Staurosporineisaverypotentuniversalinhibitorofproteinkinasesbutshowinglittleselectivity,withIC₅₀of6nM,15nM,2nM,and3nMforPKC,PKA,c-Fgr,andPhosphorylasekinase,respectively.

IC50:6nM/15nM/2nM/3nM(PKC/PKA/c-Fgr/Phosphorylasekinase)^[1]

Staurosporine,widelyusedasaproteinkinaseC(PKC)inhibitorwithabroadspectrumofactivity,isanalkaloidisolatedfromtheculturebrothofStreptomycesstaurospores.MC3T3E-1osteoblasts,exposetoStaurosporine(100nM)for12h,releaseanamountofLDH(12.4±3.1%)thatissimilartothatreleasebythecontrolcells(10.0±2.4%),indicatingtherelativeabsenceoflyticdeath,whichoccursinnecrosis.Inaddition,treatmentwithStaurosporine(100nM)resultsinmorphologicalchanges,characteristicofapoptosis:abrightbluefluorescentcondensednucleiseenthroughafluorescencemicroscopeafterHoechst33258-staining,andareductionofcellvolume^[2].

TheinhibitoryeffectofStaurosporineisstatisticallysignificantataroundWk10oftumorpromotion.Althoughstatisticallysignificantinhibitionisnotobtainedwith10ngofStaurosporineinlaterweeksoftheexperiment,adecreasingtendencyinthepercentagesoftumorbearingmiceandinaveragenumbersoftumorspermouseisapparent.Thus,StaurosporineslightlyinhibitstumorpromotionofTeleocidin,evenatthedoseatwhichStaurosporineitselfinducedtumors^[3].Staurosponne(0.05and0.1mg/kgintraperitoneal)attenuatestheimpairedperlormanceofwatermazeandpassiveavoidancetasks,eventhoughthedrugadmiNISTrationbegan2weeksafterthelesion.Moreover,Staurosporine(0.1mg/kg)partiallyreversedthedecreaseofcholineacetyltransferaseactivityinthefronto-parietalcortexinducedbybasalforebrain-lesion.TheseresultssuggestthatStaurosporineattenuatesimpairmentoflearningthroughreversalofdamagetocholinergicneuronsinducedbybasalforebrain-lesion^[4].

• [1].MeggioF,etal.Differentsusceptibilityofproteinkinasestostaurosporineinhibition.KineticstudiesandmolecularbasesfortheresistanceofproteinkinaseCK2.EurJBiochem.1995Nov15;234(1):317-22.

  [2].ChaeHJ,etal.Molecularmechanismofstaurosporine-inducedapoptosisinosteoblasts.PharmacolRes.2000Oct;42(4):373-81.

  [3].YoshizawaS,etal.Tumor-promotingactivityofstaurosporine,aproteinkinaseinhibitoronmouseskin.CancerRes.1990Aug15;50(16):4974-8.

  [4].NabeshimaT,etal.Staurosporinefacilitatesrecoveryfromthebasalforebrain-lesion-inducedimpairmentoflearninganddeficitofcholinergicneuroninrats.JPharmacolExpTher.1991May;257(2):562-6.

MC3T3E-1cells(2×10⁶cells/group)aretreatedwith100nMStaurosporineforvarioustimeperiodsandlysedinalysisbuffer(EBbuffer:1%TritonX-100,10mMTris,pH7.6,50mMNaCl,1mg/mLAprotinin,5mMEDTA,50mMNaF,0.1%2-mercaptoethanol,and100μMsodiumorthovanadate).Thelysateofthecellsissubjectedtocentrifugationat12000gat4°Cfor30min.Solublefractioniscollectedandincubatedwithanti-JNK1antibodies.Afterincubationonicefor3h,100μLofa10%solutionofformalin-fixedStaphylococcusaureusisaddedtotheanti-JNK1immunoprecipitatesandfurtherincubatedonicefor1h.TheabsorbedimmunecomplexiswashedtwicewithEBbufferandPANbuffer(10mMPIPESbuffer,pH7.0,1%aprotinin,100mMNaCl).Theimmunecomplexismixedwith2μgofGST-c-JunNT_1-79proteinsasasubstratein30μLofthereactionbuffercontaining2μMcoldATP,2mMDTT,20mMMgCl₂,2μCi[γ³³-P]-ATP,and20mMTris-HCl,pH7.5at30°Cfor20min.Thereactionisterminatedbyadding15μLof3×SDS-PAGEsamplebufferandboilingat98°Cfor5min.Theproteinsareseparatedon12%SDS-PAGEandtransferredontoanitrocellulosemembraneviathesemi-dryelectrotransfersystem.Themembraneisimmunoblottedwithrabbitanti-JNK1antibodiesandhorserADIshpeoxidaseconjugatedanti-rabbitantibodiestovisualizethesignalsmeasuredbyanenhancedchemiluminescencesystem.Thegelisdriedunderavacuum,andthephosphotransferaseactivityisvisualizedbyautoradiographyandquantifiedbyaPhosphoImageranalyzer^[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

StaurosporineissUSPendedin0.3%ofsodiumcarboxymethylcellulose(Rat)^[4].

