Introduction.Candidaspp. are commensal fungal pathogens of humans, but when there is an imbalance in the microbiota, or weak host immunity, these yeasts can become pathogenic, generating high medical costs.Gap Statement.With the increase in resistance to conventional antifungals, the development of new therapeutic strategies is necessary.This study evaluated thein vitroantifungal activity of chlorogenic acid against fluconazole-resistant strains ofCandidaspp.Mechanism of action through flow cytometry andin silicoanalyses, as well as molecular docking assays with ALS3 and SAP5, important proteins in the pathogenesis ofCandida albicansassociated with the adhesion process and biofilm formation.Results.The chlorogenic acid showedin vitroantifungal activity against the strains tested, causing reduced cell viability, increased potential for mitochondrial depolarization and production of reactive oxygen species, DNA fragmentation and phosphatidylserine externalization, indicating an apoptotic process. Concerning the analysis through docking, the complexes formed between chlorogenic acid and the targetsThymidylate Kinase, CYP51, 1Yeast Cytochrome BC1 ComplexeExo-B-(1,3)-glucanasedemonstrated more favourable binding energy. In addition, chlorogenic acid presented significant interactions with the ALS3 active site residues ofC. albicans,important in the adhesion process and resistance to fluconazole. Regarding molecular docking with SAP5, no significant interactions were found between chlorogenic acid and the active site of the enzyme.Conclusion.We concluded that chlorogenic acid has potential use as an adjuvant in antifungal therapies, due to its anti-Candidaactivity and ability to interact with important drug targets.

Aim: To evaluate the antifungal activity of gallic acid (GA) against the strains of Candida spp. resistant to fluconazole and to determine its mechanism of action. Materials & methods: Antifungal a...

This study evaluated the effect of etomidate against biofilms of Candida spp. and analysed through molecular docking the interaction of this drug with ALS3, an important protein for fungal adhesion. Three fluconazole-resistant fungi were used: Candida albicans, Candida parapsilosis and Candida tropicalis. Growing biofilms were exposed to etomidate at 31.25–500 µg ml⁻¹. Then, an ALS3 adhesive protein from C. albicans was analysed through a molecular mapping technique, composed of a sequence of algorithms to perform molecular mapping simulation based on classic force field theory. Etomidate showed antifungal activity against growing biofilms of resistant C. albicans, C. parapsilosis and C. tropicalis at all concentrations used in the study. The etomidate coupling analysis revealed three interactions with the residues of interest compared to hepta-threonine, which remained at the ALS3 site. In addition, etomidate decreased the expression of mannoproteins on the surface of C. albicans. These results revealed that etomidate inhibited the growth of biofilms.