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

Mutant forms of the Epidermal growth factor receptor (EGFR) are cell-surface receptor tyrosine kinases affected by somatic mutations primarily within their kinase domain, most notably exon 19 deletions, L858R substitution (exon 21), and exon 20 insertions. These mutations lead to constitutive, growth factor-independent activation of signaling pathways crucial for cell survival, proliferation, and oncogenesis. EGFR mutants are critical drivers in non-small cell lung cancer and other malignancies, making them high-priority therapeutic targets; numerous drugs have been developed to target and inhibit their kinase activity, and specific mutant forms (e.g., T790M) are associated with acquired resistance to initial EGFR inhibitors[2][4]. Identification of EGFR mutations serves as both a predictive and prognostic biomarker to guide patient selection and therapy monitoring. Notable safety concerns for EGFR-targeted drugs include skin rash and lung toxicity[4].

Other names

EGFR mutantmutated EGFREGFR mutantsErbB1 mutantHER1 mutant

Inhibition of kinase activity (competitive ATP binding); Irreversible inhibition (covalent bonding, e.g., osimertinib)