k-ras(g12c)

K-Ras(G12C) inhibitor 9 is an allosteric inhibitor of oncogenic K-Ras(G12C).

K-Ras(G12C) inhibitor 12 is an allosteric inhibitor of the oncogenic K-Ras(G12C) protein.

6H05 (K-Ras inhibitor) is a selective, allosteric inhibitor of oncogenic mutant K-Ras(G12C).

ARS-853 is an inhibitor of K-RASG12C(IC50 : 2.5 μM), a mutant form of K-RAS that accumulates in the active GTP-bound state in certain cancer cells

K-Ras(G12C) inhibitor 6 is an irreversible, allosteric inhibitor of the K-Ras(G12C) mutant, achieving 100% protein modification at 10 μM after 24 hours in vitro.

KRASG12C IN-13 (LY3499446), a potent inhibitor of KRAS G12C, shows potential in the study of advanced solid tumors, specifically non-small cell lung cancer and colorectal cancer.

KRASG12C IN-16 (Compound SK-17) is a selective, covalent, and orally active KRASG12C inhibitor. It can induce apoptosis and effectively prevent the activation of the MAPK and PI3K/mTOR signaling pathways. Additionally, KRASG12C IN-16 exhibits antitumor activity against pancreatic cancer.

KRASG12C IN-15 (Compound 21) is an orally active KRASG12C inhibitor that effectively blocks SOS1-mediated GDP/GTP exchange with an IC50 of 19 nM. It inhibits ERK phosphorylation with an IC50 of 0.051 μM and reduces the viability of KRASG12C mutant MIA PaCa-2 cells with an IC50 of 0.023 μM. Additionally, KRASG12C IN-15 demonstrates antitumor activity in a MIA PaCa-2 xenograft mouse model.

KRASG12C ligand-1 is a PROTAC target protein ligand utilized in synthesizing PROTAC YN14-H. YN14-H acts as a PROTAC degrader targeting KRASG12C, exhibiting antitumor activity.

KRASG12C IN-17 is an orally active covalent inhibitor of KRASG12C, demonstrating potent inhibitory activity in KRASG12C-mutant cancer cells (NCI-H23 IC50 = 0.7 nM; NCI-H358 IC50 = 0.5 nM). It efficiently and irreversibly forms a covalent bond with KRASG12C in both GDP-bound and GMPPNP-bound states, with a modification rate exceeding 96%. KRASG12C IN-17 is applicable for research on KRAS-driven tumors, including colorectal cancer.

KRASG12C IN-18 is an orally active covalent inhibitor of KRASG12C, achieving complete covalent binding to KRASG12C in both GDP- and GMPPNP-bound states. It exhibits significant antiproliferative activity against KRASG12C and its resistant mutations (including KRASG12C/R68S) with an IC50 in the low nanomolar range. KRASG12C IN-18 demonstrates notable in vivo efficacy in KRASG12C-driven solid tumors and KRASG12C/R68S xenograft models, making it applicable for colorectal adenocarcinoma research.

KRASG12C IN-19 is a selective inhibitor of KRASG12C. It exhibits potent antiproliferative activity against the KRASG12C-mutant non-small cell lung cancer (NSCLC) cell line H358, with an IC50 of 7.6 nM, and effectively inhibits downstream ERK phosphorylation (IC50= 24.06 nM). It shows no significant inhibitory activity on KRASG12V and KRASG12D mutant cancer cells (PANC 1, Panc 03.27, AsPC 1, and GP2d cells) with IC50 values greater than 10,000 nM. KRASG12C IN-19 rapidly forms a covalent bond with KRASG12V-GDP, leading to dose-dependent inhibition of the downstream KRAS pathway. This compound is suitable for research on KRASG12C-driven cancers, including non-small cell lung cancer, pancreatic cancer, and colorectal cancer.

LC-2 (PROTAC KRASG12C Degrader-LC-2) is a novel von Hippel-Lindau-based PROTAC degrader of endogenous KRAS G12C with a DC50 between 0.25 and 0.76 μM.LC-2 is a PROTAC that covalently binds KRAS G12C with MRTX849 and recruits the E3 ligase, VH, to induce a rapid and sustained degradation of KRAS G12C. LC-2 inhibits MAPK signaling in pure and heterozygous KRAS G12C cell lines.

KRASG12C IN-2 (compound 17) is an orally active KRAS G12C inhibitor that effectively suppresses tumor growth in mice [1].

KRASG12C IN-12 (compound-1) acts as an inhibitor of KRASG12C. It forms a ternary complex with intracellular CYPA and the activated mutant of KRASG12C.

BI-2865 is a non-covalent pan-KRAS inhibitor.BI-2865 binds to KRAS WT, G12C, G12D, G12V, and G13D mutants with KD values of 6.9, 4.5, 32, 26, and 4.3 nM, respectively.BI-2865 showed antiproliferative activity in BaF3 cells expressing KRAS G12C, G12D, or G12V mutants[1] . BI-2865 showed antiproliferative activity on BaF3 cells expressing KRAS G12C, G12D or G12V mutants, with an average IC50 value of approximately 140 nM.[1]

Adagrasib (MRTX849) is an orally active and selective covalent inhibitor of KRAS G12C. Adagrasib binds to the GDP state of the inactive conformation of KRAS G12C and inhibits KRAS and its downstream signaling. Adagrasib exhibits inhibitory activity against KRAS G12C mutant tumors.

Sotorasib (AMG-510) is an orally active and selective covalent inhibitor of KRAS G12C. Sotorasib binds to the GDP state of the inactive conformation of KRAS G12C and inhibits KRAS and its downstream signaling. Sotorasib exhibits inhibitory activity against KRAS G12C mutant tumors.

Divarasib (GDC-6036) is an investigational, oral, high-potency and selective KRAS G12C inhibitor with an IC50 of <0.01 μM. Divarasib irreversibly locks KRAS G12C oncoprotein in an inactive state and inhibits tumor cell growth. It is being investigated for use in solid tumors, including non-small cell lung and colorectal cancers and other types of cancer.

BI-2852 is a KRAS inhibitor targeting the switch I/II pocket (SI/II-pocket) with nanomolar affinity, leading to inhibition of downstream signaling and an antiproliferative effect in KRAS mutant cells.

KRAS G12C inhibitor 16 is a potent inhibitor of KRAS G12C.

KRas G12C inhibitor 1 is a compound that selectively inhibits the KRas G12C protein.

RMC-6291 is an orally active, covalent inhibitor of KRAS G12C (ON) that forms a tri-complex within tumor cells between KRAS G12C (ON) and cyclophilin A (CypA), thereby preventing KRAS G12C (ON) from signaling via steric blockade of RAS effector binding and eliciting deep and durable suppression of RAS pathway activity in KRAS G12C tumor models [1].

ARS-1323 is the racemate of ARS-1620 and a mutant K-ras G12C inhibitor.