Medchemexpress/(+)-MK 801 Maleate(Synonyms: Dizocilpine maleate; Dizocilpine hydrogen maleate; (+)-MK 801; MK 801)/HY-15084/1-免疫在线蚂蚁淘旗下平台

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商品详细Medchemexpress/(+)-MK 801 Maleate(Synonyms: Dizocilpine maleate; Dizocilpine hydrogen maleate; (+)-MK 801; MK 801)/HY-15084/1

Medchemexpress/(+)-MK 801 Maleate(Synonyms: Dizocilpine maleate; Dizocilpine hydrogen maleate; (+)-MK 801; MK 801)/HY-15084/1

商品编号： HY-15084-10mM*1mLinDMSO

品牌： MedChemExp

市场价： ¥1320.00

美元价： 792.00

产地：美国(厂家直采)

公司：

产品分类：小分子

公司分类： Small_molecule

联系Q Q： 3392242852

电话号码： 4000-520-616

电子邮箱： info@ebiomall.com

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商品介绍

(+)-MK801(Maleate)isapotent,selectiveandnon-competitive NMDA receptorantagoNISTwith K_d of37.2nMinratbrainmembranes.

CustomerValidation

•Neuroreport.2017May24;28(8):444-450.

Description	(+)-MK801(Maleate)isapotent,selectiveandnon-competitive NMDA receptorantagonistwith K_d of37.2nMinratbrainmembranes.
IC₅₀&Target	Ki:30.5nM
InVitro	[³H]MK-801labelshigh-affinitybindingsitesinratcerebralcorticalmembranesinasaturablemanner.MK-801producesapotentblockadeofdepolarizingresponsestoNMDAinratcerebralcorticalslices.Theonlycompoundsthatareabletocompetefor[³H]MK-801bindingsitesaresubstancesknowntoblocktheresponsesofexcitatoryaminoacidsmediatedbytheNMDAreceptorsubtype^[1].MK-801inhibitsN-methyl-D-aspartate-induced[³H]norepinephrine(NE)releaseand[³H]TCPbindinginthehippocampuswithIC₅₀of20nMand9nM,respectively^[2]. MK-801causesaprogressive,long-lastingblockadeofcurrentinducedbyNMDA.Mg²⁺ (10mM)preventsMK-801fromblockingtheN-Me-D-Asp-inducedcurrent,evenwhenMK-801isappliedforalongtimeinthepresenceofNMDA.MK-801isalsoeffectiveatblockingNMDA-activatedsingle-channelactivityinoutside-outpatches^[3]. MK-801(<500=""μm)=""prevents=""lps-induced=""activation=""of=""microglia=""in=""a=""concentration-dependent=""manner=""with=""increased=""cox-2=""protein=""expression=""in=""bv-2=""cells.=""mk-801=""><500=""μm)=""reduces=""microglial=""tnf-α=""output=""with="">₅₀of400μMinBV-2cells^[4].
InVivo	TreatmentofmicewithMK-801(1mg/kg)beforeeachMETHinjectionreducestheextentofDAdepletionby55%instriatalofmice.MK-801(1mg/kg)attenuatestheeffectsofMETHonmicroglialactivationinstriatalofmice^[4].MK-801(0.05mg/kgor0.2mg/kg,i.p.)inratsjustpriortoreactivationofthecocaine-associatedmemoryintheCPPcontextattenuatessubsequentcocaine-primedreinstatement,whilenodisruptionoccurresinratsthatdonotreceivereactivationintheCPPcontext.MK-801(0.2mg/kg,i.p.)priortotworeactivationsessionsinthehomecagedoesnotsuppresssubsequentcocaine-primedreinstatement^[5].
References	[1].WongEH,etal.TheanticonvulsantMK-801isapotentN-methyl-D-aspartateantagonist.ProcNatlAcadSciUSA.1986Sep;83(18):7104-8. [2].SnellLD,etal.ComparisonoftheeffectsofMK-801andphencyclidineoncatecholamineuptakeandNMDA-inducednorepinephrinerelease.EurJPharmacol.1988Jan12;145(2):223-6. [3].HuettnerJE,etal.BlockofN-methyl-D-aspartate-activatedcurrentbytheanticonvulsantMK-801:selectivebindingtoopenchannels.ProcNatlAcadSciUSA.1988Feb;85(4):1307-11. [4].ThomasDM,etal.MK-801anddextromethorphanblockmicroglialactivationandprotectagainstmethamphetamine-inducedneurotoxicity.BrainRes.2005Jul19;1050(1-2):190-8. [5].BrownTE,etal.TheNMDAantagonistMK-801disruptsreconsolidationofacocaine-associatedmemoryforconditionedplacepreferencebutnotforself-administrationinrats.LearnMem.2008Dec2;15(12):857-65. [6].JiangL,etal.Decreaseofgrowthanddifferentiationfactor10contributestoneuropathicpainthroughN-methyl-D-aspartatereceptoractivation.Neuroreport.2017May24;28(8):444-450.

PreparingStockSolutions

ConcentrationVolumeMass	1mg	5mg	10mg

1mM	2.9641mL	14.8205mL	29.6410mL
5mM	0.5928mL	2.9641mL	5.9282mL
10mM	0.2964mL	1.4821mL	2.9641mL

Pleaserefertothesolubilityinformationtoselecttheappropriatesolvent.

