FDA approved drugs:
(show top 50)
(show all 125)
| # |
|
Drug Name |
Active Ingredient(s) 18
|
Company |
Approval Date |
| 1 |
|
Abraxane
18
49
|
PACLITAXEL |
Celgene |
October 2012 |
Disease/s that Drug Treats:non-small cell lung cancer
Indications and Usage:
18
ABRAXANE is a microtubule inhibitor indicated for the treatment of: Metastatic breast cancer, after failure of combination chemotherapyfor metastatic disease or relapse within 6 months of adjuvantchemotherapy. Prior therapy should have included an anthracyclineunless clinically contraindicated. (1.1) Locally advanced or metastatic non-small cell lung cancer (NSCLC),as first-line treatment in combination with carboplatin, in patients whoare not candidates for curative surgery or radiation therapy. (1.2) Metastatic adenocarcinoma of the pancreas as first-line treatment, incombination with gemcitabine. (1.3), ABRAXANE is a microtubule inhibitor indicated for the treatment of: * Metastatic breast cancer, after failure of combination chemotherapy for metastatic disease or relapse within 6 months of adjuvant chemotherapy. Prior therapy should have included an anthracycline unless clinically contraindicated. (1.1) * Locally advanced or metastatic non-small cell lung cancer (NSCLC), as first-line treatment in combination with carboplatin, in patients who are not candidates for curative surgery or radiation therapy. (1.2) * Metastatic adenocarcinoma of the pancreas as first-line treatment, in combination with gemcitabine. (1.3)
DrugBank Targets:
16
1. Apoptosis regulator Bcl-2;;2. Tubulin beta-1 chain;;3. Nuclear receptor subfamily 1 group I member 2;;4. Microtubule-associated protein 4;;5. Microtubule-associated protein 2; ;6. Microtubule-associated protein tau, Apoptosis regulator Bcl-2|Tubulin beta-1 chain|Nuclear receptor subfamily 1 group I member 2|Microtubule-associated protein 4|Microtubule-associated protein 2|Microtubule-associated protein tau|
Mechanism of Action:
18
Target: microtubule , microtubule
Action: inhibitor
FDA: ABRAXANE is a microtubule inhibitor that promotes the assembly of microtubules from tubulin dimers and stabilizes microtubulesby preventing depolymerization. This stability results in the inhibition of the normal dynamic reorganization of the microtubulenetwork that is essential for vital interphase and mitotic cellular functions. Paclitaxel induces abnormal arrays or âbundlesâ ofmicrotubules throughout the cell cycle and multiple asters of microtubules during mitosis. , ABRAXANE is a microtubule inhibitor that promotes the assembly of microtubules from tubulin dimers and stabilizes microtubules by preventing depolymerization. This stability results in the inhibition of the normal dynamic reorganization of the microtubule network that is essential for vital interphase and mitotic cellular functions. Paclitaxel induces abnormal arrays or âbundlesâ of microtubules throughout the cell cycle and multiple asters of microtubules during mitosis.
|
| 2 |
|
Abstral
18
|
FENTANYL (citrate) |
ProStrakan |
January 2011 |
Disease/s that Drug Treats:breakthrough cancer pain in opiod-tolerant patients
Indications and Usage:
18
ABSTRAL is an opioid agonist indicated for the management of breakthrough pain in cancer patients 18 years of age and older who are already receiving and who are tolerant to opioid therapy for their underlying persistent cancer pain. (1) Limitations of Use: ABSTRAL may be dispensed only to patients enrolled in the TIRF REMS Access program.
DrugBank Targets:
16
1. Mu-type opioid receptor ;2. Delta-type opioid receptor;3. Kappa-type opioid receptor
Mechanism of Action:
18
Target: µ-opioid receptor (possible mechanism of action)
Action: agonist
FDA: Fentanyl is a pure opioid agonist whose principal therapeutic action is analgesia. Other members of the classknown as opioid agonists include substances such as morphine, oxycodone, hydromorphone, codeine, andhydrocodone.
|
| 3 |
|
Actiq
18
|
FENTANYL (citrate) |
Anesta Corporation |
November 1998 |
Disease/s that Drug Treats:cancer pain
Indications and Usage:
18
ACTIQ is an opioid agonist indicated for the management of breakthrough pain in cancer patients 16 years of age and older who are already receiving and who are tolerant to around-the-clock opioid therapy for their underlying persistent cancer pain. (1) Limitations of Use: ACTIQ may be dispensed only to patients enrolled in the TIRF REMS Access program. (1)
DrugBank Targets:
16
1. Mu-type opioid receptor ;2. Delta-type opioid receptor;3. Kappa-type opioid receptor
Mechanism of Action:
18
Target: -
Action: agonist
FDA: Fentanyl is a pure opioid agonist whose principal therapeutic action is analgesia. Other members of the class known as opioid agonists include substances such as morphine, oxycodone, hydromorphone, codeine, and hydrocodone.
|
| 4 |
|
Adcetris
18
49
|
BRENTUXIMAB VEDOTIN |
Seattle Genetics |
August 2011 |
Disease/s that Drug Treats:Hodgkin lymphoma and anaplastic large cell lymphoma
Indications and Usage:
18
ADCETRIS is a CD30-directed antibody-drug conjugate indicated fortreatment of patients with: Hodgkin lymphoma after failure of autologous stem cell transplant(ASCT) or after failure of at least two prior multi-agent chemotherapyregimens in patients who are not ASCT candidates (1.1). Systemic anaplastic large cell lymphoma after failure of at least oneprior multi-agent chemotherapy regimen (1.2).Accelerated approval was granted for the above indications based onoverall response rate. An improvement in patient-reported outcomes orsurvival has not been established. Continued approval for these indicationsmay be contingent upon verification and description of clinical benefit inconfirmatory trials.
DrugBank Targets:
16
Tumor necrosis factor receptor superfamily member 8
Mechanism of Action:
18
Target: microtubule
Action: disruptor
FDA: Brentuximab vedotin is an ADC. The antibody is a chimeric IgG1 directed against CD30. Thesmall molecule, MMAE, is a microtubule disrupting agent. MMAE is covalently attached to theantibody via a linker. Nonclinical data suggest that the anticancer activity of ADCETRIS is dueto the binding of the ADC to CD30-expressing cells, followed by internalization of theADC-CD30 complex, and the release of MMAE via proteolytic cleavage. Binding of MMAE totubulin disrupts the microtubule network within the cell, subsequently inducing cell cycle arrestand apoptotic death of the cells.
|
| 5 |
|
Arimidex
18
49
|
ANASTROZOLE |
AstraZeneca |
January 1996 |
Disease/s that Drug Treats:post menopausal breast cancer
Indications and Usage:
18
ARIMIDEX is an aromatase inhibitor indicated for: Adjuvant treatment of postmenopausal women withhormone receptor-positive early breast cancer (1.1) First-line treatment of postmenopausal women withhormone receptor-positive or hormone receptor unknownlocally advanced or metastatic breast cancer (1.2) Treatment of advanced breast cancer in postmenopausalwomen with disease progression following tamoxifentherapy. Patients with ER-negative disease and patientswho did not respond to previous tamoxifen therapy rarelyresponded to ARIMIDEX (1.3)
DrugBank Targets:
16
Cytochrome P450 19A1
Mechanism of Action:
18
Target: oral aromatase
Action: inhibitor
FDA: The growth of many cancers of the breast is stimulated or maintained by estrogens.In postmenopausal women, estrogens are mainly derived from the action of the aromataseenzyme, which converts adrenal androgens (primarily androstenedione and testosterone) toestrone and estradiol. The suppression of estrogen biosynthesis in peripheral tissues and inthe cancer tissue itself can therefore be achieved by specifically inhibiting the aromataseenzyme.Anastrozole is a selective non-steroidal aromatase inhibitor. It significantly lowers serumestradiol concentrations and has no detectable effect on formation of adrenal corticosteroidsor aldosterone.
|
| 6 |
|
Arranon
18
49
|
NELARABINE |
GlaxoSmithKline |
October 2005 |
Disease/s that Drug Treats:Lymphoblastic Leukemia
Indications and Usage:
18
ARRANON is a nucleoside metabolic inhibitor indicated for the treatment ofpatients with T-cell acute lymphoblastic leukemia and T-cell lymphoblasticlymphoma whose disease has not responded to or has relapsed followingtreatment with at least two chemotherapy regimens. This use is based on theinduction of complete responses. Randomized trials demonstrating increasedsurvival or other clinical benefit have not been conducted. (1)
Mechanism of Action:
18
Target: DNA synthesis
Action: disruptor --> apoptosis
FDA: Nelarabine is a pro-drug of the deoxyguanosine analogue 9-β-D-arabinofuranosylguanine266 (ara-G), a nucleoside metabolic inhibitor. Nelarabine is demethylated by adenosine deaminase267 (ADA) to ara-G, mono-phosphorylated by deoxyguanosine kinase and deoxycytidine kinase, and268 subsequently converted to the active 5â-triphosphate, ara-GTP. Accumulation of ara-GTP in269 leukemic blasts allows for incorporation into deoxyribonucleic acid (DNA), leading to inhibition270 of DNA synthesis and cell death. Other mechanisms may contribute to the cytotoxic and271 systemic toxicity of nelarabine.
|
| 7 |
|
Arzerra
18
49
|
OFATUMUMAB |
GlaxoSmithKline |
October 2009 |
Disease/s that Drug Treats:chronic lymphocytic leukemia
Indications and Usage:
18
ARZERRA (ofatumumab) is a CD20-directed cytolytic monoclonal antibodyindicated: in combination with chlorambucil, for the treatment of previouslyuntreated patients with chronic lymphocytic leukemia (CLL) for whomfludarabine-based therapy is considered inappropriate. (1.1) for the treatment of patients with CLL refractory to fludarabine andalemtuzumab. (1.2)
DrugBank Targets:
16
no entry
Mechanism of Action:
18
Target: B-cell
Action: promotes lysis
FDA: Ofatumumab binds specifically to both the small and large extracellular loops of the CD20402 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B- to mature403 B-lymphocyte) and on B-cell CLL. The CD20 molecule is not shed from the cell surface and is404 not internalized following antibody binding.405406 The Fab domain of ofatumumab binds to the CD20 molecule and the Fc domain mediates407 immune effector functions to result in B-cell lysis in vitro. Data suggest that possible408 mechanisms of cell lysis include complement-dependent cytotoxicity and antibody-dependent,409 cell-mediated cytotoxicity.
|
| 8 |
|
Beleodaq
18
49
|
BELINOSTAT |
Spectrum Pharmaceuticals |
July 2014 |
Disease/s that Drug Treats:relapsed or refractory peripheral T-cell lymphoma
Indications and Usage:
18
Beleodaq is a histone deacetylase inhibitor indicated for the treatment ofpatients with relapsed or refractory peripheral T-cell lymphoma (PTCL). Thisindication is approved under accelerated approval based on tumor responserate and duration of response. An improvement in survival or disease-relatedsymptoms has not been established. Continued approval for this indicationmay be contingent upon verification and description of clinical benefit in theconfirmatory trial. (1)
DrugBank Targets:
16
no entry
Mechanism of Action:
18
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: Beleodaq is a histone deacetylase (HDAC) inhibitor. HDACs catalyze the removal of acetyl groups from thelysine residues of histones and some non-histone proteins. In vitro, belinostat caused the accumulation ofacetylated histones and other proteins, inducing cell cycle arrest and/or apoptosis of some transformed cells.Belinostat shows preferential cytotoxicity towards tumor cells compared to normal cells. Belinostat inhibitedthe enzymatic activity of histone deacetylases at nanomolar concentrations (<250 nM).
|
| 9 |
|
Blincyto
18
49
|
BLINATUMOMAB |
Amgen |
December 2014 |
Disease/s that Drug Treats:Philadelphia chromosome-negative relapsed /refractory B cell precursor acute lymphoblastic leukemia
Indications and Usage:
18
BLINCYTO is a bispecific CD19-directed CD3 T-cell engager indicated forthe treatment of Philadelphia chromosome-negative relapsed or refractory Bcellprecursor acute lymphoblastic leukemia (ALL). This indication isapproved under accelerated approval. Continued approval for this indicationmay be contingent upon verification of clinical benefit in subsequent trials. (1)
DrugBank Targets:
16
1. B-lymphocyte antigen CD19;2. T-cell surface glycoprotein CD3 delta chain
Mechanism of Action:
18
Target: CD19-directed CD3 T-cell
Action: engager
FDA: Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on thesurface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenousT cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant Bcells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell,upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatorycytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells.
|
| 10 |
|
Bosulif
18
49
|
BOSUTINIB MONOHYDRATE |
Pfizer |
September 2012 |
Disease/s that Drug Treats:Ph+ chronic myelogenous leukemia
Indications and Usage:
18
BOSULIF is a kinase inhibitor indicated for the treatment of adult patientswith chronic, accelerated, or blast phase Ph+ chronic myelogenous leukemia(CML) with resistance or intolerance to prior therapy. (1)
DrugBank Targets:
16
1. Breakpoint cluster region protein;2. Tyrosine-protein kinase ABL1;3. Tyrosine-protein kinase Lyn;4. Tyrosine-protein kinase HCK;5. Proto-oncogene tyrosine-protein kinase Src;6. Cyclin-dependent kinase 2;7. Dual specificity mitogen-activated protein kinase kinase 1;8. Dual specificity mitogen-activated protein kinase kinase 2;9. Mitogen-activated protein kinase kinase kinase 2;10. Calcium/calmodulin-dependent protein kinase type II subunit gamma
Mechanism of Action:
18
Target: tyrosine kinase/ Src-family kinases including Src, Lyn, and Hck
Action: inhibitor
FDA: Bosutinib is a tyrosine kinase inhibitor. Bosutinib inhibits the Bcr-Abl kinase that promotes CML; it is also aninhibitor of Src-family kinases including Src, Lyn, and Hck. Bosutinib inhibited 16 of 18 imatinib-resistant forms ofBcr-Abl expressed in murine myeloid cell lines. Bosutinib did not inhibit the T315I and V299L mutant cells. In mice,treatment with bosutinib reduced the size of CML tumors relative to controls and inhibited growth of murine myeloidtumors expressing several imatinib-resistant forms of Bcr-Abl.
|
| 11 |
|
Busulfex
18
49
|
BUSULFAN |
Orphan Medical |
February 1999 |
Disease/s that Drug Treats:leukemia
Indications and Usage:
18
BUSULFEX is an alkylating drug indicated for: Use in combination with cyclophosphamide as a conditioning regimenprior to allogeneic hematopoietic progenitor cell transplantation forchronic myelogenous leukemia (CML) (1)
Mechanism of Action:
18
Target: DNA
Action: alkylyzer
FDA: Busulfan is a bifunctional alkylating agent in which two labile methanesulfonate groups are attached to opposite ends of afour-carbon alkyl chain. In aqueous media, busulfan hydrolyzes to release the methanesulfonate groups. This producesreactive carbonium ions that can alkylate DNA. DNA damage is thought to be responsible for much of the cytotoxicity ofbusulfan.
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| 12 |
|
Campath
18
49
|
ALEMTUZUMAB |
Berlex Laboratories |
May 2001 |
Disease/s that Drug Treats:Leukemia
Indications and Usage:
18
LEMTRADA is a CD52-directed cytolytic monoclonal antibody indicated dizziness, abdominal pain, flushing, and vomiting. (6.1) for the treatment of patients with relapsing forms of multiple sclerosis(MS).
DrugBank Targets:
16
1. CAMPATH-1 antigen;2. Low affinity immunoglobulin gamma Fc region receptor III-B;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Low affinity immunoglobulin gamma Fc region receptor III-A;8. High affinity immunoglobulin gamma Fc receptor I;9. Low affinity immunoglobulin gamma Fc region receptor II-a;10. Low affinity immunoglobulin gamma Fc region receptor II-b;11. Low affinity immunoglobulin gamma Fc region receptor II-c;;
Mechanism of Action:
18
Target: CD52 antigen
Action: after binding, induces cell lysis
FDA: The precise mechanism by which alemtuzumab exerts its therapeutic effects in multiple490 sclerosis is unknown but is presumed to involve binding to CD52, a cell surface antigen491 present on T and B lymphocytes, and on natural killer cells, monocytes, and492 macrophages. Following cell surface binding to T and B lymphocytes, alemtuzumab493 results in antibody-dependent cellular cytolysis and complement-mediated lysis.
|
| 13 |
|
Cervarix
18
49
|
Human Papillomavirus Bivalent (Types 16 and 18) Vaccine, Recombinant |
GlaxoSmithKline |
October 2009 |
Disease/s that Drug Treats:prevention of cervical cancer and cervical intraepithelial neoplasia caused by HPV types 16 and 18
Indications and Usage:
18
DrugBank Targets:
-
Mechanism of Action:
18
Target: IgG neutralizing antibodies directed against HPV-L1 capsid proteins
Action: activates/ provokes production
FDA: -
|
| 14 |
|
Cometriq
18
49
|
CABOZANTINIB S-MALATE |
Exelixis |
November 2012 |
Disease/s that Drug Treats:thyroid cancer
Indications and Usage:
18
COMETRIQ is a kinase inhibitor indicated for the treatment ofpatients with progressive, metastatic medullary thyroid cancer(MTC). (1)
DrugBank Targets:
16
1. Hepatocyte growth factor receptor;2. Vascular endothelial growth factor receptor 2;3. Proto-oncogene tyrosine-protein kinase receptor Ret
Mechanism of Action:
18
Target: tyrosine kinase activity of RET, MET, VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, and TIE-2
Action: inhibitor
FDA: In vitro biochemical and/or cellular assays have shown that cabozantinib inhibits the tyrosinekinase activity of RET, MET, VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, and TIE-2.These receptor tyrosine kinases are involved in both normal cellular function and pathologicprocesses such as oncogenesis, metastasis, tumor angiogenesis, and maintenance of the tumormicroenvironment.
