, followed by 5-fluorouracil 400 mg/m 2 bolus then 2400 mg/m 2 46-h infusion) every 2 weeks, and oral sunitinib 37.5 mg/day on Schedule 4/2 (4 weeks on, 2 weeks off), until disease progression or treatment withdrawal. Progression-free survival (PFS) was the primary endpoint, with a target median of 10.8 months (35% improvement over FOLFIRI alone). Seventy-one patients started a median of 3 (range 1-11) sunitinib cycles (median relative dose intensity, <60%). The median PFS was 6.7 months (95% confidence interval, 4.7-9.2) by independent review, 7.2 months (95% confidence interval, 5.4-9.5) by investigator assessment. Objective response rate (complete responses + partial responses) was 36.6% (independent review) and 42.3% (investigator assessment). Clinical benefit rate (complete responses + partial responses + stable disease) was 83.1% (independent review) and 88.7% (investigator assessment). Common all-causality, any-grade, adverse events were: neutropenia and leukopenia (both 97.2%); thrombocytopenia (84.5%); diarrhea and nausea (both 78.9%); decreased appetite (74.6%); and fatigue (66.2%). Neutropenia (96%) was the most frequent grade 3/4 adverse event. This study was closed early due to findings from a concurrent phase III study of sunitinib + FOLFIRI in non-Japanese patients with metastatic colorectal cancer. In conclusion, the median PFS for sunitinib + FOLFIRI in Japanese patients was shorter than the 10.8 month target, indicating that sunitinib did not add to the antitumor activity of FOLFIRI. This study was registered with ClinicalTrials.gov (NCT00668863). (Cancer Sci 2012; 103: 1502-1507 T he median survival of patients with metastatic CRC has improved over the past decade, from approximately 1 year with 5-FU-based monotherapy to approximately 2 years with combination systemic therapy.(1) FOLFIRI is now a standard first-line treatment for metastatic CRC.(1) The addition of other agents (typically the anti-VEGF mAb, bevacizumab) to FOLFIRI has improved patient outcomes.Sunitinib malate (SUTENT; Pfizer, New York, NY, USA) is an oral, multitargeted tyrosine kinase inhibitor of VEGFR-1, -2, and -3, platelet-derived growth factor receptors (-a and -b), stem cell factor receptor, FMS-like tyrosine kinase 3, colonystimulating factor 1 receptor, and glial cell line-derived neurotrophic receptor.(2-7) Sunitinib is currently approved multinationally for the treatment of advanced renal cell carcinoma and imatinib-resistant/-intolerant gastrointestinal stromal tumor. (8) It is also now approved for the treatment of unresectable or metastatic, well-differentiated pancreatic neuroendocrine tumors. (9) Sunitinib has shown antitumor activity in non-clinical CRC models, both as a single agent (4) and in combination with chemotherapy (Pfizer, unpublished data, 2002). In a phase II study of patients with previously treated metastatic CRC, singleagent sunitinib showed some evidence of efficacy (median OS, 10.2 months in patients with bevacizumab-naïve tumors; 7.1 months in patients with bevacizumab-pretreated tumors) and ...