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Zengen's new study reviews novel approach to control inflammation using melanocortin receptors

WOODLAND HILLS, Calif. (March 3, 2004) Zengen, Inc. announced today that its researchers have discovered that activation of melanocortin receptors (MCR) subtypes MC1R and MC3R could be a novel strategy to control inflammatory disorders.

The findings, "Targeting Melanocortin Receptors as a Novel Strategy to Control Inflammation," appear in the March 2004 issue of Pharmacological Reviews, a publication of the American Society for Pharmacology and Experimental Therapeutics (ASPET).

"MCR activation causes a collective reduction of the major molecules involved in the inflammatory process," said Anna Catania, M.D., professor of endocrinology, School of Internal Medicine, University of Milan and lead author of the study. "This discovery is significant because it shows that treatment with melanocortin peptides doesn't abolish the inflammatory response but instead modulates it. An advantage of melanocortins in the treatment of inflammation is that their influences are broad and are not restricted to a specific mediator or chemical pathway."

Recognition and cloning of five melanocortin receptors has greatly improved understanding of peptide-target cell interactions. Preclinical investigations indicate that activation of certain MCR subtypes, primarily MC1R and MC3R, could be useful in treatment of localized and systemic inflammatory disorders. These include: organ transplantation, chronic inflammatory diseases, acute inflammation, inflammation within the brain and neurogenerative disorders, peripheral neuropathies, systemic host reactions, ischemia and reperfusion injury and infections.

"The study results also indicate that certain melanocortin peptides have antimicrobial effects," said James Lipton, Ph.D., chief scientific officer and director of Zengen and study author. "Unlike corticosteroids, melanocortins do not reduce microbial killing activity, but enhance it. We are encouraged by these findings and will continue our res
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3-Mar-2004


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