Home Apoptosis KRas

KRas Inhibitors

Cat.No. Product Name Information Product Use Citations Product Validations
S8826 BAY-293 BAY-293 selectively inhibits the KRAS-SOS1 interaction with an IC50 of 21 nM.
iScience, 2025, 28(9):113374
Int J Mol Sci, 2023, 24(2)997
Clin Cancer Res, 2022, clincanres.4291.2021
S8156 ARS-853 ARS-853 is a selective, covalent KRAS(G12C) inhibitor that inhibits mutant KRAS-driven signaling by binding to the GDP-bound oncoprotein and preventing activation. This compound also induces apoptosis.
Sci Rep, 2023, 10.1038/s41598-023-46623-w
Cell Mol Gastroenterol Hepatol, 2022, S2352-345X(22)00216-8
SLAS Discov, 2022, S2472-5552(22)12517-7
S7331 K-Ras(G12C) inhibitor 12 K-Ras(G12C) inhibitor 12 is an allosteric inhibitor of oncogenic K-Ras(G12C).
Cancers -Basel), 2023, 15(19)4772
Biomedicines, 2022, 10(3)592
Oncotarget, 2016, 7(9):10064-72
Verified customer review of K-Ras(G12C) inhibitor 12
S8955 Sotorasib (AMG510) racemate Sotorasib (AMG510) racemate is a racemic of AMG-510 which is a potent KRAS G12C covalent inhibitor with potential antineoplastic activity.
Mol Cancer Ther, 2023, 22(12):1422-1433
Commun Biol, 2021, 4(1):834
Mol Clin Oncol, 2021, 15(1):148
S8499 KRpep-2d KRpep-2d is a K-Ras(G12D) selective inhibitory cyclic peptide with selectivity against wild-type (WT) K-Ras and the K-Ras(G12C) mutant. The IC50 value of this compound is 1.6 nM.
J Exp Clin Cancer Res, 2022, 41(1):73
Heliyon, 2022, 8(12):e12518
E1187 Divarasib (GDC-6036) Divarasib (GDC-6036, RG6330) is a KRAS G12C inhibitor that binds irreversibly to switch II pocket of KRAS G12C (when in the inactive GDP-bound state) thereby blocking GTP binding and activation.
Cancer Lett, 2024, 611:217414
E1606 RMC-6291 (Elironrasib) RMC-6291 is an orally active and covalent inhibitor of KRASG12C(ON). RMC-6291 forms a tri-complex within tumor cells between KRASG12C(ON) and cyclophilin A (CypA).
Mol Cancer Ther, 2025, 10.1158/1535-7163.MCT-25-0022
E1056 Opnurasib (JDQ-443) Opnurasib (JDQ-443,NVP-JDQ443) , a potent and selective, orally bioavailable covalent inhibitor of GDP-bound KRASG12C with an IC50 of 0.012 µM for inhibition of c-Raf recruitment.
J Biol Chem, 2025, 301(7):110331
E1677 Glecirasib Glecirasib (JAB-21822, KRAS G12C inhibitor 36) is a potent, and highly selective, covalent inhibitor of KRAS G12C. It exhibits promising anti-tumor activity in KRAS G12C-mutated pancreatic ductal adenocarcinoma (PDAC) , Non-Small Cell Lung Cancer(NSCLC), Colorectal Cancer (CRC) and other solid tumors.
J Exp Clin Cancer Res, 2025, 44(1):68
E1157 Pan-RAS-IN-1 Pan-RAS-IN-1, a pan-Ras inhibitor, binds to KRasG12D-GppNHp with a Kd less than 20 μM in MST, ITC and NMR assays, also binds to Ras proteins and exhibits lethality in cells partially dependent on expression of Ras proteins.
Cancer Discov, 2025, 10.1158/2159-8290.CD-24-1317
S7332 K-Ras(G12C) inhibitor 9 K-Ras(G12C) inhibitor 9 is an allosteric inhibitor of oncogenic K-Ras(G12C).
E1474 BI-2865 BI-2865 is a none-covalent pan-KRAS Inhibitor. It binds to WT, G12C, G12D, G12V and G13D mutant KRAS with KDs of 6.9, 4.5, 32, 26, 4.3 nM respectively and inhibits the proliferation of G12C, G12D or G12V mutant KRAS expressing BaF3 ce
S6996 LC-2 LC-2 is a first PROTAC capable of degrading endogenous KRASG12C with DC50s between 0.25 μM and 0.76 μM. This compound covalently binds KRASG12C with a MRTX849 warhead and recruits the E3 ligase VHL, inducing rapid and sustained KRASG12C degradation leading to suppression of MAPK signaling.
S0023 K-Ras-IN-1 K-Ras-IN-1 (MDK-3017) inhibits K-Ras by binding to K-Ras in a hydrophobic pocket that is occupied by Tyr-71 in the apo-Ras crystal structure.
