Abstract

Osimertinib (Osi), a 3rd generation EGFR-TKI, has shown great efficacy in advanced NSCLC patients (pts) with EGFR sensitizing mutations and EGFR T790M resistance mutation, but the acquisition of resistance is inevitable and the treatment regimen is limited. As an oral multi-targeted tyrosine kinase inhibitor, anlotinib effectively inhibits tumor growth and angiogenesis. We found that anlotinib plus Osi showed favorable efficacy in a subset of Osi-resistant NSCLC pts in clinical practice. However, the underlying mechanism remains unclear.

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