PeS-9-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors • ScreeningLibraries • Proteinswww.MedChemEPeS-9Cat.No.:HY-174377分子式:C₂₆H₂₈O₁₃S分子量:580.56作用靶点:AndrogenReceptor;p38MAPK;Caspase;CytochromeP450;CalciumChannel;ReactiveOxygenSpecies(ROS);Apoptosis;MitochondrialMetabolism;GLUT作用通路:VitaminDRelated/NuclearReceptor;MAPK/ERKPathway;Apoptosis;MetabolicEnzyme/Protease;MembraneTransporter/IonChannel;NeuronalSignaling;Immunology/Inflammation;NF-κB储存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性PeS-9是一种雄激素受体(AR)降解剂，可诱导雄激素受体降解。PeS-9通过促进细胞毒性ROS产生，诱导线粒体和内质网应激，导致线粒体细胞色素C和AIF释放。PeS-9可激活caspase-9和caspase-3，引起DNA片段化和细胞凋亡(apoptosis)。PeS-9具有抗前列腺癌活性，并在体内表现出抗肿瘤和抗转移活性，且副作用较小。PeS-9可用于GLUT-1过表达肿瘤的研究[1]。体外研究PeS-9(48h)showscytotoxicityincancercellswithIC50sof0.49μM(DU145),and0.58μM(LNCaP),whilehaslowcytotoxicityfornoncancercellswithIC50sof3.41μM(PNT2),3.53μM(MRC-9),11.7μM(HUVEC)and7.51μM(HEK)[1].PeS-9(0-2.5μM,4-48h)downregulatestheARsignalingpathway,producesROS,anddamagesDNAin22Rv1cells[1].PeS-9(48h)synergizeswithantiandrogenEnzalutamide(HY-70002)andPARPinhibitorOlaparib(HY-10162)withCI＜0.75in22Rv1cells[1].PeS-9(0-1μM,1h)activatestheMAPKsignalingpathwaysbyincreasingthelevelofstresskinasesp-p38,p-JNK,andp-ERKin22Rv1cells,whichcanbeantagonizedbythetestedMAPKinhibitor[1].PeS-9(0-2.5μM,1-48h)inducesapoptosisin22Rv1cellsthroughmitochondrialtargetingandcytotoxicROSinduction[1].PeS-9(0-2.5μM,1-48h)causesincreasedcytosolicCa2+levels,expansionoftheendoplasmicreticulum(ER),alteredmitochondrialmembranepermeability,andDNAdamage,asquantifiedbyanelevatedsub-G1cellpopulation[1].PeS-9(0.5-4μM,24h)inhibitstheuptakeofglucosein22Rv1cells,andthiseffectcanbeinhibitedby1/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemEGLUT-1inhibitorPhloretin(HY-N0142)[1].PeS-9(0.1-10μM,every5daysover20days)reducesthesurvivalfractionsoftumoroidsupondose-dependently[1].WesternBlotAnalysis[1]CellLine:22Rv1cellsConcentration:1,2μMIncubationTime:48hResult:DownregulatedAR-FL,AR-V7,PSA,IGF-1proteinsdose-dependently.RealTimeqPCR[1]CellLine:22Rv1cellsConcentration:0,0.5,1,2μMIncubationTime:48hResult:InhibitedthetranscriptionofTMPRSS2,FKBP5andPSAgenesdose-dependently.Immunofluorescence[1]CellLine:22Rv1cellsConcentration:1.25,2.5μMIncubationTime:4,24h,48hResult:InducedDNAdouble-strandbreaks(DSBs),asdemonstratedbyγH2AX/53BP1fociformationTriggeredprimaryDNAdamagewithin4hoursoftreatment,reachedpeakdamagelevelsat24hours,andshowedsignsofDNArepairactivationby48hours.WesternBlotAnalysis[1]CellLine:22Rv1cellsConcentration:0.5-4μMIncubationTime:48hResult:IncreasedBax/Bcl-2ratio(0.5,1,2,4,8μM).Downregulatedofantiapoptoticsurviving-survivin(1,2μM).Releasedcytotoxicmitochondrialproteinssuchasapoptosis-inducingfactor(AIF)andcytochromeCtocellularcytoplasm(2,4μM).Increasedthelevelofcaspase-9,caspase-3andPRAP(2,4μM).2/3 MasterofBioactiveMolecules—您身边的抑制剂大师www.MedChemE体内研究PeS-9(27.9mg/kg,i.p.,dailyfor15days)exertsinvivoantitumorandantimetastaticactivitywithminorsideeffectsinimmunocompromisedNOD/SCIDgamma(NSG)micebearingsubcutaneouslyxenotransplantedhumanprostatecancer22Rv1cells[1].AnimalModel:NOD/SCIDgamma(NSG)8-12weeksmicebearingsubcutaneouslyxenotransplantedhumanprostatecancer22Rv1cells[1].Dosage:27.9mg/kgAdministration:Dailyi.p.administrationfor15daysResult:Reduced40.0%tumorvolumecomparedwiththecontrolgroup(1069.5mm3vs.646.6mm3).Reduced4.4-foldlungmicrometastases.Showednosignificantdifferenceontheweightsofthebody,heart,lungs,liver,andkidney.Enlargedspleenthatindicateanimmunostimulatoryeffectofthetreatment.Showednosignificantdifferenceonthewhiteandredbloodcells,platelets,hemoglobincontent,andhematocrit.Revealednosignsoftissuedamage,inflammationorgranuloma.REFERENCESBusenbenderT,etal.6-((1,4-naphthoquinone-2-yl)methyl)thio-glucoseconjugates,anoveltargetedapproachforadvancedprostatecancer.MolCancerTher.2025