Kirsten rat sarcoma virus GTPase (KRas)

Kirsten rat sarcoma virus GTPase (KRas) is a small enzyme belonging to the Ras family of small GTPases. It acts as a molecular switch cycling between an active form bound to guanosine triphosphate (GTP) and an inactive form bound to guanosine diphosphate (GDP). In its active state, KRas relays signals from outside the cell through various signaling pathways—most notably the RAS/MAPK pathway—to regulate essential cellular processes such as proliferation, differentiation, and apoptosis. Mutations in the *KRAS* gene can result in constitutive activation of this protein; these mutations are among the most common genetic alterations found in human cancers including pancreatic ductal adenocarcinoma, colorectal carcinoma, and lung adenocarcinoma. The oncogenic activity arises because mutated forms remain locked in their active state and continuously signal cells to grow uncontrollably. Targeting mutant forms like KRas(G12C) has become a major focus for new anticancer drugs[1][3][4].

Other names

K-RasKRASc-K-rasRASK2GTPase KRas

Covalent inhibition of mutant KRas G12C by locking it in the inactive GDP-bound state and preventing downstream signaling pathways that drive tumor growth[3][4].