PLAGL2-IN-1-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEPLAGL2-IN-1Cat.No.:HY-180281CASNo.:3099026-16-8分⼦式:C₃₀H₃₅Cl₂N₅O₄S分⼦量:632.6作⽤靶点:ZincFingerProtein;Apoptosis;PI3K;Akt作⽤通路:CellCycle/DNADamage;Apoptosis;PI3K/Akt/mTOR储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性PLAGL2-IN-1⼀种多形性腺瘤样蛋⽩2(PLAGL2)抑制剂，其Kd值为2.23µM。PLAGL2-IN-1可抑制PLAGL2的转录活性，诱导G0/G1期细胞周期阻滞和细胞凋亡(apoptosis)，从⽽抑制肝细胞癌(HCC)细胞增殖。PLAGL2-IN-1可破坏细胞外质结构，并通过降低AKT磷酸化⽔平抑制PI3K-AKT信号通路。PLAGL2-IN-1可抑制HCCLM3异种移植⼩⿏模型中的肿瘤⽣长。PLAGL2-IN-1可⽤于肝细胞癌的研究[1]。IC50&TargetPLAGL22.23μM(Kd)体外研究PLAGL2-IN-1(compoundC8)(72h)demonstratesbroad-spectrumantiproliferativeactivityinapanelofcancercells,withIC50sof0.96(A549),1.35(NCI-H1650),1.03(NCI-H460),3.31(MGC803),3.28(HGC27),7.63(SW620),0.92(HT29),1.64(MDA-MB-231),2.21(HCC1937),1.43(U87-MG),24.96(LN229),8.83(U937),5.67(K562),5.33(MEG01),19.54(Jurkat),4.14(PC-3),and16.19μM(SKOV3),respectively[1].PLAGL2-IN-1(0-1μM,14days)inhibitscolonyformationofMHCC-97HandHCCLM3cellsinaconcentration-dependentmanner[1].PLAGL2-IN-1(10μM,48h)inducesapoptosisinMHCC-97HandHCCLM3cells[1].PLAGL2-IN-1(5μM,24h)inducesG0/G1phasearrestinMHCC-97Hcells[1].PLAGL2-IN-1(0-10μM,48h)inhibitscellmigrationandinvasioninHCCLM3andMHCC-97Hcellsinadose-dependentmanner,anddemonstratessignificantinhibitionofcelldivisioninHCCLM3HCCcells[1].PLAGL2-IN-1(5-10μM,24-48h)disruptsextracellularmatrixorganizationandsuppressesthePI3K-AKTpathwaybyreducingAKTphosphorylationinHCCLM3cells[1].CellProliferationAssay[1]1/4MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemECellLine:MHCC-97HandHCCLM3Concentration:0,0.01,0.1,1μMIncubationTime:14daysResult:Resultedinamarkedreductionincolonyformation.Showedconcentration-dependentinhibitioninbothcells.ApoptosisAnalysis[1]CellLine:MHCC-97HandHCCLM3Concentration:10μMIncubationTime:48hResult:Inducedlate-stageapoptosisinbothcells.Exhibitedstrongerpro-apoptoticeffectsthanthe5μM5-FU(HY-90006)positivecontrol.CellCycleAnalysis[1]CellLine:MHCC-97HandHCCLM3Concentration:5μMIncubationTime:24hResult:InducedG0/G1phasearrestinMHCC-97Hcells.DidnotinducecellcyclearrestinHCCLM3cells.CellMigrationAssay[1]CellLine:MHCC-97HandHCCLM3Concentration:0,5,10μMIncubationTime:48hResult:Showedadose-dependentinhibitionofcellwoundhealinginHCCLM3andMHCC-97Hcells.InhibitedcellmigrationinHCCLM3andMHCC-97Hcells.CellInvasionAssay[1]CellLine:MHCC-97HandHCCLM3Concentration:0,5,10μM2/4MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEIncubationTime:48hResult:InhibitedcellinvasioninHCCLM3andMHCC-97Hcellsinadose-dependentmanner.Immunofluorescence[1]CellLine:HCCLM3Concentration:5μMIncubationTime:48hResult:ReducedtheproteinexpressionlevelsVimentin.IncreasedE-cadherinexpression.WesternBlotAnalysis[1]CellLine:HCCLM3Concentration:5,10μMIncubationTime:48hResult:ReducedtheproteinexpressionlevelsofZEB1,Vimentin,MMP2,andMMP9.IncreasedE-cadherinexpression.SignificantlyinhibitedPLAGL2-dependentAKTphosphorylationatbothThr308andSer473.体内研究PLAGL2-IN-1(compoundC8)(15mg/kg,i.p.,dailyfor19days)significantlyinhibitstumorgrowthinaHCCLM3xenograftmousemodelwithoutobservabletoxicity[1].AnimalModel:MaleBALB/Cnudemice(6-8weeksold)subcutaneouslyinjectedwithHCCLM3cells[1]Dosage:15mg/kgAdministration:i.p.,dailyfor19daysResult:Effectivelyinhibitedtumorgrowth,withaTGIof63.27%.Significantlyreducedtumorweightandvolume.Showednoobservabletoxicityinmajororgansbutinducednoticeabletumornecrosis.ReducedexpressionofKi-67andα-SMAintumortissues.Demonstratedastablebodyweightduringadministration.REFERENCES[1].DingY,etal.DiscoveryofnovelsmallmoleculeinhibitortargetingthetumorpromotingeffectoftranscriptionfactorPLAGL2.EurJMed3/4MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEChem.2026;303:118471.