Cargando…

An update on the anxiolytic and neuroprotective properties of etifoxine: from brain GABA modulation to a whole-body mode of action

Treating the signs and symptoms of anxiety is an everyday challenge in clinical practice. When choosing between treatment options, anxiety needs to be understood in the situational, psychiatric, and biological context in which it arises. Etifoxine, a non-benzodiazepine anxiolytic drug belonging to t...

Descripción completa

Detalles Bibliográficos
Autores principales: Nuss, Philippe, Ferreri, Florian, Bourin, Michel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6615018/
https://www.ncbi.nlm.nih.gov/pubmed/31308671
http://dx.doi.org/10.2147/NDT.S200568
_version_ 1783433286748471296
author Nuss, Philippe
Ferreri, Florian
Bourin, Michel
author_facet Nuss, Philippe
Ferreri, Florian
Bourin, Michel
author_sort Nuss, Philippe
collection PubMed
description Treating the signs and symptoms of anxiety is an everyday challenge in clinical practice. When choosing between treatment options, anxiety needs to be understood in the situational, psychiatric, and biological context in which it arises. Etifoxine, a non-benzodiazepine anxiolytic drug belonging to the benzoxazine class, is an effective treatment for anxiety in response to a stressful situation. In the present review, we focused on several aspects of the cerebral and somatic biological mechanisms involved in anxiety and investigated the extent to which etifoxine’s mode of action can explain its anxiolytic activity. Its two mechanisms of action are the modulation of GABAergic neurotransmission and neurosteroid synthesis. Recent data suggest that the molecule possesses neuroprotective, neuroplastic, and anti-inflammatory properties. Etifoxine was first shown to be an effective anxiolytic in patients in clinical studies comparing it with clobazam, sulpiride, and placebo. Randomized controlled studies have demonstrated its anxiolytic efficacy in patients with adjustment disorders (ADs) with anxiety, showing it to be superior to buspirone and comparable to lorazepam and phenazepam, with a greater number of markedly improved responders and a better therapeutic index. Etifoxine’s noninferiority to alprazolam has also been demonstrated in a comparative trial. Significantly less rebound anxiety was observed after abrupt cessation of etifoxine compared with lorazepam or alprazolam. Consistent with this finding, etifoxine appears to have a very low dependence potential. Unlike lorazepam, it has no effect on psychomotor performance, vigilance, or free recall. Severe adverse events are in general rare. Skin and subcutaneous disorders are the most frequently reported, but these generally resolve after drug cessation. Taken together, its dual mechanisms of action in anxiety and the positive data yielded by clinical trials support the use of etifoxine for treating the anxiety signs and symptoms of individuals with ADs.
format Online
Article
Text
id pubmed-6615018
institution National Center for Biotechnology Information
language English
publishDate 2019
publisher Dove
record_format MEDLINE/PubMed
spelling pubmed-66150182019-07-15 An update on the anxiolytic and neuroprotective properties of etifoxine: from brain GABA modulation to a whole-body mode of action Nuss, Philippe Ferreri, Florian Bourin, Michel Neuropsychiatr Dis Treat Review Treating the signs and symptoms of anxiety is an everyday challenge in clinical practice. When choosing between treatment options, anxiety needs to be understood in the situational, psychiatric, and biological context in which it arises. Etifoxine, a non-benzodiazepine anxiolytic drug belonging to the benzoxazine class, is an effective treatment for anxiety in response to a stressful situation. In the present review, we focused on several aspects of the cerebral and somatic biological mechanisms involved in anxiety and investigated the extent to which etifoxine’s mode of action can explain its anxiolytic activity. Its two mechanisms of action are the modulation of GABAergic neurotransmission and neurosteroid synthesis. Recent data suggest that the molecule possesses neuroprotective, neuroplastic, and anti-inflammatory properties. Etifoxine was first shown to be an effective anxiolytic in patients in clinical studies comparing it with clobazam, sulpiride, and placebo. Randomized controlled studies have demonstrated its anxiolytic efficacy in patients with adjustment disorders (ADs) with anxiety, showing it to be superior to buspirone and comparable to lorazepam and phenazepam, with a greater number of markedly improved responders and a better therapeutic index. Etifoxine’s noninferiority to alprazolam has also been demonstrated in a comparative trial. Significantly less rebound anxiety was observed after abrupt cessation of etifoxine compared with lorazepam or alprazolam. Consistent with this finding, etifoxine appears to have a very low dependence potential. Unlike lorazepam, it has no effect on psychomotor performance, vigilance, or free recall. Severe adverse events are in general rare. Skin and subcutaneous disorders are the most frequently reported, but these generally resolve after drug cessation. Taken together, its dual mechanisms of action in anxiety and the positive data yielded by clinical trials support the use of etifoxine for treating the anxiety signs and symptoms of individuals with ADs. Dove 2019-07-03 /pmc/articles/PMC6615018/ /pubmed/31308671 http://dx.doi.org/10.2147/NDT.S200568 Text en © 2019 Nuss et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Review
Nuss, Philippe
Ferreri, Florian
Bourin, Michel
An update on the anxiolytic and neuroprotective properties of etifoxine: from brain GABA modulation to a whole-body mode of action
title An update on the anxiolytic and neuroprotective properties of etifoxine: from brain GABA modulation to a whole-body mode of action
title_full An update on the anxiolytic and neuroprotective properties of etifoxine: from brain GABA modulation to a whole-body mode of action
title_fullStr An update on the anxiolytic and neuroprotective properties of etifoxine: from brain GABA modulation to a whole-body mode of action
title_full_unstemmed An update on the anxiolytic and neuroprotective properties of etifoxine: from brain GABA modulation to a whole-body mode of action
title_short An update on the anxiolytic and neuroprotective properties of etifoxine: from brain GABA modulation to a whole-body mode of action
title_sort update on the anxiolytic and neuroprotective properties of etifoxine: from brain gaba modulation to a whole-body mode of action
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6615018/
https://www.ncbi.nlm.nih.gov/pubmed/31308671
http://dx.doi.org/10.2147/NDT.S200568
work_keys_str_mv AT nussphilippe anupdateontheanxiolyticandneuroprotectivepropertiesofetifoxinefrombraingabamodulationtoawholebodymodeofaction
AT ferreriflorian anupdateontheanxiolyticandneuroprotectivepropertiesofetifoxinefrombraingabamodulationtoawholebodymodeofaction
AT bourinmichel anupdateontheanxiolyticandneuroprotectivepropertiesofetifoxinefrombraingabamodulationtoawholebodymodeofaction
AT nussphilippe updateontheanxiolyticandneuroprotectivepropertiesofetifoxinefrombraingabamodulationtoawholebodymodeofaction
AT ferreriflorian updateontheanxiolyticandneuroprotectivepropertiesofetifoxinefrombraingabamodulationtoawholebodymodeofaction
AT bourinmichel updateontheanxiolyticandneuroprotectivepropertiesofetifoxinefrombraingabamodulationtoawholebodymodeofaction