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News--
Scientists Discover Secret of Tylenol's Success
By Merritt McKinney Sep 16, 2002
NEW YORK (Reuters Health) - Acetaminophen,
better known as the active ingredient in Tylenol and certain cold remedies, has
been used for more than a century to relieve pain and fever, but exactly how the
drug worked was a bit of a mystery. Now, Utah researchers have found that the
drug seems to target a variant form of an inflammation-related enzyme.
Ibuprofen, aspirin and other so-called
nonsteroidal anti-inflammatory drugs, or NSAIDs, work in part by targeting a
pair of enzymes called COX-1 and COX-2. Although acetaminophen relieves pain and
fever, unlike NSAIDs it does not have a strong anti-inflammatory effect nor does
it target COX-1 and COX-2.
Acetaminophen has "never had a clearly defined mechanism of action," Dr.
Daniel L. Simmons, of Brigham Young University in Provo, who led the new
research, told Reuters Health in an interview.
But according to Simmons, scientists have suspected that there might be a
type of COX enzyme in the brain that is more sensitive to acetaminophen. In
experiments in dogs, Simmons and his colleagues seemed to detect two different
types of COX-1. This variation of COX-1, which the researchers dubbed COX-3, was
most abundant in the brains of the dogs.
Unlike COX-1 and COX-2, this newly discovered enzyme, COX-3, was strongly
inhibited by acetaminophen.
"Thus, inhibition of COX-3 in the brain and the spinal cord may be the long
sought-after mechanism of action of acetaminophen," Simmons and his colleagues
state in a report that is published in the advance online edition of the journal
Proceedings of the National Academy of Sciences.
What's more, Simmons said in the interview, "not only was it sensitive to
acetaminophen, it was sensitive to other drugs that have a similar sort of
action."
Besides shedding light on the workings of a drug that is a staple of the
modern medicine cabinet, the discovery of COX-3 could advance research on pain
in general, according to the report. Since the newly identified enzyme is a
variant form of COX-1, the fact that COX-3 is blocked by acetaminophen, a pain
and fever reliever, suggests that the gene for COX-1 may play an important role
in pain and fever.
Simmons and his colleagues also found that besides acetaminophen, several
types of NSAIDs inhibited COX-3. This raises the possibility, according to the
report, that some of the pain-relieving effects of these drugs might stem from
their effect on the newly identified enzyme.
The findings represent a "very interesting and exciting start," according to
Simmons, but much more research needs to be done. One of the next steps, he
said, is to identify COX-3 in humans and prove that acetaminophen blocks it.
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