磷酸氯喹作用機制 - Medchemexpress - MCE中國

ProductDataSheetChloroquinephosphateCat.No.:HY-17589CASNo.:50-63-5分?式:C??H??ClN?O?P?分?量:515.86作?靶點:Parasite;Autophagy;SARS-CoV;Toll-likeReceptor(TLR);HIV作?通路:Anti-infection;Autophagy;Immunology/Inflammation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H2O:≥33mg/mL(63.97mM)DMSO:<1mg/mL(insolubleorslightlysoluble)*"≥"meanssoluble,butsaturationunknown.SolventMass1mg5mg10mgConcentration制備儲備液1mM1.9385mL9.6926mL19.3851mL5mM0.3877mL1.9385mL3.8770mL10mM0.1939mL0.9693mL1.9385mL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(protectfromlight)。-80°C儲存時，請在6個?內(nèi)使?，-20°C儲存時，請在1個?內(nèi)使?。BIOLOGICALACTIVITY?物活性Chloroquinephosphate?種?泛?于治療瘧疾和類風濕性關節(jié)炎的抗瘧疾和抗炎劑。Chloroquinephosphate是autophagy和toll-likereceptors(TLRs)的抑制劑。Chloroquinephosphate有效抑制SARS-CoV-2(COVID-19)感染(

EC50=1.13μM)。IC??&TargetTLRs,HIV,SARS-COV-2,Autophagy[1][2][3][4]體外研究Chloroquine(CHQ,20μM)inhibitsIL-12p70releaseandreducesTh1-primingcapacityofactivatedhumanmonocyte-derivedLangerhans-likecells(MoLC).Chloroquine(CHQ,20μM)enhancesIL-1–inducedIL-23secretioninMoLCandsubsequentlyincreasesIL-17AreleasebyprimedCD4+Tcells[1].Chloroquine(25μM)suppressesMMP-9mRNAexpressioninnormoxiaandhypoxiainparentalMDA-MB-231cells.Chloroquinehascell-,dose-andhypoxia-dependenteffectsonMMP-2,MMP-9andMMP-13mRNAexpression[2].TLR7andTLR9inhibitionusingIRS-954orchloroquinesignificantlyreducesHuH7cellproliferationinvitro[3].Page1of2www.MedChemEChloroquine(0.01-100μM;48hours)potentlyblocksvirusinfection(veroE6cellsinfectedwithSARS-CoV-2)atlow-micromolarconcentration(EC50=1.13μM).ChloroquineblocksvirusinfectionbyincreasingendosomalpHrequiredforvirus/cellfusion,aswellasinterferingwiththeglycosylationofcellularreceptorsofSARS-CoV[4].體內(nèi)研究Chloroquine(80mg/kg,i.p.)doesnotpreventthegrowthofthetriple-negativeMDA-MB-231cellswithhighorlowTLR9expressionlevelsintheorthotopicmousemodel[2].TLR7andTLR9inhibitionusingIRS-954orchloroquine

significantlyinhibitstumourgrowthinthemousexenograftmodel.HCCdevelopmentintheDEN/NMORratmodelis

alsosignificantlyinhibitedbychloroquine[3].PROTOCOLCellAssay[2]Thecellsareculturedin6-wellplateswithnormalculturemediuminthepresenceofvehicleor25or50μMchloroquine,untilnearconfluency,afterwhichtheyarerinsedwithsterilephosphate-bufferedsaline(PBS)andculturedfurtherfortheindicatedtimesinserum-freeculturemedium.Atthedesiredtime-points,theculturemediumisdiscardedandthecellsarequicklyharvestedinlysisbufferandclarifiedbycentrifugation.Subsequenttoboilingthesupernatantsinreducingsodiumdodecylsulphate(SDS)samplebuffer,equalamountsofprotein(100μg)areloadedperlaneandthesamplesareelectrophoresedinto10or4-20%gradientpolyacrylamideSDSgels,thentransferredtoanitrocellulosemembrane.TodetectTLR9,theblotsareincubatedovernightat4°Cwithanti-TLR9antibodies,diluted1:500inTris-bufferedsalinewith0.1%(v/v)Tween-20(TBST).Equalloadingisconfirmedwithpolyclonalrabbitanti-actin.Secondarydetectionisperformedwithhorseradishperoxidase-linkedsecondaryantibodies.TheproteinbandsarevisualizedbychemiluminescenceusinganECLkit.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalControlandTLR9siRNAMDA-MB-231cells(5×105cellsin100μL)areinoculatedintothemammaryfatpadsoffour-Administration[2]week-old,immune-deficientmice(athymicnude/nuFoxn1).Treatmentsarestartedsevendaysaftertumorcellinoculation.Themicearetreateddailyeitherwithintraperitoneal(i.p.)chloroquine(80mg/kg)orvehicle(PBS).Theanimalsaremonitoreddailyforclinicalsigns.TumormeasurementsareperformedtwiceaweekandtumorvolumeiscalculatedaccordingtotheformulaV=(π/6)(d1×d2)3/2,whered1andd2areperpendiculartumordiameters.Thetumorsareallowedtogrowfor22days,atwhichpointthemicearesacrificedandthetumorsaredissectedforafinalmeasurement.Throughouttheexperiments,theanimalsaremaintainedundercontrolledpathogen-freeenvironmentalconditions(20-21°C,30-60%relativehumidityanda12-hlightingcycle).Themicearefedwithsmall-animalfoodpelletsandsuppliedwithsterilewateradlibitum.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻?CircRes.2018May25;122(11):1532-1544.?AdvSci(Weinh).2019Mar25;6(10):1801862.?JClinInvest.2020May.?NucleicAcidsRes.2018Apr20;46(7):3284-3297.?Autophagy.2020May20;1-22.Seemorecustomervalidationsonwww.MedChemEREFERENCESPage2of3www.MedChemE[1].SaidA,etal.ChloroquinepromotesIL-17productionbyCD4+Tcellsviap38-dependentIL-23releasebymonocyte-derivedLangerhans-likecells.JImmunol.2014Dec15;193(12):6135-43.[2].TuomelaJ,etal.Chloroquinehastumor-inhibitoryandtumor-promotingeffectsintriple-negativebreastcancer.OncolLett.2013Dec;6(6):1665-1672.[3].MohamedFE,etal.Effectoftoll-likereceptor7and9targetedtherapytopreventthedevelopment