Hotline:400-820-3792Inhibitors ? ScreeningLibraries ? Proteinswww.MedChemEHDAC1/6-IN-3Cat.No.:HY-175176CASNo.:3038691-85-6分子式:C??H??N?O?S分子量:453.55作用靶點:HDAC;Apoptosis;Pyroptosis作用通路:CellCycle/DNADamage;Epigenetics;Apoptosis;Immunology/Inflammation儲存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性HDAC1/6-IN-3是一種強效的HDAC抑制劑。HDAC1/6-IN-3對HDAC1(IC50=1.1nM)和HDAC6(IC50=2.7nM)具有出色的抑制作用。HDAC1/6-IN-3能顯著使HepG2細胞停滯在G0/G1期，并誘導細胞凋亡(apoptosis)和細胞焦亡(pyroptosis)。HDAC1/6-IN-3在HepG2腫瘤移植模型中顯示出顯著的抗腫瘤活性。HDAC1/6-IN-3可用于癌癥研究，如肝癌、肺癌、結腸癌、乳腺癌[1]。IC50&TargetHDAC1HDAC61.1nM(IC50)2.7nM(IC50)體外研究HDAC1/6-IN-3(Compound15a)(72h)showsexcellentinhibitoryactivitiesagainstHepG2(IC50=0.12μM),PC9(IC50=0.53μM),HCT116(IC50=1.12μM)andMCF7cell(IC50=3.12μM)[1].HDAC1/6-IN-3(0.2-0.5μM,24h)increasesthelevelofacetyl-H3andH4inadose-dependentmannerinHepG2cells[1].HDAC1/6-IN-3(0.2-0.5μM,10-14d)suppressestheformationofcoloniesofHepG2cellsinadose-dependentmanner.[1].HDAC1/6-IN-3(0.2-0.5μM,24h)inducesG0/G1arrestinHepG2cellsmaybecorrelatedthedownregulationofwithCDK4andCyclinD1proteins[1].HDAC1/6-IN-3(0.2-0.5μM,48h)enhancesROSgenerationandDNAdamageaccumulationtoinduceapoptosisinHepG2cells[1].HDAC1/6-IN-3(0.2-0.5μM,24-48h)triggerspyroptosisinHepG2cellsthroughcaspase-3cleavageofGSDME[1].CellCycleAnalysis[1]1/3 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemECellLine:HepG2cellsConcentration:0.2and0.5μMIncubationTime:24hResult:SignificantlyinhibitedHepG2cellsinG0/G1phaseinadose-dependentmanner.TheG2/Mratiodecreasedfrom25.34to22.85%andtheS-phasevaluedecreasedfrom32.99to13.72%.ApoptosisAnalysis[1]CellLine:HepG2cellsConcentration:0.2and0.5μMIncubationTime:48hResult:Inducedapoptosisin28.2%at0.2μMand46.5%at0.5μM.Immunofluorescence[1]CellLine:HepG2cellsConcentration:0.2and0.5μMIncubationTime:24hResult:TheROSlevelsweredose-dependentlyincreased.Showeddose-dependentγH2AXfociformation.WesternBlotAnalysis[1]CellLine:HepG2cellsConcentration:0.2and0.5μMIncubationTime:24hResult:increasedthelevelofacetyl-H3andH4inadose-dependentmanner.Down-regulatedtheexpressionofCyclinD1andCDK4.UpregulatedtheexpressionofCl-PARP,Cl-caspase3inadose-dependentmanner.ResultedinelevatedlevelsoftheN-terminalfragmentofgasderminE(GSDME)andcaspase-3.體內研究HDAC1/6-IN-3(Compound15a)(10mg/kg,i.p.,twiceaweekfor3weeks)showsthesignificantantitumorefficacyinHepG2xenograftmodel,coupledwithanacceptablesafetyprofile[1].2/3 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemEAnimalModel:HepG2inducedxenograftmodelestablishedinmaleBALB/cnudemice[1]Dosage:10mg/kgAdministration:Intraperitonealinjection(i.p.),twiceaweekfor3weeksResult:Thegrowthoftumorswasdose-dependentlyinhibited.Adose-dependentreductioninKi67immunostainingwasobserved.InducedtheincreaseofAc-H3/H4Cl-caspase3andGSDME-Ninadose-dependentmanner.REFERENCESLiZ,etal.Designandsynthesisofthiazole-basedhydroxamatehistonedeacetylaseinhibitorswithpotentantitumorefficacybyinducingapoptosis,pyroptosisandcellcyclearrest.SciRep.2025Jul9;15(1):24589.McePdfHeightCaution:Producthasnotbeen