FDA approved drugs:
(show top 50)
(show all 250)
| # |
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Drug Name |
Active Ingredient(s) 18
|
Company |
Approval Date |
| 1 |
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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.
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| 2 |
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Abstral
18
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FENTANYL (citrate) |
ProStrakan |
January 2011 |
Disease/s that Drug Treats:breakthrough cancer pain in opiod-tolerant patients
Indications and Usage:
18
ABSTRAL is an opioid agonist indicated for the management of breakthrough pain in cancer patients 18 years of age and older who are already receiving and who are tolerant to opioid therapy for their underlying persistent cancer pain. (1) Limitations of Use: ABSTRAL may be dispensed only to patients enrolled in the TIRF REMS Access program.
DrugBank Targets:
16
1. Mu-type opioid receptor ;2. Delta-type opioid receptor;3. Kappa-type opioid receptor
Mechanism of Action:
18
Target: µ-opioid receptor (possible mechanism of action)
Action: agonist
FDA: Fentanyl is a pure opioid agonist whose principal therapeutic action is analgesia. Other members of the classknown as opioid agonists include substances such as morphine, oxycodone, hydromorphone, codeine, andhydrocodone.
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| 3 |
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Actiq
18
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FENTANYL (citrate) |
Anesta Corporation |
November 1998 |
Disease/s that Drug Treats:cancer pain
Indications and Usage:
18
ACTIQ is an opioid agonist indicated for the management of breakthrough pain in cancer patients 16 years of age and older who are already receiving and who are tolerant to around-the-clock opioid therapy for their underlying persistent cancer pain. (1) Limitations of Use: ACTIQ may be dispensed only to patients enrolled in the TIRF REMS Access program. (1)
DrugBank Targets:
16
1. Mu-type opioid receptor ;2. Delta-type opioid receptor;3. Kappa-type opioid receptor
Mechanism of Action:
18
Target: -
Action: agonist
FDA: Fentanyl is a pure opioid agonist whose principal therapeutic action is analgesia. Other members of the class known as opioid agonists include substances such as morphine, oxycodone, hydromorphone, codeine, and hydrocodone.
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| 4 |
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Adcetris
18
49
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BRENTUXIMAB VEDOTIN |
Seattle Genetics |
August 2011 |
Disease/s that Drug Treats:Hodgkin lymphoma and anaplastic large cell lymphoma
Indications and Usage:
18
ADCETRIS is a CD30-directed antibody-drug conjugate indicated fortreatment of patients with: Hodgkin lymphoma after failure of autologous stem cell transplant(ASCT) or after failure of at least two prior multi-agent chemotherapyregimens in patients who are not ASCT candidates (1.1). Systemic anaplastic large cell lymphoma after failure of at least oneprior multi-agent chemotherapy regimen (1.2).Accelerated approval was granted for the above indications based onoverall response rate. An improvement in patient-reported outcomes orsurvival has not been established. Continued approval for these indicationsmay be contingent upon verification and description of clinical benefit inconfirmatory trials.
DrugBank Targets:
16
Tumor necrosis factor receptor superfamily member 8
Mechanism of Action:
18
Target: microtubule
Action: disruptor
FDA: Brentuximab vedotin is an ADC. The antibody is a chimeric IgG1 directed against CD30. Thesmall molecule, MMAE, is a microtubule disrupting agent. MMAE is covalently attached to theantibody via a linker. Nonclinical data suggest that the anticancer activity of ADCETRIS is dueto the binding of the ADC to CD30-expressing cells, followed by internalization of theADC-CD30 complex, and the release of MMAE via proteolytic cleavage. Binding of MMAE totubulin disrupts the microtubule network within the cell, subsequently inducing cell cycle arrestand apoptotic death of the cells.
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| 5 |
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Afinitor
18
49
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EVEROLIMUS |
Novartis |
March 2009 |
Disease/s that Drug Treats:renal cell carcinoma/ renal angiomyolipoma associated with tuberous sclerosis complex/ advanced pancreatic neuroendocrine tumors/ hormone receptor-positive, HER2-negative breast cancer
Indications and Usage:
18
AFINITOR is a kinase inhibitor indicated for the treatment of: postmenopausal women with advanced hormone receptor-positive, HER2- negative breast cancer (advanced HR+ BC) in combination with exemestane after failure of treatment with letrozole or anastrozole. (1.1) adults with progressive neuroendocrine tumors of pancreatic origin (PNET) that are unresectable, locally advanced or metastatic. AFINITOR is not indicated for the treatment of patients with functional carcinoid tumors. (1.2) adults with advanced renal cell carcinoma (RCC) after failure of treatment with sunitinib or sorafenib. (1.3) adults with renal angiomyolipoma and tuberous sclerosis complex (TSC), not requiring immediate surgery. The effectiveness of AFINITOR in the treatment of renal angiomyolipoma is based on an analysis of durable objective responses in patients treated for a median of 8.3 months. Further follow-up of patients is required to determine long-term outcomes. (1.4) AFINITOR and AFINITOR DISPERZ are kinase inhibitors indicated for the treatment of: pediatric and adult patients with tuberous sclerosis complex (TSC) who have subependymal giant cell astrocytoma (SEGA) that requires therapeutic intervention but cannot be curatively resected. The effectiveness is based on demonstration of durable objective response, as evidenced by reduction in SEGA tumor volume. Improvement in diseaserelated symptoms and overall survival in patients with SEGA and TSC has not been demonstrated. (1.5)
DrugBank Targets:
16
Serine/threonine-protein kinase mTOR
Mechanism of Action:
18
Target: mTOR
Action: inhibitor
FDA: Everolimus is an inhibitor of mammalian target of rapamycin (mTOR), a serine-threonine kinase, downstream of thePI3K/AKT pathway. The mTOR pathway is dysregulated in several human cancers. Everolimus binds to an intracellularprotein, FKBP-12, resulting in an inhibitory complex formation with mTOR complex 1 (mTORC1) and thus inhibition ofmTOR kinase activity. Everolimus reduced the activity of S6 ribosomal protein kinase (S6K1) and eukaryotic initiationfactor 4E-binding protein (4E-BP1), downstream effectors of mTOR, involved in protein synthesis. S6K1 is a substrate ofmTORC1 and phosphorylates the activation domain 1 of the estrogen receptor which results in ligand-independentactivation of the receptor. In addition, everolimus inhibited the expression of hypoxia-inducible factor (e.g., HIF-1) andreduced the expression of vascular endothelial growth factor (VEGF). Inhibition of mTOR by everolimus has been shownto reduce cell proliferation, angiogenesis, and glucose uptake in in vitro and/or in vivo studies.Constitutive activation of the PI3K/Akt/mTOR pathway can contribute to endocrine resistance in breast cancer. In vitrostudies show that estrogen-dependent and HER2+ breast cancer cells are sensitive to the inhibitory effects of everolimus,and that combination treatment with everolimus and Akt, HER2, or aromatase inhibitors enhances the anti-tumor activityof everolimus in a synergistic manner.Two regulators of mTORC1 signaling are the oncogene suppressors tuberin-sclerosis complexes 1 and 2 (TSC1, TSC2).Loss or inactivation of either TSC1 or TSC2 leads to activation of downstream signaling. In TSC, a genetic disorder,inactivating mutations in either the TSC1 or the TSC2 gene lead to hamartoma formation throughout the body.
