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// Neuropeptide Research

Semax

CAS No. 80714-61-0
Molecular Formula C37H51N9O10S
Molecular Weight 813.92 g/mol
Sequence Met-Glu-His-Phe-Pro-Gly-Pro

Synthetic heptapeptide derived from the N-terminal ACTH(4-7) fragment and extended with a Pro-Gly-Pro stabilising tail. Studied in CNS research models for neurotrophin induction and neuroprotective signalling without the steroidogenic effects of full ACTH.

// 01 — Mechanism

Mechanism of Action

Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. The first four residues reproduce the N-terminal ACTH(4-7) fragment of adrenocorticotropic hormone, while the C-terminal Pro-Gly-Pro extension confers peripheral enzymatic stability. This stabilisation has enabled investigation of intranasal administration in preclinical CNS research, a route that would rapidly inactivate the unmodified ACTH(4-7) fragment. Semax lacks the C-terminal residues of full-length ACTH required for steroidogenic activity at melanocortin receptors and accordingly does not stimulate cortisol release.

Mechanistically, a central and consistently reported effect of Semax is rapid upregulation of neurotrophin expression. Published rodent studies describe increased brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mRNA and protein levels in hippocampal and cortical tissue within hours of administration, implicating Semax as a research tool for investigating neurotrophin-dependent plasticity mechanisms.

Additional lines of research have characterised Semax-induced modulation of the dopaminergic, serotonergic, and cholinergic systems, with reported changes in monoamine release, receptor expression, and metabolite profiles in specific brain regions. Related work has examined interactions with the melanocortin system relevant to CNS function, inhibition of enkephalin-degrading enzymes, and neuroprotective activity in rodent models of ischaemic CNS injury.

// 02 — Research Findings

Key Research Findings

  1. Rapid (within hours) upregulation of BDNF and NGF mRNA and protein in rodent hippocampal and cortical tissue following Semax administration has been described across multiple published studies. Levitskaya, Kaplan and colleagues, Institute of Molecular Genetics RAS, Semax neurotrophin literature.
  2. Neuroprotective activity has been characterised in rodent middle cerebral artery occlusion (MCAO) models of ischaemic CNS injury, with reported reductions in infarct volume and improved behavioural recovery parameters. Ashmarin, Romanova and colleagues, Russian Academy of Sciences ischaemic stroke model literature.
  3. Modulation of monoaminergic neurotransmission, including altered dopamine and serotonin turnover in striatal and cortical tissue, has been reported in microdialysis and tissue-content studies. Eremin, Kolomin and colleagues, Semax microdialysis and neurochemistry literature.
  4. Inhibition of enkephalin-degrading enzymes has been described as a peripheral mechanism relevant to Semax activity. Ashmarin research group, regulatory peptide enzymatic mechanism literature.
  5. Investigation of effects on attention, learning and cognitive processing parameters in experimental rodent models has featured across research from the original Russian academic groups and subsequent international follow-up studies. Ashmarin research group and international Semax cognitive research literature, 1990s–2010s.

Citations last reviewed: 1 October 2026

// 03 — Specifications

As Supplied by BasedPeps

Molecular Weight 813.92 g/mol
Purity ≥99% HPLC · mass spectrometric identity confirmed
Sequence Met-Glu-His-Phe-Pro-Gly-Pro (heptapeptide)
Storage Lyophilised at −20 °C · reconstituted at 2–8 °C
Format Lyophilised white powder · also available as intranasal solution (10 mg/mL, aqueous) for in-vitro and preclinical intranasal-administration research models
Documentation Third-party CoA available on request
Use In-vitro / in-vivo research only — not for human administration
// 04 — FAQ

Researcher FAQ

What is Semax?

Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. Its first four residues correspond to the N-terminal fragment of adrenocorticotropic hormone (ACTH residues 4–7). A C-terminal Pro-Gly-Pro extension confers peripheral stability and has enabled investigation of intranasal administration in preclinical CNS research.

Does Semax affect cortisol or the HPA axis?

Semax lacks the C-terminal residues of full-length ACTH required for steroidogenic activity at melanocortin receptors. Published research describes Semax as retaining the behavioural and neurotrophic activity of the ACTH(4-7) fragment without the cortisol-releasing action of full ACTH.

What effect does Semax have on neurotrophin expression?

Published rodent studies describe rapid upregulation of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mRNA and protein levels in hippocampal and cortical tissue within hours of Semax administration. Neurotrophin induction is among the most consistent findings across published investigations.

How is Semax reconstituted for laboratory use?

Semax is supplied as a lyophilised white powder. Reconstitution in sterile bacteriostatic water or 0.9% sodium chloride is standard in research protocols, with gentle swirling until fully dissolved. Once reconstituted, the peptide is typically stored at 2–8 °C.

Is a Certificate of Analysis provided?

Yes. BasedPeps publishes a third-party Certificate of Analysis per lot documenting HPLC purity (≥99%) and mass spectrometric identity confirmation. Certificates are available on the product page.

View BasedPeps Semax

Research-grade Semax. Third-party HPLC and mass spectrometry verification per lot. Certificate of Analysis available on request. Dispatched from Riga, Latvia within 24 hours.

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