XOMA announced results demonstrating that a murine equivalent of XOMA 052 significantly reduced adverse consequences that usually lead to the development of congestive heart failure in a mouse model of acute myocardial infarction (heart attack)
BERKELEY, CA, USA | March 14, 2010 | 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 today at the American College of Cardiology 59th 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."
Presentation details: Interleukin-1 Beta Neutralization Ameliorates Post-infarction Cardiac Remodeling in the Mouse, Abbate, A., et al., March 14, 2010, 9:30 — 10:30 am, Presentation # 1015-70
About XOMA 052
XOMA 052 is a potent monoclonal antibody with the potential to improve the treatment of patients with a wide variety of inflammatory diseases. XOMA 052 binds strongly to interleukin-1 beta (IL-1 beta), a pro-inflammatory cytokine involved in the development of Type 2 diabetes, cardiovascular disease, rheumatoid arthritis, gout and other diseases. By binding to IL-1 beta, XOMA 052 inhibits the activation of the IL-1 receptor, thereby preventing the cellular signaling events that produce inflammation. XOMA 052 has a half-life, binding properties and specificity for IL-1 beta that may provide for convenient dosing of once per month or less frequently.
About XOMA
XOMA discovers, develops and manufactures novel antibody therapeutics for its own proprietary pipeline as well as through license and collaborative agreements with pharmaceutical and biotechnology companies, and under its contracts with the U.S. government. The company’s proprietary product pipeline includes:
— XOMA 052, an anti-IL-1 beta antibody in Phase 2 clinical development for Type 2 diabetes, Type 1 diabetes and cardiovascular disease, with potential for the treatment of a wide range of inflammatory conditions.
— XOMA 3AB, an antibody candidate in pre-IND studies to neutralize the botulinum toxin, among the most deadly potential bioterror threats, under development through funding provided by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health (Contract # HHSN266200600008C).
— A preclinical pipeline with candidates in development for several diseases.
In addition to its proprietary pipeline, XOMA develops products with premier pharmaceutical companies including Novartis AG, Schering Corporation, a subsidiary of Merck & Co., Inc. and Takeda Pharmaceutical Company Limited.
XOMA’s technologies have contributed to the success of marketed antibody products, including LUCENTIS(R) (ranibizumab injection) for wet age-related macular degeneration and CIMZIA(R) (certolizumab pegol) for rheumatoid arthritis and Crohn’s disease.
The company has a premier antibody discovery and development platform that incorporates an unmatched collection of antibody phage display libraries and proprietary Human Engineering(TM), affinity maturation, Bacterial Cell Expression (BCE) and manufacturing technologies. BCE is a key breakthrough biotechnology for the discovery and manufacturing of antibodies and other proteins. As a result, more than 50 pharmaceutical and biotechnology companies have signed BCE licenses, and several licensed product candidates are in clinical development.
XOMA has a fully integrated product development infrastructure, extending from pre-clinical science to approval, and a team of about 200 employees at its Berkeley, California location. For more information, please visit http://www.xoma.com.
SOURCE: XOMA Ltd.
Post Views: 599
XOMA announced results demonstrating that a murine equivalent of XOMA 052 significantly reduced adverse consequences that usually lead to the development of congestive heart failure in a mouse model of acute myocardial infarction (heart attack)
BERKELEY, CA, USA | March 14, 2010 | 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 today at the American College of Cardiology 59th 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."
Presentation details: Interleukin-1 Beta Neutralization Ameliorates Post-infarction Cardiac Remodeling in the Mouse, Abbate, A., et al., March 14, 2010, 9:30 — 10:30 am, Presentation # 1015-70
About XOMA 052
XOMA 052 is a potent monoclonal antibody with the potential to improve the treatment of patients with a wide variety of inflammatory diseases. XOMA 052 binds strongly to interleukin-1 beta (IL-1 beta), a pro-inflammatory cytokine involved in the development of Type 2 diabetes, cardiovascular disease, rheumatoid arthritis, gout and other diseases. By binding to IL-1 beta, XOMA 052 inhibits the activation of the IL-1 receptor, thereby preventing the cellular signaling events that produce inflammation. XOMA 052 has a half-life, binding properties and specificity for IL-1 beta that may provide for convenient dosing of once per month or less frequently.
About XOMA
XOMA discovers, develops and manufactures novel antibody therapeutics for its own proprietary pipeline as well as through license and collaborative agreements with pharmaceutical and biotechnology companies, and under its contracts with the U.S. government. The company’s proprietary product pipeline includes:
— XOMA 052, an anti-IL-1 beta antibody in Phase 2 clinical development for Type 2 diabetes, Type 1 diabetes and cardiovascular disease, with potential for the treatment of a wide range of inflammatory conditions.
— XOMA 3AB, an antibody candidate in pre-IND studies to neutralize the botulinum toxin, among the most deadly potential bioterror threats, under development through funding provided by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health (Contract # HHSN266200600008C).
— A preclinical pipeline with candidates in development for several diseases.
In addition to its proprietary pipeline, XOMA develops products with premier pharmaceutical companies including Novartis AG, Schering Corporation, a subsidiary of Merck & Co., Inc. and Takeda Pharmaceutical Company Limited.
XOMA’s technologies have contributed to the success of marketed antibody products, including LUCENTIS(R) (ranibizumab injection) for wet age-related macular degeneration and CIMZIA(R) (certolizumab pegol) for rheumatoid arthritis and Crohn’s disease.
The company has a premier antibody discovery and development platform that incorporates an unmatched collection of antibody phage display libraries and proprietary Human Engineering(TM), affinity maturation, Bacterial Cell Expression (BCE) and manufacturing technologies. BCE is a key breakthrough biotechnology for the discovery and manufacturing of antibodies and other proteins. As a result, more than 50 pharmaceutical and biotechnology companies have signed BCE licenses, and several licensed product candidates are in clinical development.
XOMA has a fully integrated product development infrastructure, extending from pre-clinical science to approval, and a team of about 200 employees at its Berkeley, California location. For more information, please visit http://www.xoma.com.
SOURCE: XOMA Ltd.
Post Views: 599
