Rosiglitazone-hydrochloride-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•Agonists•ScreeningLibrariesRosiglitazonehydrochlorideCat.No.:HY-17386ACASNo.:302543-62-0分⼦式:C₁₈H₂₀ClN₃O₃S分⼦量:393.89作⽤靶点:PPAR;TRPChannel;Autophagy;Ferroptosis作⽤通路:CellCycle/DNADamage;MembraneTransporter/IonChannel;NeuronalSignaling;Autophagy;Apoptosis储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性Rosiglitazonehydrochloride(BRL49653hydrochloride)⼀种选择性的，具有⼝服活性PPARγ激动剂，对PPARγ1、PPARγ2和PPARγ的EC50值分别为30nM、100nM和60nM。Rosiglitazonehydrochloride与PPARγ结合，Kd约为40nM。Rosiglitazonehydrochloride也TRPC5的激活剂(EC50=-30μM)和TRPM3的抑制剂[1][2][3][4]。IC50&TargetPPARγ1PPARγ2TRPC5TRPM230nM(EC50)100nM(EC50)TRPM3体外研究RosiglitazoneisapotentandselectiveactivatorofPPARγ,withEC50sof30nMand100nMforPPARγ1andPPARγ2,respectively,andaKdofappr40nMforPPARγ.Rosiglitazone(BRL49653,0.1,1,10μM)promotesdifferentiationofC3H10T1/2stemcellstoadipocytes[1].Rosiglitazone(Compound6)activatesPPARγ,withanEC50of60nM[2].Rosiglitazone(1μM)activatesPPARγ,whichbindstoNF-α1promotertoactivategenetranscriptioninneurons.Rosiglitazone(1μM)alsoprotectsNeuro2Acellsandhippocampalneuronsagainstoxidativestress,andup-regulatesBCL-2expressioninanNF-α1-dependentmanner[3].RosiglitazonecompletelyinhibitsTRPM3withIC50valuesof9.5and4.6μMagainstnifedipine-andPregS-evokedactivity,butsucheffectsarenotviaPPARγ.RosiglitazoneinhibitsTRPM2athigherconcentration,withanIC50ofappr22.5μM.RosiglitazoneisastrongstimulatorofTRPC5channels,withanEC50of~30μM[4].体内研究Rosiglitazone(5mg/kg,p.o.)decreasestheserumglucoseindiabeticrats.RosiglitazonealsodecreasesIL-6,TNF-α,andVCAM-1levelsindiabeticgroup.RosiglitazoneincombinationwithlosartanincreasesglucosecomparedtodiabeticandLos-treatedgroups.RosiglitazonesignificantlyamelioratesendothelialdysfunctionindicatedbyasignificantlylowercontractileresponsetoPEandAngIIandenhancementofACh-provoked1/2relaxationinaortasisolatedfromdiabeticrats[5].户使⽤本产品发表的科研⽂献•CellMetab.2021Mar2;33(3):581-597.e9.•BrJPharmacol.2020May;177(10):2286-2302.•FreeRadicBiolMed.2018Aug21;126:259-268.•PharmacolRes.2020Mar;153:104679.•JCellPhysiol.2019Nov;234(11):20694-20703.REFERENCES[1].LehmannJM,etal.Anantidiabeticthiazolidinedioneisahighaffinityligandforperoxisomeproliferator-activatedreceptorgamma(PPARgamma).JBiolChem.1995Jun2;270(22):12953-6.[2].WillsonTM,etal.Thestructure-activityrelationshipbetweenperoxisomeproliferator-activatedreceptorgammaagonismandtheantihyperglycemicactivityofthiazolidinediones.JMedChem.1996Feb2;39(3):665-8.[3].ThouennonE,etal.Rosiglitazone-activatedPPARγinducesneurotrophicfactor-α1transcriptioncontributingtoneuroprotection.JNeurochem.2015Aug;134(3):463-70.[4].MajeedY,etal.RapidandcontrastingeffectsofrosiglitazoneontransientreceptorpotentialTRPM3andTRPC5channels.MolPharmacol.2011Jun;79(6):1023-30.[5].AteyyaH,etal.Beneficialeffectsofrosiglitazoneandlosartancombinationindiabeticrats.CanJPhysiolPharmacol.2018Mar;96(3):215