Epidermal growth factor receptor (mutant selective) (EGFR (mutant selective))

The **epidermal growth factor receptor (EGFR) (mutant selective)** refers to a family of targeted therapeutic approaches and inhibitors that specifically bind and inhibit mutated forms of EGFR, a transmembrane receptor tyrosine kinase overactive in many cancers, especially non-small cell lung cancer (NSCLC)[1][2][4][9]. Mutations in EGFR—such as L858R, exon 19 deletions, T790M, and C797S—confer sensitivity or resistance to various generations of EGFR tyrosine kinase inhibitors (TKIs)[2][4][5][9]. Mutant-selective EGFR inhibitors are designed to selectively block only mutant variants, sparing wild-type EGFR to minimize side effects, and are used to overcome acquired drug resistance to earlier TKIs, including resistance mutations like T790M and C797S[2][8][9]. Drugs in this class include osimertinib, dacomitinib, BLU-945, BBT-176, and others, each with varying selectivity and clinical application[2][8][9][10]. EGFR mutation assays (by PCR or NGS) guide therapeutic selection, monitoring, and resistance profiling as biomarkers[4][5][9]. Safety concerns center on resistance development, toxicity related to wild-type EGFR inhibition (most notably rash and diarrhea), and managing CNS metastases[4][7][9].

Other names

EGFR (mutant selective)ErbB-1 (mutant selective)HER1 (mutant selective)Mutant EGFREGFR-activating mutationsMutant-selective EGFREGFR-TKI-sensitive EGFR

Inhibition of EGFR tyrosine kinase activity (mutation-selective); Irreversible binding to mutant EGFR kinase domain; Allosteric inhibition of EGFR mutants; Competitive ATP binding inhibition