July 13, 2005
For immediate release
Contact: Bob Beard
(434) 982-4490
UVa Doctors Publish Findings on new Therapy for People with Inflammatory Bowel Disease
Hope to begin clinical trials
An experimental anti-inflammatory drug prevented inflammatory bowel disease in research tests, according to scientists at the University of Virginia Health System. The drug, called ATL-146e, acts on a receptor for the compound adenosine, which is an important regulator of the immune system.
ATL-146e may be a new therapy for the treatment of inflammatory bowel disease in patients, say doctors at UVa, who hope to plan human studies of the drug in the near future. Their findings are detailed in the July 2005 issue of the journal Gastroenterology found on the web at: www.gastrojournal.org.
Inflammatory bowel disease, or IBD, is the collective term for two chronic diseases that cause inflammation of the intestines- ulcerative colitis and Crohn’s disease. It is believed that the body’s own immune system goes haywire and attacks intestinal cells. Common symptoms are diarrhea and abdominal pain. IBD affects an estimated one million Americans, according to the Crohn’s & Colitis Foundation of America. Anyone can get it, but adolescents and young adults between the ages of 15 and 35 are most susceptible.
“Since the cause of IBD is still unknown, currently available treatments for the disease are non-specific and may cause side-effects,” said Dr. Fabio Cominelli, chief of the division of gastroenterology and hepatology at UVa and lead author of the study. “The adenosine receptor pathway identified in this research can provide a new therapy with similar efficacy to current IBD treatments, but without the side effects such as osteoporosis and suppression of the immune system.” Cominelli said side effects are common with current IBD treatments, including the steroid prednisone and a recently-approved IBD drug, remicade.
ATL-146e works by activating a specific receptor to adenosine. This receptor, one of four identified in the body, sends molecular signals to intestinal cells, which protect them from inflammation and tissue death. The study suggests that activating the receptor interferes with the function of lymphocytes, the main means of providing the body with immunity against disease. The receptor also suppresses the production of inflammatory cytokines, proteins that regulate cell growth and function during the immune response.
The study was carried out in cooperation with researchers at Cedars-Sinai Medical Center in Los Angeles and the Akita University School of Medicine in Akita, Japan. Financial support came from the National Institutes of Health, the UVa Digestive Health Research Center, the Crohn’s and Colitis Foundation of America and the Small Business Innovation Research Program (SBIR) in cooperation with Adenosine Therapeutics, LLC of Charlottesville, Va.
###