Ras

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  1. Azathioprine is an immunosuppressive drug, inhibiting purine synthesis and GTP-binding protein Rac1 activation, used in the treatment of organ transplantation and autoimmune diseases.
  2. osteoclastic bone resorption inhibitor

    Zoledronic acid is a bisphosphonate which used to multiple myeloma and prostate cancer treament.
  3. PPMTase inhibitor

    Salirasib is an inhibitor of prenylated protein methyltransferase (PPMTase) with Ki value of 2.6 uM.
  4. KRAS G12C inhibitor

    ARS-853 is a cell-active, selective, covalent KRAS G12C inhibitor with an IC50 of 2.5 μM. ARS-853 inhibits mutant KRAS-driven signaling by binding to the GDP-bound oncoprotein and preventing activation.
  5. Rac1 activation inhibitor

    NSC 23766 is a selective inhibitor of Rac1-GEF interaction. Prevents Rac1 activation by Rac-specific guanine nucleotide exchange factors (GEFs) TrioN and Tiam1 (IC50 ~ 50 μM) without affecting Cdc42 or RhoA activation.
  6. Ras?€?Raf inhibitor

    Kobe2602 is an analog of Kobe0065. Exhibits potent activity to competitively inhibit the binding of H-Ras??GTP to c-Raf-1 RBD with a Ki value of 149 ?? 55 μM.
  7. Rac GTPase Inhibitor

    EHop-016 is a potent and specific inhibitor of Rac1 and Rac3 GTPase activity that inhibits Vav2 interaction with Rac, Rac-activated PAK1, lamellipodia formation, and cell migration.
  8. Cdc42 GTPase inhibitor

    CASIN is a novel and potent Cdc42 inhibitor.
  9. KRas G12C inhibitor

    KRas G12C inhibitor 1 is a compound that inhibits KRas G12C, extracted from patent US 20180072723 A1.
  10. Kras-G12C inhibitor

    KRas G12C inhibitor 3 is a compound that inhibits KRas G12C, extracted from patent US 20180072723 A1.
  11. Kras-G12C inhibitor

    KRas G12C inhibitor 2 is a compound that inhibits KRas G12C, extracted from patent US 20180072723 A1.
  12. GGTase inhibitor

    GGTI-2418 is a synthetic peptidomimetic inhibitor of geranylgeranyltransferase I (GGTase I) that appears to induce apoptosis by downregulating several pivotal oncogenic and tumor survival pathways.
  13. Ras/Raf/MEK inhibitor

    Balamapimod, also known as MKI-822, is a Ras/Raf/MEK inhibitor.
  14. Ras-Raf interaction inhibitor

    Kobe0065 inhibits anchorage-dependent and -independent growth, blocks MEK/ERK activity and induces apoptosis in H-rasG12V transformed NIH3T3 cells.
  15. Kras-G12C inhibitor 1

    KRas G12C inhibitor 1 is a compound that inhibits KRas G12C, extracted from patent US 20180072723 A1.
  16. SOS1 inhibitor

    SOS1-IN-1 is a SOS1 inhibitor.
  17. Cdc42 GTPase inhibitor

    ZCL-278 is a selective inhibitor of Cdc42. Targets the binding site of the Cdc42 guanine nucleotide exchange factor, intersectin (ITSN). Inhibits Cdc42-mediated cellular effects, including microspike formation in 3T3 fibroblasts and neuronal branching in primary neonatal cortical neurons. Also suppresses cell motility and migration in PC3 cells, without cytotoxic effects.
  18. PDE-KRAS inhibitor

    Deltarasin is a novel small molecule inhibiting the KRAS PDEδ interaction and thus impairing oncogenic KRAS signalling.
  19. Rac family GTPase inhibitor

    EHT 1864 is an antiproliferative chemical shown to inhibit Rac family GTPases.
  20. Rac GTPase inhibitor

    NSC 23766 is a cell-permeable, reversible inhibitor of Rac1 activation by the Rac-specific GEFs TrioN and Tiam 1 (IC50 = 50 uM).
  21. K-Ras(G12C) inhibitor

    K-Ras(G12C) inhibitor 6 is an irreversible inhibitor of oncogenic K-Ras(G12C), subverting the native nucleotide preference to favour GDP over GTP.
  22. K-Ras(G12C) inhibitor

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

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

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

    CCG-1423 is a specific inhibitor of Rho pathway-mediated signaling and activation of serum response factor (SRF) transcription.
  26. GTPase Ral inhibitor