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| 6 |
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Akynzeo
18
49
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NETUPITANT AND PALONOSETRON (hydrochloride) |
Helsinn |
October 2014 |
Disease/s that Drug Treats:chemotherapy-induced nausea and vomiting
Indications and Usage:
18
AKYNZEO is a fixed combination of netupitant, a substance P/neurokinin 1(NK1) receptor antagonist, and palonosetron, a serotonin-3 (5-HT3) receptorantagonist indicated for the prevention of acute and delayed nausea andvomiting associated with initial and repeat courses of cancer chemotherapy,including, but not limited to, highly emetogenic chemotherapy. Oralpalonosetron prevents nausea and vomiting during the acute phase andnetupitant prevents nausea and vomiting during both the acute and delayedphase after cancer chemotherapy. (1)
DrugBank Targets:
16
1. Substance-P receptor;2. 5-hydroxytryptamine receptor 3A
Mechanism of Action:
18
Target: neurokinin 1 (NK1) receptors/ substance P mediated responses [netupitant] & 5-HT3 receptor [palonosetron]
Action: activator/ inhibitor & agonist
FDA: Netupitant is a selective antagonist of human substance P/neurokinin 1 (NK1) receptors.Palonosetron is a 5-HT3 receptor antagonist with a strong binding affinity for this receptor and little or noaffinity for other receptors. Cancer chemotherapy may be associated with a high incidence of nausea andvomiting, particularly when certain agents, such as cisplatin, are used. 5-HT3 receptors are located on thenerve terminals of the vagus in the periphery and centrally in the chemoreceptor trigger zone of the areapostrema. Chemotherapeutic agents produce nausea and vomiting by stimulating the release of serotoninfrom the enterochromaffin cells of the small intestine. Serotonin then activates 5-HT3 receptors located onvagal afferents to initiate the vomiting reflex. The development of acute emesis is known to depend onserotonin and its 5-HT3 receptors have been demonstrated to selectively stimulate the emetic response.Delayed emesis has been largely associated with the activation of tachykinin family neurokinin 1 (NK1)receptors (broadly distributed in the central and peripheral nervous systems) by substance P. As shown inin vitro and in vivo studies, netupitant inhibits substance P mediated responses.
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| 7 |
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Alimta
18
49
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PEMETREXED (also Pemetrexed Disodium) |
Eli Lilly |
February 2004 |
Disease/s that Drug Treats:Mesothelioma
Indications and Usage:
18
ALIMTA® is a folate analog metabolic inhibitor indicated for: Locally Advanced or Metastatic Nonsquamous Non-Small CellLung Cancer: Initial treatment in combination with cisplatin. (1.1) Maintenance treatment of patients whose disease has notprogressed after four cycles of platinum-based first-linechemotherapy. (1.2) After prior chemotherapy as a single-agent. (1.3) Mesothelioma: in combination with cisplatin. (1.4)Limitations of Use: ALIMTA is not indicated for the treatment of patients withsquamous cell non-small cell lung cancer. (1.5)
DrugBank Targets:
16
1. Thymidylate synthase;2. Bifunctional purine biosynthesis protein PURH;3. Dihydrofolate reductase;4. Trifunctional purine biosynthetic protein adenosine-3
Mechanism of Action:
18
Target: folic acid/ thymidylate synthase, dihydrofolate reductase, and glycinamide ribonucleotide formyltransferase
Action: antagonist/ inhibitor
FDA: ALIMTA, pemetrexed for injection, is a folate analog metabolic inhibitor that exerts its action by disrupting folatedependentmetabolic processes essential for cell replication. In vitro studies have shown that pemetrexed inhibitsthymidylate synthase (TS), dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT),which are folate-dependent enzymes involved in the de novo biosynthesis of thymidine and purine nucleotides.Pemetrexed is taken into cells by membrane carriers such as the reduced folate carrier and membrane folate bindingprotein transport systems. Once in the cell, pemetrexed is converted to polyglutamate forms by the enzymefolylpolyglutamate synthetase. The polyglutamate forms are retained in cells and are inhibitors of TS and GARFT.Polyglutamation is a time- and concentration-dependent process that occurs in tumor cells and, is thought to occur to alesser extent, in normal tissues. Polyglutamated metabolites are thought to have an increased intracellular half-liferesulting in prolonged drug action in malignant cells.
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| 8 |
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Aloxi
18
49
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PALONOSETRON (hydrochloride) |
MGI Pharma, Helsinn Healthcare |
August 2003 |
Disease/s that Drug Treats:Chemotherapy side effects
Indications and Usage:
18
ALOXI is a serotonin-3 (5-HT3) receptor antagonist indicated in adults for: Moderately emetogenic cancer chemotherapy -- prevention ofacute and delayed nausea and vomiting associated with initial andrepeat courses (1.1) Highly emetogenic cancer chemotherapy -- prevention of acutenausea and vomiting associated with initial and repeat courses(1.1) Prevention of postoperative nausea and vomiting (PONV) for upto 24 hours following surgery. Efficacy beyond 24 hours has notbeen demonstrated (1.3)ALOXI is indicated in pediatric patients aged 1 month to less than 17 yearsfor: Prevention of acute nausea and vomiting associated with initialand repeat courses of emetogenic cancer chemotherapy, includinghighly emetogenic cancer chemotherapy (1.2)
DrugBank Targets:
16
5-hydroxytryptamine receptor 3A
Mechanism of Action:
18
Target: serotonin subtype 3 (5-HT3) receptor/ ion channels involved in ventricular polarization
Action: antagonist/ blocker
FDA: Palonosetron is a 5-HT3 receptor antagonist with a strong bindingaffinity for this receptor and little or no affinity for other receptors.Cancer chemotherapy may be associated with a high incidence ofnausea and vomiting, particularly when certain agents, such as cisplatin, areused. 5-HT3 receptors are located on the nerve terminals of the vagus in theperiphery and centrally in the chemoreceptor trigger zone of the areapostrema. It is thought that chemotherapeutic agents produce nausea andvomiting by releasing serotonin from the enterochromaffin cells of the smallintestine and that the released serotonin then activates 5-HT3 receptorslocated on vagal afferents to initiate the vomiting reflex.Postoperative nausea and vomiting is influenced by multiple patient,surgical and anesthesia related factors and is triggered by release of 5-HT ina cascade of neuronal events involving both the central nervous system andthe gastrointestinal tract. The 5-HT3 receptor has been demonstrated toselectively participate in the emetic response.
