STA-013-生命科学试剂-MCE

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemESTA-013Cat.No.:HY-179572分⼦式:C₂₄H₁₇N₃O₂S分⼦量:411.48作⽤靶点:EGFR;Akt;MitochondrialMetabolism作⽤通路:JAK/STATSignaling;ProteinTyrosineKinase/RTK;PI3K/Akt/mTOR;MetabolicEnzyme/Protease储存⽅式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY⽣物活性STA-013⼀种EphB酪氨酸激酶抑制剂。STA-013显⽰出针对EphB1(IC50=0.69µM)、EphB2(IC50=1.73µM)和EphB4(IC50=1.02µM)酪氨酸激酶的潜在抑制效⼒。STA-013的抑制了EphB磷酸化信号，同时增强了p-AKT/AKT信号提⽰其激活了胰岛素信号通路。STA-013通过增强胰岛素受体β信号和降低⼼脏中TGF-β⽔平来抑制EphB酪氨酸激酶。STA-013可⽤于研究2型糖尿病及其⼼脏并发症(糖尿病⼼肌病)[1]。IC50&TargetErbB1ErbB2ErbB40.69μM(IC50)1.73μM(IC50)1.02μM(IC50)体外研究STA-013(5µM)inhibitsEphB1(54%),EphB2(42%),EphB4(52%),SGK1(47%),andPKBb(43%)withoutaffectingtherestof140kinasesviakinomeprofilingassay[1].STA-013(0.032-20µM,96h)significantlyinhibitslipidaccumulationinadose-dependentmannerintheembryonicmouse3T3-L1cells[1].STA-013(1µM,30min)resultsasignificantreductioninbasalrespiration,protonleak,ATPproduction,andnon-mitochondrialoxygenconsumption,increasesmaximalrespirationandsparerespiratorycapacity,exhibitsasignificantincreaseinglycolysisandglycolyticcapacityandreducespalmitateoxidationin3T3-L1cells[1].体内研究STA-013(12.5,25and50mg/kg,i.p.,dailyfor6weeks)promotesweightloss,improvesglucoseclearanceandinsulinsensitivity,andenhancesinsulinsignalinginisolatedbrownadiposetissueandliverinhigh-fatdiet-inducedC57BL/6Jmice.Intheseobesemice[1].STA-013(12.5,25and50mg/kg,i.p.,dailyfor6weeks)inducesweightlossnotthroughreducedfoodintakeorelevatedmetabolicratesinDIOmice[1].1/2MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEAnimalModel:HFD(for10weeks)inducedmaleC57BL/6Jmice(16-20weeksold)[1]Dosage:12.5,25and50mg/kgAdministration:i.p.,dailyfor6weeksResult:Showedasignificantreductioninwhole-bodyweight,improvedglucoseclearanceintheIPglucosetolerancetest(GTT),andinsulinsensitivityintheIPinsulintolerancetest(ITT).ShowedasignificantreductioninthefatmassassociatedwithpreservingtheleanmusclemassinHFD-obesemice.Inducedintrascapularbrownadiposetissue(BAT)-specificthermogenesisinHFDobesemice.Showedsignificantreductioninwhole-bodyweightassociatedwithreductioninthefatmass(%)aswellasincreaseintheleanmass(%),improvedglucoseclearance,andrestoredinsulinsensitivityinHFDobesemice.InhibitedphosphorylationofephbtyrosinekinaseforwardsignalinginboththeliverandBATat25mg/kg.Increasedthep-AKT/AKTsignaling,whichsuggeststheactivationofinsulinsignalinginBATandliverinHFDobesemice.Increasedinsr-βproteinlevelscomparedtovehicleinBATandliverlysates.AnimalModel:HFD(for10weeks)inducedmaleC57BL/6JDIOmice(16-20weeksold)[1]Dosage:12.5,25and50mg/kgAdministration:i.p.,dailyfor6weeksResult:Significantlyincreasedoxygen(VO2andcarbondioxide(VCO2)consumption)productioninthelightcycle.Decreasedprofileintherespiratoryexchangerates(RER)duringthedarkcycle.Decreaseinthetotalenergyexpenditure(EE)forSTA-013treatedHFDmice.Inducedweightlossoccurredwithoutachangeinfoodintake,suggestingitwasduetoanelevatedmetabolicrate.REFERENCES[1].TareqS,etal.Discoveryofpan-EphBtyrosinekinaseinhibitorformetabolicsyndromesparingEphB3signalinginmice.PharmacolRes.2025Sep;219:107900.McePdfHeightCaution:Productha