Medchemexpress/Reparixin(Synonyms: Repertaxin; DF 1681Y)/HY-15251/10mg-免疫在线蚂蚁淘旗下平台

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商品详细Medchemexpress/Reparixin(Synonyms: Repertaxin; DF 1681Y)/HY-15251/10mg

Medchemexpress/Reparixin(Synonyms: Repertaxin; DF 1681Y)/HY-15251/10mg

商品编号： HY-15251-10mM*1mLinDMSO

品牌： MedChemExp

市场价： ¥3360.00

美元价： 2016.00

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

ReparixinisapotentinhibitorofbothCXCL8receptorsCXCR1/2,itinhibitsweaklyCXCR2-mediatedcellmigration(IC₅₀=100nM),whereasitstronglyblocksCXCR1-mediatedchemotaxis(IC₅₀=1nM).

CustomerValidation

•AnnRheumDis.2016Apr;75(4):730-8.
•NatCommun.2017May26;8:15584.
•CellDeathDis.2017Jul13;8(7):e2932.
•StemCells.2015Dec;33(12):3558-68.
•BiochimBiophysActa.2017Jan;1863(1):220-230.
•Oncotarget.2017Jul21;8(36):60210-60222.

•Oncogenesis.2016Jun13;5(6):e234.
•JGastroenterolHepatol.2017May8.
•VetImmunolImmunopathol.2016Dec;182:52-58.

Description	ReparixinisapotentinhibitorofbothCXCL8receptorsCXCR1/2,itinhibitsweaklyCXCR2-mediatedcellmigration(IC₅₀=100nM),whereasitstronglyblocksCXCR1-mediatedchemotaxis(IC₅₀=1nM).
IC₅₀&Target	IC50:5.6/80nM(CXCR1^wt/CXCR1^Ile43Val,inL1.2cell)^[1]
InVitro	ReparixinisapotentfunctionalinhibitorofCXCL8-inducedBIOLOGicalactivitiesonhumanPMNswithamarkedselectivity(around400-fold)forCXCR1,asshowninspecificexperimentsonCXCR1/L1.2andCXCR2/L1.2transfectedcellsandonhumanPMNs.TheefficacyofReparixinissignificantlylowerinL1.2cellsexpressingIle43ValCXCR1mutant(IC₅₀valuesof5.6nMand80nMforCXCR1wtandCXCR1Ile43Val,respectively)^[1].Reparixinisanon-competitiveallostericinhibitorofIL-8receptorswitha400-foldhigherefficacyininhibitingCXCR1activitythanCXCR2^[2].
InVivo	ReparixinisaninhibitorofCXCL8receptorCXCR1andCXCR2activation,hasbeenshowntoattenuateinflammatoryresponsesinvariousinjurymodels.Spontaneouslyhypertensiverats(SHR)areadmiNISTeredasubcutaneousinjectionofReparixin(5mg/kg)dailyfor3weeks.Reparixineffectivelydecreasessystolicbloodpressureandincreasedthebloodflow^[3].ReparixinreducesthelevelsofIL-1βinthebrainaftermiddlecerebralarteryocclusion/reperfusion(MCAo)inmice.BarsrepresentlevelsofIL-1β(pg/100mg)measuredbyELISAinthebraintissuesofmicesubjectedornot(SHAM)toMCAoandpretreatedwithvehicleorReparixin(30mg/kg,s.c.)^[4].
References	[1].MoriconiA,etal.Designofnoncompetitiveinterleukin-8inhibitorsactingonCXCR1andCXCR2.JMedChem.2007Aug23;50(17):3984-4002. [2].BertiniR,etal.ReceptorbindingmodeandpharmacologicalcharacterizationofapotentandselectivedualCXCR1/CXCR2non-competitiveallostericinhibitor.BrJPharmacol.2012Jan;165(2):436-54. [3].KimHY,etal.Reparixin,aninhibitorofCXCR1andCXCR2receptoractivation,attenuatesbloodpressureandhypertension-relatedmediatorsexpressioninspontaneouslyhypertensiverats.BiolPharmBull.2011;34(1):120-7. [4].SousaLF,etal.BlockadeofCXCR1/2chemokinereceptorsprotectsagainstbraindamageinischemicstrokeinmice.Clinics(SaoPaulo).2013;68(3):391-4. [5].KrishnamurthyA,etal.Identificationofanovelchemokine-dependentmolecularmechanismunderlyingrheumatoidarthritis-associatedautoantibody-mediatedboneloss.AnnRheumDis.2016Apr;75(4):721-9.

PreparingStockSolutions

ConcentrationVolumeMass	1mg	5mg	10mg

1mM	3.5287mL	17.6435mL	35.2871mL
5mM	0.7057mL	3.5287mL	7.0574mL
10mM	0.3529mL	1.7644mL	3.5287mL

Pleaserefertothesolubilityinformationtoselecttheappropriatesolvent.

CellAssay
^[1]

Reparixinisdissolvedinsalineattheappropriatedilution^[1].

