Product R, The Immunomodulator from Advanced Viral Research Corp., Enhances Secretion of Proinflammatory Chemokines IL-8 and MCP-1 in Human Monocytes.
YONKERS, N.Y.--(BUSINESS WIRE)--July 17, 2001
Advanced Viral Research Corp. (OTCBB: ADVR) today announced the publication of a scientific research paper showing that Product R, the Company's peptide-nucleic acid immunomodulator, enhances the production of two proteins that boost the immune response during viral infection.
The paper, entitled "IL-8 and MCP-1 Secretion is Enhanced by the Peptide-Nucleic Acid Immunomodulator, Product R, in U937 Cells and Primary Human Monocytes", was based on work done by the Company's Immunology Group, and was published in the scientific journal Cytokine (Volume 14, Number 4, pages 234-239).
Interleukin-8 (IL-8) and monocyte chemoattractant protein (MCP-1) are among the small proteins, termed chemokines, produced by immune system cells in response to microbial infections, especially viral infections. These proteins, in turn, attract additional immune system cells to the site of infection. The work reported in this research paper revealed that Product R increases the production and secretion of both IL-8 and MCP-1 by a human monocytic cell line and by primary human monocytes. In monocytes activated by treatment with bacterial lipopolysaccharide, however, Product R reduced MCP-1 secretion.
"We believe that enhanced secretion of proinflammatory chemokines is an important component of Product R therapy," stated Shalom Z. Hirschman, MD, President and CEO of Advanced Viral Research Corp.
"In this paper our scientists have begun to lay the intellectual ground-work for understanding the "switch-type" activity of Product R on immune function. Product R stimulates the proinflammatory responses that are required to clear viral infections. Alternatively, if there already exists an aberrant proinflammatory reaction such as in autoimmune diseases like rheumatoid arthritis, Product R appears to dampen this reaction. Therefore, the stimulatory or inhibitory activity of Product R may depend upon the state of activation of the immune system in the patient. This may explain, in part, the broad-based effects of Product R on immune function and the promising therapeutic properties of Product R for devastating diseases such as AIDS, cancers and rheumatoid arthritis."
ABOUT PRODUCT R
Product R is a peptide nucleic acid-type immunomodulator that, in both laboratory and clinical studies, has been shown to stimulate the proinflammatory responses required to combat viral infections such as AIDS and human papilloma virus and to dampen aberrant autoimmune-type inflammatory responses, such as occurs in patients with rheumatoid arthritis. Therefore, Product R has been termed a "switch-type" immunomodulator. Product R also has shown promise in its ability to mitigate the toxic side-effects of other drugs, including those employed to treat HIV infection and chemotherapeutic drugs used in the treatment of cancers.
ABOUT ADVANCED VIRAL RESEARCH CORP.
Advanced Viral Research Corp., based in Yonkers, New York, is a biopharmaceutical firm committed to researching, developing and bringing to market new, effective therapies for viral and other diseases. Its flagship drug, Product R, is a non-toxic peptide nucleic acid type immunomodulator, which has direct anti-viral effects against select viruses such as adenovirus and human papilloma virus, and has been shown to have beneficial therapeutic effects against viral diseases such as AIDS and autoimmune diseases like rheumatoid arthritis.
For further information regarding Advanced Viral Research Corp., please visit our website at www.adviral.com
Note: This news release contains forward-looking statements that involve risks associated with clinical development, regulatory approvals, including application to the FDA, product commercialization and other risks described from time to time in the SEC reports filed by ADVR. Product R is not approved by the U.S. Food and Drug Administration or any comparable agencies of any other countries.
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|Date:||Jul 17, 2001|
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