KRAS inhibitor 11 is a first-in-class, high-affinity, noncovalent allosteric KRAS inhibitor, disrupts KRAS-Raf interaction with Kd of 1.2 uM; binds to activated KRAS with sub-micromolar affinity and disrupts effector binding, thereby inhibiting KRAS signaling and cancer cell growth; dose-dependently decreases both p-ERK and p-cRaf levels in BHK cells expressing KRASG12D and KRASG12V, suggesting inhibition of RAS signaling via the MAPK pathway.
LUNA18 is an orally active KRAS inhibitor with an IC50 of ＜2 nM against KRASG12D-SOS. LUNA18 can be used for the research of cancer[1].
KRAS inhibitor-15 (compound 3-19) is a potent KRAS G12C inhibitor with an IC50 of 0.954 µM. KRAS inhibitor-15 shows p-ERK inhibition activities with IC50s of 2.03, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-15 has the potential for the research of pancreatic, colorectal, and lung cancers[1].
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].
BI-2865 is a none-covalent pan-KRAS Inhibitor. BI-2865 binds to WT, G12C, G12D, G12V and G13D mutant KRAS with KDs of 6.9, 4.5, 32, 26, 4.3 nM respectively. BI-2865 inhibits the proliferation of G12C, G12D or G12V mutant KRAS expressing BaF3 cells (mean IC50: roughly 140 nM)[1].
MLS000532223 is a high affinity, selective inhibitor of Rho family GTPases, with EC50 ranging from 16 μM to 120 μM. MLS000532223 prevents GTP binding to several GTPases. Small GTPases are key regulators of cellular activity [1].
JDQ-443 (example 1a) is a covalent KRAS G12C inhibitor (extracted from patent WO2021120890A1)[1].
MRTX849 is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. MRTX849 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[1][2].
Salirasib is a Ras inhibitor that inhibits specifically both oncogenically activated Ras and growth factor receptor-mediated Ras activation, resulting in the inhibition of Ras-dependent tumor growth.
pan-KRAS-IN-4 (compound 5) is a potent inhibitor of KRAS with IC50s of 0.37 nM (Kras G12C), 0.19 nM (Kras G12V), respectively[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].
TH-Z816 is a reversible inhibitor againstKRAS(G12D)mutation with an IC50 value of 14 μM, which can be used in cancer research[1].
PROTAC K-Ras Degrader-1 (Compound 518) is potent K-Ras degrader based PROTAC, exhibits ≥70% degradation efficacy in SW1573 cells[1].
KY1022 is a ras destabilizer. KY1022 targets the Wnt/ß-catenin pathway and inhibits development of metastatic colorectal cancer.
KRAS G12D inhibitor 16 is a KRAS G12D inhibitor. KRAS G12D inhibitor 16 has inhibitory activity against KRAS G12D and KRAS G12D mutation with IC50 value of 0.7 nM and 0.35 μM, respectively. KRAS G12D inhibitor 16 can be used for the research of many malignant tumor, such as pancreatic ductal adenocarcinomas (PDAC), colon and rectal carcinomas (CRC), non-small cell lung carcinomas (NSCLC)[1].
RMC-4998 is a molecular glue compound with good antitumor activity. RMC-4998 is able to form a ternary complex with CYPA and an activated KRAS G12C mutant. Furthermore, CYPA binding to KRAS G12C blocks the interaction between activated KRAS mutants and downstream effector proteins, thereby inhibiting signaling that promotes cell proliferation[1].
KRAS degrader-1 (compound 1) is a potent KRAS degrader. KRAS degrader-1 target specific proteins for degradation through the autophagy-lysosomal degradation pathway[1].
SOS1-IN-16 (Comp 54) is a selective inhibitor of SOS1 with an IC50 of 7.2 nM. SOS1-IN-16 has inhibitory activity of CYP3A4 when using testosterone as a substrate, with an IC50 of 8.9μM. SOS1-IN-16 can be used for cancer research[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].
XRP44X inhibits Ras-induced transcription activation with the IC50 of 10 nM. XRP44X inhibits activation of the Ras-Erk-1/2 pathway by FGF-2[1]. XRP44X is an inhibitor of Ras/Erk activation of Elk3 that also affects microtubules[2].
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.
Rac1-IN-3 (Compound 2) is a Rac1 inhibitor with an IC50 of 46.1 μM[1].
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.
CX-5011 is a CK2 inhibitor. CX-5011 also induces Rac1 activation. CX-5011 induces apoptosis and induces cancer cell death[1][2].
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[1][2].
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].