U-73122isaninhibitorofphospholipaseC(PLC),phospholipaseA2,and5-LO(5-lipoxygenase). 

U-73122potentlyinhibitsreceptor-coupledactivationofPLCinmembranesisolatedfromPMNs^[1].U-73122inhibitsN-formyl-methionyl-leucyl-phenylalanine-inducedaggregationofhumanpolymorphonuclearneutrophils(PMN)andtheassociatedproductionofIP₃anddiacyglycerol^[2].U-73122markedlyinhibitsinositolphosphatereleaseelicitedbyeitheroxotremorine-Morguanosine-5"-O-(3-thiotriphosphate)thanthatinducedbyaddedCa²⁺indigitonin-permeABIlizedcells^[3].

U73122significantlyattenuatesTNF-αmRNAexpression,hasnoeffectonshamanimals,butsignificantlyincreasesheartworkandrateofcontractionandrelaxationwithoutaffectingheartrateinendotoxemicmice^[4].U73122(400nM/µL)significantlyreducestotallordosisdurations,comparedtovehicleinfusionstotheVTA,ofoestrADIolandprogesterone-primedhamsters.VTAinfusionsofU73122donotaltermotorbehaviourofhamstersintheactivitymonitor,butthereisasignificanteffectofmuscimoltodecreasetotalnumberofbeambreakscomparedtohamstersadmiNISTeredSKF38393^[5].

• [1].SmithRJ,etal.Receptor-coupledsignaltransductioninhumanpolymorphonuclearneutrophils:effectsofanovelinhibitorofphospholipaseC-dependentprocessesoncellresponsiveness.JPharmacolExpTher.1990May;253(2):688-97.

  [2].BleasdaleJE,etal.Selectiveinhibitionofreceptor-coupledphospholipaseC-dependentprocessesinhumanplateletsandpolymorphonuclearneutrophils.JPharmacolExpTher.1990Nov;255(2):756-68.

  [3].ThompsonAK,etal.TheaminosteroidU-73122inhibitsmuscarinicreceptorsequestrationandphosphoinositidehydrolysisinSK-N-SHneuroblastomacells.AroleforGpinreceptorcompartmentation.JBiolChem.1991Dec15;266(35):23856-62.

  [4].PengT,etal.DisruptionofphospholipaseCgamma1signallingattenuatescardiactumornecrosisfactor-alphaexpressionandimprovesmyocardialfunctionduringendotoxemia.CardiovascRes.2008Apr1;78(1):90-7.Epub2007Dec12.

  [5].FryeCA,etal.Intheventraltegmentalarea,themembrane-mediatedactionsofprogestinsforlordosisofhormone-primedhamstersinvolvephospholipaseCandproteinkinaseC.JNeuroendocrinol.2007Sep;19(9):717-24.

PMNs(4×10⁷/4mL)areincubatedwithU-73122accordingtoprotocols.Thereactionsarestoppedwithcoldcalcium-freePBS.Thecellsarecentrifugedat750×g(4°C)andresUSPendedin1mLofTritonX-100-freeextractionbuffer(50mMTris,pH7.5,50mMfimercaptoethanol,2mMEGTA,1mMphenylmethylsulfonylfluorideand4μg/mLofleupeptin,soybeantrypsininhibitorandaprotinin),andthensonicatedfor10-and5-secconsecutiveburstsat20%output.Thelysatesarecentrifugedat240×g(4°C)for20mminaTL-100ultracentrifugewiththesupernatantdesignatedasthecytosolfraction.Thepelletisresuspendedin1%Triton-containingextractionbuffer,sonicated,shakenfor30mmat4°Candcentrifuged(240×gfor20mmat4°C).Thesupernatantconstitutestheextractableparticulatefraction,andthepelletissonicatedinextractionbufferwithTritonandconstitutedthenonextractableparticulatefraction.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

U-73122isdissolvedinDMSO.

Agonist-inducedproductionofIP₃inPMNismeasuredbyuseofthecompetitiveradiobindingassy.PMN(2x10⁶-10⁷)in0.2mLofphosphate-bufferedsaline,pH7.4[NaC1(138mM),Na₂HPO₄(8.1mM),KH₂PO₄(1.5mM),KCI(2.7mM),CaCl₂(1.0mM),MgC1₂(1.0mM)andglucose(0.1%,w/v)]areincubatedinconicalpolypropylenetubesat37°Cinashakingwaterbath.U-73122orU-73343isadded(in1μLofDMSO)3minbeforetheadditionofagonist,FMLP(0.1μM)pluscytochalasinB(5μg/mL).FMLPandcytochalasinBareaddedin1μLeachofDMSOandethanol,respectively.Appropriatevehiclecontrolsareincludedineachexperiment.PMNincubationmixturesarequenchedwiththeadditionof0.07mLofice-coldTCA(20%,w/v)andaportion(0.2mL)oftheTCAextractisprocessedforthemeasurementofIP₃bycompetitiveradiobindingasdescribedaboveforplatelets.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

U-73122isformulatedinsaline.

