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Semax

Also known as: ACTH(4-7)-PGP, Heptapeptide Semax

Research Only

Molecular Formula

C37 H51 N9 O10 S

Molecular Weight

813.92 Da

Half-Life

~1–2 hours (estimated from animal models; no human PK data available)

Sequence

Met-Glu-His-Phe-Pro-Gly-Pro

Clinical Applications & Evidence

Mechanism of Action

In rodent models, Semax upregulates mRNA expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in brain tissue, and modulates dopaminergic and serotonergic neurotransmission. In animal stroke models, it alters gene expression associated with inflammatory response and vascular repair. In vitro experiments suggest copper-chelating properties that may inhibit amyloid-beta aggregation, though these findings have not been demonstrated in clinical human trials.

Investigated Uses

  • Ischemic stroke recovery (registered in Russia; not FDA-approved)
  • Cognitive function (preclinical; limited human evidence)
  • Attention disorders (no FDA-supporting literature found)
  • Optic nerve disease
  • Neuroprotection (animal models)
Early Clinical / Animal Models

Regulatory & Safety Status

FDA Status

Research Only

WADA / Athletic Status

Not Explicitly Prohibited

Known Side Effects

Nasal irritationMild headache (rare)Insufficient safety data — human PK, long-term toxicity, and carcinogenicity studies are lacking

Contraindications

  • Pregnancy
  • Acute psychosis
  • Known allergy to ACTH derivatives

Drug Interactions

  • May potentiate stimulant medications (observed in mice; unconfirmed in humans)

Citations & Clinical Trials

Alzheimer's Drug Discovery Foundation Semax — Cognitive Vitality For Researchers Europe PMC The efficacy of semax in the treatment of patients at different stages of ischemic stroke FDA FDA Briefing Document: Semax — Pharmacy Compounding Advisory Committee BMC Genomics Genomic effects of Semax in rats with cerebral ischemia Genes (MDPI) Semax gene expression study in rat hippocampus