Aurora-A-IN-5-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors • ScreeningLibraries • Proteinswww.MedChemEAuroraA-IN-5Cat.No.:HY-178343分子式: C₂₅H₂₉N₇O₂分子量: 459.54作用靶点: AuroraKinase;Apoptosis作用通路: CellCycle/DNADamage;Epigenetics;Apoptosis储存方式: PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性AuroraA-IN-5是一种高效且高选择性的AuroraA抑制剂(IC50=0.02μM)，其对AuroraA的选择性比AuroraB高362倍。AuroraA-IN-5的选择性源于其独特的C−H/π相互作用、增强的疏水接触、开放的结合口袋以及更紧密的蛋白质堆积。AuroraA-IN-5可抑制AuroraA的自身磷酸化，从而通过诱导G2/M期阻滞、触发细胞凋亡(apoptosis)和抑制克隆形成来抑制癌细胞增殖。AuroraA-IN-5可抑制MDA-MB-231异种移植小鼠模型中的肿瘤生长。AuroraA-IN-5可用于乳腺癌、宫颈癌、前列腺癌和淋巴瘤的相关研究[1]。IC50&TargetAuroraA0.02μM(IC50)体外研究AuroraA-IN-5(compound5h)(48h)showsstrongantiproliferativeactivityagainstapanelofcancercelllines,withIC50valuesof2.87μM(K562),1.50μM(MCF-7),0.85μM(HeLa),1.85μM(DU145),2.25μM(MOLT-4),and2.04μM(MDA-MB-231)[1].AuroraA-IN-5(0.5μM,48h)causesabnormalitiesinspindlemorphologyandchromosomalorganizationinMDA-MB-231cells[1].AuroraA-IN-5(2.5-10μM,24h)effectivelyinhibitsMDA-MB-231celldivisionbyhaltingcellcycleprogressionattheG2/Mphase[1].AuroraA-IN-5(2-20μM,24h)inducesapoptosisinMDA-MB-231cellsinadose-dependentmanner[1].AuroraA-IN-5(2μM,14days)effectivelysuppressescolonyformationinMDA-MB-231cells,thusinhibitingtheirproliferation[1].AuroraA-IN-5(0-1μM)exhibitspotent,selective,anddose-dependentinhibitionofAuroraAphosphorylationatThr288,withconcurrentdemonstrationoftargetengagementinMDA-MB-231cellsthroughsignificantstabilizationofAuroraAproteininacellularthermalshiftassay(46-62°C)[1].AuroraA-IN-5exhibitstoxicityinmouseembryonicosteoblastMC3T3-E1cells(IC50=7.135μM)butexhibits1/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEminimaltoxicitytowardnormalliverLO2cells(IC50=43.86μM)[1].CellProliferationAssay[1]CellLine:MDA-MB-231cellsConcentration:2.0μMIncubationTime:14daysResult:Showedconsiderablyfewercolonies(26±3)comparedtotheuntreatedcontrolgroup(106±3).ApoptosisAnalysis[1]CellLine:MDA-MB-231cellsConcentration:2.0and20.0μMIncubationTime:24hResult:Displayedaconcentration-dependentincreaseinapoptoticcells,rangingfrom11.5%at2.0μMto88.6%at20.0μM.CellCycleAnalysis[1]CellLine:MDA-MB-231cellsConcentration:2.5,5.0and10.0μMIncubationTime:24hResult:ShowedasignificantabilitytoarrestMDA-MB-231cellsintheG2/Mphase.ThepercentageofcellsintheG2/Mphasegraduallyincreasedfrom24.2%to61.8%at2.5μM.Immunofluorescence[1]CellLine:MDA-MB-231cellsConcentration:0.5μMIncubationTime:48hResult:Displayedabnormalspindleconfigurations,eithermonopolarormultipolar,accompaniedbyvariousaberrationsinchromosomealignment.体内研究AuroraA-IN-5(30mg/kg,i.p.,everytwodaysfor20days)inhibitstumorgrowthinMDA-MB-231xenograftmousemodel[1].2/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEAnimalModel:FemaleBALB/cnudemice(1-5weeks)subcutaneouslyinjectedwithMDA-MB-231cells[1]Dosage:30mg/kgAdministration:i.p.,everytwodaysfor20daysResult:Achievedatumorgrowthinhibitionrateof73.0%.Exhibitedslightlyincreasedbodyweightwithoutanysignificantfluctuationsthroughoutthetreatmentduration.Revealednosignificantparenchymaldamageorinflammatorycellinfiltrationinvitalorganssuchastheheart,liver,spleen,lung,andkidney.REFERENCESLongL,etal.DiscoveryofaPotentandHighlySelectiveInhibitorofAuroraAKinase.ACSMedChemLett.2025Sep17;16(10):2057-2069.McePdfHeightCaution:Produc