Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEL-AscorbicacidsodiumsaltCat.No.:HY-B0166ACASNo.:134-03-2Synonyms:Sodiumascorbate;SodiumL-ascorbate;VitaminCsodiumsalt分?式:C?H?NaO?分?量:198.11作?靶點:CalciumChannel;ReactiveOxygenSpecies;Apoptosis;EndogenousMetabolite作?通路:MembraneTransporter/IonChannel;NeuronalSignaling;Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB;Apoptosis儲存?式:4°C,sealedstorage,awayfrommoistureandlight*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoistureandlight)溶解性數(shù)據(jù)體外實驗H2O:100mg/mL(504.77mM;Needultrasonic)DMSO:1mg/mL(5.05mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM5.0477mL25.2385mL50.4770mL5mM1.0095mL5.0477mL10.0954mL10mM0.5048mL2.5239mL5.0477mL請根據(jù)產(chǎn)品在不同溶劑中的溶解度選擇合適的溶劑配制儲備液；?旦配成溶液，請分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲備液的保存?式和期限：-80°C,6months;-20°C,1month(sealedstorage,awayfrommoistureandlight)。-80°C儲存時，請在6個?內(nèi)使?，-20°C儲存時，請在1個?內(nèi)使?。體內(nèi)實驗請根據(jù)您的實驗動物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請先按照InVitro?式配制澄的儲備液，再依次添加助溶劑：(為保證實驗結(jié)果的可靠性，澄的儲備液可以根據(jù)儲存條件，適當(dāng)保存；體內(nèi)實驗的?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1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1.請依序添加每種溶劑：PBSSolubility:50mg/mL(252.39mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY?物活性L-Ascorbicacidsodiumsalt(Sodiumascorbate)，?種電?供體，?種內(nèi)性抗氧化劑。L-Ascorbicacidsodiumsalt選擇性抑制Cav3.2通道(Cav3.2channels)，IC50為6.5μM。L-Ascorbicacidsodiumsalt還是?種膠原沉積促進(jìn)劑和彈性?成抑制劑。IC50&TargetT-typecalciumchannelMicrobialMetaboliteHumanEndogenousMicrobialMetaboliteMetaboliteHumanEndogenousMetabolite體外研究TheconditionedmediumforB16F10cellssignificantlyinhibitscellapoptosisinducedbyL-Ascorbicacidsodiumsalt(SodiumL-ascorbate)(10mM),andtheeffectiveingredientsinthemediumshowarelativemolecularmassbelow5,000[4].體內(nèi)研究TgratstreatedwithL-Ascorbicacidsodiumsalt(SodiumL-ascorbate)showahigherincidenceofcarcinoma(29.6%),comparedtothosewithoutL-Ascorbicacidsodiumsalt(15.4%).IndependentoftheL-Ascorbicacidsodiumsalttreatment,transgenicratsexhibitvariouskindsofmalignanttumorsinvariousorgans[5].After12weeksofPEITC-treatment,bothsimplehyperplasiaandpapillaryornodular(PN)hyperplasiahavedevelopedinallanimals,butthemajorityoftheselesionshavedisappearedatweek48,irrespectiveoftheL-Ascorbicacidsodiumsalt-treatment.Thesamelesionsafter24weeksofPEITC-treatmenthaveprogressedtodysplasiaandcarcinoma,inasmallnumberofcasesbyweek48,butenhancementbytheL-Ascorbicacidsodiumsalt-treatmentisevidentonlywithsimplehyperplasiasandPNhyperplasiasinrats[6].PROTOCOLAnimalAtotalof407-week-oldmaleTgratsaredividedinto2groups.Twenty-seven(group1)and13(group2)ratsAdministration[3]aregivenapowderedMFdietwithorwithout5%sodiumL-ascorbate,respectively.Similarly,atotalof427-week-oldmaleNon-tgratsaredividedinto2groups,and30(group3)and12(group4)animalsaregivenadietwithorwithout5%sodiumL-ascorbate,respectively.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?MilMedRes.2020Nov1;7(1):52.?RedoxBiol.2022Aug;54:102392.?SciChinaLifeSci.2018Oct;61(10):1151-1167.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE?FreeRadicBiolMed.2020Feb1;147:220-230.?AntioxidRedoxSignal.2020Dec10;33(17):1191-1208.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].HinekA,etal.SodiumL-ascorbateenhanceselasticfibersdepositionbyfibroblastsfromnormalandpathologichumanskin.JDermatolSci.2014Sep;75(3):173-82.[2].YangX,etal.MousemelanomacelllineB16F10-derivedconditionedmediuminhibitssodiumL-ascorbate-inducedB16F10cellapoptosis.NanFangYiKeDaXueXueBao.2012Feb;32(2):146-50.[3].MorimuraK,etal.LackofurinarybladdercarcinogenicityofsodiumL-ascorbateinhumanc-Ha-rasproto-oncogenetransgenicrats.ToxicolPathol.2005;33(7):764-7.[4].TakagiH,etal.Limitedtumor-initiatingactivityofphenylethylisothiocyanatebypromotionwithsodiumL-ascorbateinarattwo-stageurinarybladdercarcinogenesismodel.CancerLett.2005Mar10;219(2):147-53.[5].AleksanderHinek,etal.SodiumL-ascorbateenhanceselasticfibersdepositionbyfibroblastsfromnormalandpathologichumanskin.JDermatolSci.2014Sep;75(3):173-82.[6].MichaelTNelson,etal.Molecularmechanismsofsubtype-specificinhibitionofneuronalT-typecalciumchannelsbyascorbate.JNeurosci.20