APTO-253-LOR-253-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEAPTO-253Cat.No.:HY-16291CASNo.:916151-99-0Synonyms:LOR-253;LT-253分?式:C??H??FN?分?量:367.38作?靶點(diǎn):c-Myc;KLF;Apoptosis作?通路:Apoptosis;MAPK/ERKPathway儲(chǔ)存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實(shí)驗(yàn)DMSO:60mg/mL(163.32mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM2.7220mL13.6099mL27.2198mL5mM0.5444mL2.7220mL5.4440mL10mM0.2722mL1.3610mL2.7220mL請(qǐng)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(chǔ)備液；?旦配成溶液，請(qǐng)分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲(chǔ)備液的保存?式和期限：-80°C,6months;-20°C,1month。-80°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?，-20°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請(qǐng)先按照InVitro?式配制澄的儲(chǔ)備液，再依次添加助溶劑：(為保證實(shí)驗(yàn)結(jié)果的可靠性，澄的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)的?作液，建議您現(xiàn)?現(xiàn)配，當(dāng)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.請(qǐng)依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%saline1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESolubility:2.3mg/mL(6.26mM);Suspendedsolution;Needultrasonicandwarming2.請(qǐng)依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:2.08mg/mL(5.66mM);Suspendedsolution;NeedultrasonicBIOLOGICALACTIVITY?物活性APTO-253(LOR-253)?種?分?，可抑制c-Myc表達(dá)，穩(wěn)定G-四鏈體DNA并誘導(dǎo)急性髓樣??病細(xì)胞的細(xì)胞周期停滯和凋亡。APTO-253通過誘導(dǎo)Kruppel-likefactor4(KLF4)抑癌因?介導(dǎo)抗癌活性。APTO-253具有抗關(guān)節(jié)炎活性。IC50&Targetc-Myc[1];KLF4[2]體外研究APTO-253(LOR-253)isaninducerofKLF4.APTO-253(5μM)inducesKLF4expression,andenhancesapoptosisinducedbyNSC119875inbothSKOV3andOVCAR3cells.APTO-253(5μM)alsoleadstoG1phasearrestandreducesSandG2/MphasecellsinSKOV3andOVCAR3cells[1].APTO-253iscytotoxictoRajiandRaji/253Rcelllines,withIC50sof105±2.4nMand1387±94nM,respectively.APTO-253(0.5μM)alsocausesDNAdamageinRajicells.BRCA1/2deficientcellsarehypersensitivetoAPTO-253.ABCG2overexpressedHEK-293cellsareresistanttoAPTO-253andinhibitionofABCG2reversesresistancetoAPTO-253inRaji/253R[2].APTO-253suppressestheproliferationofacutemyeloidleukemia(AML)celllinesandvariousformsoflymphomacelllineswithIC50srangingfrom57nMto1.75μM.APTO-253(500nM)alsocausesG0/G1cellcyclearrest,inducesapoptosis,anddownregulatesMYCRNAandproteinexpressioninAMLlines.APTO-253(500nM)leadstoDNAdamageresponsepathwaysinMV4-11cells.Futhermore,APTO-253isapotentstabilizerofGquadruplex(G4)motifs,anddemonstratesthegreatestpropensityforstabilizingtheMYCG4sequences[3].體內(nèi)研究APTO-253(LOR-253;15mg/kg;IV;twiceperdayfor2consecutivedaysperweekfor14days)hasantiarthriticactivityinaCIAmodel[3].AnimalModel:DBA/1Jmalemice(6weeks)withcollageninducedarthritis(CIA)[3]Dosage:15mg/kgAdministration:IV;twiceperdayfor2consecutivedaysperweekfor14daysResult:Demonstratedsignificantpreventiveandtherapeuticactivityonarthritisformation.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?AnnRheumDis.2020Nov2;annrheumdis-2020-218189.?NatCommun.2019Sep25;10(1):4369.?JCIInsight.2022Jul19;e160688.?Genes(Basel).2021,12(4),539.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE?JDiabetesRes.15Sep2021.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].LocalA,etal.APTO-253StabilizesG-quadruplexDNA,InhibitsMYCExpression,andInducesDNADamageinAcuteMyeloidLeukemiaCells.MolCancerTher.2018Jun;17(6):1177-1186.[2].HongyingZhang,etal.Inhibitionofc-MycByApto-253AsanInnovativeTherapeuticApproachtoInduceCellCycleArrestandApoptosisinAcuteMyeloidLeukemia.Blood2016128:1716.[3].HarukaTsuchiya,etal.Parsingmultiomicslandscapeofactivatedsynovialfibroblastshighlightsdrugtargetslinkedtogeneticriskofrheumatoidarthritis.AnnRheumDis.2020Nov2;annrheumdis-2020-218189.McePdfHeightCautio