Kirsten rat sarcoma viral oncogene homolog mutated protein (KRAS)

KRAS (Kirsten rat sarcoma viral oncogene homolog) encodes a small GTPase involved in cellular signal transduction within the RAS/MAPK pathway. The KRAS protein acts as a molecular switch, cycling between active (GTP-bound) and inactive (GDP-bound) forms, relaying proliferative signals from membrane receptors to the nucleus. Mutations—especially at codons 12, 13, 61, and 146—render KRAS constitutively active, driving uncontrolled cell division and cancer pathogenesis. Activated KRAS influences major growth and survival pathways; its mutation is among the most common genetic drivers of human solid tumors, and it is a major focus of drug development for oncology. Several drugs have recently achieved clinical success in selectively inhibiting KRAS mutant forms, especially G12C, yet therapeutic targeting remains challenging due to KRAS’s role in essential normal functions and adaptive resistance mechanisms

Other names

KRASK-RasKRAS2Kirsten rat sarcoma viral oncogene homologKi-ras2c-KRASv-KRAS (viral form)

Covalent inhibition of KRAS mutant protein (G12C) by locking it in an inactive GDP-bound state; Inhibition of downstream signaling pathways such as MAPK/ERK and PI3K/AKT cascades; Disruption of KRAS membrane localization