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Crizotinib is a c-MET inhibitor that has demonstrated potent inhibitory activity against ALK fusion cells. The document discusses clinical trials of crizotinib in patients with ALK-positive non-small cell lung cancer (NSCLC). Results from Phase I and II trials showed an objective response rate of 57% and disease control rate of 87% with crizotinib. Current ongoing trials are evaluating crizotinib versus chemotherapy as first-line or second-line treatment in ALK-positive NSCLC.

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Crizotinib (PF-02341066 ) c-MET inhibitor in Patient with Alk ( anaplastic lymphoma kinase ) -positive NSCLC ,[object Object],[object Object],[object Object],[object Object],Inamura K et al. J Thorac Oncol 2008;3:13–17 Soda M et al. Proc Natl Acad Sci U S A 2008;105:19893–19897 Chiarle R et al. Nat Rev Cancer 2008;8(1):11–23; Mossé YP et al. Clin Cancer Res 2009;15(18):5609–5614 Shaw AT et al. J Clin Oncol 2009;27:4247–4253 ; Inversion Translocation OR Break-apart FISH assay for ALK -fusion genes Non-split signal Split signal
Available data with crizotinib ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],ORR according to previous line therapies No. prior regimens* ORR % (n/N) 0 80 (4/5) 1 52 (14/27) 2 67 (10/15) ≥ 3 56 (19/34)
Current crizotinib clinical trials Available at: www.clinicaltrials.gov . NCT00890825 . http://www.clinicaltrials.gov/ct2/show/NCT00890825?term=NCT00890825&rank=1 ,[object Object],[object Object],[object Object],PHASE III PHASE II ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],R ,[object Object],PHASE III ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],R R ,[object Object],[object Object],[object Object],Primary Endpoint: PFS Primary Endpoint: PFS Primary Endpoint: ORR
 

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Editor's Notes

  1. Wilhelm SM, Carter C, Tang L, et al. BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis. Cancer Res . 2004;64:7099-7109. Liu L, Cao Y, Chen C, et al. Sorafenib blocks the RAF/MEK/ERK pathway, inhibits tumor angiogenesis, and induces tumor cell apoptosis in hepatocellular carcinoma model PLC/PRF/5. Cancer Res. 2006;66:11851-11858. Avila MA, Berasain C, Sangro B, Prieto J. New therapies for hepatocellular carcinoma. Oncogene . 2006;25:3866-3884. Semela D, Dufour JF. Angiogenesis and hepatocellular carcinoma. J Hepatol . 2004;41:864-880.