"We found a new way to treat a chronic and debilitating form of pain suffered by hundreds of millions of people on Earth," says J. Michael McIntosh, a University of Utah research professor of biology, and research director and professor in the Department of Psychiatry. "It is a previously unrecognized mechanism for treating pain."
The findings are being published the week of Nov. 13 in the online edition of the journal Proceedings of the National Academy of Sciences.
The study in rats found that cone snail toxins named RgIA and Vc1.1 can treat nerve hypersensitivity and pain by blocking a molecule in cells known as the "alpha9alpha10 nicotinic acetylcholine receptor."
"The numerous analgesic compounds currently available are largely ineffective" for chronic nerve pain, McIntosh and colleagues write. "Our findings not only suggest a previously unrecognized molecular mechanism for the treatment of neuropathic pain, but also demonstrate the involvement of alpha9alpha10 nicotinic receptors" in nerve injury.
McIntosh emphasized neither substance will be on the market soon. Vc1.1, also known as ACV1, is being developed by an Australian company, Metabolic, and is undergoing trials of its effectiveness in human patients. While Metabolic has said the drug targets nicotinic receptors, McIntosh says alpha9alpha10 nicotinic receptors have not been reported previously as a target for any kind of painkilling medication. McIntosh says Vc1.1 is administered by subcutaneous (under the skin) injection.
McIntosh hopes the new findings make it feasible to develop a painkiller based on RgIA that could be taken orally, but he believes that will take at least 10 years.
Source:University of Utah