Cognitive ⏱ Half-life: Short plasma half-life, but CNS effects are sustained for hours due to neurotrophic cascades. Approved Abroad

Semax

Semax (ACTH 4-10 Analog)

Updated March 15, 2026
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Evidence at a Glance

Regulatory statusApproved Abroad
Registered in Russia/Ukraine for stroke, TIA and cognitive disorders; never FDA-reviewed.
Human evidenceLimited
Animal evidenceModerate

An ACTH(4-10) analog used clinically in Russia for stroke and cognitive indications, but the supporting human trials are small, mostly Russian-language, and not independently replicated to Western standards.

What the research does not support

  • It is not FDA-approved and has undergone no US review of safety or efficacy.
  • Cognitive-enhancement claims in healthy people are not backed by rigorous double-blind trials.
  • It does not repair the brain or reverse established neurodegeneration.
  • It is not a proven treatment for ADHD, depression, or anxiety despite marketing.
Half-Life
Short plasma half-life, but CNS effects are sustained for hours due to neurotrophic cascades.
Mol. Weight
813.93 g/mol

What is Semax?

Semax is a synthetic peptide based on the ACTH (4-10) fragment, modified for stability and stripped of hormonal activity. It has become one of the most studied nootropic peptides, with particular interest in its robust neurotrophic factor expression effects.

Research Applications

Neuroprotection (stroke, TBI models), cognitive enhancement, BDNF expression research, attention and memory studies, and optic nerve damage models.

Dosage Information (Research Use)

Research protocols: 200-600 mcg/day, intranasal or subcutaneous. Courses of 10-30 days in published studies. Research use only.

Reconstitution & Handling

Standard BAC water reconstitution.

Half-Life & Pharmacokinetics

Short plasma half-life, but CNS effects are sustained for hours due to neurotrophic cascades.

Reported Observations in Literature

Minimal adverse effects in published research. No adrenal stimulation despite ACTH origin. Occasional mild headache reported.

Key Research References

  • Dolotov OV, et al. “Semax, an ACTH(4-10) analog with nootropic properties, activates BDNF and trkB in the hippocampus.” Brain Res. 2006
  • Ashmarin IP, et al. “The Mechanisms of Interaction Between Semax and Enkephalin-Degrading Enzymes.” Neurosci Behav Physiol. 2001

How Semax Works

Semax is a synthetic heptapeptide analog of the ACTH (4-10) fragment with a C-terminal Pro-Gly-Pro extension for stability. Despite being derived from ACTH, it lacks hormonal (adrenocorticotropic) activity and does not affect cortisol. Mechanism involves BDNF/NGF/GDNF upregulation, modulation of serotonergic and dopaminergic systems, and enhancement of neuronal survival signaling pathways.

Research Findings

Approved in Russia for stroke recovery and cognitive enhancement. Research shows BDNF expression increases of 1.4-3x in hippocampal regions, neuroprotection in ischemic models, and attention/memory improvement in cognitive testing paradigms.

Dosage & Administration

Research protocols: 200-600 mcg/day, intranasal or subcutaneous. Courses of 10-30 days in published studies. Research use only.

Safety & Side Effects

Minimal adverse effects in published research. No adrenal stimulation despite ACTH origin. Occasional mild headache reported.

Important: All safety information is derived from published research, primarily animal studies. No controlled human clinical trial data exists unless explicitly noted. This compound is sold for research purposes only.

Quick Facts

Sequence Met-Glu-His-Phe-Pro-Gly-Pro
Molecular Weight 813.93 g/mol
Half-Life Short plasma half-life, but CNS effects are sustained for hours due to neurotrophic cascades.
Available Sizes 5mg
Storage Lyophilized: -20°C. Reconstituted: 2-8°C.

Key Research References

  • Dolotov OV, et al. "Semax, an ACTH(4-10) analog with nootropic properties, activates BDNF and trkB in the hippocampus." Brain Res. 2006
  • Ashmarin IP, et al. "The Mechanisms of Interaction Between Semax and Enkephalin-Degrading Enzymes." Neurosci Behav Physiol. 2001

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