Abstract
First- and third-generation epidermal growth factor receptor (EGFR) inhibitors such as gefitinib and osimertinib, respectively, have improved survival outcomes for patients with advanced EGFR-mutant NSCLC. However, acquired resistance invariably emerges, leading to disease progression. The predominant mechanism of acquired resistance is a tertiary mutation at C797 position of EGFR gene added to T790M mutation which is the most well-known resistance mechanism to 1st generation EGFR inhibitors. BBT-176 specifically and non-covalently inhibits triple-mutant EGFR (exon19del/T790M/C797S and L858R/T790M/C797S).
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