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

ARS-1323 is a novel inhibitor of mutant K-ras G12C.

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

ARS-1630 is the R-conformational atropisomer of ARS-1620, 1,000-fold less potent than ARS-1620 (1.2 ± 0.6 M-1s-1) and thus acts as a unique inactive control compound..

ARS-853 is a selective, covalent inhibitor of KRAS-G12C that inhibits mutant KRAS driven signaling by binding to the GDP bound oncoprotein and preventing activation.

KBFM123 (KBFM-123) is a small molecule, allosteric inhibitor of GTP-bound form of H-Ras, weakly inhibits the association of H-RasG12V-GppNHp with c-Raf-1 RBD (Kd=10-100 uM).

KRAS inhibitor C6ME is a small-molecule compound that blocks biochemical and cellular functions of KRASG12V in vitro..

KRAS inhibitor Cmpd2 is a small-molecule compound that blocks biochemical and cellular functions of KRASG12V with IC50 of 0.8 uM in vitro.

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

K-Ras-IN-1 is a K-Ras inhibitor, by binding to K-Ras in a hydrophobic pocket that is occupied by Tyr-71 in the apo-Ras crystal structure.

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).

NSC 23766 is a specific inhibitor of the binding and activation of RAC GTPase with IC50 of ~50 μM; does not inhibit the closely related targets, Cdc42 or RhoA.

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

Pan-RAS-IN-1 is a pan-Ras inhibitor that disrupts the interaction of Ras proteins and their effectors.

RAS inhibitor Abd-7 is a potent RAS-binding compound (Kd=51 nM) that interacts with RAS in cells, prevents RAS-effector interactions and inhibits endogenous RAS-dependent signalling.

RasGRP3 ligand 96 is a potent, selective ligand of Ras guanine-releasing protein 3 (RasGRP3) with Ki of 1.75 nM, showed 73-fold and 45-fold selectivity relative to PKCα and PKCε for in vitro binding activity resepctively.

SOS1 activator 17 is a small molecule activator of guanine nucleotide exchange factor SOS1 with EC50 of 0.8 uM, modulates RAS signaling in vitro.

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

RAS GTPase inhibitor 1 (example 51) is a RAS GTPase inhibitor with anti-tumor activity, extracted from patent WO2018212774A1. RAS GTPase inhibitor 1 (example 51) exhibits an EC50 less than 1 μM for at least one nucleotide exchange and an IC50 less than 1 μM in H727 cells.

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

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

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.

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.

KRAS inhibitor-9, a potent KRAS inhibitor (Kd=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.

Rac1 Inhibitor W56 is a peptide comprising residues 45-60 of the guanine nucleotide exchange factor (GEF) recognition/activation site of Rac1. Rac1 Inhibitor W56 selectively inhibits Rac1 interaction with Rac1-specific GEFs TrioN, GEF-H1 and Tiam1.

Rac1 Inhibitor W56 TFA is a peptide comprising residues 45-60 of the guanine nucleotide exchange factor (GEF) recognition/activation site of Rac1. Rac1 Inhibitor W56 TFA selectively inhibits Rac1 interaction with Rac1-specific GEFs TrioN, GEF-H1 and Tiam1.

Antineoplaston A10 is a naturally occurring substance in the human body that that can be potentially used for the treatment of glioma, lymphoma, astrocytoma and breast cancer. The main ingredient active of antineoplaston A10 (Phenylacetylglutamine, PG) inhibits RAS and promotes apoptosis.

RAS/RAS-RAF-IN-1 is a potent RAS and RAS-RAF inhibitor. RAS/RAS-RAF-IN-1 has a KD of 5.0 μΜ-15 μΜ for cyclophilin A (CYPA) binding affinity. RAS/RAS-RAF-IN-1 has antitumor activity.

KRAS inhibitor-10 selectively and effectively inhibit RAS proteins, and particularly KRAS proteins. KRAS inhibitor-10 is an orally active anti-cancer agent and can be used for cancer research, such as pancreatic cancer, breast cancer, multiple myeloma, leukemia and lung cancer. KRAS inhibitor-10 is a tetrahydroisoquinoline compound (compound 11) extracted from patent WO2021005165 A1.

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.

SAH-SOS1A TFA is a peptide-based SOS1/KRAS protein interaction inhibitor. SAH-SOS1A TFA binds to wild-type and mutant KRAS (G12D, G12V, G12C, G12S, and Q61H) with nanomolar affinity (EC50=106-175 nM), directly and independently blocks nucleotide association, impairs KRAS-driven cancer cell viability, and exerts its effects by on-mechanism blockade of the ERK-MAPK phosphosignaling cascade downstream of KRAS.

