Etifoxine
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| AHFS/Drugs.com | International Drug Names |
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| Routes of administration |
Oral |
| ATC code | N05BX03 (WHO) |
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| Pharmacokinetic data | |
| Bioavailability | 90% |
| Metabolism | Hepatic (no CYP450 interactions) |
| Biological half-life | 2 to 6 hours (etifoxine), 20 to 30 hours (active metabolite)[1] |
| Excretion | Renal |
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| CAS Number | 21715-46-8  |
| PubChem (CID) | 30768 |
| IUPHAR/BPS | 5468 |
| DrugBank | DB08986  |
| ChemSpider | 28547 |
| UNII | X24X82MX4X |
| KEGG | D07320 |
| ChEMBL | CHEMBL2106227 |
| Chemical and physical data | |
| Formula | C17H17ClN2O |
| Molar mass | 300.782 g/mol |
| 3D model (Jmol) | Interactive image |
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Etifoxine (INN,[2] also known as etafenoxine; trade name Stresam) is an anxiolytic and anticonvulsant drug[3][4] developed by Hoechst in the 1960s.[2] It is used in some countries for anxiety disorders.[5] It has similar effects to benzodiazepine drugs, but is structurally distinct and does not bind to the benzodiazepine receptor.[6] It is more effective than lorazepam as an anxiolytic, and has fewer side effects.[7] Etifoxine is not approved by the U.S. Food and Drug Administration or the European Medicines Agency.
Side effects[edit]
The most common adverse effect is drowsiness at the initial stage. It does not usually cause any withdrawal syndromes. In conclusion, etifoxine shows less adverse effects of anterograde amnesia, sedation, impaired psychomotor performance, and withdrawal syndromes than those of benzodiazepines Etifoxine for Pain Patients with Anxiety[8]
Mechanism of action[edit]
Unlike benzodiazepines, etifoxine appears to produce its anxiolytic effects by binding to β2 and β3 subunits of the GABAA receptor complex, and so is acting at a different target site to benzodiazepines, although the physiological effect that is produced is similar to that of benzodiazepines.[9] This difference in binding means that etifoxine can be used alongside benzodiazepines to potentiate their effects without competing for binding sites;[10] however, it also means that the effects of etifoxine are not reversed by the benzodiazepine antagonist flumazenil.[11]
Etifoxine has been shown to stimulate the biosynthesis of endogenous neurosteroids, namely 17-hydroxypregnenolone, dehydroepiandrosterone, progesterone and tetrahydroprogesterone.[12] This is likely to contribute to the drug's effects, to what extent however, is unclear.
References[edit]
- ^ "Stresam PI" (PDF). Adcock Ingram. n.d. Retrieved 2008-08-30.[dead link]
- ^ a b U.S. Patent 3,725,404
- ^ Kruse HJ, Kuch H (1985). "Etifoxine: evaluation of its anticonvulsant profile in mice in comparison with sodium valproate, phenytoin and clobazam". Arzneimittelforschung. 35 (1): 133–135.
- ^ The Merck Index, 12th Edition. 3910.
- ^ Girard C, Liu S, Cadepond F, Adams D, Lacroix C, Verleye M, Gillardin JM, Baulieu EE, Schumacher M, Schweizer-Groyer G (2008). "Etifoxine improves peripheral nerve regeneration and functional recovery". Proc Natl Acad Sci U S A. 105 (51): 20505–10. doi:10.1073/pnas.0811201106.
- ^ Schlichter R, Rybalchenko V, Poisbeau P, Verleye M, Gillardin J (2000). "Modulation of GABAergic synaptic transmission by the non-benzodiazepine anxiolytic etifoxine". Neuropharmacology. 39 (9): 1523–35. doi:10.1016/s0028-3908(99)00253-1.
- ^ Nguyen N, Fakra E, Pradel V, Jouve E, Alquier C, Le Guern ME, Micallef J, Blin O (2006). "Efficacy of etifoxine compared to lorazepam monotherapy in the treatment of patients with adjustment disorders with anxiety: a double-blind controlled study in general practice". Human Psychopharmacology. 21 (3): 139–49.
- ^ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293506/
- ^ Hamon A, Morel A, Hue B, Verleye M, Gillardin JM (2003). "The modulatory effects of the anxiolytic etifoxine on GABA(A) receptors are mediated by the beta subunit". Neuropharmacology. 45 (3): 293–303. doi:10.1016/s0028-3908(03)00187-4.
- ^ Kruse HJ, Kuch H (1986). "Potentiation of clobazam's anticonvulsant activity by etifoxine, a non-benzodiazepine tranquilizer, in mice. Comparison studies with sodium valproate". Arzneimittelforschung. 36 (9): 1320–2.
- ^ Verleye M, Schlichter R, Gillardin JM (1999). "Interactions of etifoxine with the chloride channel coupled to the GABA(A) receptor complex". Neuroreport. 10 (15): 3207–10. doi:10.1097/00001756-199910190-00015.
- ^ do Rego, Jean Luc; Vaudry, David; Vaudry, Hubert. "The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis". PLOS. Retrieved 24 December 2016.
