Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEScutellarinCat.No.:HY-N0751CASNo.:27740-01-8分?式:C??H??O??分?量:462.36作?靶點:STAT;Akt;HIV作?通路:JAK/STATSignaling;StemCell/Wnt;PI3K/Akt/mTOR;Anti-infection儲存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數據體外實驗DMSO:100mg/mL(216.28mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM2.1628mL10.8141mL21.6282mL5mM0.4326mL2.1628mL4.3256mL10mM0.2163mL1.0814mL2.1628mL請根據產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，避免反復凍融造成的產品失效。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?內使?，-20°C儲存時，請在1個?內使?。體內實驗請根據您的實驗動物和給藥?式選擇適當的溶解?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：(為保證實驗結果的可靠性，澄的儲備液可以根據儲存條件，適當保存；體內實驗的?作液，建議您現?現配，當天使?；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沉淀、析出現象，可以通過加熱和/或超聲的?式助溶)1.請依序添加每種溶劑：0.5%CMC-Na/salinewater1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESolubility:10mg/mL(21.63mM);Suspendedsolution;NeedultrasonicBIOLOGICALACTIVITY?物活性Scutellarin從芩中分離到的酮類物質，在HCC細胞中，能夠下調STAT3/Girdin/Akt信號通路，在破?細胞中，能夠抑制RANKL介導的MAPK/NF-κB信號通路。Scutellarin具有抗HIV-1IIIB，HIV-1(74V)和HIV-1KM018的活性，EC50分別為26μM，253μM和136μM。IC50&TargetSTAT3HIV-1體外研究ScutellarintreatmentsignificantlyreducesHepG2cellviabilityinadose-dependentmanner,andinhibitsmigrationandinvasionofHCCcellsinvitro.ScutellarintreatmentsignificantlyreducesSTAT3andGirdersofactinfilaments(Girdin)expression,STAT3andAktphosphorylationinHCCcells.IntroductionofSTAT3overexpressionrestoresthescutellarin-downregulatedGirdinexpression,Aktactivation,migrationandinvasionofHCCcells.Furthermore,inductionofGirdinoverexpressioncompletelyabrogatestheinhibitionofscutellarinontheAktphosphorylation,migrationandinvasionofHCCcells.ScutellarincaninhibitHCCcellmetastasisinvivo,andmigrationandinvasioninvitrobydown-regulatingtheSTAT3/Girdin/Aktsignaling[1].ScutellarinselectivelyenhancesAktphosphorylation[2].Scutellarinisaputativetherapeuticagentasithasbeenfoundtonotonlysuppressmicroglialactivationthusamelioratingneuroinflammation,butalsoenhanceastrocyticreaction.Acutellarinamplifiestheastrocyticreactionbyupregulatingtheexpressionofneurotrophicfactorsamongothersthusindicatingitsneuroprotectiverole.Remarkably,theeffectsofscutellarinonreactiveastrocytesaremediatedbyactivatedmicrogliasupportingafunctional"cross-talk"betweenthetwoglialtypes[3].ScutellarincansuppressRANKL-mediatedosteoclastogenesis,thefunctionofosteoclastboneresorption,andtheexpressionlevelsofosteoclast-specificgenes(tartrate-resistantacidphosphatase(TRAP),cathepsinK,c-Fos,NFATc1).FurtherinvestigationindicatesthatScutellarincaninhibitRANKL-mediatedMAPKandNF-κBsignalingpathway,includingJNK1/2,p38,ERK1/2,andIκBαphosphorylation[5].體內研究Scutellarin(50mg/kg/day)significantlymitigatesthelungandintrahepaticmetastasisofHCCtumorsinvivo.Thenumbersofthelungandintrahepaticmetastatictumorsinthescutellarin-treatedgrouparesignificantlylessthanthatinthecontrols[1].TheratstreatedwithScutellarindisplayasignificantalleviationinneurobehavioraldeficitscomparedtotheSAHgroup.ScutellarinenhancedeNOSexpressioncomparedwithSAHrats[4].PROTOCOLCellAssay[1]HepG2cells(1×105/well)areculturedin96-wellplatesandtreatedintriplicatewithscutellarinatconcentrationsof5,10,20,30,and100μMorvehiclealonefor24h.Thecellularviabilityistestedby3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide(MTT)assay,andisexpressedasapercentageofproliferationversuscontrols.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEAnimalToestablishanorthotopicliverxenograftmodel,individualmiceareanesthetizedwithisofluraneandasmallAdministration[1]incisionismadeintheirabdomen.Individualmiceareinjectedwith2×106SK-Hep1cellsin30μLMatrigelintotheirleftlobeoftheliver.Twenty-fourhoursafterorthotopicliverimplantation,themicearerandomizedandinjectedintraperitoneallywithscutellarin(50mg/kg/day)orvehicle(0.9%NaCl,normalsaline)dailyfor35consecutivedays(n=10pergroup).Subsequently,themicearesacrificed,andtheirlungsandliversareexcised,fixedin10%bufferedformalinandparaffin-embeddedforhematoxylinandeosinstaining.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產品發表的科研?獻?CellDeathDis.2020Nov13;11(11):978.?PhytotherRes.2021Dec2.?CellBiolInt.2022Jun28.?ThoracCancer.2019Mar;10(3):492-500.?Bioengineered.2022Jan;13(1):1013-1024.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].KeY,etal.ScutellarinsuppressesmigrationandinvasionofhumanhepatocellularcarcinomabyinhibitingtheSTAT3/Girdin/Aktactivity.BiochemBiophysResCommun.2016Dec18.pii:S0006-291X(16)32174-X[2].YangLL,etal.DifferentialregulationofbaicalinandscutellarinonAMPKandAktinpromotingadiposecellglucosedisposal.BiochimBiophysActa.2016Nov27;1863(2):598-606.[3].WuCY,etal.Scutellarinattenuatesmicroglia-mediatedneuroinflammationandpromotesastrogliosisincerebralischemia-atherapeuticconsideration.CurrMedChem.2016Nov18.[Epubaheadofprint][4].LiQ,etal.ScutellarinattenuatesvasospasmthroughtheErk5-KLF2-eNOS