Sunitinib, developed by Pfizer, is a novel multitargeted oral small molecule receptor tyrosine kinase inhibitor that inhibits multiple receptor tyrosine kinases associated with tumor proliferation, angiogenesis, and metastasis. Specifically, sunitinib is a potent ATP-competitive inhibitor that inhibits the catalytic activity of a closely related set of multiple receptor tyrosine kinases, including VEGFR-1, -2, and -3, PDGFR-α and -β, KIT, CSF-1R, FLT-3, and RET. Because of its multi-target profile, the pharmacological activity of sunitinib may be mediated by inhibition of multiple RTK targets and pathways mediated. Separate clinical pharmacokinetic studies were conducted for single and multiple dosing regimens of 25-50 mg per day. Treatment regimens included daily dosing for 4 or 2 consecutive weeks and discontinuation for 2 or 1 week (4/2, 2/2 and 2/1 regimens). The maximum blood concentration (Cmax) and area under the curve (AUC) of sunitinib increased proportionally with different doses over the dose range studied. Time to peak (Tmax) and half-life (T1/2) were not dose-dependently altered. Sunitinib is mainly metabolized by cytochrome enzyme P450 (CYP3A4) to produce the active N-desethyl metabolite SU012662. No other major metabolites have been identified so far. The terminal clearance half-lives of sunitinib are approximately 40 hours and 80 hours, respectively. A plateau of minimum blood concentrations was reached within the first 2 weeks of dosing. No dose accumulation was observed in multiple cycles of treatment. In two studies of sunitinib in Asian populations, primarily with Chinese and Japanese participants, pharmacokinetic and safety analyses were performed and no racial differences were found with data from Caucasians. Overall, the most common adverse events associated with sunitinib treatment were systemic symptoms (malaise/weakness), gastrointestinal reactions (nausea, diarrhea, stomatitis, dyspepsia), bone marrow suppression (neutropenia, thrombocytopenia) and skin reactions (dermatitis, skin color changes and hair discoloration). Few patients with solid tumors present with clinically significant granulocyte decline, and rare granulocyte-deficient fever.