L1.2CellsUSPension(1.5-3×10⁶cells/mL)isincubatedat37°Cfor15mininthepresenceofvehicleorofReparixin(1nM-1μM)andnextseededintriplicatesintheuppercompartmentofthechemotacticchamber.Differentagonistsareseededinthelowercompartmentofthechamberatthefollowingconcentrations:1nMCXCL8,0.03nMfMLP,10nMCXCL1,2.5nMCCL2,30nMC5a.Thechemotacticchamberisincubatedat37°Cinairwith5%CO₂for45min(humanPMNs)or2h(monocytes).Attheendofincubation,thefilterisremoved,fixed,andstainedandfiveoilimmersionfieldsathighmagnification(100×)arecountedforeachmigrationwellaftersamplecoding.L1.2migrationisevaluatedusing5μmporesizeTranswellfilters^[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

AnimalAdministration
^[3]^[4]

Reparixinisdissolvedinsalineandadministeredsubcutaneously(MiceandRat).

Rat^[3]
TheReparixin-treatedgroupcontained5SHR(SHR-R),whereequalnumbersofnormalsaline-treatedSHR(SHR-N)andWKY(WKY-N)servedascontrols.Eighteen-week-oldSHRreceivedasubcutaneousinjectionofReparixin(5mg/kg)onceperdayfor3weeks.Reparixineffectsonbloodflow,bloodpressureandbodyweightaremeasuredbeforetreatmentandthenweeklyuntil1weekafterthefinalinjection.TheeffectofReparixinontheexpressionofhypertension-relatedmediatorsinthoracicaortas,aswellasnitricoxide(NO)plasmalevels,isexamined1weekafterthefinalinjection.Attheendofthe4weekperiod,bothcontrolandReparixin-treatedratsareanesthetizedviaintraperitonealinjectionofthiopental(50mg/kg),andbloodandtissuesamplesarecollected.
Mice^[4]
C57BL/6Jmice(8-10weeksold/20-25g)areused.ThesubcutaneousadministrationofReparixin(30mg/kg)isperformed60minutesbeforecerebralischemiainduction.Theanimalsaredividedintothefollowingthreeexperimentalgroups:Sham(i.e.,thegroupinwhichthearteriesarevisualized,butthereisnoocclusionofthemiddlecerebralartery),Vehicle(i.e.,thegrouppre-treatedwiththevehicle,phosphatebuffersolution,60minutesbeforeMCAo)andReparixin(i.e.,thegrouppre-treatedwiththedrug60minutesbeforeMCAo).ToevaluateneurologicalsignssecondarytoMCAo,theanimalsareassessedwiththeSHIRPAbattery24hafterreperfusion.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

References

[1].MoriconiA,etal.Designofnoncompetitiveinterleukin-8inhibitorsactingonCXCR1andCXCR2.JMedChem.2007Aug23;50(17):3984-4002.
[2].BertiniR,etal.ReceptorbindingmodeandpharmacologicalcharacterizationofapotentandselectivedualCXCR1/CXCR2non-competitiveallostericinhibitor.BrJPharmacol.2012Jan;165(2):436-54.
[3].KimHY,etal.Reparixin,aninhibitorofCXCR1andCXCR2receptoractivation,attenuatesbloodpressureandhypertension-relatedmediatorsexpressioninspontaneouslyhypertensiverats.BiolPharmBull.2011;34(1):120-7.
[4].SousaLF,etal.BlockadeofCXCR1/2chemokinereceptorsprotectsagainstbraindamageinischemicstrokeinmice.Clinics(SaoPaulo).2013;68(3):391-4.
[5].KrishnamurthyA,etal.Identificationofanovelchemokine-dependentmolecularmechanismunderlyingrheumatoidarthritis-associatedautoantibody-mediatedboneloss.AnnRheumDis.2016Apr;75(4):721-9.

MolecularWeight

283.39

Formula

C₁₄H₂₁NO₃S

CASNo.

266359-83-5

Storage

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

Shipping

RoomtemperatureincontinentalUS;mayvaryelsewhere

Solvent&Solubility

DMSO:≥500mg/mL

Reparixinisprepareinvehicle(sterilesaline)^[5].

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

References

[1].MoriconiA,etal.Designofnoncompetitiveinterleukin-8inhibitorsactingonCXCR1andCXCR2.JMedChem.2007Aug23;50(17):3984-4002.
[2].BertiniR,etal.ReceptorbindingmodeandpharmacologicalcharacterizationofapotentandselectivedualCXCR1/CXCR2non-competitiveallostericinhibitor.BrJPharmacol.2012Jan;165(2):436-54.
[3].KimHY,etal.Reparixin,aninhibitorofCXCR1andCXCR2receptoractivation,attenuatesbloodpressureandhypertension-relatedmediatorsexpressioninspontaneouslyhypertensiverats.BiolPharmBull.2011;34(1):120-7.
[4].SousaLF,etal.BlockadeofCXCR1/2chemokinereceptorsprotectsagainstbraindamageinischemicstrokeinmice.Clinics(SaoPaulo).2013;68(3):391-4.
[5].KrishnamurthyA,etal.Identificationofanovelchemokine-dependentmolecularmechanismunderlyingrheumatoidarthritis-associatedautoantibody-mediatedboneloss.AnnRheumDis.2016Apr;75(4):721-9.

Purity:99.88%ee.:100.00%

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