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.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.