Selank and Semax Research: Two Synthetic Regulatory Peptides

Published September 27, 2026 · ROVIQ Research

Selank and Semax are short synthetic peptides, each built on a fragment of a naturally occurring regulatory peptide. Most of the research on both comes from Russian research institutes. This overview summarizes the English-language animal and molecular studies: what they measured, in which models, and who carried them out.

A shared design: a natural fragment plus Pro-Gly-Pro

• Semax is the heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro, an analogue of the adrenocorticotropin (ACTH) fragment 4–10 (Dolotov et al., 2006a). It is also described as ACTH(4–7) followed by Pro-Gly-Pro, abbreviated ACTH(4-7)PGP (Dergunova et al., 2021).
• Selank is Thr-Lys-Pro-Arg-Pro-Gly-Pro. It is built on tuftsin (Thr-Lys-Pro-Arg), a short fragment of the human immunoglobulin G heavy chain, extended at the C-terminus with Pro-Gly-Pro to improve its metabolic stability (Volkova et al., 2016).

So both peptides end in the same three residues, Pro-Gly-Pro. For Selank, the published rationale is metabolic stability (Volkova et al., 2016).

Semax and BDNF in the rat brain (in vivo)

Two 2006 studies examined Semax and brain-derived neurotrophic factor (BDNF), a protein involved in synaptic plasticity. In the rat hippocampus, Semax increased BDNF protein levels and the activation of its receptor, trkB, along with the mRNAs for both. Treated rats also showed more conditioned avoidance responses in a learning task (Dolotov et al., 2006a). A companion study found specific, reversible, calcium-dependent binding sites for Semax on cell membranes from the rat basal forebrain. Semax increased BDNF there, but not in the cerebellum (Dolotov et al., 2006b).

Semax and gene expression in a rat ischemia model

A 2014 genome-wide study compared gene expression in rat brain cortex after an experimental focal ischemia (permanent occlusion of the middle cerebral artery), with and without Semax. Semax predominantly changed the expression of immune-system genes, including those encoding immunoglobulins and chemokines. These made up over half of the genes it affected. It also altered the expression of genes related to the vascular system, at 3 and 24 hours after the occlusion (Medvedeva et al., 2014).

Selank and neurotransmission genes (in vivo)

A 2016 study measured the expression of 84 neurotransmission-related genes in rat frontal cortex after Selank or GABA. These included GABA receptor subunits, transporters, ion channels, and dopamine and serotonin receptors. Selank changed the expression of 45 of them at 1 hour and 22 at 3 hours, and its early changes correlated positively with those produced by GABA. The authors suggest that allosteric modulation of the GABAergic system may be one of Selank's molecular mechanisms (Volkova et al., 2016). That is framed as a possibility the data point toward, not an established mechanism.

Selank and immune-related genes (in vivo)

In mouse spleen, Selank changed the expression of several inflammation-related genes within 30 to 90 minutes, including a roughly threefold drop in C3 mRNA at 30 minutes. Its short fragment Gly-Pro produced largely similar expression profiles, which the authors read as a sign that the fragment contributes to Selank's overall effect (Kolomin et al., 2014).

Who did the research

Selank was designed and produced at the Institute of Molecular Genetics of the Russian Academy of Sciences, in cooperation with the V.V. Zakusov Research Institute of Pharmacology (Volkova et al., 2016). Every study cited in this overview includes N.F. Myasoedov of that institute among its authors. There are also clinical studies of both peptides, published mostly in Russian-language journals, which this overview does not summarize. A literature concentrated in one institution isn't wrong for that reason, but independent replication by unaffiliated groups is what establishes a finding. For these two peptides, most of that work hasn't been done yet.