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Semax
Semax

Semax

Semax is a synthetic heptapeptide derived from the ACTH(4-10) fragment and modified with a stabilizing C-terminal Pro-Gly-Pro sequence. Originally developed in Russia, Semax is described in research literature as a nootropic and neuroprotective peptide with reported effects on cognitive pathways, neuroplasticity, stress response, and neuronal signaling.
It is studied for its potential influence on melanocortin pathways and its ability to modulate expression of genes involved in neuroprotection, oxidative stress balance, and synaptic plasticity.

Mechanism of Action
(Mechanistic descriptions from published research; not clinical claims.)

  • Melanocortin system modulation — Partial agonist/antagonist activity at MC4 and MC5 receptors with MC3 sparing.
  • BDNF/TrkB upregulation — Increases BDNF levels and TrkB phosphorylation, supporting synaptic plasticity.
  • Neurotransmitter modulation — Influences serotonergic and dopaminergic pathways.
  • Immunomodulation — Reduces inflammatory cytokine expression in neural tissue.
  • Enkephalinase inhibition — Prolongs endogenous neuropeptide signaling.
  • Calcium homeostasis modulation — Regulates intracellular Ca²⁺ signaling to support neuroprotection.

Clinical References

  1. Vedunova, E.V., et al. (2014). Gene expression modulation in rat brain following ischemia. BMC Genomics, 15, 228.
  2. Dolotov, O.V., et al. (2006). Semax increases BDNF in forebrain regions. J. Neurochem., 97(Suppl 1), 62–86.
  3. Kolomin, T., et al. (2021). Semax protection in cerebral ischemia. Int. J. Mol. Sci., 22(21), 11979.
  4. Lukoyanov, N.G., et al. (2004). Semax effects in MPTP-induced dysfunction. Neurosci. Behav. Physiol., 34(3), 399–405.
  5. Knyazev, O., et al. (2015). Semax mitigation of metal-induced toxicity. J. Inorg. Biochem., 142, 1–4.
  • Cognitive Enhancement: Research suggests Semax may support memory, learning, attention, and mental clarity.
  • Neuroprotection: May help protect neurons from ischemic, excitotoxic, or oxidative stress–related damage.
  • Stress Resilience: Modulates neurotransmitter pathways associated with anxiolytic- and antidepressant-like effects in research models.
  • Recovery Support: Studies indicate potential support for post-injury neural recovery.
  • Immune Modulation: May modulate inflammatory markers and immune signaling in neural tissue.
  • Metal Toxicity Protection: Research indicates a protective effect against heavy-metal-induced neurotoxicity.
  • Brain Circulation: May enhance microcirculation and oxygen delivery to neural tissues.

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