AMG 510
Covalent KRASG12C Inhibitor / AMG 510 is a potent (IC50’s = 6 nM NCI-H358; 9 nM MIA PaCa-2) covalent KRASG12C inhibitor.1,2 It significantly inhibited tumor growth in NCI-H358 and MIA PaCa-2 cell lines as well as CT-26 tumors (mouse syngeneic model) and caused tumor regression at higher doses.1 AMG 510 improved the efficacy of various other chemotherapeutic agents including inhibitors of HER kinases, EGFR, SHP2, PI3K, AKT, and MEK 1,3 and synergized with immune checkpoint reagents1. FDA approved for use in KRASG12C-positive non-small cell lung cancer. AMG 510 displayed efficacy alone4,5 and in combination5 with trametinib and/or buparlisib in pancreatic ductal adenocarcinoma cell lines.
Biochemicals & reagents
2296729-00-3
Sotorasib
1) Canon et al. (2019), The clinical KRAS(G12C) inhibitor AMG 510 drives anti-tumor immunity; Nature 575 217 2) Lanman et al. (2020); Discovery of a Covalent Inhibitor of KRASG12C (AMG 510) for the Treatment of Solid Tumors, J. Med. Chem., 63 52 3) Barrios-Bernal et al. (2023); A Novel Combination of Sotorasib and Metformin Enhances Cytotoxicity and Apoptosis in KRAS-Mutated Non-Small Cell Lung Cancer Cell Lines through MAPK and P70S6K Inhibition, Int. J. Mol. Sci., 24 4331 4) Strickler et al. (2023); Sotorasib in KRASp.G12C-Mutated Advanced Pancreatic Cancer, N. Engl. J. Med., 388 33 5) Ma et al. (2022); Inhibition of KRAS, MEKI, and PI3K Demonstrate Synergistic Anti-Tumor Effects in Pancreatic Ductal Adenocarcinoma Cell Lines, Cancers (Basel), 14 4467
-20°C
TARGET: GTPase -- PATHWAY: ERK -- RESEARCH AREA: Immunology -- DISEASE AREA: Cancer