Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (COX) enzyme. Cyclooxygenase is required for prostaglandin and thromboxane synthesis.

While the platelet-dependent effects of aspirin have been extensively studied in the context of COX-1, the role of non-canonical (e.g., non-COX) aspirin-mediated acetylation in platelets remains largely unknown.

Feb 28, 2024 · COX inhibitors divide into non-selective nonsteroidal anti-inflammatory drugs (NSAIDs), COX-2 selective nonsteroidal anti-inflammatory drugs (c2s NSAIDs), and aspirin. NSAIDs include ibuprofen, naproxen, ketorolac, and indomethacin.

Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A (2) synthesis in platelets and reducing platelet aggregation. This mechanism of action accounts for the effect of aspirin on prevention of coronary artery and cerebrovascular thrombosis.

Mar 14, 2000 · Aspirin imparts its primary antithrombotic effects through the inhibition of PGH-synthase/COX by the irreversible acetylation of a specific serine moiety (serine 530 of COX-1 and serine 516 of COX-2) 11 12 and is ≈170-fold more potent in inhibiting COX-1 than COX-2. 13 In the presence of aspirin, COX-1 is completely inactivated, whereas COX-2 ...

Jan 21, 2025 · #Aspirin MOA Cyclooxygenase Inhibition. Aspirin’s hallmark property is irreversible inactivation of cyclooxygenase (COX) enzymes—namely COX-1 and COX-2—through acetylation of a key serine residue within their active sites.

Acetylsalicylic acid (aspirin) represents a prototypic antiplatelet agent. The aim of this chapter is to integrate our current understanding of the molecular mechanism of action of aspirin with the results of clinical trials and epidemiological studies assessing its efficacy and safety.

These results provide evidence that orally consumed aspirin can inhibit the COX pathway and reduce the inflammatory mediator PGE 2 in human skeletal muscle.

Jun 15, 2003 · He proved that aspirin and other non-steroid anti-inflammatory drugs (NSAIDs) inhibit the activity of the enzyme now called cyclooxygenase (COX) which leads to the formation of prostaglandins (PGs) that cause inflammation, swelling, pain and fever.

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis via the cyclooxygenase (COX) enzyme, the key to both therapeutic benefits and toxicity. COX enzyme exists in 2 isoforms, COX-1 and COX-2.