Plerixafor-octahydrochloride-AMD3100-octahydrochloride-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEPlerixaforoctahydrochlorideCat.No.:HY-50912CASNo.:155148-31-5Synonyms:AMD3100octahydrochloride;JM3100octahydrochloride;SID791octahydrochloride分?式:C??H??Cl?N?分?量:794.47作?靶點:CXCR;HIV;VirusProtease作?通路:GPCR/GProtein;Immunology/Inflammation;Anti-infection儲存?式:4°C,sealedstorage,awayfrommoisture*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoisture)溶解性數(shù)據(jù)體外實驗H2O:100mg/mL(125.87mM;Needultrasonic)DMSO:<1mg/mL(insolubleorslightlysoluble)MassSolvent1mg5mg10mgConcentration制備儲備液1mM1.2587mL6.2935mL12.5870mL5mM0.2517mL1.2587mL2.5174mL10mM0.1259mL0.6294mL1.2587mL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,awayfrommoisture)。-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?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，適當保存；體內(nèi)實驗的?作液，建議您現(xiàn)?現(xiàn)配，當天使?；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)1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE1.請依序添加每種溶劑：PBSSolubility:120mg/mL(151.04mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY?物活性Plerixaforoctahydrochloride(AMD3100octahydrochloride)?種選擇性的CXCR4拮抗劑，IC50為44nM。IC50&Target125I-CXCL12-CXCR4125I-CXCL12-CXCR7HIV-1HIV-244nM(IC50)1-10nM(EC50)1-10nM(EC50)體外研究TheCXCR4inhibitorPlerixafor(AMD3100)isapotentinhibitorofCXCL12-mediatedchemotaxis(IC50,5.7nM)withapotencyslightlybetterthanitsaffinityforCXCR4.TreatingthecellswithCCX771orCXCL11hasnoeffectonCXCL12-mediatedMOLT-4orU937TEM.Incontrast,10μMPlerixaforinhibitsCXCL12-mediatedTEMinbothcellslines[1].Plerixafor(10μM)-treatedcellsshowamoderatereductionincellproliferationcomparedtoCXCL12-stimulatedcells,whichdonotreachstatisticalsignificance[2].體內(nèi)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?邊的抑制劑?師www.MedChemE6mg/kg/d)onregulatoryTcellnumbersisexamined.Forthesestudies,AMD3100orvehicleisdeliveredviaminipumpforaperiodofoneweek.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻?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