Semax

Mechanism (plain language)

Derived from the central-nervous-system-active fragment of ACTH with steroidogenic activity removed, plus a stabilizing Pro-Gly-Pro tail. Proposed to act through BDNF/TrkB upregulation and modulation of dopaminergic, serotonergic, and cholinergic signaling rather than through classical hormone receptors.

What research suggests

Russian human trials—mostly non-randomized or open-label—report improved attention, working memory, and EEG changes consistent with nootropic effects, plus a multicenter RCT in acute ischemic stroke reporting reduced neurological deficit progression. It has decades of Russian clinical use for stroke and optic neuropathy.

Uncertainties & risks

Not FDA-approved; almost all rigorous trial data comes from a small number of Russian research groups rather than independent international replication. Most of the human literature predates modern trial-reporting standards (open-label, unblinded, or small samples). Long-term safety data outside Russian clinical use is limited.

STACKD study summaries

Start with our in-house roundups—plain-language synthesis of the research, with primary sources cited at the bottom of each.

• STACKD summaryLimited human data
  Semax, Selank, and Noopept: the Russian nootropic peptidesDecades of domestic clinical use, but almost no independent international replication.

• Semax in Acute Ischemic Stroke: Effects on Neurological Deficit and Recovery

  2007 · human

  Multicenter trial in 184 acute ischemic stroke patients reported reduced neurological deficit progression versus standard care.

• Effectiveness of Semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)

  1997 · human

  Early controlled clinical trial describing neurological and EEG outcomes with intranasal Semax after stroke.