N-Salicyloyltryptamine-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEN-SalicyloyltryptamineCat.No.:HY-147377CASNo.:31384-98-2分⼦式:C₁₇H₁₆N₂O₂分⼦量:280.32作⽤靶点:CalciumChannel;ERK;PotassiumChannel;GuanylateCyclase;NF-κB作⽤通路:MembraneTransporter/IonChannel;NeuronalSignaling;MAPK/ERKPathway;StemCell/Wnt;GPCR/GProtein;NF-κB储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性N-Salicyloyltryptamine⼀种电压依赖性离⼦通道抑制剂，包括Na+、Ca2+、K+通道。N-Salicyloyltryptamine抑制K+电流的IC50为34.6μM(Ito)。N-Salicyloyltryptamine还具有抗惊厥、抗炎、镇痛，和⾎管舒张的作⽤。IC50&TargetL-typecalciumchannelpotassiumchannel34.6μM(IC50)体外研究N-Salicyloyltryptamine(1ng/mL-1μg/mL;24h)presentsnocytotoxicityandcausesnooxidativestressinRAW264.7cellsatlowconcentration,but(50and100μg/mL)inhibitscellviabilitywithanIC50valueof22.75μg/mL[1].N-Salicyloyltryptamine(1μg/mL;24h)reversessomeredoxandinflammatoryparametersinducedbyLPSwithoutinterferingincellviability[1].N-Salicyloyltryptamine(1μg/mL;24h)inhibitsLPS-inducedTNF-αandIL-1βrelease,aswellasCD40andTNF-αproteinup-regulation[1].N-Salicyloyltryptamine(1μg/mL;24h)inhibitsphosphorylationofERK1/2andIκBαandp65nucleartranslocation(NF-kBactivation)[1].N-Salicyloyltryptamine(17μM)inhibitsK+currentby59.27%(Ito)and73.18%(IKD),inhibitsL-typeCa2+currentsby54.9%,andshowsfewinhibitionwithhighconcentration(170μM)onTTX-sensitiveNa+currentby22.1%inGH3cells[2].N-Salicyloyltryptamine(0.01nM-100µM)producesvasorelaxationthroughactivationoftheNO/sGC/cGMPpathwayandreductionofcalciuminflux[3].1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemECellViabilityAssay[1]CellLine:RAW264.7cellConcentration:0.001,0.05,1,50,100μg/mLIncubationTime:24hoursResult:ResultednoeffectonRAW264.7cellviabilityat1μg/mL;however,concentrationsof50and100μg/mLsignificantlydecreasedbothMTTreductionandSRBincorporation.RT-PCR[1]CellLine:RAW264.7cellConcentration:1μg/mLIncubationTime:24hoursResult:ReducedCD40,TNF-α,andRAGEimmunocontent.InhibitedERK1/2andIκBαphosphorylationandnucleartranslocationofp65.体内研究N-Salicyloyltryptamine(100mg/kg;i.p.;60minbeforestimulationchallenge)significantlyinhibitspentylenetetrazol(PTZ)-inducedseizuresandpartiallyeliminatestheextensorreflexofmaximalelectric-inducedseizurestest[4].N-Salicyloyltryptamine(100mg/kg,200mg/kg;i.p.;singledose)showsantinociceptiveandnerveexcitabilityeffects[5].AnimalModel:MaleSwissmice(25-35g)[4]Dosage:50,100,200mg/kgAdministration:Intraperitonealinjection;singledose;60minbeforestimulationchallengeResult:Reducedtheincidenceofclonicpentylenetetrazol(PTZ)seizuresandmortalityat50mg/kg,anddecreasedtheincidenceoftonichindlimbextension(THE)producedbyMESat100,200mg/kg.AnimalModel:MaleSwissmice(25-35g)[5]Dosage:100mg/kg;200mg/kgAdministration:Intraperitonealinjection;singledoseResult:Reducedtheaceticacid-inducedlickingresponseoftheinjectedpaw.REFERENCES2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE[1].GasparottoJ,etalEffectofN-salicyloyltryptamine(STP),anoveltryptamineanalogue,onparametersofcellviability,oxidativestress,andimmunomodulationinRAW264.7macrophages.CellBiolToxicol.2013Jun;29(3):175-87.[2].AraújoDA,etal.N-salicyloyltryptamine,anewanticonvulsantdrug,actsonvoltage-dependentNa+,Ca2+,andK+ionchannels.BrJPharmacol.2003Dec;140(7):1331-9.[3].VerasRC,etal.N-Salicyloyltryptamine,anN-BenzoyltryptamineAnalogue,InducesVasorelaxationthroughActivationoftheNO/sGCPathwayandReductionofCalciumInflux.Molecules.2018Jan28;23(2):253.[4].OliveiraFA,etal.AnticonvulsantpropertiesofN-salicyloyltryptamineinmice.PharmacolBiochemBehav.2001Feb;68(2):199-202.[5].QuintansLJJr,etal.Bioassay-guidedevaluationofantinociceptiveeffectofN-salicyloyltryptamine:abehavioralandelectrophysiologicalapproach.JBiomedBiotechnol.2010;2010:230745.M