kras inhibitor-7

KRAS inhibitor-7 is a potent inhibitor of KRAS G12C. (KRAS inhibitor-7 specifically targets the G12C mutation in KRAS, a protein involved in cell signaling and cancer development.) [KRAS inhibitor-7 exhibits high binding affinity and selectivity for the mutant KRAS protein.]

KRAS G12C inhibitor 69 (Compound K09) is an inhibitor of the mutant RAS protein KRAS G12C with an IC50 of 4.36 nM. In the cell lines NCI-H358 and MIA-PACA-2, it suppresses ERK phosphorylation with IC50 values of 12 nM and 7 nM, respectively. Additionally, KRAS G12C inhibitor 69 hinders the proliferation of NCI-H358 and MIA-PACA-2 cancer cells, with IC50 values of 3.15 nM and 2.33 nM, respectively.

pan-KRAS-IN-7 (Compound 25) is an inhibitor of the human tumorigenic mutant gene KRAS. It effectively suppresses the proliferation of KRAS mutant cells AsPC-1 (G12D mutant) and SW480 (G12V mutant) with an IC50 of 0.35 nM and 0.51 nM, respectively.

RAS inhibitor Abd-7 is a powerful compound (Kd=51 nM) that binds to RAS and inhibits the protein-protein interaction (PPI) between RAS and its effectors. By interacting with RAS within cells, RAS inhibitor Abd-7 hinders RAS-effector interactions and suppresses endogenous RAS-dependent signaling. Additionally, RAS inhibitor Abd-7 disrupts the PPI of different mutant KRAS proteins with PI3K, CRAF, RALGDS, as well as NRAS Q61H and HRAS G12V[1].

KRAS G12D inhibitor 7, is a highly potent inhibitor specifically targeting KRAS G12D.

GDC-0623 (RG 7421) is a potent, ATP-uncompetitive MEK1 inhibitor with a Ki of 0.13 nM, currently in Phase 1.

KRAS G12D inhibitor 19 (Compound 7) is used in cancer research [1]. As a specific inhibitor of KRAS G12D, it targets and potentially suppresses this mutation, which is frequently associated with various cancers.

PAWI-2 functions as both a p53 activator and a Wnt inhibitor. It suppresses β3-KRAS signaling independently of KRAS and selectively inhibits the phosphorylation of TBK1. Additionally, PAWI-2 triggers apoptosis (activation of caspase-3/7) and induces PARP cleavage. It facilitates the translocation of retinoblastoma protein into the nucleus, leading to G2/M cell cycle arrest. PAWI-2 reverses the cancer stem cell-like properties of KRAS-dependent human pancreatic cancer stem cells (hPCSC) and overcomes drug resistance. Moreover, it inhibits the growth of hPCSC tumors in an orthotopic xenograft mouse model.

KRAS G12C inhibitor 68 (compound I-063) serves as a potent inhibitor of KRAS G12C, exhibiting an IC50 of 7 nM and demonstrating antitumor activity.

GNE-9815 (3-(2-cyanopropan-2-yl)-N-[2-fluoro-4-methyl-5-(7-methyl-8-oxo-7,8-dihydropyrido[2,3-d]pyridazin-3-yl)phenyl]benzamide) is a high kinase-selective inhibitor of RAF and targets KRAS-mutant cancers through combination therapy.

KRAS G12D-IN-35 (example 7) is a potent, orally active inhibitor of KRAS G12D. It effectively suppresses p-ERK in AGS cells and significantly inhibits the proliferation of various KRAS G12D mutant cancer cell lines. Additionally, KRAS G12D-IN-35 reduces tumor growth in HPAC and GP2D mouse models. This compound is applicable for cancer research, including studies on pancreatic and colorectal cancer.