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Introduction lung successful reversible reversible, reversible, reversible, irreversible active conf active irreversible as active conf. active Frequency in Frequency NSCLC in biochemical inactive conf. inactive a (ATP-bdg (ATP-bdg site) mutant Binding mode Binding kinases cell (ATP-bdg site; C797)) (ATP-bdg site; (ATP-bdg site; C797)) (ATP-bdg site; upon clinical well against towards their approved as used in the study the to of small different became - in a inhibitor non generation - mutations selectivity mutants an in respect analysis Resistence mutation Resistence mutation Resistence mutation Resistence Function activating activating activating activating activation next mutants of Introduction targeting of EGFR of EGFR inhibitors of challenge EGFR overall with Structure resistance the especially resistant potency . on of inhibitor comparative different 3) common the - a an a of generations Ref 1 Ref kinome Table 1: Overview of selected EGFR mutation found in NSCLC Table ( Ref. 4 modified) Ref. G718S L861Q P753S T790M C797S L718Q Mutation L853 d746 750 - d747 749 - d752 759 - Development Brigatinib (4th Gen. inh.) EGFR Afatinib Gen.(2nd inh.) EGFR Osimertinib Gen. inh.) (3rd EGFR Gefitinib (1st Gen. inh.) EGFR Lapatinib EGFR/HER2) (dual Drug Erlotinib (1st Gen. inh.) EGFR Table 2: Overview Table ( impact is induced - show . against therapies, four we towards occurrence human of ) the significant Here 1 potency inhibitors treatment cancer Modulation form The inhibitors