ArticleTranslational cancer research2025
A novel mesenchymal epithelial transition (MET) inhibitor, CB538, relieves acquired resistance in
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is the first-line standard therapy for metastatic Methods: The cellular inhibitory effects of single and co-treatment of CB538 with EGFR-TKIs were evaluated in the established EGFR-TKI-resistant cells [PC9/ER (erlotinib resistance), HCC827/OR (osimertinib resistance)]. The preclinical activities of CB538 were investigated by evaluating Results: We confirmed that activated MET/Axl signaling pathways and EMT-related proteins were inhibited by CB538 in established EGFR-TKI-resistant NSCLC cells. CB538, a novel c-MET inhibitor, decreased the growth, migration, and invasive properties of these EGFR-TKI-resistant NSCLC cells. CB538 also inhibited tumor growth and expression of activated proteins (MET and Axl) in Conclusions: Additional treatment with CB538 enhanced sensitivity to EGFR-TKIs in two EGFR-TKI-resistant NSCLC cells by inhibiting EGFR/MET/Axl pathway axis. Overall, the treatment effects of CB538 were confirmed to relieve EGFR-TKI-driven resistance in
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