XOMA 052 reduces adverse consequences that lead to development of congestive heart failure

XOMA Ltd. (Nasdaq:XOMA), a leader in the discovery and development of antibody therapeutics, announced results demonstrating that a murine equivalent of XOMA 052, its novel, high-affinity antibody to interleukin-1 beta (IL-1 beta), significantly reduced adverse consequences that usually lead to the development of congestive heart failure in a mouse model of acute myocardial infarction (heart attack). The results were presented at the American College of Cardiology 59^th Annual Scientific Sessions in Atlanta.

In the study, mice were randomly assigned to treatment with one of three doses of a murine equivalent of XOMA 052, a control antibody or saline immediately after surgery and again seven days later. Treatment with the two higher doses of XOMA 052 resulted in statistically significant improvements in measurements of left ventricular cardiac function including the ability to pump blood, which is related to an individual's chance of developing congestive heart failure. No signs of cardiac toxicity were observed.

Following a heart attack, IL-1 beta is produced at the site of tissue injury and is responsible for endothelial activation, leukocyte recruitment, and amplification of the inflammatory response. In the context of myocardial infarction, IL-1 beta leads to further tissue damage, resulting in an enlargement and weakening of the heart ("cardiac remodeling").  A weaker heart cannot pump blood as efficiently, leading to congestive heart failure. The consequences of congestive heart failure include shortness of breath, reduced exertion capacity, edema (swelling), and changes in kidney function.

People who have suffered a heart attack have substantially higher risk of developing congestive heart failure than those who have not had a heart attack. Approximately 5.7 million people in the U.S. have been diagnosed with congestive heart failure. Its incidence is increasing as survival following heart attack has increased (American Heart Association Statistical Update, 2009).

"These results demonstrate the significant role of IL-1 beta inhibition in preventing adverse cardiac remodeling in this animal model," said Antonio Abbate, M.D., Assistant Professor of Medicine at the VCU Pauley Heart Center at Virginia Commonwealth University, principal investigator for the study. "Today our group at VCU also presented the first clinical results demonstrating that anakinra, an approved IL-1 targeting agent, reduced adverse cardiac remodeling following acute cardiac events. If further studies of IL-1 targeting support these early results, patients may ultimately benefit from reduced post-heart attack complications and improved recovery."

"Despite many recent advances in prevention and treatment, cardiovascular disease remains the leading cause of death in the United States, demonstrating the ongoing need for new therapies," said Steven Engle, XOMA Chairman and Chief Executive Officer. "In addition to this study of the positive effects of IL-1 beta modulation on cardiac remodeling in this mouse model, other preclinical studies with XOMA 052 have demonstrated promising results in models of atherosclerosis and dyslipidemia. We are delighted that XOMA 052 continues to demonstrate positive results in both Type 2 diabetes and in cardiovascular diseases."