Interleukin-1β (IL-1β) is a potent mediator of inflammatory responses and plays 
a role in the differentiation of a number of lymphoid cells. In several 
inflammatory and autoimmune diseases, serum levels of IL-1β are elevated and 
correlate with disease development and severity. The central role of the IL-1 
pathway in several diseases has been validated by inhibitors currently in 
clinical development or approved by the FDA. However, the need to effectively 
modulate IL-1β-mediated local inflammation with the systemic delivery of an 
efficacious, safe and convenient drug still exists. To meet these challenges, we 
developed XOMA 052 (gevokizumab), a potent anti-IL-1β neutralizing antibody that 
was designed in silico and humanized using Human Engineering™ technology. XOMA 
052 has a 300 femtomolar binding affinity for human IL-1β and an in vitro 
potency in the low picomolar range. XOMA 052 binds to a unique IL-1β epitope 
where residues critical for binding have been identified. We have previously 
reported that XOMA 052 is efficacious in vivo in a diet-induced obesity mouse 
model thought to be driven by low levels of chronic inflammation. We report here 
that XOMA 052 also reduces acute inflammation in vivo, neutralizing the effect 
of exogenously administered human IL-1β and blocking peritonitis in a mouse 
model of acute gout. Based on its high potency, novel mechanism of action, long 
half-life, and high affinity, XOMA 052 provides a new strategy for the treatment 
of a number of inflammatory, autoimmune and metabolic diseases in which the role 
of IL-1β is central to pathogenesis.