GSK-872-DataSheet-生命科學試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEGSK-872Cat.No.:HY-101872CASNo.:1346546-69-7分?式:C??H??N?O?S?分?量:383.49作?靶點:RIPkinase作?通路:Apoptosis儲存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實驗DMSO:100mg/mL(260.76mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM2.6076mL13.0381mL26.0763mL5mM0.5215mL2.6076mL5.2153mL10mM0.2608mL1.3038mL2.6076mL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?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，適當保存；體內(nèi)實驗的?作液，建議您現(xiàn)?現(xiàn)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(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>>90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(6.52mM);Clearsolution1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE2.請依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(6.52mM);ClearsolutionBIOLOGICALACTIVITY?物活性GSK-872RIPK3抑制劑，?親和?結(jié)合RIP3激酶結(jié)構(gòu)域，IC50為1.8nM，并抑制激酶活性，IC50為1.3nM。GSK-872降低RIPK3介導的壞死(necroptosis)和隨后的HMGB1的細胞質(zhì)易位和表達，并改早期腦損傷中的腦?腫和神經(jīng)功能缺損。IC50&TargetIC50:1.3nM(RIPK3)[1]體外研究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.體內(nèi)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.戶使?本產(chǎn)品發(fā)表的科研?獻?Nature.2020Apr;580(7803):386-390.?SignalTransductTargetTher.2020Oct9;5(1):235.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師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