ADH-1-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEADH-1Cat.No.:HY-13541CASNo.:229971-81-7分?式:C??H??N?O?S?分?量:570.69作?靶點:Others作?通路:Others儲存?式:Powder-80°C2years-20°C1year*該產(chǎn)品在溶液狀態(tài)不穩(wěn)定，建議您現(xiàn)?現(xiàn)配，即刻使?。溶解性數(shù)據(jù)體外實驗DMSO:250mg/mL(438.07mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲備液1mM1.7523mL8.7613mL17.5226mL5mM0.3505mL1.7523mL3.5045mL10mM0.1752mL0.8761mL1.7523mL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；該產(chǎn)品在溶液狀態(tài)不穩(wěn)定，建議您現(xiàn)?現(xiàn)配，即刻使?.體內(nèi)實驗請根據(jù)您的實驗動物和給藥?式選擇適當(dāng)?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(jié)果的可靠性，澄的儲備液可以根據(jù)儲存條件，適當(dāng)保存；體內(nèi)實驗的?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.請依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.08mg/mL(3.64mM);Clearsolution2.請依序添加每種溶劑：10%DMSO>>90%(20%SBE-β-CDinsaline)Solubility:≥2.08mg/mL(3.64mM);Clearsolution1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE3.請依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.08mg/mL(3.64mM);ClearsolutionBIOLOGICALACTIVITY?物活性ADH-1?種N-cadherin的拮抗劑，能夠抑制N-cadherin介導(dǎo)的細(xì)胞黏附。體外研究ADH-1(0.2mg/mL)blockscollagenI-mediatedchangesinpancreaticcancercells,andishighlyeffectiveatpreventingcellmotilitythatisinducedbyexpressionofN-cadherin.ADH-1(0,0.1,0.2,0.5and1.0mg/mL)inducesapoptosisinadose-dependentandN-cadherin-dependentmanner[1].體內(nèi)研究ADH-1(50mg/kg)significantlypreventstumorgrowthandmetastasisinamousemodelforpancreaticcancer.ADH-1preventstumorcellinvasionandmetastasisinanorthotopicmodelforpancreaticcancerusingN-cadherinoverexpressingBxPC-3cells[1].ADH-1,atthedosagesevaluated,doesnotdisplayeitherantiangiogenicactivityinarataorticringassayorantitumorpotentialinaPC3subcutaneousxenografttumormodel[2].ADH-1(10mL/kg,i.p.)augmentationofmelanomatumorgrowthisovercomethroughitsabilitytomakeregionallyinfusedmelphalanmoreeffective.ADH-1mediatedaugmentationofmelanomatumorgrowthisnotalteredbyregionallyinfusedtemozolomide.InA375,butnotDM443xenografts,ADH-1treatmentincreasesphosphorylationofAKTatserine473.ADH-1slightlydiminishesN-cadherinexpressioninbothxenografts[3].PROTOCOLAnimalAnimalsareanesthetized,and40μLofasinglecellsuspensioncontaining50,000cellsisinjectedintotheAdministration[1]pancreas.Micearerandomizedintotreatmentgroups10daysaftersurgery.Fortreatment,miceareinjectedintraperitoneallyonceperdaywithADH-1at50mg/kgin100μLPBS(×1perday,×5perweekfor4weeks).Forinvivobioluminescence,D-Luciferinisadministeredbyintraperitonealinjection.Dataareacquired20minafterinjectionusingtheIVISsystem.Tumorgrowthismonitoredevery10daysfromday10today50aftersurgery.LuciferaseactivityisquantifiedusingtheIVISsystem.Twomonthsaftersurgery,themicearekilled,andthepancreas,liver,lung,anddisseminatednodulesareharvested,fixedin10%bufferedformalin,andembeddedinparaffin.Serial5-μMsectionsarecut,mountedonslides,andstainedwithH&Eusingstandardprocedures.SectionsarealsostainedforTUNEL.SectionsareexaminedusingaZeissAxioscop40microscopeequippedwithanAxioCamMRdigitalcameraandsoftware.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?CellDeathDis.2022Jun20;13(6):557.?Oncogene.2022Oct12.?JCellMolMed.2022Feb27.?SciRep.2019Feb6;9(1):1517.?BiochemBiophysResCommun.2019Oct5.pii:S0006-291X(19)31851-0.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESeemorecustomervalidationsonwww.MedChemEREFERENCES[1].ShintaniY,etal.ADH-1suppressesN-cadherin-dependentpancreaticcancerprogression.IntJCancer.2008Jan1;122(1):71-7.[2].LiH,etal.ADH1,anN-cadherininhibitor,evaluatedinpreclinicalmodelsofangiogenesisandandrogen-independentprostatecancer.AnticancerDrugs.2007Jun;18(5):563-8.[3].TurleyRS,etal.TargetingN-cadherinincreasesvascularpermeabilityanddifferentiallyactivatesAKTinmelanoma.AnnSurg.2015Feb;261(2):368-77