Summary

Semax is a synthetic heptapeptide analogue of adrenocorticotropic hormone (ACTH) fragments, developed at Moscow State University. It has been studied for cognitive enhancement, neuroprotection, and attention improvement, with a body of research primarily from Russian institutions. It is registered as a medicine in Russia but is not licensed in the UK. Evidence is predominantly from Russian animal and clinical studies with limited international replication.

Mechanism

Semax is a synthetic ACTH(4–7) analogue that upregulates BDNF and NGF expression in the brain, modulates dopaminergic and serotonergic systems, interacts with melanocortin receptors (without steroidogenic effects), and inhibits enkephalin degradation. These combined mechanisms are thought to underlie its cognitive-enhancing, neuroprotective, and attention-improving effects.

Evidence base

Evidence is predominantly from Russian institutions. Animal studies show cognitive enhancement and neuroprotection in ischaemia models. Small Russian clinical studies report benefits in stroke recovery, cognitive impairment, and optic nerve pathology. No large-scale international RCTs published. Evidence quality is limited by small samples, single-group origin, and lack of independent replication.

Protocols

Commonly discussed in research contexts: intranasal 100–300 mcg, 2–3 times daily; subcutaneous 200–500 mcg. Cycles of 7–14 days. Based on Russian clinical literature and community discussion.

Not controlled under the Misuse of Drugs Act 1971. Not a POM. Not licensed as a medicine in the UK (registered in Russia, but this has no UK or EMA standing). Legal to purchase and possess for research purposes; not approved for human consumption.

Vendor notes

Semax is available from some UK research peptide vendors, typically in lyophilised form or as intranasal solutions. No vendors have been independently verified by Peptide Data at this time.

References

  1. Dolotov, O.V. et al. (2006). Semax alters the expression of neurotrophin genes. Brain Research, 1123(1), 94–99. DOI: 10.1016/j.brainres.2006.09.024
  2. Levitskaya, N.G. et al. (2005). Semax: Effects on dopamine and serotonin systems. Doklady Biological Sciences, 401, 185–188.
  3. Gusev, E.I. et al. (1997). Semax in the treatment of acute ischaemic stroke. Neuroscience and Behavioural Physiology, 27(6), 680–685.
  4. Shadrina, M. et al. (2010). Semax and melanocortin receptors: Molecular interactions. Journal of Molecular Neuroscience, 42(3), 346–350.
  5. Loseva, E.V. et al. (2009). Gene expression changes in the brain following Semax administration in a model of focal ischaemia. Molecular Genetics and Microbiology, 24(3), 120–127.
  6. Asadulaeva, Z.M. et al. (2006). Semax therapy in patients with mild cognitive impairment. Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 106(9), 70–74.
  7. Polunin, G.S. et al. (2003). Semax in the treatment of optic nerve pathology. Vestnik Oftalmologii, 119(4), 20–23.