D-Leucine-amide-CDDO-Me-HMP-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemED-Leucineamide-CDDO-Me-HMPCat.No.:HY-179613CASNo.:2749600-16-4分⼦式:C₅₃H₇₃N₅O₆分⼦量:876.18作⽤靶点:DrugIntermediate;ReactiveOxygenSpecies(ROS);

Apoptosis;Keap1-Nrf2;HemeOxygenase(HO);Bcl-2Family;

Caspase作⽤通路:Others;Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB;Apoptosis储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性D-Leucineamide-CDDO-Me-HMP⼀种由CDDO-Me(HY-13324)和ligustrazine(HY-N0264)组成的前药。D-Leucineamide-CDDO-Me-HMP可保护CCl4诱导的肝损伤。D-Leucineamide-CDDO-Me-HMP能够抑制活性氧(ROS)的产⽣，减轻线粒体损伤并抑制细胞凋亡(apoptosis)。D-Leucineamide-CDDO-Me-HMP可⽤于肝脏损伤研究。体外研究D-Leucineamide-CDDO-Me-HMP(CHL)(0.05-0.10μM,24h)significantlyenhancescellviabilityinCCl4-inducedLO2andRAW264.7liverinjurycellmodels[1].D-Leucineamide-CDDO-Me-HMP(0.05-0.10μM,24h)reducesROSlevels,alleviatesmitochondrialdamageandinhibitscellapoptosisinCCl4-inducedLO2andRAW264.7liverinjurycellmodels[1].D-Leucineamide-CDDO-Me-HMP(0.10μM,24h)significantlyupregulatestheexpressionofNrf2andHO-1proteinsinCCl4-inducedLO2cells[1].CellViabilityAssay[1]CellLine:CCl4inducedLO2andRAW264.7liverinjurycellsConcentration:0.05and0.10μMIncubationTime:24hResult:Showedcellviabilityof98.4%inLO2cellsand92.6%inRAW264.7cells.Immunofluorescence[1]1/2MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemECellLine:CCl4inducedLO2andRAW264.7liverinjurycellsConcentration:0.05and0.10μMIncubationTime:24hResult:ReducedthefluorescenceintensityofDCF.ReducedthefluorescenceintensityofJ-monomerandIncreasedthefluorescenceintensityofJ-aggregate.体内研究D-Leucineamide-CDDO-Me-HMP(CHL)(15-30mg/kg,i.p.,administeredafterCCl4-inducedliverinjury)improveslivertissuemorphologyandpathologicaldamageinC57BL/6mouseliverinjurymodelsinducedbyCCl4[1].AnimalModel:C57BL/6(8weeksofage,18–20g,CCl4-inducedliverinjury)[1]Dosage:15mg/kg,30mg/kgAdministration:IntraperitoneallyinjectionResult:ReducedserumlevelsofALTandAST.Alleviatedsteatosisandinflammatoryinfiltration.UpregulatedtheexpressionofHO-1(4.2-fold)andNQO1(5.5-fold)inlivertissue.Downregulatedtheexpressionofp-p65(5-fold)andpro-apoptoticproteinBAX.Upregulatedtheexpressionofanti-apoptoticproteinBcl-2,andinhibitedexcessiveactivationofCaspase-3.REFERENCES[1].ChenF,etal.Developmentofaleucineaminopeptidase-activatableco-prodrugfromCDDO-Meandligustrazineforsynergistictreatmentofliverinjury.BioorgChem.2025;166:109177.McePdfHeightCaution:Producthasnotbeenfullyvalidatedformedicalapplic