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| 9 |
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Anexsia
18
|
ACETAMINOPHEN; HYDROCODONE BITARTRATE |
Mallinckrodt Group |
August 1996 |
Disease/s that Drug Treats:chronic pain
Indications and Usage:
18
DrugBank Targets:
16
1. Prostaglandin G/H synthase 2;2. Prostaglandin G/H synthase 1;3. Prostaglandin G/H synthase 3;4. Mu-type opioid receptor;5. Delta-type opioid receptor
Mechanism of Action:
18
Target: cyclooxygenase (COX); OP1, OP2, and OP3 opiate receptors
Action: inhibitor; agonist
FDA: -
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| 10 |
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Anzemet
18
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DOLASETRON MESYLATE |
Hoechst Marion Roussel |
February 1998 |
Disease/s that Drug Treats:prevention of nausea and vomiting associated with chemotherapy and surgery/ Treatment for chemotherapy induced emesis
Indications and Usage:
18
ANZEMET Tablets are indicated for the prevention of nausea and vomiting associated withmoderately emetogenic cancer chemotherapy, including initial and repeat courses in adults andchildren 2 years and older.
DrugBank Targets:
16
5-hydroxytryptamine receptor 3A
Mechanism of Action:
18
Target: seratonin 5-HT3 receptor
Action: antagonist
FDA: Dolasetron mesylate and its active metabolite, hydrodolasetron (MDL 74,156), are selectiveserotonin 5-HT3 receptor antagonists not shown to have activity at other known serotoninreceptors and with low affinity for dopamine receptors. The serotonin 5-HT3 receptors arelocated on the nerve terminals of the vagus in the periphery and centrally in the chemoreceptortrigger zone of the area postrema. It is thought that chemotherapeutic agents produce nausea andvomiting by releasing serotonin from the enterochromaffin cells of the small intestine, and thatthe released serotonin then activates 5-HT3 receptors located on vagal efferents to initiate thevomiting reflex.In healthy volunteers (N=64), dolasetron mesylate in single intravenous doses up to 5 mg/kgproduced no effect on pupil size or meaningful changes in EEG tracings. Results fromneuropsychiatric tests revealed that dolasetron mesylate did not alter mood or concentration.Multiple daily doses of dolasetron have had no effect on colonic transit in humans. Dolasetronhas no effect on plasma prolactin concentrations.
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| 11 |
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Aredia
18
49
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PAMIDRONATE DISODIUM |
Chiron |
August 1996 |
Disease/s that Drug Treats:osteolytic bone metastases of breast cancer
Indications and Usage:
18
Hypercalcemia of MalignancyAredia, in conjunction with adequate hydration, is indicated for the treatment of moderate or severehypercalcemia associated with malignancy, with or without bone metastases. Patients who have eitherepidermoid or non-epidermoid tumors respond to treatment with Aredia. Vigorous saline hydration, anintegral part of hypercalcemia therapy, should be initiated promptly and an attempt should be made torestore the urine output to about 2 L/day throughout treatment. Mild or asymptomatic hypercalcemia maybe treated with conservative measures (i.e., saline hydration, with or without loop diuretics). Patientsshould be hydrated adequately throughout the treatment, but overhydration, especially in those patientswho have cardiac failure, must be avoided. Diuretic therapy should not be employed prior to correction ofhypovolemia. The safety and efficacy of Aredia in the treatment of hypercalcemia associated withhyperparathyroidism or with other non-tumor-related conditions has not been established.Pagetâs DiseaseAredia is indicated for the treatment of patients with moderate to severe Pagetâs disease of bone. Theeffectiveness of Aredia was demonstrated primarily in patients with serum alkaline phosphatase â¥3 timesthe upper limit of normal. Aredia therapy in patients with Pagetâs disease has been effective in reducingserum alkaline phosphatase and urinary hydroxyproline levels by â¥50% in at least 50% of patients, and byâ¥30% in at least 80% of patients. Aredia therapy has also been effective in reducing these biochemicalmarkers in patients with Pagetâs disease who failed to respond, or no longer responded to othertreatments.Osteolytic Bone Metastases of Breast Cancer and Osteolytic Lesions of MultipleMyelomaAredia is indicated, in conjunction with standard antineoplastic therapy, for the treatment of osteolyticbone metastases of breast cancer and osteolytic lesions of multiple myeloma. The Aredia treatment effectappeared to be smaller in the study of breast cancer patients receiving hormonal therapy than in the studyof those receiving chemotherapy, however, overall evidence of clinical benefit has been demonstrated(see CLINICAL PHARMACOLOGY, Osteolytic Bone Metastases of Breast Cancer and OsteolyticLesions of Multiple Myeloma, Clinical Trials section).
DrugBank Targets:
16
1. Farnesyl pyrophosphate synthase;2. Hydroxylapatite
Mechanism of Action:
18
Target: bone resorption; FPP synthase
Action: inhibitor
FDA: The principal pharmacologic action of Aredia is inhibition of bone resorption. Although the mechanism ofantiresorptive action is not completely understood, several factors are thought to contribute to this action.Aredia adsorbs to calcium phosphate (hydroxyapatite) crystals in bone and may directly block dissolutionof this mineral component of bone. In vitro studies also suggest that inhibition of osteoclast activitycontributes to inhibition of bone resorption. In animal studies, at doses recommended for the treatment ofhypercalcemia, Aredia inhibits bone resorption apparently without inhibiting bone formation andmineralization. Of relevance to the treatment of hypercalcemia of malignancy is the finding that Arediainhibits the accelerated bone resorption that results from osteoclast hyperactivity induced by varioustumors in animal studies.
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| 12 |
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Arimidex
18
49
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ANASTROZOLE |
AstraZeneca |
January 1996 |
Disease/s that Drug Treats:post menopausal breast cancer
Indications and Usage:
18
ARIMIDEX is an aromatase inhibitor indicated for: Adjuvant treatment of postmenopausal women withhormone receptor-positive early breast cancer (1.1) First-line treatment of postmenopausal women withhormone receptor-positive or hormone receptor unknownlocally advanced or metastatic breast cancer (1.2) Treatment of advanced breast cancer in postmenopausalwomen with disease progression following tamoxifentherapy. Patients with ER-negative disease and patientswho did not respond to previous tamoxifen therapy rarelyresponded to ARIMIDEX (1.3)
DrugBank Targets:
16
Cytochrome P450 19A1
Mechanism of Action:
18
Target: oral aromatase
Action: inhibitor
FDA: The growth of many cancers of the breast is stimulated or maintained by estrogens.In postmenopausal women, estrogens are mainly derived from the action of the aromataseenzyme, which converts adrenal androgens (primarily androstenedione and testosterone) toestrone and estradiol. The suppression of estrogen biosynthesis in peripheral tissues and inthe cancer tissue itself can therefore be achieved by specifically inhibiting the aromataseenzyme.Anastrozole is a selective non-steroidal aromatase inhibitor. It significantly lowers serumestradiol concentrations and has no detectable effect on formation of adrenal corticosteroidsor aldosterone.
