Kirsten rat sarcoma viral oncogene homolog with glycine-to-cysteine mutation at codon 12 (KRAS G12C)

KRAS G12C is a specific mutation in the Kirsten rat sarcoma viral oncogene homolog gene where glycine at codon 12 is replaced by cysteine. This alteration causes abnormal activation of the encoded small GTPase enzyme, resulting in continuous signaling for cell growth and division. The persistent "on" state driven by this mutation leads to uncontrolled cellular proliferation and tumor formation. The KRAS G12C mutation is found most commonly in cancers such as non-small cell lung cancer and colorectal cancer. It serves as both a biomarker for diagnosis and patient selection, as well as a therapeutic target for drugs like sotorasib that specifically inhibit this mutated form of the protein[1][2].

Other names

KRAS G12CKRAS p.G12CKirsten rat sarcoma viral oncogene homolog, G12C mutantKRAS glycine 12 to cysteine mutant

Covalent inhibition of the mutant cysteine residue in the active site, locking the protein in an inactive GDP-bound state[1]