Abstract

MET amplification can arise as a bypass mechanism of resistance to EGFR tyrosine kinase inhibitors (TKIs) occurring in ∼5–26% of patients (pts) with EGFR TKI resistant EGFR-mutant non-small cell lung cancer (NSCLC). Few treatment options exist for these pts, particularly in the EGFR T790M negative (T790M−) setting. Capmatinib, a MET inhibitor, is approved in more than 10 countries for the treatment of metastatic MET exon 14 skipping NSCLC. Preliminary studies have shown that capmatinib plus EGFR TKIs demonstrated antitumor activity in pts with EGFR TKI resistant EGFR-mutant NSCLC.

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