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semax selank

Semax vs Selank: what each peptide has been researched for

Research overview 7 min read

On this page
  1. What are Semax and Selank?
  2. What is Semax used for, and what does Selank do?
  3. Semax and Selank research at a glance
  4. How are Semax and Selank thought to work?
  5. What kind of studies are these?
  6. Sources

Semax and Selank are two short, lab-made peptides: in research, Semax has mainly been studied in rat models of stroke and of brain growth-factor signalling [G1, G3–G5], and Selank mainly in rodent models of anxiety-related behaviour and in gene-activity work on brain-signalling and immune genes [G6, G8–G10]. Both were developed at the Institute of Molecular Genetics of the Russian Academy of Sciences [G6, G11]. The two were studied in different areas, so setting them side by side shows what was looked at for each, not which does more.

What are Semax and Selank?

A peptide is a short chain of amino acids, the building blocks of proteins. Semax and Selank each have seven.

Semax. Its sequence is Met-Glu-His-Phe-Pro-Gly-Pro, and Dolotov et al. describe it as an analogue of ACTH(4-10), a short piece of ACTH, a hormone made by the pituitary gland [G1]. Its first four amino acids come from ACTH [G5]. The last three, Pro-Gly-Pro, were added so enzymes break it down less easily [G5]. It was synthesised by scientists at the Institute of Molecular Genetics (IMG) [G11].

Selank. Its sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro [G6]. It is a synthetic analogue of tuftsin, a natural four-amino-acid piece (Thr-Lys-Pro-Arg) of an antibody protein [G6]. Pro-Gly-Pro was added to its end so enzymes break it down less easily [G6]. It was designed at IMG in cooperation with the V.V. Zakusov Research Institute of Pharmacology [G6].

So the two share an institute and a Pro-Gly-Pro tail, but they come from different parent molecules: a hormone fragment for Semax and an antibody fragment for Selank [G5, G6].

What is Semax used for, and what does Selank do?

In research, Semax has mainly been studied for:

  • Brain growth factors in rats. Researchers measured BDNF, a growth factor for nerve cells, and related growth-factor genes in rat brain [G1, G2, G3].
  • Gene activity in rat models of stroke. In these models an artery supplying the brain is blocked, cutting off its blood flow (ischaemia). Researchers then looked at which genes became more or less active [G3, G4, G5].
  • A learning task. In one study, rats given Semax made more conditioned avoidance responses, a learned response to a warning signal [G1].

In research, Selank has mainly been studied for:

  • Anxiety-related behaviour in rats and mice, measured in stress models [G8, G9].
  • GABA-related gene activity in rat brain. GABA is the brain's main inhibitory chemical messenger, meaning it damps down nerve-cell signalling. Researchers compared gene activity after Selank with gene activity after GABA [G6].
  • Enkephalin breakdown in the lab. Enkephalins are natural signalling peptides involved in pain and stress responses. Researchers measured how fast they were broken down in blood plasma with Selank present [G7].
  • Immune-related gene activity in mouse spleen [G10].

In the behaviour work, Kozlovskaya et al. compared Selank with ten other tuftsin-family peptides in rats and two inbred mouse strains under conflict-situation stress, and reported effects on stress-related behaviour that differed with each peptide's structure [G8]. In a chronic mild stress model with 48 male rats, Kasian et al. reported that in the unstressed rats the maze's anxiety-related measures moved in the less favourable direction in the saline (control) group, and less so in the Selank group [G9].

