How do allylamines inhibit fungal growth?

Allylamines, such as terbinafine, primarily function by inhibiting squalene epoxidase, an enzyme critical in the ergosterol biosynthetic pathway. Ergosterol is a vital component of the fungal cell membrane, analogous to cholesterol in mammalian cells. By blocking squalene epoxidase, allylamines prevent the conversion of squalene to lanosterol, eventually leading to a reduction in ergosterol production. This disruption not only undermines the structural integrity of the fungal cell membrane but also affects numerous biological functions necessary for fungal survival and replication.

In contrast, the other options do not pertain to the mechanism of action of allylamines. While the inhibition of lanosterol demethylase is relevant to azole antifungals, it is not the target of allylamines. Disrupting DNA synthesis involves different mechanisms typically associated with other classes of antifungals, and the blockage of cell wall formation pertains more to agents like echinocandins that target glucan synthesis specifically. Therefore, inhibiting squalene epoxidase distinctly highlights the unique mechanistic action of allylamines in combating fungal infections.