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| 15 |
|
Cyramza
18
49
|
RAMUCIRUMAB |
Eli Lilly |
April 2014 |
Disease/s that Drug Treats:gastric cancer
Indications and Usage:
18
CYRAMZA® is a human vascular endothelial growth factor receptor 2antagonist indicated as a single agent or in combination with paclitaxel, for treatmentof advanced gastric or gastro-esophageal junctionadenocarcinoma, with disease progression on or after priorfluoropyrimidine- or platinum-containing chemotherapy. (1.1) in combination with docetaxel, for treatment of metastatic nonsmallcell lung cancer with disease progression on or afterplatinum-based chemotherapy. Patients with EGFR or ALKgenomic tumor aberrations should have disease progression onFDA-approved therapy for these aberrations prior to receivingCYRAMZA. (1.2) in combination with FOLFIRI, for the treatment of metastaticcolorectal cancer with disease progression on or after priortherapy with bevacizumab, oxaliplatin, and a fluoropyrimidine.(1.3)
DrugBank Targets:
-
Mechanism of Action:
18
Target: ligand-stimulated activation of VEGF Receptor 2
Action: inhibitor
FDA: Ramucirumab is a vascular endothelial growth factor receptor 2 antagonist that specifically binds VEGF Receptor2 and blocks binding of VEGFR ligands, VEGF-A, VEGF-C, and VEGF-D. As a result, ramucirumab inhibits ligandstimulatedactivation of VEGF Receptor 2, thereby inhibiting ligand-induced proliferation, and migration of humanendothelial cells. Ramucirumab inhibited angiogenesis in an in vivo animal model.
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| 16 |
|
Degarelix
18
49
|
degarelix |
Ferring Pharmaceuticals |
December of 2008 |
Disease/s that Drug Treats:Prostate Cancer
Indications and Usage:
18
DrugBank Targets:
16
1. Gonadotropin-releasing hormone receptor
Mechanism of Action:
18
Target: Gonadotropin-releasing hormone (GnRH) receptor
Action: antagonist
FDA: -
|
| 17 |
|
Elliotts B Solution
18
|
CALCIUM CHLORIDE; DEXTROSE; MAGNESIUM SULFATE; POTASSIUM CHLORIDE; SODIUM BICARBONATE; SODIUM CHLORIDE; SODIUM PHOSPHATE, DIBASIC, HEPTAHYDRATE |
Orphan Medical |
October 1996 |
FDA Label: Elliotts B Solution
Disease/s that Drug Treats:meningeal leukemia or lymphocytic lymphoma
Indications and Usage:
18
DrugBank Targets:
-
Mechanism of Action:
18
Target: cerebrospinal fluid
Action: comparable in pH, electrolyte composition, glucose content, and osmolarity
FDA: -
|
| 18 |
|
Eloxatin
18
49
|
OXALIPLATIN |
Sanofi-aventis |
August 2002 |
Disease/s that Drug Treats:Metastatic colon or rectum carcinomas that have recurred or progressed within six months folowing first-line treatment
Indications and Usage:
18
ELOXATIN is a platinum-based drug used in combination with infusional 5-fluorouracil /leucovorin, which is indicated for: adjuvant treatment of stage III colon cancer in patients who haveundergone complete resection of the primary tumor. (1) treatment of advanced colorectal cancer. (1)
DrugBank Targets:
16
1. DNA
Mechanism of Action:
18
Target: DNA replication and transcription
Action: inhibitor
FDA: Oxaliplatin undergoes nonenzymatic conversion in physiologic solutions to active derivatives viadisplacement of the labile oxalate ligand. Several transient reactive species are formed, includingmonoaquo and diaquo DACH platinum, which covalently bind with macromolecules. Both interandintrastrand Pt-DNA crosslinks are formed. Crosslinks are formed between the N7 positions oftwo adjacent guanines (GG), adjacent adenine-guanines (AG), and guanines separated by anintervening nucleotide (GNG). These crosslinks inhibit DNA replication and transcription.Cytotoxicity is cell-cycle nonspecific.In vivo studies have shown antitumor activity of oxaliplatin against colon carcinoma. Incombination with 5-fluorouracil, oxaliplatin exhibits in vitro and in vivo antiproliferative activitygreater than either compound alone in several tumor models [HT29 (colon), GR (mammary), andL1210 (leukemia)].
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| 19 |
|
Emend
18
49
|
APREPITANT FOSAPREPITANT DIMEGLUMINE |
Merck |
March 2003 |
Disease/s that Drug Treats:Chemotherapy-induced Nausea and Vomiting
Indications and Usage:
18
EMEND® is a substance P/neurokinin 1 (NK1) receptor antagonist,indicated: in combination with other antiemetic agents for the:o prevention of acute and delayed nausea and vomitingassociated with initial and repeat courses of highly emetogeniccancer chemotherapy (HEC) including high-dose cisplatin (1.1)o prevention of nausea and vomiting associated with initial andrepeat courses of moderately emetogenic cancer chemotherapy(MEC) (1.1) for the prevention of postoperative nausea and vomiting (PONV)(1.2)Limitations of Use (1.3) Not studied for the treatment of established nausea and vomiting. Chronic continuous administration is not recommended.
DrugBank Targets:
16
1. Substance-P receptor
Mechanism of Action:
18
Target: emesis induced by cytotoxic chemotherapeutic agents, such as cisplatin
Action: inhibitor
FDA: Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors.Aprepitant has little or no affinity for serotonin (5-HT3), dopamine, and corticosteroid receptors, the targetsof existing therapies for chemotherapy-induced nausea and vomiting (CINV) and postoperative nauseaand vomiting (PONV).Aprepitant has been shown in animal models to inhibit emesis induced by cytotoxicchemotherapeutic agents, such as cisplatin, via central actions. Animal and human Positron EmissionTomography (PET) studies with aprepitant have shown that it crosses the blood brain barrier and occupiesbrain NK1 receptors. Animal and human studies show that aprepitant augments the antiemetic activity ofthe 5-HT3-receptor antagonist ondansetron and the corticosteroid dexamethasone and inhibits both theacute and delayed phases of cisplatin-induced emesis.
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| 20 |
|
Erbitux
18
49
|
CETUXIMAB |
Imclone, Bristol-Myers Squibb |
February 2004 |
Disease/s that Drug Treats:Colorectal Cancer
Indications and Usage:
18
Erbitux® is an epidermal growth factor receptor (EGFR) antagonist indicatedfor treatment of:Head and Neck Cancer Locally or regionally advanced squamous cell carcinoma of the headand neck in combination with radiation therapy. (1.1, 14.1) Recurrent locoregional disease or metastatic squamous cell carcinomaof the head and neck in combination with platinum-based therapy with5-FU. (1.1, 14.1) Recurrent or metastatic squamous cell carcinoma of the head and neckprogressing after platinum-based therapy. (1.1, 14.1)Colorectal CancerK-Ras wild-type, EGFR-expressing, metastatic colorectal cancer asdetermined by FDA-approved tests in combination with FOLFIRI for first-line treatment, in combination with irinotecan in patients who are refractory toirinotecan-based chemotherapy, as a single agent in patients who have failed oxaliplatin- andirinotecan-based chemotherapy or who are intolerant to irinotecan.(1.2, 5.7, 12.1, 14.2)Limitation of Use: Erbitux is not indicated for treatment of Ras-mutantcolorectal cancer. (5.7, 14.2)
DrugBank Targets:
16
1. Epidermal growth factor receptor;2. Low affinity immunoglobulin gamma Fc region receptor III-B;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Low affinity immunoglobulin gamma Fc region receptor III-A;8. Complement C1s subcomponent;9. High affinity immunoglobulin gamma Fc receptor I;10. Low affinity immunoglobulin gamma Fc region receptor II-a;11. Low affinity immunoglobulin gamma Fc region receptor II-b;12. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:
18
Target: binding of epidermal growth factor (EGF) and other ligands to epidermal growth factor receptor (EGFR, HER1, c-ErbB-1)
Action: inhibitor
FDA: The epidermal growth factor receptor (EGFR, HER1, c-ErbB-1) is a transmembraneglycoprotein that is a member of a subfamily of type I receptor tyrosine kinases including EGFR,HER2, HER3, and HER4. The EGFR is constitutively expressed in many normal epithelialtissues, including the skin and hair follicle. Expression of EGFR is also detected in many humancancers including those of the head and neck, colon, and rectum. Cetuximab binds specifically to the EGFR on both normal and tumor cells, and competitivelyinhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforminggrowth factor-alpha. In vitro assays and in vivo animal studies have shown that binding ofcetuximab to the EGFR blocks phosphorylation and activation of receptor-associated kinases,resulting in inhibition of cell growth, induction of apoptosis, and decreased matrixmetalloproteinase and vascular endothelial growth factor production. Signal transduction throughthe EGFR results in activation of wild-type Ras proteins, but in cells with activating Ras somaticmutations, the resulting mutant Ras proteins are continuously active regardless of EGFRregulation.In vitro, cetuximab can mediate antibody-dependent cellular cytotoxicity (ADCC) against certainhuman tumor types. In vitro assays and in vivo animal studies have shown that cetuximabinhibits the growth and survival of tumor cells that express the EGFR. No anti-tumor effects ofcetuximab were observed in human tumor xenografts lacking EGFR expression. The addition ofcetuximab to radiation therapy or irinotecan in human tumor xenograft models in mice resultedin an increase in anti-tumor effects compared to radiation therapy or chemotherapy alone.
|
| 21 |
|
Erivedge
18
49
|
VISMODEGIB |
Genentech |
January 2012 |
Disease/s that Drug Treats:basal cell carcinoma
Indications and Usage:
18
ERIVEDGE (vismodegib) capsule is a hedgehog pathway inhibitor indicatedfor the treatment of adults with metastatic basal cell carcinoma, or with locallyadvanced basal cell carcinoma that has recurred following surgery or who arenot candidates for surgery, and who are not candidates for radiation. (1)
DrugBank Targets:
16
1. Smoothened homolog
Mechanism of Action:
18
Target: hedgehog (Hh) signaling pathway
Action: innhibitor
FDA: Vismodegib is an inhibitor of the Hedgehog pathway. Vismodegib binds to and inhibitsSmoothened, a transmembrane protein involved in Hedgehog signal transduction.
|
| 22 |
|
Farydak
18
49
|
PANOBINOSTAT LACTATE |
Novartis |
February 2015 |
Disease/s that Drug Treats:Multiple myeloma
Indications and Usage:
18
FARYDAK, a histone deacetylase inhibitor, in combination with bortezomiband dexamethasone, is indicated for the treatment of patients with multiplemyeloma who have received at least 2 prior regimens, including bortezomiband an immunomodulatory agent. This indication is approved underaccelerated approval based on progression free survival. Continued approvalfor this indication may be contingent upon verification and description ofclinical benefit in confirmatory trials. (1)
DrugBank Targets:
-
Mechanism of Action:
18
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: FARYDAK is a histone deacetylase (HDAC) inhibitor that inhibits the enzymatic activity of HDACs atnanomolar concentrations. HDACs catalyze the removal of acetyl groups from the lysine residues of histonesand some non-histone proteins. Inhibition of HDAC activity results in increased acetylation of histone proteins,an epigenetic alteration that results in a relaxing of chromatin, leading to transcriptional activation. In vitro,Reference ID: 3699607 panobinostat caused the accumulation of acetylated histones and other proteins, inducing cell cycle arrest and/orapoptosis of some transformed cells. Increased levels of acetylated histones were observed in xenografts frommice that were treated with panobinostat. Panobinostat shows more cytotoxicity towards tumor cells comparedto normal cells.
|
| 23 |
|
Faslodex
18
49
|
FULVESTRANT |
AstraZeneca |
April 2002 |
Disease/s that Drug Treats:Hormone receptor positive metastatic breast cancer
Indications and Usage:
18
FASLODEX is an estrogen receptor antagonist indicated for the: Treatment of hormone receptor positive metastatic breast cancer inpostmenopausal women with disease progression followingantiestrogen therapy.
DrugBank Targets:
16
1. Estrogen receptor
Mechanism of Action:
18
Target: estrogen receptors on tumor cells
Action: antagonist
FDA: Many breast cancers have estrogen receptors (ER) and thegrowth of these tumors can be stimulated by estrogen.Fulvestrant is an estrogen receptor antagonist that binds to theestrogen receptor in a competitive manner with affinitycomparable to that of estradiol and downregulates the ERprotein in human breast cancer cells.In vitro studies demonstrated that fulvestrant is a reversibleinhibitor of the growth of tamoxifen-resistant, as well asestrogen-sensitive human breast cancer (MCF-7) cell lines. Inin vivo tumor studies, fulvestrant delayed the establishment oftumors from xenografts of human breast cancer MCF-7 cellsin nude mice. Fulvestrant inhibited the growth of establishedMCF-7 xenografts and of tamoxifen-resistant breast tumorxenografts.Fulvestrant showed no agonist-type effects in in vivouterotropic assays in immature or ovariectomized mice andrats. In in vivo studies in immature rats and ovariectomizedmonkeys, fulvestrant blocked the uterotrophic action ofestradiol. In postmenopausal women, the absence of changesin plasma concentrations of FSH and LH in response tofulvestrant treatment (250 mg monthly) suggests no peripheralsteroidal effects.
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| 24 |
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Folotyn
18
49
|
PRALATREXATE |
Allos Therapeutics |
September 2009 |
Disease/s that Drug Treats:peripheral T-cell lymphoma
Indications and Usage:
18
FOLOTYN is a folate analog metabolic inhibitor indicated for the treatment ofpatients with relapsed or refractory peripheral T-cell lymphoma (PTCL). Thisindication is based on overall response rate. Clinical benefit such asimprovement in progression-free survival or overall survival has not beendemonstrated. (1)
DrugBank Targets:
16
1. Dihydrofolate reductase;2. Thymidylate synthase
Mechanism of Action:
18
Target: dihydrofolate reductase
Action: inhibitor
FDA: Pralatrexate is a folate analog metabolic inhibitor that competitively inhibits dihydrofolate reductase. It is also acompetitive inhibitor for polyglutamylation by the enzyme folylpolyglutamyl synthetase. This inhibition resultsin the depletion of thymidine and other biological molecules the synthesis of which depends on single carbontransfer.
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| 25 |
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Gardasil
18
49
|
quadrivalent human papillomavirus (types 6, 11, 16, 18) recombinant vaccine |
Merck |
June 2006 |
Disease/s that Drug Treats:Cervical Cancer Caused by Human Papillomavirus
Indications and Usage:
18
GARDASIL is a vaccine indicated in girls and women 9 through 26years of age for the prevention of the following diseases caused byHuman Papillomavirus (HPV) types included in the vaccine: Cervical, vulvar, vaginal, and anal cancer caused by HPV types 16and 18 (1.1) Genital warts (condyloma acuminata) caused by HPV types 6 and11 (1.1)And the following precancerous or dysplastic lesions caused by HPVtypes 6, 11, 16, and 18: Cervical intraepithelial neoplasia (CIN) grade 2/3 and Cervicaladenocarcinoma in situ (AIS) (1.1) Cervical intraepithelial neoplasia (CIN) grade 1 (1.1) Vulvar intraepithelial neoplasia (VIN) grade 2 and grade 3 (1.1) Vaginal intraepithelial neoplasia (VaIN) grade 2 and grade 3 (1.1) Anal intraepithelial neoplasia (AIN) grades 1, 2, and 3 (1.1)GARDASIL is indicated in boys and men 9 through 26 years of age forthe prevention of the following diseases caused by HPV types includedin the vaccine: Anal cancer caused by HPV types 16 and 18 (1.2) Genital warts (condyloma acuminata) caused by HPV types 6 and11 (1.2)And the following precancerous or dysplastic lesions caused by HPVtypes 6, 11, 16, and 18: Anal intraepithelial neoplasia (AIN) grades 1, 2, and 3. (1.2)Limitations of GARDASIL Use and Effectiveness: GARDASIL does not eliminate the necessity for women tocontinue to undergo recommended cervical cancer screening.(1.3, 17) Recipients of GARDASIL should not discontinue anal cancerscreening if it has been recommended by a health care provider.(1.3, 17) GARDASIL has not been demonstrated to provide protectionagainst disease from vaccine and non-vaccine HPV types to whicha person has previously been exposed through sexual activity.(1.3, 14.4, 14.5) GARDASIL is not intended to be used for treatment of activeexternal genital lesions; cervical, vulvar, vaginal, and analcancers; CIN; VIN; VaIN, or AIN. (1.3) GARDASIL has not been demonstrated to protect againstdiseases due to HPV types not contained in the vaccine. (1.3,14.4, 14.5) Not all vulvar, vaginal, and anal cancers are caused by HPV, andGARDASIL protects only against those vulvar, vaginal, and analcancers caused by HPV 16 and 18. (1.3) GARDASIL does not protect against genital diseases not causedby HPV. (1.3) Vaccination with GARDASIL may not result in protection in allvaccine recipients. (1.3) GARDASIL has not been demonstrated to prevent HPV-relatedCIN 2/3 or worse in women older than 26 years of age. (14.7)
DrugBank Targets:
-
Mechanism of Action:
18
Target: humoral immune response
Action: inducer
FDA: HPV only infects human beings. Animal studies with analogous animal papillomaviruses suggest thatthe efficacy of L1 VLP vaccines may involve the development of humoral immune responses. Humanbeings develop a humoral immune response to the vaccine, although the exact mechanism of protectionis unknown.
