Mianserin is most probably not an inhibitor or an inducer of any major CYP enzymes.

Mianserin is a racemic mixture, in which S-mianserin is considered as the more potent enantiomer.

Mianserin is indicated for the treatment of depression.

Mianserin is metabolised via 8-hydroxylation, N-demethylation, N-oxidation and glucuronidation (Eap 1999). In vitro data indicates that mianserin is metabolised by CYP2D6, CYP3A and CYP1A (Koyama 1996 and Wang 2009). In vivo data indicates that CYP2D6 is involved in the metabolism of mianserin with enantioselectivity for S(+)-mianserin (Dahl 1994, Yasui 1997 and Wang 2009). Mianserin has two main metabolites, 8-hydroxymianserin and desmethylmianserin. 8-hydroxymianserin contributes to the pharmacological activity of the drug (Eap 1999). The half-life elimination is 21-61 hours (SPC). Co-administration of carbamazepine and mianserin, reduced the AUC of mianserin. Carbamazepine is a known inducer of CYP3A4 and the data therefore indicates that mianserin is a substrate of CYP3A (Eap 1999). Mianserin is not listed as an inducer or inhibitor of any major CYP enzymes (FDA, Hisaka 2010, Isoherranen 2009 and Pelkonen 2008) and no drug-drug interaction with mianserin as a perpetrator has been reported in the literature.

Mianserin is listed as unsafe because it has been shown to be porphyrinogenic in animals or in vitro systems, or to have been associated with acute attacks in humans (Moore 1997).

Uneventful use reported in 3 patients with acute porphyria.