FDA approved drugs:
(show top 50)
(show all 86)
| # |
|
Drug Name |
Active Ingredient(s) 18
|
Company |
Approval Date |
| 1 |
|
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.
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| 2 |
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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.
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| 3 |
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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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| 4 |
|
Aredia
18
49
|
PAMIDRONATE DISODIUM |
Chiron |
August 1996 |
Disease/s that Drug Treats:osteolytic bone metastases of breast cancer
Indications and Usage:
18
Hypercalcemia of MalignancyAredia, in conjunction with adequate hydration, is indicated for the treatment of moderate or severehypercalcemia associated with malignancy, with or without bone metastases. Patients who have eitherepidermoid or non-epidermoid tumors respond to treatment with Aredia. Vigorous saline hydration, anintegral part of hypercalcemia therapy, should be initiated promptly and an attempt should be made torestore the urine output to about 2 L/day throughout treatment. Mild or asymptomatic hypercalcemia maybe treated with conservative measures (i.e., saline hydration, with or without loop diuretics). Patientsshould be hydrated adequately throughout the treatment, but overhydration, especially in those patientswho have cardiac failure, must be avoided. Diuretic therapy should not be employed prior to correction ofhypovolemia. The safety and efficacy of Aredia in the treatment of hypercalcemia associated withhyperparathyroidism or with other non-tumor-related conditions has not been established.Pagetâs DiseaseAredia is indicated for the treatment of patients with moderate to severe Pagetâs disease of bone. Theeffectiveness of Aredia was demonstrated primarily in patients with serum alkaline phosphatase â¥3 timesthe upper limit of normal. Aredia therapy in patients with Pagetâs disease has been effective in reducingserum alkaline phosphatase and urinary hydroxyproline levels by â¥50% in at least 50% of patients, and byâ¥30% in at least 80% of patients. Aredia therapy has also been effective in reducing these biochemicalmarkers in patients with Pagetâs disease who failed to respond, or no longer responded to othertreatments.Osteolytic Bone Metastases of Breast Cancer and Osteolytic Lesions of MultipleMyelomaAredia is indicated, in conjunction with standard antineoplastic therapy, for the treatment of osteolyticbone metastases of breast cancer and osteolytic lesions of multiple myeloma. The Aredia treatment effectappeared to be smaller in the study of breast cancer patients receiving hormonal therapy than in the studyof those receiving chemotherapy, however, overall evidence of clinical benefit has been demonstrated(see CLINICAL PHARMACOLOGY, Osteolytic Bone Metastases of Breast Cancer and OsteolyticLesions of Multiple Myeloma, Clinical Trials section).
DrugBank Targets:
16
1. Farnesyl pyrophosphate synthase;2. Hydroxylapatite
Mechanism of Action:
18
Target: bone resorption; FPP synthase
Action: inhibitor
FDA: The principal pharmacologic action of Aredia is inhibition of bone resorption. Although the mechanism ofantiresorptive action is not completely understood, several factors are thought to contribute to this action.Aredia adsorbs to calcium phosphate (hydroxyapatite) crystals in bone and may directly block dissolutionof this mineral component of bone. In vitro studies also suggest that inhibition of osteoclast activitycontributes to inhibition of bone resorption. In animal studies, at doses recommended for the treatment ofhypercalcemia, Aredia inhibits bone resorption apparently without inhibiting bone formation andmineralization. Of relevance to the treatment of hypercalcemia of malignancy is the finding that Arediainhibits the accelerated bone resorption that results from osteoclast hyperactivity induced by varioustumors in animal studies.
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| 5 |
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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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| 6 |
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Bosulif
18
49
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BOSUTINIB MONOHYDRATE |
Pfizer |
September 2012 |
Disease/s that Drug Treats:Ph+ chronic myelogenous leukemia
Indications and Usage:
18
BOSULIF is a kinase inhibitor indicated for the treatment of adult patientswith chronic, accelerated, or blast phase Ph+ chronic myelogenous leukemia(CML) with resistance or intolerance to prior therapy. (1)
DrugBank Targets:
16
1. Breakpoint cluster region protein;2. Tyrosine-protein kinase ABL1;3. Tyrosine-protein kinase Lyn;4. Tyrosine-protein kinase HCK;5. Proto-oncogene tyrosine-protein kinase Src;6. Cyclin-dependent kinase 2;7. Dual specificity mitogen-activated protein kinase kinase 1;8. Dual specificity mitogen-activated protein kinase kinase 2;9. Mitogen-activated protein kinase kinase kinase 2;10. Calcium/calmodulin-dependent protein kinase type II subunit gamma
Mechanism of Action:
18
Target: tyrosine kinase/ Src-family kinases including Src, Lyn, and Hck
Action: inhibitor
FDA: Bosutinib is a tyrosine kinase inhibitor. Bosutinib inhibits the Bcr-Abl kinase that promotes CML; it is also aninhibitor of Src-family kinases including Src, Lyn, and Hck. Bosutinib inhibited 16 of 18 imatinib-resistant forms ofBcr-Abl expressed in murine myeloid cell lines. Bosutinib did not inhibit the T315I and V299L mutant cells. In mice,treatment with bosutinib reduced the size of CML tumors relative to controls and inhibited growth of murine myeloidtumors expressing several imatinib-resistant forms of Bcr-Abl.
