Selank: What the Research Shows, and Who Did It

This is the study everything else rests on. Sixty-two patients were studied. All had generalised anxiety disorder or neurasthenia.¹

Thirty received selank. Thirty-two received medazepam, a benzodiazepine. Researchers scored patients on three standard scales: Hamilton, Zung and CGI.¹

The headline finding is unusually direct. The anxiolytic effects of both drugs were similar. Selank also showed antiasthenic and psychostimulant effects, which the comparison drug did not.¹

The study tracked one more thing: enkephalin activity in blood serum. Enkephalins are the body's own signalling peptides.¹

Patients in the study had a lower level on one enkephalin measure. That level tracked with how long they had been ill and how severe their symptoms were. Selank raised it.¹

62

patients in the clinical study¹

30

received selank; 32 received a benzodiazepine¹

2008

year of publication, in Russian

Read the author lists below and a pattern appears. N. F. Myasoedov is an author on all five papers cited here. That is the clinical trial, the rat gene work, the cell work, the rat behaviour study and the brain scan.¹²³⁴⁵

Most of that work comes from the Institute of Molecular Genetics at the Russian Academy of Sciences.²³⁴

The mechanism question came straight out of the clinic. If selank behaves like a benzodiazepine, does it work like one?²

GABA is the brain's main calming signal. Benzodiazepines strengthen it by acting on GABA-A receptors.³ So researchers went looking at GABA-related genes.

• In rat cortex. Researchers measured 84 genes at 1 and 3 hours after selank or GABA. The set covered the major GABA receptor subunit, transporters, ion channels, and dopamine and serotonin receptors. Many changed significantly.²
• In human cells. The same question was put to IMR-32 cells, a human neuroblastoma line, comparing GABA, selank and olanzapine.³
• In rat behaviour. Selank and diazepam were tested alone and together, in rats under unpredictable chronic mild stress and without it, using the elevated plus maze.⁴

None of this proves selank binds the same receptor a benzodiazepine does. It shows the GABA system is where the signal turns up. Those are different claims, and the gap between them is the honest summary.

One study looked at people instead of tissue. Fifty-two healthy participants had resting-state fMRI scans, taken before, then at 5 and at 20 minutes.⁵

The researchers picked their regions in advance. The amygdala is central to regulating anxiety. The dorsolateral prefrontal cortex handles executive functions, including working memory. Both were examined in each hemisphere.⁵

Differences turned up in one place: the connection between the right amygdala and parts of the right temporal cortex. The authors call these the first described effects of selank and semax on that link.⁵

• The clinical trial has not been replicated abroad. It was published in Russian, in a Russian journal, in 2008, with 62 patients.¹
• Most mechanism work is gene expression. Measuring which genes change is a long way from knowing what a compound does to a person.²³
• The comparison drug is unfamiliar here. Medazepam is a benzodiazepine. It is not one commonly prescribed in the US, which makes the result harder to place against a drug you know.¹
• Purity and identity are per-lot facts. They come from the certificate for the vial you hold, not from any paper on this page.