MitomycinCisaDNA-damagingagentandsmall-moleculeinhibitoreffectivelysensitizecancercellstotumornecrosisfactor(TNF)-relatedapoptosis-inducingligand(TRAIL).

DNAsynthesis^[1]

TheHCT116(p53-/-)cellsareminimallysensitivetoeitherMitomycinCorTRAILalone.However,surprisingly,combinationtreatmentwithMMCandTRAILdecreasescellviABIlitysignificantly.AlthoughMitomycinCandTRAILalonearemoderatelyeffective,MitomycinCsubstantiallyenhancestheeffectofTRAILonsuppressionofthecellproliferation.MitomycinCandTRAILtreatmentaloneinduces9.5%and35.0%apoptosis,respectively.However,combinationtreatmentwithMitomycinCandTRAILenhancesapoptosisto66.6%^[1].MitomycinCisacytotoxicchemotherapeuticagentthatcausesDNAdamageintheformofDNAcross-linksaswellasavarietyofDNAmonoadductsandisknowntoinducep53^[2].

MicebearingxenograftedHCT116(p53-/-)colontumorsandHT-29colontumorsaretreatedwithMitomycinC(i.p.,1mg/kg)andTRAIL(i.v.,100μg)everyotherday.Animalsaretreatedwith10consecutivecyclesofthecombinationtherapyregimen.Thecombinationtherapysuppressestumorgrowthsignificantlyanddoesnotimpacttheweightofthemice,indicatingthatthetherapeuticcombinationofMitomycinCandTRAILiswell-toleratedandhasanti-tumoractivityinvivo^[1].IntravesicalMitomycinCinstillationshasaneffectonbodyweightthatisnotobservedinnormal,NaClinstilledorEpirubicininstilledrats.After3consecutiveweeklyinstillationsof1mg/mLMitomycinCthereisalmostnoweightgain,whereasratsintheother3groupshasastatisticallysignificantweightgaincomparedwithMMCtreatedrats^[3].

• [1].ChengH,etal.MitomycinCpotentiatesTRAIL-inducedapoptosisthroughp53-independentupregulationofdeathreceptors:Evidencefortheroleofc-JunN-terminalkinaseactivation.CellCycle.2012Sep1;11(17):3312-23.

  [2].AbbasT,etal.Differentialactivationofp53bythevariousadductsofmitomycinC.JBiolChem.2002Oct25;277(43):40513-9.

  [3].MichielsenD,etal.MitomycinCandepirubicin:functionalbladderdamageinratsafterrepeatintravesicalinstillations.JUrol.2005Jun;173(6):2166-70.

MitomycinCisdissolvedinDMSOandstored,andthendilutedwithappropriatemediumbeforeuse^[1].

ColonadenocarcinomaHCT116andHT-29humancoloncancercellsareused.TheCellTiter-GloLuminescentCellViabilityAssayisusedtomeasurecellviability,whichuseaunique,stableformofluciferasetomeasureATPasanindicatorofviablecells,andtheluminescentsignalproducedisproportionaltothenumberofviablecellspresentinculture.CellsarepretreatedwithMitomycinC(5μM)for12hor24h,andthenexposedtodifferentconcentrationsofTRAILfor12h.Anequalvolume(100μL)ofCellTiter-Glo^TMreagentisaddedandthesolutionismixedgentlyfor2minonanorbitalshaker.Mixtureisincubatedatroomtemperaturefor10mintoallowluminescentsignaltostabilize,andthenimagingisperformedusingtheXenogenIVISsystemtoquantifythecellviability^[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

MitomycinCispreparedinsaline(0.9%NaCl).

Mice^[1]
Four-to6-wk-oldNCrnudemicearetreatedwithMitomycinC(1mg/kg)byintraperitonealinjectionfor24h,followedbyoneintravenousdoseofpurifiedrhTRAIL(100μg).Asanegativecontrol,asubsetofthemiceareinjected(i.p.andi.v.)withsaline(vehicle)atthesamefrequencyoftreatment.Animalsaretreatedfor3consecutiveweeks.Thetumorsizeismonitoredeveryweekusingcalipermeasurementsofthetumorvolume.
Rats^[3]
YoungadultfemaleWistarratsatage13weekswithamedianweightof217g(range187to255)arerandomizedinto4groupsof10each,namelyanormalgroupwithnoinstillations,anNaCl0.9%orplacebogroupthatreceivedinstillationswiththesolventofthechemotherapeuticagents,anMitomycinC(1mg/mL)groupandanEpirubicin(1mg/mL)group.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

• [1].ChengH,etal.MitomycinCpotentiatesTRAIL-inducedapoptosisthroughp53-independentupregulationofdeathreceptors:Evidencefortheroleofc-JunN-terminalkinaseactivation.CellCycle.2012Sep1;11(17):3312-23.

