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Enzyme mimetic reduces tissue damage in colitis animal study

Study further demonstrates selective, anti-inflammatory properties of small-molecule compounds

St. Louis, MO, December 12, 2001 The estimated 1 to 2 million Americans suffering from inflammatory bowel disease may benefit from a potential new treatment, using small-molecule enzyme mimetics, based on research published in the European Journal of Pharmacology.

The preclinical study conducted by MetaPhore Pharmaceuticals, Inc. of St. Louis, MO and the University of Messina (Italy) showed that a superoxide dismutase (SOD) enzyme mimetic significantly reduced the extent and severity of inflammation and tissue damage to the intestinal wall in an animal model of colitis. Researchers also observed a marked reduction in the diarrhea and body weight loss typical of this disease.

The SOD mimetic, M40403, was also shown to reduce elevated levels of two pro-inflammatory cytokines, tumor necrosis factor alpha (TNF-) and interleukin-1 (IL-1), implicated in the development of inflammatory bowel disease. M40403 is one of a proprietary family of small-molecule SOD mimetics developed by MetaPhore that are designed to selectively remove superoxide, a free radical that, in excess, has been shown to contribute to inflammatory pathways and to regulate cytokine release.

In addition, M40403 reduced the production of adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and P-selectin, in the intestinal wall of the animals. These adhesion molecules appear to play a major role in the development and persistence of inflammatory bowel disease in humans by promoting infiltration of inflammatory cells (neutrophils) into the intestine wall.

Inflammatory bowel disease includes two specific disorders: Ulcerative colitis, which affects the inner lining of the lower colon, and Crohns disease, which extends into the deeper layers of the intestinal wall. In Crohns disease, the damage to the intestine can be so great that large open
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Contact: Punnie Donohue
pdonohue@kupperparker.com
314-290-2014
Kupper Parker Communications
12-Dec-2001


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