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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

The in vitro effects of 6-methoxy-2-naphthylacetic acid, the active metabolite of nabumetone, on rat gastric mucosal eicosanoid synthesis and metabolism.

Nabumetone is a neutral non-steroidal anti-inflammatory drug with a low propensity to cause gastrointestinal (GI) damage. Previous studies, in vivo, have shown that the drug has weak effects on gastric mucosal cyclooxygenase activity, which may help to explain its favourable GI profile. The present study set out to determine whether the observed effects of nabumetone on cyclooxygenase, in vivo, parallel those of its active metabolite, 6-methoxy-2-naphthylacetic acid (6MNA), in vitro. We have also studied nabumetone and 6MNA on two other systems, namely 15-prostaglandin dehydrogenase (15-PGDH) and 5-lipoxy-genase (5-LO), which when inhibited may confer mucosal protection. The results showed that 6MNA had variable effects on cyclooxygenase activity, depending on the concentration and was less potent and less effective than indomethacin. Cyclooxygenase activity was not inhibited by the reversible inhibitor, aminopyrine, but at low concentrations stimulation was observed. Sulphasalazine inhibited 15-PGDH in a concentration-dependent manner whereas 6MNA inhibited it only at high concentrations. Nabumetone was devoid of activity. Basal 5-LO activity was attenuated by phenidone and unaltered by 6MNA but increased by nabumetone at the highest concentration. In the presence of arachidonic acid, to raise 5-LO activity, nabumetone, 6MNA, BW755C and phenidone apparently inhibited this activity. However, it was possible that both nabumetone and 6MNA inhibited a prostanoid-mediated stimulatory effect on 5-LO rather than effecting enzyme inhibition per se. Nabumetone's favourable GI profile may, therefore, relate to 6MNA having weak effects on mucosal cyclooxygenase and is unlikely to involve inhibition of prostanoid metabolism or 5-LO.[1]


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