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| 13 |
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Aromasin Tablets
18
49
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EXEMESTANE |
Pharmacia & Upjohn |
October 21. 1999 |
Disease/s that Drug Treats:advanced breast cancer in postmenopausal women whose disease has progressed following tamoxifen therapy
Indications and Usage:
18
AROMASIN is an aromatase inhibitor indicated for: Incidences of cardiac ischemic events (myocardial infarction, angina, adjuvant treatment of postmenopausal women with estrogen-receptor and myocardial ischemia) were AROMASIN 1.6%, tamoxifen 0.6%.positive early breast cancer who have received two to three years of Incidence of cardiac failure: AROMASIN 0.4%, tamoxifen 0.3% (6,tamoxifen and are switched to AROMASIN for completion of a total of 6.1).five consecutive years of adjuvant hormonal therapy (14.1). Advanced breast cancer: Most common adverse events were mild to treatment of advanced breast cancer in postmenopausal women whose moderate and included hot flushes (13% vs. 5%), nausea (9% vs. 5%),disease has progressed following tamoxifen therapy (14.2).
DrugBank Targets:
16
Cytochrome P450 19A1
Mechanism of Action:
18
Target: steroidal aromatase
Action: inactivator
FDA: Breast cancer cell growth may be estrogen-dependent. Aromatase is the principal enzyme that convertsandrogens to estrogens both in pre- and postmenopausal women. While the main source of estrogen (primarilyestradiol) is the ovary in premenopausal women, the principal source of circulating estrogens in postmenopausalwomen is from conversion of adrenal and ovarian androgens (androstenedione and testosterone) to estrogens(estrone and estradiol) by the aromatase enzyme in peripheral tissues. Estrogen deprivation through aromataseinhibition is an effective and selective treatment for some postmenopausal patients with hormone-dependent breastcancer.Exemestane is an irreversible, steroidal aromatase inactivator, structurally related to the natural substrateandrostenedione. It acts as a false substrate for the aromatase enzyme, and is processed to an intermediate that bindsirreversibly to the active site of the enzyme, causing its inactivation, an effect also known as âsuicide inhibition.âExemestane significantly lowers circulating estrogen concentrations in postmenopausal women, but has nodetectable effect on adrenal biosynthesis of corticosteroids or aldosterone. Exemestane has no effect on otherenzymes involved in the steroidogenic pathway up to a concentration at least 600 times higher than that inhibitingthe aromatase enzyme.
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| 14 |
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Arranon
18
49
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NELARABINE |
GlaxoSmithKline |
October 2005 |
Disease/s that Drug Treats:Lymphoblastic Leukemia
Indications and Usage:
18
ARRANON is a nucleoside metabolic inhibitor indicated for the treatment ofpatients with T-cell acute lymphoblastic leukemia and T-cell lymphoblasticlymphoma whose disease has not responded to or has relapsed followingtreatment with at least two chemotherapy regimens. This use is based on theinduction of complete responses. Randomized trials demonstrating increasedsurvival or other clinical benefit have not been conducted. (1)
Mechanism of Action:
18
Target: DNA synthesis
Action: disruptor --> apoptosis
FDA: Nelarabine is a pro-drug of the deoxyguanosine analogue 9-β-D-arabinofuranosylguanine266 (ara-G), a nucleoside metabolic inhibitor. Nelarabine is demethylated by adenosine deaminase267 (ADA) to ara-G, mono-phosphorylated by deoxyguanosine kinase and deoxycytidine kinase, and268 subsequently converted to the active 5â-triphosphate, ara-GTP. Accumulation of ara-GTP in269 leukemic blasts allows for incorporation into deoxyribonucleic acid (DNA), leading to inhibition270 of DNA synthesis and cell death. Other mechanisms may contribute to the cytotoxic and271 systemic toxicity of nelarabine.
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| 15 |
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Arzerra
18
49
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OFATUMUMAB |
GlaxoSmithKline |
October 2009 |
Disease/s that Drug Treats:chronic lymphocytic leukemia
Indications and Usage:
18
ARZERRA (ofatumumab) is a CD20-directed cytolytic monoclonal antibodyindicated: in combination with chlorambucil, for the treatment of previouslyuntreated patients with chronic lymphocytic leukemia (CLL) for whomfludarabine-based therapy is considered inappropriate. (1.1) for the treatment of patients with CLL refractory to fludarabine andalemtuzumab. (1.2)
DrugBank Targets:
16
no entry
Mechanism of Action:
18
Target: B-cell
Action: promotes lysis
FDA: Ofatumumab binds specifically to both the small and large extracellular loops of the CD20402 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B- to mature403 B-lymphocyte) and on B-cell CLL. The CD20 molecule is not shed from the cell surface and is404 not internalized following antibody binding.405406 The Fab domain of ofatumumab binds to the CD20 molecule and the Fc domain mediates407 immune effector functions to result in B-cell lysis in vitro. Data suggest that possible408 mechanisms of cell lysis include complement-dependent cytotoxicity and antibody-dependent,409 cell-mediated cytotoxicity.
