GTPase KRas G13A (KRAS G13A)

KRas is a member of the small GTPase family that acts as a critical molecular switch in cellular signaling pathways, including the MAPK/ERK and PI3K/AKT cascades. The G13A mutation is a somatic missense mutation where glycine at position 13 is replaced by alanine, leading to impaired intrinsic and GAP-mediated GTP hydrolysis. This results in the protein being locked in a constitutively active, GTP-bound state, which drives uncontrolled cell proliferation and survival. KRAS G13A is frequently identified in colorectal, lung, and pancreatic cancers and is associated with poor prognosis and resistance to standard EGFR-targeted therapies. While direct G13A-selective inhibitors are currently in development, therapeutic strategies often involve pan-RAS inhibitors or combination treatments targeting downstream effectors like MEK and mTOR.

Other names

Kirsten rat sarcoma virus oncogene homolog G13AKRAS proto-oncogene, GTPase G13Ap.Gly13AlaKRAS2RASK2c-K-ras

Inhibition of constitutively active GTPase signaling through pan-RAS inhibition, RAF/MEK clamping, or blockade of upstream EGFR and downstream mTOR effectors.