Semax

Semax
Systematic (IUPAC) name
L-Methionyl-L-α-glutamylhistidyl-L-phenylalanyl-L-prolylglycyl-L-proline
Clinical data
Trade names Ladasten
Legal status
Legal status
  • US: Unscheduled
Identifiers
CAS Number 4037-01-8 80714-61-0 (free base)
ATC code N06BX
PubChem CID 122178
ChemSpider 108969
Synonyms (Pro8,Gly9,Pro10)ACTH-(4-10)
Chemical data
Formula C37H51N9O10S
Molar mass 813.920 g/mol

Semax is a drug produced and prescribed mostly in Russia and Ukraine for a broad range of conditions but predominantly for its purported nootropic, neuroprotective, and neurogenic/neurorestorative properties. It is a heptapeptide, synthetic analog of a fragment of adrenocorticotropic hormone (ACTH), ACTH (4-10), of the following structure: Met-Glu-His-Phe-Pro-Gly-Pro. Semax has not been evaluated by the U.S. FDA. It is unscheduled in the U.S. and legal to import by private citizens for personal use.[1]

Semax has undergone extensive study in Russia and is on the Russian List of Vital & Essential Drugs approved by the Russian Federation government on December 7, 2011.[2] Medical uses for Semax include treatment of stroke, transient ischemic attack, memory and cognitive disorders, peptic ulcers, optic nerve disease, and to boost the immune system.[1][1][3][4][5]

In animals, Semax rapidly elevates the levels and expression of brain-derived neurotrophic factor (BDNF) and its signaling receptor TrkB in the hippocampus,[6] and rapidly activates serotonergic and dopaminergic brain systems.[7][8] In accordance, it has been found to produce antidepressant-like and anxiolytic-like effects,[9][10] attenuate the behavioral effects of exposure to chronic stress,[9][10] and potentiate the locomotor activity produced by D-amphetamine.[8][11] As such, it has been suggested that Semax may be effective in the treatment of depression,[12] as well as in attention deficit hyperactivity disorder (ADHD).[13]

Though the exact mechanism of action of Semax is unclear, there is evidence that it may act through melanocortin receptors. Specifically, there is a report of Semax competitively antagonizing the action of the melanocortin receptor full agonist α-melanocyte-stimulating hormone (α-MSH) at the MC4 and MC5 receptors in both in vitro and in vivo experimental conditions, indicating that it may act as an antagonist (or partial agonist) of these receptors.[14] Semax did not antagonize α-MSH at the MC3 receptor, though this receptor could still be a target of the drug.[14] As for the MC1 and MC2 receptors, they were not assayed.[14] In addition to actions at receptors, Semax, as well as a related peptide drug, Selank, have been found to inhibit enzymes involved in the degradation of enkephalins and other endogenous regulatory peptides, and this action may also be involved in their effects.[15]

See also

References

  1. 1 2 3 Institute of Molecular Genetics, Russian Academy of Sciences website (http://old.img.ras.ru/semax1-e.htm)
  2. ↑ "ПЕРЕЧЕНЬ. жизненно необходимых и важнейших лекарственных препаратов на 2012 год. (Vital and Essential Drugs List, 2012) - Russian Federation". World Health Organization. 2012.
  3. ↑ Kurysheva NI, Shpak AA, Ioĭleva EE, Galanter LI, Nagornova ND, Shubina NIu, Shlyshalova NN (2001). "Semax in the treatment of glaucomatous optic neuropathy in patients with normalized ophthalmic tone". Vestnik oftalmologii 117 (4): 5–8. PMID 11569188.
  4. ↑ Ivanikov IO, Brekhova ME, Samonina GE, Myasoedov NF, Ashmarin IP (2002). "Therapy of peptic ulcer with semax peptide". Bulletin of experimental biology and medicine 134 (1): 73–4. doi:10.1023/A:1020621124776. PMID 12459874.
  5. ↑ Korneev, EA; Kazakova, TB (1999). "Current approaches to the analysis of the effects of stress on metabolic processes in cells of the nervous and immune systems". Med. Immunology 1 (1–2): 17–22.
  6. ↑ Dolotov OV, Karpenko EA, Inozemtseva LS, Seredenina TS, Levitskaya NG, Rozyczka J, Dubynina EV, Novosadova EV, Andreeva LA, Alfeeva LY, Kamensky AA, Grivennikov IA, Myasoedov NF, Engele J (October 2006). "Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus". Brain Res. 1117 (1): 54–60. doi:10.1016/j.brainres.2006.07.108. PMID 16996037.
  7. ↑ Eremin KO, Kudrin VS, Grivennikov IA, Miasoedov NF, Rayevsky KS (2004). "Effects of Semax on dopaminergic and serotoninergic systems of the brain". Dokl. Biol. Sci. 394: 1–3. doi:10.1023/b:dobs.0000017114.24474.40. PMID 15088389.
  8. 1 2 Eremin KO, Kudrin VS, Saransaari P, Oja SS, Grivennikov IA, Myasoedov NF, Rayevsky KS (December 2005). "Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents". Neurochem. Res. 30 (12): 1493–500. doi:10.1007/s11064-005-8826-8. PMID 16362768.
  9. 1 2 Vilenskiĭ DA, Levitskaia NG, Andreeva LA, Alfeeva LIu, Kamenskiĭ AA, Miasoedov NF (June 2007). "[Effects of chronic Semax administration on exploratory activity and emotional reaction in white rats]". Ross Fiziol Zh Im I M Sechenova (in Russian) 93 (6): 661–9. PMID 17850024.
  10. 1 2 Yatsenko KA, Glazova NY, Inozemtseva LS, Andreeva LA, Kamensky AA, Grivennikov IA, Levitskaya NG, Dolotov OV, Myasoedov NF (November 2013). "Heptapeptide semax attenuates the effects of chronic unpredictable stress in rats". Dokl. Biol. Sci. 453: 353–7. doi:10.1134/S0012496613060161. PMID 24385169.
  11. ↑ Volodina MA, Sebentsova EA, Glazova NY, Levitskaya NG, Andreeva LA, Manchenko DM, Kamensky AA, Myasoedov NF (March 2012). "Semax attenuates the influence of neonatal maternal deprivation on the behavior of adolescent white rats". Bull. Exp. Biol. Med. 152 (5): 560–3. doi:10.1007/s10517-012-1574-2. PMID 22803132.
  12. ↑ Pae CU (January 2008). "Therapeutic possibility of "Semax" for depression". CNS Spectr 13 (1): 20–1. PMID 18204410.
  13. ↑ Tsai SJ (2007). "Semax, an analogue of adrenocorticotropin (4-10), is a potential agent for the treatment of attention-deficit hyperactivity disorder and Rett syndrome". Med. Hypotheses 68 (5): 1144–6. doi:10.1016/j.mehy.2006.07.017. PMID 16996699.
  14. 1 2 3 Bertolini A (March 2012). "Drug-induced activation of the nervous control of inflammation: a novel possibility for the treatment of hypoxic damage". Eur. J. Pharmacol. 679 (1-3): 1–8. doi:10.1016/j.ejphar.2012.01.004. PMID 22293371.
  15. ↑ Kost NV, Sokolov OIu, Gabaeva MV, Grivennikov IA, Andreeva LA, Miasoedov NF, Zozulia AA (2001). "Semax and Selank Inhibit the Enkephalin-Degrading Enzymes of Human Serum". Bioorg. Khim. (in Russian) 27 (3): 180–3. doi:10.1023/A:1011373002885. PMID 11443939.


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