Target intelligence / Profile preview

KRAS Glycine-to-Cysteine Mutant Protein (KRAS G12C)

Target
KRAS G12C
Molecular classification
Small GTPase, Oncoprotein
01

Overview

KRAS G12C is a mutant form of the KRAS protein, a small GTPase that acts as a molecular switch in cell signaling pathways controlling proliferation, survival, and differentiation. The "G12C" mutation refers to the substitution of glycine (G) with cysteine (C) at codon 12. This specific mutation is highly prevalent in certain cancers, especially lung adenocarcinoma. The G12C mutation impairs GAP-mediated hydrolysis, resulting in constitutive activation. Recent advances have led to the development of selective covalent inhibitors that bind specifically to the cysteine introduced by this mutation, offering a targeted therapeutic approach.

Other names
KRAS G12C MutantKRAS G12CKRAS(G12C)
02

Mechanism of action

Covalent binding to cysteine residue at position 12, locking KRAS in inactive GDP-bound state.

03

Biological functions

Signal transductionCell proliferationCell survivalCell differentiation
04

Disease associations

CancerLung adenocarcinoma
05

Safety considerations

Potential for off-target effectsDrug resistance developmentLimited efficacy in patients with co-occurring mutationsGastrointestinal side effects
06

Interacting drugs

Covalent KRAS G12C inhibitors
07

Biomarkers

KRAS G12C mutation status in tumor tissue

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