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| 7 |
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Bromfenac
18
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BROMFENAC SODIUM |
Duract, Wyeth-Ayerst Laboratories |
July 1997 |
Disease/s that Drug Treats:acute pain
Indications and Usage:
18
Bromfenac Ophthalmic Solutionis a nonsteroidal anti-inflamatory drug (NSAID) indicated for the treatment of postoperative inflammation and reduction of ocular pain in patients who have undergone cataract extraction (1).
DrugBank Targets:
16
1. Prostaglandin G/H synthase 2;2. Prostaglandin G/H synthase 1
Mechanism of Action:
18
Target: cyclooxygenas 1 and 2
Action: inhibitor
FDA: Bromfenac is a non-steroidal anti-inflamatory drug (NSAID) that has anti-inflammatory activity. The mechanism of its action is thought to be due to its ability to block prostaglandin synthesis bby inhibiting cyclooxygenase 1 and 2. Prostaglandins have been shown in many animal models to be mediators of certain kinds of intraocular inflammation. In studies performed in animal eyes, prostaglandins have been shown to produces disruption of the blood aqueous humor barrier, vasodilation, increased vascular permeability, leukocytosis, and increased intraocular pressure.
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| 8 |
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Campath
18
49
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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.
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| 9 |
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Cometriq
18
49
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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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| 10 |
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Degarelix
18
49
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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: -
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| 11 |
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Elitek
18
49
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RASBURICASE |
sanofi-aventis |
October 2009 |
Disease/s that Drug Treats:management of plasma uric acid levels in adults with malignancies
Indications and Usage:
18
Elitek is a recombinant urate-oxidase indicated for initial management ofplasma uric acid levels in pediatric and adult patients with leukemia,lymphoma, and solid tumor malignancies who are receiving anti-cancertherapy expected to result in tumor lysis and subsequent elevation of plasmauric acid (1).Limitation of use: Elitek is indicated only for a single course of treatment (1).
DrugBank Targets:
16
1. Uric acid
Mechanism of Action:
18
Target: uric acid
Action: converter to alantoin
FDA: In humans, uric acid is the final step in the catabolic pathway of purines. Rasburicase catalyzesenzymatic oxidation of poorly soluble uric acid into an inactive and more soluble metabolite(allantoin).
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| 12 |
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Erbitux
18
49
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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.
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| 13 |
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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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| 14 |
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Femara
18
49
|
LETROZOLE |
Novartis |
January 2001 |
Disease/s that Drug Treats:Hormone receptor positive or hormone receptor unknown locally advanced or metastatic breast cancer
Indications and Usage:
18
Femara is an aromatase inhibitor indicated for: Adjuva nt treatment of postmenopausal women with hormone receptorpositive early brea st cancer (1.1) Extended adjuvant treatment of postmenopausal women with early brea stcancer who have received prior standard adju vant ta moxifen thera py (1.2) First a nd second-line treatment of postmenopausal women with hormonereceptor positive or unknown advanced breast cancer (1.3)
DrugBank Targets:
16
1. Cytochrome P450 19A1
Mechanism of Action:
18
Target: aromatase enzyme system
Action: inhibitor
FDA: The growth of some cancers of the breast is stimulated or maintained by estrogens. Treatment of breastcancer thought to be hormonally responsive (i.e., estrogen and/or progesterone receptor positive orreceptor unknown) has included a variety of efforts to decrease estrogen levels (ovariectomy,adrenalectomy, hypophysectomy) or inhibit estrogen effects (antiestrogens and progestational agents).These interventions lead to decreased tumor mass or delayed progression of tumor growth in somewomen.In postmenopausal women, estrogens are mainly derived from the action of the aromatase enzyme, whichconverts adrenal androgens (primarily androstenedione and testosterone) to estrone and estradiol. Thesuppression of estrogen biosynthesis in peripheral tissues and in the cancer tissue itself can therefore beachieved by specifically inhibiting the aromatase enzyme.Letrozole is a nonsteroidal competitive inhibitor of the aromatase enzyme system; it inhibits theconversion of androgens to estrogens. In adult nontumor- and tumor-bearing female animals, letrozole isas effective as ovariectomy in reducing uterine weight, elevating serum LH, and causing the regression ofestrogen-dependent tumors. In contrast to ovariectomy, treatment with letrozole does not lead to anincrease in serum FSH. Letrozole selectively inhibits gonadal steroidogenesis but has no significant effecton adrenal mineralocorticoid or glucocorticoid synthesis.Letrozole inhibits the aromatase enzyme by competitively binding to the heme of the cytochrome P450subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues. Treatment of womenwith letrozole significantly lowers serum estrone, estradiol and estrone sulfate and has not been shown tosignificantly affect adrenal corticosteroid synthesis, aldosterone synthesis, or synthesis of thyroidhormones.
