Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-10-27
pubmed:abstractText
Imatinib is a clinically important inhibitor of tyrosine kinases that are dysregulated in chronic myelogenous leukaemia and gastrointestinal stromal tumours. Inter-individual variation in imatinib pharmacokinetics is extensive, and influences drug safety and efficacy. Hepatic cytochrome P450 (CYP) 3A4 has been implicated in imatinib N-demethylation, but the clearance of imatinib decreases during prolonged therapy. CYP3A phenotype correlates with imatinib clearance at the commencement of therapy, but not at steady state. The present study evaluated the possibility that multiple CYPs may contribute to imatinib oxidation in liver.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1476-5381
pubmed:author
pubmed:copyrightInfo
© 2010 The Authors. British Journal of Pharmacology © 2010 The British Pharmacological Society.
pubmed:issnType
Electronic
pubmed:volume
161
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1059-69
pubmed:dateRevised
2011-11-1
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Participation of CYP2C8 and CYP3A4 in the N-demethylation of imatinib in human hepatic microsomes.
pubmed:affiliation
Pharmacogenomics and Drug Development Group, Faculty of Pharmacy, University of Sydney, NSW, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't