Selank
A Russian-developed synthetic heptapeptide registered as an anxiolytic in Russia — with consistent animal data and small human trials, but no independent replication outside Russian research groups
🧑🐀 Both
- Full name
- Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro)
- Class
- Synthetic heptapeptide; tuftsin analogue with C-terminal Pro-Gly-Pro stabiliser
- Molecular weight
- ~863.0 g/mol
- CAS number
- 129954-34-3
- Sequence
- Thr-Lys-Pro-Arg-Pro-Gly-Pro
- First synthesized
- 1990s, Institute of Molecular Genetics and Zakusov Research Institute of Pharmacology, Russian Academy of Sciences
- Regulatory status
- Registered prescription anxiolytic in Russia (nasal spray formulation). Not approved for medical use in the US, EU, UK, Australia, Canada, or any other Western jurisdiction.
What it is
Selank is a synthetic heptapeptide developed in Russia during the 1990s at the Institute of Molecular Genetics and the Zakusov Research Institute of Pharmacology. It is based on tuftsin, a natural tetrapeptide (Thr-Lys-Pro-Arg) with immunomodulatory activity, extended at the C-terminus with Pro-Gly-Pro to resist enzymatic breakdown and prolong activity. The result is a molecule with both immune-modulating and central nervous system effects. In Russia, Selank is registered as a prescription anxiolytic nasal spray for generalised anxiety disorder and neurasthenia. Outside Russia it has no regulatory standing — it is not approved in the US, EU, UK, Australia, or Canada and circulates in grey markets as a research chemical.
How it works
Selank acts through several overlapping systems. The best-supported mechanism is allosteric modulation of GABA-A receptors combined with changes in GABA receptor gene expression — producing anxiolytic effects in rodent models without the sedation or dependency seen with classical benzodiazepines. The developers attribute this to a distinct subunit-expression profile, though this claim comes from the same groups that developed the compound and has not been independently verified. A second pathway involves the enkephalinergic system: patients with GAD were found to have reduced leucine-enkephalin half-life, which Selank partially normalised. Selank also upregulates BDNF in the rat hippocampus and modulates serotonin and noradrenaline metabolism across several brain regions, suggesting nootropic effects on top of its anxiolytic profile. How these mechanisms translate to the human brain is not established.
What the research shows
The animal literature on Selank is extensive and consistent. The human evidence is a small set of clinical trials conducted by Russian research groups, published mostly in Russian-language journals; some have English abstracts on PubMed. None have been independently replicated outside Russia. Read the following findings with that context in mind.
Zozulia et al. (2008) — Clinical trial in generalised anxiety disorder and neurasthenia
Zozulia A.A. et al., 2008, Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova 🧑 Human (clinical trial, Russia)
Sixty-two patients with GAD or neurasthenia: 30 received Selank (intranasal, 400 mcg twice daily, 14 days); 32 received medazepam (benzodiazepine comparator). Anxiety was measured with Hamilton, Zung, and CGI scales.
Both drugs reduced anxiety scores comparably. Selank additionally showed antiasthenic and mild psychostimulant effects absent with medazepam, without the sedation or rebound anxiety typical of benzodiazepines. A biological sub-study found reduced leucine-enkephalin half-life at baseline that improved with Selank and correlated with symptom improvement.
Limitations: 62-patient, single-centre study from a group with institutional interest in the compound; no placebo arm; not replicated outside Russia — results are preliminary and hypothesis-generating.
Uchakina et al. (2008) — Immunomodulatory effects in anxiety-asthenic patients
Uchakina O.N. et al., 2008, Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova 🧑 Human (clinical observation, Russia)
This companion study to the Zozulia trial examined immunological parameters in patients treated with Selank. Given Selank's structural derivation from tuftsin — a peptide known to stimulate macrophage and natural killer cell activity — the authors measured cytokine profiles and immune cell markers before and after treatment.
Selank treatment was associated with normalisation of several immune parameters that were dysregulated at baseline in anxious patients, including T-lymphocyte subsets and cytokine levels. The authors proposed that Selank exerts a dual anxiolytic-immunomodulatory action, potentially relevant to the immune dysregulation sometimes seen in anxiety and stress disorders.
Limitations: Same small Russian trial context as Zozulia et al.; immune parameters vary widely across patients and no independent replication exists.
Kolomin et al. (2016) — GABAergic gene expression in rat brain
Kolomin T. et al., 2016, Frontiers in Pharmacology 🐀 Animal (rats)
This study used RT-PCR and microarray analysis to quantify changes in the expression of genes encoding GABA-A receptor subunits, GABA transporter proteins, and related scaffolding molecules in rat brain tissue following Selank administration. Twelve rats received intranasal Selank; twelve received vehicle control.
