H)-one
4-amino-1-beta-D-Arabinofuranosylpyrimidin-2(1H)-one
4-amino-1-β-D-arabinofuranosyl-2(1H)-pyrimidinone
4-amino-1β-D-ribofuranosyl-2(1H)-pyrimidinone
4-amino-1-β-D-ribofuranosylpyrimidin-2(1H)-one
69-74-9 (hydrochloride)
AC-1075
AC1L1M4F
AC1Q52OJ
AI3-52329
Alexan
AR3
Arabinocytidine
Arabinofuranosylcytosine
Arabinoside, cytosine
Arabinosyl Cytosine
Arabinosylcytosine
Arabitin
AraC
Ara-C
Ara-C, Cytosine Arabinoside, Cytosar-U, Cytarabine
Aracytidine
Ara-Cytidine
Aracytin
Aracytine
Arafcyt
beta -Arabinosylcytosine
beta -Cytosine arabinoside
beta -D-Arabinosylcytosine
beta-Ara c
beta-Ara C
beta-Arabinosylcytosine
beta-Cytosine arabinoside
Beta-cytosine arabinoside
beta-D-Arabinosylcytosine
BIDD:GT0371
BIDD:PXR0139
BTB15125
C02961
C1768_SIGMA
C2035
C9H13N3O5
CCRIS 913
CHEBI:28680
CHEMBL803
CHX 3311
CID6253
Citarabina
|
Citarabina [INN-Spanish]
Citidina
CPD000449317
Cytarabin
Cytarabina
cytarabine
Cytarabine
Cytarabine (JP15/USP/INN)
CYTARABINE (SEE ALSO CYTARABINE HYDROCHLORIDE 69-74-9)
Cytarabine [USAN:INN:BAN:JAN]
Cytarabine hydrochloride
cytarabine liposome injection
Cytarabine liposome injection
Cytarabinoside
Cytarabinum
Cytarabinum [INN-Latin]
Cytarbel
Cytidin
Cytonal
Cytosar
Cytosar u
Cytosar-u
CytosarU
Cytosar-U
Cytosine 1-beta-D-arabinofuranoside
Cytosine arabinofuranoside
Cytosine arabinose
Cytosine arabinoside
Cytosine arabinoside (VAN)
Cytosine beta-D-arabinofuranoside
Cytosine beta-D-arabinofuranoside hydrochloride
Cytosine beta-D-arabinoside
Cytosine riboside
Cytosine, beta -D-arabinoside
Cytosine, beta-D-arabinoside
Cytosine-1-b-D-arabinofuranoside
Cytosine-1-beta-D-arabinofuranoside
Cytosine-1-beta-D-arabinofuranoside hydrochloride
Cytosine-1-β-D-arabinofuranoside
Cytosinearabinoside
Cytosine-b-D-arabinofuranoside
Cytosine-beta -arabinoside
Cytosine-beta -D-arabinofuranoside
Cytosine-beta-arabinoside
Cytosine-beta-D-arabinofuranoside
cytosine-β-D-arabinofuranoside
Cytosine-β-D-arabinofuranoside
D00168
DB00987
Depocyt
Depocyt (liposomal)
Depocyt (TN)
Depocyte
DepoCyte
EINECS 205-705-9
Erpalfa
FT-0082880
HMS2051K19
HMS2090A18
HSDB 3049
Hydrochloride, cytarabine
Intrathecal (injected into the spinal fluid) DepoCyt
Intrathecal cytarabine (also known as ara-C)
Iretin
Lopac0_000316
LS-860
MLS000758310
MLS001066340
MolPort-001-792-509
NCGC00093356-03
NCGC00093356-04
NCGC00093356-05
NCI-C04728
NSC 287459
NSC287459
S1648_Selleck
SAM001247012
SMR000449317
Spongocytidine
SR-01000075773-3
Tarabine
TL8001048
U 19920A
U-19,920
U-19920
Udicil
UNII-04079A1RDZ
ZINC03795098
Zytidin
|
|
Interventional clinical trials:
(show top 50)
(show all 1302)
| # |
Name |
Status |
NCT ID |
Phase |
Drugs |
| 1 |
Surgery Alone, Surgery With Cyclophosphamide, Vinblastine, and Prednisolone (CVP), or CVP Alone in Treating Young Patients With Stage IA or Stage IIA Nodular Lymphocyte-Predominant Hodgkin Lymphoma |
Unknown status |
NCT01088750
|
Phase 4 |
cyclophosphamide;prednisolone;vinblastine sulfate |
