KM11060-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEKM11060Cat.No.:HY-19970CASNo.:774549-97-2分?式:C??H??Cl?N?O?S分?量:422.33作?靶點(diǎn):CFTR;Autophagy作?通路:MembraneTransporter/IonChannel;Autophagy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:50mg/mL(118.39mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM2.3678mL11.8391mL23.6782mL5mM0.4736mL2.3678mL4.7356mL10mM0.2368mL1.1839mL2.3678mL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(guò)程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過(guò)加熱和/或超聲的?式助溶)1.請(qǐng)依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥5mg/mL(11.84mM);Clearsolution1/2MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemEBIOLOGICALACTIVITY?物活性KM11060F508缺失-囊性纖維化跨膜電導(dǎo)調(diào)節(jié)劑(F508del-CFTR)轉(zhuǎn)運(yùn)缺陷的校正劑。KM11060可?于F508del-CFTR加?缺陷的研究和囊性纖維化治療劑的開發(fā)。體外研究Small-moleculecorrectorssuchasKM11060mayserveasusefulpharmacologicaltoolsinstudiesoftheF508del-CFTRprocessingdefectandinthedevelopmentofcysticfibrosistherapeutics.KM11060rescuesF508del-CFTRtraffickinginculturedcellsandnativeepithelialtissues.KM11060partiallycorrectsF508del-CFTRprocessingandincreasessurfaceexpressionto75%ofthatobservedincellsincubatedatlowtemperature.Upto50%oftheF508del-CFTRincellstreatedwithKM11060wascomplex-glycosylated,indicatingpassagethroughtheGolgi.KM11060asapromisingcompoundforfurtherdevelopmentofCFtherapeutics.[1]體內(nèi)研究InLPS-inducedacutelunginflammation,blockadeofPSGL-1(P-selectinglycoproteinligand-1)orP-selectin,antagonismofPAFbyWEB2086,orcorrectionofmutatedCFTRtraffickingbyKM11060couldsignificantlyincreaseplasmalipoxinA4levelsinF508delrelevanttowildtypemice.[2]戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?Patent.US9987256B2.?Patent.US20150328217A1.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].RobertR,etal.StructuralanalogofsildenafilidentifiedasanovelcorrectoroftheF508del-CFTRtraffickingdefect.MolPharmacol.2008Feb;73(2):478-89.[2].WuH,etal.LipoxinA4andplateletactivatingfactorareinvolvedinE.coliorLPS-inducedlunginflammationinCFTR-deficientmice.PLoSOne.2014Mar26;9(3):e93003.McePdfHeightCaution:Producthasnotbeenfullyvalidatedformedicalapplications.For