Dyrk1A-IN-16-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEDyrk1A-IN-16Cat.No.:HY-179600CASNo.:2805339-74-4分⼦式:C₁₄H₉NO₅S分⼦量:303.29作⽤靶点:DYRK;EGFR作⽤通路:ProteinTyrosineKinase/RTK;JAK/STATSignaling储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性Dyrk1A-IN-16⼀种选择性、可透过⾎脑屏障的ATP竞争性DYRK抑制剂，其对Dyrk1A的IC50为53nM。Dyrk1A-IN-16在⼴泛的激酶组中(对DYRK激酶具有特异性)表现出纳尔级效⼒和⾼选择性。Dyrk1A-IN-16在体外可损害神经球的⾃我更新能⼒、细胞侵袭能⼒以及EGFR的稳定性。Dyrk1A-IN-16在体内能抑制肿瘤⽣长并延长⽣存期。Dyrk1A-IN-16在胶质母细胞瘤的研究中具有应⽤潜⼒[1]。IC50&TargetDYRK1A50nM(IC50)体外研究Dyrk1A-IN-16(compoundFC-3)(0-100nM)isareversibleandATP-competitiveinhibitor,couldbeovercomeathigherconcentrationsofATP[1].Dyrk1A-IN-16(5-20µM,72h)primarilytargetsatDYRK1AintheGBMcelllineU87MG[1].Dyrk1A-IN-16(5-10µM,24h)exertsinhibitoryeffectsoninvasionthroughanon-targeteffectonDYRK1AintheGBMcelllineU87MG[1].Dyrk1A-IN-16(1-10µM,20h)acceleratesEGFRdestabilization,causingthelysosomaldegradationinEGFRdependentglioblastomaintheGBMcelllineU87MG[1].CellProliferationAssay[1]CellLine:GBMcelllineU87MGConcentration:5,10,20µMIncubationTime:72h1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEResult:Wasresistanttothemutantbutthemutantretaineditskinaseactivity,whenDYRK1A-knockoutcloneswereRescuedwiththeDYRK1Awild-typeandtheF238L-M240Rdoublemutant[1].Dyrk1a-in-16reducedneurospheresizeandnumberonlyinthepopulationsrescuedwithwild-typeDYRK1A,butnotinthoseexpressingtheF238L-M240Rmutant[1].Notdecreasedneurosphereproliferation,unliketheDYRK1AknockoutclonesinDYRK2andDYRK3-knockoutclones[1].CellInvasionAssay[1]CellLine:GBMcelllineU87MGConcentration:5or10µMIncubationTime:24hResult:ReducedinvasionofU87MGcellsinadose-dependentmanner[1].DidnotobserveanysignificantreductionofinvasionincellsrescuedwiththeDYRK1AF238L-M240RmutantasopposedtorescuewithDYRK1Awildtype[1].WesternBlotAnalysis[1]CellLine:GBMcelllineU87MGConcentration:1or10µMIncubationTime:20hResult:ObservedareductionintotalEGFRandERKphosphorylationlevelsinU87MGDYRK1A-knockoutcelllines.InducedtheaccumulationofEGFRwhenlysosomaldegradationwasinhibitedbyBaFA1.IncreasedEGFRdegradation,aphenotypealsoobservedinDYRK1A-knockoutcells.体内研究Dyrk1A-IN-16(2mg/kg,i.p.,dailyfor30days)inhibitstumorgrowthandprolongsanimalsurvivalinU87MGorU87MG-DYRK1AKOcells(1x106)inducedsubcutaneousxenograftmicemodels[1].AnimalModel:U87MGorU87MG-DYRK1AKOcells(1x106)induced-NuJnudemice[1]Dosage:2mg/kgAdministration:i.p.,dailyfor30daysResult:Observedthetumorssubstantiallysmaller.FailedtodevelopanytumorsinthetheDYRK1A-knockoutlinecohort.HadmarkedlylowerEGFRlevels.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEREFERENCES[1].VenkataramaniP,etal.Novelsmall-moleculeinhibitorsoftheproteinkinaseDYRK:Potentialtherapeuticcandidatesincancer.bioRxiv[Preprint].2025Nov7:2025.11.05.686653.McePdfHeightCaution:Producthasnotbeenfullyvali