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|Metabolism||Via catechol-O-methyltransferase pathway|
|Elimination half-life||11–17 hours|
|Excretion||40% feces, <15% urine|
|Chemical and physical data|
|Molar mass||1270.28 g/mol|
|‹See TfM› (what is this?)|
Micafungin (trade name Mycamine) is an echinocandin antifungal drug used to treat and prevent invasive fungal infections including candidemia, abscesses and esophageal candidiasis. It inhibits the production of beta-1,3-glucan, an essential component of fungal cell walls. Micafungin is administered intravenously. It received final approval from the U.S. Food and Drug Administration on March 16, 2005, and gained approval in the European Union on April 25, 2008.
Micafungin is indicated for the treatment of candidemia, acute disseminated candidiasis, Candida peritonitis, abscesses and esophageal candidiasis. Since January 23, 2008, micafungin has been approved for the prophylaxis of Candida infections in patients undergoing hematopoietic stem cell transplantation (HSCT).
Micafungin works by way of concentration-dependent inhibition of 1,3-beta-D-glucan synthase resulting in reduced formation of 1,3-beta-D-glucan, which is an essential polysaccharide comprising one-third of the majority of Candida spp. cell walls. This decreased glucan production leads to osmotic instability and thus cellular lysis.  
Known hypersensitivity to micafungin or any other ingredient contained in the formulation is a contraindication for its use.
The metabolism of micafungin occurs hepatically as the drug molecule is a substrate of CYP3A4, a liver enzyme. Precautions should be taken with regards to dosing, as micafungin also inhibits its own clearance via weak CYP3A4 inhibition.
Micafungin is a natural antifungal product derived from other fungi as a defense mechanism for competition of nutrients, etc. To be specific, micafungin is derived from FR901379, and is produced by Coleophoma empetri.