Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEBTT-3033Cat.No.:HY-110112CASNo.:1259028-99-3分?式:C??H??FN?O?S分?量:465.5作?靶點(diǎn):Integrin;Apoptosis作?通路:Cytoskeleton;Apoptosis儲(chǔ)存?式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY?物活性BTT-3033?種具有?服活性的構(gòu)象選擇性的α2β1(EC50:130nM)抑制劑，可與α2Idomain結(jié)合。BTT-3033抑制??板與collagenⅠ結(jié)合和細(xì)胞增殖，并誘導(dǎo)細(xì)胞凋亡(apoptosis)。BTT-3033可?于前列腺癌、炎癥和??管疾病的研究。IC50&Targetα2β1130nM(EC50)體外研究BTT-3033(1nM-100μM,2h)inhibitsCHO-α2wtcelladhesiontorattailcollagenⅠ(EC50:130nM),exhibitsselectivityforα2β1overα3β1,α4β1,α5β1andαv[1].BTT-3033(10μM,5min)inhibitshumanplateletbindingtocollagenⅠcoatedcapillariesunderflow,withthe

EC50valueformousewholebloodtobe6μM[1].BTT-3033(10μM,5min)inhibitsbindingofα2-expressingCHOcellstocollagenⅠundershearstressconditions[1].BTT-3033(1μM,60min)inhibitsofneurogenicandthromboxaneA2‐inducedhumanprostatesmoothmusclecontraction[3].BTT-3033(25and50μM,48h)inhibitscellviabilityandproliferationbyinducingG1cellcyclearrestinLNcap‐FGC,andDU‐145cells[4].BTT-3033(50μM,48h)inducesapoptosisthroughtheactivationofROS,Baxproteinupregulation,caspase‐3activation,anddepletionofΔΨm[4].BTT-3033(10μM,15/28days)suppressesMMP13expression,increasestheexpressionofMMP1andMT-MMP1inhumanarticularcartilage?derivedchondrocytes[5].CellViabilityAssay[4]1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemECellLine:LNcap‐FGC,andDU‐145cellsConcentration:0.05,0.55,25,and50μMIncubationTime:48hResult:Decreasedthecellviabilityat25μMand50μM.CellViabilityAssay[4]CellLine:LNcap‐FGC,andDU‐145cellsConcentration:5,25,and50μMIncubationTime:48hResult:Inll,25about20%,32%,and47%(LNcap‐FGC)and26%,41%,and59%μM.WesternBlotAnalysis[4]CellLine:LNcap‐FGC,andDU‐145cellsConcentration:25μMIncubationTime:48hResult:teit.indown-regulationofN‐cadherinandupregulationofE‐cadherin(EMT‐associated體內(nèi)研究BTT-3033(oraladministration,10mg/kg,at24hand2hbeforePAFinduction)showsanti-inflammatoryeffectsinmouseairpouchmodel[2].BTT-3033(oraladministration,10mg/kg,at48,24and2hbeforeearswelling)showsanti-inflammatoryeffectsinarachidonicacid-inducedearedemamodel[2].AnimalModel:PAF(platelet-activatingfactor)-inducedmouseairpouchmodel[2]Dosage:1,10mg/kgat24hand2hbeforePAFinductionAdministration:OraladministrationResult:Reducedtheinfiltrationofleukocytesbyabout50%at10mg/kg.AnimalModel:MaleDBA/1mice(Pharmacokineticassay)[2]Dosage:10mg/kgforasingledose2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEAdministration:OraladministrationResult:Plasmalevels:about1ng/mLat24hpost-dose.REFERENCES[1].LiisaNissinen,etal.Novelα2β1integrininhibitorsrevealthatintegrinbindingtocollagenundershearstressconditionsdoesnotrequirereceptorpreactivation.JBiolChem.2012Dec28;287(53):44694-702.[2].LiisaNissinen,etal.Sulfonamideinhibitorsofα2β1integrinrevealtheessentialroleofcollagenreceptorsininvivomodelsofinflammation.PharmacolResPerspect.2015Jun;3(3):e00146.[3].BingshengLi,etal.InhibitionofneurogenicandthromboxaneA2-inducedhumanprostatesmoothmusclecontractionbytheintegrinα2β1inhibitorBTT-3033andtheintegrin-linkedkinaseinhibitorCpd22.Prostate.2020Aug;80(11):831-849.[4].ZahraSalemi,etal.Integrinα2β1inhibitionattenuatesprostatecancercellproliferationbycellcyclearrest,promotingapoptosisandreducingepithelial-mesenchymaltransition.JCellPhysiol.2021Jul;236(7):4954-4965.[5].TakashiKanamoto,etal.Integrinα2β1playsanimportantroleintheinteractionbetweenhumanarticularcartilage-derivedchondrocytesandatelocollagengel.SciRep.2021Jan19;11(1):1757.McePdfHeigh