Kirsten rat sarcoma viral oncogene homolog Q61H mutant (KRAS Q61H)

Kirsten rat sarcoma viral oncogene homolog Q61H mutant (*KRAS Q61H*) refers to a specific point mutation in the *KRAS* gene, resulting in the substitution of glutamine (Q) by histidine (H) at codon 61. *KRAS* encodes a small GTPase that acts as a molecular switch in key signal transduction pathways regulating cell growth and survival. Mutations at Q61, including Q61H, impair intrinsic GTPase activity and result in persistent activation of KRAS and downstream pathways—especially the MAPK cascade—thereby promoting oncogenesis. Although Q61H mutations are less frequent than those at codons 12 or 13, they are detected in significant subsets of lung, pancreatic, and colorectal cancers[1][3][4][6]. Q61H produces distinct biochemical changes compared to other KRAS mutations—altering switch regions, effector binding, and preference for RAF signaling[1][5]. No selective therapies are currently approved for KRAS Q61H; therapies are investigational or non-specific pathway inhibitors. Detection of KRAS Q61H serves as a diagnostic and prognostic biomarker and is a focal point of novel drug development[1][4][6].

Other names

KRAS Q61HKRAS Q61H mutantKRAS Gln61HisKRAS Q61 mutant

Inhibitors aim to block aberrant KRAS-driven signal transduction (primarily through the MAPK pathway). Some compounds may bind mutated KRAS and prevent GTP binding/hydrolysis or disrupt effector interactions.