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Statements

Subject Item
n2:DB00619
rdf:type
n11:Drug
n11:description
Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells.
n11:dosage
n26:271B576C-363D-11E5-9242-09173F13E4C5 n26:271B576B-363D-11E5-9242-09173F13E4C5
n11:generalReferences
# Deininger MW, Druker BJ: Specific targeted therapy of chronic myelogenous leukemia with imatinib. Pharmacol Rev. 2003 Sep;55(3):401-23. Epub 2003 Jul 17. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/12869662 # Vigneri P, Wang JY: Induction of apoptosis in chronic myelogenous leukemia cells through nuclear entrapment of BCR-ABL tyrosine kinase. Nat Med. 2001 Feb;7(2):228-34. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/11175855 # Droogendijk HJ, Kluin-Nelemans HJ, van Doormaal JJ, Oranje AP, van de Loosdrecht AA, van Daele PL: Imatinib mesylate in the treatment of systemic mastocytosis: a phase II trial. Cancer. 2006 Jul 15;107(2):345-51. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/16779792 # Lassila M, Allen TJ, Cao Z, Thallas V, Jandeleit-Dahm KA, Candido R, Cooper ME: Imatinib attenuates diabetes-associated atherosclerosis. Arterioscler Thromb Vasc Biol. 2004 May;24(5):935-42. Epub 2004 Feb 26. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/14988091 # Reeves PM, Bommarius B, Lebeis S, McNulty S, Christensen J, Swimm A, Chahroudi A, Chavan R, Feinberg MB, Veach D, Bornmann W, Sherman M, Kalman D: Disabling poxvirus pathogenesis by inhibition of Abl-family tyrosine kinases. Nat Med. 2005 Jul;11(7):731-9. Epub 2005 Jun 26. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/15980865
n11:group
approved
n11:halfLife
Following oral administration in healthy volunteers, the elimination half-lives of imatinib and its major active metabolite, the N-demethyl derivative (CGP74588) are approximately 18 and 40 hours, respectively.
n11:indication
For the treatment of Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML), Ph+ acute lymphoblastic leukaemia, myelodysplastic/myeloproliferative diseases, aggressive systemic mastocytosis, hypereosinophilic syndrome and/or chronic eosinophilic leukemia (CEL), dermatofibrosarcoma protuberans, and malignant gastrointestinal stromal tumors (GIST).
n11:manufacturer
n25:271B5768-363D-11E5-9242-09173F13E4C5
owl:sameAs
n23:DB00619 n28:DB00619
dcterms:title
Imatinib
adms:identifier
n4:DB00619 n7:45783 n8:5101 n9:STI n10:PA10804 n13:D01441 n14:0078-0401-34 n29:13530 n30:5291 n31:46505055 n32:Imatinib
n11:mechanismOfAction
Imatinib mesylate is a protein-tyrosine kinase inhibitor that inhibits the Bcr-Abl tyrosine kinase, the constitutive abnormal tyrosine kinase created by the Philadelphia chromosome abnormality in chronic myeloid leukemia (CML). It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia. Imatinib also inhibits the receptor tyrosine kinases for platelet derived growth factor (PDGF) and stem cell factor (SCF) - called c-kit. Imatinib was identified in the late 1990s by Dr Brian J. Druker. Its development is an excellent example of rational drug design. Soon after identification of the bcr-abl target, the search for an inhibitor began. Chemists used a high-throughput screen of chemical libraries to identify the molecule 2-phenylaminopyrimidine. This lead compound was then tested and modified by the introduction of methyl and benzamide groups to give it enhanced binding properties, resulting in imatinib.
n11:packager
n25:271B5767-363D-11E5-9242-09173F13E4C5 n25:271B5765-363D-11E5-9242-09173F13E4C5 n25:271B5766-363D-11E5-9242-09173F13E4C5
n11:patent
n15:6958335 n15:5521184 n15:2093203
n11:routeOfElimination
Imatinib elimination is predominately in the feces, mostly as metabolites. 81% of the dose is eliminated within 7 days, in feces (68% of the dose) and urine (13% of the dose). Unchanged imatinib accounted for 25% of the dose (5% urine, 20% faces), the remainder being metabolites.
