Comparison of dapaconazole with miconazole in the treatment of <i>Tinea cruris</i>

Gobbato, André Alves Moraes; Babadópulos, Tainah; Gobbato, Cintia Aparecida Rodrigues Santiago; Ilha, Jocemar; Antunes, Nilson; Moreno, Ronílson Agnaldo; Campos, Rafael; Nucci, Gilberto De

doi:10.1111/jdv.15116

Cited by 2 publications

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“…Dapaconazole, a novel imidazole, has shown antifungal activity against several pathogenic fungi, such as Tricophyton verrucosum , Tricophyton rubrum , Trycophyton mantagrophutes , Microsporum gypseum , Microsporum canis , and Aspergillus niger [ 1 , 2 , 3 , 4 , 5 , 6 , 7 ]. Dapaconazole demonstrated noninferior efficacy to miconazole for the topical treatment of tinea cruris [ 4 ], to ketoconazole for treating interdigital tinea pedis [ 3 ], and pityriasis versicolor [ 5 ]. In addition, dapaconazole has shown a good safety profile in all trials.…”

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confidence: 99%

Prospective Prediction of Dapaconazole Clinical Drug–Drug Interactions Using an In Vitro to In Vivo Extrapolation Equation and PBPK Modeling

et al. 2022

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This study predicted dapaconazole clinical drug–drug interactions (DDIs) over the main Cytochrome P450 (CYP) isoenzymes using static (in vitro to in vivo extrapolation equation, IVIVE) and dynamic (PBPK model) approaches. The in vitro inhibition of main CYP450 isoenzymes by dapaconazole in a human liver microsome incubation medium was evaluated. A dapaconazole PBPK model (Simcyp version 20) in dogs was developed and qualified using observed data and was scaled up for humans. Static and dynamic models to predict DDIs following current FDA guidelines were applied. The in vitro dapaconazole inhibition was observed for all isoforms investigated, including CYP1A2 (IC50 of 3.68 µM), CYP2A6 (20.7 µM), 2C8 (104.1 µM), 2C9 (0.22 µM), 2C19 (0.05 µM), 2D6 (0.87 µM), and 3A4 (0.008–0.03 µM). The dynamic (PBPK) and static DDI mechanistic model-based analyses suggest that dapaconazole is a weak inhibitor (AUCR > 1.25 and <2) of CYP1A2 and CYP2C9, a moderate inhibitor (AUCR > 2 and <5) of CYP2C8 and CYP2D6, and a strong inhibitor (AUCR ≥ 5) of CYP2C19 and CYP3A, considering a clinical scenario. The results presented may be a useful guide for future in vivo and clinical dapaconazole studies.

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