Laquinimod-ABR-215062-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemELaquinimodCat.No.:HY-13010CASNo.:248281-84-7Synonyms:ABR-215062分?式:C??H??ClN?O?分?量:356.8作?靶點(diǎn):NF-κB;Apoptosis作?通路:NF-κB;Apoptosis儲(chǔ)存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實(shí)驗(yàn)DMSO:100mg/mL(280.27mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM2.8027mL14.0135mL28.0269mL5mM0.5605mL2.8027mL5.6054mL10mM0.2803mL1.4013mL2.8027mL請(qǐng)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(chǔ)備液；?旦配成溶液，請(qǐng)分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲(chǔ)備液的保存?式和期限：-80°C,6months;-20°C,1month。-80°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?，-20°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請(qǐng)先按照InVitro?式配制澄的儲(chǔ)備液，再依次添加助溶劑：(為保證實(shí)驗(yàn)結(jié)果的可靠性，澄的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)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(guò)程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過(guò)加熱和/或超聲的?式助溶)1.請(qǐng)依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%saline1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESolubility:≥2.5mg/mL(7.01mM);Clearsolution2.請(qǐng)依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(7.01mM);ClearsolutionBIOLOGICALACTIVITY?物活性Laquinimod(ABR-215062)?種可?服的羧酰胺衍?物，?種有效的免疫調(diào)節(jié)劑，可防?中樞神經(jīng)系統(tǒng)的神經(jīng)變性和炎癥。Laquinimod減少形膠質(zhì)細(xì)胞NF-κB的活化以防?銅酮(Cuprizone)誘導(dǎo)的脫髓鞘。Laquinimod具有?于多發(fā)性硬化癥(MS；RRMS或CPMS)的復(fù)發(fā)緩解(RR)和慢性進(jìn)?性(CP)形式以及神經(jīng)退?性疾病研究的潛?。IC50&TargetNF-κB體外研究LaquinimodreversesEAEandinhibitspathogenicTcellimmuneresponses.LaquinimodreversesRR-EAEandinhibitsinflammatoryTcellresponsesviaadirecteffectonmyeloidAPC.LaquinimodaltersmyeloidAPCsubsetsandinhibitsTh1andTh17polarizationofmyelin-specificTcells.Laquinimod-inducedtypeII(M2)monocytesreverseestablishedEAE[1].LaquinimodmodulatesthephenotypeofBcellsofhealthydonors.LaquinimodmodulatesexpressionofmarkersrelatedtoregulatorycapacityinBcellsofRRMSpatients.LaquinimodreducesIFNγcytokineexpressioninCD4+Tcells[2].體內(nèi)研究Laquinimodtreatmentinhibitsdonormyelin-specificTcellsfromtransferringEAEtonaiverecipientmice.Invivolaquinimodtreatmentalterssubpopulationsofmyeloidantigenpresentingcells(APC)thatincludeadecreaseinCD11c+CD11b+CD4+dendriticcells(DC)andanelevationofCD11bhiGr1himonocytes[1].PROTOCOLCellAssay[1]PurifiedCD11b+cellsfromlaquinimod-orvehicle-treatedmiceareculturedwithnaiveCD4+cellsisolatedfromlaquinimod-orvehicle-treated2D2miceandantigen(MOGp35-55,20μg/mL).Cellsareculturedin96-wellmicrotitreplatesataconcentrationof0.25×106cells/mL.CulturemediumconsistedofRPMI1640supplementedwithL-glutamine(2mM),sodiumpyruvate(1mM),penicillin(100U/mL),streptomycin(0.1mg/mL),2-mercaptoethanol(5×10-5M)and10%(v/v)fetalbovineserum.Cellsareincubatedfor48handpulsedfor18hwith1μCiperwellof[3H]-thymidinebeforeharvesting.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalSevento10-week-oldfemaleC57BL/6,DBA/1orSJL/Jmiceareinjectedsubcutaneouslywith50μgMOGAdministration[1]p35-55,50μgrMOGor100μgPLPp139-151,respectively,incompleteFreund'sadjuvant.Afterimmunizationand2dayslater,micereceive200ng(C57BL/6)or100ng(SJL/J)pertussistoxinintraperitoneally(i.p.).Foradoptivetransfer,donorSJL/Jmiceareimmunizedasdescribedaboveandtreateddailywithlaquinimodorvehicle.10dayslater,cellsfromdraininglymphnodesandspleenareisolated,re-stimulatedfor48h(20μg/mLPLPp139-151),onaiveSJL/Jrecipients(107cellspermouse).Animalsareobserveddailyandclinicalscoresareassessedasfollows:0,nosigns;1,decreasedtailtone;2,mildmonoparesisorparaparesis;3,severeparaparesis;4,paraplegiaand/or2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEquadraparesis;and5,moribundordeath.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?JNeuroimmunol.2020Feb20;342:577195.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].Schulze-Topphoff,Ulf.,etal.Laquinimod,aquinoline-3-carboxamide,inducestypeIImyeloidcellsthatmodulatecentralnervoussystemautoimmunity.PLoSOne(2012),7(3),e33797.[2].ToubiE,etal.LaquinimodmodulatesBcellsandtheirregulatoryeffectsonTcellsinMultipleSclerosis.JNeuroimmunol.2012Oct15;251(1-2):45-54.[3].BrückW,etal.ReducedastrocyticNF-κBactivationbylaquinimodprotectsfromcuprizone-induceddemyelination.ActaNeuropathol.2012Sep;124(3):411-24.[4].JanTh?ne,etal.Laquinimodinthetreatmentofmultiplesclerosis:areviewofthedatasofar.DrugDesDevelT