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KRAS proto-oncogene, GTPase, G12V mutant peptide presented by human leukocyte antigen (KRAS G12V neoantigen (when referring to the peptide); KRAS (for the gene/protein); G12V (specifying mutation); HLA (for the presenting molecule))

Target
KRAS G12V neoantigen (when referring to the peptide); KRAS (for the gene/protein); G12V (specifying mutation); HLA (for the presenting molecule)
Molecular classification
Enzyme, Oncogenic protein, Neoantigen, Protein, Receptor ligand
01

Overview

The KRAS G12V neoantigen presented by HLA is a mutated peptide resulting from a glycine to valine substitution at codon 12 in the KRAS proto-oncogene. This mutant peptide, when processed and presented on the cell surface by human leukocyte antigen molecules, is recognized as foreign by the immune system, making it a promising target for cancer immunotherapy and mutation-selective drug development. KRAS G12V is a frequent and aggressive driver mutation in several major cancers, such as lung, colon, and pancreatic cancers. Targeted therapies—including RNA interference molecules and T cell-based immunotherapies—are being researched to exploit the unique presence of this neoantigen in cancer cells. No direct clinical inhibitors for KRAS G12V are approved as of 2025, but advances in mutation-selective therapies are underway, leveraging both EGFR-directed delivery and neoantigen-specific immune approaches[3][4][5][6].

Other names
KRAS G12V mutantKRAS G12V neoantigenKRAS G12V mutant peptideKRAS G12V peptide presented by HLAmutant KRAS G12V epitope
02

Mechanism of action

RNA interference: siRNA or RNAi selectively silences KRAS G12V mRNA, reducing protein/neoantigen expression; T cell-mediated cytotoxicity: T cells engineered to recognize the KRAS G12V peptide presented on HLA kill tumor cells; Small molecule inhibition: attempts at direct KRAS G12V inhibitors (none yet FDA-approved)

03

Biological functions

Signal transductionCell proliferationTumorigenesisImmune responseApoptosis
04

Disease associations

CancerOncogenesis
05

Safety considerations

Off-target effectsTumor heterogeneityDelivery limitationsTumor immune escape
06

Interacting drugs

EFTX-G12V

2 more in the full profile.

07

Biomarkers

KRAS G12V mutation detectionNeoantigen-specific T cell responsePD-L1 expression

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