Selank and Semax are the two peptides most often grouped together as "Russian neuropeptides", and the grouping is defensible. Both are synthetic heptapeptides carrying a C-terminal Pro-Gly-Pro tail, both were developed by Russian research institutes, and both rest on a mechanism literature that is overwhelmingly rodent-based. This explainer separates what is actually published from what is commonly claimed, and grades each compound on the same scale used across Peptide Data. Nothing here is consumption or dosing advice; both compounds are research-use-only in the UK.

Semax: an ACTH fragment analogue

What it is

Semax is a synthetic heptapeptide, Met-Glu-His-Phe-Pro-Gly-Pro, described in the literature as an analogue of the ACTH(4-10) fragment (some sources give it as ACTH(4-7) extended with a Pro-Gly-Pro tail). It was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences and has been studied principally as a neuroprotective and nootropic candidate. It is not a licensed medicine in the UK.

What the mechanism work shows

The neurotrophic story is the strongest part of the Semax literature, and it is preclinical. Dolotov and colleagues reported that tritium-labelled Semax binds specifically, reversibly and calcium-dependently in the rat basal forebrain, and that intranasal application raises brain-derived neurotrophic factor (BDNF) protein in that region [R4]. A companion study found that a single application in rats produced a maximal roughly 1.4-fold increase in BDNF protein, a roughly 1.6-fold rise in trkB tyrosine phosphorylation, and increases in exon III BDNF and trkB transcripts in the hippocampus [R5]. Eremin and colleagues reported activation of dopaminergic and serotonergic systems in rodents after Semax administration [R6]. A genome-wide transcriptional study in a rat focal-ischaemia model found that Semax altered the expression of gene sets related to the immune and vascular systems, including genes involved in calcium signalling and inflammation [R7]. None of this establishes a human effect; it establishes a plausible mechanism worth testing.

What the human data shows

The human dataset is small, open-label and Russian-language. The earliest controlled comparison is Gusev and colleagues' 1997 study, which gave Semax to 30 patients in the acute period of hemispheric ischaemic stroke and compared them with 80 conventionally treated controls of similar stroke severity and location; the authors used clinical rating scales to quantify neurological deficit and described a favourable effect on functional recovery [R1]. Allocation was not randomised and blinding is not described. The largest and most recent study is the same group's 2018 open clinical study of 110 patients after ischaemic stroke, which assessed plasma BDNF, motor performance on the Medical Research Council scale and the Barthel index in early and late rehabilitation subgroups. Semax was administered intranasally at 6,000 microgram/day as two 10-day courses separated by a 20-day interval — this is trial methodology, not a recommendation — with outcomes assessed at approximately 89 and 214 days [R2]. The study was non-randomised and not placebo-controlled, and the published abstract does not report numerical effect sizes. On the nootropic side, an early report by Kaplan and colleagues described nootropic-like activity in humans [R3]; the hypothesis that Semax might be relevant to ADHD or Rett syndrome remains a published hypothesis rather than a tested claim [R8].

Evidence grade: Limited

Open comparative and non-randomised studies with no blinding, no placebo control and no independent replication outside the originating group. The mechanism literature is coherent and reproducible in animals; the human literature does not yet meet the bar for Moderate. No MHRA marketing authorisation exists, and no UK licence is in prospect.

Selank: a tuftsin analogue

What it is

Selank is a synthetic heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro, built on the immunomodulatory tetrapeptide tuftsin and extended with a Pro-Gly-Pro tail. It is described in the literature as a Russian-developed anxiolytic and is marketed in Russia on that basis [R17]. Like Semax, it is not a licensed medicine in the UK.

What the mechanism work shows

The Selank mechanism literature centres on GABAergic signalling and on enkephalin metabolism. The anxiolytic activity of the tuftsin analogue was characterised in inbred mouse strains with differing emotional-stress phenotypes [R10]. A rat study found that Selank altered the expression of genes encoding major GABA-A receptor subunits, GABA transporters and related neurotransmission proteins in frontal cortex, and that the changes overlapped with those seen after GABA itself [R11]. In the unpredictable chronic mild stress rat model, Selank enhanced the anxiolytic effect of diazepam, and no tolerance was observed over 14 days of administration [R12]. These are animal and cell-culture findings; they explain why an anxiolytic hypothesis was testable in humans, but they are not human evidence.

What the human data shows

The principal human study is Zozulia and colleagues' 2008 open comparative trial in 62 patients with generalised anxiety disorder and neurasthenia, in which Selank (30 patients) was compared with medazepam (32 patients) using the Hamilton and Zung scales and the Clinical Global Impression. The authors reported similar anxiolytic effects for the two drugs, with Selank additionally showing antiasthenic and psychostimulant effects, and measured serum enkephalin activity: the half-life of leu-enkephalin was reduced at baseline in patients with GAD and neurasthenia, correlated with symptom severity, and increased during treatment, most clearly in the GAD subgroup [R9]. The trial was open-label with an active comparator and no placebo arm, and the between-drug comparison rests on psychometric scales rather than blinded endpoints. A separate Russian-language occupational study examined peptide correction of neurotic disorders among professional truck drivers, using Selank in a working cohort [R13].

Evidence grade: Limited

One active-comparator, open-label human trial plus an occupational cohort study, both Russian-language, with no randomised placebo-controlled replication and no independent Western pharmacovigilance data. The GABA-A and enkephalin mechanism work is internally consistent but preclinical. Limited is the appropriate grade.

How the two compare

  • Scaffold. Both are heptapeptides ending in Pro-Gly-Pro, the modification that is generally credited with conferring resistance to peptidase degradation and prolonging action relative to their parent peptides.
  • Origin. Both were developed in Russian institutes and are studied predominantly by Russian groups.
  • Human literature. Both have human data confined to open-label studies without independent replication; neither has an adequately powered randomised, placebo-controlled trial published in English.
  • Mechanism depth. Semax has the larger neurotrophic (BDNF/trkB) literature; Selank has the more coherent GABA-A and enkephalin-metabolism story.
  • Regulatory position. Neither is licensed in the UK or by the EMA; neither appears on the MHRA's licensed medicines list.

UK legal status

Neither Selank nor Semax is a licensed medicine in the UK, and neither is scheduled under the Misuse of Drugs Act 1971. Both are generally supplied as "research chemicals" or "research-use-only" materials. That framing does not immunise supply: under the Human Medicines Regulations 2012, a product presented for human use with a medicinal claim is an unlicensed medicine, and supplying an unlicensed medicinal product in the UK without the relevant licence is an offence [R14][R15]. The MHRA has signalled that products marketed with research-only labelling can still fall within medicines law where their presentation implies human use, and has tightened its guidance on research-peptide labelling [R16]. Anyone handling these compounds in a laboratory context should treat the research-use-only designation as substantive, not as a formality.

What would move the grade

For both compounds, the gap is the same: an adequately powered, randomised, placebo-controlled trial with preregistered endpoints and independent analysis, replicated outside the originating group and published in English with full effect sizes and adverse-event reporting. Until then, the honest position is that both peptides have interesting preclinical mechanism data and a thin, uncontrolled human literature. That is a real research base; it is not a licence, a therapeutic claim, or a reason to assume an effect size.

A note on reading this

Trial regimens described above are historical trial methodology reported for interpretability. Peptide Data does not provide consumption, dosing or self-administration guidance for any compound, and no compound described here is approved for human use in the UK. Research use only.

This article is AI-researched and editorially reviewed. It is provided for research and educational purposes only and is not medical advice. Research peptides are not licensed for human consumption in the UK.