| 2 |
Optimization of the Primary Therapy for Patients With Hodgkin's Disease and Evaluation of PET |
Unknown status |
NCT00188149
|
Phase 4 |
Combined chemotherapy (ABVD, BACOPP-D) |
| 3 |
Doxorubicin Pharmacokinetics and Response in Non Hodgkin's Lymphoma |
Completed |
NCT00969462
|
Phase 4 |
Doxorubicin |
| 4 |
Bone Marrow Transplantation in Treating Patients With Hematologic Cancer |
Completed |
NCT00003398
|
Phase 4 |
cyclophosphamide;thiotepa |
| 5 |
Pediatric Hodgkin Lymphoma Treatment Trial With Low Cumulative Doses of Chemotherapy Agents and Reduced Radiation. |
Recruiting |
NCT03500133
|
Phase 4 |
Low risk with complete early response after two cycles of ABVD chemotherapy schedule. Only one more ABVD course is delivered.;Low risk with partial remisssion after 4 cycles of ABVD chemotherapy schedule. Two ESHAP courses are delivered.;Intermediate risk with complete early response after two cycles of ABVD chemotherapy schedule. Three more ABVD courses are delivered.;Intermediate risk with partial remission after two cycles of ABVD chemotherapy schedule. Four more chemotherapy courses are delivered alternating ESHAP and ABVD.;High risk with complete early response after 1 ABVD and 1 ESHAP courses. Four more chemotherapy courses are delivered alternating ESHAP and ABVD.;High risk with partial remission after 1 ABVD and 1 ESHAP courses. Six more chemotherapy courses are delivered alternating ESHAP and ABVD.;Low risk with partial remission at early response assessment after two cycles of ABVD chemotherpay schedule. Two ABVD courses are delivered. |
| 6 |
A Safety Study of Growth Factor Use in Treatment With Brentuximab Vedotin Plus Chemotherapy |
Recruiting |
NCT03646123
|
Phase 4 |
brentuximab vedotin;doxorubicin;vinblastine;dacarbazine;G-CSF |
| 7 |
Clinical Application of Polyethylene Glycol Liposome Doxorubicin (PLD) in Primary Lymphoma |
Recruiting |
NCT02526823
|
Phase 4 |
R-CHOP/CHOPE or ABVD chemotherapy regimen;R-CDOP/CDOPE or DBVD chemotherapy regimen |
| 8 |
A Study of Brentuximab Vedotin in Participants With Relapsed or Refractory Hodgkin Lymphoma |
Active, not recruiting |
NCT01990534
|
Phase 4 |
Brentuximab vedotin |
| 9 |
Study Evaluating the Effect of R-mabHDI in Lymphocytic Predominant Hodgkin's Lymphoma |
Unknown status |
NCT00816959
|
Phase 3 |
R-mabHDI and ABVD;ABVD |
| 10 |
Randomized Trial of G-CSF Alone Versus Intermediate-dose Ara-C Plus G-CSF Mobilization in Hodgkin's Lymphoma or Non-Hodgkin's Lymphoma |
Unknown status |
NCT02722733
|
Phase 3 |
G-CSF (filgrastim);Cytosine arabinoside with G-CSF (filgrastim) |
| 11 |
Combination Chemotherapy and Peripheral Stem Cell Transplant in Treating Patients With Relapsed Hodgkin's Lymphoma |
Unknown status |
NCT00025636
|
Phase 3 |
carmustine;cisplatin;cyclophosphamide;cytarabine;dexamethasone;etoposide;melphalan;methotrexate;vincristine sulfate |
| 12 |