StRIP16, bioavailable StRIP3 analogue, is a double-stapled peptide which can bind to Rab8a GTPase, with a Kd of 12.7 μM.

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).

MRTX1133 is a highly selective, first-in-class inhibitor of KRAS G12D. MRTX1133 targets the KRAS G12D protein in both active and inactive states. MRTX1133 selectively inhibits KRAS G12D mutant, but not KRAS wild-type, tumor cells.

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

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.

KRAS mutant protein inhibitor 1 is a KRAS mutant protein inhibitor for potential treatment in cancer.

KRAS G12C inhibitor 18 is a potent and orally active KRAS G12C inhibitor. Anti-tumor activities.

RTIL 13 is a potent inhibitor of dynamin GTPase, with an IC50 of 2.3 µM for dynamin I GTPase. RTIL 13 also targets pleckstrin homology lipid binding domain. RTIL 13 can inhibit receptor-mediated and synaptic vesicle endocytosis, with IC50s of 9.3 μM and 7.1 μM, respectively.

RM-018 is a potent, functionally distinct tricomplex KRASG12C active-state inhibitor. RM-018 retains the ability to bind and inhibit KRASG12C/Y96D and could overcome resistance. RM-018 binds specifically to the GTP-bound, active [“RAS(ON)”] state of KRASG12C.

HG106 is a potent SLC7A11 inhibitor and enhances ROS generation, ER stress, and ultimately growth arrest specifically in KRAS-mutant lung adenocarcinoma (LUAD).

8-CPT-2Me-cAMP sodium is a selective activator of exchange proteins activated by cAMP (Epac), the cAMP sensitive guanine nucleotide exchange factors (GEFs) for the small GTPases Rap1 and Rap2. 8-CPT-2Me-cAMP sodium activates Epac1 (EC50 = 2.2 μM), but not PKA (EC50> 10 μM). 8-CPT-2Me-cAMP sodium stimulates Epac-mediated Ca2+ release in pancreatic β-cells in vitro.

SOS1-IN-3 is a potent SOS1 (son of sevenless homolog 1) inhibitor with an IC50 of 5 nM. SOS1-IN-3 has anticancer effects (WO2019122129A1; compound I-1).

SOS1-IN-4 is a potent SOS1 inhibitor with an IC50 of 56 nM for KRAS-C12C/SOS1 interaction (WO2021228028 A1, example 65).

SOS1-IN-5 is a potent inhibitor of SOS1. SOS1-IN-5 is a pyrimidobicyclic derivative. SOS1-IN-5 blocks the activation of KRAS by interfering with RAS-SOS1 interaction, and achieves the purpose of broad-spectrum inhibition of KRAS activity. SOS1-IN-5 has the potential for the research of cancer diseases (extracted from patent WO2021203768A1, compound 4).

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).

KRAS G12C inhibitor 27 is a KRAS G12C inhibitor with antitumor effects (WO2021109737).

KRAS G12C inhibitor 26 is a KRAS G12C inhibitor with antitumor effects (WO2021109737).

KRAS G12C inhibitor 23 is a KRAS G12C inhibitor. KRAS G12C inhibitor 23 inhibits H358 cells with an IC50 of 491 nM (WO2021218939A1, compound 1).

KRAS G12C inhibitor 25 is a KRAS G12C inhibitor. KRAS G12C inhibitor 25 inhibits SOSl-assisted GDP/GTP exchanging activity of KRAS-G12C mutant (IC50=0.48 nM). From WO2021216770A1 compound 3.

KRAS G12C inhibitor 22 is a KRAS G12C inhibitor extracted from patent WO2021219072A1, example 120.

KRAS G12C inhibitor 28 is a KRAS G12C inhibitor with an IC50 of 57 nM. KRAS G12C inhibitor 28 has antitumor effects (WO2021113595A1; Example 1).

KRAS G12C inhibitor 20 is a KRAS G12C inhibitor extracted from patent CN112694475A, example 1.

KRAS G12C inhibitor 21 is a KRAS G12C inhibitor extracted from patent WO2021219090A1, example 7.

KRAS G12C inhibitor 29 is a KRAS G12C inhibitor extracted from patent WO2021252339A1, compound 3. KRAS G12C inhibitor 29 can be used for the research of cancer.

KRAS inhibitor-11 (compound 12) is a KRAS inhibitor.

