HDAC-IN-98-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEHDAC-IN-98Cat.No.:HY-181009分⼦式:C₂₄H₂₁N₃O₄分⼦量:415.44作⽤靶点:HDAC;Apoptosis;Autophagy作⽤通路:CellCycle/DNADamage;Epigenetics;Apoptosis;Autophagy储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性HDAC-IN-98⼀种HDAC1、HDAC2、HDAC3抑制剂(属于最具有选择性的I类HDAC抑制剂之⼀)，其IC50值分别为41.2nM、52.5nM和74.3nM。HDAC-IN-98可诱导H3K9⼄酰化，上调p21表达，引起G2/M期阻滞，诱导细胞凋亡(apoptosis)，在结直肠癌细胞中表现出强烈的抗增殖活性，对正常结肠上⽪细胞毒性较低，通过⾃噬(autophagy)调控短期体外效应，并在鸡胚绒⽑膜尿囊膜模型(CAM)试验中展现出显著的抗肿瘤效果。HDAC-IN-98可⽤于结直肠癌研究[1]。IC50&TargethHDAC1hHDAC2hHDAC3hHDAC641.2nM(IC50)52.5nM(IC50)74.3nM(IC50)>10000nM(IC50)hHDAC8hHDAC10hHDAC11>10000nM(IC50)4261nM(IC50)>10000nM(IC50)体外研究HDAC-IN-98(compound5d)selectivelyinhibitsclassIHDACenzymes(HDAC1,HDAC2,HDAC3)withsub-nanomolartolow-nanomolarIC50valuesandweakornoactivityagainstotherHDACisoforms(IC50:HDAC1=41.2nM,HDAC2=52.5nM,HDAC3=74.3nM,HDAC10=4261nM,HDAC5/8/11>10000nM)[1].HDAC-IN-98(1μM;upto60min)inhibitstotalHDACactivityinacomplexnuclearextractsystem[1].HDAC-IN-98(0.1-100μM;48h)selectivelyreducesviabilityofCRCcellswithIC50valuesrangingfrom14μMandminimaltoxicitytonormalcoloncells(IC50:HCT116=1μM,HT29=4μM,DLD1=4μM,HCEC>100μM)[1].HDAC-IN-98(1-4μM;48h)modulatesepigeneticmarkers(H3K9acetylation)andapoptoticpathways(PARPcleavage)inCRCcellswithoutinhibitingclassIIHDACs[1].HDAC-IN-98(1-4μM;48h)disruptscellcycleprogression,inducingsubG1accumulation(apoptosis)inHCT116andG1arrestinHT29/DLD1cells[1].1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEHDAC-IN-98(1-4μM;48h)triggersapoptosisselectivelyinHCT116cellswithoutinducingnecrosis[1].HDAC-IN-98(upto10μM)showsminimalhERGliabilityatconcentrationsrelevanttoitsanticanceractivity[1].HDAC-IN-98(1μM;invitropretreatment;48h)exhibitspotentantitumorefficacyinchickenembryoswithcolorectalcancerchorioallantoicmembranemodel(CAM)modelsindependentofp21status.IntheHCT116p21wildtypeCAMmodel,HDAC-IN-98confirmesarobustupregulationofp21.IntheHCT116p21−/−CAMmodel,HDAC-IN-98significantlyreducesthevesselarea,thevessellength,andthenumberofbranchingpointswhereasthevesselthicknessisnotaffected[1].CellViabilityAssay[1]CellLine:ColorectalCancerCellLines(HCT116,HT29,DLD1)andNormalColonEpithelialCells(HCEC)Concentration:0.1-100μMIncubationTime:48hResult:Showeddose-dependentcytotoxicitywithanIC₅₀of1μM(HCT116);showeddose-dependentcytotoxicitywithanIC₅₀of4μM(HT29);showeddose-dependentcytotoxicitywithanIC₅₀of4μM(DLD1);showedlowtoxicityinHCECwithanIC₅₀>100μMWesternBlotAnalysis[1]CellLine:CRCCellLines(HCT116,HT29,DLD1)Concentration:1μM,4μMIncubationTime:48hResult:SlightlyincreasedH3K9acetylationinHCT116cells;didnotaffectHDAC1/HDAC6proteinlevelsorα-tubulinacetylation;upregulatedp21inHCT116cells;inducedPARPcleavageinHCT116/HT29cells.CellCycleAnalysis[1]CellLine:CRCCellLines(HCT116,HT29,DLD1)Concentration:1μM,4μMIncubationTime:48hResult:InducedsubG1accumulation(apoptosis)inHCT116cells;increasedG1-phasepopulationinHT29/DLD1cells;reducedS-phasepopulationacrossalllines;correlatedwithupregulatedp21andreducedCyclinB1inHCT116cells.ApoptosisAnalysis[1]CellLine:CRCCellLines(HCT116,HT29,DLD1)2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEConcentration:1μM,4μMIncubationTime:48hResult:InducedsignificantapoptosisinHCT116cells(AnnexinV-positive/PI-negativecells);inducedminimalapoptosisinHT29/DLD1cells;showednonecrosis.REFERENCES[1].CarulloG,etal.TargetingClassIHistoneDeacetylasesTriggersAntitumorResponsesinColorectalCancerInVitroandInVivo.JMedChem.2026;69(2):1049-1074.McePdfHe