Target intelligence / Profile preview

Ras Protein (Mutant) (Ras (Mutant))

Target
Ras (Mutant)
Molecular classification
Small GTPase, Oncoprotein
01

Overview

Mutant Ras proteins are constitutively active GTPases that drive uncontrolled cell proliferation and survival, playing a critical role in cancer development. Common oncogenic mutations occur at positions 12, 13, and 61, impairing GTPase activity and locking Ras in its active GTP-bound state. Therapeutic strategies aim to inhibit Ras signaling by targeting post-translational modifications, directly binding mutant Ras, or inhibiting downstream effector pathways. The three main isoforms are HRAS, NRAS and KRAS (with splice variants 4A and 4B).

Other names
Mutant Ras GTPaseOncogenic RasKRAS (Mutant)HRAS (Mutant)NRAS (Mutant)
02

Mechanism of action

Inhibition of Ras signaling by targeting post-translational modifications (farnesylation), direct binding to mutant Ras (e.g., KRAS G12C), or inhibiting downstream effectors (e.g., RAF, MEK, PI3K)

03

Biological functions

Signal transductionCell proliferationCell survivalCell differentiationRegulation of gene expression
04

Disease associations

CancerTumorigenesis
05

Safety considerations

Drug resistanceOff-target effectsLimited efficacy in Ras-driven cancers beyond KRAS G12CDevelopment of alternative signaling pathwaysToxicities associated with targeting essential cellular processes
06

Interacting drugs

Farnesyltransferase inhibitors (FTIs)

5 more in the full profile.

07

Biomarkers

KRAS mutation status (e.g., G12C, G12D, G13D)NRAS mutation statusHRAS mutation statusExpression levels of Ras effector pathway components (e.g., p-ERK, p-AKT)

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