Costunolide-plus-Costunolide-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemECostunolideCat.No.:HY-N0036CASNo.:553-21-9Synonyms:(+)-Costunolide;Costuslactone分?式:C??H??O?分?量:232.32作?靶點:Apoptosis;EndogenousMetabolite作?通路:Apoptosis;MetabolicEnzyme/Protease儲存?式:-20°C,sealedstorage,awayfrommoistureandlight*Insolvent:-80°C,6months;-20°C,1month(sealed

storage,awayfrommoistureandlight)溶解性數(shù)據(jù)體外實驗DMSO:≥49mg/mL(210.92mM)Ethanol:25mg/mL(107.61mM;ultrasonicandwarmingandheatto60°C)*"≥"meanssoluble,butsaturationunknown.MassSolvent1mg5mg10mgConcentration制備儲備液1mM4.3044mL21.5220mL43.0441mL5mM0.8609mL4.3044mL8.6088mL10mM0.4304mL2.1522mL4.3044mL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(sealedstorage,awayfrommoistureandlight)。-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、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1/4MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE1.請依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.08mg/mL(8.95mM);Clearsolution2.請依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.08mg/mL(8.95mM);Clearsolution3.請依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.08mg/mL(8.95mM);Clearsolution4.請依序添加每種溶劑：10%EtOH>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.5mg/mL(10.76mM);Clearsolution5.請依序添加每種溶劑：10%EtOH>>90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(10.76mM);Clearsolution6.請依序添加每種溶劑：10%EtOH>>90%cornoilSolubility:≥2.5mg/mL(10.76mM);ClearsolutionBIOLOGICALACTIVITY?物活性Costunolide((+)-Costunolide)?種天然的倍半萜內(nèi)酯，它具有抗氧化、抗炎、抗過敏、?重塑、神經(jīng)保護、促進?發(fā)?長、抗癌和抗糖尿病的特性。Costunolide可誘導(dǎo)乳腺癌細胞周期阻滯和凋亡(apoptosis)[1][2][3]。IC50&TargetHumanEndogenousMetabolite體外研究Costunolideinhibitsthecolonyformation,migrativeandinvasiveabilitiesoftheH1299cellsinadoseortimedependentmanner[2].Costunolide(6.7-215.2μM;24hours)inhibitstheviabilityofH1299cellsinadose-dependentmanner,withanIC50of23.93μM[2].Costunolide(12.0-48.0μM;48hours)inducesapoptosisinH1299cells[2].Costunolide(12-48.0μM;6-12hours)regulatesmetastasis-andproliferation-associatedmRNAexpression[2].Costunolideregulatesepithelial-to-mesenchymaltransition(EMT)-associatedproteinexpression[2].Costunolideregulatesc-Mycmediatedapoptosissignalingand14-3-3-mediatedsignalingpathwaysinbreastcancercells[3].CellViabilityAssay[2]CellLine:H1299cellsConcentration:6.7μM,13.5μM,26.9μM,107.6μM,215.2μMIncubationTime:24hoursResult:InhibitedtheviabilityofH1299cells(MTTassay).ApoptosisAnalysis[2]2/4MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemECellLine:H1299cellsConcentration:0μM,12.0μM,24.0μM,48.0μMIncubationTime:48hoursResult:Significantlypromotedapoptosisat24.0μMand48.0μM.RT-PCR[2]CellLine:H1299cellsConcentration:0μM,12.0μM,24.0μM,48.0μMIncubationTime:6hours,12hoursResult:Regulatedthemetastasis-andproliferation-associatedmRNAlevelsinadose-dependentmanner.WesternBlotAnalysis[2]CellLine:H1299cellsConcentration:0μM,12.0μM,24.0μM,48.0μMIncubationTime:48hoursResult:SignificantlyinhibitedtheEMTofH1299cells.體內(nèi)研究Costunolide(20?mg/kg;i.p;daily;for30days)inhibitsbreastcancerthroughc-Myc/p53andAKT/14-3-3pathway[3].AnimalModel:4weeksoldfemaleBALB/cnudemice,MDA-MB-231cellsxenograftmousemodels[3]Dosage:20?mg/kgAdministration:Intraperitonealinjection,daily,for30daysResult:Reducedtheexpressionlevelsofc-Mycandp-AKTandelevatedtheexpressionlevelsofp53andp-14-3-3.戶使?本產(chǎn)品發(fā)表的科研?獻?CellMolBiolLett.2019Aug14;24:52.?Molecules.2020Jun19;25(12):2840.?Gene.2018Dec15;678:261-269.3/4MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESeemorecustomervalidationsonwww.MedChemEREFERENCES[1].DaeYongKim,etal.Costunolide-ABioactiveSesquiterpeneLactonewithDiverseTherapeuticPotential.IntJMolSci.2019Jun;20(12):2926.[2].MinyanWei,etal.CostunolideinducesapoptosisandinhibitsmigrationandinvasioninH1299lungcancercells.OncolRep.2020Jun;43(6):1986-1994.[3].ZhangxiaoPeng,etal.Costunolideanddehydrocostuslactonecombinationtreatmentinhibitbreastcancerbyinducingcellcyclearrestandapoptosisthroughc-Myc/p53andAKT/14-3-3pathway.Sci