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| 16 |
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Avastin
18
49
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BEVACIZUMAB |
Genentech |
July 2009 |
Disease/s that Drug Treats:renal cell carcinoma & Colorectal Cancer
Indications and Usage:
18
Avastin is a vascular endothelial growth factor-specific angiogenesisinhibitor indicated for the treatment of: Metastatic colorectal cancer, with intravenous 5-fluorouracil-basedchemotherapy for first- or second-line treatment. (1.1) Metastatic colorectal cancer, with fluoropyrimidine- irinotecan- orfluoropyrimidine-oxaliplatin-based chemotherapy for second-linetreatment in patients who have progressed on a first-line Avastincontainingregimen. (1.1) Non-squamous non-small cell lung cancer, with carboplatin and paclitaxelfor first line treatment of unresectable, locally advanced, recurrent ormetastatic disease. (1.2) Glioblastoma, as a single agent for adult patients with progressive diseasefollowing prior therapy. (1.3)-Effectiveness based on improvement in objective response rate. No dataavailable demonstrating improvement in disease-related symptoms orsurvival with Avastin. Metastatic renal cell carcinoma with interferon alfa (1.4) Cervical cancer, in combination with paclitaxel and cisplatin or paclitaxeland topotecan in persistent, recurrent, or metastatic disease. (1.5) Platinum-resistant recurrent epithelial ovarian, fallopian tube or primaryperitoneal cancer, in combination with paclitaxel, pegylated liposomaldoxorubicin or topotecan (1.6) Limitation of Use: Avastin is not indicated for adjuvant treatment of coloncancer. (1.1)
DrugBank Targets:
16
1. Vascular endothelial growth factor A;2. Low affinity immunoglobulin gamma Fc region receptor III-B;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Low affinity immunoglobulin gamma Fc region receptor III-A;8. High affinity immunoglobulin gamma Fc receptor I;9. Low affinity immunoglobulin gamma Fc region receptor II-a;10. Low affinity immunoglobulin gamma Fc region receptor II-b;11. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:
18
Target: VEGF
Action: inhibitor
FDA: Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR)697 on the surface of endothelial cells. The interaction of VEGF with its receptors leads to endothelial698 cell proliferation and new blood vessel formation in in vitro models of angiogenesis. Administration699 of bevacizumab to xenotransplant models of colon cancer in nude (athymic) mice caused reduction700 of microvascular growth and inhibition of metastatic disease progression
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| 17 |
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Beleodaq
18
49
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BELINOSTAT |
Spectrum Pharmaceuticals |
July 2014 |
Disease/s that Drug Treats:relapsed or refractory peripheral T-cell lymphoma
Indications and Usage:
18
Beleodaq is a histone deacetylase inhibitor indicated for the treatment ofpatients with relapsed or refractory peripheral T-cell lymphoma (PTCL). Thisindication is approved under accelerated approval based on tumor responserate and duration of response. An improvement in survival or disease-relatedsymptoms has not been established. Continued approval for this indicationmay be contingent upon verification and description of clinical benefit in theconfirmatory trial. (1)
DrugBank Targets:
16
no entry
Mechanism of Action:
18
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: Beleodaq is a histone deacetylase (HDAC) inhibitor. HDACs catalyze the removal of acetyl groups from thelysine residues of histones and some non-histone proteins. In vitro, belinostat caused the accumulation ofacetylated histones and other proteins, inducing cell cycle arrest and/or apoptosis of some transformed cells.Belinostat shows preferential cytotoxicity towards tumor cells compared to normal cells. Belinostat inhibitedthe enzymatic activity of histone deacetylases at nanomolar concentrations (<250 nM).
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| 18 |
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Bexxar
18
49
|
TOSITUMOMAB; IODINE I 131 TOSITUMOMAB |
Corixa |
June 2003 |
Disease/s that Drug Treats:Non-Hodgkin's Lymphoma
Indications and Usage:
18
BEXXAR (tositumomab and Iodine I 131 tositumomab) is a CD20-directedradiotherapeutic antibody indicated for the treatment of patients with CD20-positive, relapsed or refractory, low-grade, follicular, or transformed nonHodgkin'slymphoma who have progressed during or after rituximab therapy,including patients with rituximab-refractory non-Hodgkin's lymphoma. (1.1)Determination of the effectiveness of the BEXXAR therapeutic regimen isbased on overall response rates in patients whose disease is refractory tochemotherapy and rituximab. The effects of the BEXXAR therapeuticregimen on survival are not known. (1.1)Important Limitation of Use BEXXAR therapeutic regimen is only indicated for a single course oftreatment and is not indicated for a first-line treatment. (1.2)
DrugBank Targets:
16
1. B-lymphocyte antigen CD20;2. Low affinity immunoglobulin gamma Fc region receptor III-B;3. Complement C1r subcomponent;4. Complement C1q subcomponent subunit A;5. Complement C1q subcomponent subunit B;6. Complement C1q subcomponent subunit C;7. Low affinity immunoglobulin gamma Fc region receptor III-A;8. High affinity immunoglobulin gamma Fc receptor I;9. Low affinity immunoglobulin gamma Fc region receptor II-a;10.Low affinity immunoglobulin gamma Fc region receptor II-b;11. Low affinity immunoglobulin gamma Fc region receptor II-c
Mechanism of Action:
18
Target: CD20
Action: cytotoxic antibody
FDA: Tositumomab binds specifically to an epitope within the extracellular domain of the586 CD20 molecule. The CD20 molecule is expressed on normal B lymphocytes (pre-B lymphocytes587 to mature B lymphocytes) and on B-cell non-Hodgkin's lymphomas. The CD20 molecule is not588 shed from the cell surface and is not internalized following antibody binding. The BEXXAR589 therapeutic regimen induces cell death by emitting ionizing radiation to CD20-expressing590 lymphocytes or neighboring cells. In addition to cell death mediated by the radioisotope, other591 possible mechanisms of action include antibody-dependent cellular cytotoxicity, complement-592 dependent cytotoxicity, and CD20-mediated apoptosis.
|
| 19 |
|
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.
|
| 20 |
|
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.
|
| 21 |
|
Bromfenac
18
|
BROMFENAC SODIUM |
Duract, Wyeth-Ayerst Laboratories |
July 1997 |
Disease/s that Drug Treats:acute pain
Indications and Usage:
18
Bromfenac Ophthalmic Solutionis a nonsteroidal anti-inflamatory drug (NSAID) indicated for the treatment of postoperative inflammation and reduction of ocular pain in patients who have undergone cataract extraction (1).
DrugBank Targets:
16
1. Prostaglandin G/H synthase 2;2. Prostaglandin G/H synthase 1
Mechanism of Action:
18
Target: cyclooxygenas 1 and 2
Action: inhibitor
FDA: Bromfenac is a non-steroidal anti-inflamatory drug (NSAID) that has anti-inflammatory activity. The mechanism of its action is thought to be due to its ability to block prostaglandin synthesis bby inhibiting cyclooxygenase 1 and 2. Prostaglandins have been shown in many animal models to be mediators of certain kinds of intraocular inflammation. In studies performed in animal eyes, prostaglandins have been shown to produces disruption of the blood aqueous humor barrier, vasodilation, increased vascular permeability, leukocytosis, and increased intraocular pressure.
|
| 22 |
|
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.
|
| 23 |
|
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.
|
| 24 |
|
Campostar
18
49
|
IRINOTECAN HYDROCHLORIDE |
Pharmacia & Upjohn |
June 1996 |
Disease/s that Drug Treats:metastatic colorectal cancer
Indications and Usage:
18
CAMPTOSAR is a topoisomerase inhibitor indicated for: First-line therapy in combination with 5-fluorouracil and leucovorin forpatients with metastatic carcinoma of the colon or rectum. (1) Patients with metastatic carcinoma of the colon or rectum whose diseasehas recurred or progressed following initial fluorouracil-based therapy. (1)
DrugBank Targets:
16
1. DNA topoisomerase I, mitochondrial;2. DNA topoisomerase 1
Mechanism of Action:
18
Target: topoisomerase I-DNA complex
Action: inhibitor of repairs to DNA
FDA: Irinotecan is a derivative of camptothecin. Camptothecins interact specifically with the enzymetopoisomerase I, which relieves torsional strain in DNA by inducing reversible single-strandbreaks. Irinotecan and its active metabolite SN-38 bind to the topoisomerase I-DNA complexand prevent religation of these single-strand breaks. Current research suggests that thecytotoxicity of irinotecan is due to double-strand DNA damage produced during DNA synthesiswhen replication enzymes interact with the ternary complex formed by topoisomerase I, DNA,and either irinotecan or SN-38. Mammalian cells cannot efficiently repair these double-strandbreaks.
