Tumor lysis syndrome (TSL) is an electrolyte and metabolic disturbance that occurs as a consequence of chemotherapeutic treatment of fast-growing tumors, leading to the release of large amount of cellular content as a result of tumor cell lysis, raising uric acid levels and thus inducing renal failure. TSL may occur mainly in patients undergoing treatment for hematological diseases such as chronic myeloid leukemia (CML). The treatment of TLS, which is done in parallel with chemotherapy treatment, involves the use of a recombinant urate oxidase enzyme, which is responsible for converting high serum levels of uric acid into allantoin, a compound considered to be inert. However, there are no studies on the possible effects of high amount of allantoin produced from urate oxidase during chemotherapy of resistant hematologic tumors. One of the studies by our group shows that allantoin interferes with the antitumor activity of cisplatin in non-small cell lung cancer. Our objective with this study is to investigate whether allantoin interferes with the action of cisplatin on the in vitro treatment of multidrug-resistant chronic myeloid leukemia cells.  LUCENA-1 cells were treated with cisplatin and allantoin, and we evaluated cell viability through the MTT assay, the mitochondrial membrane potential by spectrofluorimetry with the aid of the JC-1 probe, the induction of cell death by fluorescence microscopy (Annexin V/PI), the activity of efflux pumps (P-gp) and the expression of P-gp by flow cytometry. We observed that cisplatin-induced death in LUCENA-1 cells was significantly reduced by the presence of allantoin, but the activity of the resistance protein Pgp was not affected. We conclude that allantoin reduces apoptosis induced by cisplatin in multidrug resistant chronic myeloid leukemia cells, and that this effect was not related to the efflux pump activity.