1. Signaling Pathways
  2. GPCR/G Protein
    MAPK/ERK Pathway
  3. Ras

Ras

Ras is the name given to a family of related proteins which is ubiquitously expressed in all cell lineages and organs. All Ras protein family members belong to a class of protein called small GTPase, and are involved in transmitting signals within cells. Ras is the prototypical member of the Ras superfamily of proteins, which are all related in 3D structure and regulate diverse cell behaviours. When Ras is 'switched on' by incoming signals, it subsequently switches on other proteins, which ultimately turn on genes involved in cell growth, differentiation and survival. As a result, mutations in ras genes can lead to the production of permanently activated Ras proteins. This can cause unintended and overactive signalling inside the cell, even in the absence of incoming signals. Because these signals result in cell growth and division, overactive Ras signaling can ultimately lead to cancer. The 3 Ras genes in humans (HRAS,KRAS, and NRAS) are the most common oncogenes in human cancer; Ras inhibitors are being studied as a treatment for cancer, and other diseases with Ras overexpression.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-114277
    Sotorasib
    Inhibitor 99.94%
    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 is the first KRAS G12C inhibitor in clinical development and leads to the regression of KRAS G12C tumors.
    Sotorasib
  • HY-134813
    MRTX1133
    Inhibitor 99.42%
    MRTX1133 is a noncovalent, potent, and selective 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.
    MRTX1133
  • HY-130149
    Adagrasib
    Inhibitor 99.93%
    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.
    Adagrasib
  • HY-153724
    BI-2865
    99.65%
    BI-2865 is a none-covalent pan-KRAS Inhibitor. BI-2865 binds to WT, G12C, G12D, G12V and G13D mutant KRAS with KDs of 6.9, 4.5, 32, 26, 4.3 nM respectively. BI-2865 inhibits the proliferation of G12C, G12D or G12V mutant KRAS expressing BaF3 cells (mean IC50: roughly 140 nM).
    BI-2865
  • HY-126247
    BI-2852
    Inhibitor 99.57%
    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.
    BI-2852
  • HY-156498
    RMC-7977
    Inhibitor 98.82%
    RMC-7977 is a reversible, tri-complex RAS inhibitor with broad spectrum activity for both mutant and wild-type (WT) KRAS, NRAS, and HRAS variants.RMC-7977 can lead to tumor regressions and was well tolerated in diverse RAS-addicted preclinical cancer models. RMC-7977 also can inhibit the growth of KRASG12C cancer models.
    RMC-7977
  • HY-153723
    BI-2493
    Inhibitor 99.70%
    BI-2493 is a structural analogue of BI-2865 and a highly selective pan-KRAS inhibitor. BI-2493 can attenuate tumor growth. BI-2493 can be used for cancer iseases research.
    BI-2493
  • HY-156002
    LUNA18
    Inhibitor 99.26%
    LUNA18 is an orally active KRAS inhibitor with an IC50 of <2 nM against KRASG12D-SOS. LUNA18 can be used for the research of cancer.
    LUNA18
  • 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.
    BI-3406
  • HY-B0105
    Ketoconazole
    Inhibitor 99.86%
    Ketoconazole (R-41400) is an imidazole anti-fungal agent, a CYP3A4 and CYP24A1 inhibitor.
    Ketoconazole
  • HY-15723A
    NSC 23766 trihydrochloride
    Inhibitor 99.32%
    NSC 23766 trihydrochloride is an inhibitor of Rac1 activation.
    NSC 23766 trihydrochloride
  • HY-12755
    ML141
    Inhibitor 99.87%
    ML141 (CID-2950007) is a potent, allosteric, selective and reversible non-competitive inhibitor of Cdc42 GTPase. ML141 inhibits Cdc42 wild type and Cdc42 Q61L mutant with EC50s of 2.1 and 2.6 μM, respectively. ML141 shows low micromolar potency and selectivity against other members of the Rho family of GTPases (Rac1, Rab2, Rab7). ML141 do not show cytotoxicity in multiple cell lines.
    ML141
  • HY-12646
    Rhosin hydrochloride
    Inhibitor 99.93%
    Rhosin hydrochloride is a potent, specific RhoA subfamily Rho GTPases inhibitor. Rhosin hydrochloride specifically binds to RhoA to inhibit RhoA-GEF interaction with a Kd of ~ 0.4 uM, and does not interact with Cdc42 or Rac1, nor the GEF, LARG. Rhosin hydrochloride induces cell apoptosis. Rhosin hydrochloride promotes stress resiliency through enhancing D1-MSN plasticity and reducing hyperexcitability.
    Rhosin hydrochloride
  • HY-13452
    CID-1067700
    Inhibitor 98.06%
    CID-1067700 (ML282) is a pan GTPase inhibitor, and competitively inhibits Ras-related in brain 7 (Rab7) with a Ki of 13 nM.
    CID-1067700
  • HY-15136
    Lonafarnib
    Inhibitor 99.87%
    Lonafarnib (Sch66336) is a potent and orally active farnesyl transferase (FTase) inhibitor. Lonafarnib inhibits the activities of H-ras, K-ras and N-ras with IC50 values of 1.9 nM, 5.2 nM and 2.8 nM, respectively. Lonafarnib also has anti-hepatitis delta virus (HDV) activities.
    Lonafarnib
  • HY-16659
    EHT 1864
    Inhibitor 99.85%
    EHT 1864 is an inhibitor of Rac family small GTPases. EHT 1864 directly binds and impairs the ability of this small GTPase to engage critical downstream effectors required for growth transformation. The Kd values are 40, 50, 60, and 230 nM for Rac1, Rac1b, Rac2 and Rac3, respectively. EHT 1864 also potently inhibits other Rac-dependent transformation processes, Tiam1- and Ras-mediated growth transformation. EHT 1864 prevents Aβ 40 and Aβ 42 production in vivo. EHT 1864 dependently suppresses the release of migrasomes from podocytes induced by LPS, PAN, or HG.
    EHT 1864
  • HY-145928
    Divarasib
    Inhibitor 99.46%
    Divarasib (GDC-6036) is an orally bioavailable, highly potent, and selective KRAS G12C inhibitor with an IC50 of <0.01 μM. Divarasib covalently binds to the switch II (SW-II) pocket of KRAS G12C and irreversibly locks it in the inactive GDP-bound state.
    Divarasib
  • HY-114398
    BAY-293
    Inhibitor 98.06%
    BAY-293, a valuable chemical probe, blocks RAS activation via disruption of the KRAS-SOS1 interaction with an IC50 of 21 nM. BAY-293 is a potent inhibitor of Son of Sevenless 1 (SOS1). SOS1 is the guanine nucleotide exchange factor (GEF) and activator of RAS.
    BAY-293
  • HY-15871
    GGTI298 Trifluoroacetate
    Inhibitor 99.87%
    GGTI298 Trifluoroacetate is a CAAZ peptidomimetic geranylgeranyltransferase I (GGTase I) inhibitor, which can inhibit Rap1A with IC50 of 3 μM; little effect on Ha-Ras with IC50 of >20 μM.
    GGTI298 Trifluoroacetate
  • HY-139612
    Opnurasib
    Inhibitor 98.94%
    Opnurasib (JDQ-443) (NVP-JDQ443) is an orally active, potent, selective, and covalent KRAS G12C inhibitor (extracted from patent WO2021120890A1). Opnurasib shows antitumor activity.
    Opnurasib
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