Salinomycin-sodium-salt-Salinomycin-sodium-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemESalinomycinsodiumsaltCat.No.:HY-17439CASNo.:55721-31-8Synonyms:Salinomycinsodium;Sodiumsalinomycin分⼦式:C₄₂H₆₉NaO₁₁分⼦量:772.98作⽤靶点:Wnt;β-catenin;Bacterial;Autophagy;Apoptosis;Antibiotic;Parasite作⽤通路:StemCell/Wnt;Anti-infection;Autophagy;Apoptosis储存⽅式:4°C,storedundernitrogen*Insolvent:-80°C,6months;-20°C,1month(storedunder

nitrogen)溶解性数据体外实验DMSO:100mg/mL(129.37mM;Needultrasonic)H2O:1mg/mL(1.29mM;ultrasonicandwarmingandheatto80°C)MassSolvent1mg5mg10mgConcentration制备储备液1mM1.2937mL6.4685mL12.9369mL5mM0.2587mL1.2937mL2.5874mL10mM0.1294mL0.6468mL1.2937mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；⼀旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存⽅式和期限：-80°C,6months;-20°C,1month(storedundernitrogen)。-80°C储存时，请在6个⽉内使⽤，-20°C储存时，请在1个⽉内使⽤。体内实验请根据您的实验动物和给药⽅式选择适当的溶解⽅案。以下溶解⽅案都请先按照InVitro⽅式配制澄的储备液，再依次添加助溶剂：(为保证实验结果的可靠性，澄的储备液可以根据储存条件，适当保存；体内实验的⼯作液，建议您现⽤现配，当天使⽤；以下溶剂前显⽰的百分⽐指该溶剂在您配制终溶液中的体积占⽐；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的⽅式助溶)1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE1.请依序添加每种溶剂：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.5mg/mL(3.23mM);Clearsolution2.请依序添加每种溶剂：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(3.23mM);ClearsolutionBIOLOGICALACTIVITY⽣物活性Salinomycinsodiumsalt(Salinomycinsodium)，⼀种钾离⼦载体抗⽣素，Wnt/β-catenin信号传导的有效抑制剂。Salinomycinsodiumsalt(Salinomycinsodium)作⽤于Wnt/Fzd/LRP复合物，阻断Wnt诱导的LRP6磷酸化，导致LRP6蛋⽩降解。Salinomycinsodiumsalt(Salinomycinsodium)选择性抑制⼈肿瘤⼲细胞。IC50&TargetWnt/β-catenin[1]体外研究Salinomycin(0.1-8µM)inhibitsthegrowthofHUVECsinadose-dependentmanner,accountingfor32.1and59.2%inhibitionat4and8µM,respectively.HUVECsexposedto2,4and8µMofSalinomycinfor48h

showadose-dependentreductionincellnumberandachangeincellmorphology.Salinomycin(4µM)

treatmenteffectivelyinhibitsHUVECmigrationandinvasion,andsignificantlydisruptthecapillary-liketube

formationofHUVECs.Salinomycinsignificantlysuppressestheexpressionlevelsofphosphorylated(p)-FAK

inatime-anddose-dependentmannerinHUVECs.SalinomycininhibitsHUVECangiogenesisbydisturbing

theVEGF-VEGFR2-AKTsignalingaxis[1].CombinationofRSVLandSalinomycinsynergisticallyinhibitsthe

proliferationofTNBC(MDA-MB-231)cells.RSVLandSalinomycineffectivelyreducewoundhealing,colony

andtumorosphereformingcapabilityinTNBCcells.SynergisticcombinationofRSVLandSalinomycin

inducesapoptosisinbothcultureconditionsbysignificantupregulationofBaxwithdecreasedBcl-2

expressionascomparisontountreatedandalonedrugtreatments[2].Salinomycin(0,2,4,8and16μM)

significantlyinhibitstheproliferationofA2780andSK-OV-3celllinesinadose-andtime-dependentmanner,

(IC5024h:13.8μM,IC5048h:6.888μMandIC5072h:4.382μMforA2780celllines),(IC5024h:12.7μM,

IC5048h:9.869μMandIC5072h:5.022μMforSK-OV-3celllines).SalinomycinblockstheWnt/β-catenin

pathwayinEOCcells[3].Salinomycin(2μM)reducescancercellproliferation,inhibitsSTAT3

phosphorylationandP38andβ-cateninexpressions,andsuppressesepithelial-mesenchymaltransitionin

colorectalcancercells.Salinomycin(1-5μM)inhibitscancercellproliferationandSTAT3signalingin

colorectalcancercells.Furthermore,SalinomycinactivatesAkt(Ser473)anddown-regulatesHsp27(Ser

82)phosphorylationinHT-29andSW480.Salinomycindown-regulateshTERTandreducestelomerase

activitywhencombinedwithtelomeraseinhibitor[4].体内研究Salinomycin(5and10mg/kg)significantlysupressestheaveragetumorvolumeandtumorweight.SalinomycinhinderstheU251humangliomacellgrowthinvivoviainhibitionofangiogenesiswithinvolvementofAKTandFAKdephosphorylation[1].Salinomycin(0.5mg/kgb.wt.)enhancesthemeansurvivaltimeofthetumorbearingSwissalbinomice[2].PROTOCOL2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemECellAssay[1]TheeffectofSalinomycinonHUVECgrowthisdeterminedbyMTTassay.Briefly,HUVECs(6,000cells/well)areseededin96-wellcultureplatesfor24handincubatedwithdifferentconcentrationsofSalinomycin.Inthepreliminaryexperiments,Salinomycintreatmentfor12,24,48and72hshowstime-dependenteffectsoncellgrowthinhibition.However,treatmentfor48histheoptimaltimeandisselectedforfurthermechanismevaluation.AfterSalinomycintreatmentfor48h,20µL/wellofMTTsolution(5mg/mL)isaddedandincubatedfor5h.Themediumisaspiratedandreplacedwith200µL/wellofDMSOtodissolvetheformazanSalinomycintformed.Thecolorintensityoftheformazansolutionismeasuredat570nmbyamicroplatespectrophotometer.Thecellviabilityisexpressedas%ofthecontrol(as100%).MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalHumangliomaU251cells(1×107)suspendedin100µLPBSareinjectedintotherightlowerhindflankofAdministration[1]each6-week-oldmalenudemouse.Themicearethenrandomlyassignedintothreegroupsof10miceineachgroup.Afteroneweek,Salinomycin(5and10mg/kg)isadministeredintothecaudalveineveryotherdayfor16days.Controlmicereceiveanequalvolumeofvehicle(Salinomycinine)only.Bodyweightandtumorvolumearemonitoredeverytwodays.Attheendoftheexperiments,tumorsareexcised,photographed,andweighed.Tumorsfromeachgroupareusedforwesternblottingandimmunohistochemical(IHC)assay.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.户使⽤本产品发表的科研⽂献•EMBOMolMed.2019Oct;11(10):e9930.•JControlRelease.2020Oct10;326:387-395.•ActaBiomater.2022Aug23;S1742-7061(22)00501-3.•PharmacolRes.2020May;155:104751.•CellBiosci.2021Aug4;11(1):156.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].LuD,etal.SalinomycininhibitsWntsignalingandselectivelyinducesapoptosisinchroniclymphocyticleukemiacells.ProcNatlAcadSciUSA.2011Aug9;108(32):13253-7.[2].ZhouJ,etal.Salinomycininducesapoptosisincisplatin-resistantcolorectalcancercellsbyaccumulationofreactiveoxygenspecies.Toxi