Favipiravir-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•Agonists•ScreeningLibrarieswww.MedChemEFavipiravirCat.No.:HY-14768CASNo.:259793-96-9分⼦式:C₅H₄FN₃O₂分⼦量:157.1作⽤靶点:DNA/RNASynthesis;InfluenzaVirus;SARS-CoV作⽤通路:CellCycle/DNADamage;Anti-infection储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验DMSO:≥100mg/mL(636.54mM)扫描⼆维码，H2O:6.25mg/mL(39.78mM;Needultrasonic)运⽤溶解⽅案计算器*"≥"meanssoluble,butsaturationunknown.获得适合您实验体系的溶解⽅案MassSolvent1mg5mg10mgConcentration制备储备液1mM6.3654mL31.8269mL63.6537mL5mM1.2731mL6.3654mL12.7307mL10mM0.6365mL3.1827mL6.3654mL请根据产品在不同溶剂中的溶解度，选择合适的溶剂配制储备液，并请注意储备液的保存⽅式和期限。体内实验请根据您的实验动物和给药⽅式选择适当的溶解⽅案。以下溶解⽅案都请先按照InVitro⽅式配制澄的储备液，再依次添加助溶剂：为保证实验结果的可靠性，澄的储备液可以根据储存条件，适当保存；体内实验的⼯作液，建议您现⽤现配，当天使⽤；以下溶剂前显⽰的百分⽐指该溶剂在您配制终溶液中的体积占⽐；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的⽅式助溶1.请依序添加每种溶剂：1%DMSO99%saline2.Solubility:≥0.5mg/mL(3.18mM);Clearsolution请依序添加每种溶剂：10%DMSO40%PEG3005%Tween-8045%salineSolubility:≥2.5mg/mL(15.91mM);Clearsolution此⽅案可获得≥2.5mg/mL(15.91mM，饱和度未知)的澄溶液。1/4www.MedChemEwww.MedChemE以1mL⼯作液为例，取100μL25.0mg/mL的澄DMSO储备液加到400μLPEG300中，混合均匀；向上述3.体系中加⼊50μLTween-80，混合均匀；然后继续加⼊450μL⽣理盐⽔定容⾄1mL。请依序添加每种溶剂：10%DMSO90%(20%SBE-β-CDinsaline)Solubility:≥2.5mg/mL(15.91mM);Clearsolution此⽅案可获得≥2.5mg/mL(15.91mM，饱和度未知)的澄溶液。以1mL⼯作液为例，取100μL25.0mg/mL的澄DMSO储备液加到900μL20%的SBE-β-CD⽣理盐⽔⽔溶4.液中，混合均匀。请依序添加每种溶剂：10%DMSO90%cornoilSolubility:≥2.5mg/mL(15.91mM);Clearsolution此⽅案可获得≥2.5mg/mL(15.91mM，饱和度未知)的澄溶液，此⽅案不适⽤于实验周期在半个⽉以上的实验。5.以1mL⼯作液为例，取100μL25.0mg/mL的澄DMSO储备液加到900μL⽟⽶油中，混合均匀。请依序添加每种溶剂：5%DMSO40%PEG3005%Tween-8050%saline6.Solubility:≥2.5mg/mL(15.91mM);Clearsolution请依序添加每种溶剂：5%DMSO95%(20%SBE-β-CDinsaline)7.Solubility:≥2.5mg/mL(15.91mM);Clearsolution请依序添加每种溶剂：PBSSolubility:4.55mg/mL(28.96mM);Clearsolution;NeedultrasonicBIOLOGICALACTIVITY⽣物活性Favipiravir(T-705)⼀种病毒RNA聚合酶(RNApolymerase)抑制剂，可转变为其活性形式Favipiravir-ribofuranosyl-5′-triphosphate(RTP)。Favipiravir-RTP抑制流感病毒RNA依赖性的RNA聚合酶(RdRP)活性，IC50为341nM。IC50&TargetIC50:341nM(RdRP)[1]体外研究Favipiravir(T705)isanantiviraldrugthatselectivelyinhibitstheRNA-dependentRNApolymeraseofinfluenzavirus.Favipiravir(T705)isanovelantiviralcompoundthatselectivelyandpotentlyinhibitstheRNA-dependentRNApolymerase(RdRP)ofinfluenzaandmanyotherRNAviruses.Favipiravir-RTPdoesnotinhibitthehumanDNApolymeraseα,βorγwithIC50>1mM.TheIC50forthehumanRNApolymeraseIIis905μM;Favipiraviristherefore2,650timesmoreselectivefortheinfluenzavirusRdRP,consistentwiththelackofinhibitionofhost-cellDNAandRNAsynthesis[1].Favipiravir(T705)actsasapro-drug,itscytotoxicityisexpectedtobecell-linedependent.Favipiravirinhibitsinadose-dependentmannerMNV-inducedCPE(EC50:250±11μM)andMNVRNAsynthesisincellculture(EC50:124±42μM).Despitethisrathermodestantiviralactivity,Favipiravir(T705)isabletocompletelyinhibitnorovirusreplicationataconcentrationof100μg/mL,whichisaconcentrationthathaslittleornoadverseeffectonthehostcell(cellviability>80%)[2].