Plerixafor-octahydrochloride-AMD3100-octahydrochloride-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEPlerixaforoctahydrochlorideCat.No.:HY-50912CASNo.:155148-31-5Synonyms:AMD3100octahydrochloride;JM3100octahydrochloride;SID791octahydrochloride分⼦式:C₂₈H₆₂Cl₈N₈分⼦量:794.47作⽤靶点:CXCR;HIV;VirusProtease作⽤通路:GPCR/GProtein;Immunology/Inflammation;Anti-infection储存⽅式:4°C,sealedstorage,awayfrommoisture*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoisture)溶解性数据体外实验H2O:100mg/mL(125.87mM;Needultrasonic)DMSO:<1mg/mL(insolubleorslightlysoluble)MassSolvent1mg5mg10mgConcentration制备储备液1mM1.2587mL6.2935mL12.5870mL5mM0.2517mL1.2587mL2.5174mL10mM0.1259mL0.6294mL1.2587mL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,awayfrommoisture)。-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、析出现象，可以通过加热和/或超声的⽅式助溶)1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE1.请依序添加每种溶剂：PBSSolubility:120mg/mL(151.04mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY⽣物活性Plerixaforoctahydrochloride(AMD3100octahydrochloride)⼀种选择性的CXCR4拮抗剂，IC50为44nM。IC50&Target125I-CXCL12-CXCR4125I-CXCL12-CXCR7HIV-1HIV-244nM(IC50)1-10nM(EC50)1-10nM(EC50)体外研究TheCXCR4inhibitorPlerixafor(AMD3100)isapotentinhibitorofCXCL12-mediatedchemotaxis(IC50,5.7nM)withapotencyslightlybetterthanitsaffinityforCXCR4.TreatingthecellswithCCX771orCXCL11hasnoeffectonCXCL12-mediatedMOLT-4orU937TEM.Incontrast,10μMPlerixaforinhibitsCXCL12-mediatedTEMinbothcellslines[1].Plerixafor(10μM)-treatedcellsshowamoderatereductionincellproliferationcomparedtoCXCL12-stimulatedcells,whichdonotreachstatisticalsignificance[2].体内研究Plerixafor(2mg/kg)administrationtoUUOmiceexacerbatesrenalinterstitialTcellinfiltration,resultinginincreasedproductionofthepro-inflammatorycytokinesIL-6andIFN-γanddecreasedexpressionoftheanti-inflammatorycytokineIL-10[3].BothperivascularandinterstitialfibrosisaresignificantlyreducedbytheCXCR4antagonist,Plerixafor(AMD3100)at8weeks[4].LD50,mouse,SC:16.3mg/kg;LD50,rat,SC:>50mg/kg;LD50,mouseandrat,IVinjection:5.2mg/kg.PROTOCOLCellAssay[2]U87MGcellsareseededin96-wellplatesatthedensityof6×103cellsin200μL/wellandtreatedwithCXCL12,PlerixafororwithpeptideR,asdescribedintheprevious“Treatments”section.MTT(5μg/mL)isaddedateachtimepoint(24,48,72h)duringthefinal2hoftreatment.Afterremovingcellmedium,100μLDMSOareaddedandopticaldensitiesmeasuredat595nmwithaLT-4000MSMicroplateReader.Measurementsaremadeintriplicatesfromthreeindependentexperiments[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMice[3]Administration[3][4]MaleC57bl/6mice(6-7weeksold,weighing20g)areused.Theanimalsareacclimatedtothehousingenvironment,whichisSPFandhadatemperatureof22°Canda12h/12hlight/darkcycleforaweek.Then,theyarerandomlydividedintofollowingexperimentalgroups,with8miceineachgroup:normal(nospecificintervention),UUO+AMD3100(micereceivedUUOsurgeryand2mg/kgAMD3100),andUUO+PBS(micereceivedUUOsurgeryandthesamevolumeofPBS).AMD3100andPBSareadministeredviaintraperitonealinjectioneverydayuntilsacrifice.Rats[4]TheCXCR4antagonist,AMD3100dissolvedinH2O,isdeliveredinthetype2diabeticsandratmodelatadoseof6mg/kgperdayfor8weeks.Incomplementarystudies,theeffectofCXCR4antagonism(AMD31002/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE6mg/kg/d)onregulatoryTcellnumbersisexamined.Forthesestudies,AMD3100orvehicleisdeliveredviaminipumpforaperiodofoneweek.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.户使⽤本产品发表的科研⽂献•CellMolImmunol.2020Mar;17(3):283-299.•AdvFunctMater.2020,2000309.•BrainBehavImmun.2017Jan;59:322-332.•NanoToday.2022,47:101689.•BioactMater.2021Jan7;6(7):2039-2057.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].ZabelBA,etal.ElucidationofCXCR7-mediatedsignalingeventsandinhibitionofCXCR4-mediatedtumorcelltransendothelialmigrationbyCXCR7ligands.JImmunol.2009Sep1;183(5):3204-11.[2].MercurioL,etal.TargetingCXCR4byaselectivepeptideantagonistmodulatestumormicroenvironmentandmicrogliareactivityinahumanglioblastomamodel.JExpClinCancerRes.2016Mar25;35:55.[3].YangJ,etal.ContinuousAMD3100TreatmentWorsensRenalFibrosisthroughRegulationofBoneMarrowDerivedPro-AngiogenicCellsHomingandT-Cell-RelatedInflammation.PLoSOne.2016Feb22;11(2):e0149926.[4].ChuPY,etal.CXCR4AntagonismAttenuatestheDevelopmentofDiabeticCardiacFibrosis.PLoSOne.2015Jul27;10(7):e0133616.[5].ScholsD,etal.HIVco-receptorinhibitorsasnovelclassofan