| Summary: | The opportunistic human fungal pathogen <i>Candida albicans</i> relies on cell morphological transitions to develop biofilm and invade the host. In the current study, we developed new regulatory molecules, which inhibit the morphological transition of <i>C. albicans</i> from yeast-form cells to cells forming hyphae. These compounds, benzyl α-<span style="font-variant: small-caps;">l</span>-fucopyranoside and benzyl β-<span style="font-variant: small-caps;">d</span>-xylopyranoside, inhibit the hyphae formation and adhesion of <i>C. albicans</i> to a polystyrene surface, resulting in a reduced biofilm formation. The addition of cAMP to cells treated with α-<span style="font-variant: small-caps;">l</span>-fucopyranoside restored the yeast-hyphae switch and the biofilm level to that of the untreated control. In the β-<span style="font-variant: small-caps;">d</span>-xylopyranoside treated cells, the biofilm level was only partially restored by the addition of cAMP, and these cells remained mainly as yeast-form cells.
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