Hotline:400-820-3792Inhibitors ? ScreeningLibraries ? Proteinswww.MedChemENF-κB-IN-20Cat.No.:HY-175833分子式:C??H??NO?分子量:353.41作用靶點(diǎn):NF-κB;Keap1-Nrf2;HemeOxygenase(HO);InterleukinRelated;TNFReceptor;ReactiveOxygenSpecies(ROS);SOD作用通路:NF-κB;MetabolicEnzyme/Protease;Immunology/Inflammation;Apoptosis儲(chǔ)存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性 NF-κB-IN-20是一種口服有效的NF-κB抑制劑。NF-κB-IN-20會(huì)直接與Keap1蛋白結(jié)合，激活Keap1/Nrf2/HO-1抗氧化途徑，同時(shí)抑制NF-κB炎癥途徑，從而協(xié)同降低氧化應(yīng)激和炎癥反應(yīng)。NF-κB-IN-20M11可抑制IL-6、IL-1β和TNF-α的表達(dá)，顯著降低ROS的水平，并恢復(fù)線粒體膜電位。NF-κB-IN-20可用于急性肺損傷(ALI)的研究。IC50&Target NF-κB IL-6 IL-1β HO-1體外研究NF-κB-IN-20(CompoundM11)(0.01?100μM,5h)exhibitsgoodinvitrosafety(CC50>100μM)inLPS(HY-D1056)-inducedRaw264.7cells,attenuatesthemRNAexpressionlevelsoftheinflammatoryandoxidativestressmarkersIL-6(IC50=6.55μM),IL-1β,TNF-α,andSODinadose-dependentmannerandinhibitsROSexpression,enhancesmitochondrialmembranepotential,thereforemitigatingLPS-inducedcellulardamage[1].RT-PCR[1]CellLine:Raw264.7cellsConcentration:25,50and100μMIncubationTime:1handstimulatedwithLPSfor4h.Result:ReducedthemRNAexpressionsofIL-6,IL-1β,andTNF-αandincreasedthemRNAexpressionofSOD.1/3 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemE體內(nèi)研究NF-κB-IN-20(CompoundM11)(15-60mg/kg,i.g.,oncedailyfor7days)alleviatesALIinducedlunginjuryandoxidativestressinmice,andinhibitscollagenformationandpolarizationofM1macrophages[1].NF-κB-IN-20(15-60mg/kg,i.g.,oncedailyfor7days)enhancessputumsecretionandmitigatedcoughinginmice,therebycontributingtothemanagementofpulmonarydiseases[1].NF-κB-IN-20(500mg/kg,i.g.,singledose)exhibitsgoodinvivosafetyprofileinSDratsduringthe14-dayDuringthe14-dayobservationperiod[1].AnimalModel:LPSinducedALImodelestablishedinfive-tosix-week-oldmaleBALB/cmice[1]Dosage:15,30and60mg/kgAdministration:Oralgavage(i.g.),oncedailyfor7daysResult:SignificantlyreducedthetotalnumberofinflammatorycellsinBALF.EnhancedtheactivitiesofSODandGSH-Pxinlungtissue,whilereducingthelevelofROS,effectivelyreversingtheoxidativestresscausedbyLPS.Improvedthepathologicalphenomenasuchasinflammatorycellinfiltration,destructionofalveolarstructure,andthickeningofalveolarsepta.InhibitedtheexpressionofM1-typemacrophagemarkers(iNOS,CD86),whilepromotingtheexpressionofM2-typemarkers(Arg-1,CD163).AnimalModel:CecalpunctureinducedALImodelestablishedinfive-tosix-week-oldmaleBALB/cmice[1]Dosage:15,30and60mg/kgAdministration:Oralgavage(i.g.),oncedailyfor7daysResult:Alleviatedlunginjurycausedbysepsisinfection.Amelioratedinflammatorycellinfiltration,alleviatedalveolaratrophy,andinhibitedcollagenformationandfibrosis.Reversedtheexpressionofinflammatorycytokineandoxidativestressrelatedfactors.AnimalModel:5%ammonia-inducedcoughassayestablishedinfive-tosix-week-oldmaleBALB/cmice[1]Dosage:15,30and60mg/kgAdministration:Oralgavage(i.g.),oncedailyfor7daysResult:DemonstratedasignificantincreaseinphenolredsecretionintheBALF.Ledtoaprolongedcoughlatencyperiodandadecreasedfrequencyofcoughs.REFERENCES2/3 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemESongL,etal.SynthesisandevaluationoflansiumamideBanaloguestoameliorateacutelunginjurybyreducingoxidativestressandinflammationviaKeap1/Nrf2/NF-κBpathway.EurJMedChem.2025Dec5;299:118052.McePdfHeightCaution:Product