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| 26 |
|
Gilotrif
18
49
|
AFATINIB DIMALEATE |
Boehringer Ingelheim |
July 2013 |
Disease/s that Drug Treats:metastatic non-small cell lung cancer with EGFR mutations
Indications and Usage:
18
GILOTRIF is a kinase inhibitor indicated for the first-line treatment ofpatients with metastatic non-small cell lung cancer (NSCLC) whose tumorshave epidermal growth factor receptor (EGFR) exon 19 deletions or exon 21(L858R) substitution mutations as detected by an FDA-approved test (1)Limitation of Use: Safety and efficacy of GILOTRIF have not beenestablished in patients whose tumors have other EGFR mutations (1)
DrugBank Targets:
16
1. Epidermal growth factor receptor;2. Receptor tyrosine-protein kinase erbB-2;3. Receptor tyrosine-protein kinase erbB-4
Mechanism of Action:
18
Target: tyrosine kinase autophosphorylation
Action: inhibitor
FDA: Afatinib covalently binds to the kinase domains of EGFR (ErbB1), HER2 (ErbB2), and HER4 (ErbB4) andirreversibly inhibits tyrosine kinase autophosphorylation, resulting in downregulation of ErbB signaling.Afatinib demonstrated inhibition of autophosphorylation and in vitro proliferation of cell lines expressing wildtypeEGFR or those expressing selected EGFR exon 19 deletion mutations or exon 21 L858R mutations,including some with a secondary T790M mutation, at afatinib concentrations achieved, at least transiently, inpatients. In addition, afatinib inhibited in vitro proliferation of cell lines overexpressing HER2.Treatment with afatinib resulted in inhibition of tumor growth in nude mice implanted with tumors eitheroverexpressing wild type EGFR or HER2 or in an EGFR L858R/T790M double mutant model.
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| 27 |
|
Gleevec
18
49
|
IMATINIB MESYLATE |
Novartis |
May 2001 |
Disease/s that Drug Treats:chronic myeloid leukemia/Gastrointestinal stromal tumors (GISTs)
Indications and Usage:
18
Gleevec⢠(imatinib mesylate) is indicated for the treatment of newly diagnosed adultpatients with Philadelphia chromosome positive chronic myeloid leukemia (CML) in chronicphase. Follow-up is limited. Page 10Gleevec is also indicated for the treatment of patients with Philadelphia chromosomepositive chronic myeloid leukemia (CML) in blast crisis, accelerated phase, or in chronicphase after failure of interferon-alpha therapy. Gleevec is also indicated for the treatment ofpediatric patients with Ph+ chronic phase CML whose disease has recurred after stem celltransplant or who are resistant to interferon alpha therapy. There are no controlled trialsdemonstrating a clinical benefit, such as improvement in disease-related symptoms orincreased survival.Gleevec is also indicated for the treatment of patients with Kit (CD117) positiveunresectable and/or metastatic malignant gastrointestinal stromal tumors (GIST). (SeeCLINICAL STUDIES: Gastrointestinal Stromal Tumors.) The effectiveness of Gleevec inGIST is based on objective response rate (see CLINICAL STUDIES). There are no controlledtrials demonstrating a clinical benefit, such as improvement in disease-related symptoms orincreased survival.
DrugBank Targets:
16
1. BCR/ABL fusion protein isoform X9;2. Mast/stem cell growth factor receptor Kit;3. RET proto-oncogene;4. High affinity nerve growth factor receptor;5. Macrophage colony-stimulating factor 1 receptor;6. Platelet-derived growth factor receptor alpha;7. Epithelial discoidin domain-containing receptor 1;8. Tyrosine-protein kinase ABL1;9. Platelet-derived growth factor receptor beta
Mechanism of Action:
18
Target: protein-tyrosine kinase
Action: inhibitor
FDA: Imatinib mesylate is a protein-tyrosine kinase inhibitor that inhibits the Bcr-Abl tyrosinekinase, the constitutive abnormal tyrosine kinase created by the Philadelphia chromosomeabnormality in chronic myeloid leukemia (CML). It inhibits proliferation and inducesapoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphiachromosome positive chronic myeloid leukemia. In colony formation assays using ex vivoperipheral blood and bone marrow samples, imatinib shows inhibition of Bcr-Abl positivecolonies from CML patients.In vivo, it inhibits tumor growth of Bcr-Abl transfected murine myeloid cells as wellas Bcr-Abl positive leukemia lines derived from CML patients in blast crisis.Imatinib is also an inhibitor of the receptor tyrosine kinases for platelet-derivedgrowth factor (PDGF) and stem cell factor (SCF), c-kit, and inhibits PDGF- andSCF-mediated cellular events. In vitro, imatinib inhibits proliferation and induces apoptosis ingastrointestinal stromal tumor (GIST) cells, which express an activating c-kit mutation.
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| 28 |
|
Ibrance
18
49
|
PALBOCICLIB |
Pfizer |
February 2015 |
Disease/s that Drug Treats:ER-positive, HER2-negative breast cancer
Indications and Usage:
18
IBRANCE is a kinase inhibitor indicated in combination with letrozole for thetreatment of postmenopausal women with estrogen receptor (ER)-positive,human epidermal growth factor receptor 2 (HER2)-negative advanced breastcancer as initial endocrine-based therapy for their metastatic disease. Thisindication is approved under accelerated approval based on progression-freesurvival (PFS). Continued approval for this indication may be contingentupon verification and description of clinical benefit in a confirmatory trial. (1)
DrugBank Targets:
16
1. Cyclin-dependent kinase 4;2. Cyclin-dependent kinase 6
Mechanism of Action:
18
Target: cyclin-dependent kinase (CDK) 4 and 6
Action: inhibitor
FDA: Palbociclib is an inhibitor of cyclin-dependent kinase (CDK) 4 and 6. Cyclin D1 and CDK4/6 aredownstream of signaling pathways which lead to cellular proliferation. In vitro, palbociclib reducedcellular proliferation of estrogen receptor (ER)-positive breast cancer cell lines by blocking progressionof the cell from G1 into S phase of the cell cycle. Treatment of breast cancer cell lines with thecombination of palbociclib and antiestrogens leads to decreased retinoblastoma protein (Rb)phosphorylation resulting in reduced E2F expression and signaling and increased growth arrestcompared to treatment with each drug alone. In vitro treatment of ER-positive breast cancer cell lineswith the combination of palbociclib and antiestrogens leads to increased cell senescence, which wassustained for up to 6 days following drug removal. In vivo studies using a patient-derived ER-positivebreast cancer xenograft model demonstrated that the combination of palbociclib and letrozole increasedthe inhibition of Rb phosphorylation, downstream signaling and tumor growth compared to each drugalone.
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| 29 |
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Iclusig
18
49
|
PONATINIB HYDROCHLORIDE |
Ariad Pharmaceuticals |
December 2012 |
Disease/s that Drug Treats:chronic myeloid leukemia and Philadelphia chromosome positive acute lymphoblastic leukemia
Indications and Usage:
18
Iclusig is a kinase inhibitor indicated for the: Treatment of adult patients with T315I-positive chronic myeloidleukemia (chronic phase, accelerated phase, or blast phase) or T315IpositivePhiladelphia chromosome positive acute lymphoblasticleukemia (Ph+ ALL). Treatment of adult patients with chronic phase, accelerated phase, orblast phase chronic myeloid leukemia or Ph+ ALL for whom no othertyrosine kinase inhibitor (TKI) therapy is indicated. (1)These indications are based upon response rate. There are no trials verifying animprovement in disease-related symptoms or increased survival with Iclusig.
DrugBank Targets:
16
1. Tyrosine-protein kinase ABL1;2. Breakpoint cluster region protein;3. Mast/stem cell growth factor receptor Kit;4. Proto-oncogene tyrosine-protein kinase receptor Ret;5. Angiopoietin-1 receptor;6. Receptor-type tyrosine-protein kinase FLT3;7. Fibroblast growth factor receptor 1;8. Fibroblast growth factor receptor 2;9. Fibroblast growth factor receptor 3;10. Fibroblast growth factor receptor 4;11. Tyrosine-protein kinase Lck;12. Proto-oncogene tyrosine-protein kinase Src;13. Tyrosine-protein kinase Lyn;14. Vascular endothelial growth factor receptor 2;15. Platelet-derived growth factor receptor alpha
Mechanism of Action:
18
Target: tyrosine kinase activity of ABL and T315I mutant ABL
Action: inhibitor
FDA: Ponatinib is a kinase inhibitor. Ponatinib inhibited the in vitro tyrosine kinase activity of ABL and T315I mutant ABL withIC50 concentrations of 0.4 and 2.0 nM, respectively. Ponatinib inhibited the in vitro activity of additional kinases with IC50concentrations between 0.1 and 20 nM, including members of the VEGFR, PDGFR, FGFR, EPH receptors and SRCfamilies of kinases, and KIT, RET, TIE2, and FLT3. Ponatinib inhibited the in vitro viability of cells expressing native ormutant BCR-ABL, including T315I. In mice, treatment with ponatinib reduced the size of tumors expressing native orT315I mutant BCR-ABL when compared to controls.
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| 30 |
|
Imbruvica
18
49
|
IBRUTINIB |
Pharmacyclics |
November of 2013/February 2014 |
Disease/s that Drug Treats:mantle cell lymphoma/chronic lymphocytic leukemia
Indications and Usage:
18
IMBRUVICA is a kinase inhibitor indicated for the treatment of patients with: Mantle cell lymphoma (MCL) who have received at least one priortherapy (1.1).Accelerated approval was granted for this indication based on overallresponse rate. Continued approval for this indication may be contingentupon verification of clinical benefit in confirmatory trials. Chronic lymphocytic leukemia (CLL) who have received at least oneprior therapy (1.2). Chronic lymphocytic leukemia with 17p deletion (1.3). Waldenströmâs macroglobulinemia (WM) (1.4).
DrugBank Targets:
16
1. Tyrosine-protein kinase BTK
Mechanism of Action:
18
Target: Bruton's tyrosine kinase (Btk)
Action: selective inhibitor
FDA: Ibrutinib is a small-molecule inhibitor of BTK. Ibrutinib forms a covalent bond with a cysteineresidue in the BTK active site, leading to inhibition of BTK enzymatic activity. BTK is asignaling molecule of the B-cell antigen receptor (BCR) and cytokine receptor pathways. BTKâsrole in signaling through the B-cell surface receptors results in activation of pathways necessaryfor B-cell trafficking, chemotaxis, and adhesion. Nonclinical studies show that ibrutinib inhibitsmalignant B-cell proliferation and survival in vivo as well as cell migration and substrateadhesion in vitro.
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| 31 |
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Intron A
18
49
|
INTERFERON ALFA-2B |
Schering-Plough |
December 1997/ December 1995/ March 1997 |
Disease/s that Drug Treats:non-Hodgkin's lymphoma/ malignant melanoma / Hepatitis C
Indications and Usage:
18
Hairy Cell Leukemia INTRON® A is indicated for the treatment of patients 18 years ofage or older with hairy cell leukemia.Malignant Melanoma INTRON A is indicated as adjuvant to surgical treatment inpatients 18 years of age or older with malignant melanoma who are free of disease butat high risk for systemic recurrence, within 56 days of surgery.Follicular Lymphoma INTRON A is indicated for the initial treatment of clinicallyaggressive (see Clinical Pharmacology) follicular Non-Hodgkinâs Lymphoma inconjunction with anthracycline-containing combination chemotherapy in patients 18years of age or older. Efficacy of INTRON A therapy in patients with low-grade, lowtumorburden follicular Non-Hodgkinâs Lymphoma has not been demonstrated.Condylomata Acuminata INTRON A is indicated for intralesional treatment of selectedpatients 18 years of age or older with condylomata acuminata involving externalsurfaces of the genital and perianal areas (see DOSAGE AND ADMINISTRATION).The use of this product in adolescents has not been studied.AIDS-Related Kaposi's Sarcoma INTRON A is indicated for the treatment of selectedpatients 18 years of age or older with AIDS-Related Kaposi's Sarcoma. The likelihoodof response to INTRON A therapy is greater in patients who are without systemic symptoms, who have limited lymphadenopathy and who have a relatively intact immunesystem as indicated by total CD4 count.Chronic Hepatitis C INTRON A is indicated for the treatment of chronic hepatitis C inpatients 18 years of age or older with compensated liver disease who have a history ofblood or blood-product exposure and/or are HCV antibody positive. Studies in thesepatients demonstrated that INTRON A therapy can produce clinically meaningful effectson this disease, manifested by normalization of serum alanine aminotransferase (ALT)and reduction in liver necrosis and degeneration.A liver biopsy should be performed to establish the diagnosis of chronic hepatitis.Patients should be tested for the presence of antibody to HCV. Patients with othercauses of chronic hepatitis, including autoimmune hepatitis, should be excluded. Priorto initiation of INTRON A therapy, the physician should establish that the patient hascompensated liver disease. The following patient entrance criteria for compensated liverdisease were used in the clinical studies and should be considered before INTRON Atreatment of patients with chronic hepatitis C: No history of hepatic encephalopathy, variceal bleeding, ascites, or otherclinical signs of decompensation Bilirubin Less than or equal to 2 mg/dL Albumin Stable and within normal limits Prothrombin Time Less than 3 seconds prolonged WBC Greater than or equal to 3000/mm3 Platelets Greater than or equal to 70,000/mm3Serum creatinine should be normal or near normal.Prior to initiation of INTRON A therapy, CBC and platelet counts should beevaluated in order to establish baselines for monitoring potential toxicity. These testsshould be repeated at Weeks 1 and 2 following initiation of INTRON A therapy, andmonthly thereafter. Serum ALT should be evaluated at approximately 3-month intervalsto assess response to treatment (see DOSAGE AND ADMINISTRATION).Patients with preexisting thyroid abnormalities may be treated if thyroidstimulatinghormone (TSH) levels can be maintained in the normal range by medication.TSH levels must be within normal limits upon initiation of INTRON A treatment and TSHtesting should be repeated at 3 and 6 months (see PRECAUTIONS, LaboratoryTests).INTRON A in combination with REBETOL® is indicated for the treatment ofchronic hepatitis C in patients 3 years of age and older with compensated liver diseasepreviously untreated with alpha interferon therapy and in patients 18 years of age andolder who have relapsed following alpha interferon therapy. See REBETOL prescribinginformation for additional information. Chronic Hepatitis B INTRON A is indicated for the treatment of chronic hepatitis B inpatients 1 year of age or older with compensated liver disease. Patients who have beenserum HBsAg positive for at least 6 months and have evidence of HBV replication(serum HBeAg positive) with elevated serum ALT are candidates for treatment. Studiesin these patients demonstrated that INTRON A therapy can produce virologic remissionof this disease (loss of serum HBeAg) and normalization of serum aminotransferases.INTRON A therapy resulted in the loss of serum HBsAg in some responding patients.Prior to initiation of INTRON A therapy, it is recommended that a liver biopsy beperformed to establish the presence of chronic hepatitis and the extent of liver damage.The physician should establish that the patient has compensated liver disease. Thefollowing patient entrance criteria for compensated liver disease were used in theclinical studies and should be considered before INTRON A treatment of patients withchronic hepatitis B: No history of hepatic encephalopathy, variceal bleeding, ascites, or othersigns of clinical decompensation Bilirubin Normal Albumin Stable and within normal limits Prothrombin Time Adults less than 3 seconds prolongedPediatrics less than or equal to 2 seconds prolonged WBC Greater than or equal to 4000/mm3 Platelets Adults greater than or equal to 100,000/mm3Pediatrics greater than or equal to 150,000/mm3Patients with causes of chronic hepatitis other than chronic hepatitis B or chronichepatitis C should not be treated with INTRON A. CBC and platelet counts should beevaluated prior to initiation of INTRON A therapy in order to establish baselines formonitoring potential toxicity. These tests should be repeated at treatment Weeks 1, 2,4, 8, 12, and 16. Liver function tests, including serum ALT, albumin, and bilirubin,should be evaluated at treatment Weeks 1, 2, 4, 8, 12, and 16. HBeAg, HBsAg, andALT should be evaluated at the end of therapy, as well as 3- and 6-months posttherapy,since patients may become virologic responders during the 6-month periodfollowing the end of treatment. In clinical studies in adults, 39% (15/38) of respondingpatients lost HBeAg 1 to 6 months following the end of INTRON A therapy. Ofresponding patients who lost HBsAg, 58% (7/12) did so 1 to 6 months post-treatment.A transient increase in ALT greater than or equal to 2 times baseline value (flare)can occur during INTRON A therapy for chronic hepatitis B. In clinical trials in adultsand pediatrics, this flare generally occurred 8 to 12 weeks after initiation of therapy andwas more frequent in responders (adults 63%, 24/38; pediatrics 59%, 10/17) than innonresponders (adults 27%, 13/48; pediatrics 35%, 19/55). However, in adults andpediatrics, elevations in bilirubin greater than or equal to 3 mg/dL (greater than or equalto 2 times ULN) occurred infrequently (adults 2%, 2/86; pediatrics 3%, 2/72) duringtherapy. When ALT flare occurs, in general, INTRON A therapy should be continued unless signs and symptoms of liver failure are observed. During ALT flare, clinicalsymptomatology and liver function tests including ALT, prothrombin time, alkalinephosphatase, albumin, and bilirubin, should be monitored at approximately 2-weekintervals (see WARNINGS).
DrugBank Targets:
16
1. Interferon alpha/beta receptor 2;2. Interferon alpha/beta receptor 1
Mechanism of Action:
18
Target: intracellular oncogene expression, natural killer and cytotoxic T-cells, microphage, cytokine production
Action: stimulation, induction (unspecified effects on oncogene expression)
FDA: -
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| 32 |
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Iressa
18
49
|
GEFITINIB |
AstraZeneca |
May 2003 |
Disease/s that Drug Treats:Non-Small-Cell Lung Cancer
Indications and Usage:
18
IRESSA is indicated as monotherapy for the continued treatment of patients with locally advanced ormetastatic non-small cell lung cancer after failure of both platinum-based and docetaxelchemotherapies who are benefiting or have benefited from IRESSA.In light of positive survival data with other agents including another oral EGFR inhibitor, physiciansshould use other treatment options in advanced non-small cell lung cancer patient populations whohave received one or two prior chemotherapy regimens and are refractory or intolerant to their mostrecent regimen. The effectiveness of IRESSA was initially based on objective response rates (see CLINICALPHARMACOLOGY-Clinical Studies section). Subsequent studies intended to demonstrate anincrease in survival have been unsuccessful. Specifically, results from a large placebo-controlledrandomized trial in patients with advanced NSCLC who progressed while receiving or within 90 daysof the last dose of chemotherapy or were intolerant to the most recent prior chemotherapy regimen, didnot show an improvement in survival (see CLINICAL PHARMACOLOGY- Clinical Studiessection).Results from two large, controlled, randomized trials in first-line treatment of non-small cell lungcancer showed no benefit from adding IRESSA to doublet, platinum-based chemotherapy. , IRESSA is indicated as monotherapy for the continued treatment of patients with locally advanced or metastatic non-small cell lung cancer after failure of both platinum-based and docetaxel chemotherapies who are benefiting or have benefited from IRESSA. In light of positive survival data with other agents including another oral EGFR inhibitor, physicians should use other treatment options in advanced non-small cell lung cancer patient populations who have received one or two prior chemotherapy regimens and are refractory or intolerant to their most recent regimen. The effectiveness of IRESSA was initially based on objective response rates (see CLINICAL PHARMACOLOGY-Clinical Studies section). Subsequent studies intended to demonstrate an increase in survival have been unsuccessful. Specifically, results from a large placebo-controlled randomized trial in patients with advanced NSCLC who progressed while receiving or within 90 days of the last dose of chemotherapy or were intolerant to the most recent prior chemotherapy regimen, did not show an improvement in survival (see CLINICAL PHARMACOLOGY- Clinical Studies section). Results from two large, controlled, randomized trials in first-line treatment of non-small cell lung cancer showed no benefit from adding IRESSA to doublet, platinum-based chemotherapy.
