Mechanism of impaired glucose metabolism during nilotinib therapy in patients with chronic myelogenous leukemia

Abstract

Nilotinib, a 2nd generation tyrosin kinase inhibitor (TKI), is efficacious in the treatment of chronic myelogenous leukemia (CML). Impaired glucose metabolism with hyperglycemia represents one of the most frequently observed adverse events (AEs) during nilotinib therapy.

However, the mechanism of glucose metabolism impairment remains unknown.

Keywords

• Nilotinib
• tyrosin kinase inhibitor
• glucose metabolism