K20 is a potent and selective KRas G12C inhibitor with an IC50 of 1.16 µM. K20 shows anticancer activity in H358 cells (IC50= 0.78 µM). K20 decreases the levels of phosphorylated Erk and leads to cancer cell apoptosis. K20 suppresses NCI-H358 tumor growth with a TGI of 41% without causing obvious toxicity.

KRAS G12D inhibitor 14 is a potent KRAS G12D inhibitor with a KD of 33 nM for binding to KRAS G12D protein. KRAS G12D inhibitor 14 decreases the active form of KRAS G12D (KRAS G12D-GTP) but not KRAS G13D.

SOS1-IN-9 is a potent SOS1 inhibitor with an IC50 of 116.5 nM for SOS1-KRAS G12C (WO2022028506A1, compound 302).

SOS1-IN-10 is a potent SOS1 inhibitor with an IC50 of 13 nM for KRAS G12C-SOS1 (WO2022017519A1, compound 8).

KRAS G12C inhibitor 32, an eight membered heterocyclic compound containing N, is a potent KRAS G12C inhibitor.

ZINC09659342 (compound 13) is an inhibitor of Lbc-RhoA interaction with an IC50 of 3.6 μΜ.

KRAS G12C inhibitor 33 is a KRAS G12C inhibitor extracted from patent WO2021244603A1, compound 1. KRAS G12C inhibitor 33 can be used for the research of cancer.

SOS1-IN-11 is a potent SOS1 inhibitor with an IC50 value of 30 nM.

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

KRAS G12C inhibitor 34 is a KRAS G12C inhibitor extracted from patent WO2021239058A1, compound Z1. KRAS G12C inhibitor 34 can be used for the research of cancer.

SOS1-IN-6 (compound 33-P1) is a potent SOS1 inhibitor with IC50s of 14.9 and 73.3 nM for SOS1-G12D and SOS1-G12V, respectively.

KRAS G12C inhibitor 31 is a KRAS G12C inhibitor extracted from patent WO2021252339A1, compound 1. KRAS G12C inhibitor 31 can be used for the research of cancer.

KRAS G12C inhibitor 30 is a KRAS G12C inhibitor extracted from patent WO2021252339A1, compound 2. KRAS G12C inhibitor 30 can be used for the research of cancer.

SOS1-IN-7 (compound 18-p1) is a potent SOS1 inhibitor with IC50s of 20 and 67 nM for SOS1-G12D and SOS1-G12V, respectively.

KRAS G12D inhibitor 3 is a KRAS G12D inhibitor with an IC50 of <500 nM. KRAS G12D inhibitor 3 has antitumor effects (WO2022002102A1; compound 146).

KRAS G12D inhibitor 3 TFA is a KRAS G12D inhibitor with an IC50 of <500 nM. KRAS G12D inhibitor 3 TFA has antitumor effects (WO2022002102A1; compound 146).

SOS1-IN-8 is a potent SOS1 inhibitor with IC50s of 11.6 and 40.7 nM for SOS1-G12D and SOS1-G12V, respectively (WO2022017339A1, compound 2).

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.

DW0254 (DW-0254,DW 0254) is a small molecules capable of inhibiting RAS-related C3 botulinum toxin substrate (RAC) small GTPase activation in ALL cell lines, directly binds to the hydrophobic pocket of PDE6D (Kd=436 nM, ITC), a RAS chaperone protein.DW0254 demonstrated dose-dependent RAC inhibition, arrest of proliferation and induced apoptosis in human leukemic cell lines (RS4;11 IC50=1.5-1.8 uM), also showed promising anti-leukemic activity in RAS-mutated cells (CCRF-CEM NRAS G12D, IC50=3.3-4.2 uM).DW0254 disrupted the interaction between PDE6D and RAS, disturbing RAS subcellular localization.DW0254 demonstrated anti-leukemic activity, decreased tumor progression in a murine xenograft model.

IODVA1 is a small molecule with cellular inhibitory activity against several transformed cell lines including Ras-driven cells, targets Rac activation and signaling instead of Ras; IODVA1 inhibits ST8814 cell proliferation with GI50 of 1 uM, similar results were observed with MCF7, MDA-MB-231, and T47D cells with estimated GI50s <1 uM. IODVA1 significantly decreases number of colonies of the breast cancer cells in soft agar at 1 and 3 uM. IODVA1 probably does not bind Ras and that its mechanism of action is likely Ras-independent, inhibits lamellipodia and circular dorsal ruffle (CDR) formation in MDA-MB-231 cells and decreases Rac activation. IODVA1 inhibits Rac activation and downstream signaling leading to inhibition of lamellipodia and CDR formation; IODVA1 inhibits cell-substratum and cell-cell interactions, does not target kinases, and reduces tumor burden of solid tumors in vivo.

