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Novel molecule blocks pain receptor system

Discovery May Lead to New Treatments for Pain

Researchers with Banyu Pharmaceutical Co. in Japan have designed a synthetic molecule that can block a molecular pathway, allowing researchers a closer look at what makes some people less sensitive to pain.

This finding will appear in the Dec. 16 issue of the peer-reviewed Journal of Medicinal Chemistry, published by the American Chemical Society, the world's largest scientific society. The article was initially published Nov. 19 on the journal's web site.

Scientists have been studying a nerve receptor called the "opiod receptor-like 1" (ORL-1), which is widely distributed throughout the central nervous system. Like other opiod receptors, ORL-1 was believed to play a key role in pain regulation. However, the natural compounds that activate ORL-1 are different than those that activate the opiod receptors, the researchers say.

In 1995, scientists found a novel hormone, called nociceptin or orphanin FQ, that binds to the ORL-1 receptor. They theorized that blocking the hormone may make a person less sensitive to pain. It has been difficult to test this theory because researchers have lacked an agent to block the hormone-receptor system so its functions could be observed and tested.

Now, the Japanese researchers believe they have found that agent. While there are many different ways to prevent pain, this discovery represents a new avenue for pain research and could be key to development of new and improved drugs to treat pain, says Yoshikazu Iwasawa, Ph.D., research director at Banyu Pharmaceutical Co.

Studies in mice suggest that the ORL-1 receptor and its corresponding hormones may also play important roles in anxiety, learning and memory and other neurological responses. Further understanding of the roles of this hormone-receptor system may lead to drugs not just for pain, but for a variety of neurological disorders, Dr. Iwasawa and hi
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Contact: Beverly Hassell
b_hassell@acs.org
202-872-4065
American Chemical Society
14-Dec-1999


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