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Ref Type Journal Article
PMID (40304209)
Authors Wang P, Sun X, He X, Kang D, Liu X, Liu D, Li A, Yang G, Lin Y, Li S, Wang Y, Wang Y
Title Glecirasib, a Potent and Selective Covalent KRAS G12C Inhibitor Exhibiting Synergism with Cetuximab or SHP2 Inhibitor JAB-3312.
Journal Vol Issue Date Pages Journal Short Title
Cancer research communications 5 5 2025 May 01 792-803 Cancer Res Commun
URL
Abstract Text Glecirasib potently and selectively inhibits KRAS G12C and reduces ERK and AKT phosphorylation in KRAS G12C-mutant cancer cells, further inducing cell-cycle arrest and apoptosis. Glecirasib monotherapy leads to tumor regression in KRAS G12C-mutant animal models and shows synergistic effects with cetuximab or JAB-3312 (sitneprotafib).

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Molecular Profile Treatment Approach
Gene Name Source Synonyms Protein Domains Gene Description Gene Role
Therapy Name Drugs Efficacy Evidence Clinical Trials
JAB-3312 JAB-3312 5 0
Drug Name Trade Name Synonyms Drug Classes Drug Description
JAB-3312 JAB3312|JAB 3312|sitneprotafib SHP2 Inhibitor 20 JAB-3312 is a SHP2 inhibitor, which potentially decreases tumor growth (PMID: 40304209).
Gene Variant Impact Protein Effect Variant Description Associated with drug Resistance
Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References
NRAS G12C Advanced Solid Tumor sensitive Glecirasib Preclinical - Cell culture Actionable In a preclinical study, Glecirasib (JAB-21822) treatment inhibited viability of cells expressing NRAS G12C in culture (PMID: 40304209). 40304209
HRAS G12C Advanced Solid Tumor sensitive Glecirasib Preclinical - Cell culture Actionable In a preclinical study, Glecirasib (JAB-21822) treatment inhibited viability of cells expressing HRAS G12C in culture (PMID: 40304209). 40304209