6-Methoxydihydrosanguinarine-hydrochloride-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemE6-MethoxydihydrosanguinarinehydrochlorideCat.No.:HY-N3000A分子式:C₂₁H₁₈ClNO₅分子量:399.82作用靶点:JNK;IRE1;Akt;mTOR;YAP;ReactiveOxygenSpecies(ROS);Autophagy;Apoptosis;Ferroptosis;Fungal;Caspase;DNA/RNASynthesis作用通路:MAPK/ERKPathway;CellCycle/DNADamage;PI3K/Akt/mTOR;StemCell/Wnt;Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB;Autophagy;Apoptosis;Anti-infection储存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性6-Methoxydihydrosanguinarinehydrochloride是一种对多种癌细胞系均具有活性的生物碱。6-Methoxydihydrosanguinarinehydrochloride可激活IRE1/JNK信号通路，阻断Akt/mTOR与PI3K/AKT/mTOR通路，降低Cdc25C、CyclinB1、Cdc2、YAP/TAZ、Survivin、GPX4及EGFR的表达水平，上调IRE1与DR5的表达，并激活JNK与caspases。6-Methoxydihydrosanguinarinehydrochloride可诱导细胞凋亡(apoptosis)、G2/M期阻滞、DNA损伤、ROS生成、脂质过氧化、铁死亡(ferroptosis)、自噬(autophagy)抑制癌细胞生长。6-Methoxydihydrosanguinarinehydrochloride可破坏Candidaalbicans(C.albicans)的生物膜形成。6-Methoxydihydrosanguinarinehydrochloride可用于非小细胞肺癌、肝细胞癌、黑色素瘤、结肠癌、卵巢癌及乳腺癌的相关研究[1][2][3][4][5][6][7]。体外研究6-Methoxydihydrosanguinarine(0.15625-10μM;24h)hydrochloridesuppressestheviabilityofA549andH1299NSCLCcellsinadose-dependentmanner,withIC50valuesof2.154μMand2.586μMrespectivelyafter24htreatment[1].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochlorideinducesG2/MphasearrestinA549andH1299NSCLCcellsafter24htreatmentat2μM,andG1phasearrestinH1299cellsatlowerconcentrations[1].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochloridedownregulatescellcycle-relatedproteinsCdc25C,p-Cdc25C,cyclinB1,andCdc2inA549andH1299NSCLCcellsafter24htreatment[1].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochloridedose-dependentlyactivatesthecaspasecascadeandinducesPARPcleavageinA549andH1299NSCLCcellsafter24htreatment,promotingapoptoticcelldeath[1].1/4 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemE6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochloridedose-dependentlyinhibitstheAkt/mTORsignalingpathwayinA549andH1299NSCLCcellsafter24htreatmentbyreducingAktandp70S6Kphosphorylationandtotalproteinlevels[1].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochloridedose-dependentlyblockstheYAP/TAZoncogenicsignalingaxisinA549andH1299NSCLCcellsafter24htreatmentbyreducingYAP,TAZ,andsurvivinexpressionandincreasingLATS1/2phosphorylation[1].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochloridedose-dependentlyinducesapoptosisinA549andH1299NSCLCcellsafter24htreatment[1].6-Methoxydihydrosanguinarine(0.5-2μM;12h)hydrochloridedose-dependentlyelevatesintracellularROSlevelsinA549andH1299NSCLCcellsafter12htreatment[1].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochloridedose-dependentlyactivatestheIRE1/JNKsignalingpathwayinA549andH1299NSCLCcellsafter24htreatment[1].6-Methoxydihydrosanguinarine(0.125-8μM;24h)hydrochloridedose-dependentlyreducescellviabilityinHepG2andHuh7cells,withIC50valuesof2.83μMand3.46μMafter24hoftreatment[2].6-Methoxydihydrosanguinarinehydrochloride(6-MS)(1-2μM;12h)hydrochloridedose-dependentlyincreasesintracellularROSproductioninHepG2andHuh7cellsafter12hoftreatment[2].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochloridedose-dependentlyinhibitstheEGFR/Aktsignalingpathway,asmeasuredbyreducedEGFRexpressionandAktphosphorylation,inHepG2andHuh7cellsafter24hoftreatment[2].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochlorideactivatestheJNKandp38MAPKpathwaysinHepG2andHuh7cellsafter24hoftreatment,withJNKactivationbeingrequiredfor6-MS-inducedPARPcleavage(amarkerofapoptosis)[2].6-Methoxydihydrosanguinarine(0.5-2μM;24h)hydrochloridedose-dependentlyupregulatesDR4andDR5expressioninHepG2andHuh7cellsafter24hoftreatment,andDR5upregulationisrequiredfor6-Methoxydihydrosanguinarinehydrochloride-mediatedsensitizationtoTRAIL-inducedapoptosis[2].6-Methoxydihydrosanguinarine(0-1.5μM;12h)hydrochloridepotentlyinhibitstheviabilityofHLEandHCCLM3hepatocellularcarcinomacellswithIC50valuesof1.129μMand1.308μMrespectivelyafter12h,andislesscytotoxictonormalLX-2hepaticstellatecells[3].6-Methoxydihydrosanguinarine(1μM(HLE),1.5μM(HCCLM3);12