2. Signaling Pathways
  3. GPCR/G Protein
    MAPK/ERK Pathway
  4. Ras
  5. K-Ras Isoform
  6. K-Ras Inhibitor

K-Ras Inhibitor

K-Ras Inhibitors (224):

Cat. No. Product Name Effect Purity
  • HY-148439
    Daraxonrasib
    		Inhibitor 99.96%
    Daraxonrasib (RMC-6236) is an orally active, non-covalent RAS (ON) inhibitor. Daraxonrasib disrupts the interaction of wild-type or mutant RAS proteins with the RAS binding domain of BRAF, with EC50 values ranging from 28-220 nM for wild-type KRAS, NRAS, HRAS, and multiple oncogenic RAS variants. Daraxonrasib inhibits pERK. Daraxonrasib has anti-tumor activity against KRAS mutant tumors.
  • HY-134813
    MRTX1133
    		Inhibitor 99.97%
    MRTX1133 is a noncovalent, potent, and selective alkyne-based KRAS G12D inhibitor. MRTX1133 optimally fills the switch II pocket and extends three substituents to favorably interact with the protein, resulting in an estimated KD against KRAS G12D of 0.2 pM. MRTX1133 prevents SOS1-catalyzed nucleotide exchange and/or formation of the KRAS G12D/GTP/RAF1 complex, thereby inhibiting mutant KRAS-dependent signal transduction. MRTX1133 selectively inhibits KRAS G12D mutant, but not KRAS wild-type, tumor cells. MRTX1133 has single digit nanomolar activity in cellular assays and marked in vivo efficacy in tumor models harboring KRAS G12D mutations.
  • HY-114277
    Sotorasib
    		Inhibitor 99.70%
    Sotorasib (AMG-510) is a first-in-class, orally bioavailable, and selective KRAS G12C covalent inhibitor. Sotorasib irreversibly inhibits KRAS G12C by locking it in an inactive GDP-bound state. Sotorasib leads to the regression of KRAS G12C‑mutated locally advanced or metastatic non‑small cell lung cancer (NSCLC).
  • HY-130149
    Adagrasib
    		Inhibitor 99.96%
    Adagrasib (MRTX849) is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. Adagrasib covalently binds to KRAS G12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction.
  • HY-156819
    Zoldonrasib
    		Inhibitor 99.73%
    Zoldonrasib (RMC-9805) is a potent and orally active KRAS G12D inhibitor.Zoldonrasib induces apoptosis in KRAS G12D mutant cancer cells. Zoldonrasib has the potential for the research of KRAS G12D mutant cancer.
  • HY-181420A
    BBO-11818
    		Inhibitor 99.77%
    BBO-11818 is an orally active, highly selective (relative to NRAS and HRAS), non-covalent pan-KRAS inhibitor (IC50=28-120 nM). BBO-11818 specifically binds to the Switch-II/Helix 3 pocket, disrupts the KRAS:RAF1 interaction by inducing conformational changes, and blocks the MAPK signaling pathway. BBO-11818 exhibits significant anti-tumor activity, which not only inhibits cell proliferation and induces apoptosis, but also drives tumor regression in xenograft models. BBO-11818 produces synergistic effects when combined with Cetuximab (HY-P9905), anti-PD-1 antibody or PI3Kα inhibitor. BBO-11818 is used in the research of KRAS mutation-related malignancies such as pancreatic cancer, non-small cell lung cancer and colorectal cancer.
  • HY-176954
    RSC-1255
    		Inhibitor 99.91%
    RSC-1255 is a potent and selective Vacuolar H⁺-ATPase (V-ATPase) inhibitor that directly binds the mammalian V-ATPase complex with a Kd = 23 nM. RSC-1255 exhibits preferential cytotoxicity toward KRAS-mutant cancer cells, especially KRASG13D and KRASG12V cells. RSC-1255 induces apoptosis and blocks lysosomal acidification, autophagy, and macropinocytosis in cancer cells. RSC-1255 can be used for the study of KRAS-driven lung and colon cancers.
  • HY-159474A
    (1R)-KRAS inhibitor-24
    		Inhibitor 98.29%
    (1R)-KRAS inhibitor-24 (compound 115c) is a pyridopyrimidine KRAS inhibitor, with an IC50 of < 100 nM for KRas G12V, KRas WT and KRas G12R.
  • HY-156498
    RMC-7977
    		Inhibitor 99.48%
    RMC-7977 is an orally active triple-complex RAS inhibitor that can simultaneously bind to cyclophilin A (CYPA) (Kd = 195 nM) and KRAS (G12V) (Kd = 292 μM). It exhibits broad-spectrum inhibitory activity against KRAS, NRAS, and HRAS proteins and their various wild-type and mutant variants. RMC-7977 induces apoptosis by inhibiting the phosphorylation of ERK, CRAF, and RSK, as well as increasing PARP cleavage. This leads to tumor regression, reduces resistance in KRASG12C cancer models, and demonstrates good tolerability across various RAS cancer models.
  • HY-153346
    Elironrasib
    		Inhibitor 99.65%
    Elironrasib is an orally active and covalent inhibitor of KRASG12C(ON). Elironrasib forms a tri-complex within tumor cells between KRASG12C(ON) and cyclophilin A (CypA). Thus, Elironrasib prevents KRASG12C(ON) from signaling via steric blockade of RAS effector binding. Elironrasib inhibits ERK signaling and induced apoptosis in KRASG12C-mutant H358 cells. Elironrasib also inhibits the proliferation of KRASG12C mutant cells with a median IC50 of 0.11 nM.
