Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEARL67156trisodiumCat.No.:HY-103265CASNo.:1021868-83-6Synonyms:FPL67156trisodium分?式:C??H??Br?N?Na?O??P?分?量:785.05作?靶點(diǎn):Phosphatase作?通路:MetabolicEnzyme/Protease儲(chǔ)存?式:-20°C,sealedstorage,awayfrommoisture*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoisture)溶解性數(shù)據(jù)體外實(shí)驗(yàn)H2O:25mg/mL(31.85mM;Needultrasonic)DMSO:1mg/mL(1.27mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM1.2738mL6.3690mL12.7380mL5mM0.2548mL1.2738mL2.5476mL10mM0.1274mL0.6369mL1.2738mL請(qǐng)根據(jù)產(chǎn)品在不同溶劑中的溶解度選擇合適的溶劑配制儲(chǔ)備液；?旦配成溶液，請(qǐng)分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲(chǔ)備液的保存?式和期限：-80°C,6months;-20°C,1month(sealedstorage,awayfrommoisture)。-80°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?，-20°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?。BIOLOGICALACTIVITY?物活性ARL67156(FPL67156)trisodium?種ecto-ATPase抑制劑。ARL67156trisodium競(jìng)爭(zhēng)性NTPDase1(CD39)，NTPDase3和NPP1抑制劑，Ki分別為11，18和12μM。ARL67156trisodium可?于鈣化性主動(dòng)脈瓣疾病、哮喘等疾病的研究。1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEIC50&TargetKi:11μM(NTPDase1),18μM(NTPDase3),12μM(NPP1)[1]體外研究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].體內(nèi)研究ARL67156trisodium(1.1μg/kg/day,administeredwithosmoticpumpsimplantedsubcutaneously,for28days)preventsthedevelopmentofcalcificaorticvalvediseaseinWarfarin(HY-B0687)-treatedrats[2].ARL67156trisodium(intraperitonealinjection,2?mg/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:2?mg/kgAdministration:Intraperitonealinjection,1?hbeforeadministrationofFBP(100?mg/kg)Result:Completelyabolishedtheanti-inflammatoryeffectsofFBP(observedbytheneutrophilinfiltration,hyperalgesiaandoedemaofthejoint).戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?Neuron.2021Dec17;S0896-6273(21)00988-0.?FrontImmunol.04October2022.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].CKennedy,etal.ATPasaco-transmitterwithnoradrenalineinsympatheticnerves--functionandfate.CibaFoundSymp.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師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].NancyC?té,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