Combination Chemotherapy Followed by Radiation Therapy in Treating Young Patients With Newly Diagnosed Hodgkin's Lymphoma |
Unknown status |
NCT00302003
|
Phase 3 |
doxorubicin hydrochloride;vincristine sulfate;prednisone;cyclophosphamide;ifosfamide;vinorelbine tartrate;dexamethasone;etoposide phosphate;cisplatin;cytarabine |
| 13 |
Combination Chemotherapy in Treating Patients With Previously Untreated Advanced Hodgkin's Lymphoma |
Unknown status |
NCT00041210
|
Phase 3 |
ABVD regimen;Stanford V regimen;dacarbazine;doxorubicin hydrochloride;etoposide;mechlorethamine hydrochloride;prednisone;vinblastine sulfate;vincristine sulfate |
| 14 |
Combination Chemotherapy Given With Radiation Therapy or Radiation Therapy Alone in Treating Patients With Early-Stage Hodgkin's Disease |
Unknown status |
NCT00002987
|
Phase 3 |
cyclophosphamide;doxorubicin hydrochloride;etoposide;prednisolone;vincristine sulfate |
| 15 |
Ketamine Hydrochloride and Best Pain Management in Treating Cancer Patients With Neuropathic Pain |
Unknown status |
NCT01316744
|
Phase 3 |
ketamine hydrochloride |
| 16 |
Levofloxacin Compared With Cefepime in Treating Cancer Patients With Fever and Neutropenia |
Unknown status |
NCT00020865
|
Phase 3 |
cefepime hydrochloride;levofloxacin |
| 17 |
Early Hospital Discharge or Standard Inpatient Care in Cancer Patients Receiving Antibiotics for Febrile Neutropenia |
Unknown status |
NCT00445497
|
Phase 3 |
amoxicillin-clavulanate potassium;ciprofloxacin |
| 18 |
Study of Fixed vs. Flexible Filgrastim to Accelerate Bone Marrow Recovery After Chemotherapy in Children With Cancer |
Unknown status |
NCT01987596
|
Phase 3 |
|
| 19 |
Interferon Alfa-2b Following Chemotherapy and Peripheral Stem Cell Transplantation in Treating Patients With Recurrent or Refractory Hodgkin's Disease or Non-Hodgkin's Lymphoma |
Unknown status |
NCT00003924
|
Phase 3 |
|
| 20 |
Exercise During Chemotherapy for Patients With Hematological Malignancies |
Unknown status |
NCT00884364
|
Phase 3 |
|
| 21 |
Study Comparing ABVD vs BEACOPP in Advanced Hodgkin's Lymphoma |
Completed |
NCT01251107
|
Phase 3 |
Bleomycin;Etoposide;Doxorubicin;Cyclophosphamide;Vincristine;Procarbazine;Prednisone;Doxorubicin;Bleomycin;Vinblastine;Dacarbazine |
| 22 |
Combination Chemotherapy and Radiation Therapy in Treating Young Patients With Newly Diagnosed Hodgkin Lymphoma |
Completed |
NCT01026220
|
Phase 3 |
doxorubicin hydrochloride;liposomal vincristine sulfate;vinorelbine tartrate;cyclophosphamide;etoposide phosphate;prednisone;ifosfamide |
| 23 |
A Phase III Randomized, Double Blind, Placebo Controlled Multi-center Study of Panobinostat for Maintenance of Response in Patients With Hodgkin's Lymphoma (HL) |
Completed |
NCT01034163
|
Phase 3 |
Panobinostat;Placebo |
| 24 |
Fludeoxyglucose F 18 PET Scan-Guided Therapy or Standard Therapy in Treating Patients With Previously Untreated Stage I or Stage II Hodgkin's Lymphoma |
Completed |
NCT00433433
