CADD522-DataSheet-生命科学试剂-MedChemExpress

Hotline:400-820-3792Inhibitors•ScreeningLibraries•Proteinswww.MedChemECADD522Cat.No.:HY-107999CASNo.:199735-88-1分⼦式:C₁₅H₁₃Cl₂NO₃分⼦量:326.17作⽤靶点:ReactiveOxygenSpecies作⽤通路:Immunology/Inflammation;MetabolicEnzyme/Protease;NF-κB储存⽅式:4°C,storedundernitrogen*Insolvent:-80°C,6months;-20°C,1month(storedunder

nitrogen)溶解性数据体外实验DMSO:250mg/mL(766.47mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制备储备液1mM3.0659mL15.3294mL30.6589mL5mM0.6132mL3.0659mL6.1318mL10mM0.3066mL1.5329mL3.0659mL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(storedundernitrogen)。-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.请依序添加每种溶剂：10%DMSO>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.17mg/mL(6.65mM);Clearsolution2.请依序添加每种溶剂：10%DMSO>>90%cornoilSolubility:≥2.17mg/mL(6.65mM);Clearsolution1/5MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEBIOLOGICALACTIVITY⽣物活性CADD522⼀种RUNX2-DNA结合抑制剂(下调RUNX2介导的下游靶因的转录)，其IC50值为10nM。CADD522还可通过增加线粒体驱动的细胞ROS⽔平发挥其抗肿瘤活性。CADD522能抑制体内原发肿瘤的⽣长和免疫受损⼩⿏肺部肿瘤细胞的实验性转移，可⽤于癌症的研究。IC50&TargetRUNX2-DNAbinding[1]体外研究CADD522(0-100μM;24-72h)exhibitsastronginhibitoryeffectonBCcellgrowthandsurvival[1].CADD522(50μM;72h)showsanti-proliferativeeffectbyinducingcellcyclearrest(G1phase)[1].CADD522(50μM;8days)inhibitstumorsphereformationand(50μM;24h)invitroinvasionofBCcells(withoutcellulartoxicity)[1].CADD522(2,10,25,50,100μM;48h)inhibitsRUNX2transcriptionalactivitybyinhibitingRUNX2-DNAbindinginT47D-RUNX2andT47D-Emptycells[1].CADD522(50μM;72h)upregulatesRUNX2levelsthroughincreasedRUNX2stabilityincells[1].CADD522(50μM;6or24h)increasesROSgenerationofmitochondrialinMCF7andMDA-468cells[2].CADD522(0-2000nM,30min)inhibitsmitochondrialATPsynthaseactivityinMDA-231andMDA-468cells[2].CellViabilityAssay[1]CellLine:MDA-MB-468,MCF7,MCF10A,IEC-6,GES-1andC2C12cellsConcentration:0-100μMIncubationTime:24-72hResult:Displayedadose-andtime-dependentcellgrowthinhibitionover72h.Exhibitedlowcytotoxicityfornormalcellgrowth.CellCycleAnalysis[1]CellLine:MCF7,MDA-468andMDA-231cellsConcentration:50μMIncubationTime:72hResult:InducedMDA-231cellsaccumulatedattheG1andG2/MphasewhereasMCF7andMDA-468cellswereattheG1phase.CellViabilityAssay[1]CellLine:MCF7,MCF7-tet-offcellsConcentration:50μM2/5MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEIncubationTime:8daysResult:Dramaticallydecreasedthesizeaswellasthenumberoftumorspheres,andseverelydisruptedtumorspheresatday4.ShowedarelativelyselectiveeffectonBCcells(didnothaveasignificantinfluenceonmammosphereformationoftheMCF10Anon-malignantmammaryepithelialcells).CellInvasionAssay[1]CellLine:MCF7-tet-off(+Doxy),MCF7-tet-off(-Doxy)cellsConcentration:50μMIncubationTime:24hResult:AlmostabrogatedtheinvasivenessofbothMCF7-tet-off(+Doxy)andMCF7-tet-off(-Doxy)cellswithoutcellulartoxicity.CellViabilityAssay[1]CellLine:T47D-RUNX2andT47D-EmptycellsConcentration:2,10,25,50,100μMIncubationTime:48hResult:Resultedinadramaticdecreaseofthepromoter-luciferase(Luc)activitiesofRUNX2downstreamtargetgenessuchasMMP13andVEGF(metastasismarkers)andOC(osteogenesismarker).RT-PCR[1]CellLine:T47DandMCF7cells(ectopicexpressingRUNX2)Concentration:50μMIncubationTime:72hResult:SignificantlyinhibitedthemRNAlevel(RUNX2-mediated)ofGlut-1andLDHA.WesternBlotAnalysis[1]CellLine:T47D-RUNX2andMCF7-RUNX2cellsConcentration:50μMIncubationTime:72hResult:EnhancedbothmRNAandproteinexpressionofRUNX2.3/5MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEWesternBlotAnalysis[1]CellLine:MDA-468andMDA-231cellsConcentration:50μMIncubationTime:2,4,6hResult:IncreasedRUNX2stabilitybydelayingproteindegradation.CellViabilityAssay[2]CellLine:MCF7andMDA-468cellsConcentration:50μMIncubationTime:6or24hResult:IncreasedthelevelofmitochondrialROS,whichwasmoreevidentinserum-freethanserum-containingcondition.CellViabilityAssay[2]CellLine:MDA-231andMDA-468cellsConcentration:50,250,2000nM(forMDA-231);500,2000nM(forMDA-468)IncubationTime:30minResult:InhibitedtheactivityofATPsynthase.体内研究CADD522(1,5and20mg/kg;i.p.;twiceaweekfor45days)delaystheonsetofthetumorsandsuppressestumorgrowthinmice[1].CADD522(10mg/kg;i.p.;twiceaweekfor11days)suppressestumormetastasisandinhibitsexpressionofKi-67inmice[1].AnimalModel:Femalemice(6-week-old;MMTV-PyMTtransgenicmodel)[1].Dosage:1,5and20mg/kgAdministration:Intraperitonealinjection;twiceaweekfor45days.Result:Delayedtheonsetofthetumors,delayedtumordevelopmentandreducedtumorburdenintransgenicMMTV-PyMTmice.Reducedthetumorweightinmice.AnimalModel:FemaleNODscidgamma(NSG)miceandnudemice(TNBC-PDXBr-001model)[1].4/5MasterofBioactiveMolecules—您⾝边的抑制剂⼤师www.MedChemEDosage:10mg/kgAdministration:Intraperitonealinjection;twiceaweekfor11days.Result:SignificantdecreasedtumorvolumeandmarkedlyinhibitedexpressionofKi-67.InhibitedexperimentalmetastasisofBCcellsinvivo.(didnotsignificantlydecreasebodyweightorinfluencethegeneralhealthofanimals).户使⽤本产品发表的科研⽂献•NatCommun.