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Entia Receives Notices Of Allowance For Its Ergothioneine And Genetic Transporter Patents From The United States, Canada, And Israel

Stocks in this article: ERGO

SHERWOOD, Ore., April 2, 2013 /PRNewswire/ -- Entia Biosciences (OTCQB: ERGO), a food science biotechnology company and emerging leader in the field of Nutrigenomics, has now received three Patent Notices of Allowance covering the use of Ergothioneine and its genetic transporter in the treatment of a wide variety of diseases, including those affecting the immune and central nervous systems.  Notices from the United States Patent and Trademark Office and the Israel Patent Office were received in March and from the Canadian Intellectual Property Office in December.

Ergothioneine is a powerful amino acid and master antioxidant that is acquired exclusively from the diet and carried by a unique and specific transporter (human gene symbol SLC22A4) to cells throughout the body that are fighting damage and death from oxidative stress and toxic free radical reactions.  Research conducted by Entia since 2011 has confirmed significant transporter activity in diabetes, arthritis, and several other serious non-communicable chronic conditions, suggesting an important physiologic role for Ergothioneine and its transporter in diseases affecting millions of people world-wide.   

Discovered in 2005 by Dr. Dirk Grundemann at the University of Cologne ( Germany), SLC22A4 is a sodium-ion dependent transporter that efficiently and specifically carries Ergothioneine across the cell membrane to erythrocytes (red blood cells), progenitor stem cells, and monocytes (white blood cells) (Grundemann, 2005).  Variations in SLC22A4 have been associated with susceptibility to inflammatory disorders, such as rheumatoid arthritis and Crohn's disease, and expression has been documented in a variety of human tissues.  Entia licensed the exclusive world-wide diagnostic and therapeutic rights to the discovery from the University of Cologne in 2010 and Dr. Grundemann currently serves on Entia's Scientific Advisory Board.

Found in naturally high concentrations almost exclusively in mushrooms and other fungi, Ergothioneine is transferred directly from these sources into the soil, where it is taken up by plants and grazing mammals.  For thousands of years, our hunter/gatherer genetics have relied on this process to maintain adequate levels of Ergothioneine to prevent or delay the onset and progression of disease.  Entia theorizes introduction of modern agricultural practices in the past century, such as the heavy use of chemical fertilizers, herbicides, pesticides, and over tilling of the soil, has been gradually eradicating mushrooms from our farmland and depleting Ergothioneine from the food supply.   During this same period, our dietary habits have been changing,  which Entia believes is further accelerating deficiency in the general population and may be a contributing factor in the dramatic increases we are now seeing in diabetes, arthritis, neurodegenerative, and other debilitating diseases.  This deficiency theory is supported by human blood testing conducted in the late 1920s (Salt, 1931) that showed "normal" Ergothioneine levels nearly double those found by Pennsylvania State University in 2010 (Weigand-Heller, 2012).

Dr. Solomon Snyder of Johns Hopkins University School of Medicine has suggested that Ergothioneine is as potent as glutathione and because of its dietary origin and the toxicity associated with its depletion, it may represent a new vitamin whose physiologic roles include antioxidant cytoprotection.  Dr. Snyder further believes that the high density of Ergothioneine within mitochondria implies a unique role in protecting mitochondrial DNA from damage induced by free radicals and reactive oxygen species (Snyder, 2009).  Mitochondria are cytoplasmic organelles responsible for life and death.  Evidence from animal and clinical studies suggest that mitochondria play a critical role in aging, cancer, diabetes and neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease (Simon, 2004; Lin, 2006; Reddy, P.H., 2009).   

About Entia Biosciences, Inc.

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