Forskolin-DataSheet-生命科學試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?Agonists?ScreeningLibrarieswww.MedChemEForskolinCat.No.:HY-15371CASNo.:66575-29-9分?式:C??H??O?分?量:410.5作?靶點:AdenylateCyclase;FXR;Autophagy作?通路:GPCR/GProtein;MetabolicEnzyme/Protease;Autophagy儲存?式:4°C,protectfromlight*Insolvent:-80°C,6months;-20°C,1month(protectfromlight)溶解性數(shù)據(jù)體外實驗DMSO:100mg/mL(243.61mM;Needultrasonic)掃描?維碼，H2O:<0.1mg/mL(insoluble)運?溶解?案計算器獲得適合您實驗體系的溶解?案MassSolvent1mg5mg10mgConcentration制備儲備液1mM2.4361mL12.1803mL24.3605mL5mM0.4872mL2.4361mL4.8721mL10mM0.2436mL1.2180mL2.4361mL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，并請注意儲備液的保存?式和期限。體內(nèi)實驗請根據(jù)您的實驗動物和給藥?式選擇適當?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，適當保存；體內(nèi)實驗的?作液，建議您現(xiàn)?現(xiàn)配，當天使?；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.請依序添加每種溶劑：10%DMSO40%PEG3005%Tween-8045%salineSolubility:≥2.5mg/mL(6.09mM);Clearsolution此?案可獲得≥2.5mg/mL(6.09mM，飽和度未知)的澄溶液。以1mL?作液為例，取100μL25.0mg/mL的澄DMSO儲備液加到400μLPEG300中，混合均勻；向上述2.體系中加?50μLTween-80，混合均勻；然后繼續(xù)加?450μL?理鹽?定容?1mL。請依序添加每種溶劑：10%DMSO90%cornoil1/4www.MedChemEwww.MedChemESolubility:≥2.5mg/mL(6.09mM);Clearsolution此?案可獲得≥2.5mg/mL(6.09mM，飽和度未知)的澄溶液，此?案不適?于實驗周期在半個?以上的實驗。以1mL?作液為例，取100μL25.0mg/mL的澄DMSO儲備液加到900μL??油中，混合均勻。BIOLOGICALACTIVITY?物活性Forskolin(Coleonol)?種有效的腺苷酸環(huán)化酶(adenylatecyclase)激活劑，對于I型腺苷酸環(huán)化酶，IC50為41nM，EC50為0.5μM。Forskolin也?種細胞內(nèi)cAMP形成的誘導劑。Forskolin誘導多種細胞類型的分化并激活孕烷X受體(PXR)和FXR。Forskolin對?臟產(chǎn)?正性肌?作?，并具有??板抗凝集和降壓作?。Forskolin也可誘導細胞?噬(autophagy)。IC50&TargetIC50:41nM(Adenylylcyclase)[1]EC50:0.5μM(Adenylylcyclase)[1]體外研究Forskolin(Coleonol)isalsoapotentexosomebiogenesisand/orsecretionactivatorinprostatecancer(PC)cells[8].Forskolin(Fsk)isanaturallyoccurringditerpeneisolatedfromColeusforskholii,directlyactivatesadenylylcyclase(AC)throughitscatalyticsubunittoincreaseintracellularlevelsofcyclicadenosinemonophosphate(cAMP)[1].Forskolin(Fsk)affectstheproliferationofthehumanT-celllinessuchasKit225andMT-2.ForskolintreatmentinhibitstheproliferationofbothKit225andMT-2cellsinadose-dependentmannerwithanIC50equalto~5μMFsk.Forskolintreatment(10-100μM)increasescAMPilevels~5-to20-foldabovebasallevels,whichreachemaximumlevelsbetween50-100μMForskolin[6].體內(nèi)研究TheForskolin(Coleonol)-treatedMrp4-/-miceshowsanincreasednumberofKi67-positiveandcleavedcaspase3-positiveECs,asignificantdecreaseintheamountofpericytecoverage,andareducednumberofemptysleeves.Inpupsexposedtohyperoxia(75%oxygen)fromP7toP12,theMrp4-/-miceshowsasignificantincreaseintheunvascularizedretinalarea[2].Theaveragebloodglucoseinthehealthyratgroupis102.12±1.94mg/dL,101.25±3.56forcontrolgroupand103±2.08inforskolingroup.Thedatashowsthatglucoselevelsattheendofthestudyarelowerinforskolingroup,withasignificantdifferenceaccordingtothestatisticaltestsapplied(p=0.03)[7].