  • HY-145928
    Divarasib
    		Inhibitor 99.31%
    Divarasib (GDC-6036) is an orally active, selective KRASG12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds Cys12 in GDP-bound KRASG12C, occupies the switch II pocket, blocks GTP binding and SOS-mediated reactivation, and inhibits oncogenic KRAS signaling. Divarasib induces tumor shrinkage and robust tumor growth inhibition in KRASG12C-positive models and cancer cells. Divarasib can be used for the research of non-small cell lung cancer, colorectal adenocarcinoma, pancreatic ductal adenocarcinoma, and other KRASG12C-mutated solid tumors.
  • HY-125817
    BI-3406
    		Inhibitor 99.95%
    BI-3406 (compound I-6) is an orally active, highly potent and selective inhibitor of the interaction between KRAS and Son of Sevenless 1 (SOS1) with an IC50 of 6 nM. BI-3406 potently reduces the formation of GTP-loaded KRAS, and inhibits MAPK pathway signaling. BI-3406 has anticancer activity.
  • HY-173632
    AMG410
    		Inhibitor 99.75%
    AMG410 is a non-covalent and selective pan-KRAS inhibitor with IC50 values of 1-4 nM for KRAS G12D, KRAS G12V, and KRAS G13D. AMG410 shows greater than 100-fold selectivity against both HRAS and NRAS. AMG410 is a dual GTP(on)- and GDP(off)-state inhibitor (Kd(GDP-state) of 1 nM; Kd(GTP-state) of 22 nM). AMG410 blocks KRAS signaling in a cycling state-independent manner and also blocks proliferation in wildtype KRAS-amplified tumor cells. AMG410 can be used for the study of colorectal, pancreatic, and lung cancers.
  • HY-126247
    BI-2852
    		Inhibitor 99.46%
    BI-2852 is a KRAS inhibitor for the switch I/II pocket (SI/II-pocket) by structure-based agent design with nanomolar affinity. BI-2852 is mechanistically distinct from covalent KRASG12C inhibitor (binds to switch II pocket) and binds ten-fold more strongly to active KRASG12D versus KRASwt (740 nM vs 7.5 μM). BI-2852 blocks GEF, GAP, and effector interactions with KRAS, leading to inhibition of downstream signaling and an antiproliferative effect in KRAS mutant cells.
  • HY-173629
    RMC-5127
    		Inhibitor 99.96%
    RMC-5127 is a small molecule inhibitor that binds to GTP-targeted KRASG12V, with oral bioavailability and blood-brain barrier permeability. RMC-5127 inhibits the activities of the RAS and MAPK pathways, suppresses the proliferation of KRASG12V-mutant cancer cells and induces their apoptosis. RMC-5127 can be used for the research of KRASG12V-mutant non-small cell lung cancer, pancreatic ductal adenocarcinoma, colorectal cancer and intracranial KRASG12V tumors.
  • HY-148273
    Setidegrasib
    		Inhibitor 99.65%
    Setidegrasib (KRAS G12D inhibitor 17, ASP3082) is a PROTAC KRAS degrader (DC50: 37 nM). Setidegrasib induces the degradation of G12D-mutation KRAS protein. Setidegrasib suppresses p-ERK, p-AKT, p-S6 levels in AsPC-1 cells. Setidegrasib exhibits anti-tumor activity in various cancer xenograft models in mice. Setidegrasib can be used for the study of KRAS(G12D)-mutated solid tumors. (Blue: VHL ligase ligand (HY-168699); Black: linker (HY-168698); Pink: G12D ligand (HY-168700)).
  • HY-160699
    DCC-3116
    		Inhibitor 99.84%
    DCC-3116 is an orally active ULK1/2 inhibitor. DCC-3116 can inhibit autophagy in lung cancer cells by inhibiting KRASG12C signaling, thereby inhibiting the proliferation of lung cancer cells and exerting anti-cancer effects.
  • HY-159127
    HRS-4642
    		Inhibitor 98.38%
    HRS-4642 is a high affinity, selective, long-acting, and non-covalent KRASG12D inhibitor with a Kd value of 0.083 nM. HRS-4642 inhibits the binding of KRASG12D to SOS1 or RAF1, thereby blocking the downstream MEK-ERK signaling pathway. HRS-4642 promotes Apoptosis. HRS-4642 alone or combined with Carfilzomib (HY-10455) effectively shapes the tumor microenvironment. HRS-4642 has an anti-cancer effect on pancreatic and colorectal cancers carrying the KRASG12D mutation[1][2][3].
  • HY-158107
    BBO-8520
    		Inhibitor 99.90%
    BBO-8520 is a direct small molecule covalent inhibitor targeting KRAS G12C with high oral availability. BBO-8520 has the characteristics of KRAS G12C (OFF) inhibitor and the function of blocking KRASG12C (ON) signal. BBO-8520 inhibits cell proliferation by inhibiting KRAS G12C (ON) by binding GTP protein. BBO-8520 can block RAS-RAF1 interaction and return KRAS G12C to the inactive (OFF) state. BBO-8520 can be used for the research of cancer.
  • HY-153723
    BI-2493
    		Inhibitor 99.79%
    BI-2493 is a structural analogue of BI-2865 and a highly selective and orally active pan-KRAS inhibitor. BI-2493 can attenuate tumor growth. BI-2493 can be used for cancer iseases research.