Acute　myeloid　leukemia　(AML)　is　an　aggressive　hematopoietic　malignancy　with　poor　prognosis　and　high　recurrence　rate.　The　discovery　of　more　effective　therapeutic　strategies　for　AML　plays　a　crucial　role.　The　present　work　showed　that　E35,　a　novel　derivative　of　emodin,　significantly　inhibited　cell　proliferation　and　induced　autophagy　and　apoptosis　in　AML　cells.　Treatment　with　E35　markedly　induced　Beclin-1,　LC3-II,　cleaved　Caspase-9　and　PARP,　and　suppressed　mitogen-activated　protein　kinase　(MAPK)　pathway.　E35　exposure　evoked　autophagic　activity　prior　to　apoptosis　induction,　and　autophagy　inhibition　by　3-methyladenine　(3-MA)　dramatically　increased　E35-induced　apoptosis　in　both　AML　cell　lines　and　patient-derived　AML　cells.　Nevertheless,　study　on　AML　xenograft　model　showed　that　the　combination　E35　with　3-MA　exhibited　much　more　inhibitory　effects　on　leukemia　cell　growth　in　vivo.　No　obvious　adverse　reactions　occurred　in　the　xenograft　animals　administered　E35　alone　or　its　cotreatment　with　3-MA.　These　findings　suggest　that　E35　could　exert　anti-leukemia　effects,　and　that　the　combination　of　E35　and　autophagy　inhibitor　might　prove　a　more　highly　efficient　strategy　for　AML　treatment.