|
Phase 3 |
ABVD q4 weeks;BEACOPP escalated q3 weeks |
| 25 |
Combination Chemotherapy in Treating Young Patients With Hodgkin's Lymphoma |
Completed |
NCT00433459
|
Phase 3 |
cyclophosphamide;dacarbazine;prednisolone;prednisone;procarbazine hydrochloride;vincristine sulfate |
| 26 |
Study of a Treatment Driven by Early PET Response to a Treatment Not Monitored by Early PET in Patients With AA Stage 3-4 or 2B HL |
Completed |
NCT01358747
|
Phase 3 |
BEACOPPesc;BEACOPPesc - ABVD - PET2 |
| 27 |
High-dose Chemotherapy and Stem Cell Transplantation, in Patients PET-2 Positive, After 2 Courses of ABVD and Comparison of RT Versus no RT in PET-2 Negative Patients |
Completed |
NCT00784537
|
Phase 2, Phase 3 |
ABVD;ABVD and Radiotherapy |
| 28 |
Immunotherapy Using Cyclosporine, Interferon Gamma, and Interleukin-2 After High-Dose Myeloablative Chemotherapy With Autologous Stem Cell Transplantation in Treating Patients With Refractory or Relapsed Hodgkin's Lymphoma |
Completed |
NCT00070187
|
Phase 2, Phase 3 |
carmustine;cyclosporine;cytarabine;etoposide;melphalan |
| 29 |
Combination Chemotherapy With or Without Radiation Therapy in Treating Patients With Hodgkin's Lymphoma |
Completed |
NCT00003389
|
Phase 3 |
Doxorubicin;Bleomycin;Vinblastine;Dacarbazine;Vincristine;Mechlorethamine;Etoposide;Prednisone;Cyclophosphamide |
| 30 |
HD12 for Advanced Stages |
Completed |
NCT00265031
|
Phase 3 |
Cyclophosphamide;Adriamycin;Etoposide;Procarbazine;Prednisone;Vincristine;Bleomycin |
| 31 |
HD10 for Early Stages |
Completed |
NCT00265018
|
Phase 3 |
Adriamycin;Bleomycin;Vinblastine;DTIC |
| 32 |
HD11 for Intermediate Stages |
Completed |
NCT00264953
|
Phase 3 |
Adriamycin;Bleomycin;Vinblastine;DTIC;Etoposide;Procarbazine;Prednisone;Vincristine |
| 33 |
Radiation Therapy and Chemotherapy in Treating Patients With Hodgkin's Disease |
Completed |
NCT00002561
|
Phase 3 |
dacarbazine;doxorubicin hydrochloride;vinblastine |
| 34 |
Tacrolimus/Sirolimus/Methotrexate vs Tacrolimus/Methotrexate or Cyclosporine/Mycophenolate Mofetil for GVHD Prophylaxis After Reduced Intensity Allogeneic Stem Cell Transplantation for Patients With Lymphoma |
Completed |
NCT00928018
|
Phase 3 |
Sirolimus;Methotrexate;Tacrolimus;Cyclosporine;MMF |
| 35 |
Prophylactic Use of Filgrastim SD/01 in Patients With Hodgkin's Disease Receiving ABVD Chemotherapy |
Completed |
NCT00038558
|
Phase 3 |
Filgrastim SD/01;Adriamycin;Bleomycin;Vinblastine;DTIC |
| 36 |
SWOG-9133 RT w/ or w/o Doxorubicin and Vinblastine in Stage I or Stage II Hodgkin's Disease |
Completed |
NCT00002495
|
Phase 3 |
doxorubicin hydrochloride;vinblastine |
| 37 |
An International Study to Evaluate Recombinant Interleukin-2 in HIV Positive Patients Taking Anti-retroviral Therapy |
Completed |
NCT00004978
|
Phase 3 |
Recombinant interleukin-2 (rIL-2) |
| 38 |
Combination Chemotherapy in Treating Patients With Advanced Hodgkin's Disease |
Completed |
