| Description | RM-018 is a powerful tricomplex inhibitor that specifically targets the active state of KRAS G12C. It exhibits unique functional characteristics and possesses the ability to bind and inhibit both KRAS G12C and KRAS G12C/Y96D, potentially overcoming resistance. |
| In vitro | RM-018 is a “tricomplex” KRAS inhibitor, which exploits a highly abundant chaperone protein, cyclophilin A, to bind and inhibit KRAS G12C[1]. RM-018 (0.01-1000 nM; 72 hours) has IC 50 s of 1.4-3.5 nM (KRAS G12C ) and 2.8-7.3 nM (KRAS G12C/Y96D ) in NCI-H358, MIA PaCa-2, Ba/F3, and MGH1138-1 cells[1]. RM-018 (0-100 nM; 4 hours) inhibits the expression of KRAS, pERK, and pRSK protein[1]. Cell Viability Assay[1]Cell Line: NCI-H358, MIA PaCa-2, Ba/F3, and MGH1138-1 cells, which stably infected with KRAS G12C or KRAS G12C/Y96D . Concentration: 0.01-1000 nM Incubation Time: 72 hours Result: Inhibited the cell activity, but largely unaffected by KRAS G12C/Y96D expression. Western Blot Analysis[1]Cell Line: MIA PaCa-2, HEK293T and MGH1138-1 cells, which expressing KRAS G12C or KRAS G12C/Y96D . Concentration: 0-100 nM Incubation Time: 4 hours Result: Inhibited KRAS, pERK and pRSK levels with similar potency. |
| molecular weight | 985.24 |
| Molecular formula | C56H72N8O8 |
| CAS | 2641993-55-5 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| References | 1. Tanaka N, et.al. Clinical Acquired Resistance to KRAS G12C Inhibition through a Novel KRAS Switch-II Pocket Mutation and Polyclonal Alterations Converging on RAS-MAPK Reactivation. Cancer Discov. 2021 Aug;11(8):1913-1922. |