Rosiglitazone-hydrochloride-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?Agonists?ScreeningLibrariesRosiglitazonehydrochlorideCat.No.:HY-17386ACASNo.:302543-62-0分?式:C??H??ClN?O?S分?量:393.89作?靶點(diǎn):PPAR;TRPChannel;Autophagy;Ferroptosis作?通路:CellCycle/DNADamage;MembraneTransporter/IonChannel;NeuronalSignaling;Autophagy;Apoptosis儲(chǔ)存?式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY?物活性Rosiglitazonehydrochloride(BRL49653hydrochloride)?種選擇性的，具有?服活性PPARγ激動(dòng)劑，對(duì)PPARγ1、PPARγ2和PPARγ的EC50值分別為30nM、100nM和60nM。Rosiglitazonehydrochloride與PPARγ結(jié)合，Kd約為40nM。Rosiglitazonehydrochloride也TRPC5的激活劑(EC50=-30μM)和TRPM3的抑制劑[1][2][3][4]。IC50&TargetPPARγ1PPARγ2TRPC5TRPM230nM(EC50)100nM(EC50)TRPM3體外研究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].體內(nèi)研究Rosiglitazone(5mg/kg,p.o.)decreasestheserumglucoseindiabeticrats.RosiglitazonealsodecreasesIL-6,TNF-α,andVCAM-1levelsindiabeticgroup.RosiglitazoneincombinationwithlosartanincreasesglucosecomparedtodiabeticandLos-treatedgroups.RosiglitazonesignificantlyamelioratesendothelialdysfunctionindicatedbyasignificantlylowercontractileresponsetoPEandAngIIandenhancementofACh-provoked1/2relaxationinaortasisolatedfromdiabeticrats[5].戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?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