KAL-21404358 (KAL21404358) is a small-molecule, allosteric inhibitor of K-Ras(G12D), binds to K-Ras(G12D) P110 site with KD of 88 uM in MST assay; KAL-21404358 disrupts the K-RasG12D-B-Raf interaction using a NanoBiT split luciferase assay, and to impair the Raf-MEK-ERK and the PI3K-AKT signaling pathways. KAL-21404358 exhibited specificity for K-RasG12D over K-RasWT, H-RasWT, Rap1a, R-Ras and R-Ras2.

KRAS G12C Pipetide (LVVVGACGVGK)

K-Ras G12D inhibitor KS-58 is the first K-Ras(G12D) selective, bicyclic peptide inhibitor with binding Ki of 22 nM; KS-58 suppressed growth of A427 cells and PANC-1 cells (human pancreas carcinoma, G12D mutant) down to 21.1% and 50.1% at 30 uM. KS-58 showed significantly weaker cell growth suppression activities against A549 (human lung carcinoma, G12S mutant), H1975 (human lung carcinoma, WT), MIA PaCa-2 (human pancreas carcinoma, G12C mutant), and Capan-1 (human pancreas carcinoma, G12V mutant) cells. KS-58 reduced the phosphorylation of ERK down to 26.0% and 57.6% at 30 uM, respectively. Biotin-KS-58 exhibited stronger binding to K-Ras(G12D) than to other Ras proteins; KS-58 enters cells, binds to both forms of intracellular K-Ras(G12D)GDP/GTP, and inhibits K-Ras(G12D)GDP/GTP-effector protein interactions, thus preventing downstream Ras signal pathways, such as ERK, and suppressing cell proliferation. KS-58 exhibits anti-cancer activity when given as an intravenous injection to mice with subcutaneous or orthotropic PANC-1 cell xenografts.

KRpep-2d (Ac-RRCPLYISYDPVCRR-NH2) is a potent, selective, cell-membrane permeable, cyclic peptide inhibitor of K-Ras(G12D) with IC50 of 1.6 nM, >10-fold selectivity over WT and G12C KRas; KRpep-2d significantly suppressed ERK-phosphorylation, downstream of K-Ras(G12D), along with A427 cancer cell proliferation at 30 μM peptide concentration.

K-tetracosapeptide (K-TC) is a peptide of 24 amino acids corresponding to the helix a5 in KRAS4B, potent inhibitor of KARATE (KRAS4B-RHOA-mTORC2 Ensemble), specifically targets the KRAS4B-RHOA interaction.

LY-3537982 (LY3537982) is a highly selective and potent KRAS-G12C inhibitor, selectively inhibits growth of KRAS G12C mutant cells (IC50=1-60 nM).LY-3537982 does not inhibit growth of KRAS G12S/G13C/G12D mutant cells and WT KRAS cells (CI50>10 uM).LY-3537982 displays high selectivity for proteome-wide cysteine residues was evaluated using competitive chemical proteomics (8866 peptides).LY3537982 inhibits the growth of subcutaneous EL3187 NSCLC PDX tumors in nude mice in a dose dependent manner.LY3537982 demonstrates robust tumor regression in combination with other agents in KRAS G12C in vivo models.LY3537982 is a promising KRAS G12C inhibitor predicted to deliver >90% KRAS G12C target occupancy in the clinic.

MRTX-EX185 (EX185) is a novel potent small-molecule inhibitor of KRAS mutants, exhibits target engagement against KRAS(G12D) with IC50 of 90 nM, binds to GDP-loaded KRAS and KRAS(G12D), as well as the active GNP state.MRTX-EX185 also bound GDP-loaded HRAS.MRTX-EX185 engages both nucleotide states-albeit with preference for the inactive GDP-loaded protein-and might present an opportunity to inhibit even constitutively active (GTP-loaded) KRAS hotspot mutants MRTX-EX185 engages numerous KRAS Q61, G12 and G13 mutant proteins and drives antiproliferation.

NSC290956 is a small molecule inhibitor of KRas with Kd of 21.3 uM.NSC290956 inhibits KRas activity and downstream signaling events in KRas-driven nuytant NSCLC cells, decreases the cellular viability, cell cycle, and migration.NSC290956 changes KRas-dependent metabolic phenotype in Non-small-cell lung cancer cells, regulates mitochondrial dysfunction for apoptosis in both A549 and H358 cells.NSC290956 shows activity in the KRas mutant cell line xenograft.

