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KRAS G12C is a specific mutation in the KRAS gene, where glycine at codon 12 is replaced by cysteine. This mutation causes the K-Ras protein to become constitutively active, driving uncontrolled cell growth and contributing to tumorigenesis, particularly in non-small cell lung cancer, colorectal cancer and other solid tumors. It is a target for small molecule inhibitors like sotorasib and adagrasib.
Covalent binding to the cysteine residue introduced by the G12C mutation, inhibiting KRAS G12C activity.
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