STRESAM ® [Etifoxine]

In general, it can be argued that the etifoxine anxiolytic Stresam® is effective in treating a very wide range of anxiety-neurotic disorders and psychosomatic pathologies, sleep disorders, vegetative-vascular dystonia, etc. The drug does not adversely affect psychomotor and cognitive functions and muscle tone; it does not cause dependence, tolerance and does not have a withdrawal syndrome.

Dosage and Administration 

Very few side effects in Stresam® administration provide possibilities for dose variations in accordance with the therapeutic necessity (taken existings recommendations, patients' peculiarities and the specifics of symptoms). The usual dose is 1-2 capsules 2-3 times a day from 1 week to 2 months. For the full information on the administration, please refer to the official description.

Side effects 

Stresam® is devoid of a significant amount of side effects of its precursors (benzodiazepines). Rare side effects include dizziness, insomnia and the development of skin allergic reactions.

Contraindications

Liver / kidney disease is a contraindication as well as pregnancy / lactation and child age.

Overdose 

Overdose is noted only in doses many times higher than the recommended ones, and is limited to the effects of hypotension, eliminated by the appropriate treatment.

Analogs

Stresam® does not have structural analogues. Sedatives with a similar mechanism of action are:

  • Xanax;
  • Ativan;
  • Valium; 
  • Atarax, etc.

You can read the full instruction here

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Stresam® is a drug manufactured by the French company Biocodex. Its active substance - etifoxine, a benzoxazine derivative - has an original mechanism of action that distinguishes it from all other anxiolytics. It is characterized by maximum selectivity and physiological action in relation to the influence on the development of the symptom complex of anxiety.

Active substance was developed back in the 1960s by the German pharmaceutical company, when benzodiazepines (psychoactive substances with sedative effects), dominated the market of sedatives and drugs for anxiety disorders. However, despite their popularity, tranquilizers of the benzodiazepine structure have significant side effects: psychomotor inhibition, drowsiness, lethargy, dizziness, muscle relaxation, memory impairment, development of addiction, etc. An alternative way to develop drugs to eliminate anxiety was the synthesis and implementation of new generation anxiolytics of non-benzodiazepine nature. Etifoxine was one of several anxiolytics with enough potential to replace benzodiazepine drugs.

It has anxiolytic properties and can relieve various psychosomatic disorders (anxiety, internal tension, sleep disturbances, irritability, inadequate emotional reactions), without a negative effect on psychomotor and cognitive domains. The compound produces neurosteroids in the brain that can indirectly modulate the activity of GABAA response. Enhancing neurosteroids in the brain has a lot of potential in keeping the functional yet calm state of body and mind. Stresam® which is an official trade name of etifoxine demonstrates the following effects:  

  • The drug effectively eliminates manifestations of anxiety (stress, discomfort, insomnia, a sense of fear, etc.).
  • Since the active substance of Stresam® does not have a withdrawal syndrome and does not cause dependence, etifoxine is of great interest for narcologists: the drug has shown its effectiveness in reducing manifestation of alcohol withdrawal syndrome, reducing tremor, anxiety and paroxysmal sweating. Stresam® helps to reduce the pathological craving for alcohol, improving the quality of life in the post-withdrawal period. 
  • Additional effects of Stresam® are due to the fact that the drug has a mediated effect at the intracellular level: it stimulates mitochondrial benzodiazepine receptors, thereby enhancing the synthesis of neurosteroids. According to preliminary data, these effects stipulate an improvement in concentration and memory functions, which increases the ability to learn.
  • Another property of Stresam® that has been recently discovered is neuroprotection. Stresam® was shown to promote neuron growth; in particular, it accelerates axonal regeneration and might serve as a treatment for polyneuropathy.
  • Stresam® was also proven to have the ability to alleviate mild depressions which are widespread nowadays.
  • Stresam® has an indirect effect on the course of cardiovascular, pulmonary, gastroenterological and other diseases of psychosomatic nature.

The facts mentioned above make this drug a decent alternative to other anxiolytics currently used in everyday medical practice in the treatment of anxiety disorders of various origins. The drug is approved in more than 40 countries.

  1. Micallef et al (2001) A double blind parallel group placebo controlled comparison of sedative and mnesic effects of etifoxine and lorazepam in healthy subjects [corrected] https://www.ncbi.nlm.nih.gov/pubmed/11468032
  2. Hamon et al (2003) The modulatory effects of the anxiolytic etifoxine on GABA(A) receptors are mediated by the beta subunit https://www.ncbi.nlm.nih.gov/pubmed/12871647
  3. Nhuyen et al (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 https://www.ncbi.nlm.nih.gov/pubmed/16625522
  4. Ugale et al (2007) Neurosteroid allopregnanolone mediates anxiolytic effect of etifoxine in rats https://www.ncbi.nlm.nih.gov/pubmed/17950705
  5. Girard et al (2008) Etifoxine improves peripheral nerve regeneration and functional recovery https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2629330/
  6. Verleye et al (2011) Differential effects of etifoxine on anxiety-like behaviour and convulsions in BALB/cByJ and C57BL/6J mice: any relation to overexpression of central GABAA receptor beta2 subunits? https://www.ncbi.nlm.nih.gov/pubmed/20943351
  7. Zhou et al (2013) Etifoxine promotes glial derived neurotrophic factor induced neurite outgrowth in PC12 cells https://www.spandidos-publications.com/10.3892/mmr.2013.1474
  8. Aouad et al (2014) Etifoxine stimulates allopregnanolone synthesis in the spinal cord to produce analgesia in experimental mononeuropathy https://www.ncbi.nlm.nih.gov/pubmed/23881562
  9. Choi et al (2015) Etifoxine for pain patients with anxiety https://www.ncbi.nlm.nih.gov/pubmed/25589941
  10. Y Choi, K Kim (2015) Etifoxine for Pain Patients with Anxiety https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293506/
  11. Rego et al (2015) The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364751/
  12. D Stein (2015) Etifoxine Versus Alprazolam for the Treatment of Adjustment Disorder with Anxiety: a Randomized Controlled Trial https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4311065/
  13. Simon-O’Brien et al (2016) Etifoxine improves sensorimotor deficits and reduces glial activation, neuronal degeneration, and neuroinflammation in a rat model of traumatic brain injury https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5002207/
  14. Ravikumar et al (2016) Differential efficacy of the TSPO ligands etifoxine and XBD-173 in two rodent models of Multiple Sclerosis http://europepmc.org/abstract/med/27039042
  15. Bouillot et al (2016) A microPET comparison of the effects of etifoxine and diazepam on [(11)C]flumazenil uptake in rat brains https://www.ncbi.nlm.nih.gov/pubmed/26644334
  16. Costa et al (2017) The Anxiolytic Etifoxine Binds to TSPO Ro5-4864 Binding Site with Long Residence Time Showing a High Neurosteroidogenic Activity https://www.ncbi.nlm.nih.gov/pubmed/28362078
  17. Poisbeau et al (2018) Anxiolytics targeting GABAA receptors: Insights on etifoxine https://www.ncbi.nlm.nih.gov/pubmed/30204559
  18. Deplanque et al (2018) Etifoxine impairs neither alertness nor cognitive functions of the elderly: A randomized, double-blind, placebo-controlled crossover study https://www.ncbi.nlm.nih.gov/pubmed/30135030


Type: Nootropics




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