iCRT3-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEiCRT3Cat.No.:HY-103705CASNo.:901751-47-1分?式:C??H??N?O?S分?量:394.53作?靶點(diǎn):Wnt;Apoptosis作?通路:StemCell/Wnt;Apoptosis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:150mg/mL(380.20mM;Needultrasonicandwarming)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM2.5347mL12.6733mL25.3466mL5mM0.5069mL2.5347mL5.0693mL10mM0.2535mL1.2673mL2.5347mL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>>40%PEG300>>5%Tween-80>>45%salineSolubility:≥2.5mg/mL(6.34mM);Clearsolution1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE2.請(qǐng)依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.5mg/mL(6.34mM);ClearsolutionBIOLOGICALACTIVITY?物活性iCRT3Wnt和β-連環(huán)蛋?應(yīng)答轉(zhuǎn)錄(β-catenin-responsivetranscription)的抑制劑。IC50&TargetWnt[1],β-catenin-responsivetranscription[2]體外研究iCRT3isaninhibitorofbothWntandβ-catenin-responsivetranscription.iCRT3significantlydecreasesTOPFlashactivityandreducesthelevelofNTSR1.Theanti-apoptoticeffectsofNeurotensin(NTS)andWnt3acanbelargelyabrogatedbyiCRT3[1].CellsmaintainedlongtermwithiCRT3showenhancedexpressionofclassicpluripotencygenescomparewiththeDMSOcontrol,whereasexpressionofdifferentiationmarkersandT-cellfactor(TCF)targetgenesisconcomitantlyreduced[2].TreatmentwithiCRT3atdosesof12.5,25,50,and75μMdecreasesTNF-αlevelsby14.7%,18.5%,44.9%and61.3%,respectively.WithiCRT3treatment,IκBlevelsareincreasedinadose-dependentmannercomparetothevehicle[3].體內(nèi)研究ThetumorgrowthratesaremarkedlyretardedbyiCRT3treatment.Consistently,thetumor-suppressiveroleofiCRT3isaccompaniedwithareductioninKi67index,aproliferationmarker[1].TheIL-6levelsinthe10?mg/kgiCRT3treatmentgroupare82.9%lowerthanthoseinthevehiclegroup.IL-1βlevelsareundetectableintheshambutreach371?pg/mLinsepticmiceandaredownby30.2%and53.2%,respectively,with5and10?mg/kgiCRT3.WithiCRT3treatmentatdosesof5and10?mg/kg,ASTlevelsinthesesepticmiceare15.4%and44.2%lower,respectively,thanthoseinthevehicle-treatedmice.Aftertreatmentwith10?mg/kgiCRT3,lungmorphologyisimprovedwithmuchreducedmicroscopicdeterioration,comparetothevehiclegroup.ThenumberofapoptoticcellsinthelungtissuesoftheiCRT3-treatedmiceissignificantlyreducedby92.7%incomparisonwiththevehiclegroup[3].PROTOCOLCellAssay[1]Cellsareseededinto96-wellplatestoadensityof5×103cellsperwellandincubatedintheculturemediumwithiCRT3foranadditional48h.CellviabilityandcellapoptosisassaysarecarriedoutusingaCellCountingkit-8andaCaspase-Glo3/7assaykitaccordingtothemanufacturer’sinstructions,respectively[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.AnimalNOD-SCIDBALB/cmiceareinoculatedsubcutaneouslyintherightbackwith2×106A172cells.ThegrowthAdministration[1]oftheprimarytumorsisrecordedevery4days.iCRT3(5mg/kg)isdilutedinPBSi.p.triweeklywhentumorsgrowto~200mm3.ThecontrolmicearetreatedwithblankPBScontaining5%(v/v)DMSO.Tumorvolumeisevaluatedwiththefollowingformula:volume=tumorlength×width2/2.Themicearesacrificed24daysafterpharmaceuticaltreatment.Thetumorsareresectedandembeddedinparaffin,andtheKi67stainingisanalyzedbyimmunohistochemistry[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemE戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?NatCommun.2022Nov2;13(1):6552.?NatCommun.2022Jul28;13(1):4364.?NatCommun.2021Nov24;12(1):6831.?BMCBiol.2020Oct27;18(1):151.Seemorecustomervalidationsonwww.MedChemEREFERENCES[1].XiaoH,etal.ANovelPositiveFeedbackLoopBetweenNTSR1andWnt/β-CateninContributestoTumorGrowthofGlioblastoma.CellPhysiolBiochem.2017Oct24;43(5):2133-2142.[2].ChatterjeeSS,etal.Inhibitionofβ-catenin-TCF1interactiondelaysdifferentiationofmouseembryonicstemcells.JCellBiol.2015Oct12;211(1):39-51.[3].SharmaA,etal.Mitigationofsepsis-inducedinflammatoryresponsesandorganinjurythroughtargetingWnt/β-cateninsignaling.doi: