Micafungin, a potent inhibitor of 1,3-b-D-glucan synthase, has become the second available agent in the echinocandins class that is approved for use in clinical practice. This agent shares with caspofungin an identical spectrum of in vitro activity against Candida albicans, non-albicans species of Candida, and Aspergillus species, as well as several but not all pathogenic molds. If anything, its in vitro activity appears to be superior to that of caspofungin, although the clinical relevance of this observation is unclear. The clinical role of micafungin appears to be similar to that of caspofungin, although clinical data are still lacking at this stage, with initial approval only for treatment of esophageal candidiasis and prophylaxis in subjects with neutropenia. Pharmacokinetic and pharmacodynamic studies and reports of adverse effects and safety have reported similar but not identical results to those of other agents in the echinocandin class. Factors such as acquisition costs and the potential for resistance development may be more relevant to its widespread use than in vitro and in vivo data comparisons with caspofungin.The echinocandins are a novel class of antifungals. Caspofungin was the first echinocandin agent approved by the US Food and Drug Administration (FDA), and anidulafungin is currently in phase 3 development. Micafungin is a promising echinocandin that was recently approved by the FDA and has demonstrated activity against Candida and Aspergillus species.
MECHANISM OF ACTIONMicafungin is a water-soluble antifungal agent (molecular weight, 1292.26 Da) that is derived from Coleoptioma empedri via enzymatic cleavage of the hexapeptide FR901370, a natural product of the fungus; the addition of a fatty N-acyl side chain improves its antifungal potency [1,2]. Micafungin acts in a concentration-dependent manner as a noncompetitive inhibitor of the formation of the enzyme 1,3-b-d glucan synthase, an enzyme necessary for synthesis of 1,3-b-d glucan, a glucose polymer crucial to the structure and integrity of the cell wall of several common fungal pathogens [3][4][5]. Fungal cells unable to synthesize this polysaccharide cannot maintain their shape and lack adequate rigidity to resist osmotic pressure, which results in fungal cell lysis. This mechanism is unique to the echinocandin class of antifungal agents and has the potential to be either additive or synergistic with polyenes and azoles. Glucan is essential not only to cell-wall structure and integrity but also to cell growth and division [6]. Micafungin demonstrates a prolonged concentration-dependent postantifungal effect.Most fungal cell walls contain chitin, a-or b-linked glucans, and a variety of mannoproteins, although the quantity and relative importance of each component varies among different fungal species-thus, the selective antifungal effect on echinocandins [7]. Of significance, the cell walls of zygomycetes and cryptococcus lack 1,3-b-d glucan, which explains the poor activity of echinocandins, including micafungin, against these fungi ...