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| 15 |
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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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| 16 |
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Gliadel Wafer
18
49
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CARMUSTINE |
Rhone-Poulenc Rorer, Guilford Pharmaceuticals |
February 1997 |
Disease/s that Drug Treats:brain cancer
Indications and Usage:
18
GLIADELWaferisanalkylatingdrugindicatedforthetreatmentof: newly-diagnosedhigh-grade-malignantgliomaasanadjuncttosurgeryandradiation(1)and recurrentglioblastomamultiformeasanadjuncttosurgery(1)
DrugBank Targets:
16
1. Glutathione reductase, mitochondrial;2. DNA;3. RNA
Mechanism of Action:
18
Target: DNA and RNA
Action: alkylating agent
FDA: The activity of GLIADEL Wafer is due to release of cytotoxic concentrations of carmustine, aDNA and RNA alkylating agent, into the tumor resection cavity. On exposure to the aqueousenvironment of the resection cavity, the anhydride bonds in the copolymer are hydrolyzed,releasing carmustine, carboxyphenoxypropane, and sebacic acid into the surrounding braintissue.
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| 17 |
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Iclusig
18
49
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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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| 18 |
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Imbruvica
18
49
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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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| 19 |
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Ixempra
18
49
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IXABEPILONE |
Bristol-Myers Squibb |
October 2007 |
Disease/s that Drug Treats:Breast cancer
Indications and Usage:
18
IXEMPRA, a microtubule inhibitor, in combination with capecitabine isindicated for the treatment of metastatic or locally advanced breastcancer in patients after failure of an anthracycline and a taxane (1). IXEMPRA as monotherapy is indicated for the treatment of metastaticor locally advanced breast cancer in patients after failure of ananthracycline, a taxane, and capecitabine (1).
DrugBank Targets:
16
1. Tubulin beta-3 chain
Mechanism of Action:
18
Target: β-tubulin subunits on microtubules
Action: suppressor of dynamics
FDA: Ixabepilone is a semi-synthetic analog of epothilone B. Ixabepilone binds directlyto β-tubulin subunits on microtubules, leading to suppression of microtubule dynamics.Ixabepilone suppresses the dynamic instability of αβ-II and αβ-III microtubules.Ixabepilone possesses low in vitro susceptibility to multiple tumor resistance mechanisms including efflux transporters, such as MRP-1 and P-glycoprotein (P-gp). Ixabepiloneblocks cells in the mitotic phase of the cell division cycle, leading to cell death.
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| 20 |
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Jevtana
18
49
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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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| 21 |
|
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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| 22 |
|
Kadian
18
|
MORPHINE SULFATE |
Purepac Pharmaceutical |
July 1996 |
Disease/s that Drug Treats:chronic pain
Indications and Usage:
18
KADIAN is an opioid agonist indicated for the management of pain severeenough to require daily, around-the-clock, long-term opioid treatment and forwhich alternative treatment options are inadequate.Limitations of Use Because of the risks of addiction, abuse, and misuse with opioids, even atrecommended doses, and because of the greater risks of overdose anddeath with extended-release opioid formulations, reserve KADIAN foruse in patients for whom alternative treatment options (e.g., non-opioidanalgesics or immediate-release opioids) are ineffective, not tolerated, orwould be otherwise inadequate to provide sufficient management of pain. KADIAN is not indicated as an as-needed (prn) analgesic.
DrugBank Targets:
16
1. Mu-type opioid receptor;2. Kappa-type opioid receptor;3. Delta-type opioid receptor
Mechanism of Action:
18
Target: opioid receptors
Action: agonist
FDA: Morphine sulfate, an opioid agonist, is relatively selective for the mu receptor, although it can interactwith other opioid receptors at higher doses. In addition to analgesia, the widely diverse effects ofmorphine sulfate include analgesia, dysphoria, euphoria, somnolence, respiratory depression, diminishedgastrointestinal motility, altered circulatory dynamics, histamine release, physical dependence, andalterations of the endocrine and autonomic nervous systems.Morphine produces both its therapeutic and its adverse effects by interaction with one or more classes ofspecific opioid receptors located throughout the body. Morphine acts as a full agonist, binding with andactivating opioid receptors at sites in the peri-aqueductal and peri-ventricular grey matter, the ventromedialmedulla and the spinal cord to produce analgesia.
