New preclinical data of XOMA 052 in animal model of Type 2 diabetes to be presented at ADA 2010

XOMA Ltd. (Nasdaq:XOMA), a leader in the discovery and development of therapeutic antibodies, will be presenting new preclinical data in an animal model of Type 2 diabetes in which its anti-inflammatory therapeutic antibody candidate, XOMA 052, was used as monotherapy and in combination with the marketed anti-diabetic drugs exendin-4 (Byetta®) or sitagliptin (Januvia®). The new results, to be presented at the American Diabetes Association 70^th Scientific Sessions add to the growing body of research supporting the development of XOMA 052, an inhibitor of the pro-inflammatory cytokine interleukin-1 beta (IL-1 beta), in Type 2 diabetes.

Two posters will be presented on Monday, June 28 from 12:00 PM to 2:00 PM in the Orange County Convention Center, Hall C. Abstract 1811-P is entitled "Combination Studies of the Anti-Interleukin-1 beta Monoclonal Antibody XOMA 052 with Exendin-4 or Sitagliptin in a Diet-Induced Obesity Mouse Model of Type 2 Diabetes Mellitus." XOMA 052 was evaluated in combination with either exendin-4 or sitagliptin. As previously reported, researchers demonstrated that, in a mouse model, XOMA 052 had significant beneficial effects on fasting insulin, stimulated insulin secretion, beta-cell proliferation and beta-cell mass. The results also demonstrated no deleterious effects with the two-drug combinations and improved insulin tolerance with a combination of XOMA 052 and sitagliptin. The results support the evaluation of XOMA 052 in combination with either sitagliptin or exendin-4 in Type 2 diabetes patients.

Abstract 1820-P is entitled "Inhibition of Interleukin-1 beta with the Monoclonal Antibody XOMA 052 Reveals the Differential Sensitivities of Glycemic and Pancreatic Function Parameters to Chronic Inflammation." The poster details an extended pharmacological study of XOMA 052 in the diet-induced obesity mouse model. This study examined different doses of XOMA 052 and suggests that pancreatic function parameters in the diet-induced obesity model may be differentially sensitive to locally available IL-1 beta.

The final abstract 2467-PO, accepted as published-only, is entitled "The Role of Interleukin-1 beta in Insulin Resistance." Examined in the abstract were in vitro models that support the hypothesis that IL-1 beta interferes with normal insulin signaling and that XOMA 052 may prevent this interference.

Previously, XOMA has reported results showing  that mice treated with XOMA 052 both prophylactically and therapeutically experienced improvement in measures associated with diabetes and cardiovascular disease including reduction in glycosylated hemoglobin (HbA1c) levels, improvement in glucose control, improved beta-cell survival and function, and a reduction in total cholesterol without reduction in high density lipoprotein. Each of these parameters is an important goal for the management of Type 2 diabetes, and well-controlled blood glucose levels and reductions in lipid levels can help minimize the risk of long-term consequences associated with diabetes.