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Discovery may lead to first medical treatment for Celiac disease

WOODLAND HILLS, Calif. (February 19, 2003) - Results from a new study may lead to the first medical treatment for celiac disease, a hereditary digestive disease that can damage the small intestine and interfere with the absorption of nutrients from food. Celiac disease sufferers cannot tolerate gluten, a protein that is found in wheat, barley and rye. Celiac disease affects an estimated one in 250 Americans, mostly those of European descent, and there is no known medical treatment or cure.

Zengen, Inc. researchers discovered that a synthetic form of alpha-Melanocyte-Stimulating Hormone (a-MSH) has an anti-inflammatory effect in celiac mucosa, the inside lining of the intestinal tract that absorbs food into the body. A naturally occurring molecule, a-MSH modulates inflammatory and immune responses. Data confirming the presence of a-MSH in celiac mucosa suggests the presence of a local reaction of the molecule to control the inflammatory response elicited by gliadin. Gliadin is the subfraction of gluten that acts as a toxin or poison in people with celiac disease; it causes an immune reaction, resulting in damage to the small intestine and an inability to digest and absorb nutrients necessary for health and growth (malabsorption).

The findings, "Anti-Inflammatory Effects of a-Melanocyte-Stimulating Hormone in Celiac Intestinal Mucosa," appear in the February 20, 2003 issue of NeuroImmunoModulation, the official journal of the International Society for Neuroimmunomodulation.

"Our research suggests that locally-produced a-MSH modulates inflammation and perhaps limits epithelial damage in patients with celiac disease," stated James M. Lipton, Ph.D, study investigator, chief scientific officer and director of Zengen. "We are particularly excited by these findings as these data, coupled with abundant evidence of the anti-inflammatory and anti-infective activity of Zengen's novel molecules based on a-MSH, further validate our research and deve
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19-Feb-2003


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