Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEAdenosine5′-diphosphoribosesodiumCat.No.:HY-100973ACASNo.:68414-18-6Synonyms:ADPribosesodium分?式:C??H??N?NaO??P?分?量:581.3作?靶點(diǎn):TRPChannel;Autophagy作?通路:MembraneTransporter/IonChannel;NeuronalSignaling;Autophagy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:125mg/mL(215.04mM;Needultrasonic)DMSO:25mg/mL(43.01mM;ultrasonicandwarmingandheatto80°C)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM1.7203mL8.6014mL17.2028mL5mM0.3441mL1.7203mL3.4406mL10mM0.1720mL0.8601mL1.7203mL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?。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請(qǐng)先按照InVitro?式配制澄的儲(chǔ)備液，再依次添加助溶劑：(為保證實(shí)驗(yàn)結(jié)果的可靠性，澄的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)的?作液，建議您現(xiàn)?現(xiàn)配，當(dāng)天使?；以下溶劑前顯?的百分?指該溶劑在您配制終溶液中的體積占?；如在配制過程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1/2MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE1.請(qǐng)依序添加每種溶劑：PBSSolubility:100mg/mL(172.03mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY?物活性Adenosine5′-diphosphoribosesodium(ADPribosesodium)?種煙酰胺腺嘌呤核苷酸(NAD+)的代謝產(chǎn)物，也?種最有效和最主的細(xì)胞內(nèi)Ca2+滲透性陽離?TRPM2通道激活劑，還可以增強(qiáng)?噬(autophagy)。IC50&TargetTRPM2channel[1][2]Autophagy[1]體外研究Inmouseembryonicfibroblasts(MEFs),H2O2treatmentdemonstratesthattheactivationofpoly(ADP-ribose)(PAR)polymerase-1(PARP-1)producedAdenosine5′-diphosphoribose(ADPribose),whichisanactivatingsignalforTRPM2channels,therebypromotingCa2+elevationthroughextracellularCa2+influxand(or)lysosomalCa2+release.Thisprocesseventuallyactivatesearlyorlateautophagyinresponsetodifferentdegreesofoxidativestress[1][1].TRPM2channelsareactivatedbybindingofAdenosine5′-diphosphoribose(ADPribose)totheintracellularNUDT9-homology(NUDT9-H)domainuniquetoTRPM2andlocatedatitsCterminus.InadditiontoADPR,intracellularCa2+isanessentialcoactivator:TRPM2channelsopenonlyinthecombinedpresenceofbothligands[2].REFERENCES[1].ZhangDX,etal.ThepotentialregulatoryrolesofNAD(+)anditsmetabolisminautophagy.Metabolism.2016Apr;65(4):454-62.[2].TóthB,etal.PorecollapseunderliesirreversibleinactivationofTRPM2cationchannelcurrents.ProcNatlAcadSciUSA.2012Aug14;109(33):13440-5.McePdfHeightCaution:Producthasnotbeenfullyvalidatedformedicalapplications.For