DrugBank Targets:
16
1. Epidermal growth factor receptor, Epidermal growth factor receptor
Mechanism of Action:
18
Target: EGFR tyrosine kinase and other tyrosine kinases, EGFR tyrosine kinase
Action: inhibitor
FDA: The mechanism of the clinical antitumor action of gefitinib is not fully characterized. Gefitinibinhibits the intracellular phosphorylation of numerous tyrosine kinases associated with transmembranecell surface receptors, including the tyrosine kinases associated with the epidermal growth factorreceptor (EGFR-TK). EGFR is expressed on the cell surface of many normal cells and cancer cells.No clinical studies have been performed that demonstrate a correlation between EGFR receptorexpression and response to gefitinib., The mechanism of the clinical antitumor action of gefitinib is not fully characterized. Gefitinib inhibits the intracellular phosphorylation of numerous tyrosine kinases associated with transmembrane cell surface receptors, including the tyrosine kinases associated with the epidermal growth factor receptor (EGFR-TK). EGFR is expressed on the cell surface of many normal cells and cancer cells. No clinical studies have been performed that demonstrate a correlation between EGFR receptor expression and response to gefitinib.
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| 33 |
|
Istodax
18
49
|
ROMIDEPSIN |
Gloucester Pharmaceuticals |
November 2009 |
Disease/s that Drug Treats:cutaneous T-cell lymphoma
Indications and Usage:
18
ISTODAX is a histone deacetylase (HDAC) inhibitor indicated for: Treatment of cutaneous T-cell lymphoma (CTCL) in patients who havereceived at least one prior systemic therapy (1). Treatment of peripheral T-cell lymphoma (PTCL) in patients who havereceived at least one prior therapy (1).These indications are based on response rate. Clinical benefit such asimprovement in overall survival has not been demonstrated (1).
DrugBank Targets:
-
Mechanism of Action:
18
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: Romidepsin is a histone deacetylase (HDAC) inhibitor. HDACs catalyze the removal of acetyl groups from acetylated lysine residues in histones, resulting in themodulation of gene expression. HDACs also deacetylate non-histone proteins, such as transcription factors. In vitro, romidepsin causes the accumulation of acetylatedhistones, and induces cell cycle arrest and apoptosis of some cancer cell lines with IC50 values in the nanomolar range. The mechanism of the antineoplastic effect ofromidepsin observed in nonclinical and clinical studies has not been fully characterized.
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| 34 |
|
Jevtana
18
49
|
CABAZITAXEL |
sanofi aventis |
June 2010 |
Disease/s that Drug Treats:prostate cancer
Indications and Usage:
18
JEVTANA is a microtubule inhibitor indicated in combination withprednisone for treatment of patients with hormone-refractory metastaticprostate cancer previously treated with a docetaxel-containing treatmentregimen. (1)
DrugBank Targets:
16
1. Tubulin alpha-4A chain;2. Tubulin beta-1 chain
Mechanism of Action:
18
Target: microtubule
Action: inhibitor
FDA: Cabazitaxel is a microtubule inhibitor. Cabazitaxel binds to tubulin and promotes its assemblyinto microtubules while simultaneously inhibiting disassembly. This leads to the stabilization ofmicrotubules, which results in the inhibition of mitotic and interphase cellular functions.
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| 35 |
|
Kadcyla
18
49
|
ADO-TRASTUZUMAB EMTANSINE |
Genentech |
February 2013 |
Disease/s that Drug Treats:HER2-positive metastatic breast cancer
Indications and Usage:
18
KADCYLA is a HER2-targeted antibody and microtubule inhibitor conjugateindicated, as a single agent, for the treatment of patients with HER2-positive,metastatic breast cancer who previously received trastuzumab and a taxane,separately or in combination. Patients should have either: Received prior therapy for metastatic disease, or Developed disease recurrence during or within six months ofcompleting adjuvant therapy. (1)
DrugBank Targets:
16
1. Receptor tyrosine-protein kinase erbB-2
Mechanism of Action:
18
Target: microtubule
Action: inhibitor
FDA: Ado-trastuzumab emtansine is a HER2-targeted antibody-drug conjugate. The antibody is thehumanized anti-HER2 IgG1, trastuzumab. The small molecule cytotoxin, DM1, is a microtubuleinhibitor. Upon binding to sub-domain IV of the HER2 receptor, ado-trastuzumab emtansineundergoes receptor-mediated internalization and subsequent lysosomal degradation, resulting inintracellular release of DM1-containing cytotoxic catabolites. Binding of DM1 to tubulindisrupts microtubule networks in the cell, which results in cell cycle arrest and apoptotic celldeath. In addition, in vitro studies have shown that similar to trastuzumab, ado-trastuzumabemtansine inhibits HER2 receptor signaling, mediates antibody-dependent cell-mediatedcytotoxicity and inhibits shedding of the HER2 extracellular domain in human breast cancer cellsthat overexpress HER2.
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| 36 |
|
Keytruda
18
49
|
PEMBROLIZUMAB |
Merck |
September 2014 |
Disease/s that Drug Treats:unresectable or metastatic melanoma
Indications and Usage:
18
KEYTRUDA is a human programmed death receptor-1 (PD-1)-blockingantibody indicated for the treatment of patients with unresectable ormetastatic melanoma and disease progression following ipilimumaband, if BRAF V600 mutation positive, a BRAF inhibitor.This indication is approved under accelerated approval based on tumorresponse rate and durability of response. An improvement in survivalor disease-related symptoms has not yet been established. Continuedapproval for this indication may be contingent upon verification anddescription of clinical benefit in the confirmatory trials. (1)
DrugBank Targets:
16
1. Programmed cell death protein 1
Mechanism of Action:
18
Target: PD-1 receptor
Action: blocks interaction withPD-L1 and PD-L2
FDA: Binding of the PD-1 ligands, PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibits T cellproliferation and cytokine production. Upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors.Pembrolizumab is a monoclonal antibody that binds to the PD-1 receptor and blocks its interaction withPD-L1 and PD-L2, releasing PD-1 pathway-mediated inhibition of the immune response, including theanti-tumor immune response. In syngeneic mouse tumor models, blocking PD-1 activity resulted indecreased tumor growth.
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| 37 |
|
Kyprolis
18
49
|
CARFILZOMIB |
Onyx Pharmaceuticals |
July 2012 |
Disease/s that Drug Treats:multiple myeloma
Indications and Usage:
18
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:
18
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.
|
| 38 |
|
Lazanda
18
|
FENTANYL CITRATE |
Archimedes |
June 2011 |
Disease/s that Drug Treats:breakthrough cancer pain
Indications and Usage:
18
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:
18
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.
|
| 39 |
|
Lenvima
18
49
|
LENVATINIB MESYLATE |
Eisai |
February 2015 |
Disease/s that Drug Treats:thyroid cancer
Indications and Usage:
18
LENVIMA is a kinase inhibitor indicated for the treatment of patients with locally recurrent or metastatic, progressive, radioactive iodine-refractory differentiated thyroid cancer (1).
DrugBank Targets:
16
1. Vascular endothelial growth factor receptor 1;2. Vascular endothelial growth factor receptor 2;3. Vascular endothelial growth factor receptor 3;4. Fibroblast growth factor receptor 1;5. Fibroblast growth factor receptor 2;6. Fibroblast growth factor receptor 3;7. Fibroblast growth factor receptor 4;8. Platelet derived growth factor receptor alpha;9. RET;10. Mast/stem cell growth factor receptor Kit
Mechanism of Action:
18
Target: kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4)
Action: inhibitor
FDA: Lenvatinib is a receptor tyrosine kinase (RTK) inhibitor that inhibits the kinase activities ofvascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR),and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs that have been implicated inpathogenic angiogenesis, tumor growth, and cancer progression in addition to their normalcellular functions, including fibroblast growth factor (FGF) receptors FGFR1, 2, 3, and 4; theplatelet derived growth factor receptor alpha (PDGFRα), KIT, and RET.
|
| 40 |
|
Leukine
18
|
SARGRAMOSTIM |
Immunex |
on November 24, 1995/ November 1996 |
Disease/s that Drug Treats:transplantation/ replenishment of white blood cells, fungal infections
Indications and Usage:
18
DrugBank Targets:
16
1. Granulocyte-macrophage colony-stimulating factor receptor subunit alpha;2. Interleukin-3 receptor subunit alpha;3. Cytokine receptor common subunit beta;4. Syndecan-2;5. Bone marrow proteoglycan
Mechanism of Action:
18
Target: -
Action: -
FDA: -
|
| 41 |
|
Lynparza
18
49
|
OLAPARIB |
AstraZeneca |
December 2014 |
Disease/s that Drug Treats:previously treated BRCA mutated advanced ovarian cancer
Indications and Usage:
18
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:
18
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.
|
| 42 |
|
Mekinist
18
49
|
TRAMETINIB DIMETHYL SULFOXIDE |
GlaxoSmithKline |
May of 2013 |
Disease/s that Drug Treats:unresectable or metastatic melanoma with BRAF V600E or V600K mutations
Indications and Usage:
18
MEKINIST is a kinase inhibitor indicated as a single agent and incombination with dabrafenib for the treatment of patients with unresectable ormetastatic melanoma with BRAF V600E or V600K mutations as detected byan FDA-approved test. The use in combination is based on the demonstrationof durable response rate. Improvement in disease-related symptoms or overallsurvival has not been demonstrated for MEKINIST in combination withdabrafenib. (1, 14.1)Limitation of use: MEKINIST as a single agent is not indicated for treatmentof patients who have received prior BRAF-inhibitor therapy. (1)
DrugBank Targets:
16
1. Dual specificity mitogen-activated protein kinase kinase 1;2. Dual specificity mitogen-activated protein kinase kinase 2
Mechanism of Action:
18
Target: mitogen-activated extracellular signal regulated kinase 1 (MEK1) and MEK2 activation and of MEK1 and MEK2 kinase
Action: inhibitor
FDA: Trametinib is a reversible inhibitor of mitogen-activated extracellular signal-regulated kinase 1(MEK1) and MEK2 activation and of MEK1 and MEK2 kinase activity. MEK proteins areupstream regulators of the extracellular signal-related kinase (ERK) pathway, which promotescellular proliferation. BRAF V600E mutations result in constitutive activation of the BRAFpathway which includes MEK1 and MEK2. Trametinib inhibits BRAF V600 mutation-positivemelanoma cell growth in vitro and in vivo.Trametinib and dabrafenib target two different tyrosine kinases in the RAS/RAF/MEK/ERKpathway. Use of trametinib and dabrafenib in combination resulted in greater growth inhibitionof BRAF V600 mutation-positive melanoma cell lines in vitro and prolonged inhibition of tumorgrowth in BRAF V600 mutation positive melanoma xenografts compared with either drug alone.
|
| 43 |
|
Miraluma Test
18
|
TECHNETIUM TC-99M SESTAMIBI KIT |
DuPont Merck Pharmaceutical Company |
May 1997 |
Disease/s that Drug Treats:breast imaging
Indications and Usage:
18
Breast Imaging: MIRALUMA, Kit for the Preparation of Technetium Tc99m Sestamibi for Injection, is indicated for planar imaging as a second line diagnostic drug after mammography to assist in the evaluation of breast lesions in patients with an abnormal mammogram or a palpable breast mass. MIRALUMA is not indicated for breast cancer screening, to confirm the presence or absence of malignancy, and it is not an alternative to biopsy.
DrugBank Targets:
-
Mechanism of Action:
18
Target: malignant cells
Action: accumulates
FDA: The mechanism of Tc99m Sestanibi localization in various types of breast tissue (e.g. beinign, inflammatory, malignant, fiborous) has not been established.
|
| 44 |
|
Nolvadex
18
49
|
TAMOXIFEN CITRATE |
AstraZeneca |
October 1998 |
Disease/s that Drug Treats:Breast Cancer
Indications and Usage:
18
Metastatic Breast Cancer:NOLVADEX is effective in the treatment of metastatic breast cancer in women and men. Inpremenopausal women with metastatic breast cancer, NOLVADEX is an alternative tooophorectomy or ovarian irradiation. Available evidence indicates that patients whose tumorsare estrogen receptor positive are more likely to benefit from NOLVADEX therapy.Adjuvant Treatment of Breast Cancer:NOLVADEX is indicated for the treatment of node-positive breast cancer in women followingtotal mastectomy or segmental mastectomy, axillary dissection, and breast irradiation. In someNOLVADEX adjuvant studies, most of the benefit to date has been in the subgroup with four ormore positive axillary nodes.NOLVADEX is indicated for the treatment of axillary node-negative breast cancer in womenfollowing total mastectomy or segmental mastectomy, axillary dissection, and breast irradiation.The estrogen and progesterone receptor values may help to predict whether adjuvantNOLVADEX therapy is likely to be beneficial.NOLVADEX reduces the occurrence of contralateral breast cancer in patients receiving adjuvantNOLVADEX therapy for breast cancer.Ductal Carcinoma in Situ (DCIS):In women with DCIS, following breast surgery and radiation, NOLVADEX is indicated toreduce the risk of invasive breast cancer (see BOXED WARNING at the beginning of thelabel). The decision regarding therapy with NOLVADEX for the reduction in breast cancerincidence should be based upon an individual assessment of the benefits and risks ofNOLVADEX therapy.Current data from clinical trials support five years of adjuvant NOLVADEX therapy for patientswith breast cancer. Reduction in Breast Cancer Incidence in High Risk Women:NOLVADEX is indicated to reduce the incidence of breast cancer in women at high risk forbreast cancer. This effect was shown in a study of 5 years planned duration with a medianfollow-up of 4.2 years. Twenty-five percent of the participants received drug for 5 years. Thelonger-term effects are not known. In this study, there was no impact of tamoxifen on overall orbreast cancer-related mortality (see BOXED WARNING at the beginning of the label).NOLVADEX is indicated only for high-risk women. âHigh riskâ is defined as women at least35 years of age with a 5-year predicted risk of breast cancer ⥠1.67%, as calculated by the GailModel.Examples of combinations of factors predicting a 5-year risk ⥠1.67% are:Age 35 or older and any of the following combination of factors: One first degree relative with a history of breast cancer, 2 or more benign biopsies, and ahistory of a breast biopsy showing atypical hyperplasia; or At least 2 first degree relatives with a history of breast cancer, and a personal history of atleast one breast biopsy; or LCISAge 40 or older and any of the following combination of factors: One first degree relative with a history of breast cancer, 2 or more benign biopsies, age at firstlive birth 25 or older, and age at menarche 11 or younger; or At least 2 first degree relatives with a history of breast cancer, and age at first live birth 19 oryounger; or One first degree relative with a history of breast cancer, and a personal history of a breastbiopsy showing atypical hyperplasia.Age 45 or older and any of the following combination of factors: At least 2 first degree relatives with a history of breast cancer and age at first live birth 24 oryounger; or One first degree relative with a history of breast cancer with a personal history of a benignbreast biopsy, age at menarche 11 or less and age at first live birth 20 or more.Age 50 or older and any of the following combination of factors: At least 2 first degree relatives with a history of breast cancer; or History of one breast biopsy showing atypical hyperplasia, and age at first live birth 30 orolder and age at menarche 11 or less; or History of at least two breast biopsies with a history of atypical hyperplasia, and age at firstlive birth 30 or more.Age 55 or older and any of the following combination of factors: One first degree relative with a history of breast cancer with a personal history of a benignbreast biopsy, and age at menarche 11 or less; or History of at least 2 breast biopsies with a history of atypical hyperplasia, and age at first livebirth 20 or older.Age 60 or older and: 5-year predicted risk of breast cancer ⥠1.67%, as calculated by the Gail Model.For women whose risk factors are not described in the above examples, the Gail Model isnecessary to estimate absolute breast cancer risk. Health Care Professionals can obtain a GailModel Risk Assessment Tool by dialing 1-800-544-2007.There are insufficient data available regarding the effect of NOLVADEX on breast cancerincidence in women with inherited mutations (BRCA1, BRCA2) to be able to make specificrecommendations on the effectiveness of NOLVADEX in these patients.After an assessment of the risk of developing breast cancer, the decision regarding therapy withNOLVADEX for the reduction in breast cancer incidence should be based upon an individualassessment of the benefits and risks of NOLVADEX therapy. In the NSABP P-1 trial,NOLVADEX treatment lowered the risk of developing breast cancer during the follow-up periodof the trial, but did not eliminate breast cancer risk (See Table 3 in CLINICALPHARMACOLOGY).
