American College of Rheumatology/Association of Rheumatology Health Professionals (ACR/ARHP) 2015 Meeting Highlights: New Data on Canakinumab

Abstract

Interleukin (IL)-1 is a messenger for the regulation of inflammatory responses, but it can be harmful when in excess, such as in the inflammation observed in patients with autoinflammatory disease. Cryopyrinassociated periodic syndromes (CAPS) are a group of rare autoinflammatory diseases with an estimated population frequency ranging from 1–3 people per million.>1 These hereditary cytokine dysregulation syndromes encompass a spectrum of three cryopyrinopathies, including familial cold autoinflammatory syndrome (FCAS), Muckle–Wells syndrome (MWS), and neonatal-onset multisystemic inflammatory disease. In such genotypes, the NLRP3 gene that encodes cryopyrin, an inflammation mediator involved in IL-1β processing, is mutated. Canakinumab (CAN) is a humanised monoclonal antibody, which is administered subcutaneously and acts as an IL-β inhibitor drug, with a long plasma half-life (21–28 days) and an activity in the picomolar range. In the USA, CAN is indicated for the treatment of CAPS, including FCAS and MWS in adults and children. CAN was subsequently approved in 2013 for the treatment of active systemic juvenile idiopathic arthritis (SJIA) in patients aged ≥2.2-4 The European Medicines Agency (EMA) approved CAN for the management of CAPS, gouty arthritis (GA), and SJIA in October 2009.5 New data on CAN use in CAPS is still emerging and CAN is also currently being evaluated in the treatment of other autoinflammatory diseases, including SJIA, as well as hereditary periodic fever syndromes and a range of other conditions, such as GA.6-8 This article reviews the new preclinical and clinical evidence on CAN presented at the American College of Rheumatology/Association of Rheumatology Health Professionals (ACR/ARHP) meeting held in San Francisco, California, USA from 6th–11th November 2015.