Hamstersarehormone-primedwith17β-oestradiolath 0andprogesteroneath 45.Ath 48,hamstersarepretestedformotorbehaviour,followedbysexualbehaviourtesting,andbilateralinfusionsofU73122(400nM/µL)orsalinevehicle.Thirtyminutesafterinfusions,hamstersarere-testedforsexualbehaviour(postinhibitorinfusiontest)and,immediatelyaftertesting,infusedbilaterallywithSKF38393(100ng/µL),muscimol(100ng/µL),orsalinevehicle.Thirtyminutesaftertheagonistorvehicleinfusions,lordosisandmotorbehaviourofhamstersisreassessed(postagonistinfusiontest).Allhamstersareassignedtoonepretreatmentcondition,U73122orvehicle,andaretestedonceaweekfor3weeksuntilallinfusionconditions(SKF38393,muscimolorvehicle),arereceived.TheorderinwhichhamstersreceiveSKF38393,muscimolorvehicleinfusionsiscounterbalancedacrossthegroup. MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

• [1].SmithRJ,etal.Receptor-coupledsignaltransductioninhumanpolymorphonuclearneutrophils:effectsofanovelinhibitorofphospholipaseC-dependentprocessesoncellresponsiveness.JPharmacolExpTher.1990May;253(2):688-97.

  [2].BleasdaleJE,etal.Selectiveinhibitionofreceptor-coupledphospholipaseC-dependentprocessesinhumanplateletsandpolymorphonuclearneutrophils.JPharmacolExpTher.1990Nov;255(2):756-68.

  [3].ThompsonAK,etal.TheaminosteroidU-73122inhibitsmuscarinicreceptorsequestrationandphosphoinositidehydrolysisinSK-N-SHneuroblastomacells.AroleforGpinreceptorcompartmentation.JBiolChem.1991Dec15;266(35):23856-62.

  [4].PengT,etal.DisruptionofphospholipaseCgamma1signallingattenuatescardiactumornecrosisfactor-alphaexpressionandimprovesmyocardialfunctionduringendotoxemia.CardiovascRes.2008Apr1;78(1):90-7.Epub2007Dec12.

  [5].FryeCA,etal.Intheventraltegmentalarea,themembrane-mediatedactionsofprogestinsforlordosisofhormone-primedhamstersinvolvephospholipaseCandproteinkinaseC.JNeuroendocrinol.2007Sep;19(9):717-24.

464.64

C₂₉H₄₀N₂O₃

112648-68-7

RoomtemperatureincontinentalUS;mayvaryelsewhere

DMSO:<4.8="">

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

Purity:>98.0%

SelectBatch:HY-13419-14812

DataSheet(125KB)SDS(389KB)

COA(94KB)HNMR(459KB)

HandlingInstructions(1252KB)

• [1].SmithRJ,etal.Receptor-coupledsignaltransductioninhumanpolymorphonuclearneutrophils:effectsofanovelinhibitorofphospholipaseC-dependentprocessesoncellresponsiveness.JPharmacolExpTher.1990May;253(2):688-97.

  [2].BleasdaleJE,etal.Selectiveinhibitionofreceptor-coupledphospholipaseC-dependentprocessesinhumanplateletsandpolymorphonuclearneutrophils.JPharmacolExpTher.1990Nov;255(2):756-68.

  [3].ThompsonAK,etal.TheaminosteroidU-73122inhibitsmuscarinicreceptorsequestrationandphosphoinositidehydrolysisinSK-N-SHneuroblastomacells.AroleforGpinreceptorcompartmentation.JBiolChem.1991Dec15;266(35):23856-62.

  [4].PengT,etal.DisruptionofphospholipaseCgamma1signallingattenuatescardiactumornecrosisfactor-alphaexpressionandimprovesmyocardialfunctionduringendotoxemia.CardiovascRes.2008Apr1;78(1):90-7.Epub2007Dec12.

  [5].FryeCA,etal.Intheventraltegmentalarea,themembrane-mediatedactionsofprogestinsforlordosisofhormone-primedhamstersinvolvephospholipaseCandproteinkinaseC.JNeuroendocrinol.2007Sep;19(9):717-24.

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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