E1433 LY3537982 (KRAS G12C Inhibitor 67) LY3537982 (KRAS G12C inhibitor 19) is a highly selective and potent inhibitor of the  KRAS-G12C protein. LY3537982 selectively inhibits the growth of KRAS G12C mutant cells H23 G12C, H358 G12C, and H2122 G12C with IC50s of 1.04 nM, 1.16 nM, and 11.38 nM, respectively.
E1578 garsorasib (D-1553) Garsorasib (D-1553 ) is a potent and selective oral KRASG12C inhibitor with antitumor activity. It has the potential to treat KRAS G12C-mutated non-small cell lung cancer (NSCLC).
E8295New LY3499446 LY3499446 (KRASG12C IN-13) is a potent inhibitor of KRAS G12C. It can be used in research on advanced solid tumors, including non-small cell lung cancer (NSCLC) and colorectal cancer (CRC).
S7330 6H05 6H05 is a selective, and allosteric inhibitor of oncogenic K-Ras(G12C).
S7333 K-Ras(G12C) inhibitor 6 K-Ras(G12C) inhibitor 6 is an allosteric, and selective inhibitor of oncogenic K-Ras(G12C).
E4758New ACBI3 ACBI3 is a selective and potent PROTAC degrader of pan-KRAS that promotes VHL engagement, ternary complex formation, and E3 ligase-dependent KRAS degradation with high proteome-wide selectivity. It demonstrates strong anti-tumor activity, resulting in durable pathway modulation and tumor regressions in KRAS driven cancers.
E1857 TH-Z816 TH-Z816 is an inhibitor of ,KRAS(G12D) with an IC50 of 14 μM in an SOS-catalyzed nucleotide exchange assay with GDP as the incoming nucleotide.
E1356 BI-0474 BI-0474 is a potent inhibitor of KRASG12C with an IC50 value of 7.0 nM. It inhibits GDP-KRAS::SOS1 protein-protein interactions. It exhibits anti-proliferative and anti-tumour activity and can be used in cancer research.
E6405New AZD0022 AZD0022 is a potent, orally bioavailable, selective, reversible inhibitor of KRASG12D that drives robust pathway inhibition and anti-tumour activity in KRASG12D models.
E6406New AMG 410 AMG410 is a non-covalent, selective inhibitor of pan-KRAS with IC50 of 1–4 nM for KRAS G12D, G12V, and G13D. It binds both GDP- and GTP-bound KRAS with Kd of 1 nM and 22 nM, respectively. AMG410 inhibits KRAS signaling in a nucleotide cycling-independent manner. It also suppresses proliferation in KRAS-amplified wild-type tumor cells.
E1959New RMC-4998 RMC-4998 is a tri-complex inhibitor that selectively targets the GTP-bound state of mutant KRASG12C, with high potency for KRASG12C-CYPA tri-complex formation with an IC50 of 28 nM. It strongly inhibits ERK signaling with an IC50 of 1–10 nM and attenuates AKT/MTOR and RAL pathways, leading to potent suppression of KRASG12C-driven tumor growth and can used in cancer research.
E1843New Fulzerasib Fulzerasib (IBI351, GFH925) is an irreversible small molecule inhibitor for KRAS G12C mutation blocking KRAS pathway signaling pERK with an IC50 of 37 nM. It demonstrates potent anti-tumor activity in multiple KRAS G12C-mutant tumor models including human pancreatic cancer, human lung adenocarcinoma, colorectal adenocarcinoma, and lung cancer models.
E1576New LUNA18 LUNA18 (Paluratide) is an orally bioavailable 11-mer cyclic peptide KRAS inhibitor for the intracellular tough target RAS. It binds to KRASG12D with a kd of 0.043 nM and blocks KRASG12D–SOS1 interaction at IC50 of < 2.2 nM. It also exhibits antiproliferative activity in KRAS-mutant cancer cell lines with an IC50 of 1.4 nM in AsPC-1 pancreatic cancer cells.
E4697 RGT-018 RGT-018, is a potent and selective inhibitor of SOS1. It blocks the interaction of KRAS:SOS1 with an IC50 of 8 nM and inhibited KRAS signaling and the proliferation of KRAS-driven cancer cells. It may exhibit potent anticancer activity against NSCLC, colorectal cancer, and pancreatic cancer.
E1829New Calderasib (MK-1084) Calderasib (MK-1084) is a selective KRAS G12C inhibitor demonstrating antitumor efficacy. It can be utilized as monotherapy or in combination with pembrolizumab () for oncology research.
E2540New Salvianolic acid F Salvianolic acid F acts as a KRAS inhibitor, with activity against KRAS G12D. It suppresses NF-kB, MMP-9, and NO production. In vitro studies show it reduces cancer cell proliferation, invasion, and migration while promoting apoptosis through the EP300/PI3K/AKT pathway. In vivo experiments demonstrate its inhibition of KRAS-dependent lung cancer cell growth via PI3K/AKT signaling. This compound has potential applications in studying multiple cancer types, particularly KRAS G12D-associated NSCLC and ovarian cancer.
