Micafungin is not an inhibitor or an inducer of CYP3A4 in vivo and it is not an inhibitor or inducer of CYP1A2 or CYP2C9 in vitro. Risk for gastrointestinal adverse events in the form of nausea, vomiting, diarrhoea and abdominal pain motivates vigilance against insufficient intake of food, especially of carbohydrate.

Micafungin is an antifungal agent. 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, vomiting, diarrhea and abdominal pain. Other common side effects are increased levels of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and abnormal liver function tests. In rodent studies are found premalignant foci and tumors in the liver after > 3 month exposure to micafungin concentrations also being reached in human therapy with micafungin. Care and monitoring of markers for hepatocellular damage is thus motivated in carriers of acute porphyria (AIP) because of the high incidence of hepatocellular carcinoma in this disorder. Because of nephrotoxic effects, care is also recommended in carriers with affected kidney function or in the risk zone for such. For these reasons micafungin is not a first order drug for use in candididosis or aspargillosis.

Micafungin is hydroxylated to several compounds. It is a CYP3A4 substrate in vivo, but hydroxylation by CYP3A4 is not a major pathway for micafungin metabolism in vivo (SPC). Elimination half-life is 10-17 hours. Micafungin is listed as a mild inhibitor of CYP3A4 in vitro (Fukuoka 2010). In vitro studies indicate that it is not an inhibitor or an inducer of CYP2C9 or CYP1A2 (Niwa 2005, Niwa 2005). The AUC of itraconazole, sirolimus and nifepidine (substrates of CYP3A4) were increased about 20%, when co-administrated with micafungin (Ikeda 2007 and SPC). The increases caused by micafungin are however, according to the FDA, too small to qualify it to be a weak inhibitor of CYP3A4. In a drug-drug interaction study with micafungin and tacrolimus (CYP3A4 substrate) the authors concluded that there is no drug interaction between the two drugs (Fukuoka 2010). This indicates that micafungin is not an inhibitor or an inducer of CYP3A4 in vivo.