Ras 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.

CFL-137 is a potent KRas^G12C inhibitor. CFL-137 shows an antiproliferative effect. CFL-137 shows anticancer activity. CFL-137 has the potential for the research of lung cancer.

Broussoflavonol F is a potent dual inhibitor of the HER2-RAS-MEK-ERK signaling pathway and mushroom tyrosinase with an IC₅₀ value of 82.3 μM. Broussoflavonol F downregulates the expression of RAS, HER2, phosphorylated BRAF, phosphorylated MEK and phosphorylated Erk proteins. Broussoflavonol F induces cell cycle arrest and apoptosis, and exhibits cytotoxicity in colon cancer cells. Broussoflavonol F inhibits endothelial proliferation, migration and tube formation, suppresses subintestinal vascular development, and reduces the mRNA levels of angiogenesis-associated genes.Broussoflavonol F can be used for colon cancer research.

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.

KRAS inhibitor-3 is an inhibitor of KRAS inhibitor. KRAS inhibitor-3 binds to WT and oncogenic KRAS mutants with high affinity (K_D: 0.28 μM for KRAS WT, 0.63 μM for KRAS G12C, 0.37 μM for KRAS G12D, 0.74 μM for KRAS Q61H). KRAS inhibitor-3 also disrupts interaction of KRAS with Raf.

VVD-699 is a covalent blocker of the RAS-p110α interaction with oral activity. VVD-699 inhibits activation of PI3Kα (IC₅₀: 104 nM in H358 cells) . VVD-699 inhibits phosphorylated AKT. VVD-699 can be used for the research of KRAS mutant/amplified cancer.

(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.

ARS-1323-alkyne is a covalent inhibitor probe that covalently binds to the Switch-II pocket (S-IIP) of the KRAS G12C mutant protein. ARS-1323-alkyne visualizes the covalent modification of KRAS G12C and quantitatively measures the binding efficiency of the inhibitor to the target. ARS-1323-alkyne can be used to validate the target occupancy of KRAS G12C inhibitors and the synergistic mechanism of combination therapy.

KRAS G12D inhibitor 29 (Compound Formula (I)) is an orally active and selective KRAS^G12D mutant inhibitor. KRAS G12D inhibitor 29 blocks downstream signaling pathways mediated by KRAS^G12D, suppressing tumor cell proliferation. KRAS G12D inhibitor 29 is promising for research of KRAS^G12D mutation-related cancers (such as pancreatic cancer, lung cancer, colorectal cancer).

l-Naproxen ((R)-Naproxen) is an enantiomer of (S)-Naproxen. l-Naproxen can inhibit Cdc42 and Rac1 (EC₅₀=96 μM and 212 μM, respectively), and show anti-tumor activity. l-Naproxen is a nonsteroidal antiinflammatory agent (NSAID).

ZINC69391, a specific Rac1 inhibitor, interferes with Rac1-GEF interaction by masking Trp56 residue on Rac1 surface. ZINC69391 interferes with the interaction of Rac1 with Dock180 and reduces Rac1-GTP levels. ZINC69391 induces apoptosis, and shows antiproliferative and antimetastatic effects.