G9a-IN-4-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors • ScreeningLibraries • Proteinswww.MedChemEG9a-IN-4Cat.No.:HY-178378分子式:C₃₅H₄₈N₆O₄分子量:616.79作用靶点:HistoneMethyltransferase;GLPReceptor;ReactiveOxygenSpecies(ROS);Autophagy;Apoptosis作用通路:Epigenetics;GPCR/GProtein;Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB;Autophagy;Apoptosis储存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性G9a-IN-4是一种G9a特异性抑制剂(IC50=32nM)。G9a-IN-4对其他测试的赖氨酸/精氨酸甲基转移酶表现出很高的选择性。G9a-IN-4展示出较高的酶活性，并且对所有测试的癌细胞均表现出更强的抗增殖作用。G9a-IN-4显著抑制了H3K9me2的水平。G9a-IN-4通过诱导ROS的产生来触发自噬(autophagy)，从而导致CT26结肠癌细胞凋亡(apoptosis)和G0/G1期细胞周期阻滞。G9a-IN-4可用于结肠癌的研究[1]。体外研究G9a-IN-4(Compound31)isaspecificG9a/GLPinhibitor(IC50=0.2nM;IC50=0.43nM)withhighselectivityforothertestedepigenetictargetsinAlphaLISA[1].G9a-IN-4(72h)displaysmorepotentsuppressingeffectsagainstalltestedcancercells,includinghematologicalcancercells:RPMI8226(IC50=0.85μM),MV-4-11(IC50=0.49μM),Jeko-1(IC50=0.7μM),Molt4(IC50=1.34μM),andsolidtumorcells:HeLa(IC50=1.55μM),U2OS(IC50=3μM),CT26(IC50=3.31μM)[1].G9a-IN-4(1.25-2.5μM,72h)inducesamarkedreductioninthedimethylationofH3K9inCT26cellsinadose-dependentmanner[1].G9a-IN-4(2.5-5μM,48h)significantlyinducestheROSaccumulationinCT26cellsinadose-dependentmanner[1].G9a-IN-4(2.5-10μM,12h)significantlydecreasesLC3-Iexpressionat10μMandincreasestheLC3-IIlevelatalltestedconcentrations,thusleadingtoanincreasedratioofLC3-IItoLC3-Iinadose-dependentmanner,effectivelyinduceautophagyinCT26cells[1].G9a-IN-4(2.5-10μM,24h)canincreasetheproportionofapoptoticcellsdose-dependentlyto91.37%from5.48%inCT26cells[1].G9a-IN-4(2.5-5μMfor24h)inducesG0/G1phasearrestinCT26cells[1].WesternBlotAnalysis[1]1/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemECellLine:CT26cellsConcentration:1.25μM,2.5μMIncubationTime:72hResult:InducedamarkedreductioninthedimethylationofH3K9inCT26cellsinadose-dependentmanner.CellAutophagyAssay[1]CellLine:CT26cellsConcentration:2.5μM,5μM,10μMIncubationTime:72hResult:SignificantlydecreasedLC3-Iexpressionat10μMandincreasedtheLC3-IIlevelatalltestedconcentrations,thusleadingtoanincreasedratioofLC3-IItoLC3-Iinadose-dependentmanner.EffectivelyinducedautophagyinCT26cells.CellCycleAnalysis[1]CellLine:CT26cellsConcentration:2.5μM,5μMIncubationTime:24hResult:InducedamarkedreductioninthedimethylationofH3K9inCT26cellsinadose-dependentmanner.体内研究G9a-IN-4(10mg/kg,I.p.,onceeverytwodaysfortwoweeks)effectivelyinhibitstumorsinthecoloncancermicemodelwithoutcausingsignificantweightlossordeath[1].AnimalModel:CT26cells(5×105cells/mouse)weresubcutaneouslyimplantedintotherightarmpitoffemaleBALB/cmice(6weeks)[1].Dosage:10mg/kgAdministration:I.p.,onceeverytwodaysfortwoweeksResult:Significantlysuppressedtumorgrowthwitha45.1%(TGI)reductionintumorweight.Exhibitedanegligibleimpactonthebodyweightofmicewithoutmortalityduringthe14-daytreatment.2/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEREFERENCESShaoM,etal.Discoveryof2-tetrahydroisoquinoline-substitutedquinazolinederivativesaslysinemethyltransferaseG9ainhibitorswithinvivoantitumorefficacy.EurJMedChem.2025Dec15;300:118113.McePdfHeightCaution:Producthasn