Galantamine is not an inhibitor or an inducer of CYP3A4. Risk for gastrointestinal adverse events in the form of reduced appetite, anorexia, weight decreased, vomiting, nausea, diarrhoea and dyspepsia motivates vigilance against insufficient intake of food, especially of carbohydrate.

Galantamine has three chiral centres and the S,R,S-form is the naturally occurring form. It is a tertiary alkaloid.

Galantamine is a reversible competitive inhibitor of acetylcholinesterase (AChE) and is indicated for the symptomatic treatment of mild to moderately severe dementia of the Alzheimer type. Very common and 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 reduced appetite, anorexia, vomiting, nausea, abdominal pain, diarrhoea, dyspepsia, stomach and abdominal discomfort, fatigue and weight decreased. Other common side effects are hallucination, depression, syncope, dizziness, tremor, headache, somnolence, bradycardia and hypertension.

Galantamine is metabolised mainly by CYP2D6 and CYP3A4 to clinically inactive metabolites (Farlow 2003 and SPC). The elimination half-life is 8-10 hours. In vitro studies indicated that the inhibition potential of galantamine with respect to the major forms of human cytochrome P450 is very low (SPC). Galantamine increased the AUC of risperidone by 10% when co-administrated. This is believed to be caused by weak inhibition by CYP2D6 (Huang 2002). The increase is however, too low for CYP enzymes to be considered as a weak inhibitor by the criteria’s of the FDA. An in vivo study also suggests that CYP3A4 contributes significantly to the metabolism of risperidone (Mahatthanatrakul 2012). The drug interaction study with galantamine and risperidone might therefore indicate that galantamine is not an inhibitor or an inducer of CYP3A4.