Mitochonic-acid-5-MA-5-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEMitochonicacid5Cat.No.:HY-111536CASNo.:1354707-41-7Synonyms:MA-5分?式:C??H??F?NO?分?量:329.3作?靶點:MitochondrialMetabolism作?通路:MetabolicEnzyme/Protease儲存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實驗DMSO:≥106.66mg/mL(323.90mM)H2O:<0.1mg/mL(insoluble)*"≥"meanssoluble,butsaturationunknown.MassSolvent1mg5mg10mgConcentration制備儲備液1mM3.0367mL15.1837mL30.3674mL5mM0.6073mL3.0367mL6.0735mL10mM0.3037mL1.5184mL3.0367mL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(fù)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(dāng)?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(dāng)保存；體內(nèi)實驗的?作液，建議您現(xiàn)?現(xiàn)配，當(dāng)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1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE、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>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.5mg/mL(7.59mM);Clearsolution2.請依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(7.59mM);Clearsolution3.請依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(7.59mM);ClearsolutionBIOLOGICALACTIVITY?物活性Mitochonicacid5與線粒體結(jié)合，并改腎?管和?肌細(xì)胞損傷。Mitochonicacid5調(diào)節(jié)線粒體ATP合成。IC50&TargetMitochondrialMetabolism[1]體外研究Mitochonicacid5(MA-5)modulatesmitochondrialATPsynthesisindependentlyofoxidativephosphorylationandtheelectrontransportchain.MitochondrialdysfunctioncausesincreasedoxidativestressanddepletionofATP,whichareinvolvedintheetiologyofavarietyofrenaldiseases[1].Mitochonicacid5(MA-5),whichisderivedfromtheplantgrowthhormoneindole-3-aceticacid,canprotectmitochondrialfunctionbyregulatingenergymetabolismandreducingmitochondrialoxidativestress.ToobservetheprotectiveroleofMitochonicacid5inmicrogliaunderinflammatoryconditions,TNFαisapplied.Subsequently,theMTTassayisusedtoevaluatecellviability.InresponsetotheTNFαtreatment,cellviabilitysignificantlydecreases.However,thiseffectisdose-dependentlyinhibitedbyMitochonicacid5treatment[2].體內(nèi)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?邊的抑制劑?師www.MedChemE戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?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