NCT00003421
|
Phase 3 |
ABVD regimen;chlorambucil;dacarbazine;doxorubicin hydrochloride;etoposide;prednisolone;procarbazine hydrochloride;vinblastine sulfate;vincristine sulfate |
| 39 |
Chemotherapy Followed by Radiation Therapy in Treating Young Patients With Newly Diagnosed Hodgkin's Disease |
Completed |
NCT00002827
|
Phase 3 |
dexrazoxane hydrochloride;doxorubicin hydrochloride;etoposide;vincristine sulfate |
| 40 |
Combination Chemotherapy With or Without Dexrazoxane in Treating Children With Hodgkin's Disease |
Completed |
NCT00005578
|
Phase 3 |
cyclophosphamide;dexrazoxane hydrochloride;doxorubicin hydrochloride;etoposide;prednisone;vincristine sulfate |
| 41 |
Chemotherapy With or Without Additional Chemotherapy and/or Radiation Therapy in Treating Children With Newly Diagnosed Hodgkin's Disease |
Completed |
NCT00025259
|
Phase 3 |
Cisplatin;Cyclophosphamide;Cytarabine;Dexamethasone;Doxorubicin Hydrochloride;Etoposide;Prednisone;Vincristine Sulfate Liposome |
| 42 |
Internet-Based Program With or Without Telephone-Based Problem-Solving Training in Helping Long-Term Survivors of Hematopoietic Stem Cell Transplant Cope With Late Complications |
Completed |
NCT00799461
|
Phase 3 |
|
| 43 |
St. John's Wort in Relieving Fatigue in Patients Undergoing Chemotherapy or Hormone Therapy for Cancer |
Completed |
NCT00005805
|
Phase 3 |
|
| 44 |
Prevention of Infection in Patients With Hematologic Cancer and Persistent Fever Caused by a Low White Blood Cell Count |
Completed |
NCT00003805
|
Phase 3 |
piperacillin sodium;piperacillin-tazobactam;tazobactam sodium;vancomycin |
| 45 |
Liposomal Amphotericin B in Treating Granulocytopenia and Persistent Unexplained Fever in Cancer Patients |
Completed |
NCT00003938
|
Phase 3 |
liposomal amphotericin B |
| 46 |
Dalteparin to Prevent Complications in Cancer Patients Receiving Chemotherapy Through a Catheter |
Completed |
NCT00006083
|
Phase 3 |
Fragmin |
| 47 |
Personalized Information or Basic Information in Helping Patients Make Decisions About Participating in a Clinical Trial |
Completed |
NCT00750009
|
Phase 3 |
|
| 48 |
Caspofungin Acetate Compared With Amphotericin B Liposomal in Treating Patients With Persistent Fever and Neutropenia Following Cancer Treatment |
Completed |
NCT00008359
|
Phase 3 |
caspofungin acetate;liposomal amphotericin B |
| 49 |
Levofloxacin to Prevent Infection Following Chemotherapy in Treating Patients With Solid Tumors or Lymphoma |
Completed |
NCT00005590
|
Phase 3 |
levofloxacin |
| 50 |
Opioid Titration Order Sheet or Standard Care in Treating Patients With Cancer Pain |
Completed |
NCT00666211
|
Phase 3 |
|
Inferred drug relations via
UMLS
74
/
NDF-RT
52
:
Cell-based therapeutics:
Data from LifeMap, the Embryonic Development and Stem Cells Database
Stem-cell-based therapeutic approaches for Lymphoma, Hodgkin, Classic:
Embryonic/Adult Cultured Cells Related to Lymphoma, Hodgkin, Classic:
|