DrugBank Targets:
16
1. Estrogen receptor;2. Estrogen receptor beta;3. 3-beta-hydroxysteroid-Delta(8),Delta(7)-isomerase;4. Protein kinase C
Mechanism of Action:
18
Target: estrogen receptors
Action: competitor with estraidiol
FDA: NOLVADEX is a nonsteroidal agent that has demonstrated potent antiestrogenic properties inanimal test systems. The antiestrogenic effects may be related to its ability to compete withestrogen for binding sites in target tissues such as breast. Tamoxifen inhibits the induction of ratmammary carcinoma induced by dimethylbenzanthracene (DMBA) and causes the regression ofalready established DMBA-induced tumors. In this rat model, tamoxifen appears to exert itsantitumor effects by binding the estrogen receptors.In cytosols derived from human breast adenocarcinomas, tamoxifen competes with estradiol forestrogen receptor protein.
|
| 45 |
|
Odomzo
18
49
|
SONIDEGIB PHOSPHATE |
Novartis |
Jul-15 |
Disease/s that Drug Treats:locally advanced basal cell carcinoma
Indications and Usage:
18
ODOMZO is a hedgehog pathway inhibitor indicated for the treatment ofadult patients with locally advanced basal cell carcinoma (BCC) that hasrecurred following surgery or radiation therapy, or those who are notcandidates for surgery or radiation therapy. (1)
DrugBank Targets:
-
Mechanism of Action:
18
Target: Smoothened
Action: inhibitor
FDA: Sonidegib is an inhibitor of the Hedgehog pathway. Sonidegib binds to and inhibits Smoothened, a transmembrane proteininvolved in Hedgehog signal transduction.
|
| 46 |
|
Onsolis
18
|
FENTANYL CITRATE |
BioDelivery Sciences |
July 2009 |
Disease/s that Drug Treats:breakthrough cancer pain
Indications and Usage:
18
Onsolis 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:Onsolis may be dispensed only to patients enrolled in the TIRF REMS Accessprogram.
DrugBank Targets:
16
1. Mu-type opioid receptor;2. Delta-type opioid receptor;3. Kappa-type opioid receptor
Mechanism of Action:
18
Target: mu-opioid receptor
Action: agonist
FDA: Fentanyl is a pure opioid agonist whose principal therapeutic action is analgesia. Other members of the class known asopioid agonists include substances such as morphine, oxycodone, hydromorphone, codeine, and hydrocodone.
|
| 47 |
|
Opdivo
18
49
|
NIVOLUMAB |
Bristol-Myers Squibb |
March 2015/ December 2014, March 2015 |
Disease/s that Drug Treats:metastatic squamous non-small cell lung cancer/ unresectable or metastatic melanoma, metastatic squamous non-small cell lung cancer
Indications and Usage:
18
OPDIVO is a programmed death receptor-1 (PD-1) blocking antibodyindicated for the treatment of patients with: unresectable or metastatic melanoma and disease progression followingipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. (1.1)This indication is approved under accelerated approval based on tumorresponse rate and durability of response. Continued approval for thisindication may be contingent upon verification and description of clinicalbenefit in the confirmatory trials. (1.1, 14.1) metastatic squamous non-small cell lung cancer with progression on orafter platinum-based chemotherapy. (1.2) , OPDIVO is a programmed death receptor-1 (PD-1) blocking antibody indicated for the treatment of patients with: * unresectable or metastatic melanoma and disease progression following ipilimumab and, if BRAF V600 mutation positive, a BRAF inhibitor. (1.1) This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. (1.1, 14.1) * metastatic squamous non-small cell lung cancer with progression on or after platinum-based chemotherapy. (1.2)
DrugBank Targets:
16
1. Programmed cell death protein 1, Programmed cell death protein 1
Mechanism of Action:
18
Target: PD-1 receptor
Action: blocker of interaction with PD-L1 and PD-L2, blocks its interaction with PD-L1 and PD-L2
FDA: Binding of the PD-1 ligands, PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibitsT-cell proliferation and cytokine production. Upregulation of PD-1 ligands occurs in sometumors and signaling through this pathway can contribute to inhibition of active T-cell immunesurveillance of tumors. Nivolumab is a human immunoglobulin G4 (IgG4) monoclonal antibodythat binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2, releasing PD-1pathway-mediated inhibition of the immune response, including the anti-tumor immuneresponse. In syngeneic mouse tumor models, blocking PD-1 activity resulted in decreased tumorgrowth. , Binding of the PD-1 ligands, PD-L1 and PD-L2, to the PD-1 receptor found on T cells, inhibits T-cell proliferation and cytokine production. Upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway can contribute to inhibition of active T-cell immune surveillance of tumors. Nivolumab is a human immunoglobulin G4 (IgG4) monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2, releasing PD-1 pathway-mediated inhibition of the immune response, including the anti-tumor immune response. In syngeneic mouse tumor models, blocking PD-1 activity resulted in decreased tumor growth.
|
| 48 |
|
Perjeta
18
49
|
PERTUZUMAB |
Genentech |
June 2012 |
Disease/s that Drug Treats:HER2+ metastatic breast cancer
Indications and Usage:
18
PERJETA is a HER2/neu receptor antagonist indicated for: Use in combination with trastuzumab and docetaxel for treatment ofpatients with HER2-positive metastatic breast cancer (MBC) who havenot received prior anti-HER2 therapy or chemotherapy for metastaticdisease. (1.1) Use in combination with trastuzumab and docetaxel as neoadjuvanttreatment of patients with HER2-positive, locally advanced,inflammatory, or early stage breast cancer (either greater than 2 cm indiameter or node positive) as part of a complete treatment regimen forearly breast cancer. This indication is based on demonstration of animprovement in pathological complete response rate. No data areavailable demonstrating improvement in event-free survival or overallsurvival. (1.2, 2.1, 14.2)Limitations of Use: The safety of PERJETA as part of a doxorubicin-containing regimenhas not been established. The safety of PERJETA administered for greater than 6 cycles forearly breast cancer has not been established.
DrugBank Targets:
16
1. Receptor tyrosine-protein kinase erbB-2
Mechanism of Action:
18
Target: mitogen-activated protein (MAP) kinase, phosphoinositide 3-kinase445 (PI3K)
Action: inhibitor of ligand-initiated intracellular signaling
FDA: Pertuzumab targets the extracellular dimerization domain (Subdomain II) of the human epidermal growth factor receptor 2 protein (HER2) and, thereby, blocks ligand-dependent heterodimerization of HER2 with other HER family members, including EGFR, HER3, and HER4. As a result, pertuzumab inhibits ligand-initiated intracellular signaling through two major signal pathways, mitogen-activated protein (MAP) kinase, and phosphoinositide 3-kinase (PI3K). Inhibition of these signaling pathways can result in cell growth arrest and apoptosis, respectively. In addition, pertuzumab mediates antibody-dependent cell-mediated cytotoxicity (ADCC). While pertuzumab alone inhibited the proliferation of human tumor cells, the combination of pertuzumab and trastuzumab augmented anti-tumor activity in HER2-overexpressing xenograft models.
|
| 49 |
|
Premarin
18
|
ESTROGENS CONJUGATED |
Wyeth |
July of 2003 |
Disease/s that Drug Treats:prevention of postmenopausal osteoporosis and treatment of vasomotor menopause symptoms
Indications and Usage:
18
PREMARIN is a mixture of estrogens indicated for: Treatment of Moderate to Severe Vasomotor Symptoms due toMenopause (1.1) Treatment of Moderate to Severe Vulvar and Vaginal Atrophy due toMenopause (1.2) Treatment of Hypoestrogenism due to Hypogonadism, Castration orPrimary Ovarian Failure (1.3) Treatment of Breast Cancer (for Palliation Only) in AppropriatelySelected Women and Men with Metastatic Disease (1.4) Treatment of Advanced Androgen-Dependent Carcinoma of theProstate (for Palliation Only) (1.5) Prevention of Postmenopausal Osteoporosis (1.6)
DrugBank Targets:
16
1. Estrogen receptor
Mechanism of Action:
18
Target: nuclear receptors in estrogen-responsive tissues
Action: reduce theelevated levels of gonadotropins
FDA: Endogenous estrogens are largely responsible for the development and maintenance of thefemale reproductive system and secondary sexual characteristics. Although circulatingestrogens exist in a dynamic equilibrium of metabolic interconversions, estradiol is theprincipal intracellular human estrogen and is substantially more potent than its metabolites,estrone and estriol, at the receptor level.The primary source of estrogen in normally cycling adult women is the ovarian follicle, whichsecretes 70 to 500 mcg of estradiol daily, depending on the phase of the menstrual cycle.After menopause, most endogenous estrogen is produced by conversion of androstenedione,secreted by the adrenal cortex, to estrone in the peripheral tissues. Thus, estrone and thesulfate-conjugated form, estrone sulfate, are the most abundant circulating estrogens inpostmenopausal women. Estrogens act through binding to nuclear receptors in estrogen-responsive tissues. To date,two estrogen receptors have been identified. These vary in proportion from tissue to tissue.Circulating estrogens modulate the pituitary secretion of the gonadotropins, luteinizinghormone (LH) and FSH, through a negative feedback mechanism. Estrogens act to reduce theelevated levels of these gonadotropins seen in postmenopausal women.
|
| 50 |
|
Provenge
18
49
|
sipuleucel-T |
Dendreon |
May 2010 |
Disease/s that Drug Treats:hormone refractory prostate cancer
Indications and Usage:
18
PROVENGE is an autologous cellularimmunotherapy indicated for the treatment ofasymptomatic or minimally symptomatic metastaticcastrate resistant (hormone refractory) prostatecancer. (1)
DrugBank Targets:
-
Mechanism of Action:
18
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.
|
Drugs for Cholangiocarcinoma (from DrugBank, HMDB, Dgidb, PharmGKB, IUPHAR, NovoSeek, BitterDB):
(show top 50)
(show all 313)
| # |
|
Name |
Status |
Phase |
Clinical Trials |
Cas Number |
PubChem Id |
| 1 |
|
Celecoxib |
Approved, Investigational |
Phase 4 |
|
169590-42-5 |
2662
|
|
Synonyms:
169590-42-5
184007-95-2
1oq5
4-(5-(4-Methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)benzenesulfonamide
4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1Hpyrazol-1-yl] benzenesulfonamide
4-[5-(4-METHYLPHENYL)-3-(TRIFLUOROMETHYL)-1H-PYRAZOL-1-YL]BENZENESULFONAMIDE
4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide
AC1L1E6K
AC-4228
AI-525
Benzenesulfonamide,4-(5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl)
BIDD:GT0408
BRD-K02637541-001-02-4
BSPBio_003596
C07589
C105934
C17H14F3N3O2S
CCRIS 8679
CEL
Celebra
Celebrex
Celebrex (TN)
Celebrex, Celebra, Celecoxib
Celecox
Celecoxi
celecoxib
Celecoxib
Célécoxib
Celecoxib (JAN/USAN/INN)
Celecoxib (SC-58635)
Celecoxib [Old RN]
Celecoxib [USAN]
Celecoxibum
Celocoxib
CEP-33222
CHEBI:41423
CHEMBL118
CID2662
cMAP_000027
CPD000550473
D00567
DB00482
DivK1c_000893
Eurocox
FT-0080064
HMS1922G14
HMS2089L18
HMS2093I07
HMS502M15
HSDB 7038
I01-1033
IDI1_000893
KBio1_000893
|
KBio2_000912
KBio2_002351
KBio2_003480
KBio2_004919
KBio2_006048
KBio2_007487
KBio3_002830
KBio3_003037
KBioGR_000723
KBioGR_002351
KBioSS_000912
KBioSS_002354
LS-31667
Medicoxib
MLS001165684
MLS001195656
MLS001304708
MolPort-002-885-815
NCGC00091455-01
NCGC00091455-02
NCGC00091455-03
NCGC00091455-04
NCI60_041049
NINDS_000893
NSC719627
Onsenal
p-(5-p-Tolyl-3-(trifluoromethyl)pyrazol-1-yl)benzenesulfonamide
P-(5-P-Tolyl-3-(trifluoromethyl)pyrazol-1-yl)benzenesulfonamide
P-(5-P-Tolyl-3-(trifluoromethyl)pyrazol-1-yl)benzenesulphonamide
Pfizer brand of celecoxib
S1261_Selleck
SAM002589995
SC 58635
SC-58553, SC-58635
SC58635
SC-58635
SMR000550473
Solexa
SPBio_001512
Spectrum_000432
SPECTRUM1503678
Spectrum2_001576
Spectrum3_001996
Spectrum4_000182
Spectrum5_001324
TL8001323
TPI-336
UNM-0000305813
Xilebao
YM 177
YM177
YM-177
ZINC02570895
|
|
| 2 |
|
Pancrelipase |
Approved, Investigational |
Phase 4,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
53608-75-6 |
|
|
Synonyms:
lipase
Pancrealipase
Pancreatic extract pancrelipase
Pancreatic protease
|
Pancreatin
Pancreatinum
Pancrelipase (amylase
protease)
|
|
| 3 |
|
Isoflurane |
Approved, Vet_approved |
Phase 4,Not Applicable |
|
26675-46-7 |
3763
|
|
Synonyms:
1-chloro-2,2,2-trifluoroethyl difluoromethyl ether
1-chloro-2,2,2-Trifluoroethyl difluoromethyl ether
1-Chloro-2,2,2-trifluoroethyl difluoromethyl ether
26675-46-7
2-Chloro-2-(difluoromethoxy)-1,1,1-trifluoroethane
2-chloro-2-difluoromethoxy-1,1,1-trifluoroethane
AC-154802
AC1L1GNN
Aerrane
AErrane (Veterinary)
BRN 1852087
C07518
CCRIS 3043
CHEBI:6015
CHEMBL1256
CID3763
Compound 469
D00545
D007530
DB00753
EINECS 247-897-7
Ethane
Ether, 1-chloro-2,2,2-trifluoroethyl difluoromethyl
|
Forane
Forane (TN)
Forene
I14-1303
IsoFlo
isoflurane
Isoflurane
Isoflurane (JP15/USP/INN)
Isoflurane [Anaesthetics, volatile]
Isoflurane [Usan:Ban:Inn:Jan]
Isoflurane [USAN:BAN:INN:JAN]
Isoflurane [USAN:INN:BAN:JAN]