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| 23 |
|
Kytril
18
|
GRANISETRON HYDROCHLORIDE |
Roche/SmithKline Beecham |
June 2001/ November 1997 |
Disease/s that Drug Treats:nausea and vomiting associated with chemotherapy
Indications and Usage:
18
KYTRIL Injection is a serotonin-3 (5-HT3) receptor antagonist indicated for: Prevention of nausea and/or vomiting associated with initial and repeatcourses of emetogenic cancer therapy, including high-dose cisplatin. (1) Prevention and treatment of postoperative nausea and vomiting in adults.(1)--------------
DrugBank Targets:
16
1. 5-hydroxytryptamine receptor 3A
Mechanism of Action:
18
Target: 5-hydroxytryptamine3 (5-HT3) receptor
Action: antagonist
FDA: Granisetron is a selective 5-hydroxytryptamine3 (5-HT3) receptor antagonist with little or no affinity for otherserotonin receptors, including 5-HT1; 5-HT1A; 5-HT1B/C; 5-HT2; for alpha1-, alpha2- or beta-adrenoreceptors; fordopamine-D2; or for histamine-H1; benzodiazepine; picrotoxin or opioid receptors. Serotonin receptors of the 5-HT3 type are located peripherally on vagal nerve terminals and centrally in thechemoreceptor trigger zone of the area postrema. During chemotherapy-induced vomiting, mucosalenterochromaffin cells release serotonin, which stimulates 5-HT3 receptors. This evokes vagal afferentdischarge and may induce vomiting. Animal studies demonstrate that, in binding to 5-HT3 receptors, granisetronblocks serotonin stimulation and subsequent vomiting after emetogenic stimuli such as cisplatin. In the ferretanimal model, a single granisetron injection prevented vomiting due to high-dose cisplatin or arrested vomitingwithin 5 to 30 seconds.In most human studies, granisetron has had little effect on blood pressure, heart rate or ECG. No evidence of aneffect on plasma prolactin or aldosterone concentrations has been found in other studies.KYTRIL Injection exhibited no effect on oro-cecal transit time in normal volunteers given a single intravenousinfusion of 50 mcg/kg or 200 mcg/kg. Single and multiple oral doses slowed colonic transit in normalvolunteers.
|
| 24 |
|
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.
|
| 25 |
|
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.
|
| 26 |
|
Lupron Depot
18
49
|
LEUPROLIDE ACETATE |
TAP Pharmaceuticals/ Abbott Laboratories |
July 1997/ January 1996 |
Disease/s that Drug Treats:prostate cancer
Indications and Usage:
18
LUPRON DEPOT is a gonadotropin releasing hormone (GnRH) agonistindicated for: palliative treatment of advanced prostatic cancer. (1)
DrugBank Targets:
16
1. Gonadotropin-releasing hormone receptor
Mechanism of Action:
18
Target: GnRH
Action: agonist
FDA: Leuprolide acetate, a GnRH agonist, acts as an inhibitor of gonadotropin secretion. Animalstudies indicate that following an initial stimulation, continuous administration of leuprolideacetate results in suppression of ovarian and testicular steroidogenesis. This effect was reversibleupon discontinuation of drug therapy.Administration of leuprolide acetate has resulted in inhibition of the growth of certain hormonedependent tumors (prostatic tumors in Noble and Dunning male rats and DMBA-inducedmammary tumors in female rats) as well as atrophy of the reproductive organs.
|
| 27 |
|
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.
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| 28 |
|
Neulasta
18
|
PEGFILGRASTIM |
Amgen |
January 2002 |
Disease/s that Drug Treats:Neutropenia
Indications and Usage:
18
Neulasta is a man-made form of granulocyte colony-stimulating factor (G-CSF), which is made using the bacteriaEscherichia coli. G-CSF is a substance produced by the body. It stimulates the growth of neutrophils (nu-tro-fils),a type of white blood cell important in the bodyâs fight against infection.
DrugBank Targets:
16
1. Granulocyte colony-stimulating factor receptor;2. Neutrophil elastase
Mechanism of Action:
18
Target: hematopoietic cells
Action: stimulates proliferation
FDA: -
|
| 29 |
|
Neutroval
18
|
tbo-filgrastim |
Teva Pharmaceutical |
August 2012 |
Disease/s that Drug Treats:severe chemotherapy-induced neutropenia
Indications and Usage:
18
DrugBank Targets:
16
1. Granulocyte colony-stimulating factor receptor;2. Neutrophil elastase
Mechanism of Action:
18
Target: G-CSF receptors
Action: stimulates proliferation of neutrofils
FDA: -
|
| 30 |
|
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.
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| 31 |
|
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.
|
| 32 |
|
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.
|
| 33 |
|
Picato gel
18
|
INGENOL MEBUTATE |
LEO Pharma |
January 2012 |
Disease/s that Drug Treats:actinic keratosis
Indications and Usage:
18
Picato® gel is an inducer of cell death indicated for the topical treatment ofactinic keratosis. (1)
DrugBank Targets:
16
1. Protein kinase C delta type;2. Protein kinase C alpha type
Mechanism of Action:
18
Target: AK lesions
Action: inducer of apoptosis (otherwise, mechanism of action is unknown)
FDA: The mechanism of action by which Picato® gel induces cell death in treating AK lesions isunknown.
|
| 34 |
|
Plenaxis
18
|
ABARELIX |
Praecis Pharmaceuticals |
December 2003 |
Disease/s that Drug Treats:Prostate Cancer
Indications and Usage:
18
Plenaxis⢠is indicated for the palliative treatment of men with advanced symptomaticprostate cancer, in whom LHRH agonist therapy is not appropriate and who refusesurgical castration, and have one or more of the following: (1) risk of neurologicalcompromise due to metastases, (2) ureteral or bladder outlet obstruction due to localencroachment or metastatic disease, or (3) severe bone pain from skeletal metastasespersisting on narcotic analgesia.
