Sulindac-sodium-MK-231-sodium-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemESulindacsodiumCat.No.:HY-B0008ACASNo.:63804-15-9Synonyms:MK-231sodium分⼦式:C₂₀H₁₆FNaO₃S分⼦量:378.39作⽤靶点:NF-κB;PD-1/PD-L1作⽤通路:NF-κB;Immunology/Inflammation储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性Sulindac(MK-231)⼀种⼝服活性⾮甾体类抗炎药。Sulindac也⼀种免疫调节剂。Sulindac可⽤于脊柱关节炎、痛风性关节炎及多种癌症如结直肠癌、肺癌的研究。体外研究Sulindac(MK-231)(500μM,48h)sodiumiseffectiveinpreventingTGF-β1-inducedEMT,asindicatedbyupregulationoftheepithelialmarker,E-cadherin,anddownregulationofmesenchymalmarkersandtranscriptionfactors[1].Sulindacsodium(500μM,48h)caninhibitTGF-β1-enhancedmigrationandinvasionofA549cells[1].Sulindacsodium(500μM,48h)enhancesthereversalofTGF-β1-inducedEMTbysulindac(sodium)andSIRT1upregulationpromotedTGF-β1-inducedEMT[1].WesternBlotAnalysis[1]CellLine:A549cellsConcentration:500μMIncubationTime:48hResult:Inhibittransforminggrowthfactor(TGF)-β1-inducedepithelial-mesenchymaltransitioninA549cells.Immunofluorescence[1]1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemECellLine:A549cellsConcentration:500μMIncubationTime:48hResult:ReversedSIRT-1expressionbyTGF-β1andinhibitedtheTGF-β1-inducedcadherinswitch.CellMigrationAssay[1]CellLine:A549cellsConcentration:500μMIncubationTime:48hResult:Inhibitedmigration,decreasedresistanceco-treatmentwithTGF-β1.CellInvasionAssay[1]CellLine:A549cellsConcentration:500μMIncubationTime:40h;48hResult:CouldeffectivelyinhibittheTGF-β1-inducedincreaseininvasionbylungcancercells.体内研究Sulindac(MK-231)sodium(15mg/kg,p.o.,bid(sulindacalone);7.5mg/kgp.o.,bid(sulindaccombinationwithPD-L1))showsasignificantreductionintumorvolumeandincreasesinfiltrationofCD8+Tlymphocytesinthetumortissueswhentreatedwithcombinationtherapy[2].Sulindacsodium(15mg/kg,p.o.,bid(sulindacalone);7.5mg/kgp.o.,bid(sulindaccombinationwithPD-L1))candownregulatePD-L1byblockingNF-κBsignaling,whichinturnledtoadecreaseinexosomalP[2].Sulindacsodium(15mg/kg,p.o.,bid(sulindacalone);7.5mg/kgp.o.,bid(sulindaccombinationwithPD-L1))leadstoincreasedavailabilityofPD-L1AbbydownregulatingPD-L1incombinationtherapy[2].SulindacsodiumhasnotasystemicinhibitoryeffectonprostaglandinE2(PGE2)inlow-dosedoes[2].AnimalModel:CT26syngeneicmousetumormodel[2]Dosage:15mg/kg;7.5mg/kgAdministration:15mg/kg,p.o.,bid(sulindacalone);7.5mg/kgp.o.,bid(sulindaccombinationwithPD-L1)Result:DownregulatedPD-L1throughtheblockadeofNF-κBsignalingandmodulatetheresponseofpMMRCRCtoanti-PD-L1immunotherapy.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEAnimalModel:CT26syngeneicmousetumormodel[2]Dosage:15mg/kg;7.5mg/kgAdministration:15mg/kg,p.o.,bid(sulindacalone);7.5mg/kgp.o.,bid(sulindaccombinationwithPD-L1)Result:DownregulatedPD-L1throughtheblockadeofNF-κBsignalingandmodulatetheresponseofpMMRCRCtoanti-PD-L1immunotherapy.CoundeffectivelyinhibitPD-L1withnosignificantsystematictoxicity.REFERENCES[1].Byong-KiCha,etal.CelecoxibandsulindacinhibitTGF-β1-inducedepithelial-mesenchymaltransitionandsuppresslungcancermigrationandinvasionviadownregulationofsirtuin1.Oncotarget.2016Aug30;7(35):57213-57227.[2].BinYi,etal.SulindacModulatestheResponseofProficientMMRColorectalCancertoAnti-PD-L1Immunotherapy.MolCancerTher.2021Jul;20(7):1295-1304.McePdfHeightCaution:Produc