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(S)-Naproxen is a non-selective COX inhibitor [1,2].

Cyclooxygenase (COX) is the key enzyme required for the conversion of arachidonic acid to prostaglandins. Cyclooxygenase enzymes have been involved in diverse physiological situations and disease processes ranging from inflammation to cancer. Until now, two cyclooxygenase isoforms have been identified, COX-1 and COX-2. The COX-1 enzyme is produced constitutively (i.e., gastric mucosa) and COX-2 is inducible (i.e., sites of inflammation) [3].

(S)-Naproxen inhibited the activity of human recombinant COX-1 and -2 with the IC50 values of 0.6-4.8 μM and 2.0-28.4 μM, respectively [1]. (S)-naproxen bound tightly to Aβfibrils with the Ki value of 5.70 ± 1.31 nM against [18F]FDDNP [2]. Pretreatment with (S)-naproxen significantly reduced the specific binding of [18F]FDDNP to regions of gray matter with SPs in AD specimens [4].

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