P-gp-inhibitor-30-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors • ScreeningLibraries • Proteinswww.MedChemEP-gpinhibitor30Cat.No.:HY-178349分子式: C₂₂H₁₅FN₄O₂分子量: 386.38作用靶点: P-glycoprotein;Apoptosis;Autophagy作用通路: MembraneTransporter/IonChannel;Apoptosis;Autophagy储存方式: PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性P-gpinhibitor30是一种强效的P-gp抑制剂，能逆转乳腺癌的多药耐药性，使耐药细胞对Doxorubicin(ADM)(HY-15142)敏感。P-gpinhibitor30与ADM联合使用时，可促进耐药乳腺癌细胞细胞凋亡(apoptosis)，诱导自噬(autophagy)，抑制细胞增殖、迁移和侵袭。P-gpinhibitor30在体外和体内均能抑制乳腺癌肿瘤生长。P-gpinhibitor30可用于耐药性乳腺癌的相关研究[1]。体外研究P-gpinhibitor30(compoundA38)(0.1μM)reversesADMresistanceinMDA-MB-231/ADMcells,potentlyreducingtheIC50ofADMfrom785.46μMto2.05μM[1].P-gpinhibitor30(0.125-4μM)significantlyinhibitsP-gpATPaseactivityatdifferentconcentrationsinaconcentration-dependentmanner[1].P-gpinhibitor30interactswithP-gptoinhibititsfunctionwithoutdownregulatingitsexpression,andstabilizestheprotein,therebyreducingitsdegradationinMCF7/ADMcellsuponincreasingtemperature[1].P-gpinhibitor30(6h)significantlyincreasesRh123intensityinMCF7/ADMcellsandincreasestheaccumulationofADMandinhibitstheeffluxofRh123inMDA-MB-231/ADMcells[1].P-gpinhibitor30(0.1-1μM,24h-15days)promotesapoptosis,inhibitscellproliferation,andsuppressesthemigrationandinvasionofbreastcancerdrug-resistantcells(MCF7/ADMandMDA-MB-231/ADMcells),whencombinedwithADM,demonstratingthatitsensitizesthesecellstoADM[1].P-gpinhibitor30(0.1μM)leadstotheaccumulationofautophagosomesandsignificantlyincreasestheexpressionofautophagy-relatedproteinsinMCF7/ADMandMDA-MB-231/ADMcellswhencombinedwithADM,therebyinducingcelldeath[1].P-gpinhibitor30(1-10days)significantlyreducesthetumorvolumeofbothMCF7/ADMandMDA-MB-231/ADMcellswhencombinedwithADMina3Dtumorspheroidmodel[1].WesternBlotAnalysis[1]1/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemECellLine:MCF7/ADMandMDA-MB-231/ADMcellsConcentration:0.1μMIncubationTime:24hResult:SignificantlyincreasestheexpressionlevelofLC3whencombinedwithADM.ApoptosisAnalysis[1]CellLine:MCF7/ADMandMDA-MB-231/ADMcellsConcentration:0.1,0.5and1μMIncubationTime:48hResult:SignificantlyincreasedADM-inducedapoptosisinadose-dependentmannercomparedtotheMCF7/ADMcontrolgroup.SignificantlyincreasedADM-inducedapoptosisonMDA-MB-231/ADMcells.CellProliferationAssay[1]CellLine:MCF7/ADMandMDA-MB-231/ADMcellsConcentration:0.1,0.5and1μMIncubationTime:15daysResult:SignificantlyinhibitedtheproliferationofMCF7/ADMcellsinadose-dependentmannercomparedtotheMCF7/ADMcontrolgroupwhencombinedwithADM.Resultedinonlyafewcellssurvivedataconcentrationof1μM.Markedlyinhibitedtheproliferationofdrug-resistantbreastcancercellswhencombinedwithADM.CellMigrationAssay[1]CellLine:MCF7/ADMandMDA-MB-231/ADMcellsConcentration:0.1μMIncubationTime:36hResult:Suppressedthemigrationabilityofbreastcancerdrug-resistantcellswhencombinedwithADM.CellInvasionAssay[1]CellLine:MCF7/ADMandMDA-MB-231/ADMcells2/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEConcentration:0.1μMIncubationTime:24hResult:Suppressedtheinvasionabilityofbreastcancerdrug-resistantcellswhencombinedwithADM.体内研究P-gpinhibitor30(2mg/kg,i.p.,every2daysfor14days)showsantitumoreffectswhencombinedwithADMinMCF-7/ADMmousemodel[1].AnimalModel:FemaleBALB/cnudemice(4-5weeksold)subcutaneouslyinjectedwithMCF-7/ADMcells[1]Dosage:2mg/kgAdministration:i.p.,every2daysfor14daysResult:SignificantlyreducedtumorsizewhencombinedwithADM(10mg/kg),withefficacycomparabletoTariquidar(HY-10550).Showedsignificantlylowertumorweightthanthatofothergroups.Showednosignificantlosscomparedtocontrol.Causednosignificanttissuecellnecrosis.REFERENCESXueWH,etal.DiscoveryofaheterocyclicaromaticamidebasedP-gpinhibitorascoadjutantregulatingautophagyagainstdrugresistanceinbreastcancer.EurJMedChem.2025Dec15;300:118151