Cytarabine-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•Agonists•ScreeningLibrarieswww.MedChemECytarabineCat.No.:HY-13605CASNo.:147-94-4分⼦式:C₉H₁₃N₃O₅分⼦量:243.22作⽤靶点:DNA/RNASynthesis;NucleosideAntimetabolite/Analog;HSV;Autophagy;EndogenousMetabolite;Apoptosis作⽤通路:CellCycle/DNADamage;Anti-infection;Autophagy;MetabolicEnzyme/Protease;Apoptosis储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验H2O:48mg/mL(197.35mM;Needultrasonic)扫描⼆维码，DMSO:17.3mg/mL(71.13mM;Needultrasonicand运⽤溶解⽅案计算器warming)获得适合您实验体系的溶解⽅案MassSolvent1mg5mg10mgConcentration制备储备液1mM4.1115mL20.5575mL41.1150mL5mM0.8223mL4.1115mL8.2230mL10mM0.4112mL2.0558mL4.1115mL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，并请注意储备液的保存⽅式和期限。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、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：10%DMSO40%PEG3005%Tween-8045%salineSolubility:≥2.08mg/mL(8.55mM);Clearsolution此⽅案可获得≥2.08mg/mL(8.55mM，饱和度未知)的澄溶液。1/4www.MedChemEwww.MedChemE以1mL⼯作液为例，取100μL20.8mg/mL的澄DMSO储备液加到400μLPEG300中，混合均匀；向上述2.体系中加⼊50μLTween-80，混合均匀；然后继续加⼊450μL⽣理盐⽔定容⾄1mL。请依序添加每种溶剂：10%DMSO90%(20%SBE-β-CDinsaline)Solubility:≥2.08mg/mL(8.55mM);Clearsolution此⽅案可获得≥2.08mg/mL(8.55mM，饱和度未知)的澄溶液。以1mL⼯作液为例，取100μL20.8mg/mL的澄DMSO储备液加到900μL20%的SBE-β-CD⽣理盐⽔⽔溶3.液中，混合均匀。请依序添加每种溶剂：10%DMSO90%cornoilSolubility:≥2.08mg/mL(8.55mM);Clearsolution此⽅案可获得≥2.08mg/mL(8.55mM，饱和度未知)的澄溶液，此⽅案不适⽤于实验周期在半个⽉以上的实验。4.以1mL⼯作液为例，取100μL20.8mg/mL的澄请依序添加每种溶剂：PBSDMSO储备液加到900μL⽟⽶油中，混合均匀。Solubility:130mg/mL(534.50mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY⽣物活性Cytarabine⼀种核苷类似物，可引起S期细胞周期停滞并抑制DNA聚合酶。Cytarabine抑制DNA合成的IC50为16nM。Cytarabine对HSV具有抗病毒作⽤。IC50&TargetHumanEndogenousHSV-1Metabolite体外研究Cytarabineisphosphorylatedintoatriphosphateform(Ara-CTP)involvingdeoxycytidinekinase(dCK),whichcompeteswithdCTPforincorporationintoDNA,andthenblocksDNAsynthesisbyinhibitingthefunctionofDNAandRNApolymerases.Cytarabinedisplaysahighergrowthinhibitoryactivitytowardswild-typeCCRF-CEMcellscomparedtootheracutemyelogenousleukemia(AML)cellswithIC50of16nM[1].Cytarabineapparentlyinducesapoptosisofratsympatheticneuronsat10μM,ofwhich100μMshowsthehighesttoxicityandkillsover80%oftheneuronsby84hours,involvingthereleaseofmitochondrialcytochrome-candtheactivationofcaspase-3,andthetoxicitycanbeattenuatedbyp53knockdownanddelayedbybaxdeletion[2].体内研究Cytarabine(250mg/kg)alsocausesplacentalgrowthretardationandincreasesplacentaltrophoblasticcellsapoptosisintheplacentallabyrinthzoneofthepregnantSlc:Wistarrats,whichincreasesfrom3hourafterthetreatmentandpeaksat6hourbeforereturningtocontrollevelsat48hour,withremarkablyenhancedp53protein,p53trancriptionaltargetgenessuchasp21,cyclinG1andfasandcaspase-3activity[3].Cytarabineishighlyeffectiveagainstacuteleukaemias,whichcausestheCytarabineteristicG1/Sblockageandsynchronization,andincreasesthesurvivaltimeforleukaemicBrownNorwayratsinaweakdose-relatedfashionindicatingthattheuseofhigherdosagesofCytarabinedoesnotcontributetoitsantileukaemiceffectivenessinman[4].PROTOCOLAnimalPregnantratsareinjectedintraperitoneally(i.p.)with250mg/kgofCytarabineonDay13ofgestation2/4www.MedChemEwww.MedChemEAdministration[3](GD13).Undertheconditionsofthisexperiment,congenitalanomaliesandgrowthretardationaredetectedatahighrateinperinatalfetuses,althoughtheincidenceoffetaldeathisnotmarkedlyincreased.At1,3,6,9,12,24,and48hafterthetreatment,sixdamseacharekilledbyheartpunctureunderetheranesthesia,andtheplacentasarecollected.Ascontrols,sixpregnantratsareinjectedi.p.withanequivalentvolumeofPBSonGD13andkilledatthesametimepointasCytarabine-treatedgroups.Ofthesixdamsobtainedateachtimepoint,threeareusedforhistopathologicalanalysesandthreeforreversetranscription-polymerasechainreaction(RT-PCR)analysis.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.户使⽤本产品发表的科研⽂献•Cell.2018Sep20;175(1):171-185.e25.•Leukemia.2021Mar29.•ClinChem.2019Dec;65(12):1522-1531.•CellDeathDis.2021Jan5;12(1):20.•ActaPharmacolSin.2021Jan;42(1):108-114.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].Tobias,S.C.andR.F.Borch,Synthesisandbiologicalevaluationofacytarabinephosphoramidateprodrug.MolPharm,2004.1(2):p.112-6.[2].Besirli,C.G.,etal.CytosinearabinosiderapidlyactivatesBax-dependentapoptosisandadelayedBax-independentdeathpathwayinsympatheticneurons.CellDeathDiffer,2003.10(9):p.1045-58.[3].Yamauchi,H.,etal.,Involvementofp53in1-beta-D-arabinofuranosylcytosine-inducedtrophoblasticcellapoptosisandimpairedproliferationinratplacenta.BiolReprod,2004.70(6):p.1762-7.[4].Richel,D.J.,etal.,Comparisonoftheantileukaemicactivityof5aza-2-deoxycytidineandarabinofuranosyl-cytosineinratswithmyelocyticleukaemia.BrJCancer,1988.58(6):p.730-3.[5].ShepshelovichD,etal.Pharmacodynamicsofcytarabineinducedleucopenia:aretrospectivecohortstudy.BrJClinPharmacol.2015Apr;79(4):685-91.[6].RenisHE.Antiviralactivityofcytarabineinherpesvir