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Medchemexpress/Deferoxamine mesylate(Synonyms: Desferrioxamine B mesylate; DFOM)/HY-B0988/10mM*1mL in Water
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Medchemexpress/Deferoxamine mesylate(Synonyms: Desferrioxamine B mesylate; DFOM)/HY-B0988/10mM*1mL in Water
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Deferoxaminemesylateisanironchelator,andeffectivelyreducesoxidativestressandneuronaldeath.
Description

Deferoxaminemesylateisanironchelator,andeffectivelyreducesoxidativestressandneuronaldeath.

InVitro

DeferoxaminetreatmentsignificantlyincreasesHIF-1αbindingunderallcultureconditions,includinghypoxicandhigh-glucose.ThemechanismofdeferoxamineisthroughimprovingHIF-1αBIOLOGicalfunctionthroughscavengingoxygenfreerADIcals[1].Deferoxamine(5μM)hassignificanteffectonthetumor-associatedstromalcellscellularmultiplication,andcellsdieatday7afterexposureto50μMand100μMdeferoxamine.Deferoxamine(5μM-100μM)inhibitstheproliferationofBMMSCs,andinducesapoptosisofMSCsinadose-dependentmanner.DeferoxamineinfluencestheexpressionofadhesionproteinsonMSCs[3].Deferoxamine(30,60,120 μM)showslowerexpressionofHIF-1αinaconcentrationdependentwayinAdMSCs[4].

InVivo

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].

ClinicalTrial
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References
  • [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.2015Jan1;584:362-7.

CellAssay
[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.

AnimalAdmiNISTration
[5]

Deferoxamineisdeliveredasa1%solutionin0.2×phosphatebufferedsalineatapHof6.0. 

Micearedividedintothreetreatmentgroupsof17each:(1)TGmicegivenINDeferoxamine(TG-DFO),(2)TGmicegivenINphosphatebufferedsaline(TG-PBS),and(3)WTmicegivenINPBS(WT-PBS).At30weeksofage,miceareacclimatedtohandlingandthentreatedintranasallyeverymonday,wednesday,andfriday,startingat36weeksofage.Micearedosedfor18weeks,untilbehaviortestsat54weeks.Dosingcontinuesduringthe4weeksofbehaviortomeasurebothchronicandacuteeffects.Afterbehaviormicearedosedafinaltime,and24hlatereuthanizedandtissuescollectedforbiochemicalanalyses.TheseincludesolubleandinsolubleamyloidasmeasuredbyELISAandIHC,quantificationofproteinswithWesternblotandoxidativeMarkers.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

References
  • [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.2015Jan1;584:362-7.

MolecularWeight

656.79

Formula

C₂₆H₅₂N₆O₁₁S

CASNo.

138-14-7

Storage
Powder-20°C3years
 4°C2years
Insolvent-80°C6months
 -20°C1month
Shipping

RoomtemperatureincontinentalUS;mayvaryelsewhere

Solvent&Solubility

H2O:≥33mg/mL

*"<1 mg/ml"="" means="" slightly="" soluble="" or="" insoluble.="" "≥"="" means="" soluble,="" but="" saturation="">

Purity:>98.0%