ERGO >>Patents from the United States, Canada, and Israel//
Entia Receives Notices of Allowance for its Ergothioneine and Genetic Transporter Patents from the United States, Canada, and Israel
PR NewswirePress Release: Entia Biosciences – Tue, Apr 2, 2013 12:10 PM EDT
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SHERWOOD, Ore., April 2, 2013 /PRNewswire/ -- Entia Biosciences (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.
Entia is an authority on the clinical effects of oxidative stress and free radical reactions and is bringing this expertise to the fields of food science biotechnology and Nutrigenomics. The Company identifies, scientifically validates, patents, and commercializes solutions that address multi-billion dollar markets for health, beauty and agriculture.
For more information, please visit our web sites at www.entiabio.com or contact:
Devin Andres
Chief Operating Officer
Entia Biosciences, Inc.
13565 SW Tualatin-Sherwood Rd Sherwood, OR, 97140
Phone: 503-334-3575 Email: info@entiabio.com
Any statements contained in this press release that relate to future plans, events or performance are forward-looking statements that involve risks and uncertainties including, but not limited to, the risks associated with the transaction described in this press release, and other risks identified in the filings by Entia Biosciences with the Securities and Exchange Commission. Further information on risks faced by the Company and its shareholders are detailed in the Form 10-K for the year ended December 31, 2012 and in its subsequent Quarterly Reports on Form 10-Q. These filings are or will become available on a website maintained by the Securities and Exchange Commission at http://www.sec.gov. The information contained in this press release is accurate as of the date indicated. Actual results, events or performance may differ materially. Entia does not undertake any obligation to publicly release the result of any revision to these forward-looking statements that may be made to reflect events or circumstances after the date hereof or to reflect the occurrence of unanticipated events.
Bibliography:
Burmer, G. (2012). TNCS001A-1/SLC22A4. Entia Biosciences.
Grigat, S. et al. (2007). Probing the Substrate Specificity of the Ergothioneine Transporter with Methimazole, Hercynine,and Organic Cations. Biochem. Pharmacol., 74, 309-316.
Grundemann, D. et al. (2005). Discovery of the Ergothioneine Transporter. Proc. Natl. Acad. Science (PNAS), 102(14), 5256-5261.
Lin, MT. & Beal, MF . (2006). Mitochondrial Dysfunction and Oxidative Stress in Neurodegenerative Diseases. Nature, 443, 787-795.
Mydel, P. et al. (2006). Roles of the Host Oxidative Immune Response and Bacterial Antioxidant Rubrerythrin During Porphyromonas gingivalis Infection. PloS. Pathog., 2(7), 71-76.
Paul, B. & Snyder, S., (2009). The Unusual Amino Acid L-Ergothioneine is a Physiologic Cytoprotectant. Cell Death & Differentiation, pp. 1-7.
Reddy, P. (2009). The Role of mitochondria in Neurodegenerative Diseases: Mitochondria as a Therapeutic Target in Alzheimer's Disease. CNS Spectr., 14(8), 8-18.
Salt, HB (1931). The Ergothioneine Content of the Blood in Health and Disease. Biochem J., 25(5):1712-1719
Simon, D. K. (2004). Somatic mitochondrial DNA Mutations in Cortex and Substantia nigra in Aging and Parkinson's Disease. Neurobiol. Aging, 25, 71-81.
Turner, E. et al. (2009). Imidazole-Based Erythrocyte Markers of Oxidative Stree in Preeclampsia - An NMR Investigation. Reprod.Sciences, 16(11), 1040-1051.
Weigand-Heller et al. (2012)The bioavailability of ergothioneine from mushrooms (Agaricus bisporus) and the acute effects on antioxidant capacity and biomarkers of inflammation. Preventive Medicine, 54:575-578.
West, A. et al. (2011). TLR Signalling Augments Macrophage Bactericidal Activity Through Mitochondrial ROS. Nature, 472, 476-480.
