Abstract

KRAS G12C mutation acts as a key oncogenic driver occurring in approximately 15% of non-small cell lung cancer (NSCLC). An activating KRAS mutation (for example, G12C mutation) results in KRAS protein accumulated in the GTP-bound, active form, which is believed to drive the abnormal growth of cancer cells in multiple tumor types. D-1553 is an orally bioavailable inhibitor of KRAS G12C that selectively and irreversibly binds KRAS G12C mutated protein in an inactive GDP-bound state.

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