Oligomycin D (Rutamycin A) is an antibiotic. Oligomycin D can be derived from a strain of S. rutgersensis. Oligomycin D also is a potent inhibitors of K-Ras PM localization. Oligomycin D can be used for the research of various cancers[1].
Neogrifolin is an inhibitor of KRAS. Neogrifolin suppress KRAS expression in human colon cancer cells. Neogrifolin has anti-cell viability activity against HeLa, SW480 and HT29 cells wih IC50s of 24.3, 34.6, and 30.1 μM, respectively[1].
KRAS G12D inhibitor 15 is a potent inhibitor of KRAS G12D. KRAS G12D inhibitor 15 has the potential for the research of various diseases or disorders, such as cancer or cancer metastasis (extracted from patent WO2022042630A1, compound 243)[1].
PROTAC K-Ras Degrader-1 (Compound 518) is potent K-Ras degrader based PROTAC, exhibits ≥70% degradation efficacy in SW1573 cells[1].
KRAS G12D inhibitor 13 is a potent inhibitor of KRAS G12D. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12D inhibitor 13 has the potential for the research of KRAS G12D-mediated cancer (extracted from patent WO2021108683A1, compound 142)[1].
Atrovastatin-PEG3-FITC (compound S31) is a KRAS-PDEδ interaction inhibitor. Atrovastatin-PEG3-FITC acts as a ligand in fluorescence anisotropy assay[1][2].
MRTX-1257 is a selective, irreversible, covalent and oral active KRAS G12C inhibitor, with an IC50 of 900 pM for KRAS dependent ERK phosphorylation in H358 cells[1].
BI-2493 is a non-covalent and pan KRAS inhibitor. BI-2493 inhibits the interaction of GDP-bound KRAS with SOS1 in a biochemical assay using recombinant proteins with IC50s < 11nM. BI-2493 can be used in studies about KRAS-driven cancers.
CID-1067700 is a pan GTPase inhibitor, and competitively inhibits Ras-related in brain 7 (Rab7) with a Ki of 13 nM.
MBQ-167 is a dual Rac/Cdc42 inhibitor, with IC50s of 103 nM for Rac 1/2/3 and 78 nM for Cdc42 in MDA-MB-231 cells, respectively.
Diazepinomicin (TLN-4601) is a secondary metabolite produced by Micromonospora sp. Diazepinomicin (TLN-4601) inhibits the EGF-induced Ras-ERK MAPK signaling pathway and induces apoptosis. An anti-tumor agent for K-Ras mutant models[1].
CCG-232601 is a potent (IC50=0.55 uM), orally bioavailable Rho/MKL1/SRF transcriptional pathway that target transcriptional factor MRTF; inhibits the development of bleomycin-induced dermal fibrosis in mice when administered at 50mg/kg.
KRAS G12C inhibitor 22 is a KRAS G12C inhibitor extracted from patent WO2021219072A1, example 120[1].
SOS1/KRAS-IN-1(Compound 2) is a SOS1/KRAS inhibitor, which can be used in the research of SOS1/KRAS-mediated diseases[1].
KRAS G12C inhibitor 5 is a KRas G12C inhibitor extracted from patent WO2017201161A1, Compound example 147[1].
GGTI-286, a potent and cell-permeable GGTase I inhibitor, is 25-fold more potent (IC50=2 μM) than the corresponding methyl ester of FTI-276 (HY-15873A). GGTI-286 selectively inhibits geranylgeranylation of Rap1A over farnesylation of H-Ras in NIH3T3 cells (IC50s =2 and >30 μM, respectively). GGTI-286 also potently inhibits oncogenic K-Ras4B stimulation with an IC50 of 1 μM[1].
SOS1 activator 1 (Compound 64) is a potent activator of SOS1-mediated nucleotide exchange with a Kd of 44 nM. SOS1 is a guanine nucleotide exchange factor that catalyzes the exchange of GDP for GTP on RAS[1].
KRAS G12C inhibitor 24 is a potent KRAS G12C inhibitor. KRAS G12C inhibitor 24 inhibits KRAS G12C/SOS1 interaction with an IC50 of＜50 nM (CN113563323A, compound 1)[1].
KRAS inhibitor-13 (compound 5-6) is a potent KRAS G12C inhibitor with an IC50 of 0.883 µM. KRAS inhibitor-13 shows p-ERK inhibition activities with IC50s of 5.9, >100 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-13 has the potential for the research of pancreatic, colorectal, and lung cancers[1].
SOS1-IN-14 is a potent, selective and orally active SOS1 inhibitor with an IC50 value of 3.9 nM. SOS1-IN-14 can be absorbed in the intestine via a P-glycoprotein-mediated efflux mechanism. SOS1-IN-14 can be used to research KRAS-mutated cancers. SOS1-IN-14 has better potent tumor suppression than BI-3406 (HY-125817)[1].
BQU57 shows selective inhibition for Ral relative to Ras or Rho and inhibit xenograft tumor growth similar to depletion of Ral by siRNA. The IC50 for BQU57 of 2.0 μM in H2122 and 1.3 μM in H358.IC50 value: 2.0 μM (H2122 cell), 1.3 μM (H358 cell)Target: Ralin vitro: BQU57 inhibits Ral binding to its effector RalBP1, Ral-mediated cell spreading in murine fibroblasts and anchorage-independent growth of human cancer cell lines.in vivo: H2122 xenograft tumors are collected 3h after a single intraperitoneal injection BQU57 (10/20/50 mg/kg) and activation of Ral in the extracts is analyzed in RalBP1 pull-down assays. Both RalA and RalB are significantly inhibited by BQU57. By contrast, no inhibition of Ras and RhoA activity is observed.
ARS-1323 is a novel inhibitor of mutant K-ras G12C extracted from patent WO 2015054572 A1.
Pan-RAS-IN-1 is a pan-Ras inhibitor that disrupts the interaction of Ras proteins and their effectors.
KRAS G12C inhibitor 59 is a KRAS G12C inhibitor with anticancer effects (WO2023036282A1, compound II)[1].
PAT-IN-2 is a protein acyl transferases (PAT) inhibitor. PAT-IN-2 competitively inhibits Erf2 autopalmitoylation (WO2017011518A1; compound 25)[1].
KRas G12C inhibitor 2 is a compound that inhibits KRas G12C, extracted from patent US 20180072723 A1.
KRAS G12C inhibitor 53 (Compound 1) is a KRAS G12C inhibitor[1].
CFL-120 is a potent KRasG12C inhibitor. CFL-120 shows an antiproliferative effect. CFL-120 shows anticancer activity. CFL-120 has the potential for the research of lung cancer[1].
KRAS G12C inhibitor 50 (Example 4) is a KRAS G12C inhibitor with an IC50 of 46.7 nM[1].
RBC10 is an anti-cancer agent. RBC10 inhibits the binding of Ral to its effector RALBP1. RBC10 also inhibits Ral-mediated cell spreading of murine embryonic fibroblasts and anchorage-independent growth of human cancer cell lines[1].