ABSTRACT
There are currently only four structurally distinct antifungal classes available for the treatment of invasive fungal infections. As both fungal cells and mammalian cells are eukaryotic, anti-infective drug targets that are fungal specic are few. The most widely exploited strategy for antifungal therapy makes use of differences in sterol biosynthesis and targets either the ergosterol biosynthesis pathway or ergosterol itself, which is incorporated into the fungal cell membrane. Other strategies include inhibiting RNA and DNA synthesis by compounds that are selectively transported into the fungal cell and inhibition of the fungal cell wall. Mortality rates in neutropenic patients for yeast and mold infections are still unacceptably high, and time to implementation of the optimal antifungal has a signicant impact on patient outcomes (Garey et al. 2006).