Isoflurano
Isoflurano [INN-Spanish]
Isofluranum
Isofluranum [INN-Latin]
Jsp005223
LS-7462
MolPort-000-153-606
NCGC00181037-01
R-E 235dal
ST51041445
UNII-CYS9AKD70P
|
|
| 4 |
|
Sevoflurane |
Approved, Vet_approved |
Phase 4 |
|
28523-86-6 |
5206
|
|
Synonyms:
1,1,1,3,3,3-hexafluoro-2-(Fluoromethoxy)propane
1,1,1,3,3,3-Hexafluoro-2-(fluoromethoxy)propane
28523-86-6
AC-15484
AC1L1JU0
Bax 3084
BRN 2041023
C009250
C07520
C4H3F7O
CHEBI:9130
CHEMBL1200694
CID5206
D00547
DB01236
F0691
Fluoromethyl 1,1,1,3,3,3-Hexafluoroisopropyl Ether
Fluoromethyl 2,2,2-trifluoro-1-(trifluoromethyl)ethyl ether
fluoromethyl hexafluoroisopropyl ether
Fluoromethyl hexafluoroisopropyl ether
fluoromethyl-2,2,2-trifluoro-1-(trifluoromethyl)ethyl ether
Fluoromethyl-2,2,2-trifluoro-1-(trifluoromethyl)ethyl ether
I14-13357
|
LS-67851
MolPort-001-775-746
MR_6S4
MR6S4
NCGC00167421-01
PC4681
Sevofluran
sevoflurane
Sevoflurane
Sevoflurane (JAN/USAN/INN)
Sevoflurane [USAN:INN:BAN:JAN]
Sevoflurano
Sevoflurano [INN-Spanish]
Sevofluranum
Sevofluranum [INN-Latin]
Sevofrane
Sevorane
Sojourn
Ultane
Ultane (TN)
UNII-38LVP0K73A
ZINC01530810
|
|
| 5 |
|
Desflurane |
Approved |
Phase 4,Not Applicable |
|
57041-67-5 |
42113
|
|
Synonyms:
(+-)-2-Difluoromethyl 1,2,2,2-tetrafluoroethyl ether
1,1,1,2-tetrafluoro-2-(difluoromethoxy)ethane
1,1,1,2-tetrafluoro-2-(Difluoromethoxy)ethane
1,1,1,2-Tetrafluoro-2-(difluoromethoxy)ethane
2-(difluoromethoxy)-1,1,1,2-tetrafluoroethane
57041-67-5
AC1L274J
AC1Q4ICY
Baxter anaesthesia brand OF desflurane
Baxter brand OF desflurane
C07519
C3H2F6O
CHEBI:4445
CHEMBL1200733
CID42113
D00546
DB01189
Desflurane
DESFLURANE
Desflurane (JAN/USP/INN)
|
Desflurane [USAN:INN]
Desflurano
Desflurano [INN-Spanish]
Desfluranum
Desfluranum [INN-Latin]
difluoromethyl 1,2,2,2-tetrafluoroethyl ether
Difluoromethyl 1,2,2,2-tetrafluoroethyl ether
I 653
I653
I-653
LS-65505
MolPort-001-776-387
Ohmeda brand OF desflurane
PC6781E
r-e 236ea1
Suprane
Suprane (TN)
UNII-CRS35BZ94Q
Zeneca brand OF desflurane
|
|
| 6 |
|
Oxaliplatin |
Approved, Investigational |
Phase 4,Phase 3,Phase 2,Phase 1 |
|
61825-94-3 |
43805
6857599
5310940
9887054
|
|
Synonyms:
CHEMBL1201055
CID9887054
D01790
DACPLAT
Diaminocyclohexane Oxalatoplatinum
Eloxatin
Eloxatin (TN)
Elplat
Foloxatine
L-OHP
Oxalatoplatin
Oxalatoplatinum
|
oxaliplatin
Oxaliplatin (JAN/USAN/INN)
Oxaliplatin [Usan:Inn:Ban]
oxaliplatine
oxaliplatino
Oxaliplatino [Spanish]
oxaliplatinum
Oxaliplatinum [Latin]
Oxaloplatine [French]
Oxaloplatino [Spanish]
Transplatin
|
|
| 7 |
|
Meperidine |
Approved |
Phase 4 |
|
57-42-1 |
4058
|
|
Synonyms:
1-Methyl-4-phenyl-4-piperidinecarboxylic acid ethyl ester
1-Methyl-4-phenylisonipecotic acid, ethyl ester
1-Methyl-4-phenyl-piperidin-4-carbon-saeure-aethylester
1-Methyl-4-phenyl-piperidin-4-carbon-saeure-aethylester [German]
1-Methyl-4-phenylpiperidine-4-carboxylic acid ethyl ester
4-Carbethoxy-1-methyl-4-phenylpiperidine
4-Piperidinecarboxylic acid, 1-methyl-4-phenyl-, ethyl ester
50-13-5 (hydrochloride)
57-42-1
610593_ALDRICH
610593_FLUKA
AC1L1HBJ
C07128
CHEBI:122528
CHEMBL607
CID4058
D008614
D08343
DB00454
DEA No. 9230
Demarol
Demerol
DivK1c_000983
Dolantin
Dolargan
Dolcontral
Dolin
Dolosal
Dolsin
EINECS 200-329-1
Ethyl 1-methyl-4-phenylisonipecotate
Ethyl 1-methyl-4-phenylpiperidine-4-carboxylate
HSDB 3116
IDI1_000983
Isonipecain
Isonipecaine
Isonipecaïne
Isonipecotic acid, 1-methyl-4-phenyl-, ethyl ester
|
KBio1_000983
L000908
Lidol
LS-85121
Lydol
meperidine
Meperidine hydrochloride
Meperidine solution
Meperidol
Methyl phenylpiperidine carbonic acid ethyl ester
MolPort-001-785-564
Nemerol
NINDS_000983
N-Methyl-4-phenyl-4-carbethoxypiperidine
Operidine epj I
Operidine EPJ I
Operidine epj-I
Operidine EPJ-I
Pethanol
Pethidin
Pethidine
Péthidine
Pethidine (INN)
Pethidine DBL
Pethidine DBL (TN)
Pethidineter
Pethidinum
Pethidinum [INN-Latin]
Petidina
Petidina [INN-Spanish]
Petydyna
Petydyna [Polish]
Phetidine
Piperosal
Pipersal
UNII-9E338QE28F
YIsonipecotic acid, 1-methyl-4-phenyl-, ethyl ester (8CI)
|
|
| 8 |
|
Midazolam |
Approved, Illicit |
Phase 4 |
|
59467-70-8 |
4192
|
|
Synonyms:
4H-Imidazo[1,5-a][1,4]benzodiazepine, 8-chloro-6-(2-fluoro-phenyl)-1-methyl-, (Z)-2-butenedioate
59467-70-8
8-Chlor-6-(2-fluorphenyl)-1-methyl-4H-imidazo(1,5-a)(1,4)benzodiazepin
8-Chloro-6-(2-fluorophenyl)-1-methyl-4H-imidazo[1,5-a][1,4]benzodiazepine
8-Chloro-6-(2-fluorophenyl)-1-methyl-4H-imidazo[1,5a][1,4]benzodiazepine hydrochloride
8-Chloro-6-(o-fluorophenyl)-1-methyl-4H-imidazo(1,5-a)(1,4)benzodiazepine
8-Chloro-6-(O-fluorophenyl)-1-methyl-4H-imidazo[1,5-a][1,4]-benzodiazepine
AC-18749
AC1L1HMA
BIDD:GT0647
BRN 0625572
Buccolam
C07524
C18H13ClFN3
CHEMBL655
CID4192
D00550
Dazolam
DB00683
Dea no. 2884
Dea No. 2884
DEA No. 2884
Dormicum
Dormicum (TN)
EINECS 261-774-5
|
Hydrochloride, midazolam
LS-77780
Maleate, midazolam
Midanium
midazolam
Midazolam
Midazolam (JAN/INN)
Midazolam [INN:BAN:JAN]
Midazolam base
Midazolam Base
Midazolam Hcl
Midazolam hydrochloride
Midazolam maleate
Midazolamum
Midazolamum [INN-Latin]
Midosed
MolPort-003-849-219
NCGC00168254-01
nchembio747-comp32
Ro 21-3981
TL8003787
UC429_SIGMA
UNII-R60L0SM5BC
Versed
ZINC00001732
|
|
| 9 |
|
Etomidate |
Approved |
Phase 4 |
|
33125-97-2 |
667484
36339
|
|
Synonyms:
(+)-Ethyl 1-(alpha-methylbenzyl)imidazole-5-carboxylate
(+)-Ethyl 1-(alpha-methylbenzyl)imidazole-5-carboxylic acid
(+)-Ethyl 1-(a-methylbenzyl)imidazole-5-carboxylate
(+)-Ethyl 1-(a-methylbenzyl)imidazole-5-carboxylic acid
(+)-ethyl 1-(α-methylbenzyl)imidazole-5-carboxylate
(+)-Ethyl 1-(α-methylbenzyl)imidazole-5-carboxylate
(+)-Ethyl 1-(α-methylbenzyl)imidazole-5-carboxylic acid
(+)-etomidate
(+)-Etomidate
(+)-Etomidic acid
(d)-Etomidate
(R)-(+)-1-(alpha-Methylbenzyl)imidazole-5-carboxylate ethyl ester
(R)-(+)-1-(alpha-Methylbenzyl)imidazole-5-carboxylic acid ethyl ester
(R)-(+)-1-(a-Methylbenzyl)imidazole-5-carboxylate ethyl ester
(R)-(+)-1-(a-Methylbenzyl)imidazole-5-carboxylic acid ethyl ester
(R)-(+)-1-(α-methylbenzyl)imidazole-5-carboxylate ethyl ester
(R)-(+)-1-(α-methylbenzyl)imidazole-5-carboxylic acid ethyl ester
(R)-1-(1-Phenylethyl)-1H-imidazole-5-carboxylate ethyl ester
(R)-1-(1-phenylethyl)-1H-imidazole-5-carboxylic acid ethyl ester
(R)-1-(1-Phenylethyl)-1H-imidazole-5-carboxylic acid ethyl ester
1-(1-Phenylethyl)-1H-imidazole-5-carboxylic acid ethyl ester
1-(1-Phenylethyl)-imidazole-5-carboxylic acid, ethyl ester
1-(alpha-Methylbenzyl)-1H-imidazole-5-carboxylic acid ethyl ester
15301-65-2
1H-Imidazole-5-carboxylic acid, 1-((1R)-1-phenylethyl)-, ethyl ester
3-((R)-1-Phenyl-ethyl)-3H-imidazole-4-carboxylate ethyl ester
3-((R)-1-Phenyl-ethyl)-3H-imidazole-4-carboxylic acid ethyl ester
3-(1-Phenyl-ethyl)-3H-imidazole-4-carboxylic acid ethyl ester
33125-97-2
Absele
AC1L1VLF
AC1Q34BV
AC1Q64LP
AC-5898
AKOS000548952
Amidate
Amidate (pharmaceutical)
Amidate (TN)
Amidate, Etomidate
BAS 01947657
BRN 0665833
C07522
C14H16N2O2
CHEBI:129025
CHEMBL23731
|
CID36339
CPD000010931
D005045
D00548
DB00292
D-Etomidate
EINECS 251-385-9
Ethnor
Ethomidate
Ethyl 1-(1-phenylethyl)-1H-imidazole-5-carboxylate
ethyl 3-(1-phenylethyl)imidazole-4-carboxylate
Etomidate
Etomidate (USAN/INN)
Etomidate [USAN:BAN:INN]
Etomidato
Etomidato [INN-Spanish]
Etomidatum
Etomidatum [INN-Latin]
Etomidic acid
HMS1571A04
HMS1612G10
HMS2093P17
Hypnomidate
LS-78232
MLS000034952
MLS001240191
MolPort-000-917-569
Prestwick0_001041
Prestwick1_001041
Prestwick2_001041
R 16659
R 26490
R-(+)-Ethyl 1-(1-phenylethyl)-1H-imidazole-5-carboxylate
R-(+)-Ethyl 1-(1-phenylethyl)-1H-imidazole-5-carboxylic acid
R26490
R-26490
Radenarcon
Radenarkon
S1329_Selleck
SAM002548930
SBB066197
SMR000010931
SPBio_002901
UNII-Z22628B598
|
|
| 10 |
|
Bilirubin |
|
Phase 4,Not Applicable |
|
635-65-4 |
5280352
|
|
Synonyms:
(4E)2,17-Diethenyl-1,10,19,22,23,24-hexahydro-3,7,13,18-tetramethyl-1,19-dioxo--21H-biline-8,12-dipropanoate
(4E)2,17-Diethenyl-1,10,19,22,23,24-hexahydro-3,7,13,18-tetramethyl-1,19-dioxo--21H-biline-8,12-dipropanoic acid
|
|
|
| 11 |
|
Analgesics |
|
Phase 4,Phase 3,Phase 1,Phase 2,Not Applicable |
|
|
|
| 12 |
|
Anti-Inflammatory Agents, Non-Steroidal |
|
Phase 4,Phase 1,Phase 2 |
|
|
|
| 13 |
|
Cyclooxygenase Inhibitors |
|
Phase 4 |
|
|
|
| 14 |
|
Cyclooxygenase 2 Inhibitors |
|
Phase 4 |
|
|
|
| 15 |
|
Anti-Inflammatory Agents |
|
Phase 4,Phase 3,Phase 1,Phase 2 |
|
|
|
| 16 |
|
Peripheral Nervous System Agents |
|
Phase 4,Phase 3,Phase 1,Phase 2,Not Applicable |
|
|
|
| 17 |
|
pancreatin |
|
Phase 4,Phase 2,Phase 1,Not Applicable,Early Phase 1 |
|
|
|
| 18 |
|
Gastrointestinal Agents |
|
Phase 4,Phase 3,Phase 2,Phase 1,Not Applicable |
|
|
|
| 19 |
|
Antirheumatic Agents |
|
Phase 4,Phase 1,Phase 2 |
|
|
|
| 20 |
|
Analgesics, Non-Narcotic |
|
Phase 4,Phase 1,Phase 2 |
|
|
|
| 21 |
|
arginine |
|
Phase 4 |
|
|
|
| 22 |
|
Omega 3 Fatty Acid |
|
Phase 4 |
|
|
|
| 23 |
|
Anesthetics, Inhalation |
|
Phase 4,Not Applicable |
|
|
|
| 24 |
|
Anesthetics, General |
|
Phase 4,Phase 3,Not Applicable |
|
|
|
| 25 |
|
Liver Extracts |
|
Phase 4,Phase 2,Phase 3,Phase 1,Not Applicable |
|
|
|
| 26 |
|
Central Nervous System Depressants |
|
Phase 4,Phase 3,Not Applicable |
|
|
|
| 27 |
|
Anesthetics |
|
Phase 4,Phase 3,Not Applicable |
|
|
|
| 28 |
|
Platelet Aggregation Inhibitors |
|
Phase 4 |
|
|
|
| 29 |
|
Cola |
|
Phase 4,Phase 3,Phase 1,Phase 2,Not Applicable |
|
|
|
| 30 |
|
Bismuth |
|
Phase 4,Phase 3 |
|
7440-69-9 |
16682734
105143
|
|
Synonyms:
17034_FLUKA
24267-48-9
25243-76-9
264008_ALDRICH
265462_ALDRICH
265470_ALDRICH
452386_ALDRICH
556130_ALDRICH
7440-69-9
83Bi
95372_ALDRICH
95372_FLUKA
95375_FLUKA
AC1NSDYX
AC1O4PN8
AR-1I0647
Bi
Bi(3+)
Bismut
bismuth
|
Bismuth standard for AAS
Bismuth standard for ICP
Bismuth(III) cation
Bismuth(III) nitrate solution
BISMUTH, 99.95%
BISMUTH, 99.999%
Bismuth, elemental
Bismuth-209
bismuto
Bisumth(3+) ion
C15471
CHEBI:33301
CID5359367
EINECS 231-177-4
HSDB 2078
LS-44708
LTBB002773
MolPort-003-925-759
Wismut
|
|
| 31 |
|
GABA Modulators |
|
Phase 4,Not Applicable |
|
|
|
| 32 |
|
GABA Agents |
|
Phase 4,Not Applicable |
|
|
|
| 33 |
|
Neurotransmitter Agents |
|
Phase 4,Phase 3,Phase 2,Not Applicable |
|
|
|
| 34 |
|
Hypnotics and Sedatives |
|
Phase 4,Not Applicable |
|
|
|
| 35 |
|
Anti-Anxiety Agents |
|
Phase 4,Phase 3 |
|
|
|
| 36 |
|
Adjuvants, Anesthesia |
|
Phase 4,Phase 3 |
|
|
|
| 37 |
|
Analgesics, Opioid |
|
Phase 4,Phase 3,Not Applicable |
|
|
|
| 38 |
|
Anesthetics, Intravenous |
|
Phase 4,Phase 3,Not Applicable |
|
|
|
| 39 |
|
Narcotics |
|
Phase 4,Phase 3,Not Applicable |
|
|
|
| 40 |
|
Tranquilizing Agents |
|
Phase 4,Phase 3 |
|
|
|
| 41 |
|
Psychotropic Drugs |
|
Phase 4,Phase 3 |
|
|
|
| 42 |
|
Capecitabine |
Approved, Investigational |
Phase 3,Phase 2,Phase 1,Not Applicable |
|
154361-50-9 |
60953
|
|
Synonyms:
(1-(5-Deoxy-b-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-carbamate pentyl ester
(1-(5-Deoxy-b-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-carbamic acid pentyl ester
(1-(5-Deoxy-beta-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-carbamate pentyl ester
(1-(5-Deoxy-beta-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-carbamic acid pentyl ester
(1-(5-Deoxy-β-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-carbamate pentyl ester
(1-(5-Deoxy-β-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-carbamic acid pentyl ester
154361-50-9
158798-73-3
5'-Deoxy-5-fluoro-N-((pentyloxy)carbonyl)cytidine
5'-deoxy-5-fluoro-N-[(pentyloxy)carbonyl]cytidine
AC1L1U83
AC1Q4KU8
Ambap154361-50-9
C110904
C12650
C15H22FN3O6
CAPE
Capecitabin
capecitabina
Capecitabina
capecitabine
CAPECITABINE
Capécitabine
Capecitabine (JAN/USAN/INN)
Capecitabine [USAN]
capecitabinum
Capecitabinum
Capecitibine
Capiibine
Carbamic acid, (1-(5-deoxy-beta-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinyl)-, pentyl ester
Caxeta
CHEBI:31348
CHEMBL1773
CID60953
D01223
|
DB01101
FT-0082472
HSDB 7656
LS-59070
MolPort-005-938-254
N(4)-Pentyloxycarbonyl-5'-deoxy-5-fluorocytidine
Pentyl [1-(5-deoxy-b-D-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl]carbamate
Pentyl [1-(5-deoxy-b-D-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl]carbamic acid
Pentyl [1-(5-deoxy-beta-D-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl]carbamate
Pentyl [1-(5-deoxy-beta-D-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl]carbamic acid
Pentyl [1-(5-deoxy-β-D-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl]carbamate
Pentyl [1-(5-deoxy-β-D-ribofuranosyl)-5-fluoro-2-oxo-1,2-dihydropyrimidin-4-yl]carbamic acid
Pentyl 1-(5-deoxy-b-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamate
Pentyl 1-(5-deoxy-b-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamic acid
Pentyl 1-(5-deoxy-beta-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamate
Pentyl 1-(5-deoxy-beta-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamic acid
pentyl 1-(5-deoxy-β-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamate
Pentyl 1-(5-deoxy-β-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamate
