Ras Inhibitor

Digeranyl bisphosphonate (DGBP) is a potent geranylgeranylpyrophosphate (GGPP) synthase inhibitor, which inhibits geranylgeranylation of Rac1.

MLS-573151 (MLS000573151) is a selective GTPase Cdc42 inhibitor with an EC₅₀ of 2 μM. MLS-573151 is inactive against other GTPases family members, such as Rab2, Rab7, H-Ras, Rac1, Rac 2 and RhoA wild-type. MLS-573151 acts by blocking the binding of GTP to Cdc42.

ML-097 (CID-2160985) is a pan Ras-related GTPases activator that can activate Rac1, cell division cycle 42, Ras, and Rab7.

Atranorin is a secondary metabolite of lichens and AKT inhibitor. Atranorin possesses multiple activities such as antibacterial, anti-inflammatory, antioxidant, anti-glycation, analgesic, and anti-tumor effects. Atranorin has IC₅₀ values for scavenging DPPH and ABTS free radicals of 117 μM and less than 10 μM, respectively. Additionally, Atranorin also exhibits effects in promoting wound healing. Atranorin can be used in the research of various diseases, including myelodysplastic syndromes, tumors, and inflammatory conditions.

AZA1 is a potent dual inhibitor of Rac1 and Cdc42. AZA1 induces prostate cancer cells apoptosis and inhibits prostate cancer cells proliferation, migration and invasion.

PRLX-93936 dihydrochloride is a molecular Glues that binds to and reprograms the TRIM21 ubiquitin ligase to degrade nuclear pore complexes. PRLX-93936 dihydrochloride binds to TRIM21, forms a ternary complex with TRIM21 and NUP98, and mediates the ubiquitination and proteasomal degradation of NUP98 and other nuclear pore complex proteins. PRLX-93936 dihydrochloride induces the loss of short-lived cytoplasmic mRNA transcripts, triggers cancer cell apoptosis (Apoptosis), and inhibits the activated Ras pathway. PRLX-93936 dihydrochloride inhibits HIF-1 under hypoxic conditions (IC₅₀ = 0.09 μM in cell-based reporter gene assay). PRLX-93936 dihydrochloride suppresses tumor growth in mouse models and improves survival rates in mouse models of multiple myeloma. PRLX-93936 dihydrochloride is applicable to research related to pancreatic cancer and multiple myeloma.

Fendiline, a diphenylalkylamine type of antianginal agent, is an L-type calcium channel blocker (IC₅₀ of 17 µM). Fendiline is also a selective K-Ras inhibitor, and has no effect on H-Ras and N-Ras. Fendiline inhibits K-Ras plasma membrane localization (IC₅₀ of 9.64 μM), inhibits K-Ras signal output and blocks the proliferation of pancreatic, colon, lung, and endometrial cancer cell lines expressing oncogenic mutant K-Ras. Fendiline is a STING agonist and is able to inhibit the growth of multiple refractory cold tumors (MC38, CT26 and B16F10).

Rasarfin is a dual Ras and ARF6 inhibitor.

K-Ras(G12C) inhibitor 12 is an irreversible inhibitor of K-Ras(G12C). K-Ras(G12C) inhibitor 12 can alter the nucleotide-binding preference of K-Ras and block its interaction with effector proteins. K-Ras(G12C) inhibitor 12 can reduce cell viability and induce apoptosis in lung cancer cell lines with G12C mutations. K-Ras(G12C) inhibitor 12 has anti-tumor activity.

Deltarasin is an inhibitor of?KRAS-PDEδ interaction with?K_d?of 38 nM for binding to purified PDEδ.

HJC0197 is a potent Epac1 (exchange protein directly activated by cAMP 1) and Epac2 (IC₅₀=5.9 μM for Epac2) antagonist. HJC0197 selectively blocks cAMP-induced Epac activation. HJC0197 inhibits Epac1-mediated Rap1-GDP exchange activity at 25 μM in the presence of equal concentration of cAMP.

(R)-Ketorolac is an orally active Cdc42 and Rac1 inhibitor. (R)-Ketorolac inhibits GTPase. (R)-Ketorolac alters ovarian cancer cell behaviors critical for invasion and metastasis. (R)-Ketorolac ameliorates cancer-associated cachexia.

CID44216842 (Cdc42-IN-1) is a potent Cdc42-selective guanine nucleotide binding lead inhibitor. The EC₅₀s for Cdc42 WT and Cdc42Q61L mutant are 1.0 and 1.2 μM in GTP binding assay, respectively. The EC₅₀s for Cdc42 WT and Cdc42Q61L mutant are 0.3 and 0.5 μM in GDP binding assay, respectively. Use as a molecular probe.

ZT-12-037-01 is a STK19-targeted inhibitor, has a high-affinity interaction with STK19 protein and inhibits oncogenic NRAS-driven melanocyte malignant transformation. ZT-12-037-01 is an ATP-competitive inhibitor, inhibiting phosphorylation of NRAS (major isoform of Ras family) with an IC₅₀ of 24 nM.

RBC8 is a selective and allosteric RALA and RALB inhibitor. RBC8 stabilizes the inactive GDP-bound state of Ral, preventing its activation. RBC8 promotes the phosphorylation of proteins related to the MAPK/JNK pathway. RBC8 has the activity of inhibiting tumor cell proliferation, migration and invasion. RBC8 is used in the study of various cancers such as lung cancer, gastric cancer, and multiple myeloma.

R-IMPP (PF-00932239) is a PCSK9 translation inhibitor and a selective 80S ribosome binder. R-IMPP inhibits the KRAS/MEK/ERK signaling cascade. R-IMPP reduces LPS-induced nuclear translocation of NFkB P65. R-IMPP increases LDL-R levels in cells, promotes LDL-C uptake, and does not alter the secretion of transferrin or albumin. R-IMPP inhibits the growth of colorectal cancer (CRC) cells, organoids and xenografts carrying APC/KRAS mutations, as well as the number and burden of spontaneous mouse tumors. R-IMPP can be used in research related to colorectal cancer with APC/KRAS mutations, hepatic ischemia-reperfusion injury and hypercholesterolemia.

RMC-0331 (RM-023) is a potent, selective and orally bioavailable SOS1 inhibitor. RMC-0331 is an in vivo tool compound that blocks RAS activation via disruption of the RAS-SOS1 interaction.

(R)-CE3F4 is a potent and selective inhibitor of exchange protein directly activated by cAMP isoform 1 (Epac1), with an IC₅₀ of 4.2 μM, with 10-fold selectivity for Epac1 over Epac2 (IC₅₀, 44 μM). (R)-CE3F4 is more potent than racemic CE3F4 and (S)-CE3F4.

Calderasib (MK-1084) is a selective KRAS G12C inhibitor. Calderasib exhibits anticancer activity and can be used either alone or in combination with Pembrolizumab (HY-P9902) for cancer research.

KRAS inhibitor-9, a potent KRAS inhibitor (K_d=92 μM), blocks the formation of GTP-KRAS and downstream activation of KRAS. KRAS inhibitor-9 binds to KRAS G12D, KRAS G12C and KRAS Q61H protein with a moderate binding affinity. KRAS inhibitor-9 causes G2/M cell cycle arrest and induces apoptosis. KRAS inhibitor-9 selectively inhibits the proliferation of NSCLC cells with KRAS mutation but not normal lung cells.