Nilotinib-induced metabolic dysfunction: insights from a translational study using in vitro adipocyte models and patient cohorts

摘要

Nilotinib, a second-generation tyrosine kinase inhibitor (TKI),has been described to be a superior drug in the frontlinetreatment of patients with Philadelphia chromosome–positive(Ph+) chronic myeloid leukemia (CML) [1]. However, withmore mature follow-up, it has become clear that nilotinib isassociated with impaired glucose and lipid metabolism [2–4]and an excess in arterial thrombotic events in comparison toimatinib [5]. The 5-year safety update of the ENESTnd trial[3] provided further confirmation; it reported significant elevations in fasting glucose and serum lipids and an increased incidence of cardiovascular events in nilotinib-treated patientsas opposed to imatinib [3].