Pentyl 1-(5-deoxy-β-D-ribofuranosyl)-5-fluoro-1,2-dihydro-2-oxo-4-pyrimidinecarbamic acid
pentyl N-[1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-methyloxolan-2-yl]-5-fluoro-2-oxopyrimidin-4-yl]carbamate
R340
R-340
RG-340
Ro 09-1978
Ro 09-1978/000
Ro-09-1978
Ro-09-1978/000
S1156_Selleck
UNII-6804DJ8Z9U
Xabine
Xeloda
Xeloda (TN)
Xeloda, Captabin, Capecitabine
ZINC03806413
|
|
| 43 |
|
Gemcitabine |
Approved |
Phase 3,Phase 2,Phase 1,Not Applicable |
|
95058-81-4 |
60750
|
|
Synonyms:
103882-84-4
122111-03-9
2',2'-DFDC
2',2'-DiF-dC
2',2'-difluoro-2'-Deoxycytidine
2',2'-Difluoro-2'-deoxycytidine
2',2'-Difluorodeoxycytidine
2'-Deoxy-.beta.-D-2',2'-difluorocytidine
2'-Deoxy-2',2'-difluorocytidine
2'-Deoxy-2',2''-difluorocytidine-5'-O-monophosphate
2'-Deoxy-2'-difluorocytidine
4-amino-1-((2R,4R,5R)-3,3-difluoro-4-hydroxy-5-(hydroxymethyl)-tetrahydrofuran-2-yl)pyrimidin-2(1H)-one
4-amino-1-((2R,4R,5R)-3,3-difluoro-4-Hydroxy-5-(hydroxymethyl)-tetrahydrofuran-2-yl)pyrimidin-2(1H)-one
4-amino-1-((2R,4R,5R)-3,3-Difluoro-4-hydroxy-5-(hydroxymethyl)-tetrahydrofuran-2-yl)pyrimidin-2(1H)-one
4-Amino-1-[(2R,4R,5R)-3,3-difluoro-4-hydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidin-2-one
4-Amino-1-[3,3-difluoro-4-hydroxy-5-(hydroxymethyl) tetrahydrofuran-2-yl]-1H-pyrimidin-2-one
95058-81-4
AB1004842
AC1L1TUQ
C07650
CCRIS 8984
CHEBI:175901
CHEMBL888
CID60750
Cytidine, 2'-deoxy-2',2'-difluoro-2'-Deoxy-.beta.-D-2',2'-difluorocytidine
D02368
DB00441
DDFC
DFdC
DFDC
DFdCyd
Folfugem
Gamcitabine
Gemcel
Gemcin
Gemcitabin
|
Gemcitabina
Gemcitabina [INN-Spanish]
gemcitabine
Gemcitabine
Gemcitabine (USAN/INN)
Gemcitabine HCl
Gemcitabine hydrochloride
Gemcitabine stereoisomer
Gemcitabine, (alpha-D-threo-pentofuranosyl)-isomer
Gemcitabine, (beta-D-threo-pentafuranosyl)-isomer
Gemcitabine, (D-threo-pentafuranosyl)-isomer
Gemcitabinum
Gemcitabinum [INN-Latin]
GemLip
Gemtro
Gemzar
Gemzar (hydrochloride)
GEO
HMS2089P10
HSDB 7567
Inno-D07001
LS-59139
LY 188011
LY188011
LY-188011
NCGC00168784-01
NChemBio.2007.10-comp25
nchembio.573-comp7
nchembio.90-comp2
NSC 613327
NSC613327
TL8005979
UNII-B76N6SBZ8R
Zefei
ZINC18279854
|
|
| 44 |
|
Trioxsalen |
Approved |
Phase 2, Phase 3,Phase 3,Not Applicable |
|
3902-71-4 |
5585
|
|
Synonyms:
2',4,8-Trimethylpsoralen
2,5,9-Trimethyl-7H-furo(3,2-g)benzopyran-7-one
4,5',8-Trimethylpsoralen
4,8,5'-Trimethylpsoralen
6-Hydroxy-b,2,7-trimethyl-5-benzofuranacrylate, delta-lactone
6-Hydroxy-b,2,7-trimethyl-5-benzofuranacrylate, δ-lactone
6-Hydroxy-b,2,7-trimethyl-5-benzofuranacrylic acid, delta-lactone
6-Hydroxy-b,2,7-trimethyl-5-benzofuranacrylic acid, δ-lactone
6-Hydroxy-beta,2,7-trimethyl-5-benzofuranacrylate, delta-lactone
6-Hydroxy-beta,2,7-trimethyl-5-benzofuranacrylic acid, delta-lactone
6-Hydroxy-β,2,7-trimethyl-5-benzofuranacrylate, δ-lactone
6-Hydroxy-β,2,7-trimethyl-5-benzofuranacrylic acid, δ-lactone
|
ICN brand OF trioxsalen
trimethylpsoralen
Trimethylpsoralen
Trioxisaleno
Trioxisalenum
Trioxsalen
trioxysalen
Trioxysalen
Trioxysalene
Trioxysalenum
trisoralen
Trisoralen
|
|
| 45 |
|
Fluorouracil |
Approved |
Phase 2, Phase 3,Phase 3,Phase 1,Not Applicable |
|
51-21-8 |
3385
|
|
Synonyms:
1004-03-1
1-fluoro-1h-pyrimidine-2,4-dione
1upf
2,4-Dihydroxy-5-fluoropyrimidine
2,4-Dioxo-5-fluoropryimidine
2,4-Dioxo-5-fluoropyrimidine
47576_FLUKA
4921-97-5
5 Fluorouracil
5 Fluorouracil biosyn
5 FU lederle
5 FU Lederle
5 FU medac
5 HU hexal
5 HU Hexal
51-21-8
5-Faracil
5-Fluor-2,4(1H,3H)-pyrimidindion
5-Fluor-2,4(1H,3H)-pyrimidindion [Czech]
5-Fluor-2,4-dihydroxypyrimidin
5-Fluor-2,4-dihydroxypyrimidin [Czech]
5-Fluor-2,4-pyrimidindiol
5-Fluor-2,4-pyrimidindiol [Czech]
5-Fluoracil
5-Fluoracil [German]
5-Fluoracyl
5-fluoro uracil
5-fluoro-1H-pyrimidine-2,4-dione
5-Fluoro-2,4(1H,3H)-pyrimidinedione
5-Fluoro-2,4-pyrimidinedione
5-Fluoropyrimidin-2,4-diol
5-fluoropyrimidine-2,4(1H,3H)-dione
5-Fluoropyrimidine-2,4-dione
5-fluorouracil
5-Fluorouracil
5-Fluorouracil-biosyn
5-Fluoruracil
5-Fluoruracil [German]
5-Fluracil
5-Ftouracyl
5FU
5-FU
5-FU (TN)
5-FU lederle
5-FU Lederle
5-FU medac
5-HU hexal
5-HU Hexal
79108-01-3
AC-11201
AC1L1FTE
AC1Q4N2X
AccuSite
Actino-Hermal
Adrucil
Adrucil (TN)
AI3-25297
AKOS000119162
AKOS003237897
Allergan brand OF fluorouracil
Allergan Brand of Fluorouracil
Arumel
BB_NC-0576
biosyn Brand of Fluorouracil
Biosyn brand OF fluorouracil
BSPBio_002048
C07649
C4H3FN2O2
Carac
Carac (TN)
Carzonal
CCRIS 2582
CHEBI:46345
CHEMBL185
CID3385
Cinco FU
CPD000038082
CPD0-1327
CSP Brand of Fluorouracil
CSP Brand OF fluorouracil
Cytosafe
D005472
D00584
Dakota brand OF fluorouracil
Dakota Brand of Fluorouracil
Dakota, fluorouracile
Dakota, Fluorouracile
DB00544
Dermatech brand OF fluorouracil
Dermatech Brand of Fluorouracil
Dermik brand OF fluorouracil
Dermik Brand of Fluorouracil
DivK1c_000054
Effluderm
Effluderm (free base)
Efudex
Efudix
Efurix
EINECS 200-085-6
EU-0100536
F 6627
F0151
F6627_SIGMA
F8423_SIGMA
Ferrer brand OF fluorouracil
Ferrer Brand of Fluorouracil
Fiverocil
Fluoro Uracil
fluoro Uracile icn
Fluoro Uracile ICN
Fluoroblastin
Fluoroplex
Fluoroplex (TN)
fluorouracil
Fluorouracil
Fluorouracil (JP15/USP/INN)
Fluorouracil [USAN:INN:BAN:JAN]
Fluorouracil gry
Fluorouracil GRY
Fluorouracil mononitrate
Fluorouracil Mononitrate
Fluorouracil monopotassium salt
Fluorouracil Monopotassium Salt
Fluorouracil monosodium salt
Fluorouracil Monosodium Salt
Fluorouracil potassium salt
Fluorouracil Potassium Salt
Fluorouracil teva brand
Fluorouracil Teva Brand
Fluorouracile
Fluoro-uracile
Fluorouracile [DCIT]
|
Fluorouracile dakota
Fluorouracile Dakota
fluoro-Uracile icn
Fluoro-Uracile ICN
Fluorouracil-gry
Fluorouracil-GRY
Fluorouracilo
Fluoro-uracilo
Fluorouracilo [INN-Spanish]
fluorouracilo Ferrer far
Fluorouracilo Ferrer Far
Fluorouracilum
Fluorouracilum [INN-Latin]
Fluoruracil
Fluouracil
Flurablastin
Fluracedyl
Fluracil
Fluracilum
Fluri
Fluril
Fluro Uracil
Fluroblastin
Flurodex
Flurouracil
Flurox
FT-0082524
Ftoruracil
FU
Gry brand OF fluorouracil
Gry Brand of Fluorouracil
haemato Brand OF fluorouracil
Haemato Brand of Fluorouracil
haemato Fu
Haemato fu
haemato-Fu
Haemato-fu
Hexal brand OF fluorouracil
Hexal Brand of Fluorouracil
HMS1920O18
HMS2090I04
HMS2091F19
HMS500C16
HSDB 3228
I07-0022
ICN brand OF fluorouracil
ICN Brand of Fluorouracil
IDI1_000054
IN1335
inhibits thymilidate synthetase
KBio1_000054
KBio2_001321
KBio2_003889
KBio2_006457
KBio3_001268
KBioGR_001253
KBioSS_001321
Kecimeton
Lopac0_000536
Lopac-F-6627
LS-153
medac Brand of Fluorouracil
Medac brand OF fluorouracil
MLS000069498
MLS002415705
MolPort-000-156-102
MolPort-003-990-447
MolPort-004-758-143
MolPort-004-758-144
MolPort-005-861-486
NCGC00015442-01
NCGC00015442-03
NCGC00015442-10
NCGC00091349-01
NCGC00091349-02
NCGC00091349-03
NCGC00091349-04
NCGC00091349-05
NCGC00091349-07
NCGC00091349-08
nchembio.90-comp3
nchembio809-comp6
NCI60_001652
Neocorp brand OF fluorouracil
Neocorp Brand of Fluorouracil
Neofluor
NINDS_000054
NSC 19893
NSC19893
NSC-19893
Onkofluor
Onkoworks brand OF fluorouracil
Onkoworks Brand of Fluorouracil
Pharmachemie brand OF fluorouracil monosodium salt
Phthoruracil
Phtoruracil
Queroplex
Ribofluor
ribosepharm Brand of Fluorouracil
Ribosepharm brand OF fluorouracil
Riemser brand OF fluorouracil
Riemser Brand of Fluorouracil
Ro 2-9757
Ro-2-9757
Roche brand OF fluorouracil
Roche Brand of Fluorouracil
S1209_Selleck
SAM002264615
SMR000038082
SPBio_000291
Spectrum_000841
SPECTRUM1500305
Spectrum2_000076
Spectrum3_000434
Spectrum4_000557
Spectrum5_000718
STK297802
T5233394
tetratogen
Teva brand OF fluorouracil
Teva Brand of Fluorouracil
Timazin
TL8006093
U 8953
U-8953
Ulup
UNII-U3P01618RT
UPCMLD-DP130
UPCMLD-DP130:001
URF
WLN: T6MVMVJ EF
ZINC00897110
|
|
| 46 |
|
Levoleucovorin |
Approved, Investigational |
Phase 2, Phase 3,Phase 3,Phase 1 |
|
68538-85-2 |
|
|
Synonyms:
(6S)-5-Formyl-5,6,7,8-tetrahydrofolic acid
(6S)-5-formyltetrahydrofolic acid
(6S)-Folinic acid
(6S)-Leucovorin
(S)-Leucovorin
|
Citrovorum factor
Levofolene
Levofolinic acid
L-Folinic acid
N-[4-({[(6S)-2-amino-5-formyl-4-oxo-1,4,5,6,7,8-hexahydropteridin-6-yl]methyl}amino)benzoyl]-L-glutamic acid
|
|
| 47 |
|
leucovorin |
Approved |
Phase 2, Phase 3,Phase 3,Phase 1 |
|
58-05-9 |
6006
143
|
|
Synonyms:
(5-formyl-5,6,7,8-tetrahydropteroyl)glutamate
(6R,S)-5-Formyltetrahydrofolate
10-Formyl-7,8-dihydrofolate
10-Formyl-7,8-dihydrofolic acid
5 Formyltetrahydrofolate
5 Formyltetrahydropteroylglutamate
5-Formyl-5,6,7,8-tetrahydrofolate
5-Formyl-5,6,7,8-tetrahydrofolic acid
5-Formyl-5,6,7,8-tetrahydropteroyl-L-glutamic acid
5-Formyltetrahydrofolate
5-formyltetrahydrofolic acid
5-Formyltetrahydrofolic acid
5-Formyltetrahydropteroylglutamate
5-Formyltetrahydropteroylglutamic acid
Acid, folinic
Acide folinique
Calcium citrovorum factor
Calcium folinate
Calcium leucovorin
Citrovorum factor
Factor, citrovorum
folinate
Folinate
Folinate, calcium
Folinic acid
Folinic acid calcium salt
Folinic acid calcium salt USP27
Folinic acid SF
Folinic acid-SF
L(-)-5-Formyl-5,6,7,8-tetrahydrofolate
|
L(-)-5-Formyl-5,6,7,8-tetrahydrofolic acid
Leucal
Leucovorin
Leucovorin calcium
Leucovorin folinic acid
Leucovorin, (D)-isomer
Leucovorin, (DL)-isomer
Leucovorin, (R)-isomer
Leucovorin, calcium
Leucovorin, calcium (1:1) salt
Leucovorin, calcium (1:1) salt, (DL)-isomer
Leucovorin, calcium (1:1) salt, pentahydrate
Leucovorin, monosodium salt
Leucovorinum
Leukovorin
Leukovorum
Levoleucovorin
L-leucovorin
L-Leucovorin
L-N-[P-[[(2-amino-5-Formyl-5,6,7,8-tetrahydro-4-hydroxy-6-pteridinyl)methyl]amino]benzoyl]-glutamic acid
Monosodium salt leucovorin
N(5)-Formyltetrahydrofolate
N-(5-formyl-5,6,7,8-tetrahydropteroyl)-L-glutamic acid
N5-Formyl-5,6,7,8-tetrahydrofolate
N5-Formyl-5,6,7,8-tetrahydrofolic acid
N5-Formyltetrahydrofolate
N5-Formyltetrahydrofolic acid
Rescuvolin
Welcovorin
Wellcovorin
|
|
| 48 |
|
Cisplatin |
Approved |
Phase 3,Phase 2,Phase 1,Not Applicable |
|
15663-27-1 |
2767
441203
84093
|
|
Synonyms:
(SP-4-1)-diamminedichloridoplatinum
(SP-4-1)-diamminedichloroplatinum
(SP-4-2)-diamminedichloridoplatinum
(SP-4-2)-diamminedichloroplatinum
Abiplatin
Biocisplatinum
Briplatin
CACP
Carboquone
CDDP
CHEBI:35852
CID441203
Cis Pt II
cis-[PtCl2(NH3)2]
cis-DDP
Cis-DDP
Cis-Diaminedichloroplatinum
cis-diamminedichloridoplatinum(II)
cis-Diamminedichloroplatinum
Cis-Diamminedichloroplatinum
cis-diamminedichloroplatinum(II)
cis-Dichlorodiammineplatinum(II)
Cismaplat
Cisplatine
cisplatino
Cisplatino
Cisplatinum
Cisplatyl
Citoplationo
CPD0-1392
CPDC
|
CPDD
DB00515
DDP
DDPT
Diamminedichloroplatinum
EU-0100918
Lederplatin
nchembio773-comp1
Neoplatin
Peyrone's chloride
Peyrone's salt
Plastin
Platamine
Platiblastin
Platidiam
Platinex
Platinol
Platinol-AQ
Platinoxan
Platinum Ammine Chloride
Platinum Ammonium Chloride
Platinum Diamine Dichloride
Randa
trans-DDP
Trans-DDP
Trans-Diaminedichloroplatinum
trans-diamminedichloridoplatinum(II)
Trans-Diamminedichloroplatinum
Trans-Dichlorodiammine Platinum
Trans-Platinumdiammine Dichloride
|
|
| 49 |
|
Ursodeoxycholic acid |
Approved, Investigational |
Phase 2, Phase 3 |
|
128-13-2 |
31401
|
|
Synonyms:
(3a,5b,7b)-3,7-Dihydroxycholan-24-Oate
(3a,5b,7b)-3,7-Dihydroxy-cholan-24-Oate
(3a,5b,7b)-3,7-Dihydroxycholan-24-Oic acid
(3a,5b,7b)-3,7-Dihydroxy-cholan-24-Oic acid
(3alpha,5beta,7beta)-3,7-Dihydroxycholan-24-Oate
(3alpha,5beta,7beta)-3,7-dihydroxycholan-24-oic acid
(3alpha,5beta,7beta)-3,7-Dihydroxycholan-24-Oic acid
(3alpha,5beta,7beta,8xi)-3,7-dihydroxycholan-24-oic acid
(3α,5β,7β)-3,7-dihydroxycholan-24-Oate
(3α,5β,7β)-3,7-dihydroxycholan-24-oic acid
(3α,5β,7β)-3,7-dihydroxycholan-24-Oic acid
(4R)-4-[(3R,5S,7S,8R,9S,10S,13R,14S,17R)-3,7-dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoic acid
128-13-2
17-beta-(1-Methyl-3-carboxypropyl)etiocholane-3-alpha,7-beta-diol
3 alpha,7 beta Dihydroxy 5 beta cholan 24 Oic acid
3 alpha,7 beta-Dihydroxy-5 beta-cholan-24-oic Acid
3 alpha,7 beta-Dihydroxy-5 beta-cholan-24-Oic acid
3,7-Dihydroxycholan-24-oic acid
3,7-Dihydroxycholan-24-Oic acid
3a,7b-Dihydroxy-5b-cholan-24-Oate
3a,7b-Dihydroxy-5b-cholan-24-Oic acid
3alpha,7beta-Dihydroxy-5beta-cholan-24-Oate
3alpha,7beta-Dihydroxy-5beta-cholan-24-oic acid
3alpha,7beta-Dihydroxy-5beta-cholan-24-Oic acid
3alpha,7beta-Dihydroxy-5beta-cholanic acid
3-alpha,7-beta-Dihydroxy-5-beta-cholanoic acid
3-alpha,7-beta-Dihydroxycholanic acid
3-alpha,7-beta-Dioxycholanic acid
3α,7β-dihydroxy-5β-cholan-24-Oate
3α,7β-dihydroxy-5β-cholan-24-Oic acid
4-10-00-01604 (Beilstein Handbook Reference)
50809-41-1
5beta-Cholan-24-oic acid-3alpha,7beta-diol
5beta-Cholanic Acid-3alpha,7beta-diol
7beta-Hydroxylithocholic acid
7-beta-Hydroxylithocholic acid
80225-86-1
AB00513977
AC-18919
AC1L1LJH
AC-2081
Acid, deoxyursocholic
Acid, ursacholic
Acid, ursodeoxycholic
Acide ursodesoxycholique
Acide ursodesoxycholique [INN-French]
Acido ursodeossicolico
Acido ursodeossicolico [Italian]
Acido ursodeoxicolico
Acido ursodeoxicolico [INN-Spanish]
Acidum ursodeoxycholicum
Acidum ursodeoxycholicum [INN-Latin]
Actigall
Actigall (TN)
Antigall
Antigen brand OF ursodeoxycholic acid
Arsacol
Aventis brand OF ursodeoxycholic acid