|
| 25 |
|
CEA-Scan
18
|
|
Immunomedics |
April 1996 |
Disease/s that Drug Treats:colorectal cancer
Indications and Usage:
18
DrugBank Targets:
16
1. Carcinoembryonic antigen-related cell adhesion molecule 1
Mechanism of Action:
18
Target: carcinoembryonic antigen (""CEA"")
Action: marks
FDA: -
|
| 26 |
|
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: -
|
| 27 |
|
Clolar
18
49
|
CLOFARABINE |
Genzyme |
December, 2004 |
Disease/s that Drug Treats:Lymphoblastic Leukemia
Indications and Usage:
18
Clolar (clofarabine) injection is a purine nucleoside metabolic inhibitorindicated for the treatment of pediatric patients 1 to 21 years old with relapsedor refractory acute lymphoblastic leukemia after at least two prior regimens.This indication is based upon response rate. There are no trials verifying animprovement in disease-related symptoms or increased survival with Clolar.(1)
DrugBank Targets:
16
1. DNA polymerase alpha catalytic subunit;2. Ribonucleoside-diphosphate reductase large subunit;3. DNA
Mechanism of Action:
18
Target: ribonucleotide reductase
Action: inhibitor
FDA: Clofarabine is sequentially metabolized intracellularly to the 5â-monophosphate metabolite bydeoxycytidine kinase and mono- and di-phospho-kinases to the active 5â-triphosphate metabolite.Clofarabine has affinity for the activating phosphorylating enzyme, deoxycytidine kinase, equalto or greater than that of the natural substrate, deoxycytidine. Clofarabine inhibits DNA synthesisby decreasing cellular deoxynucleotide triphosphate pools through an inhibitory action onribonucleotide reductase, and by terminating DNA chain elongation and inhibiting repair throughincorporation into the DNA chain by competitive inhibition of DNA polymerases. The affinity ofclofarabine triphosphate for these enzymes is similar to or greater than that of deoxyadenosinetriphosphate. In preclinical models, clofarabine has demonstrated the ability to inhibit DNArepair by incorporation into the DNA chain during the repair process. Clofarabine 5â-triphosphate also disrupts the integrity of mitochondrial membrane, leading to the release of thepro-apoptotic mitochondrial proteins, cytochrome C and apoptosis-inducing factor, leading toprogrammed cell death.Clofarabine is cytotoxic to rapidly proliferating and quiescent cancer cell types in vitro.
|
| 28 |
|
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.
|
| 29 |
|
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.
|
| 30 |
|
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: -
|
| 31 |
|
Doxil
18
49
|
DOXORUBICIN HYDROCHLORIDE |
Alza |
June 1999 |
Disease/s that Drug Treats:ovarian cancer that is refractory to other first-line therapies
Indications and Usage:
18
DOXIL is an anthracycline topoisomerase II inhibitor indicated for: Ovarian cancer (1.1)After failure of platinum-based chemotherapy. AIDS-related Kaposiâs Sarcoma (1.2)After failure of prior systemic chemotherapy or intolerance to such therapy. Multiple Myeloma (1.3)In combination with bortezomib in patients who have not previouslyreceived bortezomib and have received at least one prior therapy.
DrugBank Targets:
16
1. DNA;2. DNA topoisomerase 2-alpha
Mechanism of Action:
18
Target: nucleic acidsynthesis
Action: inhibitor
FDA: The active ingredient of DOXIL is doxorubicin HCl. The mechanism of action ofdoxorubicin HCl is thought to be related to its ability to bind DNA and inhibit nucleic acidsynthesis. Cell structure studies have demonstrated rapid cell penetration and perinuclearReference ID: 373359617 chromatin binding, rapid inhibition of mitotic activity and nucleic acid synthesis, andinduction of mutagenesis and chromosomal aberrations.
|
| 32 |
|
Eligard
18
49
|
LEUPROLIDE ACETATE |
Atrix Laboratories |
January 2002 |
Disease/s that Drug Treats:Advanced prostate cancer
Indications and Usage:
18
ELIGARD is a gonadatropin releasing hormone (GnRH) agonist indicated forthe palliative treatment of advanced prostate cancer (1)
DrugBank Targets:
16
1. Gonadotropin-releasing hormone receptor
Mechanism of Action:
18
Target: gonadotropin secretion
Action: inhibitor
FDA: Leuprolide acetate, a gonadotropin releasing hormone (GnRH) agonist, acts as a potent inhibitorof gonadotropin secretion when given continuously in therapeutic doses. Animal and humanstudies indicate that after an initial stimulation, chronic administration of leuprolide acetateresults in suppression of testicular and ovarian steroidogenesis. This effect is reversible upondiscontinuation of drug therapy.In humans, administration of leuprolide acetate results in an initial increase in circulating levelsof luteinizing hormone (LH) and follicle stimulating hormone (FSH), leading to a transientincrease in levels of the gonadal steroids (testosterone and dihydrotestosterone in males, andestrone and estradiol in premenopausal females). However, continuous administration ofleuprolide acetate results in decreased levels of LH and FSH. In males, testosterone is reduced tobelow castrate threshold (< 50 ng/dL). These decreases occur within two to four weeks afterinitiation of treatment. Long-term studies have shown that continuation of therapy withleuprolide acetate maintains testosterone below the castrate level for up to seven years.
|
| 33 |
|
Elitek
18
49
|
RASBURICASE |
sanofi-aventis |
October 2009 |
Disease/s that Drug Treats:management of plasma uric acid levels in adults with malignancies
Indications and Usage:
18
Elitek is a recombinant urate-oxidase indicated for initial management ofplasma uric acid levels in pediatric and adult patients with leukemia,lymphoma, and solid tumor malignancies who are receiving anti-cancertherapy expected to result in tumor lysis and subsequent elevation of plasmauric acid (1).Limitation of use: Elitek is indicated only for a single course of treatment (1).
DrugBank Targets:
16
1. Uric acid
Mechanism of Action:
18
Target: uric acid
Action: converter to alantoin
FDA: In humans, uric acid is the final step in the catabolic pathway of purines. Rasburicase catalyzesenzymatic oxidation of poorly soluble uric acid into an inactive and more soluble metabolite(allantoin).
|
| 34 |
|
Ellence
18
49
|
EPIRUBICIN HYDROCHLORIDE |
Pharmacia & Upjohn |
September 1999 |
Disease/s that Drug Treats:Component of adjuvant therapy in patients with evidence of axillary node tumor involvement for primary breast cancer
Indications and Usage:
18
ELLENCE Injection is an anthracycline topoisomerase II inhibitor indicatedas a component of adjuvant therapy in patients with evidence of axillary nodetumor involvement following resection of primary breast cancer (1).