Mice^[3]
FemaleCD-Imiceareused.VariousamountsofStaurosporinein10μLofacetoneareappliedtotheearsof8-wk-oldCD-Imice.Theextentofirritationisexpressedastheminimumdoseofthecompoundcausingirritation.InductionofHOCinMouseSkinStaurosporinein0.1mLofacetoneisappliedtotheskinofthebacksofCD-Imice,andacrudeenzymeextractisobtainedfromtheskin18hlater.HDCactivityisexpressedaspmolofCO₂releasedpermgofproteinperlhofincubation.InductionofODCinMouseSkinStaurosporinein0.2mLofacetoneisappliedtotheskinofthebacksofCD-Imice.After4h,acrudeenzymeextractispreparedfromtheepidermis,anditsODCactivityismeasured.EnzymeactivityisexpressedasnmolofCO₂permgofproteinper30minofincubation.
Rats^[4]
MaleKblWistarrats(weighing270to310g)areused.InthegroupwhichisgivenStaurosporinefor2weeks,thewatermazetaskandStaurosporineadministrationarestarted2weeksaftertheBF-lesion,andthepassiveavoidancetaskiscarriedout4weeksaftertheBFlesion.TheratreceivedStaurosporineatdosesof0.01,0.03,0.1,and0.3mg/kg(i.p.,N=10ineachgroupfor2weeks)30mmpriortothewatermazetrainingsessionsandthepassiveavoidancetaskacquisitiontrial.InthegroupwhichisgivenStaurosporinefor4weeks,thedrugisfirstgiven2weeksaftertheBF-lesion.Thewatermazetaskiscarriedout4weeksaftertheBF-lesion.Thepassiveavoidancetaskiscarriedout6weeksaftertheBF-lesion.TheratreceivedStaurosporineat0.05,0.1,and0.2mg/kg(i.p.,N=10ineachgroup)onceadayfor2weeksbeforetraining,andfor2weeksafterthewatermazetrainingsessionsandthepassiveavoidancetaskacquisitiontrial.Staurosporineissuspendedin0.3%ofsodiumcarboxymethylcellulose.Thevehicleisadministeredtothenon-lesionedcontrolsandthelesionedcontrolsonthesamescheduleastheStaurosporine-treatedanimals.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

• [1].MeggioF,etal.Differentsusceptibilityofproteinkinasestostaurosporineinhibition.KineticstudiesandmolecularbasesfortheresistanceofproteinkinaseCK2.EurJBiochem.1995Nov15;234(1):317-22.

  [2].ChaeHJ,etal.Molecularmechanismofstaurosporine-inducedapoptosisinosteoblasts.PharmacolRes.2000Oct;42(4):373-81.

  [3].YoshizawaS,etal.Tumor-promotingactivityofstaurosporine,aproteinkinaseinhibitoronmouseskin.CancerRes.1990Aug15;50(16):4974-8.

  [4].NabeshimaT,etal.Staurosporinefacilitatesrecoveryfromthebasalforebrain-lesion-inducedimpairmentoflearninganddeficitofcholinergicneuroninrats.JPharmacolExpTher.1991May;257(2):562-6.

466.53

C₂₈H₂₆N₄O₃

62996-74-1

RoomtemperatureincontinentalUS;mayvaryelsewhere

DMSO:≥31mg/mL

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

Purity:99.98%

SelectBatch:HY-15141-21226HY-15141-19340HY-15141-16980HY-15141-26871

DataSheet(139KB)SDS(120KB)

COA(99KB)HNMR(203KB)LCMS(211KB)

HandlingInstructions(1252KB)

• [1].MeggioF,etal.Differentsusceptibilityofproteinkinasestostaurosporineinhibition.KineticstudiesandmolecularbasesfortheresistanceofproteinkinaseCK2.EurJBiochem.1995Nov15;234(1):317-22.

  [2].ChaeHJ,etal.Molecularmechanismofstaurosporine-inducedapoptosisinosteoblasts.PharmacolRes.2000Oct;42(4):373-81.

  [3].YoshizawaS,etal.Tumor-promotingactivityofstaurosporine,aproteinkinaseinhibitoronmouseskin.CancerRes.1990Aug15;50(16):4974-8.

  [4].NabeshimaT,etal.Staurosporinefacilitatesrecoveryfromthebasalforebrain-lesion-inducedimpairmentoflearninganddeficitofcholinergicneuroninrats.JPharmacolExpTher.1991May;257(2):562-6.

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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