PROTOCOLCellAssay[2]QuiescentKit225orMT-2cellsareseededinto96-wellplatesat5×104cellsperwell.Cellsarethenpretreatedfor1hwith1%DMSO(vehicle)orForskolinat1,5,10,25,50,and100μMconcentrations.ThecellsarestimulatedwithIL-2andculturedforanadditional20hat37°C.Controlcellsaretreatedwith1%DMSOfor20h.Duringthefinal4hofincubation,thecellsarepulsedwith[3H]thymidineataconcentrationof0.5μCi/200μL.Cellsareharvestedontofiberglassfiltersandanalyzedusingliquidscintillationcounting[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMice[3]2/4www.MedChemEwww.MedChemEAdministration[3][4]C57BL/6Jmiceareused.Mrp4-knockoutmice,whichareestablishedandrepeatedlybackcrossedtotheC57BL/6Jmice.Forskolinisinjectedintraperitoneallyintoneonatalmiceatpostnataldays4(P4)and5(P5).MiceinjectedwithDMSOserveasthecontrols.ThetreatedmiceareeuthanizedatP6,andtheirretinasareisolatedforwhole-mountimmunohistochemistry(IHC).TheeffectofdifferentconcentrationsofForskolinonthesurvivalrateandretinalvasculatureisfirsttested,andtheoptimalconcentrationisdetermined,1.0μg/50μL(0.3mg/kg)atP4and1.5μg/50μL(0.5mg/kg)atP5,usedtocomparetheretinalvascularphenotypesbetweenWTmiceandMrp4-deficientmice.Rats[4]MaleWistarrats,aged10-14weeksold,withameanweightof300g±50g,aredividedintofourgroups;19areexperimentallyinducedtodevelopdiabetes,and8aremaintainedinahealthycondition.BothdiabeticandhealthyratsreceivenoForskolin(control),or6mg/kgperdayofForskolin,administeredorallyfor8weeks.BloodglucoselevelsaredeterminedineachgroupbeforeandafterForskolintreatment.Thediabeticratsaretestedtwoweeksafterconfirmingthepresenceofdiabetes(threeweeksaftertheinduction)andaftereightweeksofthedesignatedtreatment.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻?SciTranslMed.2020May6;12(542):eaba0769.?SignalTransductTargetTher.2021Feb28;6(1):91.?Biomaterials.2018Dec6;193:30-46.?BrJPharmacol.2019Aug;176(16):2962-2976.?JExpClinCancerRes.2019Sep13;38(1):404.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].RobbinsJD,etal.Forskolincarbamates:bindingandactivationstudieswithtypeIadenylylcyclase.JMedChem.1996Jul5;39(14):2745-52.[2].RodriguezG,etal.Forskolin-induciblecAMPpathwaynegativelyregulatesT-cellproliferationbyuncouplingtheinterleukin-2receptorcomplex.JBiolChem.2013Mar8;288(10):7137-46.[3].MatsumiyaW,etal.ForskolinmodifiesretinalvasculardevelopmentinMrp4-knockoutmice.InvestOphthalmolVisSci.2012Dec7;53(13):8029-35.[4].Ríos-SilvaM,etal.Effectofchronicadministrationofforskolinonglycemiaandoxidativestressinratswithandwithoutexperimentaldiabetes.IntJMedSci.2014Mar11;11(5):448-52.[5].MayatiA,etal.FunctionalpolarizationofhumanhepatomaHepaRGcellsinresponsetoforskolin.SciRep.2018Oct31;8(1):16115.[6].AwadJA,etal.Interactionsofforskolinandadenylatecyclase.EffectsonsubstratekineticsandprotectionagainstinactivationbyheatandN-ethylmaleimide.JBiolChem