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Overview
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Please contact us at for specific academic pricing.
Background
Non-small cell lung cancer (NSCLC) patients with activating epidermal growth factor receptor (EGFR) mutations respond to EGFR tyrosine kinase inhibitors (TKI) but ultimately develop resistance to these therapies. The most common resistance mechanism is a second site gate-keeper mutation within exon 20 of EGFR (T790M). EGF816 is identified as a novel covalent inhibitor of mutant-selective epidermal growth factor receptor.
In vitro: EGF816 showed sustained inhibition of pEGFR, which is consistent with the irreversible binding mechanism of EGF816. EGF816 also performs exceptionally well in long term dosing studies providing durable responses in the preclinical models [1].
In vivo: EGF816 demonstrated strong in vivo tumor regressions in several EGFR activating and resistant tumor models. In all of the models EGF816 inhibited tumor growth dose-dependently and achieved regressions of established tumors at well tolerated doses [1].
Clinical trial: A phase I/II study of EGFRmut-TKI EGF816 is being conducted to investigate the efficacy in adult patients with EGFRmut solid malignancies.
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