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At ASCO, Pfizer Presents Data on New Mutation-Targeting NSCLC Drug

ORLANDO, Fla. — An investigational drug developed by Pfizer to selectively attack certain genetic features of non-small cell lung cancer cells was able to stop or shrink tumor growth in a majority of patients enrolled in an early study, according to an abstract presented at the American Society of Clinical Oncology's annual meeting here this weekend.

PF-02341066, a dual inhibitor of mesenchymal epithelial transition growth factor (c-met) and anaplastic lymphoma kinase translocation genes, caused tumor shrinkage in 10 out of 19 patients for between two and 23 weeks in the Phase I study. The drug also stopped tumor growth in five patients for between eight weeks and 40 weeks.

The drug "is the first agent in clinical development that selectively targets a unique genetic feature of cancer cells," Pfizer said in a statement released at ASCO, where the theme of the annual meeting was personalizing cancer care.

Specifically, PF-02341066 targets echinoderm microtubule-associated protein-like 4 (EML4)-ALK translocation, which is present in some NSCLC patients. It is unclear if Pfizer is planning to market the drug with a companion diagnostic that can gauge which lung cancer patients express EML4-ALK mutations.

"Treatment with PF-02341066 resulted in promising clinical activity against tumors carrying activating ALK gene rearrangements. Further study of PF in patients with ALK-dependent tumors is warranted," concluded researchers from Massachusetts General Hospital Cancer Center and other institutions.

The abstract for the study, by Kwak et al., is available here.

For further details on this study and other personalized medicine abstracts from ASCO, see this week's issue of Pharmacogenomics Reporter.

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