Semax and Selank research at a glance

Compound Area What researchers looked at Models Kind of evidence
Semax Brain growth-factor signalling BDNF protein and activity of its receptor (trkB) in the hippocampus [G1]; BDNF in the basal forebrain but not the cerebellum, and specific binding sites in basal-forebrain tissue [G2] Rats; rat brain tissue [G1, G2] Animal and tissue studies
Semax Stroke (ischaemia) models Activity of growth-factor genes [G3], immune and blood-vessel genes [G4], and inflammation- and signalling-related genes [G5] after a brain artery was blocked Rats: permanent [G3, G4] and temporary [G5] artery blockage Animal studies, gene-activity (mRNA) level; no protein-level confirmation in G5 [G5]
Selank Anxiety-related behaviour Behaviour in a conflict stress test [G8]; elevated plus maze under chronic mild stress [G9] Rats and mice grouped by emotional reactivity [G8]; 48 rats [G9] Animal studies
Selank GABA-related genes Activity of 84 signalling genes after Selank or GABA; 45 changed at 1 hour and 22 at 3 hours across both; Selank's pattern correlated with GABA's at 1 hour [G6] Rat frontal cortex [G6] Animal study, gene-activity level
Selank Enkephalin breakdown How fast enzymes broke down enkephalin with Selank present [G7] Blood plasma, in the lab [G7] Lab (in vitro) study
Selank Immune-related genes Activity of 84 inflammation-related genes; 34 changed, including Bcl6 [G10] Mouse spleen [G10] Animal study, gene-activity level

The two peptides were studied in different models with different measures, so the rows are not a head-to-head comparison.

How are Semax and Selank thought to work?

Semax: BDNF and its receptor. BDNF (brain-derived neurotrophic factor) acts on trkB, a receptor on nerve cells. In the rat hippocampus, a brain region, Dolotov et al. observed higher BDNF protein and more trkB phosphorylation after Semax was given [G1]. Phosphorylation is a chemical tag that switches a receptor on. Levels of BDNF and trkB mRNA, the gene copies a cell reads to make a protein, also rose [G1]. The authors suggested that Semax acts by modulating this BDNF/trkB system [G1]. The same group found that BDNF protein rose in rat basal forebrain at 3 hours but not in the cerebellum [G2].

Semax: genes after ischaemia. Transcription is the step in which a gene is copied into mRNA. In rats with a permanently blocked brain artery, Dmitrieva et al. found that Semax raised transcription of neurotrophin genes (the BDNF family of growth factors) and their receptors in the affected cortex, at time points from 3 to 72 hours [G3]. A genome-wide follow-up found that over half of the genes Semax changed were immune-related, and that 24 blood-vessel-related genes changed at 3 hours and 12 at 24 hours [G4]. Those authors proposed the immune and vascular changes as likely key mechanisms of Semax's action in this model [G4]. In a temporary-blockage model, Filippenkov et al. used RNA-Seq, a method that reads all of a tissue's active genes at once, and found 394 genes changed versus saline at 24 hours [G5]. Inflammation-related genes went down and neurotransmission-related genes went up, the reverse of the pattern after ischaemia alone [G5].

Selank: GABA-related genes. Volkova et al. measured 84 neurotransmission genes in rat frontal cortex 1 and 3 hours after Selank or GABA was given [G6]. Counting both compounds, 45 genes changed at 1 hour and 22 at 3 hours [G6]. At 1 hour the changes after Selank correlated positively with those after GABA; at 3 hours the correlation was negative [G6]. The authors' hypothesis is "allosteric modulation of the GABAergic system" [G6]: an effect on GABA receptors through a site other than the one GABA itself binds.

Selank: enkephalin breakdown. Enkephalinases are the enzymes that break down enkephalins. In blood plasma in the lab, Zozulya et al. found that Selank inhibited this breakdown in a concentration-dependent way, more strongly than two reference peptidase inhibitors, bacitracin and puromycin [G7].

Selank: immune genes. Kolomin et al. measured 84 inflammation-related genes in mouse spleen 6 and 24 hours after Selank and two of its fragments were given; 34 changed [G10]. Bcl6, a gene involved in immune-cell development, changed with each peptide, along with genes it targets and a co-repressor gene that works with it [G10].

What kind of studies are these?

Lab (in vitro) studies test a compound on cells or samples, such as blood plasma, in a dish or tube; animal studies test it in living animals, here rats and mice; human (clinical) studies test it in people. The sources in this post are animal and lab studies [G1–G10].

Many of them measure gene activity (mRNA levels). That shows which genes switched on or off, but not by itself what changed in the tissue. Filippenkov et al. name this as a limitation of their own study: they did not confirm the mRNA changes at the protein level or in function [G5].

Most of the studies cited here were carried out at the institutes that developed the peptides: IMG for both [G1–G6, G9, G10], and the Zakusov institute, IMG's partner on Selank [G6, G8].

For a similar map of another research peptide, see What is BPC-157 used for in research? Back to the Limitless Science home page.

Sources

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