GSK0660-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEGSK0660Cat.No.:HY-12377CASNo.:1014691-61-2分?式:C??H??N?O?S?分?量:418.49作?靶點:PPAR作?通路:CellCycle/DNADamage儲存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實驗DMSO:≥49mg/mL(117.09mM)*"≥"meanssoluble,butsaturationunknown.MassSolvent1mg5mg10mgConcentration制備儲備液1mM2.3895mL11.9477mL23.8954mL5mM0.4779mL2.3895mL4.7791mL10mM0.2390mL1.1948mL2.3895mL請根據(jù)產(chǎn)品在不同溶劑中的溶解度選擇合適的溶劑配制儲備液；?旦配成溶液，請分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲備液的保存?式和期限：-80°C,6months;-20°C,1month。-80°C儲存時，請在6個?內(nèi)使?，-20°C儲存時，請在1個?內(nèi)使?。體內(nèi)實驗請根據(jù)您的實驗動物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請先按照InVitro?式配制澄的儲備液，再依次添加助溶劑：(為保證實驗結(jié)果的可靠性，澄的儲備液可以根據(jù)儲存條件，適當(dāng)保存；體內(nèi)實驗的?作液，建議您現(xiàn)?現(xiàn)配，當(dāng)天使?；以下溶劑前顯?的百分?指該溶劑在您配制終溶液中的體積占?；如在配制過程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1.請依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%saline1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESolubility:≥2.5mg/mL(5.97mM);ClearsolutionBIOLOGICALACTIVITY?物活性GSK0660有效的PPARβ和PPARδ拮抗劑，IC50均為155nM。IC50&TargetPPARβ/δ155nM(IC50)體外研究GSK0660isapotentantagonistofPPARβandPPARδ,withIC50sofboth155nM,andisnearlyinactiveonPPARαandPPARγwithIC50sofboth>10μM.GSK0660antagonizes100%oftheactivityofPPARβ/δwithapIC50of6.8.GSK0660(100nM)reducesCPT1a(aPPARβ/δtargetgene)expressionbelowthebasalvehicle-treatedlevelbyapproximately50%,butshowsnoeffectonPDK4expression,whichisalsoaPPARβ/δtargetgeneinskeletalmusclecells[1].GSK0660(0.5μM)reducesthelevelsofAMPKandeNOSphosphorylation,andBMP-2,Runx-2mRNAexpressioninMC3T3-E1cells.GSK0660(0.1and0.5μM)reversesthebezafibrate-inducedenchancementofALPactivityond7inMC3T3-E1cells[2].GSK0660(1μM)markedlyblocksGW501516-mediatedattenuationofglutamaterelease,andtheeffectofGW501516onROSgenerationinBV-2cellsstimulatedwithLPS.Furthermore,GSK0660significantlyreducesinhibitoryeffectofGW501516ontheLPS-inducedexpressionofgp91phoxmRNAinBV-2cells[3].PROTOCOLCellAssay[2]CellviabilityisdeterminedbytheMTTdye.MC3T3-E1cellsareincubatedwithbezafibrate(1?1000μM)for24,48,or72h,andarepretreatedwiththeAMPKinhibitorcompoundC(5μM),PPARβinhibitorGSK0660(0.5μM),PPARαinhibitorMK886(10μM),orNOSinhibitorL-NAME(1000μM)followedbybezafibrate(100μM)incubationfor48h.Aftertheincubations,10μLofMTTisaddedtoeachwellofa96-wellmicroplate,andthemicroplatesareplacedinanincubatorat37°Cfor4h.OnehundredfiftymicrolitersofDMSOisaddedtoallwellsandmixedthoroughlytolysethecellsanddissolvethedarkbluecrystals.After10min,theabsorbanceismeasuredat570nmusingamicroplatereader[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?JAdvRes.2020Jun20;27:115-125.?PPARRes.2020Dec28.?BrainResBull.2018Jun;140:378-391.Seemorecustomervalidationsonwww.MedChemEREFERENCES2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE[1].ShearerBG,etal.Identificationandcharacterizationofaselectiveperoxisomeproliferator-activatedreceptorbeta/delta(NR1C2)antagonist.MolEndocrinol.2008Feb;22(2):523-9.Epub2007Nov1.[2].ZhongX,etal.BezafibrateenhancesproliferationanddifferentiationofosteoblasticMC3T3-E1cellsviaAMPKandeNOSactivation.ActaPharmacolSin.2011May;32(5):591-600.[3].LeeWJ,etal.ActivationofPPARδattenuatesneurotoxicitybyinhibitinglipopolysaccharide-triggeredglutamatereleaseinBV-2microglialcells.JCellBiochem.2018Feb1.McePdfHeightCaution:Prod