DrugBank Targets:
16
1. Chromodomain-helicase-DNA-binding protein 1;2. DNA topoisomerase 2-alpha;3. DNA
Mechanism of Action:
18
Target: nucleic acid (DNA and RNA) and protein synthesis
Action: inhibitor
FDA: Epirubicin is an anthracycline cytotoxic agent. Although it is known that anthracyclines can interfere with a number of biochemical andbiological functions within eukaryotic cells, the precise mechanisms of epirubicinâs cytotoxic and/or antiproliferative properties have not beencompletely elucidated.Epirubicin forms a complex with DNA by intercalation of its planar rings between nucleotide base pairs, with consequent inhibition of nucleicacid (DNA and RNA) and protein synthesis.Such intercalation triggers DNA cleavage by topoisomerase II, resulting in cytocidal activity. Epirubicin also inhibits DNA helicase activity,preventing the enzymatic separation of double-stranded DNA and interfering with replication and transcription. Epirubicin is also involved inoxidation/reduction reactions by generating cytotoxic free radicals. The antiproliferative and cytotoxic activity of epirubicin is thought to resultfrom these or other possible mechanisms.Epirubicin is cytotoxic in vitro to a variety of established murine and human cell lines and primary cultures of human tumors. It is also activein vivo against a variety of murine tumors and human xenografts in athymic mice, including breast tumors.
|
| 35 |
|
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: -
|
| 36 |
|
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)].
|
| 37 |
|
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.
|
| 38 |
|
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.
|
| 39 |
|
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.
|
| 40 |
|
Erwinaze
18
49
|
asparaginase Erwinia chrysanthemi |
Eusa Pharma |
November of 2011 |
Disease/s that Drug Treats:acute lymphoblastic leukemia
Indications and Usage:
18
ERWINAZE (asparaginase Erwinia chrysanthemi) is an asparagine specificenzyme indicated as a component of a multi-agent chemotherapeutic regimenfor the treatment of patients with acute lymphoblastic leukemia (ALL) whohave developed hypersensitivity to E. coli-derived asparaginase. (1)
DrugBank Targets:
-
Mechanism of Action:
18
Target: deamidation of asparagine to aspartic acid and ammonia
Action: catalyzer
FDA: Asparaginase Erwinia chrysanthemi catalyzes the deamidation of asparagine to aspartic acid and ammonia, resultingin a reduction in circulating levels of asparagine. The mechanism of action of ERWINAZE is thought to be based onthe inability of leukemic cells to synthesize asparagine due to lack of asparagine synthetase activity, resulting incytotoxicity specific for leukemic cells that depend on an exogenous source of amino acid asparagine for theirprotein metabolism and survival.
|
| 41 |
|
Ethyol
18
|
AMIFOSTINE |
Alza |
December 8, 1995 |
Disease/s that Drug Treats:ovarian cancer
Indications and Usage:
18
ETHYOL (amifostine) is indicated to reduce the cumulative renal toxicity associated withrepeated administration of cisplatin in patients with advanced ovarian cancer.ETHYOL is indicated to reduce the incidence of moderate to severe xerostomia in patientsundergoing post-operative radiation treatment for head and neck cancer, where the radiationport includes a substantial portion of the parotid glands (see Clinical Studies).For the approved indications, the clinical data do not suggest that the effectiveness of cisplatin basedchemotherapy regimens or radiation therapy is altered by ETHYOL. There are at present only limiteddata on the effects of ETHYOL on the efficacy of chemotherapy or radiotherapy in other settings.ETHYOL should not be administered to patients in other settings where chemotherapy can produce asignificant survival benefit or cure, or in patients receiving definitive radiotherapy, except in thecontext of a clinical study (see WARNINGS).
DrugBank Targets:
16
1. Ectonucleotide pyrophosphatase/phosphodiesterase family member 1;2. Alkaline phosphatase, placental-like
Mechanism of Action:
18
Target: -
Action: -
FDA: -
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| 42 |
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Eulexin
18
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FLUTAMIDE |
Schering-Plough |
June 1996 |
Disease/s that Drug Treats:prostate cancer
Indications and Usage:
18
EULEXIN capsules are indicated for use in combination with LHRH agonists for the management of locally confined Stage B2C and Stage D2 metastatic carcinoma of the prostate. Stage B2C Prostatic Carcinoma: Treatment with EUlEXIN an the goserelin acetate implant shouls start 8 weeks prior to initiating radiation therapy and continue during radiation therapy. Stage D2 Metastatic Carcinoma: To acheive benefit from treatment, EULEXIN Capsules should be initiated with the LHRH-agonist and continued until progression.
DrugBank Targets:
16
1. Androgen receptor;2. Aryl hydrocarbon receptor
Mechanism of Action:
18
Target: androgen uptake and/or nuclear binding of angrogen in target tissues
Action: inhibitor
FDA: In animal studies, flutamide demonstrates potent anti-angrogenic effects. It exerts an antiandrogenic action by inhibiting angrogen uptake and/or by inhibiting nuclear binding of androgen in target tissues or both. Prostatic carcinoma is known to be androgen-sensitive and responds to treatment that counteracts the effect of androgen and/or removes the source of androgen, eg. castration. Elevations of plasma testosterone and estraidiol levels have been noted following flutamide administration.
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Evista
18
49
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RALOXIFENE HYDROCHLORIDE |
Eli Lilly |
September 2007 |
Disease/s that Drug Treats:osteoporosis and reduction of breast cancer risk in postmenopausal women
Indications and Usage:
18
EVISTA is an estrogen agonist/antagonist indicated for Treatment and prevention of osteoporosis in postmenopausal women.(1.1)
DrugBank Targets:
16
1. Estrogen receptor;2. Estrogen receptor beta
Mechanism of Action:
18
Target: estrogenic pathways
Action: can be an activator or antooagonist
FDA: Decreases in estrogen levels after oophorectomy or menopause lead to increases in bone resorption andaccelerated bone loss. Bone is initially lost rapidly because the compensatory increase in bone formation isinadequate to offset resorptive losses. In addition to loss of estrogen, this imbalance between resorption andformation may be due to age-related impairment of osteoblasts or their precursors. In some women, these changeswill eventually lead to decreased bone mass, osteoporosis, and increased risk for fractures, particularly of the spine,hip, and wrist. Vertebral fractures are the most common type of osteoporotic fracture in postmenopausal women.The biological actions of raloxifene are largely mediated through binding to estrogen receptors. This bindingresults in activation of certain estrogenic pathways and blockade of others. Thus, raloxifene is an estrogenagonist/antagonist, commonly referred to as a selective estrogen receptor modulator (SERM).Raloxifene decreases resorption of bone and reduces biochemical markers of bone turnover to thepremenopausal range. These effects on bone are manifested as reductions in the serum and urine levels of boneturnover markers, decreases in bone resorption based on radiocalcium kinetics studies, increases in bone mineraldensity (BMD), and decreases in incidence of fractures.
