| 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. |
| M58646 | HRS-4642 | HRS-4642 is a selective KRAS(G12D) inhibitor, with Kd value of 0.083 nM. HRS-4642 has anti-cancer activity. HRS-4642 exhibits significant in vivo potency. |
| M56328 | BI-2493 | BI-2493 is a structural analogue of BI-2865 and a highly selective and orally active pan-KRAS inhibitor. |
| M56326 | MK-1084 | Calderasib (MK-1084) is a selective KRAS G12C inhibitor. MK-1084 can be used in studies related to solid tumors. |
| 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. |
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