RSVA405-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemERSVA405Cat.No.:HY-103238CASNo.:140405-36-3分⼦式:C₁₇H₂₀N₄O₂分⼦量:312.37作⽤靶点:AMPK;STAT;Autophagy作⽤通路:Epigenetics;PI3K/Akt/mTOR;JAK/STATSignaling;StemCell/Wnt;Autophagy储存⽅式:Powder-20°C3yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验DMSO:125mg/mL(400.17mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制备储备液1mM3.2013mL16.0067mL32.0133mL5mM0.6403mL3.2013mL6.4027mL10mM0.3201mL1.6007mL3.2013mL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。-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。BIOLOGICALACTIVITY⽣物活性RSVA405⼀种有效和具有⼝服活性的AMPK激活剂，EC50值为1μM。RSVA405通过促进CaMKKβ依赖的AMPK活化，从⽽抑制mTOR，并促进⾃噬(autophagy)以增加Aβ的降解。RSVA405通过抑制STAT3功能具有抗炎作⽤。RSVA405也可⽤于肥胖症的研究。IC50&TargetAMPK1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE1μM(EC50,incell-basedassays)体外研究RSVA405(0.2-2μM;24h)inhibitsadipocytedifferentiation[2].RSVA405(0.2-2μM;24h)significantlyinhibitstheexpressionofperoxisomeproliferator-activatedreceptor(PPAR)-γ,fattyacidsynthase(FAS)andfattyacidbindingprotein4(aP2)in3T3-L1cells[2].RSVA405(1-3μM;16h)inhibitsLPS-inducedSTAT3activity,intracellularsignaling,andcytokineresponseinactivatedRAW264.7macrophages[3].RSVA405(1-3μM;24h)inhibitsmTOR,inducesautophagy,andfacilitatesthelysosomaldegradationofAβ,withanEC50of-1μMinAPP-HEK293cells[4].CellViabilityAssay[2]CellLine:3T3-L1preadipocytesConcentration:0.2,0.5,1,2μMIncubationTime:24hResult:IncreasedthephosphorylationofAMPKanditssubstrateacetyl-CoAcarboxylase(ACC).Inhibitedtheaccumulationoflipiddropletsinadose-dependentmanner,withanIC50of0.5μM.体内研究RSVA405(3mg/kg;i.p.)attenuatesrenalinjuryandprotectsrenalfunctionafterischemia-reperfusion(I/R)inrats[1].RSVA405(20-100mg/kg/d;p.o.for11weeks)significantlyreducesthebodyweightgainofmicefedahigh-fatdiet[2].AnimalModel:MaleSprague-Dawleyrats(300-350g)areinducedI/Rinjury[1]Dosage:3mg/kgAdministration:I.p.onehourbeforeinducingI/RinjuryResult:Decreasedthelevelsofcreatinineandbloodureanitrogen(BUN),by35.8%and44.3%inserum,respectively.Decreasedthelevelsofaspartateaminotransferase(AST)andlactatedehydrogenase(LDH)by33.0%and59.8%inserum,respectively.REFERENCES[1].KhaderA,et,al.Novelresveratrolanaloguesattenuaterenalischemicinjuryinrats.JSurgRes.2015Feb;193(2):807-15.[2].VingtdeuxV,et,al.Small-moleculeactivatorsofAMP-activatedproteinkinase(AMPK),RSVA314andRSVA405,inhibitadipogenesis.MolMed.Sep-Oct2011;17(9-10):1022-30.[3].CapirallaH,et,al.Identificationofpotentsmall-moleculeinhibitorsofSTAT3withanti-inflammatorypropertiesinRAW264.7macrophages.FEBSJ.2012Oct;279(20):3791-9.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE[4].VingtdeuxV,et,al.Novelsyntheticsmall-moleculeactivatorsofAMPKasenhancersofautophagyandamyloid-βpeptidedegradation.FASEBJ.2011Jan;25(1):219-31.McePdfHeightCaution:Producthasnotbeenfullyvali