Vadimezan-DMXAA-DataSheet-生命科學試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEVadimezanCat.No.:HY-10964CASNo.:117570-53-3Synonyms:DMXAA;ASA-404分?式:C??H??O?分?量:282.29作?靶點:STING;IFNAR;InfluenzaVirus作?通路:Immunology/Inflammation;Anti-infection儲存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實驗DMSO:7.14mg/mL(25.29mM;Needultrasonic)7.5%sodiumbicarbonate:6.67mg/mL(23.63mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM3.5425mL17.7123mL35.4246mL5mM0.7085mL3.5425mL7.0849mL10mM0.3542mL1.7712mL3.5425mL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。-80°C儲存時，請在6個?內使?，-20°C儲存時，請在1個?內使?。體內實驗請根據(jù)您的實驗動物和給藥?式選擇適當?shù)娜芙?案。以下溶解?案都請先按照InVitro?式配制澄的儲備液，再依次添加助溶劑：(為保證實驗結果的可靠性，澄的儲備液可以根據(jù)儲存條件，適當保存；體內實驗的?作液，建議您現(xiàn)?現(xiàn)配，當天使?；以下溶劑前顯?的百分?指該溶劑在您配制終溶液中的體積占?；如在配制過程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過加熱和/或超聲的?式助溶)1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE1.請依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥0.71mg/mL(2.52mM);Clearsolution2.請依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥0.71mg/mL(2.52mM);Clearsolution3.請依序添加每種溶劑：50%PEG300>>50%salineSolubility:5mg/mL(17.71mM);Suspendedsolution;NeedultrasonicBIOLOGICALACTIVITY?物活性Vadimezan(DMXAA;ASA-404)?管破壞劑，??擾素因(STING)刺激物，也I型IFN和其他細胞因?的強效誘導劑。Vadimezan具有抗流感病毒H1N1-PR8的活性。IC50&TargetSTING[1],typeIIFNs[2]體外研究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].體內研究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?邊的抑制劑?師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.戶使?本產(chǎn)品發(fā)表的科研?獻?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