Hotline:400-820-3792Inhibitors ? ScreeningLibraries ? Proteinswww.MedChemEFLT3-IN-36Cat.No.:HY-178996分子式:C??H??NO?分子量:331.36作用靶點(diǎn):FLT3;Apoptosis;Akt;ERK;PI3K;STAT作用通路:ProteinTyrosineKinase/RTK;Apoptosis;PI3K/Akt/mTOR;MAPK/ERKPathway;StemCell/Wnt;JAK/STATSignaling儲(chǔ)存方式:PleasestoretheproductundertherecommendedconditionsintheCertificateofAnalysis.BIOLOGICALACTIVITY生物活性FLT3-IN-36是一種強(qiáng)效的FLT3抑制劑。FLT3-IN-36對(duì)FLT3突變的急性髓系白血病(AML)細(xì)胞具有抗腫瘤活性。FLT3-IN-36可誘導(dǎo)細(xì)胞周期阻滯、降低線粒體膜電位并誘導(dǎo)細(xì)胞凋亡(apoptosis)，從而下調(diào)FLT3及其下游蛋白(包括AKT、ERK、PI3K和STAT5)的表達(dá)。FLT3-IN-36可用于AML研究[1]。體外研究FLT3-IN-36(compound8h)(24h)exhibitsselectiveantiproliferativeactivityagainstFLT3mutantAMLcells,withIC50sof2.04(MV4-11)and3.25μM(MOLM-13),whileshowingsignificantlyweakereffectsonFLT3wild-typecellssuchasTHP-1,U937,andOCI-AML2(IC50=19.59,91.49,and55.38μM)[1].FLT3-IN-36(0.1-100μM,24h)inhibitsMV4-11cellgrowthinatime-anddose-dependentmanner,whileshowinglowcytotoxicityinnormalHK-2andHepRGcells[1].FLT3-IN-36(1-10μM,24h)inducesapoptosis,G2/MphasecellcyclearrestandareductionofmitochondrialmembranepotentialinMV4-11cellsinadose-dependentmanner[1].FLT3-IN-36(0-10μM,24h)inhibitsthegrowthofMV4-11cellsbybydownregulatingFLT3proteinlevelsandinactivatingitsdownstreamsignalingpathway,includingkeyeffectorssuchasAKT,ERK,PI3K,andSTAT5[1].FLT3-IN-36fitswelltotheATPbindingpocketofFLT3andonlyinteractswiththeresiduesGlu692andCys694inthehingeregionoftheactiveconformation[1].FLT3-IN-36(1-10μM)directlytargetsFLT3kinase,exhibiting58%inhibitionofFLT3-ITDkinaseactivityat10μM[1].CellCycleAnalysis[1]CellLine:MV4-11cellsConcentration:1,2.5and5μM1/2 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemEIncubationTime:24hResult:SignificantlyincreasedtheG2/MphasearrestinMV4-11.InducedtheG2/Mphasearrestatmoderateconcentrationwithadose-dependentmanneraftertreatmentfor24h.CellViabilityAssay[1]CellLine:MV4-11,HK-2andHepRGcellsConcentration:0.1,1,2,4,8,10,16,50,and100μMIncubationTime:24and48hResult:DecreasedMV4-11cellviabilityinatime-anddose-dependentmanner.ShowedlowcytotoxicityinnormalHK-2andHepRGcells.WesternBlotAnalysis[1]CellLine:MV4-11cellsConcentration:0,2.5,5,and10μMIncubationTime:24hResult:PromotedthecleavageandactivationofCaspase-3(evidencedbyincreasedlevelsofcleavedCaspase-3).ResultedinnoobviouschangesforthelevelsofBcl-2andBax.Causedthedecreaseofthedownstream-relatedproteinlevels,includingAKT,ERK,PI3KandSTAT5.ApoptosisAnalysis[1]CellLine:MV4-11cellsConcentration:1,2.5and5μMIncubationTime:24hResult:InducedapoptosisinMV4-11cellswithadose-dependentmanner.REFERENCESXingQ,etal.Developmentandbio-evaluationofnovelindolizinederivativesinFLT3mutantacutemyeloidleukemiacells.BioorgMedChemLett.2025Oct4;130:130429.McePdfHeight2/2 MasterofBioactiveMolecules—您身邊的抑制劑大師www.MedChemECaution:Producthasnotbeenfullyvalidate