DrugBank Targets:
16
1. Gonadotropin-releasing hormone receptor
Mechanism of Action:
18
Target: GnRH receptors in the pituitary gland
Action: competitive blocker
FDA: -
|
| 35 |
|
Pomalyst
18
49
|
POMALIDOMIDE |
Celgene |
February 2013 |
Disease/s that Drug Treats:relapsed and refractory multiple myeloma
Indications and Usage:
18
POMALYST is a thalidomide analogue indicated, in combination withdexamethasone, for patients with multiple myeloma who have received atleast two prior therapies including lenalidomide and a proteasome inhibitorand have demonstrated disease progression on or within 60 days ofcompletion of the last therapy (1.1).
DrugBank Targets:
16
1. Protein cereblon;2. Tumor necrosis factor;3. Prostaglandin G/H synthase 2
Mechanism of Action:
18
Target: hematopoietic tumor cells, lenalidomide-resistant multiple myeloma cell lines/ T-cells
Action: inhibitor of proliferation/ inducer of apoptosis/ enhancer of natural killer cell-mediated immunity
FDA: Pomalidomide, an analogue of thalidomide, is an immunomodulatory agent with antineoplasticactivity. In in vitro cellular assays, pomalidomide inhibited proliferation and induced apoptosis of hematopoietic tumor cells. Additionally, pomalidomide inhibited the proliferation oflenalidomide-resistant multiple myeloma cell lines and synergized with dexamethasone in bothlenalidomide-sensitive and lenalidomide-resistant cell lines to induce tumor cell apoptosis.Pomalidomide enhanced T cell- and natural killer (NK) cell-mediated immunity and inhibitedproduction of pro-inflammatory cytokines (e.g., TNF-α and IL-6) by monocytes. Pomalidomidedemonstrated anti-angiogenic activity in a mouse tumor model and in the in vitro umbilical cordmodel.
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| 36 |
|
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.
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| 37 |
|
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.
|
| 38 |
|
Quadramet
18
|
SAMARIUM SM-153 LEXIDRONAM PENTASODIUM |
DuPont Merck Pharmaceutical Company |
March 1997 |
Disease/s that Drug Treats:pain associated with bone cancer
Indications and Usage:
18
DrugBank Targets:
-
Mechanism of Action:
18
Target: osteoblastic tumor sites
Action: irradiator
FDA: -
|
| 39 |
|
Sancuso
18
|
GRANISETRON |
ProStrakan |
September 2008 |
Disease/s that Drug Treats:chemotherapy-induced nausea and vomiting
Indications and Usage:
18
Sancuso is a serotonin subtype 3 (5-HT3) receptor antagonist indicated for theprevention of nausea and vomiting in patients receiving moderately and/orhighly emetogenic chemotherapy for up to 5 consecutive days. (1)
DrugBank Targets:
16
1. 5-hydroxytryptamine receptor 3A
Mechanism of Action:
18
Target: 5-hydroxytryptamine3 (5-HT3) receptor
Action: agonist
FDA: Granisetron is a selective 5-hydroxytryptamine3 (5-HT3) receptor antagonist with little or no affinityfor other serotonin receptors, including 5-HT1, 5-HT1A, 5-HT1B/C, 5-HT2; for alpha1-, alpha2-, or betaadrenoreceptors;for dopamine-D2; or for histamine-H1; benzodiazepine; picrotoxin or opioidreceptors.Serotonin receptors of the 5-HT3 type are located peripherally on vagal nerve terminals and centrallyin the chemoreceptor trigger zone of the area postrema. During chemotherapy that inducesvomiting, mucosal enterochromaffin cells release serotonin, which stimulates 5-HT3 receptors. Thisevokes vagal afferent discharge, inducing vomiting. Animal studies demonstrate that, in binding to5-HT3 receptors, granisetron blocks serotonin stimulation and subsequent vomiting after emetogenicstimuli such as cisplatin. In the ferret animal model, a single granisetron injection preventedvomiting due to high-dose cisplatin or arrested vomiting within 5 to 30 seconds.
|
| 40 |
|
Sclerosol Intrapleural Aerosol
18
49
|
TALC |
Bryan Corporation |
January 1998 |
Disease/s that Drug Treats:malignant pleural effusions
Indications and Usage:
18
Sclerosol® Intrapleural Aerosol, administered by aerosol during thoracoscopy or openthoracotomy, is indicated to prevent recurrence of malignant pleural effusions in symptomaticpatients. , Sclerosol® Intrapleural Aerosol, administered by aerosol during thoracoscopy or open thoracotomy, is indicated to prevent recurrence of malignant pleural effusions in symptomatic patients.
DrugBank Targets:
-
Mechanism of Action:
18
Target: pleural cavity,
Action: inducer of inflammatory reaction,
FDA: The therapeutic action of talc instilled into the pleural cavity is thought to result from inductionof an inflammatory reaction. This reaction promotes adherence of the visceral to the parietalpleura, obliterating the pleural space and preventing reaccumulation of pleural fluid. The extentof talc systemically absorbed after intrapleural administration has not been adequately studied.Systemic exposure could be affected by the integrity of the visceral pleura, and therefore couldbe increased if talc is administered immediately following lung resection or biopsy. , The therapeutic action of talc instilled into the pleural cavity is thought to result from induction of an inflammatory reaction. This reaction promotes adherence of the visceral to the parietal pleura, obliterating the pleural space and preventing reaccumulation of pleural fluid. The extent of talc systemically absorbed after intrapleural administration has not been adequately studied. Systemic exposure could be affected by the integrity of the visceral pleura, and therefore could be increased if talc is administered immediately following lung resection or biopsy.
|
| 41 |
|
Stivarga
18
49
|
REGORAFENIB |
Bayer/ Bayer HealthCare Pharmaceuticals |
February 2013/ September 2012 |
Disease/s that Drug Treats:gastrointestinal stromal tumor/ metastatic colorectal cancer
Indications and Usage:
18
Stivarga is a kinase inhibitor indicated for the treatment of patients with: Metastatic colorectal cancer (CRC) who have been previously treated withfluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, an antiVEGFtherapy, and, if KRAS wild type, an anti-EGFR therapy. (1.1) Locally advanced, unresectable or metastatic gastrointestinal stromal tumor(GIST) who have been previously treated with imatinib mesylate andsunitinib malate. (1.2)
DrugBank Targets:
16
1. Proto-oncogene tyrosine-protein kinase receptor Ret;2. Vascular endothelial growth factor receptor 1;3. Vascular endothelial growth factor receptor 2;4. Vascular endothelial growth factor receptor 3;5. Mast/stem cell growth factor receptor Kit;6. Platelet-derived growth factor receptor alpha;7. Platelet-derived growth factor receptor beta;8. Fibroblast growth factor receptor 1;9. Fibroblast growth factor receptor 2;10. Angiopoietin-1 receptor;11. Discoidin domain-containing receptor 2;12. High affinity nerve growth factor receptor;13. Ephrin type-A receptor 2;14. RAF proto-oncogene serine/threonine-protein kinase;15. Serine/threonine-protein kinase B-raf;16. Mitogen-activated protein kinase 11;17. Tyrosine-protein kinase FRK;18. Tyrosine-protein kinase ABL1
Mechanism of Action:
18
Target: RET, VEGFR1, VEGFR2, VEGFR3, KIT, PDGFR-alpha, PDGFR-beta, FGFR1, FGFR2,TIE2, DDR2, TrkA, Eph2A, RAF-1, BRAF, BRAFV600E , SAPK2, PTK5, and Abl kinases
Action: inhibitor
FDA: Regorafenib is a small molecule inhibitor of multiple membrane-bound and intracellular kinases involved in normalcellular functions and in pathologic processes such as oncogenesis, tumor angiogenesis, and maintenance of the tumormicroenvironment. In in vitro biochemical or cellular assays, regorafenib or its major human active metabolites M-2 andM-5 inhibited the activity of RET, VEGFR1, VEGFR2, VEGFR3, KIT, PDGFR-alpha, PDGFR-beta, FGFR1, FGFR2,TIE2, DDR2, TrkA, Eph2A, RAF-1, BRAF, BRAFV600E , SAPK2, PTK5, and Abl at concentrations of regorafenib thathave been achieved clinically. In in vivo models, regorafenib demonstrated anti-angiogenic activity in a rat tumor model,and inhibition of tumor growth as well as anti-metastatic activity in several mouse xenograft models including some forhuman colorectal carcinoma.
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Subsys
18
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FENTANYL |
Insys Therapeutics |
January of 2012 |
Disease/s that Drug Treats:breakthrough cancer pain
Indications and Usage:
18
SUBSYS is an opioid agonist indicated for the management of breakthroughpain in cancer patients 18 years of age and older who are already receivingand who are tolerant to opioid therapy for their underlying persistent cancerpain. Patients must remain on around-the-clock opioids when takingSUBSYS. (1)Limitations of Use:SUBSYS 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 receptors?
Action: agonist
FDA: Fentanyl is an opioid agonist whose principal therapeutic action is analgesia.Other members of the class known as opioid agonists include substances such asmorphine, oxycodone, hydromorphone, codeine, and hydrocodone.
