The antifungals known as polyenes interact with ergosterol, a lipid unique to fungus membranes.
The fungus's homeostatic regulation depends on the sterol-, sphingolipid-, and glycerophospholipid-rich fungal membrane. Azoles impair the normal stability of the fungal membrane by inhibiting the enzyme lanosterol-14-demethylase (Erg11 or CYP51), which converts lanosterol to ergosterol. Unfortunately, the widespread use of these drugs has resulted in the development of resistance mechanisms, including the activation of efflux pumps, the development of biofilms, and the overexpression or active site mutation of CYP51. The creation of novel inhibitors able to overcome the resistance was made possible by the crystal structures of mutant CYP51 enzymes from Saccharomyces cerevisiae and Candida albicans in association with azoles.
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