Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEBuChE-IN-20Cat.No.:HY-172782分?式:C??H??FN?O?分?量:484.56作?靶點(diǎn):Cholinesterase(ChE);Amyloid-β;InterleukinRelated;ReactiveOxygenSpecies;NOD-likeReceptor(NLR)作?通路:NeuronalSignaling;Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB儲(chǔ)存?式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY?物活性BuChE-IN-20?種選擇性hBuChE抑制劑(IC50=0.13μM)，具有?腦屏障(BBB)通透性。BuChE-IN-20是?種L-Tryptophan衍?物。BuChE-IN-20通過抑制?氧化氮(NO)的產(chǎn)?和降低活性氧(ROS)?平來發(fā)揮神經(jīng)保護(hù)作?。BuChE-IN-20能夠有效抑制淀粉樣β蛋?(Aβ)肽的?聚集。BuChE-IN-20可?于阿爾茨海默病的研究[1]。IC50&TargetBChE0.13nM(IC50)體外研究BuChE-IN-20(Compound4d-13)(5μM,10min)showsselectivityforBuChEthroughenzymaticactivityassaysofhAChEandhBuChE[1].BuChE-IN-20(20μM,48h)preventstheaggregationanddepositionofAβ1-42,therebyexertingneuroprotectiveeffectsbyinhibitingtheformationoftoxicamyloidplaques,andmitigatetheneurotoxicityinducedbyAβ1-42throughROSgeneration[1].BuChE-IN-20(1mM,30min)exertsscavengingcapacitiesforhydroxylradicals775timesthatofvitaminC[1].BuChE-IN-20(5-10μM,4hpretreatmentand8hcotreatmentwithLPS)decreasesintracellularreactiveoxygenspecies(ROS)concentration-dependentlyinLPS(1.5μg/mL)(HY-D1056)-inducedRAW264.7cells[1].BuChE-IN-20(6.25-12.5μM,4hpretreatmentand24hcotreatmentwithLPS)demonstratespotentinhibitoryactivityonLPS(2μg/mL)-inducedNOproductioninRAW264.7cells[1].BuChE-IN-20(1-100μM,24h)exertsinhibitoryeffectsandfreeradicalscavengingatsub-micromolarconcentrationsinmouseBV-2cellline,withasafetymarginofnearly150-foldregardingcytotoxicity[1].BuChE-IN-20(1-10μM,24hpretreatmentand24hcotreatmentwithLPS)decreasesIL-1βlevelsinLPS1/2MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE(100ng/mL)-inducedBV-2cells[1].BuChE-IN-20(1-20μM,6hpretreatmentand24hcotreatmentwithNMDA/SodiumL-Glutamate)mitigatesthecytotoxiceffectsdose-dependentlyinNMDA(20mM)/SodiumL-Glutamate(Glu)(HY-N0455B)-inducedSH-SY5Ycellinjurymodel[1].RT-PCR[1]CellLine:LPS(100ng/mL)-inducedBV-2cellsConcentration:1,5,10μMIncubationTime:24hpretreatmentand24hcotreatmentwithLPSResult:Exhibitedadose-dependentreductioninIL-1βexpression,whilehavingalessereffectonIL-6andTNF-α.Inhibitedtheproduction,release,andNLRP3-mediatedmaturationofIL-1βdirectly.InhibitedtheNF-κBandMAPKsignalingpathwaystoreduceIL-1βindirectly.體內(nèi)研究BuChE-IN-20(Compound4d-13)(10-100mg/kg,p.o.,onesingledose)showsnotoxicorabnormalsymptomswiththemaximumtolerateddoseof100mg/kginICRmicemodel[1].BuChE-IN-20(10-40mg/kg,p.o.,onesingledose)showsnotablepositiveeffectonimprovinglearningandmemoryfunctionin(-)-Scopolaminehydrobromide(HY-W010892)(3mg/kg,i.p.)-inducedICRmice[1].AnimalModel:(-)-Scopolaminehydrobromide(HY-W010892)(3mg/kg,i.p.)-inducedICRmice[1]Dosage:10-40mg/kgAdministration:Oralgavage(p.o.)Result:Recoveredtheimpairmentofhippocampus-dependentmemoryandspatiallearningfunctionsinducedby(-)-Scopolaminehydrobromide.Mitigatedthecognitiveimpairmentinducedby(-)-Scopolaminehydrobromideatthedosageof40mg/kgviagavage,evidencedbyareductioninescapelatencyandadecreaseinthetraverseddistancetotheescapeplatform.REFERENCES[1].AtlanteS,etal.,AXanthineDerivativeWithNovelHeatShockProtein90-AlphaInhibitoryandSenolyticProperties.AgingCell.2025Mar17:e70047.McePdfHeightCaution:Product