  [2].AbbasT,etal.Differentialactivationofp53bythevariousadductsofmitomycinC.JBiolChem.2002Oct25;277(43):40513-9.

  [3].MichielsenD,etal.MitomycinCandepirubicin:functionalbladderdamageinratsafterrepeatintravesicalinstillations.JUrol.2005Jun;173(6):2166-70.

334.33

C₁₅H₁₈N₄O₅

50-07-7

RoomtemperatureincontinentalUS;mayvaryelsewhere

DMSO:30mg/mL

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

Purity:98.51%

SelectBatch:HY-13316-12592HY-13316-25192HY-13316-05100HY-13316-13426

DataSheet(125KB)SDS(120KB)

COA(97KB)HNMR(357KB)LCMS(145KB)

HandlingInstructions(1252KB)

• [1].ChengH,etal.MitomycinCpotentiatesTRAIL-inducedapoptosisthroughp53-independentupregulationofdeathreceptors:Evidencefortheroleofc-JunN-terminalkinaseactivation.CellCycle.2012Sep1;11(17):3312-23.

  [2].AbbasT,etal.Differentialactivationofp53bythevariousadductsofmitomycinC.JBiolChem.2002Oct25;277(43):40513-9.

  [3].MichielsenD,etal.MitomycinCandepirubicin:functionalbladderdamageinratsafterrepeatintravesicalinstillations.JUrol.2005Jun;173(6):2166-70.

他替瑞林口服促甲状腺素释放激素他替瑞林CAS号:103300-74-9英文名称:Taltirelin英文同义词:TA0910;Taltirelin;Taltireline;Ceredist,TA-0910;TaltirelinAcetate;TA-0910,taltirelin;TaltirelininterMediate;TALTIRELININTERMEDIATES;TaltirelinAcetate,TA-0910;L-Prolinamide,(4S)-hexahydro-1-methyl-中文名称:他替瑞林中文同义词:他替瑞林;醋酸他替瑞林;1-METHYL-4,5-DIHYDROOROTYL-HIS-PRO-NH2;(4S)-N-[(2S)-1-[(2S)-2-氨基甲酰基吡咯烷-1-基]-3-(3H-咪唑-4-基)-1-氧代丙-2-基]-1-甲基-2,6-二氧代-1,3-二氮杂己环-4-甲酰胺CBNumber:CB31177191分子式:C17H23N7O5分子量:405.41MOLFile:103300-74-9.mol化学性质安全信息用途供应商86化学性质安全信息用途供应商86他替瑞林化学性质熔点:72-75°比旋光度:25D-13.6°(c=1inwater)密度:1.447±0.06g/cm3(Predicted)储存条件:Storeat+4°C酸度系数(pKa):9.32±0.40(Predicted)安全信息他替瑞林性质、用途与生产工艺口服促甲状腺素释Chemicalbook放激素他替瑞林是一种垂体激素释放兴奋药，由日本田边三菱制药株式会社研制成功，商品名Taltirelin，属于化药新药3.1类，目前临床用于改善脊髓小脑变性患者的运动失调最为有效的药物。他替瑞林（Taltirelin）是世界上第一个批准的口服促甲状腺素释放激素(TRH)，除具有内分泌作用外，还可发挥一定的中枢神经系统(CNS)作用，包括提高运动活性，拮抗利舍平诱导的体温降低，以及拮抗戊巴比妥诱导的睡眠。该品种由日本田边三菱制药株式会社开发，2000年9月首次在日本上市，用于改善脊髓小脑变性病人的共济失调。脊髓小脑共济失调(SCAs)旧称常染色体显性共济失调，是一组以共济失调、辨距不良为主要临床表现的中枢神经系统慢性变性疾病。2000年9月前，促甲状腺素释放激素（TRH）注射液是唯一用于治疗该类疾病的药物。他替瑞林是TRH的结构修饰改造药物，药理学研究显示本品经由脑TRH受体对CNS产生强而持久的多重作用。本品对CNS的兴奋作用比TRH强10～100倍，作用持续时间比TRH长约8倍。本品对TRH受体的亲和力约为TRH的1/11，因而本品的内分泌作用比TRH弱，但本品在体内比TRH稳定。另外本品对促甲状腺素(TSH)释放的作用为TRH的1/6-1/11，TSH释放是由一个包括甲状腺激素的强负反馈系统调节的，对中枢神经系统具有较强的作用，但同时其激素样作用较小，因此副作用较少。不良反应主要是消化系统反应，包括呕吐、恶心和胃不适。所有的不良反应均为轻中度，在治疗期间及(或)停药后消失。

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