Arachidonic acid (AA) (AA)

Arachidonic acid is a 20-carbon polyunsaturated omega-6 fatty acid that is a fundamental component of the phospholipid bilayer in mammalian cell membranes [1, 3]. It is liberated from membranes by the enzyme phospholipase A2 (PLA2) in response to inflammatory or physiological stimuli [2]. Once released, it serves as the primary substrate for three major enzymatic pathways: the cyclooxygenase (COX) pathway, the lipoxygenase (LOX) pathway, and the cytochrome P450 (CYP) pathway [2]. These pathways produce a diverse array of bioactive lipid mediators known as eicosanoids, including prostaglandins, thromboxanes, and leukotrienes, which regulate inflammation, blood pressure, and platelet aggregation [1, 2]. While arachidonic acid is essential for normal cellular signaling and brain health, its over-metabolism is a hallmark of chronic inflammatory conditions, asthma, and cardiovascular disease [2, 3]. Consequently, the arachidonic acid cascade is one of the most significant therapeutic targets in medicine, though drugs typically target the metabolizing enzymes rather than the fatty acid itself [1]. Common pharmacological interventions include nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit COX enzymes, and corticosteroids, which limit the availability of free arachidonic acid [2].

Other names

(5Z,8Z,11Z,14Z)-eicosa-5,8,11,14-tetraenoic acid5,8,11,14-Eicosatetraenoic acidall-cis-5,8,11,14-Eicosatetraenoic acidOmega-6 fatty acid (20:4n-6)ARA

Pharmacological agents typically modulate the arachidonic acid pathway by inhibiting the enzymes responsible for its release from membranes (e.g., Phospholipase A2) or its conversion into bioactive eicosanoids (e.g., Cyclooxygenase-1/2, 5-Lipoxygenase), or by antagonizing downstream eicosanoid receptors.