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Sutent
18
49
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SUNITINIB MALATE |
Pfizer |
May 2011/ January 2006 |
Disease/s that Drug Treats:pancreatic neuroendocrine tumors/ Kidney Cancer/Gastrointestinal Stromal Tumors
Indications and Usage:
18
SUTENT is a kinase inhibitor indicated for the treatment of: Gastrointestinal stromal tumor (GIST) after disease progression on orintolerance to imatinib mesylate. (1.1) Advanced renal cell carcinoma (RCC). (1.2) Progressive, well-differentiated pancreatic neuroendocrine tumors(pNET) in patients with unresectable locally advanced or metastaticdisease. (1.3)
DrugBank Targets:
16
1. Platelet-derived growth factor receptor beta;2. Vascular endothelial growth factor receptor 1;3. Mast/stem cell growth factor receptor Kit;4. Vascular endothelial growth factor receptor 2;5. Vascular endothelial growth factor receptor 3;6. Receptor-type tyrosine-protein kinase FLT3;7. Macrophage colony-stimulating factor 1 receptor;8. Platelet-derived growth factor receptor alpha
Mechanism of Action:
18
Target: variety of kinases, platelet-derived growth factor receptors (PDGFRα and PDGFRβ), vascular endothelial growth factorreceptors (VEGFR1, VEGFR2 and VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3(FLT3), colony stimulating factor receptor Type 1 (CSF-1R), and the glial cell-line derived neurotrophic factorreceptor (RET)
Action: inhibitor
FDA: Sunitinib is a small molecule that inhibits multiple receptor tyrosine kinases (RTKs), some of which areimplicated in tumor growth, pathologic angiogenesis, and metastatic progression of cancer. Sunitinib wasevaluated for its inhibitory activity against a variety of kinases (>80 kinases) and was identified as an inhibitorof platelet-derived growth factor receptors (PDGFRα and PDGFRβ), vascular endothelial growth factorreceptors (VEGFR1, VEGFR2 and VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3(FLT3), colony stimulating factor receptor Type 1 (CSF-1R), and the glial cell-line derived neurotrophic factorreceptor (RET). Sunitinib inhibition of the activity of these RTKs has been demonstrated in biochemical andcellular assays, and inhibition of function has been demonstrated in cell proliferation assays. The primarymetabolite exhibits similar potency compared to sunitinib in biochemical and cellular assays.Sunitinib inhibited the phosphorylation of multiple RTKs (PDGFRï¢, VEGFR2, KIT) in tumor xenograftsexpressing RTK targets in vivo and demonstrated inhibition of tumor growth or tumor regression and/orinhibited metastases in some experimental models of cancer. Sunitinib demonstrated the ability to inhibitgrowth of tumor cells expressing dysregulated target RTKs (PDGFR, RET, or KIT) in vitro and to inhibitPDGFRï¢- and VEGFR2-dependent tumor angiogenesis in vivo.
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Synercid I.V.
18
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DALFOPRISTIN; QUINUPRISTIN QUINUPRISTIN; DALFOPRISTIN |
Rhone Poulenc Rorer |
September 1999 |
Disease/s that Drug Treats:For serious or life-threatening infections associated w/ vancomycin-resistant Enterococcus faecium (VREF) bacteremia.
Indications and Usage:
18
Synercid is indicated in adults for the treatment of the following infections when caused bysusceptible strains of the designated microorganisms.Complicated skin and skin structure infections caused by Staphylococcus aureus (methicillinsusceptible) or Streptococcus pyogenes. (See CLINICAL STUDIES.)
DrugBank Targets:
16
16
1. Streptogramin A acetyltransferase| 1. 23S rRNA;2. 50S ribosomal protein L10;3. 50S ribosomal protein L22
Mechanism of Action:
18
Target: bacterial ribosome - protien synthesis
Action: inhibitor
FDA: The site of action of quinupristin and dalfopristin is the bacterial ribosome. Dalfopristin has beenshown to inhibit the early phase of protein synthesis while quinupristin inhibits the late phase ofprotein synthesis. Synercid is bactericidal against isolates of methicillin-susceptible andmethicillin-resistant staphylococci. The mode of action of Synercid differs from that of otherclasses of antibacterial agents such as Ã-lactams, aminoglycosides, glycopeptides, quinolones,macrolides, lincosamides and tetracyclines. Therefore, there is no cross resistance betweenSynercid and these agents when tested by the minimum inhibitory concentration (MIC) method.
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Taxol
18
49
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PACLITAXEL |
Bristol-Myers Squibb |
August 1997 |
Disease/s that Drug Treats:Kaposi's Sarcoma
Indications and Usage:
18
Paclitaxel Injection, USP is indicated as subsequent therapy for the treatment of advanced carcinoma ofthe ovary. As first-line therapy, Paclitaxel Injection, USP is indicated in combination with cisplatin.Paclitaxel Injection, USP is indicated for the adjuvant treatment of node-positive breast canceradministered sequentially to standard doxorubicin-containing combination chemotherapy.. In the clinicaltrial, there was an overall favorable effect on disease-free and overall survival in the total population ofpatients with receptor-positive and receptor-negative tumors, but the benefit has been specifically demonstrated by available data (median follow-up 30 months) only in the patients with estrogen andprogesterone receptor-negative tumors (see CLINICAL STUDIES, Breast Carcinoma).Paclitaxel Injection, USP is indicated for the treatment of breast cancer after failure of combinationchemotherapy for metastatic disease or relapse within 6 months of adjuvant chemotherapy. Prior therapyshould have included an anthracycline unless clinically contraindicated.Paclitaxel Injection, USP, in combination with cisplatin, is indicated for the first-line treatment of nonsmallcell lung cancer in patients who are not candidates for potentially curative surgery and/or radiationtherapy.Paclitaxel Injection, USP is indicated for the second-line treatment of AIDS-related Kaposiâs sarcoma.
