Etifoxine
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| Systematic (IUPAC) name | |
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6-Chloro-N-ethyl-4-methyl-4-phenyl-4H-benzo[d][1,3]oxazin-2-amine
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| Clinical data | |
| AHFS/Drugs.com | International Drug Names |
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| Routes of administration |
Oral |
| Legal status | |
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| Pharmacokinetic data | |
| Bioavailability | 90% |
| Metabolism | Hepatic (no CYP450 interactions)[1] |
| Biological half-life | 2 to 6 hours (etifoxine), 20 to 30 hours (active metabolite)[2] |
| Excretion | Renal[1] |
| Identifiers | |
| CAS Number | 21715-46-8  |
| ATC code | N05BX03 (WHO) |
| PubChem | CID 30768 |
| IUPHAR/BPS | 5468 |
| DrugBank | DB08986  |
| ChemSpider | 28547 |
| UNII | X24X82MX4X |
| KEGG | D07320 |
| ChEMBL | CHEMBL2106227 |
| Chemical data | |
| Formula | C17H17ClN2O |
| Molar mass | 300.782 g/mol |
| 3D model (Jmol) | Interactive image |
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Etifoxine (INN,[3] also known as etafenoxine; trade name Stresam) is an anxiolytic and anticonvulsant drug[4][5] developed by Hoechst in the 1960s.[3] It is used in some countries for anxiety disorders.[6] It has similar effects to benzodiazepine drugs, but is structurally distinct and does not bind to the benzodiazepine receptor.[7] It is more effective than lorazepam as an anxiolytic, and has fewer side effects.[8] Etifoxine is not approved by the U.S. Food and Drug Administration or the European Medicines Agency.
Side effects[edit]
Etifoxine has been associated with acute liver injury.[1]
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]
References[edit]
- ^ a b c Mennecier D, Rimlinger H, Gidenne S, et al. (November 2003). "[Etifoxine chlorhydrate-induced acute hepatitis]". Gastroenterol. Clin. Biol. (in French). 27 (11): 1050–1. PMID 14732859.
- ^ "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.
- ^ 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.
