MM927-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors • ScreeningLibraries • Proteinswww.MedChemEMM927Cat.No.:HY-175783CASNo.:3065567-21-4分子式:C₂₆H₁₈FN₃O₄S分子量:487.5作用靶点:Apoptosis作用通路:Apoptosis储存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性MM927是一种高效的NVL抑制剂，其IC50值为0.053μM。MM927阻断核仁中60S核糖体亚基的生物合成。MM927能诱导半核糖体多聚体的形成，使细胞在G1/S和G2/M期发生周期阻滞，并诱导细胞凋亡(apoptosis)。MM927在MOLM-13急性髓系白血病(AML)和HCT116结直肠癌(CRC)异种移植模型中展示了抗肿瘤活性。MM927可用于研究急性髓系白血病(AML)和HCT116结直肠癌(CRC)等癌症[1]。体外研究MM927(72h)inhibitsviabilityofHCT116cells(IC50=53nM)andMOLM-13cells(IC50=92nM)[1].MM927(0.5μM,24h)induceshalf-merpolysomesandreducesfree60S/80SpeaksinpolysomeprofilesofHCT116NVLWTcells[1].MM927(3μM,6h)shiftsnewlysynthesizedeL36-SNAP(60Ssubunitmarker)tonon-ribosomalfractionsanddepletesitfrom60S/80S/polysomefractionsinHCT116cells[1].MM927(3μM,24h)causesreductionincytoplasmicsignalofnewlysynthesizedeL36-SNAP(60S)andretainsitinnucleolarfoci(colocalizedwithFibrillarin)inHCT116NVLWTcells[1].MM927(0.5μM,24-48h)inducesG1/SandG2/McellcyclearrestinHCT116mockcells[1].MM927(3μM,2-3days)triggersapoptosisinMOLM-13cells,asshownbydecreasedprocaspase-3andincreasedcleavedcaspase-3levels,andhighAnnexinV-positivecellrates[1].MM927(0.051μM,72h)inhibitstheviabilityofHCT116NVLAID/AIDcellsexpressingectopichumanNVLwithanIC50of0.051μM,andinhibitsHCT116NVLAID/AIDcellsexpressingectopicmouseNVLwithanIC50of0.207μM[1].ApoptosisAnalysis[1]CellLine:MOLM-13cells1/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEConcentration:3μMIncubationTime:2,3daysResult:InducedapoptosisinMOLM-13cells.Decreasedprocaspase-3.Increasedcleavedcaspase-3levels,andhighAnnexinV-positivecellrates.体内研究MM927(35mg/kg,i.p.,twicedaily,21days)reducesthegrowthofHCT116NVLWTtumorxenograftsanddecreasestumorburdeninNSGmice,withnoeffectonHCT116NVLR403WCRISPRtumorxenografts[1].MM927(35mg/kg,i.p.,twicedaily,14days)causesreductioninleukemicdiseaseburdeninNSGmice[1].MM927(35mg/kg,i.p.,twicedaily,3days)increasesnuclearp53stainingandreducesKi-67-positivecellstaininginHCT116NVLWTtumorxenograftsofNSGmice[1].AnimalModel:HCT116NVLWTcellsorHCT116NVLR403WCRISPRcells(5×106in100µL)weresubcutaneouslyimplantedintotheleftandrightflanksof4-8-week-oldNSGmice[1]Dosage:35mg/kgAdministration:i.p.,twicedaily,21daysResult:Achievedtumorgrowthinhibition(TGI)inHCT116NVLWTtumorxenograftsofNSGmice.Reducedtumorburdenattheendoftreatment.ShowednoeffectonHCT116NVLR403WCRISPRtumorxenografts.Showednosignificantchangesinbodyweight,nosignificantalterationsinhemoglobin,platelets,liverEnzymes(ALT,AST).AnimalModel:Luciferase-expressingMOLM-13cells(1×106)wereintravenouslyinjectedintothetailveinof4-8-week-oldNSGmice[1]Dosage:35mg/kgAdministration:i.p.,twicedaily,14daysResult:Achieveda7-foldreductioninleukemicdiseaseburden.Causeda9-folddecreaseinMOLM-13cellpercentageinbonemarrowanda15-folddecreaseinperipheralblood.AnimalModel:HCT116NVLWTcellsorHCT116NVLR403WCRISPRcells(5×106in100µL)weresubcutaneouslyimplantedintotheleftandrightflanksof4-8-week-oldNSGmice[1]Dosage:35mg/kg2/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEAdministration: i.p.,twicedaily,3daysResult: ReducedKi-67-positive(proliferating)cellstaininginHCT116NVLWTtumorxenograftsofNSGmice,withfewcellsshowingco-localizationofp53andKi-67.REFERENCESGuoHH,etal.AsmallmoleculeinhibitorofNVLsuppressestumorgrowthbyblockingribosomebiogenesis.bioRxiv[Preprint].2025Aug1:2025.07.31.667081.McePdfHeightCaut