A novel mesenchymal epithelial transition (MET) inhibitor, CB538, relieves acquired resistance in <i>EGFR</i>-mutated <i>MET</i>-amplified non-small cell lung cancer.

ABSTRACT:

Background

Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is the first-line standard therapy for metastatic EGFR-mutated non-small cell lung cancer (NSCLC). Although osimertinib is effective, it's durable response is invariably limited by the emergence of acquired resistance. Mesenchymal epithelial transition (MET) amplification is a frequent mechanism in patients with EGFR-mutated NSCLC who are resistant to EGFR-TKIs. Consequently, combined treatment with EGFR-TKIs and MET-TKIs has been explored as a strategy for overcoming this resistance. The current study aimed to explore the single and combination inhibition effect of CB538, a novel MET inhibitor in MET-activated, EGFR-mutant NSCLC cells.

Methods

SUBMITTER: Song JY 

PROVIDER: S-EPMC11985202 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature