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

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEAdipoRonhydrochlorideCat.No.:HY-110164CASNo.:1781835-20-8分?式:C??H??ClN?O?分?量:464.98作?靶點(diǎn):AdiponectinReceptor作?通路:MetabolicEnzyme/Protease儲(chǔ)存?式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY?物活性AdipoRonhydrochloride?種可?服的，特異性的AdipoR激動(dòng)劑，能夠與AdipoR1和AdipoR2結(jié)合，Kd值分別為1.8和3.1μM。IC50&TargetKd:1.8μM(AdipoR1),3.1μM(AdipoR2)[1]體外研究AdipoRonhydrochlorideisanorallyactiveandspecificAdipoRagonist,bindstoAdipoR1andAdipoR2,withKdsof1.8and3.1μM.AdipoRon(50nM-50μM)increasesAMPKphosphorylationviaAdipoR1[1].AdipoRon(50μM)dose-dependentlyattenuatestheexpressionofTNF-αandTGF-β1intheL02cells.AdipoRonexhibitssignificantanddosage-dependentgrowthsuppressiononmacrophages[2].AdipoRontreatmentsignificantlyimprovescardiacfunctionalrecoveryafterreperfusion,andinhibitspost-MIapoptosis[3].AdipoRonexertsvasodilationbymechanismsdistincttoadiponectinandinducesvasorelaxationwithoutamarkeddecreaseinVSMC[Ca2+]i[4].體內(nèi)研究AdipoRon(50?mg/kg,i.v.)cuasessignificantphosphorylationofAMPKinskeletalmuscleandliverofwild-typemicebutnotAdipor1?/??Adipor2?/?double-knockoutmice[1].AdipoRon(0.02,0.1,and0.5mg/kg,i.g.)alleviatesD-GalNinducedhepatotoxicityinmice,andpreventshepaticarchitecturedistortionagainstD-GalNchallenge.ThehepatoprotectivepotentialofAdipoRonisparticularlyevidentinhigherdosages(0.1and0.5mg/kg)[2].EnhancedcardiomyocyteapoptosisinAPN-deficientmiceisrescuedbyAdipoRon(50mg/kg,p.o.)administration.AntiapoptoticeffectofAdipoRonisattenuatedbutnotlostinAMPK-DNmice[3].PROTOCOL1/2MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemECellAssay[2]TheeffectsofAdipoRonontheproliferationofparenchymalandnon-parenchymalhepatocytesareevaluatedinvitroviaL02andRAW264.7,byMTTassayasdescribedwithslightmodification:100μLcellssuspension(6×104/mL)areseededina96-wellplateandincubatedfor18h.FreshmediawithAdipoRonareaddedatspecifiedconcentrations,andtheincubationscontinueforafurther24h.Thencellsareincubatedfor4hwith0.5mg/mLofMTT,andanalyzedinamicroplatereaderat490nm.Eachgroupisperformedinsixreplications.Themeanabsorbancevaluescorrectedforablank(mediumonly)arecalculatedaspercentagesofsurvival[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMice[2]Administration[2]After3daysofacclimation,micearerandomLydividedintosixgroups(9miceineach):control,model,bicyclol(20mg/kg),AdipoRon(0.02mg/kg,0.1mg/kg,0.5mg/kg).ThesyntheticAdipoRonandbicyclolaredissolvedinDMSOanddilutedbysalinecontaining0.5%sodiumcarboxymethylcellulose(CMC-Na)[finalvehicle:5%DMSO(v/v)salinesolution].Alltestgroupsareadministeredwithvehicle(controlandmodelgroups)ortherapeuticagents(bicyclolorAdipoRongroups)atadosingvolumeof10mL/kg,byintragastric(i.g.)gavagetwiceperdayforthreeconsecutivedayspriortoD-GalNadministration.2hafterlasttreatment,micearechallengedwithasingleintraperitoneal(i.p.)administrationofD-GalNsalinesolutionatadoseof600mg/kgtoinduceacuteliverinjury,whilethecontrolgroupmicereceivesalineinstead.Thenmicearefastedfor20hbeforeorbitalbloodcollection.Finally,allanimalsaresacrificedbycervicaldislocation,andliversareharvestedforbiochemicalorhistopathologyanalysis[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?MolPsychiatry.2020Mar4.?ProgNeurobiol.2021Jul29;102125.?RedoxBiol.August2022,102390.?Diabetes.2021Jun;70(6):1303-1316.?ActaPharmacolSin.2022Aug2.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].Okada-IwabuM,etal.Asmall-moleculeAdipoRagonistfortype2diabetesandshortlifeinobesity.Nature.2013Nov28;503(7477):493-9.[2].WangY,etal.HepatoprotectiveeffectsofAdipoRonagainstd-galactosamine-inducedliverinjuryinmice.EurJPharmSci.2016Aug9;93:123-131.[3].ZhangY,etal.AdipoRon,thefirstorallyactiveadiponectinreceptoractivator,attenuatespostischemicmyocardialapoptosisthroughbothAMPK-mediatedandAMPK-independentsignalings.AmJPhysiolEndocrinolMetab.2015Aug1;309(3):E275-82.[4].HongK,etal.AdiponectinReceptorAgonist,AdipoRon,CausesVasorelaxationPredominantlyViaaDirectSmoothMuscleAction.Microcirculation.2016Apr;23(3):207-20.McePdfHeight2/2MasterofBio