n11:synonym
Imatinib Methansulfonate alpha-(4-Methyl-1-piperazinyl)-3'-((4-(3-pyridyl)-2-pyrimidinyl)amino)-P-toluidide Imatinibum 4-(4-METHYL-piperazin-1-ylmethyl)-N-[4-methyl-3-(4-pyridin-3-yl-pyrimidin-2-ylamino)-phenyl]-benzamide Imatinib STI 571
n11:toxicity
The most frequently reported adverse reactions (>30%) were edema, nausea, vomiting, muscle cramps, musculoskeletal pain, diarrhea, rash, fatigue and abdominal pain.
n18:hasAHFSCode
n19:92-00-00 n19:10-00-00
n11:foodInteraction
Take with food to reduce the incidence of gastric irritation. Follow with a large glass of water. A lipid rich meal will slightly reduce and delay absorption. Avoid grapefruit and grapefruit juice throughout treatment, grapefruit can significantly increase serum levels of this product.
n11:proteinBinding
95% protein bound, mostly to albumin and alpha-1-acid glycoprotein.
n11:salt
n11:synthesisReference
"DrugSyn.org":http://www.drugsyn.org/Imatinib.htm
n20:hasConcept
n21:M0424454
foaf:page
n6:gleevec.htm n16:imatinib.html
n11:IUPAC-Name
n12:271B5771-363D-11E5-9242-09173F13E4C5
n11:InChI
n12:271B5777-363D-11E5-9242-09173F13E4C5
n11:Molecular-Formula
n12:271B5776-363D-11E5-9242-09173F13E4C5
n11:Molecular-Weight
n12:271B5773-363D-11E5-9242-09173F13E4C5
n11:Monoisotopic-Weight
n12:271B5774-363D-11E5-9242-09173F13E4C5
n11:SMILES
n12:271B5775-363D-11E5-9242-09173F13E4C5
n11:Water-Solubility
n12:271B576F-363D-11E5-9242-09173F13E4C5 n12:271B5787-363D-11E5-9242-09173F13E4C5
n11:logP
n12:271B5770-363D-11E5-9242-09173F13E4C5 n12:271B576D-363D-11E5-9242-09173F13E4C5 n12:271B5789-363D-11E5-9242-09173F13E4C5
n11:logS
n12:271B576E-363D-11E5-9242-09173F13E4C5
n18:hasATCCode
n24:L01XE01
n11:H-Bond-Acceptor-Count
n12:271B577D-363D-11E5-9242-09173F13E4C5
n11:H-Bond-Donor-Count
n12:271B577E-363D-11E5-9242-09173F13E4C5
n11:InChIKey
n12:271B5778-363D-11E5-9242-09173F13E4C5
n11:Polar-Surface-Area--PSA-
n12:271B5779-363D-11E5-9242-09173F13E4C5
n11:Polarizability
n12:271B577B-363D-11E5-9242-09173F13E4C5
n11:Refractivity
n12:271B577A-363D-11E5-9242-09173F13E4C5
n11:Rotatable-Bond-Count
n12:271B577C-363D-11E5-9242-09173F13E4C5
n11:absorption
The pharmacokinetics in CML and GIST patients are similar. Imatinib is well absorbed with mean absolute bioavailability is 98% and maximum plasma levels achieved within 2-4 hours of dosing
n11:affectedOrganism
Humans and other mammals
n11:casRegistryNumber
152459-95-5
n11:category
n11:clearance
* 8 L/h [50-year-old CML and GIST patient weighing 50 kg] * 14 L/h [50-year-old CML and GIST patient weighing 100 kg]
n11:containedIn
n27:271B5769-363D-11E5-9242-09173F13E4C5 n27:271B576A-363D-11E5-9242-09173F13E4C5
n11:Bioavailability
n12:271B5783-363D-11E5-9242-09173F13E4C5
n11:Ghose-Filter
n12:271B5785-363D-11E5-9242-09173F13E4C5
n11:MDDR-Like-Rule
n12:271B5786-363D-11E5-9242-09173F13E4C5
n11:Melting-Point
n12:271B5788-363D-11E5-9242-09173F13E4C5
n11:Number-of-Rings
n12:271B5782-363D-11E5-9242-09173F13E4C5
n11:Physiological-Charge
n12:271B5781-363D-11E5-9242-09173F13E4C5
n11:Rule-of-Five
n12:271B5784-363D-11E5-9242-09173F13E4C5
n11:Traditional-IUPAC-Name
n12:271B5772-363D-11E5-9242-09173F13E4C5
n11:pKa--strongest-acidic-
n12:271B577F-363D-11E5-9242-09173F13E4C5
n11:pKa--strongest-basic-
n12:271B5780-363D-11E5-9242-09173F13E4C5