Fluvastatin is a weak inhibitor of CYP2C9, but is not listed as a mechanism-based inhibitor. It is not listed as an inducer of CYP enzymes. Risk for gastrointestinal adverse events in the form of nausea motivates vigilance against insufficient intake of food, especially of carbohydrate.

HMG-CoA reductase inhibitor

Fluvastatin is indicated for the treatment of hypercholesterolemia and cardiovascular prevention. 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 nausea, dyspepsia and abdominal pain. Another common side effect is insomnia.

Fluvastatin is mainly metabolized by CYP2C9 (Corsini 1999, Masubuchi 2007), but is also metabolized by CYP3A4, CYP2C8 and CYP2D6 (Norsk legemiddelhåndbok, Scripture 2001). The elimination half-life is 2-3 hours. In vitro studies have shown that fluvastatin increased the expression of CYP2C9 which was mediated through CAR (Bertrand-Thiebault 2007). Other in vitro studies have shown that fluvastatin induce CYP3A and CYP2B effectively (Dickins 2004, Kocarek 2002), but it is not listed as an inducer of CYP enzymes in humans (Hisaka 2010, Pelkonen 2008). Losartan is primarily converted to the metabolite E-3174 by CYP2C9. Co-administration of losartan with fluvastatin did not affect the metabolism of losartan, which may indicate that fluvastatin do not inhibit or induce CYP2C9 (Meadowcroft 1999, Scripture 2001). Fluvastatin have however, increased the AUC of tolbutamide by 23 % (Appel 1995, Meadowcroft 1999) and the AUC of glibenclamide by 19 % (Appel 1995). They are CYP2C9-substrates, which indicates that fluvastatin is an inhibitor of CYP2C9. Fluvastatin is listed as a weak inhibitor of CYP2C9 in vivo (Isoherranen 2009, Scripture 2001), but is on the other hand not listed as a mechanism-based inhibitor (Pelkonen 2008). An in vitro study has showed that it is a non-competitive inhibitor of CYP3A4 (McDonnell 2005).