CP-24879-hydrochloride-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemECP-24879hydrochlorideCat.No.:HY-115319CASNo.:10141-51-2分⼦式:C₁₁H₁₈ClNO分⼦量:215.72作⽤靶点:Others;Ferroptosis作⽤通路:Others;Apoptosis储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据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>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.08mg/mL(9.64mM);Clearsolution2.请依序添加每种溶剂：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.08mg/mL(9.64mM);ClearsolutionBIOLOGICALACTIVITY⽣物活性CP-24879(hydrochloride)⼀种有效且选择性的delta5D/delta6D联合抑制剂。CP-24879(hydrochloride)能显著降低肝细胞内脂质积聚和炎症损伤。CP-24879(hydrochloride)在脂-1和ω-3处理的肝细胞中表现出优越的抗脂变性和抗炎作⽤，可⽤于⾮精性脂性肝炎的研究[1][2]。IC50&TargetIC50:0.015μM(delta6DinABMC-7cells),0.56μM(delta6DinLivermicrosomes),0.67μM(delta5DinABMC-7cells),3.4μM(delta5DinABMC-7cells)[1]体外研究CP-24879(hydrochloride)(0-10μM,4days)inhibitsΔ6+Δ5desaturaseactivitiesinaconcentration-1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEdependentmanner,withaconcentration-dependentdepletionofAAanddecreaseinLTC4production[1].CP-24879(hydrochloride)(0-10μM,16h)showstheinhibitoryresponsesonoleicacid-inducedtriglycerideaccumulationinhepatocytes[2].CP-24879(hydrochloride)(0-10μM,16h)blocksLPS-inducedexpressionofinflammatorycytokinesinaconcentration-dependentmanner[2].CP-24879(hydrochloride)(0-2μM,4h)inhibitsdesaturaseactivityandamelioratesferroptosis[3].CellViabilityAssayCellLine:MousemastocytomaABMC-7cells[1]Concentration:0,100nM,300nM,1μM,3μM,and10μMIncubationTime:4daysResult:InhibitedΔ6+Δ5desaturaseactivitiesinaconcentration-dependentmanner,withaconcentration-dependentdepletionofAAanddecreaseinLTC4(LeukotrieneC4)production,anddidnotinhibiteither5-lipoxygenaseorLTC4synthaseactivity.体内研究CP-24879(hydrochloride)(3mg/kg,IP,threetimesaday,for6or4days)inhibitsΔ6+Δ5desaturaseactivitiesinvivo,causingdepletionofAAintheliversofchow-fedmiceandpreventingrepletionofAAintheliversofEFADmice[1].CP-24879(hydrochloride)(33mg/kg,IV,once)isclearedquiterapidlyandhasarelativelyshorthalf-life[1].AnimalModel:Chow-fedandEFADBalb/Cmice(N=5/group)[1]Dosage:3mg/kgAdministration:IP,threetimesaday,for6or4daysResult:Inhibitedapproximately80%combinedΔ6+Δ5desaturaseactivities,causingdepletionofAAintheliversofchow-fedmiceandpreventingrepletionofAAintheliversofEFADmice,andincreasedOAandLA,withahigherratioofLA/AAintheliversofmiceinjectedwithCP-24879versussaline(4.70vs2.00,Chow-fedmice;2.46vs1.40,EFADmice;respectively).AnimalModel:Swiss-Webstermice(male,25g)[1]Dosage:33mg/kgAdministration:IVinthetailvein,once(PharmacokineticAnalysis)Result:Wasreadilydistributedtotheperipheraltissues,withthevolumeofdistribution(V)of1.9mL/g,wasclearedquiterapidly(CL=0.56mL/min)andhadarelativelyshorthalf-life(T1/2=59min).REFERENCES2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE[1].ObukowiczMG,etal.Identificationandcharacterizationofanoveldelta6/delta5fattyaciddesaturaseinhibitorasapotentialanti-inflammatoryagent.BiochemPharmacol.1998Apr1;55(7):1045-58.[2].[2]López-VicarioC,etal.MolecularinterplaybetweenΔ5/Δ6desaturasesandlong-chainfattyacidsinthepathogenesisofnon-alcoholicsteatohepatitis.Gut.2014Feb;63(2):344-55.[3].[3]LeeJY,NamM,SonHY,etal.Polyunsaturatedfattyacidbiosynthesispathwaydeterminesferroptosissensitivityingastriccancer.ProcNatlAcadSciUSA.2020;117(51):32433-32442.McePdfHeightCa