Imatinib was the first FDA-approved tyrosine-kinase inhibitor. The drug was designed to block the breakpoint cluster region tyrosine kinase (BCR:ABL) produced by the Philadelphia chromosome associated with chronic myelogenous leukemia and acute lymphocytic leukemia. The pharmacokinetics of imatinib demonstrate a mean time to maximum concentration of 2 to 4 hours, with a terminal half-life of 15 hours.40 Imatinib also has shown activity against GI stroma tumors (GIST) that are positive for c-kit (CD117). Numerous drug interactions have been reported for imatinib. CYP450 3A4 inducers, such as rifampicin and St. John's wort, increase the clearance of imatinib.41,42 Ketoconazole, a CYP450 3A4 inhibitor, has been shown to decrease imatinib clearance by almost 30%.43 Imatinib also may increase the exposure of simvastatin, a CYP450 3A4 substrate.44

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