ARL67156-trisodium-FPL-67156-trisodium-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEARL67156trisodiumCat.No.:HY-103265CASNo.:1021868-83-6Synonyms:FPL67156trisodium分⼦式:C₁₅H₂₁Br₂N₅Na₃O₁₂P₃分⼦量:785.05作⽤靶点:Phosphatase作⽤通路:MetabolicEnzyme/Protease储存⽅式:-20°C,sealedstorage,awayfrommoisture*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoisture)溶解性数据体外实验H2O:25mg/mL(31.85mM;Needultrasonic)DMSO:1mg/mL(1.27mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制备储备液1mM1.2738mL6.3690mL12.7380mL5mM0.2548mL1.2738mL2.5476mL10mM0.1274mL0.6369mL1.2738mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；⼀旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存⽅式和期限：-80°C,6months;-20°C,1month(sealedstorage,awayfrommoisture)。-80°C储存时，请在6个⽉内使⽤，-20°C储存时，请在1个⽉内使⽤。BIOLOGICALACTIVITY⽣物活性ARL67156(FPL67156)trisodium⼀种ecto-ATPase抑制剂。ARL67156trisodium竞争性NTPDase1(CD39)，NTPDase3和NPP1抑制剂，Ki分别为11，18和12μM。ARL67156trisodium可⽤于钙化性主动脉瓣疾病、哮喘等疾病的研究。1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEIC50&TargetKi:11μM(NTPDase1),18μM(NTPDase3),12μM(NPP1)[1]体外研究ARL67156trisodium(1-100μM)potentiatesneurogeniccontractionsinaconcentration-dependentmanner[4].ARL67156trisodium(10μg/mL,24h)increasesthesurfaceexpressionofCXCR3onATP-treatedHMC-1cells[5].ARL67156trisodium(30μM,5s)potentiatesthenorepinephrinereleasepromotedbyATPinguineapigheartsynaptosomes[6].ARL67156trisodium(100μM,4h)significantlydecreasesHIV-1replicationinmacrophages[7].体内研究ARL67156trisodium(1.1μg/kg/day,administeredwithosmoticpumpsimplantedsubcutaneously,for28days)preventsthedevelopmentofcalcificaorticvalvediseaseinWarfarin(HY-B0687)-treatedrats[2].ARL67156trisodium(intraperitonealinjection,2ꢀmg/kg)preventstheincreaseofserumadenosineconcentrationinducedbyFructose1,6-bisphosphate(FBP)[3].AnimalModel:Warfarin-inducedmineralizationratmodel[2]Dosage:1.1μg/kg/dayAdministration:Administeredwithosmoticpumpsimplantedsubcutaneously,for28daysResult:Preventedthedevelopmentofaorticstenosisbyloweringthelevelofapoptosisandmineralizationoftheaorticvalve/aorta.NormalizedthelevelofpAkt(animportantkinaseinvolvedinthesurvivalpathway).AnimalModel:C57BL/6mice[3]Dosage:2ꢀmg/kgAdministration:Intraperitonealinjection,1ꢀhbeforeadministrationofFBP(100ꢀmg/kg)Result:Completelyabolishedtheanti-inflammatoryeffectsofFBP(observedbytheneutrophilinfiltration,hyperalgesiaandoedemaofthejoint).户使⽤本产品发表的科研⽂献•Neuron.2021Dec17;S0896-6273(21)00988-0.•FrontImmunol.04October2022.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].CKennedy,etal.ATPasaco-transmitterwithnoradrenalineinsympatheticnerves--functionandfate.CibaFoundSymp.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE1996;198:223-35;discussion235-8.[2].Ya-DongGao,etal.Th2cytokine-primedairwaysmoothmusclecellsinducemastcellchemotaxisviasecretionofATP.JAsthma.2014Dec;51(10):997-1003.[3].CasildeSesti,etal.EctoNucleotidaseincardiacsympatheticnerveendingsmodulatesATP-mediatedfeedbackofnorepinephrinerelease.JPharmacolExpTher.2002Feb;300(2):605-11.[4].JulietaSchachter,etal.Inhibitionofecto-ATPaseactivitiesimpairsHIV-1infectionofmacrophages.Immunobiology.2015May;220(5):589-96.[5].LévesqueSA,etal.Specificityoftheecto-ATPaseinhibitorARL67156onhumanandmouseectonucleotidases.BrJPharmacol.2007Sep;152(1):141-50.[6].NancyCôté,etal.InhibitionofEctonucleotidaseWithARL67156PreventstheDevelopmentofCalcificAorticValveDiseaseinWarfarin-TreatedRats.EurJPharmacol.2012Aug15;689(1-3):139-46.[7].FlávioPVeras,etal.Fructose1,6-bisphosphate,ahigh-energyintermediateofglycolysis,attenuatesexperimentalarthritisbyactivatinganti-inflammatoryadenosinergicpathway.SciRep.2015Oct19;5:15171.McePdfHeigh