    BQU57, a derivative of RBC8, is a selective GTPase Ral inhibitor relative to the GTPases Ras and RhoA.
  27. Rab7 activator

    ML-098 is an activator of the GTP-binding protein Rab7 (EC50 = 77.6 nM).
  28. Ras-Net inhibitor

    XRP44X is a Ras-Net (Elk-3) pathway inhibitor (IC50 = 10-20 nM). Indirectly inhibits Net phosphorylation upstream of Erk1/2 activation.
  29. K-Ras inhibitor

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

    APS-2-79 HCl, small molecule that stabilizes the KSR (Kinase suppressor of Ras) inactive state and antagonizes oncogenic Ras signalling (IC50 value 120 nM against ATP-biotin probe-labelling of KSR2).
  31. KSR/Ras inhibitor

    APS-2-79 is an antagonist of MEK phosphorylation by RAF through direct binding of the KSR active site.
  32. KRAS G12C inhibitor

    MRTX849 is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity.
  33. GGTase I inhibitor

    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.
  34. Ral GTPase inhibitor

    RBC8 is a novel small molecule inhibitor of Ral GTPase; has IC50 of 3.5 μM in H2122 cell and 3.4 μM in H358 cell.
  35. Dual inhibitor of Rac and Cdc42

    MBQ-167 is a potent and dual inhibitor of Rac and Cdc42 with IC50s of 103 nM and 78 nM respectively, in metastatic breast cancer cells.
  36. KRAS-G12C inhibitor

    ARS-1620 is a potent, orally bioavailable covalent inhibitor of KRAS-G12C) and could achieve rapid and sustained in vivo target occupancy to induce tumor regression.
  37. MRCK inhibitor

    BDP9066 is a potent and selective MRCK inhibitor, reducing substrate phosphorylation.
  38. SRE activation inhibitor

    CCG-203971 is an inhibitor of SRE activation in the prostate cancer cell line PC-3 (IC50 = 6.4 μM), with 87% inhibition of SRE activation achieved at 100 μM.
  39. Rac1 inhibitor

    1A-116 is a specific Rac1 inhibitor, can prevent EGF-induced Rac1 activation and block Rac1-P-Rex1 interaction. 1A-116 can induce apoptosis and inhibit cell proliferation, migration and cycle progression in a concentration-dependent manner. 1A-116 also demonstrates a high antimetastatic activity in vivo.

  40. ROCK and MRCK inhibitor

    BDP5290 is a potent inhibitor of both ROCK and MRCK with IC50s of 5 nM, 50 nM, 10 nM and 100 nM for ROCK1, ROCK2, MRCKα and MRCKβ, respectively.
  41. mutant K-ras G12C inhibitor

    ARS-1323 is a novel inhibitor of mutant K-ras G12C.
  42. mutant K-ras G12C inhibitor

    ARS-1630 is a novel inhibitor of mutant K-ras G12C.
  43. Ras inhibitor

    Antineoplaston A 10 is a Ras inhibitor potentially for the treatment of glioma, lymphoma, astrocytoma and breast cancer.
  44. pan-RAS inhibitor

    Ras-IN-3144 is a pan-RAS inhibitor which inhibits RAS signaling pathways in cancer cells and prevents the growth of RAS mutant mouse cancer xenografts.
  45. KRAS-G12C inhibitor

    MRTX1257 is a potent, selective, covalent and irreversible inhibitor of KRAS G12C, MRTX1257 inhibited KRAS dependent ERKphosphorylation in the H358cell assay with an IC50= 900 pM.
  46. SOS1 inhibitor

    BAY-293 is a potent, cell-active SOS1 inhibitor that disrupts the KRAS-SOS1 interaction with IC50 of 21 nM.
  47. ATP-competitive STK19 inhibitor

    ZT-12-037-01 is a potent, selective, ATP-competitive STK19 inhibitor. ZT-12-037-01 effectively blocks oncogenic NRAS-driven melanocyte malignant transformation and melanoma growth in vitro and in vivo.
  48. KRAS G12C inhibitor

    KRAS G12C inhibitor 17 is a potent KRAS G12C inhibitor extracted from patent WO2019110751A1, compound 82, has an IC50 of 5 nM.
  49. KRAS G12C inhibitor

    KRAS G12C inhibitor 16 is a potent KRAS G12C inhibitor extracted from patent WO2019110751A1, compound 39, has an IC50 of 97 nM.
  50. KRAS G12C inhibitor

    KRAS G12C inhibitor 15 is a potent KRAS G12C inhibitor extracted from patent WO2019110751A1, compound 22, has an IC50 of 5 nM.

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