Glecirasib, a Potent and Selective Covalent KRAS G12C Inhibitor Exhibiting Synergism with Cetuximab or SHP2 Inhibitor JAB-3312
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).
Authors
- Guiqun Yang
- Xueting He
- Yinxiang Wang
- Sujing Li
- Amin Li
- Yanping Wang (ORCID: https://orcid.org/0009-0009-9498-2124)
- Yiwei Lin (ORCID: https://orcid.org/0000-0003-1503-9082)
- Xiaoyu Liu
- Di Kang
- Xin Sun (ORCID: https://orcid.org/0000-0001-7035-593X)
- Peng Wang (ORCID: https://orcid.org/0009-0006-7782-1589)
- Dan Liu (ORCID: https://orcid.org/0000-0001-5812-8638)
Institutions
- Jacobi Medical Center (US)
- Beijing VDJBio (China) (CN)
- Sino Biological (China) (CN)
- Cubist Pharmaceuticals (United States) (US)
Publication Details
- Journal
- Cancer Research Communications
- Published
- 2025-04-30
- DOI
- https://doi.org/10.1158/2767-9764.crc-25-0001
- Citations
- 4
- Primary Topic
- PI3K/AKT/mTOR signaling in cancer
- Type
- article
- Field-Weighted Citation Impact
- 3.22