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Target intelligence / Profile preview
Kirsten Rat Sarcoma Viral Oncogene Homolog Glycine 12 Mutated to Valine (KRAS G12V)
- Target
- KRAS G12V
- Molecular classification
- Small GTPase, Oncogene
01
Overview
The Kirsten rat sarcoma viral oncogene homolog (KRAS) G12V mutation is an oncogenic alteration where glycine at position 12 is replaced by valine. This mutation impairs the intrinsic GTPase activity of KRAS, locking it in an active, GTP-bound state, leading to constitutive activation of downstream signaling pathways like RAF-MEK-ERK and PI3K-AKT-mTOR. This persistent activation drives uncontrolled cell growth and survival signals, contributing to tumorigenesis. KRAS G12V is frequently found in pancreatic, colorectal, and lung adenocarcinomas. Directly targeting KRAS G12V has been historically difficult.
- Other names
- KRAS Gly12ValKRAS G12VG12V KRAS
02
Mechanism of action
Constitutive activation of RAS/MAPK and PI3K/AKT/mTOR pathways
03
Biological functions
Signal transductionCell proliferationCell survivalRegulation of cell growthInhibition of apoptosis
04
Disease associations
CancerPancreatic cancerColorectal cancerLung adenocarcinomaUrogenital cancers
05
Safety considerations
Lack of direct inhibitorsDifficulty in targeting due to smooth protein surfaceSelectivity challenges to avoid affecting wild-type KRAS function
06
Biomarkers
KRAS G12V mutation status
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