PI3K-mTOR-IN-20-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEPI3K/mTOR-IN-20Cat.No.:HY-180556分⼦式:C₂₉H₂₄F₂N₈O₄S分⼦量:618.61作⽤靶点:mTOR;PI3K作⽤通路:PI3K/Akt/mTOR储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性PI3K/mTOR-IN-20⼀种选择性的双重PI3K/mTOR抑制剂。PI3K/mTOR-IN-20在MRC-5和Mlg2908细胞中展现出纳尔级别的抗增殖效果其IC50值分别为0.380和0.090μM。在Bleomycin诱导的肺纤维化模型中，PI3K/mTOR-IN-20能够降低Ashcroft评分、减少羟脯氨酸含量和胶原沉积，下调纤维化相关蛋⽩表达，并修复肺组织结构。PI3K/mTOR-IN-20表现出良好的安全性，⼩⿏体重稳定恢复，且未出现明显的肝、肾毒性。PI3K/mTOR-IN-20可⽤于肺成纤维细胞的相关研究[1]。IC50&TargetPI3KαPI3KβPI3KγPI3KδPI3K体外研究PI3K/mTOR-IN-20(compound11)(72h)exhibitsnanomolarantiproliferativeactivityagainstMRC-5andMlg2908cellswithIC50=0.38and0.09μMrespectively[1].PI3K/mTOR-IN-20(1μM)effectivelyinhibitshighlymTORandandclassIPI3Kisoforms(α,β,andy)whileexhibitingweakeractivityagainstPl3k(inhibitionrate=94.89,79.24,42.60and42.99%forPI3Kα,PI3Kβ,PI3Kγ,PI3KδandmTORrespectively[1].PI3K/mTOR-IN-20(1μM,48h)effectivelyinhibitsPI3KactivityandattenuatesfibroblastactivationinMRC-5cells[1].WesternBlotAnalysis[1]CellLine:MRC-5cellsConcentration:1μMIncubationTime:48h1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEResult:SignificantlyreducedAKTphosphorylation(pAKT).Suppressedtheexpressionofkeypulmonaryfibrosis-associatedproteins,fibroblastactivationprotein(FAP),fibronectin(FN),andα-smoothmuscleactin(α-SMA).体内研究PI3K/mTOR-IN-20(compound11)(15mg/kg,ip,dailyfor11days)exertsrobustantifibroticeffects,mitigatingcollagendeposition,restoringlungarchitecture,suppressingprofibroticandimprovingphysiologicaloutcomeswithsafetyprofileinaBleomycin(BLM)inducedpulmonaryfibrosismicemodel[1].PI3K/mTOR-IN-20(15-60mg/kg,i.p.,oncedailyfor3days)exhibitsnoappreciableliverorkidneytoxicityinableomycin(BLM)inducedpulmonaryfibrosismicemodel[1].AnimalModel:Bleomycin(HY-108345A)(0.75U/kg,i.p.)induced-maleC57BL/6mice(8-10weeks)[1]Dosage:15mg/kgAdministration:i.p.,dailyfor11daysResult:Significantlyattenuatedthepathologicalchanges,partiallyrestoringnormallungstructureandextensivingfibroticremodeling[1].ReducedAshcroftscores,aquantitativemeasureoffibrosisseverity[1].ReversedtheBLM-inducedincreaseinthelungindex(lung-to-bodyweightratio),whichreflectsedemaandfibroticmassaccumulation[1].RobustlysuppressedBLM-inducedincreaseindcollagendeposition(ahallmarkoffibrosisprogression)[1].MitigatedBLM-inducedweightlossandmaintainedsteadyweightrecovery[1].Significantlyinhibitedfibroblastactivationprotein(FAP)expression[1].AnimalModel:ICRmice(8weeks)[1]Dosage:15,30,or60mg/kgAdministration:i.p.,oncedailyfor3daysResult:Revealedminimaltoxicityinliverandkidneyfunction[1].RemainedSerumlevelsofalaninetransaminase(ALT)andaspartatetransaminase(AST)withinthenormalrangeatdosesof15and30mg/kg[1].Unchangedserumcreatinine(CREA)anduricacid(UA)levels(markersofkidneyfunction)[1].NoObviousstructurechangesoccurinthelivers[1].REFERENCES[1].ZengW,etal.DiscoveryofImidazo[1,2-b]pyridazineDerivativesasPotentPI3K/mTORDualInhibitorsfortheTreatmentofPulmonaryFibrosis.JMedChem.2025Dec25;68(24):26418-26431.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEMcePdfHeightCaution:Producthasnot