HDAC6-IN-67-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors • ScreeningLibraries • Proteinswww.MedChemEHDAC6-IN-67Cat.No.:HY-178351CASNo.:2196247-20-6分子式:C₁₇H₁₅N₃O₃分子量:309.32作用靶点:HDAC;Microtubule/Tubulin;Apoptosis;Caspase;Bcl-2Family作用通路:CellCycle/DNADamage;Epigenetics;Cytoskeleton;Apoptosis储存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性HDAC6-IN-67是一种选择性HDAC6抑制剂（IC50=17.15nM），其对HDAC1的选择性是HDAC1的19倍。HDAC6-IN-67通过与Ser531和His614相互作用选择性抑制HDAC6。HDAC6-IN-67通过诱导caspase9、8、3和PARP的裂解、上调Bax表达以及下调Bcl-2表达来诱导细胞凋亡(apoptosis)。HDAC6-IN-67能有效诱导MCF-7/ADR细胞中α-微管蛋白(α-tubulin)的乙酰化，而不影响组蛋白H3的乙酰化。HDAC6-IN-67可用于乳腺癌的研究[1]。体外研究HDAC6-IN-67showssignificanttime-dependentinhibitionoftumorcellsinalltestedhumancancercelllines,withGI50valuesrangingfrom2.9to24.8μM,italsoshowsstronganti-proliferativeactivityagainstMCF-7/ADRcellsafter72hours(GI50=2.4μM)[1].HDAC6-IN-67(0.01-2μM,24hours)candose-dependentlyincreasetheacetylationofα-tubulininMCF-7/ADRcellswithoutaffectingtheacetylationofhistoneH3evenathighconcentrations[1].HDAC6-IN-67(0.1-2μM,10days)resultsinasignificantdose-dependentinhibitionofcolonyformationinMCF-7/ADRcells[1].HDAC6-IN-67(0.1-2μM,24h)significantlyinducesearlyandlateapoptosis,andfurtherconfirmsitsapoptoticeffect,demonstratingadose-dependentinductionofcleavageofCaspase9,Caspase8,Caspase3,andPARP,alongwithsignificantupregulationofthepro-apoptoticproteinBaxanddownregulationoftheanti-apoptoticproteinBcl-2inMCF-7/ADRcells[1].WesternBlotAnalysis[1]CellLine:MCF-7/ADRcells1/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEConcentration:0.01μM,0.1μM,0.5μM,1μM,2μMIncubationTime:24hResult:Dose-dependentlyincreasedtheacetylationofα-tubulin.Inducedα-tubulinacetylationatconcentrationsaslowas0.1μM,withoutaffectingtheacetylationofHistoneH3evenatconcentrationsupto1μM.CellProliferationAssay[1]CellLine:MCF-7/ADRcellsConcentration:0.1μM,0.5μM,1μM,2μMIncubationTime:10daysResult:Resultedinasignificantdose-dependentinhibitionofcolonyformation.Aconcentrationof1μMwasabletosuppresscolonyformationbyapproximately65%.WesternBlotAnalysis[1]CellLine:MCF-7/ADRcellsConcentration:0.1μM,0.5μM,1μM,2μMIncubationTime:24hResult:Significantlyinducesearlyandlateapoptosisby25.4%and15.7%.ThecleavageofCaspase9,Caspase8,Caspase3,andPARPweresignificantlyinducedinadose-dependentmanner.TheapoptoticproteinBaxwassignificantlyinduced,whereastheanti-apoptoticproteinBcl-2wasremarkablydecreasedinadose-dependentmanner.体内研究HDAC6-IN-67(5mg/kg,10mg/kg,i.p.,dailyduringweekdays,followedbyweekendrestfor17days)inhibitsHCT116tumorgrowthinvivoinadose-dependentmannerwithoutshowingsignificanttoxicityinmice[1].AnimalModel:SubcutaneouslyinjectingnudemicewithHCT116humancoloncancercells(2.0×106cells/mice).Dosage:5mg/kg,10mg/kgAdministration:I.p.,dailyduringweekdays,followedbyweekendrestfor17daysResult:Showeddelayedtumorgrowthstartingrightafterthefirstmeasurement.Foundnodifferencesinbodyweight,treatment-relateddeaths,orabnormalbehaviorsbetweenthecontrolandexperimentalgroups.2/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEREFERENCESGuptaSK,etal.Design,synthesis,andbiologicalevaluationofquinazolin-4-one-basedselectiveHDAC6inhibitorstargetingserine531,histidine614residues,andtheL1andL2loop.EurJMedChem.2025Dec15;300:118184.McePdfHeightCaution:Produc