h)hydrochlorideinducescelldeathinhepatocellularcarcinomacellsafter12hoftreatment,andthiseffectismediatedviaferroptosis,asshownbyreversalwithferroptosisinhibitors[3].6-Methoxydihydrosanguinarine(1μM(HLE),1.5μM(HCCLM3);6h)hydrochloridedownregulatesGPX4expressionatthetranscriptionallevelinhepatocellularcarcinomacellsafter6hoftreatment[3].6-Methoxydihydrosanguinarine(1-50μM;24h)hydrochlorideselectivelyinhibitshumanA375melanomacellviabilityovernormalNHDFcells,withanIC50of2.85μMafter24h[4].6-Methoxydihydrosanguinarine(0-32μM;24h)hydrochloridepotentlyreducesMCF-7breastcancercellviabilityinatime-anddose-dependentmanner,withanIC50of4.21μMafter24h[5].6-Methoxydihydrosanguinarine(2-4μM;6-24h)hydrochlorideinducesapoptosisinMCF-7breastcancercellsbyupregulatingpro-apoptoticproteinsanddownregulatinganti-apoptoticproteins,inducesautophagybyupregulatingautophagy-relatedproteins,andinhibitsthePI3K/AKT/mTORpathwaybyreducingphosphorylationofkeypathwayproteins[5].6-MethoxydihydrosanguinarinehydrochloridedownregulatestheexpressionofEFG1,CDC35,RAS1,andTPK2,allofwhicharecriticalcomponentsofthecAMPpathway.Furthermore,6-2/4 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEMethoxydihydrosanguinarinehydrochloridechangesthemembranepermeabilityofC.albicansandcausedreactiveoxygenspeciesaccumulation,leadingtocelldeath[6].CellViabilityAssay[1]CellLine:A549,H1299non-smallcelllungcancer(NSCLC)cellsConcentration:0.15625μM,0.3125μM,0.625μM,1.25μM,2.5μM,5μM,10μMIncubationTime:24hResult:Causedadose-dependentreductionincellviabilityinbothcelllines,withIC50valuesof2.154μMforA549cellsand2.586μMforH1299cells.CellCycleAnalysis[1]CellLine:A549,H1299non-smallcelllungcancer(NSCLC)cellsConcentration:0.5μM,1μM,2μMIncubationTime:24hResult:InducedG2/MphasearrestinbothA549andH1299cellsat2μM,withaconcomitantreductioninG1orSphasecells.InducedG1phaseblockinH1299cellsatlowerconcentrations.WesternBlotAnalysis[1]CellLine:A549,H1299non-smallcelllungcancer(NSCLC)cellsConcentration:0.5μM,1μM,2μMIncubationTime:24hResult:SignificantlydecreasedtheproteinlevelsofCdc25C,p-Cdc25C,cyclinB1,andCdc2inbothcelllines.Significantlyincreasedtheproteinlevelsofγ-H2AXinbothA549andH1299cells,indicatinginductionofDNAdouble-strandbreaks.Causedadose-dependentincreaseinthecleavageofcaspase-3,caspase-8,caspase-9,andPARPinbothA549andH1299cells.\nCausedadose-dependentdecreaseinproteinexpressionofp-Akt,totalAkt,p-p70S6K,andtotalp70S6KinbothA549andH1299cells,indicatinginhibitionoftheAkt/mTORpathway.Causedadose-dependentdecreaseinproteinexpressionofYAP,TAZ,andsurvivin,andanincreaseinp-LATS1/2proteinexpressioninbothA549andH1299cells,indicatinginhibitionoftheYAP/TAZoncogenicaxis.WesternBlotAnalysis[5]CellLine:HumanbreastcancerMCF-7cells3/4 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEConcentration:2μM,4μMIncubationTime:6,12,24hResult:Increasedcleavedcaspase-7/caspase-7,cleavedPARP/PARP,andBAXexpression,anddecreasedBcl-2expression,indose-andtime-dependentmanners.IncreasedLC3II/LC3IandAtg5expressionindose-andtime-dependentmanners.DecreasedP-PI3K/PI3K,P-AKT/AKT,andP-mTOR/mTORratiosinadose-dependentmanner.体内研究6-Methoxydihydrosanguinarine(5mg/kg;i.p.;daily;14days)hydrochloridedecreasestumorvolumeandweightinaCaov-3ovariancancermousexenograftmodel[7].AnimalModel:FemaleBALB/c-nudemice(5-week-old)wereinjectedsubcutaneouslyventrallyCAOV3cells(5×106)[7]Dosage:5mg/kgAdministration:i.p.;daily;14daysResult:ThetumorvolumeandweightweremuchlowerShowednophysiologicallyharmfuleffectsonmice.REFERENCESQiX,etal.6-MethoxydihydrosanguinarineSuppressestheProliferationofNon-smallCellLungCancerCellsthroughElevationofROSandActivationofIRE1/JNKSignaling.CellBiochemBiophys.2025Dec;83(4):5307-5319.WangLL,etal.6-MethoxydihydrosanguinarineexhibitscytotoxicityandsensitizesTRAIL-inducedapoptosisofhepatocellularcarcinomacellsthroughROS-mediatedupregulationofDR5.MedOncol.2023;40(9):266.Published2023Aug11.HanL,etal.Bioactivenaturalalkaloid6-Methoxydihydrosanguinarineexertsanti-tumoreffectsinhepatocellularcarcinomacellsviaferroptosis.FrontPharmacol.2025;16:1500461.Published2025Apr24.ZuoC,etal.Mole