Ras Inhibitor

Ras Inhibitors (565):

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 K_D 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-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 K_d = 23 nM. RSC-1255 exhibits preferential cytotoxicity toward KRAS-mutant cancer cells, especially KRAS^G13D and KRAS^G12V 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-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-156498

RMC-7977	Inhibitor	99.48%
RMC-7977 is an orally active triple-complex RAS inhibitor that can simultaneously bind to cyclophilin A (CYPA) (K_d = 195 nM) and KRAS (G12V) (K_d = 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 KRAS^G12C cancer models, and demonstrates good tolerability across various RAS cancer models.

HY-B0105

Ketoconazole	Inhibitor	99.57%
Ketoconazole (R-41400) is an imidazole anti-fungal agent, a CYP3A4 and CYP24A1 inhibitor.

HY-12755

ML141	Inhibitor	99.96%
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.

HY-15723A

NSC 23766 trihydrochloride	Inhibitor	99.41%
NSC 23766 trihydrochloride is an inhibitor of Rac1 activation.

HY-13452

CID-1067700	Inhibitor	99.71%
CID-1067700 (ML282) is a pan GTPase inhibitor, and competitively inhibits Ras-related in brain 7 (Rab7) with a K_i of 13 nM.

HY-12646

Rhosin hydrochloride	Inhibitor	99.94%
Rhosin hydrochloride is a potent, specific RhoA subfamily Rho GTPases inhibitor. Rhosin hydrochloride specifically binds to RhoA to inhibit RhoA-GEF interaction with a K_d 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.

HY-15723

NSC 23766	Inhibitor	99.86%
NSC 23766 is a cell-permeable, reversible and specific inhibitor of Rac GTPase, used for cancer treatment.

HY-15136

Lonafarnib	Inhibitor	99.85%
Lonafarnib (Sch66336) is a potent and orally active, and CNS-penetrant 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.

HY-153346

Elironrasib	Inhibitor	99.65%
Elironrasib is an orally active and covalent inhibitor of KRAS^G12C(ON). Elironrasib forms a tri-complex within tumor cells between KRAS^G12C(ON) and cyclophilin A (CypA). Thus, Elironrasib prevents KRAS^G12C(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 KRAS^G12C mutant cells with a median IC₅₀ of 0.11 nM.

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 K_d 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.

HY-145928

Divarasib	Inhibitor	99.31%
Divarasib (GDC-6036) is an orally active, selective KRAS^G12C inhibitor with an IC₅₀ of <0.01 μM. Divarasib covalently binds Cys12 in GDP-bound KRAS^G12C, 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 KRAS^G12C-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 KRAS^G12C-mutated solid tumors.

HY-12874

CASIN	Inhibitor	99.89%
CASIN is a selective GTPase Cdc42 inhibitor with an IC₅₀ of 2 uM. CASIN can be used for the research of cancer.

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