L-Ascorbic-acid-sodium-salt-Sodium-ascorbate-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEL-AscorbicacidsodiumsaltCat.No.:HY-B0166ACASNo.:134-03-2Synonyms:Sodiumascorbate;SodiumL-ascorbate;VitaminCsodiumsalt分⼦式:C₆H₇NaO₆分⼦量:198.11作⽤靶点:CalciumChannel;ReactiveOxygenSpecies;Apoptosis;EndogenousMetabolite作⽤通路:MembraneTransporter/IonChannel;NeuronalSignaling;Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB;Apoptosis储存⽅式:4°C,sealedstorage,awayfrommoistureandlight*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoistureandlight)溶解性数据体外实验H2O:100mg/mL(504.77mM;Needultrasonic)DMSO:1mg/mL(5.05mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制备储备液1mM5.0477mL25.2385mL50.4770mL5mM1.0095mL5.0477mL10.0954mL10mM0.5048mL2.5239mL5.0477mL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,awayfrommoistureandlight)。-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。体内实验请根据您的实验动物和给药⽅式选择适当的溶解⽅案。以下溶解⽅案都请先按照InVitro⽅式配制澄的储备液，再依次添加助溶剂：(为保证实验结果的可靠性，澄的储备液可以根据储存条件，适当保存；体内实验的⼯作液，建议您现⽤现配，当天使⽤；以下溶剂前显⽰的百分⽐指该溶剂在您配制终溶液中的体积占⽐；如在配制过程中出现沉淀1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE、析出现象，可以通过加热和/或超声的⽅式助溶)1.请依序添加每种溶剂：PBSSolubility:50mg/mL(252.39mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY⽣物活性L-Ascorbicacidsodiumsalt(Sodiumascorbate)，⼀种电⼦供体，⼀种内性抗氧化剂。L-Ascorbicacidsodiumsalt选择性抑制Cav3.2通道(Cav3.2channels)，IC50为6.5μM。L-Ascorbicacidsodiumsalt还是⼀种胶原沉积促进剂和弹性⽣成抑制剂。IC50&TargetT-typecalciumchannelMicrobialMetaboliteHumanEndogenousMicrobialMetaboliteMetaboliteHumanEndogenousMetabolite体外研究TheconditionedmediumforB16F10cellssignificantlyinhibitscellapoptosisinducedbyL-Ascorbicacidsodiumsalt(SodiumL-ascorbate)(10mM),andtheeffectiveingredientsinthemediumshowarelativemolecularmassbelow5,000[4].体内研究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.户使⽤本产品发表的科研⽂献•MilMedRes.2020Nov1;7(1):52.•RedoxBiol.2022Aug;54:102392.•SciChinaLifeSci.2018Oct;61(10):1151-1167.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师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