Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemETA-02Cat.No.:HY-100115CASNo.:1784751-19-4分?式:C??H??F?N?分?量:333.33作?靶點(diǎn):p38MAPK;Autophagy作?通路:MAPK/ERKPathway;Autophagy儲(chǔ)存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實(shí)驗(yàn)DMSO:25mg/mL(75.00mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM3.0000mL15.0002mL30.0003mL5mM0.6000mL3.0000mL6.0001mL10mM0.3000mL1.5000mL3.0000mL請(qǐng)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(chǔ)備液；?旦配成溶液，請(qǐng)分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲(chǔ)備液的保存?式和期限：-80°C,6months;-20°C,1month。-80°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?，-20°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請(qǐng)先按照InVitro?式配制澄的儲(chǔ)備液，再依次添加助溶劑：(為保證實(shí)驗(yàn)結(jié)果的可靠性，澄的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)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(guò)程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過(guò)加熱和/或超聲的?式助溶)1.請(qǐng)依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.5mg/mL(7.50mM);Clearsolution1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE2.請(qǐng)依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(7.50mM);ClearsolutionBIOLOGICALACTIVITY?物活性TA-02SB203580(HY-10256)的?個(gè)類似物，p38MAPK的抑制劑，其IC50值為20nM。TA-02可抑制TGFBR-2。TA-02和SB203580、SB202190(HY-10295)具有相似的?活性。體外研究TA-02(5μM)inhibitsthephosphorylationofproteinsdownstreamofp38αMAPKsuchasMAPKAPK2andHSP27duringcardiogenesis.TA-02at5μMconcentrationinducescardiogenesis,butalsoincreasesATF-2phosphorylationandMEF2C?expressionincontrasttowhatwouldbeexpectedwithamechanismdependentonp38αMAPKinhibition[1].TA-02inducesT/BrachyurywhereasSB203580additionincreasedMESP1andT/Brachyurytranscripts[1].TA-02significantlyinduceshighNKX2-5expressionwhenappliedbetweendays0-8[1].TA-02isfoundtoinhibitmultipletargetswithsimilarpotencytop38αMAPK,suchasp38α,p38β,JNK3,JNK2,CIT,CK1ε,DMPK2,JNK1,DDR1CK1δ,MEK5,andERBB2[1].TA-02andSB203580reducethenuclearTCF/LEF-1driventranscriptionofluciferasesimilartoDKK-1[1].TA-02(5nM-5μM)inhibitsp38andincreasestheanti-inflammationeffectsofBDNFoninflammationinvitro[2].WesternBlotAnalysis[2]CellLine:ThenervecelllineAGE1.HN.Concentration:5nM-5μM.IncubationTime:44h(100ng/mlLPSfor4hat37°C).Result:Suppressedp-38proteinexpression,reducedIL-1β,IL-6,IL-18andTNF-αlevelsandinhibitediNOSandCOX-2levelsinaninvitromodelofSCIbyBDNFoverexpression,comparedwiththeBDNFoverexpressiongroup.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?ExpTherMed.2019Mar;17(3):1688-1696.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].LacoF,etal.CardiomyocytedifferentiationofpluripotentstemcellswithSB203580analoguescorrelateswithWntpathwayCK1inhibitionindependentofp38MAPKsignaling.JMolCellCardiol.2015Mar;80:56-70.[2].JiedongLiang,etal.TheactivationofBDNFreducedinflammationinaspinalcordinjurymodelbyTrkB/p38MAPKsignaling.ExpTher2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEMed.2019Mar;17(3):1688-1696.McePdfHeightCaution:Producthasnotbeenfullyvalidated