GSK-872-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEGSK-872Cat.No.:HY-101872CASNo.:1346546-69-7分⼦式:C₁₉H₁₇N₃O₂S₂分⼦量:383.49作⽤靶点:RIPkinase作⽤通路:Apoptosis储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验DMSO:100mg/mL(260.76mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制备储备液1mM2.6076mL13.0381mL26.0763mL5mM0.5215mL2.6076mL5.2153mL10mM0.2608mL1.3038mL2.6076mL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。体内实验请根据您的实验动物和给药⽅式选择适当的溶解⽅案。以下溶解⽅案都请先按照InVitro⽅式配制澄的储备液，再依次添加助溶剂：(为保证实验结果的可靠性，澄的储备液可以根据储存条件，适当保存；体内实验的⼯作液，建议您现⽤现配，当天使⽤；以下溶剂前显⽰的百分⽐指该溶剂在您配制终溶液中的体积占⽐；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的⽅式助溶)1.请依序添加每种溶剂：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(6.52mM);Clearsolution1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE2.请依序添加每种溶剂：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(6.52mM);ClearsolutionBIOLOGICALACTIVITY⽣物活性GSK-872RIPK3抑制剂，⾼亲和⼒结合RIP3激酶结构域，IC50为1.8nM，并抑制激酶活性，IC50为1.3nM。GSK-872降低RIPK3介导的坏死(necroptosis)和随后的HMGB1的细胞质易位和表达，并改早期脑损伤中的脑⽔肿和神经功能缺损。IC50&TargetIC50:1.3nM(RIPK3)[1]体外研究GSK-872(GSK'872;0.01-3μM;24hours)blocksTNF-inducednecroptosisinhumanHT-29cellsinaconcentration-dependentmanner[1].CellViabilityAssay[1]CellLine:HT-29cellsConcentration:0.01,0.03,0.1,0.3,1,and3μMIncubationTime:24hoursResult:BlockedTNF-inducednecroptosisinaconcentration-dependentmanner.体内研究GSK-872(25mM;intracerebroventricularinjection)canattenuatebrainedemaandimproveneurologicalfunctionfollowingsubarachnoidhemorrhage(SAH)andreducethenumberofnecroticcells.GSK-872canalsodecreasetheproteinlevelsofRIPK3andMLKL,andcytoplasmictranslocationandexpressionofHMGB1,animportantpro-inflammatoryprotein[3].AnimalModel:EightweeksoldSprague-Dawleymaleratswith300-320gbodyweight(ratSAHmodel)[3]Dosage:25mM/6μLAdministration:Syringepump(intracerebroventricular)at30minafterSAHResult:Attenuatedbrainedema,improvedneurologicalfunctionanddecreasedthenumberofnecroticcellsintheipsilateralcortex.DecreasedtheexpressionofRIPK3,MLKLandcytoplasmicHMGB1at72hafterSAHintheipsilateralcortex.户使⽤本产品发表的科研⽂献•Nature.2020Apr;580(7803):386-390.•SignalTransductTargetTher.2020Oct9;5(1):235.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE•NatCellBiol.2022Apr;24(4):471-482.•ClinCancerRes.2022Nov30;CCR-22-1591.•CellDeathDiffer.2022Jan22.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].MandalP,etal.RIP3inducesapoptosisindependentofpronecrotickinaseactivity.MolCell.2014Nov20;56(4):481-95.[2].AroraD,etal.DeltamethrininducedRIPK3-mediatedcaspase-independentnon-apoptoticcelldeathinratprimaryhepatocytes.BiochemBiophysResCommun.2016Oct14;479(2):217-223.[3].ChenT,etal.InhibitingofRIPK3attenuatesearlybraininjuryfollowingsubarachnoidhemorrhage:Possiblythroughalleviatingnecroptosis.BiomedPharmacother.2018;107:563-570.McePdfHeightCaution:Producthasnotbeenfullyval