For laboratory research only.

Everything sold on peptidesth.com is supplied for in-vitro research and laboratory use. These materials are not drugs, supplements, or food. They are not intended for human or animal consumption, diagnostic use, or therapeutic use.

Please confirm you are 21 or older before continuing. Our research desk ships from Bangkok to qualified buyers in Thailand and worldwide.

Your acknowledgement is remembered on this device for 24 hours.

You’re about to view data for this compound.

This compound is supplied strictly for in-vitro research. It is not a medicine and is not intended for human or animal use. By continuing, you confirm you are 21 or older and accessing this information for laboratory purposes.
Thailand Peptides
Get in Contact
Research summary4 min read

Semax and Selank research summary: BDNF and NGF modulation, ACTH(4-10) analog evidence

Curated summary of Semax and Selank primary literature: BDNF and NGF gene expression, ACTH(4-10) analog mechanism, neuroprotection, anxiolytic effects. PubMed-verified.

By TH Labs Research Desk · Research Editor ·
Key findings
  • Semax is an ACTH(4-10) analog that upregulates BDNF and TrkB expression in the rat hippocampus.
  • Dolotov et al. (2006) demonstrated direct BDNF transcript induction in rat hippocampus following intranasal Semax administration.
  • Subsequent rat studies extended the BDNF/NGF expression evidence to frontal cortex and retina.
  • Selank (a tuftsin analog) shows transcriptomic effects on rat hippocampus and spleen and is studied as a non-sedating anxiolytic.
  • Both compounds remain largely Russian-research-tradition with limited Western clinical trial replication; mechanism characterisation is the most defensible claim.

Semax and Selank are short synthetic peptides developed in the Russian research tradition. Both are administered intranasally in published rodent protocols, both target the brain, and both have a distinct evidence profile from Western-tradition nootropics.

Semax: BDNF and TrkB upregulation

Semax is a heptapeptide derived from ACTH(4-10) — an analog of the central segment of adrenocorticotropic hormone. The canonical mechanism reference is Dolotov and colleagues' 2006 Brain Research paper 1, which demonstrated that intranasal Semax administration produces measurable upregulation of both BDNF (brain-derived neurotrophic factor) and TrkB (the BDNF receptor) in the rat hippocampus. BDNF supports neuronal survival, dendritic remodelling, and synaptic plasticity, so the induction provides a plausible mechanism for the cognitive and neuroprotective effects reported in rodent studies.

Shadrina and colleagues' 2010 J Mol Neurosci paper 2 extended this with temporal-dynamics data showing both BDNF and NGF (nerve growth factor) transcript changes across hippocampus, frontal cortex, and retina. The neurotrophin program is not localised to a single brain region. Agapova and colleagues (2007, Neurosci Lett) 3 independently replicated the neurotrophin-gene-expression response.

Selank: tuftsin analog, anxiolytic profile

Selank is a heptapeptide derived from tuftsin, a naturally occurring tetrapeptide involved in immune signalling. Its research profile is dominated by Russian-tradition publications and characterises it as a non-sedating anxiolytic with effects on GABAergic signalling and stress-system modulation.

Kolomin and colleagues (2010, Dokl Biochem Biophys) 4 characterised the transcriptomic response in rat hippocampus and spleen following single and chronic Selank administration. Both single and chronic dosing produced distinct gene-expression signatures spanning neurotransmission, immune signalling, and stress-response pathways.

Why BDNF matters

The broader BDNF-neuroprotection literature 5 establishes BDNF as a credible upstream target. Compounds that upregulate BDNF — whether peptide, small-molecule, or behavioural (exercise) — are studied for depression, neurodegeneration, and cognitive aging. Semax sits in this literature as one of the more directly-characterised peptide BDNF inducers.

Limits of the evidence

Most Semax and Selank evidence is rat-model. Western clinical trial replication remains thin, and human pharmacokinetics and dose-response require their own investigation. The mechanism story is well-supported; the human-translation story is not yet at the same level of replication.

For the long-form treatment, see the Semax and Selank BDNF article.

Thailand Peptides Semax 11 MG vial, clear glass with brushed aluminum cap and clear film label
Related peptide

Semax

ACTH(4-10) analog; elevates BDNF and modulates monoaminergic tone.

Open Semax product page →

Citations

  1. Dolotov OV, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 2006. PMID: 16996037
  2. Shadrina M, et al. Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action. J Mol Neurosci. 2010. PMID: 19662538
  3. Agapova TY, et al. Neurotrophin gene expression in rat brain under the action of Semax, an analogue of ACTH 4-10. Neurosci Lett. 2007. PMID: 17353092
  4. Kolomin T, et al. Transcriptomic response of rat hippocampus and spleen cells to single and chronic administration of the peptide Selank. Dokl Biochem Biophys. 2010. PMID: 20380151
  5. Colucci-D'Amato L, et al. Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer. Int J Mol Sci. 2020. PMID: 33096634

All references verified against PubMed via NCBI E-utilities.

Research desk
Questions about Semax? WhatsApp the Bangkok research desk. Pricing, COA, and protocol questions handled in-chat.
Open a line with the research desk ≥98% HPLC purity · supplier COA on file · Bangkok-based

This summary draws on the full-length article at /articles/semax-selank-bdnf. The article is the canonical long-form treatment; this page is the research-summary re-presentation.