体内研究Favipiravir(T705)(30mg/kg/day,orally)improvessurvivalcomparetoplacebo.Favipiravir(T705)alsoprovidessignificantprotectionagainsttheA/Duck/MN/1525/81(H5N1)virusatadoseof33mg/kg/dayormore,regardlessofthenumberofdailydoses.Whengiven4timesaday,allmicesurvive[1].PROTOCOL2/4www.MedChemEwww.MedChemECellAssay[2]TheantiviralactivityofFavipiravir(T705)isdeterminedusinganMTS-basedCPEreductionassayintheMNV/RAW264.7cellline.Tothisend,RAW264.7cellsareseeded(1×104cells/well)in96-wellplatesandinfectedwithMNVatanMOIof0,001inthepresence(orabsence)ofadilutionseriesofFavipiravir(T705)(3.13-200μg/mL).Following3daysofincubation,i.e.untilcompleteCPEisobservedininfecteduntreatedcells,cellculturesupernatantsarecollectedforquantificationofviralRNAloadbyquantitativeRT-PCR(qRT-PCR).FortheMTSreductionassayanMTS/Phenazinemethosulphate(PMS)stocksolution(2mg/mLMTSand46g/mLPMSinPBSatpH6-6.5)isdiluted1/20inMEM.Toeachwell,75μLofMTS/PMSsolutionisaddedandtheopticaldensity(OD)isreadat498nm2hlater.The%CPEreductioniscalculatedas[(ODtreated)MNW−ODVC]/[ODCC-ODVC]×100,whereODCCrepresentstheODoftheuninfecteduntreatedcells,whereasODVCand(ODtreated)CCrepresenttheODofinfecteduntreatedcellsandvirus-infectedcellstreatedwithacompoundconcentration,respectively.TheEC50isdefinedasthecompoundconcentrationthatprotected50%ofcellsfromvirus-inducedCPE.AdverseeffectsofthemoleculeonthehostcellarealsoassessedbymeansoftheMTS-method,byexposinguninfectedcellstothesameconcentrationsofFavipiravirfor3days.The%cellviabilityiscalculatedas(ODtreated/ODCC)×100,whereODCCistheODofuninfecteduntreatedcellsandODtreatedareuninfectedcellstreatedwithcompound.TheCC50isdefinedasthecompoundconcentrationthatreducesthenumberofviablecellsby50%.Theselectivityindex(SI)iscalculatedasCC50/EC50[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMice[1]Administration[1]Favipiravir(T705)hasalsobeenshowntoprotectmiceagainstlethalinfectionbyavarietyofinfluenzavirusstrains.WhenFavipiravirisorallyadministered2or4timesadayfor5daysinmiceinfectedwithlethaldosesofinfluenzavirusA/Victoria/3/75(H3N2),A/Osaka/5/70(H3N2)orA/Duck/MN/1525/81(H5N1).MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.户使⽤本产品发表的科研⽂献•NucleicAcidsRes.2021Jan8;49(D1):D1113-D1121.•AntimicrobAgentsChemother.2020Jun23;64(7):e00222-20.•AntimicrobAgentsChemother.2019May24;63(6).pii:e00003-19.•IntJBiolSci.2020Oct16;16(16):3100-3115.•FrontPharma