Two mechanisms of butenafine action in Candida albicans.

Article Details

Citation

Copy to clipboard

Iwatani W, Arika T, Yamaguchi H

Two mechanisms of butenafine action in Candida albicans.

Antimicrob Agents Chemother. 1993 Apr;37(4):785-8.

PubMed ID

8494375 [ View in PubMed

]

Abstract

The mechanism of action of a new benzylamine antimycotic, butenafine hydrochloride, was studied in Candida albicans by using the thiocarbamate antimycotic tolnaftate as a reference drug. Butenafine completely inhibited the growth of a test strain of C. albicans at 25 micrograms/ml and was cidal at 50 micrograms/ml. Tolnaftate did not show any growth-inhibitory activity up to 100 micrograms/ml. Both butenafine and tolnaftate inhibited squalene epoxidation in C. albicans, with 50% inhibitory concentrations being 0.57 and 0.17 microgram/ml, respectively. Butenafine, but not tolnaftate, induced the release of appreciable amounts of Pi from C. albicans cells at 12.5 micrograms/ml. This effect of butenafine was augmented when the cells were pretreated with tolnaftate. The results suggest that the direct membrane-damaging effect of butenafine may play a major role in its anticandidal activity and that the drug-induced alteration in the cellular sterol composition renders the cell membrane more susceptible to the membrane-damaging effect of this drug.

DrugBank Data that Cites this Article

Drugs

Butenafine

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Butenafine	Squalene monooxygenase	Protein	Humans	Yes	Inhibitor	Details