Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemETat-NR2B9cCat.No.:HY-P0117CASNo.:500992-11-0Synonyms:Tat-NR2Bct;NA-1分?式:C???H???N??O??分?量:2518.88SequenceShortening:YGRKKRRQRRRKLSSIESDV作?靶點:iGluR;NOSynthase作?通路:MembraneTransporter/IonChannel;NeuronalSignaling;Immunology/Inflammation儲存?式:Powder-80°C2years-20°C1yearInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實驗H2O:≥50mg/mL(19.85mM)*"≥"meanssoluble,butsaturationunknown.MassSolvent1mg5mg10mgConcentration制備儲備液1mM0.3970mL1.9850mL3.9700mL5mM0.0794mL0.3970mL0.7940mL10mM0.0397mL0.1985mL0.3970mL請根據(jù)產品在不同溶劑中的溶解度選擇合適的溶劑配制儲備液；?旦配成溶液，請分裝保存，避免反復凍融造成的產品失效。儲備液的保存?式和期限：-80°C,6months;-20°C,1month。-80°C儲存時，請在6個?內使?，-20°C儲存時，請在1個?內使?。體內實驗Tat-NR2B9cispreparedinsaline[4].1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEBIOLOGICALACTIVITY?物活性Tat-NR2B9c(Tat-NR2Bct;NA-1)?種PSD-95的抑制劑，抑制PSD-95d2(PSD-95PDZdomain2)和PSD-95d1的EC50分別為6.7nM和670nM。Tat-NR2B9c擾亂了PSD-95/NMDAR的相互作?，抑制PSD-95和NR2A和NR2B結合的IC50值分別為0.5μM和8μM。Tat-NR2B9c還能抑制神經元?氧化氮合酶(nNOS)/PSD-95相互作?，具有神經保護作?。IC50&TargetEC50:6.7nM(PSD-95d2),670nM(PSD-95d1)[1]NOsynthase[1]體外研究Tat-NR2B9cisaPSD-95inhibitor,withanEC50of6.7nMforPSD-95d2,representinga>100-foldhigheraffinityforthisdomainthanforPSD-95d1(EC50,0.67μM).Tat-NR2B9cinhibitsNMDAR2A,NMDAR2B,andNMDAR2CbindingtoPSD-95,withIC50sof0.5μM,-8μM,and0.75μM,respectively.Tat-NR2B9calsoblockstheinteractionbetweenPSD-95andnNOSwithanIC50of-0.2μM[1].Tat-NR2B9creducesassociationofPSD-95withGluN2Bby-50%intheYAC128striatum,decreasesNMDA-inducedp38activationinYAC128striataltissue,butshowsnoeffectontheNMDA-inducedJNKactivation[2].體內研究Tat-NR2B9c(10?nmol/g,i.v.)reducesinfarctionvolumeofmaleC57BL/6mice,buthasnoeffectat3?nM/g[3].PROTOCOLCellAssay[2]Postnatalmono-culturedWTandYAC128striatalneurons(DIV9,duetotheviabilityofthesemono-culturedMSNs)arepretreatedfor1hwith200nMTat-NR2B9c,and/orSB-239063(p38inhibitor),and/orSP-600125(JNKinhibitor),thenincubatedwithorwithout500μMNMDAfor10min.AfterNMDAtreatment,striatalneuronsarewashedoncewithwarmplatingmedium(PM)andthenincubatedinconditionedPM(withoutTatpeptidesorp38,JNKinhibitors)for24h.ThencellsarewashedwithPBSonceandfixedwith4%paraformaldehyde(PFA)for30min[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMice[3]Administration[3]Ineachstudymicearerandomlyallocatedtothreetreatmentgroups(0.0,3.0,10.0nMole/gTat-NR2B9c)ortoshamtreatment.Theindividualperformingtheexperimentalprocedures,administeringtreatmentsandperformingtheanalysesisblindedtothetreatmentassignments.Tat-NR2B9cispreparedattheindicateddosesandadministeredintravenouslyviathetailveinusingapumpinavolumeof1?μL/gover5?minbeginningatreperfusion[3].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產品發(fā)表的科研?獻?JCerebBloodFlowMetab.2019Aug;39(8):1588-1601.?SciRep.2018May18;8(1):7848.?PLoSOne.2020Mar3;15(3):e0229499.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE?JNeuropatholExpNeurol.2020Jul1;79(7):800-808.?BehavBrainRes.7January2022,113537.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].CuiH,etal.PDZproteininteractionsunderlyingNMDAreceptor-mediatedexcitotoxicityandneuroprotectionbyPSD-95inhibitors.JNeurosci.2007Sep12;27(37):9901-15.[2].FanJ,etal.P38MAPKisinvolvedinenhancedNMDAreceptor-dependentexcitotoxicityinYACtransgenicmousemodelofHuntingtondisease.NeurobiolDis.2012Mar;45(3):999-1009.[3].TevesLM,etal.EfficacyofthePSD95inhibitorTat-NR2B9cinmicerequiresdosetranslationbetweenspecies.JCerebBloodFlowMetab.2016Mar;36(3):555-61.[4].JingFan,etal.N-methyl-D-aspartateReceptorSubunit-AndNeuronal-TypeDependenceofExcitotoxicSignalingThroughPost-SynapticDensity9.JNeurochem.2010Nov;115(4):1045-56