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[1].
KRAS G12C inhibitor 20 is a KRAS G12C inhibitor extracted from patent CN112694475A, example 1[1].
Cyclorasin 9A5 is an 11-residue cell-permeable cyclic peptide that orthosterically inhibits the Ras-Raf protein interaction with an IC50 of 120 nM[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[1].
ML-099 (CID-888706) is a pan Ras-related GTPases activator that can activate Rac1, cell division cycle 42, Ras, Rab7, and Rab-2A[1].
Z62954982 is a potent, specific Rac1 inhibitor, reduces the intracellular levels of Rac1-GTP in a concentration-dependent manner with IC50 of 12 uM, 4 times more effective than NSC23766 (IC50=50 uM); causes a concentration-dependent decrease in transendothelial electrical resistance (TER) in both HDMEC and HUVEC.
ARS-853 is a selective, covalent KRASG12C inhibitor with an IC50 of 2.5 μM.
Kras4B G12D-IN-1 is a Kras4B G12D inhibitor with anticancer effects. Kras4B G12D-IN-1 decreases Kras protein expression in mouse embryonic fibroblasts (MEF) expressing Kras4B G12D (WO2016179558A1, Comp 994566)[1].
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[1].
KRAS G12C inhibitor 36 is a potent inhibitor of KRAS G12C. The Ras family of proteins is an important intracellular signaling molecule that plays an important role in growth and development. KRAS G12C inhibitor 36 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2021121367A1, compound 1-2)[1].
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[1].
KRAS G12C inhibitor 61 (Example 3) inhibits phospho-ERK 1/2 in MIA PaCa-2 cells with an IC50 value of 9 nM. KRAS G12C inhibitor 61 can be used for research of pancreatic, colorectal, and lung cancers[1].
PAT-IN-1 is a protein acyl transferases (PAT) inhibitor. PAT-IN-1 competitively inhibits Erf2 autopalmitoylation (WO2017011518A1; compound 13)[1].
KRas G12C inhibitor 1 is a compound that inhibits KRas G12C, extracted from patent US 20180072723 A1.
Manumycin A is an antibiotic. Manumycin A acts as a selective, competitive inhibitor of protein farnesyltransferase (FTase) with respect to farnesylpyrophosphate (Ki =1.2 μM), and as a noncompetitive inhibitor with respect to the Ras protein. Manumycin A induces apoptosis and exerts antitumor activity[1] [2][3].
SOS1-IN-12 is a potent son of sevenless homolog 1 (SOS1) inhibitor with a Ki of 0.11 nM for SOS1 and an IC50 of 47 nM for pERK. SOS1-IN-13 can be used for researching anticancer[1].
kobe2602 is a novel and effective small-molecule compound inhibiting Ras–Raf interaction by SBDD; exhibits potent activity to competitively inhibit the binding of H-Ras·GTP to c-Raf-1 RBD with a Ki value of 149 ± 55 μM.IC50 value: 149 ± 55 uM (Ki) [1]Target: Ras-Raf These two compounds(Kobe0065 and Kobe2602), added to the culture medium at 2 and 20 μM, effectively reduced the amount of c-Raf-1 associated with H-Ras G12V in NIH 3T3 cells in a dose-dependent manner, indicating the inhibition of the cellular activity of Ras. A rough estimate of the IC50 value for the cellular Ras–Raf-binding inhibition was around 10 μM (Fig. 1B), which was not much different from the Ki values for the in vitro Ras–Raf-binding inhibition considering thequite low cellular concentration of Raf. A similar inhibitory effect was also observed with NIH 3T3 cells overexpressing K-Ras G12V. Both Kobe0065 and Kobe2602 at 20 μM efficiently inhibited the phosphorylation of MEK and ERK, downstream kinases of Raf in NIH 3T3 cells transiently expressingH-Ras G12V, although the effect was slightly weaker than that of2 μM sorafenib.
Fulzerasib is a potent KRAS inhibitor[1].
CCG-222740 is a potent and selective Rho/myocardin-related transcription factor (MRTF) pathway inhibitor[1]. CCG-222740 also is a potent inhibitor of alpha-smooth muscle actin protein expression. CCG-222740 effectively reduces fibrosis in skin and blocks melanoma metastasis[2].
Spiclomazine hydrochloride (APY-606) is an antipsychotic and antitumor agent. Spiclomazine hydrochloride inhibits KRas. Spiclomazine hydrochloride induces cancer cell apoptosis[1][2].
SOS1-IN-4 is a potent SOS1 inhibitor with an IC50 of 56 nM for KRAS-C12C/SOS1 interaction (WO2021228028 A1, example 65)[1].
ZCL278 is a selective Cdc42 modulator that directly binds to Cdc42 and inhibits its functions with Kd of 11.4 μM for Cdc42-ZCL278 affinity in surface plasmon resonance (SPR) experiment.
KRAS G12D inhibitor 17 (example 8) is a quinazoline-linked (4R)-4-hydroxy-L-prolinamide compound, inducing degradation of G12D-mutation KRAS protein[1].
KRAS G12C inhibitor 17 is a potent KRAS G12C inhibitor extracted from patent WO2019110751A1, compound 82, has an IC50 of 5 nM[1].
K-Ras (G12C) inhibitor 9 is an allosteric inhibitor of the K-Ras (G12C)[1].
PROTAC KRAS G12C degrader-2 (compound 432) is a modulator of K-Ras protein hydrolysis. PROTAC KRAS G12C degrader-2 is a bifunctional compound, which contain on one end a cereblon inhibitor of apoptosis proteins (IAP) and on the other end a moiety which binds KRAS[1].
Digeranyl bisphophonate is a potent geranylgeranylpyrophosphate (GGPP) synthase inhibitor, which inhibits geranylgeranylation of Rac1.
Oncrasin-1 is a potent and effective anticancer inhibitor that kills various human lung cancer cells with K-Ras mutations at low or submicromolar concentrations; also led to abnormal aggregationof PKCι in nucleus of sensitive cells but not in resistant cells.IC50 value: 1.0 μM(A549, K-ras 12H and p53 Wt) [1]Target: human lung cancer cells with K-Ras mutation; K-Ras/PKCiota pathway inhibitorin vitro: effectively kills various human lung cancer cells with K-Ras mutations at low or submicromolar concentrations. The cytotoxic effects correlated with apoptosis inductionas was evidenced by increase of apoptotic cells and activation of caspase-3 and caspase-8 upon the treatment of oncrasin-1 in sensitive cells.Treatment with oncrasin-1 also led to abnormal aggregationof PKCι in nucleus of sensitive cells but not in resistant cells. Furthermore, oncrasin-1 induced apoptosis was blocked by siRNA of K-Ras or PKCι suggesting that oncrasin-1 is targeted to a novel K-Ras/PKCι pathway [1]. oncrasin-1 treatment led to coaggregation of PKCiota and splicing factors into megaspliceosomes but had no obvious effects on the DNA repair molecule Rad51. Moreover, oncrasin-1 treatment suppressed the phosphorylation of the largest subunit of RNA polymerase II and the expression of intronless reporter genes in sensitive cells but not in resistant cells [2]. in vivo: The in vivo administration of oncrasin-1 suppressed the growth of K-ras mutant human lung tumor xenografts by >70% and prolonged the survival of nude mice bearing these tumors, without causing detectable toxicity [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].
PROTAC K-Ras Degrader-1 (Compound 518) is potent K-Ras degrader based PROTAC, exhibits ≥70% degradation efficacy in SW1573 cells[1].