Sunitinib blocks several tyrosine kinases, so it inhibits platelet-derived growth factor, vascular endothelial growth factor receptor, stem cell factor receptor, fms-like receptor growth factor, colony-stimulating growth factor receptor type 1, and glial-cell-line-derived neurotrophic factor receptor. The active metabolite of sunitinib blocks these same enzymes with similar potency. The pharmacokinetics of sunitinib demonstrate a time of peak concentration of about 5 hours, with a half-life of 41 to 86 hours.46 It is indicated for the treatment of GISTs after disease progression or intolerance to imat-inib. It is also indicated for the treatment of advanced renal cell cancer. Significant side effects include left ventricular dysfunction, hemorrhage, asthenia, hypertension, nausea and vomiting, and diarrhea. Approximately one-third of patients may develop a yellow color of the skin, along with dryness and cracking of the skin. Also, hair may become depigmented with doses of 50 mg/day or more, and the depigmentation is reversible when therapy is stopped. Clinically significant drug interactions exist with drugs metabolized via the CYP450 3A4 system; ketoconazole has been shown to increase concentrations of sunitinib, whereas rifampin has been shown to decrease concentrations of sunitinib.

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