Deferoxamine-mesylate-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•Agonists•ScreeningLibrarieswww.MedChemEDeferoxaminemesylateCat.No.:HY-B0988CASNo.:138-14-7分⼦式:C₂₆H₅₂N₆O₁₁S分⼦量:656.79作⽤靶点:Autophagy;Amyloid-β;Mitophagy;Ferroptosis作⽤通路:Autophagy;NeuronalSignaling;Apoptosis储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验H2O:125mg/mL(190.32mM;Needultrasonic)扫描⼆维码，运⽤溶解⽅案计算器获得适合您实验体系的溶解⽅案MassSolvent1mg5mg10mgConcentration制备储备液1mM1.5226mL7.6128mL15.2256mL5mM0.3045mL1.5226mL3.0451mL10mM0.1523mL0.7613mL1.5226mL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：PBSSolubility:33.33mg/mL(50.75mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY1/3www.MedChemEwww.MedChemE⽣物活性Deferoxaminemesylate⼀种铁螯合剂，可将游离铁与稳定的复合物结合，防⽌其发⽣化学反应。体外研究DeferoxaminetreatmentsignificantlyincreasesHIF-1αbindingunderallcultureconditions,includinghypoxicandhigh-glucose.ThemechanismofdeferoxamineisthroughimprovingHIF-1αbiologicalfunctionthroughscavengingoxygenfreeradicals[1].Deferoxamine(5μM)hassignificanteffectonthetumor-associatedstromalcellscellularmultiplication,andcellsdieatday7afterexposureto50μMand100μMdeferoxamine.Deferoxamine(5μM-100μM)inhibitstheproliferationofBMMSCs,andinducesapoptosisofMSCsinadose-dependentmanner.DeferoxamineinfluencestheexpressionofadhesionproteinsonMSCs[3].Deferoxamine(30,60,120ꢀμM)showslowerexpressionofHIF-1αinaconcentrationdependentwayinAdMSCs[4].体内研究Deferoxamine(100mg/kg,i.p.)lowersthemortalityrateofsubarachnoidhemorrhage(SAH)rat.Deferoxamine(100mg/kg,i.p.)attenuatesEvan’sblueextravasationincortex,amelioratesthetightjunctiondetachmentandpreservestheintegrityofthebasemembraneexaminedinelectronmicroscopeatday3afterSAH.DeferoxamineattenuatesdegradationofBBBproteinsafterSAHandsignificantlyreducesferritinexpressionatday3inthecortex,andimprovesneurologicbehaviorandcognitivedeficitsafterexperimental[1].TenµLof1mMdeferoxamine-treatedwoundsdisplaysignificantlyacceleratedhealingfromday7onwardandhealsignificantlyfasterthancontrol-treatedwoundsindiabeticmice.Deferoxamine-treatedwoundsanddimethyloxalylglycine-treatedwoundshealsignificantlyfasterthancontrol-treatedwoundsinagedmice[2].Indeferoxamine(10mg/mL)-treatedTGmice,thereisadecreaseinbothsolubleandinsolubleAβ40andAβ42.BothpGSK3βandβ-cateninaresignificantlyincreasedbyapproximately50%inthedeferoxamine-treatedmice[5].PROTOCOLCellAssay[3]Harvestedmurinetumorandbonemarrow-derivedMSCsareexposedtovaryingdosesofdeferoxamine.Cellviabilityisassessedbytrypanblueexclusionassay.Theviablecellsaremorethan98%beforeenrolledforexperiments.Atotalof1.5×105TAMSCs/wellor3×105BMMSCs/wellareseededin6-wellplates.ThenMSCsareexposedto5,10,25,50,and100μMdeferoxamineonthefollowingday.After7days,thenumberofTAMSCsiscounted.ToassessthecytotoxicityofdeferoxaminetoprimarybonemarrowMSCs,2×106bonemarrowcells/wellareseededin24-wellplates.After9days,thenumberofsurvivalcellsiscounted.Toassessthecellcycle,TAMSCsarestainedwithpropidiumiodide,andcellcycledistributionisanalyzedbyflowcytometry.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMicearedividedintothreetreatmentgroupsof17each:(1)TGmicegivenINDeferoxamine(TG-DFO),(2)Administration[5]TGmicegivenINphosphatebufferedsaline(TG-PBS),and(3)WTmicegivenINPBS(WT-PBS).At30weeksofage,miceareacclimatedtohandlingandthentreatedintranasallyeverymonday,wednesday,andfriday,startingat36weeksofage.Micearedosedfor18weeks,untilbehaviortestsat54weeks.Dosingcontinuesduringthe4weeksofbehaviortomeasurebothchronicandacuteeffects.Afterbehaviormicearedosedafinaltime,and24hlatereuthanizedandtissuescollectedforbiochemicalanalyses.TheseincludesolubleandinsolubleamyloidasmeasuredbyELISAandIHC,quantificationofproteinswithWesternblotandoxidativemarkers.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.2/3www.MedChemEwww.MedChemE户使⽤本产品发表的科研⽂献•CellRes.2018Dec;28(12):1171-1185.•SignalTransductTargetTher.2020May8;5(1):51.•RedoxBiol.2020Jan;29:101402.•ACSApplMaterInterfaces.2018Feb21;10(7):6180-6189.•Theranostics.2020Apr6;10(11):5107-5119.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].LiY,etal.Effectsofdeferoxamineonblood-brainbarrierdisruptionaftersubarachnoidhemorrhage.PLoSOne.2017Mar1;12(3):e0172784[2].DuscherD,etal.ComparisonoftheHydroxylaseInhibitorDimethyloxalylglycineandtheIronChelatorDeferoxamineinDiabeticandAgedWoundHealing.PlastReconstrSurg.2017Mar;139(3):695e-706e[3].WangG,etal.Invitroassessmentofdeferoxamineonmesenchymalstromalcellsfromtumorandbonemarrow.EnvironToxicolPharmacol.2017Jan;49:58-64[4].WahlEA,etal.VEGFreleasedbydeferoxaminepreconditionedmesenchymalstemcellsseededoncollagen-GAGsubstratesenhancesneovascularization.SciRep.2016Nov10;6:36879[5].FineJM,etal.IntranasaldeferoxamineengagesmultiplepathwaystodecreasememorylossintheAPP/PS1modelofamyloidaccumulation.NeurosciLett.2015Ja