MRTX0902 is a potent SOS1 inhibitor with an IC50 of 46 nM (WO2021127429A1; Example 12-10).

JDQ443 (example 1a) is a covalent KRAS G12C inhibitor (extracted from patent WO2021120890A1).

AZD4625 is a potent, selective, covalent allosteric inhibitor of mutant GTPase KRAS G12C with IC50 of 3 nM, inhibitor H358 cell proliferation with GI50 of 4 nM.AZD4625 is a clinical development candidate for the treatment of KRASG12C positive tumors.

ASP2453 is a potent, selective and covalent KRAS G12C inhibitor. ASP2453 inhibits the Son of Sevenless (SOS)-mediated interaction between KRAS G12C and Raf with an IC50 value of 40 nM.

CCG-100602 is a specific inhibitor of myocardin-related transcription factor A/serum response factor (MRTF-A/SRF) signaling. CCG-100602 specifically block MRTF-A nuclear localization and thus inhibit the fibrogenic transcription factor SRF.

Atrovastatin-PEG3-FITC (compound S31) is a KRAS-PDEδ interaction inhibitor. Atrovastatin-PEG3-FITC acts as a ligand in fluorescence anisotropy assay.

BI-0474 is a potent KRASG12C inhibitor with an IC50 value of 7.0 nM for the GDP-KRAS::SOS1 protein-protein interaction. BI-0474 exhibits good anti-proliferative activity against NCI-H358 cells carrying the G12C mutation. BI-0474 also shows good anti-tumour activity in non-small cell lung cancer xenograft models.

ARS-2102 is a potent covalent KRAS G12C inhibitor for use in cancer research.

(S)-JDQ-443 is an isomer of JDQ-443. JDQ-443 is an orally active, potent, selective, and covalent KRAS G12C inhibitor (extracted from patent WO2021120890A1). JDQ-443 shows antitumor activity.

Spiclomazine hydrochloride (APY-606) is an antipsychotic and antitumor agent. Spiclomazine hydrochloride inhibits KRas. Spiclomazine hydrochloride induces cancer cell apoptosis.

ZCL278 is a Cdc42 small molecule modulator that directly binds to Cdc42 (Kd=11.4 uM) and inhibits Cdc42-intersectin interaction.

MRTX849(Adagrasib) 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-bou

ML-098 is an activator of the GTP-binding protein Rab7 (EC50 = 77.6 nM) that demonstrates selectivity against the related GTPases cdc42, Ras, Rab-2A, and Rac1 (EC50s = 588.8, 346.7, 158.5, and 794.3 nM, respectively).

K-Ras(G12C) inhibitor 12 is an allosteric inhibitor of oncogenic K-Ras(G12C).

APS6-45 is an orally active tumor-calibrated inhibitor (TCI). APS6-45 inhibits RAS/MAPK signaling and exhibits antitumor activity.

BI-3406 (compound I-6) is a potent, selective and orally active inhibitor of the interaction between KRAS and Son of Sevenless 1 (SOS1) with IC50 of 6 nM. BI-3406 reduces the formation of GTP-loaded KRAS, and inhibits MAPK pathway signaling. BI-3406 exhib

ARS-1620 is a covalent compound with high potency and selectivity for KRAS-G12C.

6H05 is a selective, and allosteric inhibitor of oncogenic K-Ras(G12C).

ZG1077 is a covalent KRAS G12C inhibitor. ZG1077 can be used in the research of non-small cell lung cancer (NSCLC).

MRTX849 acid, a derivative of MRTX849, can be used in the synthesis of PROTAC LC-2. LC-2 is a potent and first-in-class PROTAC capable of degrading endogenous KRAS G12C (DC50s between 0.25 and 0.76 μM).

G12Si-2, an analog of G12Si-1, is a negative control tool. G12Si-2 is not a covalent inhibitor of the G12C mutant of K-Ras.

G12Si-1 is a selective K-Ras(G12S) covalent inhibitor, which can inhibit oncogenic signaling of K-Ras(G12S). G12Si-1 shows good ability to covalently engage recombinant K-Ras(G12S) at the mutant serine residue. G12Si-1 can also affect nucleotide cycling of K-Ras by blocking Sos-catalyzed exchange and decreasing the rate of EDTA promoted exchange.

(rac)-Antineoplaston A10 is the racemate of Antineoplaston A10, which is a Ras inhibitor potentially for the treatment of glioma, lymphoma, astrocytoma and breast cancer.

MRTX-EX185 formic is a potent inhibitor of GDP-loaded KRAS and KRAS(G12D), with an IC50 of 90 nM for KRAS(G12D). MRTX-EX185 formic also binds GDP-loaded HRAS.

GDC-6036-NH is from patent WO2020097537A2, and a precursor of compound 17 a/b. Compound 17 a/b is a RAS inhibitor and can be used in cancer research.

NSC 23766 is a specific inhibitor of the binding and activation of Rac GTPase.

VUBI1 is a potent activator of SOS1 which modulates the KRAS pathway, binds directly to SOS1 (Kd=44 nM); VUBI1 increase nucleotide exchange on RAS in vitro at sub-micromolar concentration, rapidly enhances cellular RAS-GTP levels, and invoke biphasic signaling changes in phosphorylation of ERK 1/2 (Hela pERK ICW EC50=5.9 uM).

TH-Z835 is a potent, mutant selective KRAS (G12D) inhibitor with IC50 of 1.6 uM.TH-Z835 binds to both GDP-bound and GMPPNP-bound KRAS G12D with similar affinities, efficiently disrupt KRAS–CRAF interaction, but do not bind to wide type and G12C mutant KRAS.TH-Z835 reduced the pERK level in PANC-1 cells with an IC50 <2.5 uM, exhibited anti-proliferative effects for KRAS(G12D)-bearing pancreatic cancer cell lines PANC-1 and KPC with IC50 of <0.5 uM, induced arrest at the G1 phase of the cell cycle.TH-Z835 displayed anti-tumor effects alone and in combination with anti-PD-L1 antibody in xenograft pancreatic tumor models.

TAT-K-tetracosapeptide is K-tetracosapeptide fused to a cell-permeable TAT peptide, K-tetracosapeptide (K-TC) is a peptide of 24 amino acids corresponding to the helix a5 in KRAS4B, potent inhibitor of KARATE.TAT-K-tetracosapeptide blocks insulin-induced phosphorylation of AKT and its downstream effector TBC1D4, a Rab GTPase-activating protein.TAT-K-tetracosapeptide strongly inhibits insulin-induced transport of GLUT4-GFP to the plasma membrane and glucose uptake in adipocytes.

Ral inhibitor 1 is a covalent inhibitor of RalB (Ras-like GTPase) activation, inhibits guanine exchange factor Rgl2-mediated nucleotide exchange of Ral GTPase, selectively inhibits Ral over Ras; Ral inhibitor 1 inhibits RalB/Rgl2 interaction through covalent reaction at Tyr-82 with IC50 of 49.5 uM; Ral (Ras-like) GTPases are directly activated by oncogenic Ras GTPases.