Axcan brand OF ursodeoxycholic acid
BB_NC-2372
BPBio1_001052
BRN 3219888
BSPBio_000956
C07880
C24H40O4
CCRIS 5502
CHEBI:9907
CHEMBL1551
CHEMBL73390
chenodeoxycholic acid
Cholan-24-oic acid, 3,7-dihydroxy-, (3-alpha,5-beta,7-beta)- (9CI)
Cholit-ursan
Cholofalk
CID11516715
CID31401
CP Brand OF ursodeoxycholic acid
CPD000058403
CPD-10534
D00734
DB01586
Delursan
Deoxyursocholic acid
Deoxyursocholic Acid
Destolit
Deursil
Dom-ursodiol c
EINECS 204-879-3
Estedi brand OF ursodeoxycholic acid
|
Falk brand OF ursodeoxycholic acid
Farmasa brand OF ursodeoxycholic acid
Galen brand OF ursodeoxycholic acid
Heumann brand OF ursodeoxycholic acid
HMS1570P18
ISO-URSODEOXYCHOLIC ACID
IU5
Litursol
LMST04010033
LS-53033
Lyeton
MLS000028461
MLS001066373
MolPort-001-794-630
MolPort-005-932-884
NCGC00179363-01
NCI60_028904
Niddapharm brand OF ursodeoxycholic acid
Norgine brand OF ursodeoxycholic acid
NSC 657950
NSC 683769
Orphan brand OF ursodeoxycholic acid
Peptarom
PHL-ursodiol c
PMS-ursodiol c
Prestwick0_000958
Prestwick1_000958
Prestwick2_000958
Prestwick3_000958
Provalis brand OF ursodeoxycholic acid
S1643_Selleck
SAM002264653
Sanofi synthelabo brand OF ursodeoxycholic acid
SMP2_000012
SMR000058403
Sodium ursodeoxycholate
Sodium Ursodeoxycholate
Solutrat
SPBio_003105
tramedico Brand OF ursodeoxycholic acid
U0030
U5127_SIGMA
U-9000
UDCA
UDCS
UNII-724L30Y2QR
Urdox
Urosdesoxycholate
Urosdesoxycholic acid
Urosiol
Ursacholic acid
Ursacholic Acid
Ursacol
Urso
UrSO
Urso (TN)
Urso 250
Urso DS
Urso Forte
urso Heumann
Ursobilane
Ursobilin
Ursochol
Ursodamor
Ursodeoxy cholic acid
ursodeoxycholate
Ursodeoxycholate
Ursodeoxycholate, sodium
Ursodeoxycholic acid
URSODEOXYCHOLIC ACID
Ursodeoxycholic acid (JP15/INN)
Ursodeoxycholic acid, UDCA, Ursosan, Ursofalk, Urso Forte, Udiliv, Ursodiol
Ursodeoxycholicacid
Ursodesoxycholic acid
Ursodexycholate
Ursodexycholic acid
Ursodexycholic Acid
ursodiol
Ursodiol
Ursodiol (USP)
Ursodiol [USAN]
Ursofalk
Ursogal
Ursolite
Ursolvan
Ursosan
Vita brand OF ursodeoxycholic acid
Zambon brand OF ursodeoxycholic acid
|
|
| 50 |
|
Fentanyl |
Approved, Illicit, Investigational, Vet_approved |
Phase 3 |
|
437-38-7 |
3345
|
|
Synonyms:
1-Phenethyl-4-(N-phenylpropionamido)piperidine
1-phenethyl-4-N-propionylanilinopiperidine
1-Phenethyl-4-N-propionylanilinopiperidine
437-38-7
5-22-08-00049 (Beilstein Handbook Reference)
80832-90-2
990-73-8 (citrate)
AC1L1FQ2
Actiq
BIDD:GT0555
BRN 0494484
Cephalon brand OF fentanyl buccal oravescent
CHEBI:119915
CHEMBL596
CID3345
D00320
DB00813
Duragesic
Duragesic (TN)
Duragesic-100
Duragesic-12
Duragesic-25
Duragesic-50
Duragesic-75
Durogesic
EINECS 207-113-6
Fentanest
Fentanil
Fentanil [DCIT]
Fentanila
Fentanila [INN-Spanish]
Fentanilo
fentanyl
Fentanyl
Fentanyl (JAN/USAN/INN)
Fentanyl [INN:BAN]
Fentanyl CII
Fentanyl citrate
Fentanyl-100
Fentanyl-12
Fentanyl-25
Fentanyl-50
|
Fentanyl-75
Fentanylum
Fentanylum [INN-Latin]
Fentora
HSDB 3329
IONSYS
Janssen pharmaceutica brand OF fentanyl
JNS020QD
L001275
LS-124439
Matrifen
MolPort-003-847-369
N-(1-phenethyl-4-piperidinyl)-N-phenylpropionamide
N-(1-Phenethyl-4-piperidinyl)-N-phenylpropionamide
N-(1-phenethyl-4-piperidyl)propionanilide
N-(1-Phenethyl-4-piperidyl)propionanilide
N-(1-phenethylpiperidin-4-yl)-N-phenylpropanamide
N-(1-phenethylpiperidin-4-yl)-N-phenylpropionamide
N-(1-Phenethylpiperidin-4-yl)-N-phenylpropionamide
N-(1-Phenethyl-piperidin-4-yl)-N-phenyl-propionamide
Nasalfent
NCGC00168252-01
N-phenethyl-4-(N-propionylanilino)piperidine
N-Phenethyl-4-(N-propionylanilino)piperidine
N-phenyl-N-(1-(2-phenylethyl)-4-piperidinyl)propanamide
N-Phenyl-N-(1-(2-phenylethyl)-4-piperidinyl)propanamide
N-phenyl-N-[1-(2-phenylethyl)piperidin-4-yl]propanamide
Oprea1_152073
Oprea1_207148
PDSP1_000860
PDSP2_000846
Pentanyl
Phentanyl
Propanamide, N-phenyl-N-(1-(2-phenylethyl)-4-piperidinyl)- (9CI)
R 4263
Rapinyl
Sentonil
Sublimase
Sublimaze
Transmucosal oral fentanyl citrate
UNII-UF599785JZ
|
|
Interventional clinical trials:
(show top 50)
(show all 493)
| # |
Name |
Status |
NCT ID |
Phase |
Drugs |
| 1 |
Quality of Life in Patients With Unresectable Hilar Cholangiocarcinoma on Palliative Metallic Stent Versus Plastic Stent |
Unknown status |
NCT00746538
|
Phase 4 |
|
| 2 |
Preoperative Biliary Drainage for Resectable Hilar Cholangiocarcinoma |
Unknown status |
NCT00797121
|
Phase 4 |
|
| 3 |
Cyclooxygenase-2 Inhibitor for Adjuvant Anticancer Effect in Patients With Biliary-pancreas Cancer |
Unknown status |
NCT01111591
|
Phase 4 |
Cox2 inhibitor (Celecoxib) |
| 4 |
Effects of Preoperative Immunonutrition in Patients Undergoing Hepatectomy |
Unknown status |
NCT01256047
|
Phase 4 |
|
| 5 |
Anesthetic Agents and Acute Kidney Injury After Liver Resection Surgery |
Unknown status |
NCT02174575
|
Phase 4 |
Sevoflurane;Desflurane |
| 6 |
Relationship Between Platinum Levels in the Blood and Neurotoxicity in Patients Who Are Receiving Oxaliplatin for Gastrointestinal Cancer |
Unknown status |
NCT00274885
|
Phase 4 |
oxaliplatin |
| 7 |
Uncovered Self-expandable Metal Stent Versus Double Layer Plastic Stent for Malignant Hilar Stricture |
Unknown status |
NCT01125865
|
Phase 4 |
|
| 8 |
Efficacy and Cost Analysis of Plastic Stent Compare to Metallic Stent in Hilar Cholangiocarcinoma |
Completed |
NCT00721175
|
Phase 4 |
|
| 9 |
Effects of Preoperative Immunonutrition in Patients Undergoing Pancreaticoduodenectomy |
Completed |
NCT01256034
|
Phase 4 |
|
| 10 |
Influence of an Oral Nutritional Supplement Rich in Omega-3 Fatty Acids on Functional State and Quality of Life in Malnourished Patients With Gastroenterological Tumors |
Completed |
NCT00168987
|
Phase 4 |
oral nutritional supplement rich in eicosapentanoic acid |
| 11 |
Etomidate vs. Midazolam for Sedation During ERCP |
Completed |
NCT02027311
|
Phase 4 |
Etomidate;Midazolam;Meperidine |
| 12 |
Biliary Metal Stent Study: Metal Stents for Management of Distal Malignant Biliary Obstruction |
Completed |
NCT00280709
|
Phase 4 |
|
| 13 |
Early Oral Versus Enteral Nutrition After Pancreatoduodenectomy |
Recruiting |
NCT01642875
|
Phase 4 |
|
| 14 |
Percutaneous Bilateral Versus Unilateral Metal Stent for Hilar Cholangiocarcinoma |
Unknown status |
NCT02108145
|
Phase 2, Phase 3 |
|
| 15 |
Oxaliplatin+Gemcitabine vs Capecitabine as Adjuvant Therapy for Intrahepatic Cholangiocarcinoma |
Unknown status |
NCT02548195
|
Phase 3 |
oxaliplatin and gemcitabine;capecitabine |
| 16 |
Comparison of Endoscopic Radiofrequency Ablation Versus Photodynamic Therapy for Inoperable Cholangiocarcinoma |
Unknown status |
NCT01739465
|
Phase 2, Phase 3 |
|
| 17 |
Unilateral Versus Bilateral Stents for Bismuth Type II and III Malignant Hilar Strictures |
Unknown status |
NCT00653978
|
Phase 3 |
|
| 18 |
Early Enteral Feeding After Pylorus Preserving Pancreatoduodenectomy |
Unknown status |
NCT00809081
|
Phase 3 |
|
| 19 |
S-1 and Photodynamic Therapy in Cholangiocarcinoma |
Completed |
NCT00869635
|
Phase 3 |
S-1 Chemotherapy |
| 20 |
Gemcitabine With or Without Cisplatin in Treating Patients With Unresectable Locally Advanced or Metastatic Cholangiocarcinoma or Other Biliary Tract Tumors |
Completed |
NCT00262769
|
Phase 3 |
cisplatin;gemcitabine hydrochloride |
| 21 |
Biliary Stenting With or Without Photodynamic Therapy in Treating Patients With Locally Advanced, Recurrent, or Metastatic Cholangiocarcinoma or Other Biliary Tract Tumors That Cannot Be Removed by Surgery |
Completed |
NCT00513539
|
Phase 3 |
porfimer sodium |
| 22 |
Fluorouracil, Cisplatin, and Radiation Therapy or Gemcitabine and Oxaliplatin in Treating Patients With Nonmetastatic Biliary Tract Cancer That Cannot Be Removed By Surgery |
Completed |
NCT00304135
|
Phase 2, Phase 3 |
cisplatin;gemcitabine hydrochloride;oxaliplatin |
| 23 |
Gemcitabine Hydrochloride and Oxaliplatin or Observation in Treating Patients With Biliary Tract Cancer That Has Been Removed by Surgery |
Completed |
NCT01313377
|
Phase 3 |
gemcitabine hydrochloride;oxaliplatin |
| 24 |
Capecitabine or Observation After Surgery in Treating Patients With Biliary Tract Cancer |
Completed |
NCT00363584
|
Phase 3 |
capecitabine |
| 25 |
Trial of High-dose Urso in Primary Sclerosing Cholangitis |
Completed |
NCT00059202
|
Phase 2, Phase 3 |
Ursodeoxycholic Acid |
| 26 |
Comprehensive Electronic Cancer Support System for the Treatment of Cancer Related Symptoms |
Completed |
NCT01640522
|
Phase 3 |
|
| 27 |
Fentanyl Sublingual Spray in Treating Patients With Breakthrough Cancer Pain |
Completed |
NCT00538850
|
Phase 3 |
Fentanyl sublingual spray;Placebo |
| 28 |
Ondansetron With or Without Dexamethasone to Prevent Vomiting in Patients Receiving Radiation Therapy to the Upper Abdomen |
Completed |
NCT00016380
|
Phase 3 |
dexamethasone;ondansetron |
| 29 |
A Study to Evaluate the Efficacy and Safety of Pemigatinib Versus Chemotherapy in Unresectable or Metastatic Cholangiocarcinoma - (FIGHT-302) |
Recruiting |
NCT03656536
|
Phase 3 |
Pemigatinib;Gemcitabine;Cisplatin |
| 30 |
Chemo Alone or in Combination With Radiation in Unresectable Cholangiocarcinoma |
Recruiting |
NCT02773485
|
Phase 3 |
Systemic chemotherapy |
| 31 |
SIRT Followed by CIS-GEM Chemotherapy Versus CIS-GEM Chemotherapy Alone as 1st Line Treatment of Patients With Unresectable Intrahepatic Cholangiocarcinoma |
Recruiting |
NCT02807181
|
Phase 2, Phase 3 |
Cisplatin-gemcitabine |
| 32 |
Study of AG-120 in Previously Treated Advanced Cholangiocarcinoma With IDH1 Mutations (ClarIDHy) |
Recruiting |
NCT02989857
|
Phase 3 |
AG-120;AG-120 matched placebo |
| 33 |
Percutaneous Hepatic Perfusion vs. Cisplatin/Gemcitabine in Patients With Intrahepatic Cholangiocarcinoma |
Recruiting |
NCT03086993
|
Phase 2, Phase 3 |
Cisplatin and Gemcitabine |
| 34 |
A Study of Second-line Treatment With Apatinib in Patients With Advanced Intrahepatic Cholangiocarcinoma |
Recruiting |
NCT03251443
|
Phase 3 |
Apatinib |
| 35 |
Photodynamic Therapy (PDT) for Palliation of Cholangiocarcinoma |
Recruiting |
NCT01755013
|
Phase 2, Phase 3 |
|
| 36 |
Bortezomib in Intrahepatic Cholangiocellular Carcinoma |
Recruiting |
NCT03345303
|
Phase 3 |
Bortezomib |
| 37 |
HAIC Versus Systemic Chemotherapy for Unresectable ICC |
Recruiting |
NCT03771846
|
Phase 3 |
gemcitabine, oxaliplatin , fluorouracil, and leucovorin;gemcitabine and oxaliplatin |
| 38 |
Adjuvant Chemotherapy With Gemcitabine and Cisplatin Compared to Standard of Care After Curative Intent Resection of Biliary Tract Cancer |
Recruiting |
NCT02170090
|
Phase 3 |
Gemcitabine;Cisplatin;Capecitabine |
| 39 |
Clinical Trial of Adjuvant Chemotherapy Followed by Concurrent Chemoradiotherapy Compared With Adjuvant Chemotherapy Alone in Patients With Gallbladder Carcinoma and Extrahepatic Cholangiocarcinoma |
Recruiting |
NCT02798510
|
Phase 3 |
capecitabine;gemcitabine |
| 40 |
Safety and Efficacy of Modified Folfirinox Versus Gemcis in Bile Duct Tumours |
Recruiting |
NCT02591030
|
Phase 2, Phase 3 |
GEMCIS;mFolfirinox |
| 41 |
Study of GEMOX(Gemcitabine/Oxaliplatin) Versus XELOX(Xeloda/Oxaliplatin) in Advanced Biliary Tract Carcinoma |
Recruiting |
NCT01470443
|
Phase 3 |
Oxaliplatin;Oxaliplatin |
| 42 |
Adjuvant Chemotherapy for Biliary Tract Cancer After Curative Resection |
Recruiting |
NCT03779035
|
Phase 3 |
Gemcitabine;Capecitabine |
| 43 |
Gemcitabine Hydrochloride and Cisplatin With or Without Nab-Paclitaxel in Treating Patients With Newly Diagnosed Advanced Biliary Tract Cancers |
Recruiting |
NCT03768414
|
Phase 3 |
Cisplatin;Gemcitabine Hydrochloride;Nab-paclitaxel |
| 44 |
Early Palliative Care in Patients With Metastatic Upper Gastrointestinal Cancers Treated With First-line Chemotherapy |
Recruiting |
NCT02853474
|
Phase 3 |
|
| 45 |
Liver Cancer Immunotherapy: Placebo-controlled Clinical Trial of Hepcortespenlisimut-L |
Recruiting |
NCT02232490
|
Phase 3 |
|
| 46 |
Radiofrquency Ablation Combined With Cytokine-induced Killer Cells for the Patients With Cholangiocarcinoma |
Active, not recruiting |
NCT02482454
|
Phase 2, Phase 3 |
|
| 47 |
Active Symptom Control Alone or With mFOLFOX Chemotherapy for Locally Advanced/ Metastatic Biliary Tract Cancers |
Active, not recruiting |
NCT01926236
|
Phase 3 |
L-folinic acid;5 FU;Oxaliplatin |
| 48 |
Early Palliative Care With Standard Care or Standard Care Alone in Improving Quality of Life of Patients With Incurable Lung or Non-colorectal Gastrointestinal Cancer and Their Family Caregivers |
Active, not recruiting |
NCT02349412
|
Phase 3 |
|
| 49 |
Study of Oral Infigratinib in First Line Cholangiocarcinoma With FGFR2 Gene Fusions/Translocations |
Not yet recruiting |
NCT03773302
|
Phase 3 |
BGJ398;Gemcitabine;Cisplatin |
| 50 |
Efficacy and Safety Study of PDT Using Photofrin in Unresectable Advanced Perihilar Cholangiocarcinoma (OPUS) |
Terminated |
NCT02082522
|
Phase 3 |
Photodynamic therapy-Photofrin;Chemotherapy regimen |
Cell-based therapeutics:
Data from LifeMap, the Embryonic Development and Stem Cells Database
Stem-cell-based therapeutic approaches for Cholangiocarcinoma:
Embryonic/Adult Cultured Cells Related to Cholangiocarcinoma:
|
