Hotline:400-820-3792Inhibitors ? ScreeningLibraries ? Proteinswww.MedChemENrf2activator-21Cat.No.:HY-175548CASNo.:1912404-14-8分子式:C??H??O?分子量:322.31作用靶點(diǎn):Keap1-Nrf2;Apoptosis;Caspase作用通路:NF-κB;Apoptosis儲(chǔ)存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性Nrf2activator-21是一種具有雙重抗氧化和神經(jīng)保護(hù)特性的Nrf2激活劑。Nrf2activator-21與Keap1Kelch結(jié)構(gòu)域結(jié)合，破壞Keap1-Nrf2相互作用，并激活抗氧化防御機(jī)制。Nrf2activator-21減少海馬神經(jīng)元的凋亡(apoptosis)并降低caspase-3活性。Nrf2activator-21通過(guò)激活Nrf2途徑靶向腦缺血/再灌注損傷(CIRI)。Nrf2activator-21改善神經(jīng)功能，緩解大鼠雙血管閉塞(2VO)誘導(dǎo)的CIRI的焦慮樣行為，并增強(qiáng)記憶。Nrf2activator-21可用于腦缺血/再灌注損傷研究[1]。體外研究Nrf2activator-21(Compound7I)(1-15μM,24h)significantlyimprovestheviabilityofhippocampalneuronalcellsexposedtoH2O2[1].Nrf2activator-21(2.5μM,24h)reducesapoptosisanddecreasescaspase-3activityinthehippocampalneurons[1].ApoptosisAnalysis[1]CellLine:hippocampalneuronsConcentration:2.5μMIncubationTime:24hResult:Reducedapoptosisanddecreasedcaspase-3activityinthehippocampalneurons.體內(nèi)研究Nrf2activator-21(Compound7I)(15mg/kg,i.p.,once,15minpost-reperfusion)significantlyimprovesneurologicalfunctioninmaleadultWistarratswith2-vesselocclusion(2VO)-inducedcerebralischemia/reperfusioninjury[1].1/2 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemEAnimalModel:MaleadultWistarrats:amidlineneckincisionwasmadetoisolatebilateralcommoncarotidarteries,whichwerethenclampedsimultaneouslyfor15mintoinducecerebralischemia,followedby15minofreperfusiontoestablishthe2-vesselocclusion(2VO)cerebralischemia/reperfusioninjurymodel[1]Dosage:15mg/kgAdministration:i.p.once15minpost-reperfusionResult:Achievedsignificantimprovementsinmotorfunction,sensoryresponse,andwirecageclimbingability,withtotalneurologicaldeficitscoresnotablyreducedin2VOmodelrats.Showedalleviationofanxiety-likebehavior.Improvedmemoryfunction,withthediscriminationindexsignificantlyincreasedintheNovelObjectRecognitionTest,reversingmemorydeficitsinducedbycerebralischemia/reperfusioninjury.PreservedhippocampalCA1neuronmorphologyandreducedthenumberofdegenerateddarkneuronsanddecreasedhippocampalcaspase-3activity.IncreasedhippocampalNrf2proteinexpression,restoredSODandCATactivitiestonear-shamlevelsandreducedMDAlevels.UpregulatedhippocampalBDNFandTrkBreceptorlevelsandenhancedneuroprotectivesignaling.REFERENCESMohammadniaM,etal.Coumarin-Chalconederivativesaspromisingantioxidantagentstargetingischemia/reperfusioninjurythroughNrf2pathwayactivation.BioorgChem.2025Jul26;164:108790.McePdfHeightCaution:Producthasnotbeenfullyvalidatedformedicalappli