Nabumetone and its metabolite is metabolised by CYP1A2 and CYP2C9, respectively in vitro. No clinical observations of CYP-induction or –inhibition. Risk for gastrointestinal adverse events in the form of nausea and diarrhoea motivates vigilance against insufficient intake of food, especially of carbohydrate.

Nabumetone is a prodrug and is metabolised to the active metabolite, 6-methoxy-2-naphtylacetic acid (6-MNA).

Nabumetone is indicated for the treatment of rheumatoid arthritis and osteoarthritis. Common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are abdominal pain, nausea, diarrhoea, dyspepsia and obstipation. A less common side effect is pseudo porphyria.

Nabumetone is a prodrug and goes through extensive first-pass metabolism. It is metabolised to 6-MNA (SPC), then hydroxylated to 6-HNA (Matsumoto 2011) and conjugated before excretion in urine (Matsumoto 2011 and SPC). In vitro data indicate that CYP1A2 have a central role in the nabumetone bioactivation and that CYP2B6, CYP2C19, CYP2D6 and CYP2E1 might act as minor metabolic pathways (Turpeinen 2009). In vitro data also suggests that CYP2C9 metabolise 6-MNA to 6-HNA (Matusmoto 2011). 6-MNA has been shown to be a very weak inhibitor of CYP2C9 in human liver microsomes and to have no significant effect on CYP1A2, CYP2A6, CYP2C, CYP2D6 and CYP3A4 (Matsumoto 2011). No drug-drug interactions has been reported with nabumetone as a perpetrator concerning CYP enzymes (DRUID and Interaktionsdatabasen), which may indicate that it is not an inducer or an inhibitor of them.

Uneventful use reported in 1 patient with acute porphyria.