E1856 ARS-1323 ARS-1323 is the racemic mixture, containing ARS-1620, and a potent inhibitor of mutant KRAS G12C. It can be used in research for biochemical binding screens as companion imaging drugs (CID) for KRAS G12C.
E6643New SS-3091 SS-3091 is a pan-KRas inhibitor that targets the interaction interfaces of KRas. By destabilizing the ARaf/KRas complex, it modulates downstream signaling pathways. This compound exhibits activity against KRas G12D, G12C, G12V, and G12S mutants in multiple cancer cell lines.
E1071 ASP2453 ASP2453, a potent, selective and covalent KRAS G12C inhibitor, inhibits the Son of Sevenless (SOS)-mediated interaction between KRAS G12C and Raf. This compound is a potential therapeutic agent for KRAS G12C-mutated cancer.
E6526New MCB-294 MCB-294 is a pan-KRAS inhibitor that targets both active (GTP-bound) and inactive (GDP-bound) KRAS states, exhibiting Kd values of about 1 pM and 10 nM, respectively. It shows preferential inhibition of KRAS over NRAS and HRAS. The compound inhibits proliferation of hTERT-HPNE cells harboring G12D, G12C, G12V, G12S, G13D, and wild-type KRAS variants, with IC50 values around 700 nM. MCB-294 triggers apoptosis in KRAS-mutated tumors and demonstrates activity against KRASG12C inhibitor-resistant cancer cells while modulating the tumor immune microenvironment. This compound serves as a research tool for pancreatic, colorectal, and lung cancer investigations.
E6411New RP03707 RP03707 is a PROTAC molecule designed to degrade KRASG12D, consisting of three components: a KRASG12D inhibitor (, red), a linker (black), and an E3 ligase ligand (blue).
E5847New olomorasib Olomorasib (KRAS G12C inhibitor 19, LY3537982) is a potent and highly selective second-generation inhibitor of GDP-bound KRAS G12C, with the potential to treat patients with advanced solid tumors carrying the KRAS G12C mutation.
E6638New VS-7375 (GFH375) VS-7375 (GFH375) is an oral small-molecule inhibitor that selectively targets KRAS G12D in both its active (GTP-bound) and inactive (GDP-bound) forms. This dual-state inhibition results in stronger tumor suppression compared to single-state inhibitors. It exhibits potent anti-proliferative and anti-tumor effects in KRAS G12D-mutant models, including an intracranial GP2D tumor model.
E1968New BBO-8520 BBO-8520 is a covalent small molecule inhibitor that selectively targets KRAS G12C with high oral bioavailability. It functions as both a KRAS G12C (OFF) inhibitor and a blocker of KRAS G12C (ON) signaling. This compound inhibits cellular proliferation by binding to GTP-bound KRAS G12C (ON), thereby preventing RAS-RAF1 interaction and promoting the transition to the inactive (OFF) state.
E5910New KRAS-533 KRAS-533 is a potent agonist of KRAS that binds to the GTP/GDP-binding pocket and prevents the hydrolysis of GTP, leading to accumulation of active GTP-bound KRAS. This triggers both apoptotic and autophagic cell death pathways in cancer cells, leading to potent suppression of mutant KRAS lung cancer in vitro and in animal models.
S8831 MRTX-1257 MRTX-1257 is a potent, selective, irreversible, covalent and orally active inhibitor of KRAS G12C with IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells.
E1564 BI-2493 BI-2493, a structural analogue of BI-2865, is a highly selective inhibitor of pan-KRAS. This compound attenuates tumor growth and can be used for cancer research.
S2797 Lonafarnib (SCH66336) Lonafarnib (SCH66336) is an orally bioavailable FPTase inhibitor for H-ras, K-ras-4B and N-ras with IC50 of 1.9 nM, 5.2 nM and 2.8 nM in cell-free assays, respectively. Phase 3.
PLoS Pathog, 2025, 21(10):e1013558
iScience, 2025, 28(2):111864
Sci Rep, 2025, 15(1):34331
Verified customer review of Lonafarnib (SCH66336)
S7224 Deltarasin Deltarasin is a small molecular inhibitor of KRAS-PDEδ interaction with Kd of 38 nM for binding to purified PDEδ.
Eur J Cell Biol, 2023, 102(2):151314
Appl. Sci, 2023, 13(1), 166
Cell Death Differ, 2019, 26(11):2400-2415
S5279 Fendiline hydrochloride Fendiline hydrochloride is the hydrochloride salt form of Fendiline, which is an L-type calcium channel blocker and also a specific inhibitor of K-Ras plasma membrane targeting with no detectable effect on the localization of H- and N-Ras.