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Etifoxine: Difference between revisions

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It is not recommended under the age of 18 years.<ref>https://www.awakebrain.com/stresam-etifoxine</ref>
It is not recommended under the age of 18 years.<ref>https://www.awakebrain.com/stresam-etifoxine</ref>


The known mechanism oof action is potentiation of GABA<sub>A</sub> receptor, via stimulation of neurosteroid production.
The known mechanism of action is potentiation of GABA<sub>A</sub> receptor, via stimulation of neurosteroid production.
The etifoxine therapy promoted the regeneration of axons
<ref>[http://www.pnas.org/content/105/51/20505.full.pdf Etifoxine improves peripheral nerve regeneration and functional recovery]</ref>
<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293506/pdf/kjpain-28-4.pdf Etifoxine for Pain Patients with Anxiety]</ref>
<ref>[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293506/pdf/kjpain-28-4.pdf Etifoxine for Pain Patients with Anxiety]</ref>
==Links==
==Links==
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[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364751/pdf/pone.0120473.pdf do Rego JL, Vaudry D, Vaudry H (2015) The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis. PLoS ONE 10(3): e0120473. doi:10.1371/journal.pone.0120473]
[http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364751/pdf/pone.0120473.pdf do Rego JL, Vaudry D, Vaudry H (2015) The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis. PLoS ONE 10(3): e0120473. doi:10.1371/journal.pone.0120473]
etifoxine therapy promoted the regeneration of axons
<ref>[http://www.pnas.org/content/105/51/20505.full.pdf Etifoxine improves peripheral nerve regeneration and functional recovery]</ref>
<references/>
<references/>
[[Category:GABAA receptor positive allosteric modulators]]

Latest revision as of 19:28, 28 November 2016

Choi, YM, and Kim, KH (2015). Etifoxine for Pain Patients with Anxiety

etifoxine is an anticonvulsant and ansiolytic agent. It is not recommended under the age of 18 years.[1]

The known mechanism of action is potentiation of GABAA receptor, via stimulation of neurosteroid production. The etifoxine therapy promoted the regeneration of axons [2] [3]

Links

Etifoxine promotes glial‑derived neurotrophic factor‑induced neurite outgrowth in PC12 cells

do Rego JL, Vaudry D, Vaudry H (2015) The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis. PLoS ONE 10(3): e0120473. doi:10.1371/journal.pone.0120473