Background.　Bortezomib　is　used　for　treating　multiple　myeloma　(MM);　however,　it　has　considerable　adverse　effects.　Emodin　has　been　reported　to　exhibit　inhibitory　effects　on　MM　cell　lines.　We　investigated　the　efficacy　of　emodin　35　(E35),　an　emodin　derivative,　using　U266　and　MM1s　cell　lines　in　treating　MM　and　the　efficacy　of　combining　bortezomib　and　E35.　Methods.　MTT　assays　were　used　to　observe　the　effects　of　E35　on　MM　cell　growth.　The　effects　on　cellular　apoptosis　were　then　observed　using　Annexin　V/propidium　iodide　(PI)　staining　assay.　The　expression　of　apoptosis-related　genes,　including　the　caspase　family,　was　examined.　The　efficacy　of　combining　bortezomib　and　E35　was　investigated　by　examining　the　expression　of　the　Akt/mTOR/4EBP1　signaling　pathway-related　proteins.　Results.　We　report　that　E35　inhibited　the　growth　of　U266　and　MM1s　cells　by　inducing　cellular　apoptosis.　Moreover,　E35　downregulated　the　expression　of　apoptosis-related　genes　and　suppressed　the　phosphorylation　of　Akt/mTOR/4EBP1　signaling　pathway-related　genes,　thus　exhibiting　synergistic　effects　with　bortezomib.　All　observed　effects　were　dose-dependent.　Conclusion.　The　results　showed　that　E35　exhibited　cytotoxic　effects　in　MM　cell　lines　in　protein　levels.　Thus,　E35,　particularly　in　combination　with　bortezomib,　may　be　considered　as　a　promising　treatment　for　MM;　however,　this　requires　further　investigation　in　vivo.