KinaseAssay
^[1]

CerebralcorticesfrommaleSprague-Dawleyrats(200-300g)arehomogenizedin9volumesofice-cold0.32mol/LsucrosebyninestrokeswithaTeflon/glasshomogenizerat500rpm.Thehomogenateiscentrifugedfor10minat1×10³g,andthesupernatantisrecentrifugedat1×10⁴gfor20minat4°C.ThepelletissUSPendedinassaybuffer(118mMNaCl/4.7mMKCl/1.2mMMgSO₄/5mMNaHCO₃/20mMHepes/1.2mMKH₂PO₄/2.5mMCaCl₂/11mMglucose,pH7.4)andincubatedat23°Cfor20minpriortofinalcentrifugationat1×10³gfor20minat4°C.Thepelletisresuspendedinassaybuffer(70mLpergramoforiginaltissue).Bindingof[³H]MK-801ismeasuredbyincubating750μLduplicatealiquotsofthiscrudemembranesuspension(=0.75mgofprotein)with100μLofbuffercontainingdisplacerorofbufferalone(totalbinding),100μLof50nM[³H]MK-801,and50μLofbufferfor60minat23°C.Nonspecificbindingisdefinedby100μM(finalconcentration)unlabeledMK-801.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

AnimalAdministration
^[5]

MK-801isformulatedinsaline.

AnimalsaregivensalineorMK-801followedbycocaine30minlaterinthehomecageinsteadofintheCPPapparatusforthetwodaysof“reactivation.”Thisisdonetodeterminewhetherreactivationofthememoryforthecocaine-associatedcontextbycocaineintheCPPcontextisnecessaryfortheABIlityofMK-801todisruptreconsolidation.Animalsundergopreconditioning,conditioning,testing,andextinctionbutanimalsareinjectedwithsalineorMK-801(0.20mg/kg,i.p.)30minpriortoacocaineinjection(10mg/kg,i.p.)inthehomecage.Animalsremaininthehomecages,andthenextday,theprocedurefromthefirstdayofreactivationisrepeated.Thefollowingday,animalsaretestedforcocaine-primedreinstatementintheirCPPboxwithoutanypriormicroinjectionofsalineorMK-801.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

References

[1].WongEH,etal.TheanticonvulsantMK-801isapotentN-methyl-D-aspartateantagonist.ProcNatlAcadSciUSA.1986Sep;83(18):7104-8.
[2].SnellLD,etal.ComparisonoftheeffectsofMK-801andphencyclidineoncatecholamineuptakeandNMDA-inducednorepinephrinerelease.EurJPharmacol.1988Jan12;145(2):223-6.
[3].HuettnerJE,etal.BlockofN-methyl-D-aspartate-activatedcurrentbytheanticonvulsantMK-801:selectivebindingtoopenchannels.ProcNatlAcadSciUSA.1988Feb;85(4):1307-11.
[4].ThomasDM,etal.MK-801anddextromethorphanblockmicroglialactivationandprotectagainstmethamphetamine-inducedneurotoxicity.BrainRes.2005Jul19;1050(1-2):190-8.
[5].BrownTE,etal.TheNMDAantagonistMK-801disruptsreconsolidationofacocaine-associatedmemoryforconditionedplacepreferencebutnotforself-administrationinrats.LearnMem.2008Dec2;15(12):857-65.
[6].JiangL,etal.Decreaseofgrowthanddifferentiationfactor10contributestoneuropathicpainthroughN-methyl-D-aspartatereceptoractivation.Neuroreport.2017May24;28(8):444-450.

MolecularWeight

337.37

Formula

C₂₀H₁₉NO₄

CASNo.

77086-22-7

Storage

Powder	-20°C	3years
	4°C	2years
Insolvent	-80°C	6months
	-20°C	1month

Shipping

RoomtemperatureincontinentalUS;mayvaryelsewhere

Solvent&Solubility

10mMinDMSO;Ethanol：6mg/mL;H₂O：<0.6="">

MK-801isdissolvedin1%dimethylsulfoxideanddilutedwithpreservative-freenormalsalineataconcentrationof2μg/μL^[6].

*"<1 mg/ml"="" means="" slightly="" soluble="" or="" insoluble.="" "≥"="" means="" soluble,="" but="" saturation="">

References

[1].WongEH,etal.TheanticonvulsantMK-801isapotentN-methyl-D-aspartateantagonist.ProcNatlAcadSciUSA.1986Sep;83(18):7104-8.
[2].SnellLD,etal.ComparisonoftheeffectsofMK-801andphencyclidineoncatecholamineuptakeandNMDA-inducednorepinephrinerelease.EurJPharmacol.1988Jan12;145(2):223-6.
[3].HuettnerJE,etal.BlockofN-methyl-D-aspartate-activatedcurrentbytheanticonvulsantMK-801:selectivebindingtoopenchannels.ProcNatlAcadSciUSA.1988Feb;85(4):1307-11.
[4].ThomasDM,etal.MK-801anddextromethorphanblockmicroglialactivationandprotectagainstmethamphetamine-inducedneurotoxicity.BrainRes.2005Jul19;1050(1-2):190-8.
[5].BrownTE,etal.TheNMDAantagonistMK-801disruptsreconsolidationofacocaine-associatedmemoryforconditionedplacepreferencebutnotforself-administrationinrats.LearnMem.2008Dec2;15(12):857-65.
[6].JiangL,etal.Decreaseofgrowthanddifferentiationfactor10contributestoneuropathicpainthroughN-methyl-D-aspartatereceptoractivation.Neuroreport.2017May24;28(8):444-450.

Purity:99.98%

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