Acetaminophen (paracetamol) is a selective cyclooxygenase‐2 inhibitor in man

@article{Hinz2008AcetaminophenI,
  title={Acetaminophen (paracetamol) is a selective cyclooxygenase‐2 inhibitor in man},
  author={Burkhard Hinz and Olga Cheremina and Kay Brune},
  journal={The FASEB Journal},
  year={2008},
  volume={22},
  pages={383 - 390},
  url={https://api.semanticscholar.org/CorpusID:9633350}
}
In contrast to previous concepts, acetaminophen inhibited COX‐2 by more than 80%, i.e., to a degree comparable to nonste‐roidal antiinflammatory drugs (NSAIDs) and selective COx‐2 inhibitors.
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52 References

Mechanism of action of acetaminophen: is there a cyclooxygenase 3?

COX-3 may be a product of the same gene that encodes COX-2, but have different molecular characteristics, because acetaminophen is a weak inhibitor in vitro of both cyclooxygenase (COX)-1 and COx-2.

Mechanism of acetaminophen inhibition of cyclooxygenase isoforms.

Results are consistent with a mechanism of inhibition of acetaminophen in which it acts to reduce the active oxidized form of COX to the resting form, consistent with the known tissue selectivity of acetamine.

Mechanism of Action of Paracetamol

There is considerable evidence that the analgesic effect of paracetamol is central and is due to activation of descending serotonergic pathways, but its primary site of action may still be inhibition of PG synthesis.

Determinants of the cellular specificity of acetaminophen as an inhibitor of prostaglandin H2 synthases

The hypothesis that the clinical action of acetaminophen is mediated by inhibition of PGHS activity, and that hydroperoxide concentration contributes to its cellular selectivity, is supported.

Actions of paracetamol on cyclooxygenases in tissue and cell homogenates of mouse and rabbit.

The hypothesis that paracetamol selectively inhibits a COX enzyme which is different from COX1 or COX-2 and may be a variant ofCOX-1 is supported.

Pharmacological analysis of cyclooxygenase-1 in inflammation.

The results suggest that, in addition to the role of peripherally produced PGs, there is a critical, centrally mediated neurological component to inflammatory pain that is mediated at least in part by COX-2.

Acetaminophen and the Cyclooxygenase-3 Puzzle: Sorting out Facts, Fictions, and Uncertainties

The aim of this review is to evaluate the literature that seeks to point out critical theoretical and methodological limitations of the COX-3 studies that led several investigators to scientifically questionable conclusions.

COX‐3—a virtual pain target in humans?

A long-sought molecule (1) was recently identified as acting independent of COX-1/-2 (2). The potent analgesic and anti-pyretic actions of acetaminophen lacking anti-inflammatory potency suggested…

COX-3, a cyclooxygenase-1 variant inhibited by acetaminophen and other analgesic/antipyretic drugs: Cloning, structure, and expression

Comparison of canineCOX-3 activity with murine COX-1 and -2 demonstrates that this enzyme is selectively inhibited by analgesic/antipyretic drugs such as acetaminophen, phenacetin, antipyrine, and dipyrone, and is potently inhibited by some nonsteroidal antiinflammatory drugs.

Dose-dependent Inhibition of Platelet Function by Acetaminophen in Healthy Volunteers

Acetaminophen, which is a weak inhibitor of platelet cyclooxygenase 1, has a dose-dependent antiaggregatory effect that may become clinically significant in patients with intrinsic or drug-induced impairment of hemostasis.
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