Table 1.

Antifungal drugs commonly used against C. auris infection and mechanisms of resistance already reported.

Antifungal Drug Class	Mode of Action	Mechanism of Resistance	Reference(s)
Azoles	Inhibit the activity of lanosterol 14-α-demethylase enzyme; prevent converting lanosterol to ergosterol, leading to damaging integrity of cell membrane.	Overexpression of ATP-binding cassette (ABC) and major facilitator superfamily (MFS) transporters. ERG11 point mutation: Y132F and K143R. Mutation in zinc cluster transcription factors Mrr1 and Tac1.	[9,32,36,45,79,82,85,86,87,88,89,91,92,93]
Polyenes	Bind ergosterol molecules in the cytoplasmic membrane; disturb the permeability of cell membrane by formation of pores, causing oxidative damage.	Induction of genes associated with sterol biosynthetic process including ERG1, ERG2, ERG6, and ERG13. SNPs in different genomic loci related to increased resistance.	[81,84,94,95]
Echinocandins	Inhibit β-(1,3)-D-glucan synthase enzyme, leading to defective cell wall formation.	Hot-spot mutation in FKS1 gene associated with S639Y, S639P, and S639Y regions and FKS2.	[32,36,76,81,96]
Flucytosine	Inhibit the nucleic acid synthesis (DNA and RNA) of fungi.	Mutation of FUR1 gene, specifically missense mutation of FUR1 causing F211I amino acid substituted in the FUR1 gene in one flucytosine-resistant isolate. Mutations in the FCY2, FCY1 genes.	[81,95,97]