Cyclooxygenase 3 Inhibition: A Probable Mechanism of Acetaminophen in Human: A Review

Abstract

The key rate-limiting step in prostanoid and thromboxane biosynthesis is catalyzed by Cyclooxygenases (COXs) and is the target of nonsteroidal anti-inflammatory drugs (NSAIDs). Until recently, the existence of only two isoforms: COX-1 and COX-2; remained under debate as the anti-pyretic and analgesic property of acetaminophen (paracetamol) could not be explained by mere COX-1 or COX-2 blockades. A novel COX-1 splice variant termed COX-3, sensitive to acetaminophen, was recently discovered in dog brain by Simmons et al., and is considered to play a major role in the biosynthesis of prostanoids known to be significant mediators in pain and fever. Drugs that preferentially block COX-1 also appear to act at COX-3. However at the nucleotide sequence level in humans, the existence of COX-3 is questionable. A functional COX-3 in humans is still perplexing, underlining that the concept of COX-3 is still attractive.

Keywords: COX, NSAIDs, acetaminophen

Cite this Article

Iswar Hazarika, Panner Selvam. Cyclooxygenase 3 inhibition: a probable mechanism of acetaminophen in human: A review. Research & Reviews: A Journal of Pharmaceutical Science. 2015; 6(3): 23–29p.