Ravoxertinib-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•Agonists•ScreeningLibrarieswww.MedChemERavoxertinibCat.No.:HY-15947CASNo.:1453848-26-4分⼦式:C₂₁H₁₈ClFN₆O₂分⼦量:440.86作⽤靶点:ERK作⽤通路:MAPK/ERKPathway;StemCell/Wnt储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验DMSO:≥35mg/mL(79.39mM)扫描⼆维码，*"≥"meanssoluble,butsaturationunknown.运⽤溶解⽅案计算器获得适合您实验体系的溶解⽅案MassSolvent1mg5mg10mgConcentration制备储备液1mM2.2683mL11.3415mL22.6829mL5mM0.4537mL2.2683mL4.5366mL10mM0.2268mL1.1341mL2.2683mL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，并请注意储备液的保存⽅式和期限。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%DMSO40%PEG3005%Tween-8045%salineSolubility:≥1.67mg/mL(3.79mM);Clearsolution此⽅案可获得≥1.67mg/mL(3.79mM，饱和度未知)的澄溶液。以1mL⼯作液为例，取100μL16.699999mg/mL的澄DMSO储备液加到400μLPEG300中，混合均匀；向上述体系中加⼊50μLTween-80，混合均匀；然后继续加⼊450μL⽣理盐⽔定容⾄1mL。1/3www.MedChemEwww.MedChemE2.请依序添加每种溶剂：10%DMSO90%(20%SBE-β-CDinsaline)Solubility:≥1.67mg/mL(3.79mM);Clearsolution此⽅案可获得≥1.67mg/mL(3.79mM，饱和度未知)的澄溶液。以1mL⼯作液为例，取100μL16.699999mg/mL的澄DMSO储备液加到900μL20%的SBE-β-CD⽣理盐3.⽔⽔溶液中，混合均匀。请依序添加每种溶剂：10%DMSO90%cornoilSolubility:≥1.67mg/mL(3.79mM);Clearsolution此⽅案可获得≥1.67mg/mL(3.79mM，饱和度未知)的澄溶液，此⽅案不适⽤于实验周期在半个⽉以上的实验。4.以1mL⼯作液为例，取100μL16.699999mg/mL的澄DMSO储备液加到900μL⽟⽶油中，混合均匀。请依序添加每种溶剂：5%DMSO40%PEG3005%Tween-8050%salineSolubility:≥2.5mg/mL(5.67mM);ClearsolutionBIOLOGICALACTIVITY⽣物活性Ravoxertinib(GDC-0994)可⼝服的ERK激酶抑制剂，抑制ERK1和ERK2的IC50分别为6.1nM和3.1nM。IC50&TargetERK2ERK1p-RSK3.1nM(IC50)6.1nM(IC50)12nM(IC50)体外研究Ravoxertinib(GDC-0994)alsoinhibitsp90RSKwithanIC50of12nM[1].Ravoxertinib(GDC-0994)ishighlyselectiveforERK1andERK2,withbiochemicalpotencyof1.1nMand0.3nM,respectively[2].Ravoxertinib(GDC0994;50nM,0.5µM,and5µM;48hours)decreasestheviabilityoflungadenocarcinomacelllines(A549,HCC827,HCC4006)[3].体内研究InCD-1mice,a10mg/kgoraldoseofRavoxertinib(GDC-0994)issufficienttoachievethedesiredtargetcoverageforatleast8h[1].Daily,oraldosingofRavoxertinibresultsinsignificantsingle-agentactivityinmultipleinvivocancermodels,includingKRAS-mutantandBRAF-mutanthumanxenografttumorsinmice[2].PROTOCOLAnimalMice[1]Administration[1]PK/PDdataforRavoxertinib(GDC-0994)intheHCT116mousexenograftmodel.HCT116tumorsareestablishedinnudemicetoatumorvolumeof400-600mm3.Micearetreatedwithasingleoraldoseof22at15,30,or100mg/kgversusvehiclecontrolalone(40%PEG400/60%(10%HPβCD))followbytumorandplasmacollectionat2,8,16,and24hpostdose.Tumorlevelsofphosphorylatedp90RSK(pRSK)relativetotalp90RSK(tRSK)aremeasuredbyquantitativeWesternblotandarenormalizedtovehiclecontrolat2hpostdose(setto100%).PlasmaandtumorconcentrationsaremeasuredbyLC−MS.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.户使⽤本产品发表的科研⽂献2/3www.MedChemEwww.MedChemE•Cell.2018Sep20;175(1):186-199.e19.•SciTranslMed.2021Jan27;13(578):eaba7308.•EnvironPollut.2021Jan1;268(PtB):115748.•MolOncol.2020Nov;14(11):2894-2919.•Cancer.2020Mar15;126(6):1339-1350.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].BlakeJF,etal.Discoveryof(S)-1-(1-(4-Chloro-3-fluorophenyl)-2-hydroxyethyl)-4-(2-((1-methyl-1H-pyrazol-5-yl)amino)pyrimidin-4-yl)pyridin-2(1H)-one(GDC-0994),anExtracellularSignal-RegulatedKinase1/2(ERK1/2)InhibitorinEarlyClinicalDevelopme[2].KirkRobarge,etal.AbstractDDT02-03:DiscoveryofGDC-0994,apotentandselectiveERK1/2inhibitorinearlyclinicaldevelopment.Proceedings:AACRAnnualMeeting2014;April5-9,2014.[3].MICHAELLAI.OpportunityforPharmaceuticalInterventioninLungCancer:SelectiveInhibitionofJAK1/2toEliminateEMT-DerivedMesenchymalCells.McePdfHeight关注MCE中国公众号，

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