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
Mechanism of Action:
18
Target: microtubules
Action: promoter of assembly & preventor of depolymerization
FDA: Paclitaxel is a novel antimicrotubule agent that promotes the assembly of microtubules from tubulindimers and stabilizes microtubules by preventing depolymerization. This stability results in the inhibitionof the normal dynamic reorganization of the microtubule network that is essential for vital interphase andmitotic cellular functions. In addition, paclitaxel induces abnormal arrays or âbundlesâ of microtubulesthroughout the cell cycle and multiple asters of microtubules during mitosis.Following intravenous administration of paclitaxel, paclitaxel plasma concentrations declined in abiphasic manner. The initial rapid decline represents distribution to the peripheral compartment andelimination of the drug. The later phase is due, in part, to a relatively slow efflux of paclitaxel from theperipheral compartment.Pharmacokinetic parameters of paclitaxel following 3- and 24-hour infusions of paclitaxel at dose levelsof 135 and 175 mg/m2 were determined in a Phase 3 randomized study in ovarian cancer patients and aresummarized in the following table:
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Trelstar Depot/ Trelstar LA
18
|
TRIPTORELIN PAMOATE |
Debio Rechereche Pharmaceutique, Target Research Associates/ Debiopharm |
June 2000/ June 2001 |
Disease/s that Drug Treats:advanced prostate cancer/ Prostate cancer
Indications and Usage:
18
TRELSTAR is a gonadotropin releasing hormone (GnRH) agonist indicated for the palliative treatmentof advanced prostate cancer. (1)
DrugBank Targets:
-
Mechanism of Action:
18
Target: gonadotropin releasing hormone (GnRH)
Action: agonist
FDA: Triptorelin is a synthetic decapeptide agonist analog of gonadotropin releasing hormone (GnRH).Comparative in vitro studies showed that triptorelin was 100-fold more active than native GnRH instimulating luteinizing hormone release from monolayers of dispersed rat pituitary cells in culture and20-fold more active than native GnRH in displacing 125I-GnRH from pituitary receptor sites. In animalstudies, triptorelin pamoate was found to have 13âfold higher luteinizing hormone-releasing activity and21-fold higher follicle-stimulating hormone-releasing activity compared to the native GnRH.
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| 47 |
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Trisenox
18
49
|
ARSENIC TRIOXIDE |
Cell Therapeutics |
September 2000 |
Disease/s that Drug Treats:Acute Promyelocytic Leukemia
Indications and Usage:
18
TRISENOX is an arsenical indicated for induction of remission andconsolidation in patients with acute promyelocytic leukemia (APL) who arerefractory to, or have relapsed from, retinoid and anthracycline chemotherapy,and whose APL is characterized by the presence of the t(15;17) translocationor PML/RAR-alpha gene expression.
DrugBank Targets:
16
1. Inhibitor of nuclear factor kappa-B kinase subunit beta;2. Thioredoxin reductase 1, cytoplasmic;3. Transcription factor AP-1;4. G1/S-specific cyclin-D1;5. Mitogen-activated protein kinase 3;6. Mitogen-activated protein kinase 1;7. RAC-alpha serine/threonine-protein kinase
Mechanism of Action:
18
Target: DNA/ promyelocytic leukemia (PML)-retinoic acid receptor (RAR)-alpha
Action: damager
FDA: The mechanism of action of TRISENOX is not completely understood. Arsenic trioxide causes morphologicalchanges and DNA fragmentation characteristic of apoptosis in NB4 human promyelocytic leukemia cells invitro. Arsenic trioxide also causes damage or degradation of the fusion protein promyelocytic leukemia (PML)-retinoic acid receptor (RAR)-alpha.
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UltraJect
18
|
MORPHINE SULFATE |
Mallinckrodt Group |
August 1996 |
Disease/s that Drug Treats:chronic pain
Indications and Usage:
18
DrugBank Targets:
16
1. Mu-type opioid receptor;2. Kappa-type opioid receptor;3. Delta-type opioid receptor
Mechanism of Action:
18
Target: -
Action: -
FDA: -
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Unituxin
18
49
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DINUTUXIMAB |
United Therapeutics |
March 2015 |
Disease/s that Drug Treats:pediatrics with high-risk neuroblastoma
Indications and Usage:
18
Unituxin is a GD2-binding monoclonal antibody indicated, incombination with granulocyte-macrophage colony-stimulating factor(GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for thetreatment of pediatric patients with high-risk neuroblastoma whoachieve at least a partial response to prior first-line multiagent,multimodality therapy. (1)
DrugBank Targets:
16
1. Ganglioside GD2
Mechanism of Action:
18
Target: GD2
Action: inducer of cell lysis through ADCC and CDC
FDA: Dinutuximab binds to the glycolipid GD2. This glycolipid is expressed on neuroblastoma cellsand on normal cells of neuroectodermal origin, including the central nervous system andperipheral nerves. Dinutuximab binds to cell surface GD2 and induces cell lysis of GD2-expressing cells through antibody-dependent cell-mediated cytotoxicity (ADCC) andcomplement-dependent cytotoxicity (CDC).
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Vandetanib
18
49
|
vandetanib |
AstraZeneca |
April 2011 |
Disease/s that Drug Treats:thyroid cancer
Indications and Usage:
18
DrugBank Targets:
16
1. Vascular endothelial growth factor A;2. Epidermal growth factor receptor;3. Protein-tyrosine kinase 6;4. Angiopoietin-1 receptor
Mechanism of Action:
18
Target: tyrosine kinases
Action: inhibitor
FDA: -
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