PHT-7.3 (Cnksr1 (Cnk1) inhibitor PHT-7.3) is a selective inhibitor of connector enhancer of kinase suppressor of Ras 1 (Cnk1) pleckstrin homology (PH) domain (Kd=4.7 μM).PHT-7.3 bound selectively to the PH domain of Cnk1, preventing plasma membrane colocalization with mut-KRas.PHT-7.3 inhibits mut-KRas, but not wild-type KRas cancer cell and tumor growth and signaling.

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.

Ras binder 2C07 is a switch-II binding ligand which binds Ras GDP and GTP states.

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.

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.

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).

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.

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.

(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.

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.

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.

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.

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

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

(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.

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

A potent, selective, covalent KRAS G12C inhibitor that selectively inhibit KRAS G12C-dependent signaling and cancer cell growth at sub-micromolar concentrations..

6H05 is a selective, allosteric inhibitor of oncogenic mutant K-Ras(G12C), an intermediate for the synthesis of other oncogenic K-Ras(G12C) inhibitors..

ACA-14 is a small molecule direct inhibitor of KRAS, impedes the interaction of KRAS with its effector Raf and reduces both intrinsic and SOS-mediated nucleotide exchange rates.

ACA22 is a small molecule KRAS inhibitor, inhibits KRAS-mediated signal transduction in cells expressing wild type (WT) and G12D mutant KRAS.

ADT-007 (ADT007) is a potent, specific pan-RAS inhibitor, shows potential to circumvent resistance to mutant-specific KRAS inhibitors and activates antitumor immunity.

ASP6918 (ASP 6918) is a highly potent, covalent KRAS G12C inhibitor with IC50 of 28 nM in cell-free assays, and pERK inhibition IC50 of 3.7 nM in NCI-H1373 cells.

BBO-8956 is a highly potent, covalent inhibitor of GTP-KRAS G12C, BBO-8956 is effective against both GDP and GTP-bound KRAS G12C.

BC-DXI-32982 is a specific small molecule DX2-KRAS inhibitor that specifically binds to the KRAS-binding region of AIMP2-DX2, inhibits interaction between DX2 and KRAS4B with IC50 of 0.18 uM.

CSC01 is a small molecule inhibitor of oncogenic KRAS mutant G13D (KRAS-G13D).

ERAS-5024 (ERAS5024) is a potent and selective KRAS G12D inhibitor with IC50 of 0.86 nM in RAS-RAF binding assays, inhibits ERK1/2 phosphorylation (pERK) formation with IC50 of 2.1 nM in AsPC-1 cell-based assays.

Fulzerasib is a potent selective inhibitor of KRAS gene mutation.

G12Si-5 is a specific small molecule that covalently target K-Ras(G12S) mutation, suppresses K-Ras(G12S) signaling, preferentially inhibits the growth of the K-Ras(G12S)-transduced cells with IC50 of 2.4 uM.

RMC-4998 (RMC4998) is a tricomplex inhibitor that targets the active state or GTP-bound state of KRAS G12C, selectively inhibits the proliferation of KRASG12C mutant cells with mean IC50 of 0.28 nM.

RSC-1255 (KRAS inhibitor 249C, V-ATPase inhibitor) is a Ras-mutant selective cytotoxic agent with nanomolar potency against a spectrum of Ras-mutant cancer cells (A549 (KRASG12S), IC50=73 nM), binds to V-ATPase (Kd=23 nM) and inhibits its activity.

SCH-53239 (SCH53239) is a small molecule inhibitor of Ras nucleotide exchange with IC50 of 0.5 uM, bind competitively with GDP in the nucleotide binding site of the Ras protein.

SIJ1772 is a potent mutated RAS (mtRAS)-signaling pathway blocker/inhibitor with IC50 of 77 and 96 nM for Ba/F3-NRAS-G12D and Ba/F3-NRAS-G12V, respectively.

SIJ1795 is a potent mutated RAS (mtRAS)-signaling pathway blocker/inhibitor with IC50 of 82 and 75 nM for Ba/F3-NRAS-G12D and Ba/F3-NRAS-G12V, respectively.

LY3537982 (KRAS G12C inhibitor 19) is a highly selective and potent inhibitor of the  KRAS-G12C protein. LY3537982 selectively inhibits the growth of KRAS G12C mutant cells H23 G12C, H358 G12C, and H2122 G12C with IC50s of 1.04 nM, 1.16 nM, and 11.38 nM, respectively.