NSD2-H3K36me2-modulator-1-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemENSD2/H3K36me2modulator-1Cat.No.:HY-179427分⼦式:C₄₁H₅₉ClN₂O₅分⼦量:695.37作⽤靶点:HistoneMethyltransferase;Apoptosis;ReactiveOxygenSpecies(ROS)作⽤通路:Epigenetics;Apoptosis;Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性NSD2/H3K36me2modulator-1⼀种⼝服有效的NSD2/H3K36me2调节剂。NSD2/H3K36me2modulator-1与NSD2的SAM⼝袋竞争性结合，有效抑制NSD2表达并抑制H3K36me2甲化。NSD2/H3K36me2modulator-1还能逆转上⽪-间质转化(EMT)，抑制细胞迁移，并诱导G0/G1期阻滞和细胞凋亡(apoptosis)。NSD2/H3K36me2modulator-1可降低线粒体膜电位(MMP)并导致活性氧(ROS)⽣成。NSD2/H3K36me2modulator-1可⽤于研究靶向NSD2的表观遗传抗癌策略在肝细胞癌(HCC)中的应⽤[1]。IC50&TargetNSD2体外研究NSD2/H3K36me2modulator-1(Compound5b)(24h)displaysIC50<5μMagainstallfivecancercelllines(IC50valuesof4.67,2.12,2.64,4.56,4.99μMinA549,HepG-2,PC-3,HCT-116,MCF-7cellsrespectively),confirmingitsexceptionalbroad-spectrumantitumoractivity[1].NSD2/H3K36me2modulator-1exhibitsahightumorselectivityforHepG-2cellsoverHaCaTcells(IC50=19.2μM)(selectivityindex(SI)=9.06)[1].NSD2/H3K36me2modulator-1(2μM,24h,37-62℃)effectivelybindstoNSD2withinHepG-2cells[1].NSD2/H3K36me2modulator-1(2,4μM,24h)inhibitsNSD2andselectivelydownregulatesitsmediatedH3K36me2inHepG-2cells[1].NSD2/H3K36me2modulator-1(2,4μM,24h)reversesEMTatthemolecularlevel,likelythroughNSD2inhibitionandsubsequentTWIST1downregulation,leadingtoalteredexpressionofEpithelial-mesenchymaltransition(EMT)masterregulators[1].NSD2/H3K36me2modulator-1(2,4μM,18,36h)significantlyinhibitsmigrationandproliferationofHepG-2cells[1].NSD2/H3K36me2modulator-1(2,4μM,24h)exertsmultipleregulatoryeffectsonHepG-2cells,includingeffectivelyinducingapoptosis,triggeringconcentration-dependentG0/G1phasearrest,reducing1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEmitochondrialmembranepotential(MMP)dose-dependently,andefficientlypromotingthegenerationofROS[1].WesternBlotAnalysis[1]CellLine:HepG-2cellsConcentration:2,4μMIncubationTime:24hResult:SuppressedNSD2expressioninadose-dependentmanner,withnotablystronginhibitionat4μM.ExhibitedhighselectiveinhibitionofH3K36me2.BoundeffectivelytoNSD2withincells.ApoptosisAnalysis[1]CellLine:HepG-2cellsConcentration:2,4μMIncubationTime:24hResult:SignificantlyincreasedthetotalapoptosisrateinHepG-2cellswiththeelevationoftheconcentration.Exhibitedslightlysuperiorapoptosis-inducingcapacityattheconcentrationof4μM.WesternBlotAnalysis[1]CellLine:HepG-2cellsConcentration:2,4μMIncubationTime:24hResult:SignificantlysuppressedTWIST1expression.Dose-dependentlydownregulatedN-CadherinandVimentin.UpregulatedE-CadherinandOccludininadose-dependentmanner.CellCycleAnalysis[1]CellLine:HepG-2cellsConcentration:0,2,4μMIncubationTime:24hResult:ElevatedtheproportionofHepG-2cellsinG0/G1phasefrom53.8%to65.7%,withtheconcentrationincreasingfrom0to2μM.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEIncreasedtheG0/G1subpopulationto79.6%,withtheconcentrationreaching4μM,andexceededthatof5-Fluorouracil(HY-90006)(73.5%).InducedamarkeddecreaseinthelevelsofcellcycleregulatorsCDK2,CDK4,andCDK6,effectivelyblockingcellcycleprogressioninaconcentration-dependentmanner.体内研究NSD2/H3K36me2modulator-1(Compound5b)(20,40mg/kg,dailyp.o.for18consecutivedays)exertsrobustantitumoreffectswitheffectivetumorgrowthinhibitionandanacceptablesafetyprofileinaHepG-2cellxenograftmodel,asevidencedbytheabsenceofsignificantdifferencesinthebodyweight,organindices,andmorphologicalfeatures[1].AnimalModel:AnHepG-2xenograftmodelestablishedinfemaleBALB/cnudemice(6-8weeksold)[1]Dosage:20,40mg/kgAdministration:dailyoralgavage(p.o.)for18consecutivedaysResult:Significantlysuppressedtumorgrowthinadose-dependentmanner.Exhibitedthestrongestantitumoreffectat40mg/kg.REFERENCES[1].LvL,etal.Synthesisofamide-linkedpanaxadiol-indolinedionederivatives:AnovelNSD2/H3K36me2epigeneticmodulatorwithsignificantantitumorefficacy.EurJMedChem.2026Jan15;302(Pt