Deferoxaminemesylateisanironchelator,andeffectivelyreducesoxidativestressandneuronaldeath.

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].

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].

• [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.

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.

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.

• [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.

656.79

C₂₆H₅₂N₆O₁₁S

138-14-7

RoomtemperatureincontinentalUS;mayvaryelsewhere

H₂O:≥33mg/mL

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

Purity:>98.0%

SelectBatch:HY-B0988-25079HY-B0988-25086HY-B0988-25080HY-B0988-20600HY-B0988-19006

DataSheet(120KB)SDS(120KB)

COA(92KB)HNMR(598KB)

HandlingInstructions(1252KB)

• [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.

品牌介绍

托烷司琼临床评价药物相关作用适应症托烷司琼CAS号:89565-68-4英文名称:Tropisetron英文同义词:icf205-930;TROPICACID;TROPISETRON;SS-TROPISETRON;BETA-TROPISETRON;Tropisetron(ICS205930);TROPISHTRONHYDROCHLORIDE;Indole-3-carbonylchloride;3-Tropanylindole-3-carboxylate;lαH，5Αh-Tropan-3α-ylindole-3-carboxylate中文名称:托烷司琼中文同义词:托普西隆;托普西龙;曲匹西龙;托烷司琼;Β-托烷司琼;CS-348;Β-内托烷司琼;吲哚-3-甲酰氯;Β-托烷司琼(光学异构体);Β-托烷司琼,托烷司琼异构体CBNumber:CB3236404分子式:C17H20N2O2分子量:284.35MOLFile:89565-68-4.mol化学性质安全信息用途供应商112化学性质安全信息用途供应商112托烷司琼化学性质熔点:201-202°C沸点:448.5±35.0°C(Predicted)密度:1.26储存条件:2-8°C溶解度:H2O:soluble形态:solid酸度系数(pKa):15.38±0.30(Predicted)颜色:whiteCAS数据库:Chemicalbook89565-68-4(CASDataBaseReference)安全信息WGKGermany:3托烷司琼化学药品说明书托烷司琼|药物应用信息托烷司琼性质、用途与生产工艺临床评价Sorbe等报道本品对含顺铂(剂量50～89mg/m2)化疗方案引起的急性呕吐完全控制率为63%。58例恶性肿瘤化疗所致恶心、呕吐者，应用托烷司琼或昂丹司琼8mg分别在同一病人前后2个化疗周期的第1d给药前30min静脉注射，并用地塞米松10mg静脉滴注。结果两药控制急性及迟发性恶心、呕吐的疗效基本相似，均可达81%～100%。本品对强致吐化疗药物顺铂的止吐疗效突出。药物相关作用饮食可略为延长本品的吸收。本品与利福平、苯巴比妥等肝酶诱导药同时使用，可加快代谢，故快代谢型者需增加剂量，慢者则不必。西咪替丁等肝酶抑制药对本品血药浓度无明显影响。适应症托烷司琼临床用于预防和治疗癌症化疗引起的恶心和呕吐。化学性质结晶，熔点201-202℃(二氯甲烷-乙酸乙酯)。单盐酸托烷司琼(TropisetronMonohydroehloride)：C17H20N2O2?HCI。[105826-92-4]。熔点283-285℃(分解)。用途有高效性和选择性的5-HT3受体拮抗剂。用于化疗所致的呕吐。用途为5-羟色胺拮抗药生产方法托品醇(I)和酰氯(Ⅱ)反应，可得托烷司琼。托烷司琼上下游产品信息上游原料托品醇下游产品

公司介绍

托烷司琼临床评价药物相关作用适应症托烷司琼CAS号:89565-68-4英文名称:Tropisetron英文同义词:icf205-930;TROPICACID;TROPISETRON;SS-TROPISETRON;BETA-TROPISETRON;Tropisetron(ICS205930);TROPISHTRONHYDROCHLORIDE;Indole-3-carbonylchloride;3-

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类固醇 生物碱 糖类和糖苷类 染料试剂 生化分析试剂

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