Vadimezan-DMXAA-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemEVadimezanCat.No.:HY-10964CASNo.:117570-53-3Synonyms:DMXAA;ASA-404分⼦式:C₁₇H₁₄O₄分⼦量:282.29作⽤靶点:STING;IFNAR;InfluenzaVirus作⽤通路:Immunology/Inflammation;Anti-infection储存⽅式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性数据体外实验DMSO:7.14mg/mL(25.29mM;Needultrasonic)7.5%sodiumbicarbonate:6.67mg/mL(23.63mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制备储备液1mM3.5425mL17.7123mL35.4246mL5mM0.7085mL3.5425mL7.0849mL10mM0.3542mL1.7712mL3.5425mL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；⼀旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存⽅式和期限：-80°C,6months;-20°C,1month。-80°C储存时，请在6个⽉内使⽤，-20°C储存时，请在1个⽉内使⽤。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)1/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemE1.请依序添加每种溶剂：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥0.71mg/mL(2.52mM);Clearsolution2.请依序添加每种溶剂：10%DMSO>>90%cornoilSolubility:≥0.71mg/mL(2.52mM);Clearsolution3.请依序添加每种溶剂：50%PEG300>>50%salineSolubility:5mg/mL(17.71mM);Suspendedsolution;NeedultrasonicBIOLOGICALACTIVITY⽣物活性Vadimezan(DMXAA;ASA-404)⾎管破坏剂，⿏⼲扰素因(STING)刺激物，也I型IFN和其他细胞因⼦的强效诱导剂。Vadimezan具有抗流感病毒H1N1-PR8的活性。IC50&TargetSTING[1],typeIIFNs[2]体外研究Vadimezan(DMXAA),thevasculardisruptingagent,isamurineagonistofthestimulatorofinterferongenes(STING)andalsoapotentinduceroftypeIIFNsandothercytokines.Vadimezan(DMXAA)hasnodetrimentaleffecton344SQ-ELuccellviability.ItisfoundthatVadimezan-mediatedupregulationoftheNF-κBpathwayasshownbyincreasedp65phosphorylationinM2macrophages[1].ResultsdemonstratethatVadimezan(DMXAA)-treatedcellsareprotectedfromVSV-inducedcytotoxicityatallMOIsincontrasttomedium-pretreatedmacrophages.Vadimezan(DMXAA)effectivelyinhibitsgrowthofbothstrainsofinfluenza,demonstratingthepotentialofVadimezanfortreatmentofdrug-resistantstrainsofhumaninfluenza[2].体内研究344SQ-ELucNSCLCsubcutaneoustumorsresponddramaticallytoVadimezan(DMXAA),withamarkeddecreaseinbioluminescence(BLI)signalspost-druginjection.Vadimezan(DMXAA)treatmentof344SQ-ELucmetastasesyieldsnodecreaseinphotonemissionrates,withthetumorsremaininghistologicallysimilartocontrolsafterthistreatment.Aswiththelargesubcutaneoustumors,Vadimezan(DMXAA)administrationtomicewithsmallsubcutaneoustumorsstillleadsto~2-logdecreasesinphotonemissionatboth6and24hours[1].Invivo,Vadimezan(DMXAA)isamorepotentinducerofIFN-βmRNAandarelativelypoorinducerofTNF-αmRNA.Vadimezan(DMXAA)administrationleadstosignificantlylessweightlossininfluenza-infectedmice[2].PROTOCOLKinaseAssay[1]M2-polarizedmacrophagesaretreatedwith20µg/mLVadimezan(ASA-404)orDMSOvehiclefor30min.CellsarethenlysedandproteindenaturedinSDSbufferandsamplessentforRPPAanalysis.Differentialabundanceofvariousproteinsand/ortheirphosphorylationstatusinresponsetoVadimezan(ASA-404)isassessed[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.CellAssay[2]RAW264.7macrophagesareculturedandplatedat1×105cells/wellina96-wellplate.Afterovernightincubationat37°C,cellsaretreatedwithmediumcontainingvehicleorVadimezan(DMXAA)(100μg/mL).2/3MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEAfter6h,theculturemediumisreplacedwithserum-freeDMEMcontainingVSVattheindicatedMOIfor1h.CellsarethenmaintainedincompleteDMEMwith10%FBS.Twenty-fourhourslater,cellsarewashedwithPBS,fixedwith10%bufferedformalin,andrinsedthoroughlywithdistilledwater.Adherentcellsarestainedwithcrystalviolet[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalMale129/Svmice(6to12weekold)areusedinthisstudy.Togeneratesubcutaneoustumors,5×105Administration[1]344SQ-ELuccellsin100µLPBSareinjectedinbothposteriorflanksofmice.Tumorgrowthismonitoredevery2to4daysviaBLI.Oncetumorsareestablished(day10forsystemicmetastases;day7orday14forsubcutaneoustumors),micearegiven25mg/kgofVadimezan(DMXAA),orDMSOvehiclebyi.p.injection.BLIiscarriedoutat6and24hours[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.户使⽤本产品发表的科研⽂献•Gastroenterology.2018May;154(6):1822-1835.e2.•Neuron.2022Nov4;S0896-6273(22)00961-8.•CellDeathDis.2022Jul28;13(7):653.•CellDeathDis.2021Jul3;12(7):673.•CellDeathDis.2020Dec11;11(12):1050.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].ShireyKA,etal.Theanti-tumoragent,5,6-dimethylxanthenone-4-aceticacid(DMXAA),inducesIFN-beta-mediatedantiviralactivityinvitroandinvivo.JLeukocBiol.2011Mar;89(3):351-7.[2].DowneyCM,etal.DMXAAcausestumorsite-specificvasculardisruptioninmurinenon-smallcelllungcancer,andliketheendogenousnon-canonicalcyclicdinucleotideSTINGagonist,2'3'-cGAMP,in