SJ-300-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemESJ-300Cat.No.:HY-179459CASNo.:1210357-06-4分⼦式:C₂₀H₂₇FN₄分⼦量:342.45作⽤靶点:Wnt;LDLR;Amyloid-β作⽤通路:StemCell/Wnt;MetabolicEnzyme/Protease;NeuronalSignaling储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性SJ-300⼀种具有选择性，⼝服活性且可透过⾎脑屏障DKK3-LRP1抑制剂。SJ300以Kd=7.9μM的结合⼒与mLRPIV结合，能够以IC50=3.2μM的效⼒抑制DKK3mLRPIV复合物，且不⼲扰Aβ与LRP1的结合。SJ-300可在阿尔茨海默病模型中恢复Aβ除功能，并在体内挽救认知功能、改神经病理(Aβ斑块减少约73.3%)。SJ300可⽤于阿尔茨海默病的相关研究[1]。体外研究SJ-300(0-5μM)exertsasubstantialreductionintheDKK3-mLRPIVinteractioninSH-SY5Ycells[1].SJ-300(1μM,2h)restoresAβinternalizationinAD-NSCcells[1].SJ-300(10μM)hasnodirectimpactonthecanonicalWnt/β-cateninsignalingpathwayinSH-SY5Ycell.[1].SJ-300(50μMin2μL0-60min)hassuperiormetabolicstabilityinmouseandhumanlivermicrosomes[1].Immunofluorescence[1]CellLine:AD-NSCcellConcentration:1μMIncubationTime:2hResult:RestoredAβinternalizationincellstreatedwithDKK3butintreatedwithDKK1.体内研究SJ-300(i.v.atadoseof2mg/kgori.g.at10mg/kg,once)demonstratesstableplasmaconcentrationsthroughoutthetimeintervalstudiedinC57mice[1].SJ-300(i.g.,10mg/kg,once)showsabrain-penetrationcapabilitywithbrain/plasma(B/P)ratio=5732%[1].1/2MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemESJ-300(i.g.,5mg/kg,oncedailyfor8weeks)improvescognitivefunctionsinthe5×FADtransgenicmouse(6months)modelofAD,andtheseimprovementsassociatewithreductionsinAβpathology.[1].SJ-300(i.g.,5mg/kg,oncedailyfor8weeks)attenuatescognitivedeficitsandADpathologiesthroughenhancingAβclearancein6-month-old5×FADmice.[1].AnimalModel:5×FADtransgenicmousemodelofAD(16weeks)[1]Dosage:5mg/kgAdministration:i.g.,oncedailyfor8weeksResult:Reducedescapelatenciesduringthe5-dayacquisitionphase.Increasedtimespentinthetargetquadrant,andnumberofplatformcrossingsduringtheprobetrials.EnhancedspatialworkingmemoryintheY-mazetest.ReducedthenumberofAβplaquesofvariousdiametersinbothbrainregions.DecreasedthetotalnumberofAβplaquesbyapproximately73.3%.Decreasedtheclusteringofastrocytesby64.1%andmicrogliaaroundtheplaques.ReducedbothsolubleandinsolubleAβlevels.DidnotaffectAPPcleavageorAβproduction.AnimalModel:5×FADtransgenicmousemodelofAD(6months)[1]Dosage:5mg/kgAdministration:i.g.,oncedailyfor8weeksResult:DidnotalterLRP1expressionbutreducedcolocalizedAβonbrainvascularbasementmembranesandendothelium.ReducedthelevelsofbothAβ40andAβ42intheplasmaandliveroftreatedmice.DidnotalterthecirculatingconcentrationsofsolubleLRP1.InhibitedtheassociationbetweensolubleLRP1(sLRP1)andDKK3.REFERENCES[1].YangR,etal.DKK3-LRP1complexandachemicalinhibitorregulateAβclearanceinmodelsofAlzheimer'sdisease.SciAdv.2025Nov7;11(45):eadz2099.McePdfHeightCaution:Producthasnotbeenfullyvalidated