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Farydak
18
49
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PANOBINOSTAT LACTATE |
Novartis |
February 2015 |
Disease/s that Drug Treats:Multiple myeloma
Indications and Usage:
18
FARYDAK, a histone deacetylase inhibitor, in combination with bortezomiband dexamethasone, is indicated for the treatment of patients with multiplemyeloma who have received at least 2 prior regimens, including bortezomiband an immunomodulatory agent. This indication is approved underaccelerated approval based on progression free survival. Continued approvalfor this indication may be contingent upon verification and description ofclinical benefit in confirmatory trials. (1)
DrugBank Targets:
-
Mechanism of Action:
18
Target: histone deacetylase (HDAC)
Action: inhibitor
FDA: FARYDAK is a histone deacetylase (HDAC) inhibitor that inhibits the enzymatic activity of HDACs atnanomolar concentrations. HDACs catalyze the removal of acetyl groups from the lysine residues of histonesand some non-histone proteins. Inhibition of HDAC activity results in increased acetylation of histone proteins,an epigenetic alteration that results in a relaxing of chromatin, leading to transcriptional activation. In vitro,Reference ID: 3699607 panobinostat caused the accumulation of acetylated histones and other proteins, inducing cell cycle arrest and/orapoptosis of some transformed cells. Increased levels of acetylated histones were observed in xenografts frommice that were treated with panobinostat. Panobinostat shows more cytotoxicity towards tumor cells comparedto normal cells.
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| 45 |
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Faslodex
18
49
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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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Femara
18
49
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LETROZOLE |
Novartis |
January 2001 |
Disease/s that Drug Treats:Hormone receptor positive or hormone receptor unknown locally advanced or metastatic breast cancer
Indications and Usage:
18
Femara is an aromatase inhibitor indicated for: Adjuva nt treatment of postmenopausal women with hormone receptorpositive early brea st cancer (1.1) Extended adjuvant treatment of postmenopausal women with early brea stcancer who have received prior standard adju vant ta moxifen thera py (1.2) First a nd second-line treatment of postmenopausal women with hormonereceptor positive or unknown advanced breast cancer (1.3)
DrugBank Targets:
16
1. Cytochrome P450 19A1
Mechanism of Action:
18
Target: aromatase enzyme system
Action: inhibitor
FDA: The growth of some cancers of the breast is stimulated or maintained by estrogens. Treatment of breastcancer thought to be hormonally responsive (i.e., estrogen and/or progesterone receptor positive orreceptor unknown) has included a variety of efforts to decrease estrogen levels (ovariectomy,adrenalectomy, hypophysectomy) or inhibit estrogen effects (antiestrogens and progestational agents).These interventions lead to decreased tumor mass or delayed progression of tumor growth in somewomen.In postmenopausal women, estrogens are mainly derived from the action of the aromatase enzyme, whichconverts adrenal androgens (primarily androstenedione and testosterone) to estrone and estradiol. Thesuppression of estrogen biosynthesis in peripheral tissues and in the cancer tissue itself can therefore beachieved by specifically inhibiting the aromatase enzyme.Letrozole is a nonsteroidal competitive inhibitor of the aromatase enzyme system; it inhibits theconversion of androgens to estrogens. In adult nontumor- and tumor-bearing female animals, letrozole isas effective as ovariectomy in reducing uterine weight, elevating serum LH, and causing the regression ofestrogen-dependent tumors. In contrast to ovariectomy, treatment with letrozole does not lead to anincrease in serum FSH. Letrozole selectively inhibits gonadal steroidogenesis but has no significant effecton adrenal mineralocorticoid or glucocorticoid synthesis.Letrozole inhibits the aromatase enzyme by competitively binding to the heme of the cytochrome P450subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues. Treatment of womenwith letrozole significantly lowers serum estrone, estradiol and estrone sulfate and has not been shown tosignificantly affect adrenal corticosteroid synthesis, aldosterone synthesis, or synthesis of thyroidhormones.
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| 47 |
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Feridex I.V.
18
|
FERUMOXIDES |
Advanced Magnetics |
February 1996 |
Disease/s that Drug Treats:liver cancer
Indications and Usage:
18
DrugBank Targets:
-
Mechanism of Action:
18
Target: -
Action: -
FDA: -
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| 48 |
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Folotyn
18
49
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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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Fusilev
18
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LEVOLEUCOVORIN CALCIUM |
Spectrum Pharmaceuticals |
March of 2008 |
Disease/s that Drug Treats:rescue after high-dose methotrexate therapy in osteosarcoma and to reduce the toxicity of methotrexate
Indications and Usage:
18
Fusilev is a folate analog indicated for: Rescue after high-dose methotrexate therapy in osteosarcoma. Diminishing the toxicity and counteracting the effects of impairedmethotrexate elimination and of inadvertent overdosage of folic acidantagonists. Use in combination chemotherapy with 5-fluorouracil in the palliativetreatment of patients with advanced metastatic colorectal cancer.(1)Limitations of UseFusilev is not approved for pernicious anemia and megaloblastic anemias.Improper use may cause a hematologic remission while neurologicmanifestations continue to progress. (1.1)
DrugBank Targets:
16
1. Thymidylate synthase
Mechanism of Action:
18
Target: therapeutic and toxic effects of folic acidantagonists / therapeutic and toxic effects of fluoropyrimidines used in cancer therapy
Action: counteract/enhance
FDA: 12.1.1 Levoleucovorin effects during high-dose methotrexate therapyLevoleucovorin is the pharmacologically active isomer of 5-formyl tetrahydrofolic acid. Levoleucovorin does not requirereduction by the enzyme dihydrofolate reductase in order to participate in reactions utilizing folates as a source of âonecarbonâmoieties. Administration of levoleucovorin can counteract the therapeutic and toxic effects of folic acidantagonists such as methotrexate, which act by inhibiting dihydrofolate reductase.12.1.2 Levoleucovorin effects in combination with 5-fluorouracilLevoleucovorin can enhance the therapeutic and toxic effects of fluoropyrimidines used in cancer therapy such as5-fluorouracil. 5-fluorouracil is metabolized to 5-fluoro-2'-deoxyuridine-5'-monophosphate (FdUMP), which binds to andinhibits thymidylate synthase (an enzyme important in DNA repair and replication). Levoleucovorin is readily convertedto another reduced folate, 5,10-methylenetetrahydrofolate, which acts to stabilize the binding of FdUMP to thymidylatesynthase and thereby enhances the inhibition of this enzyme.
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| 50 |
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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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