Mitochonic-acid-5-MA-5-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEMitochonicacid5Cat.No.:HY-111536CASNo.:1354707-41-7Synonyms:MA-5分⼦式:C₁₈H₁₃F₂NO₃分⼦量:329.3作⽤靶点:MitochondrialMetabolism作⽤通路:MetabolicEnzyme/Protease储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验DMSO:≥106.66mg/mL(323.90mM)H2O:<0.1mg/mL(insoluble)*"≥"meanssoluble,butsaturationunknown.MassSolvent1mg5mg10mgConcentration制备储备液1mM3.0367mL15.1837mL30.3674mL5mM0.6073mL3.0367mL6.0735mL10mM0.3037mL1.5184mL3.0367mL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1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE、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:≥2.5mg/mL(7.59mM);Clearsolution2.请依序添加每种溶剂：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(7.59mM);Clearsolution3.请依序添加每种溶剂：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(7.59mM);ClearsolutionBIOLOGICALACTIVITY⽣物活性Mitochonicacid5与线粒体结合，并改肾⼩管和⼼肌细胞损伤。Mitochonicacid5调节线粒体ATP合成。IC50&TargetMitochondrialMetabolism[1]体外研究Mitochonicacid5(MA-5)modulatesmitochondrialATPsynthesisindependentlyofoxidativephosphorylationandtheelectrontransportchain.MitochondrialdysfunctioncausesincreasedoxidativestressanddepletionofATP,whichareinvolvedintheetiologyofavarietyofrenaldiseases[1].Mitochonicacid5(MA-5),whichisderivedfromtheplantgrowthhormoneindole-3-aceticacid,canprotectmitochondrialfunctionbyregulatingenergymetabolismandreducingmitochondrialoxidativestress.ToobservetheprotectiveroleofMitochonicacid5inmicrogliaunderinflammatoryconditions,TNFαisapplied.Subsequently,theMTTassayisusedtoevaluatecellviability.InresponsetotheTNFαtreatment,cellviabilitysignificantlydecreases.However,thiseffectisdose-dependentlyinhibitedbyMitochonicacid5treatment[2].体内研究AdministrationofMitochonicacid5(MA-5)toanischemia-reperfusioninjurymodelandacisplatin-inducednephropathymodelimprovedrenalfunction.Toexaminethetissue-protectiveeffectofMitochonicacid5,theoralbioavailabilityisexamined.OraladministrationofMitochonicacid5increasestheplasmaconcentrationinadose-responsemanneratthepeaktimeof1hour[1].PROTOCOLCellAssay[2]ThemouseBV-2cellsusedinthisstudyareculturedinL-DMEMsupplementedwith10%fetalbovineserum(FBS)at37°Cinanatmospherewith5%CO2.Toinduceinflammatoryinjury,cellsaretreatedwith10ng/mLTNFαforabout12h.Mitochonicacid5(0-10μM)isincubatedwithBV-2cellsforabout12hwithTNFαtreatment[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMice[1]Administration[1]ForevaluationofthebloodconcentrationsofMitochonicacid5(MA-5),Mitochonicacid5isorallyadministeredatdosesof25,50,or150mg/kgtoC57/BL6mice,andbloodsamplesarecollectedatthedesignatedtimes.After1hour,themiceareeuthanized.ThebloodconcentrationofMitochonicacid5isdeterminedbyLC/MS/MS[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE户使⽤本产品发表的科研⽂献•CellDeathDis.2022Jun20;13(6):557.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].SuzukiT,etal.MitochonicAcid5BindsMitochondriaandAmelioratesRenalTubularandCardiacMyocyteDamage.JAmSocNephrol.2016Jul;27(7):1925-32.[2].LeiQ,etal.Mitochonicacid5activatestheMAPK-ERK-yapsignalingpathwaystoprotectmousemicroglialBV-2cellsagainstTNFα-inducedapoptosisviaincreasedBnip3-relatedmitophagy.CellMolBiolLett.2018Apr5;23:14.McePdf