| Cat.No. | Name | Information |
|---|---|---|
| M9428 | MRTX849 (Adagrasib) | MRTX849 (Adagrasib) is a potent, highly selective, oral available KRAS G12C inhibitor. |
| M9356 | AMG-510 | AMG-510 (Sotorasib) is a potent KRAS G12C covalent inhibitor. |
| M8999 | CCG-1423 | CCG-1423 is a novel specific inhibitor of RhoA transcriptional signaling. |
| M6282 | NSC 23766 | NSC 23766 is an inhibitor of Rac GTPase targeting Rac activation by guanine nucleotide exchange factors (GEFs) with IC50 of ~50 μM in a cell-free assay; does not inhibit the closely related targets, Cdc42 or RhoA. |
| M2562 | ZCL278 | ZCL278 is a selective Cdc42 GTPase inhibitor with Kd of 11.4 μM. |
| M66241 | ERAS-4001 | ERAS-4001 is a pan-KRAS inhibitor, it has potent antitumor activities and significantly inhibits the proliferation of wild-type and mutant (such as KRASG12D, KRASG12V and KRASG12C) cancer cells. ERAS-4001 binds to both wild-type KRAS and the KRAS G12X mutant, and inhibits downstream signalling by KRAS via effector proteins such as the RAF protein family. |
| M58664 | AMG410 | 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 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. |
| M56328 | BI-2493 | BI-2493 is a structural analogue of BI-2865 and a highly selective and orally active pan-KRAS inhibitor. |
| M56323 | Rasarfin | Rasarfin is a dual Ras and ARF6 inhibitor. |
| M56321 | Z62954982 | Z62954982 (ZINC08010136) is a potent, selective and cell-permeable Rac1 (IC50=12 μM) inhibitor that is 4 times more effective than NSC23766 (IC50=50 μM). |
| M55573 | ACBI3 | ACBI3 (compound 7) is a pan-KRAS degrader. ACBI3 achieves in vivo degradation of oncogenic KRAS. |
| M55031 | BBO-8520 | BBO-8520 is a first-in-class orally active covalent KRAS G12C inhibitor. BBO-8520 inhibits KRASG12C (ON) by locking the GTP-binding protein in state 1, a conformation incapable of binding effectors, thereby inhibiting the downstream signaling of KRASG12C (ON) that promotes cell proliferation. BBO-8520 also rapidly and completely blocks the RAS-RAF1 interaction, returning KRASG12C to its inactive (OFF) state. |
| M55018 | RMC-9805 | RMC-9805 (KRAS G12D inhibitor 18) is a first-in-class, orally active KRAS G12D inhibitor. RMC-9805 (KRAS G12D inhibitor 18) inhibits RAS signaling and induces apoptosis in KRAS G12D mutant cancer cells. |
| M54858 | RMC-7977 | RMC-7977 is a highly selective, reversible, tri-complex RAS inhibitor of the active (GTP-bound) forms of KRAS, HRAS, and NRAS, with affinity for both mutant and wild type (WT) variants. RMC-7977 demonstrated potent activity against RAS-addicted tumours carrying various RAS genotypes, particularly against cancer models with KRAS codon 12 mutations (KRASG12X). |
| M49938 | Glecirasib | Glecirasib is a potent, irreversible, orally active KRAS G12C inhibitor for studies related to KRAS G12C-mediated cancers. |
| M40832 | Daraxonrasib | Daraxonrasib (RAS-IN-2; RMC-6236) is a potent pan-KRAS inhibitor targeting activation-state KRAS for cancer-related studies. |
| M40563 | AZD4747 | AZD4747 is an orally active, potent, and selective KRAS G12C inhibitor that crosses the blood-brain barrier and can be used in studies related to solid tumors with KRAS G12C mutations. |
| M40562 | LUNA18 | LUNA18 is an orally active RAS cyclic peptide inhibitor that selectively targets, binds and inhibits Ras, thereby inhibiting Ras-dependent signaling and ultimately suppressing the proliferation of Ras-overexpressing tumor cells. It can be used in studies related to solid tumors. |
| M40499 | BI-2865 | BI-2865 is a non-covalent pan-KRAS inhibitor that binds to KRAS WT, G12C, G12D, G12V, and G13D mutants with Kd values of 6.9 nM, 4.5 nM, 32 nM, 26 nM, and 4.3 nM, respectively.It can be used in studies related to KRAS mutant tumors. |
| M30401 | 8-CPT-2Me-cAMP sodium | 8-CPT-2Me-cAMP sodium is a selective activator of exchange proteins activated by cAMP (Epac), the cAMP sensitive guanine nucleotide exchange factors (GEFs) for the small GTPases Rap1 and Rap2. 8-CPT-2Me-cAMP sodium activates Epac1 (EC50 = 2.2 μM), but not PKA (EC50> 10 μM). 8-CPT-2Me-cAMP sodium stimulates Epac-mediated Ca2+ release in pancreatic β-cells in vitro. |
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