Selank produced statistically significant changes in the expression of multiple genes in the GABAergic pathway within one to three hours of administration. The expression of GABRA1, GABRA2 (encoding GABA-A receptor alpha-1 and alpha-2 subunits), and the GABA transporter GAT-1 were all affected. Crucially, the expression profile differed from that produced by diazepam at equipotent anxiolytic doses, providing a molecular basis for why Selank might lack the sedative and dependency-inducing effects of classical benzodiazepines. A companion analysis of the hippocampal transcriptome identified changes in 36 genes after a single dose, with notable effects on orexin pathway genes (Hcrt) relevant to sleep-wake balance.
Limitations: Rodent gene expression changes do not directly predict human pharmacology; dose extrapolation to humans is not established.
Semenova et al. (2009) — Serotonin metabolism in rat brain
Semenova T.P. et al., 2009, Bulletin of Experimental Biology and Medicine 🐀 Animal (rats)
Semenova and colleagues examined how Selank affects serotonin (5-HT) metabolism in rats whose serotonin synthesis had been pharmacologically depleted using para-chlorophenylalanine (PCPA). The PCPA model creates a serotonin-depleted brain state, allowing researchers to probe whether a compound can restore or modulate 5-HT turnover.
Selank significantly enhanced 5-HT metabolism in the brainstem 30 minutes after administration in PCPA-pretreated rats, while the parent compound tuftsin had minimal effect under the same conditions. A separate study from the same group showed that a single injection of Selank activated 5-HT metabolism in the hypothalamus and caudal brainstem for up to two hours and improved learning performance — findings that positioned serotonergic modulation as a component of Selank's nootropic and anxiolytic profile distinct from its GABAergic actions.
Limitations: PCPA depletion is an artificial model; short-interval serotonin measurements in rodent brainstem may not reflect clinically meaningful changes in human 5-HT transmission.
Kolpakov et al. (2014) — Selank in alcohol withdrawal anxiety (rats)
Kolpakov V.G. et al., 2014, Bulletin of Experimental Biology and Medicine 🐀 Animal (alcohol-preferring rats)
Using a line of rats selectively bred for voluntary alcohol preference (a model of alcohol use disorder), the investigators induced a stable alcohol-dependent state and then allowed withdrawal. Selank (0.3 mg/kg, intraperitoneal) was administered at the peak of withdrawal and its effects on anxiety-related behaviour were measured in the elevated plus-maze and open-field test — the standard battery for rodent anxiolytic screening.
A single dose of Selank completely normalised elevated plus-maze behaviour in withdrawing rats, eliminating the excess anxiety caused by alcohol withdrawal. The effect was comparable to diazepam at clinically relevant doses but Selank did not produce the sedation or motor impairment seen with diazepam. The authors concluded that Selank may have utility in managing anxiety during alcohol withdrawal, though they acknowledged this would require human validation.
Limitations: Results are from a specialised inbred strain; human data on Selank in alcohol withdrawal do not exist.
Inozemtsev et al. (2016) — Selank and diazepam synergy under chronic stress (rats)
Inozemtsev A.N. et al., 2016, Neurochemical Journal 🐀 Animal (rats, chronic mild stress model)
This study placed rats in an unpredictable chronic mild stress (UCMS) protocol — a well-validated model of the affective and cognitive blunting seen in human anxiety and depression — and then tested Selank alone, diazepam alone, and the combination of both at sub-threshold doses. Anxiolytic efficacy was measured in the elevated plus-maze; cognitive performance was assessed in a conditioned avoidance task.
Selank enhanced the anxiolytic effect of a sub-effective dose of diazepam in UCMS rats, producing a synergistic response that exceeded what either compound achieved alone. Selank alone also reduced anxiety under UCMS conditions at a dose that was ineffective in non-stressed animals, suggesting stress-state dependence of its effects. The interaction was not simply additive, pointing to complementary rather than identical mechanisms.
Limitations: UCMS models incompletely capture human GAD; synergistic benzodiazepine interactions in humans — including potential enhanced side effects — have not been studied.
Reported benefits (from research)
- In the Zozulia 2008 Phase 2 RCT (n=62), intranasal Selank produced significant reductions in HAM-A anxiety scores compared with baseline, with effect sizes comparable to the benzodiazepine comparator (medazepam) but without sedation or cognitive impairment.
- In rodent open-field and elevated-plus-maze studies, Selank reduced anxiety-related behaviour at doses of 100–300 µg/kg IP without impairing locomotor activity, consistent with an anxiolytic rather than sedative mechanism.
- Selank upregulated BDNF expression in the hippocampus and prefrontal cortex of rats in several studies, suggesting a potential neuroprotective and pro-cognitive effect separate from anxiety reduction.
- In rodent studies, Selank stabilised enkephalin metabolism by inhibiting enkephalinase enzymes, offering a potential mechanism for sustained anxiolytic effects and mood modulation.
- In rat models of learned helplessness and chronic mild stress, Selank attenuated depressive-like behaviour, supporting its broader anxiolytic–antidepressant profile in rodents.
Drawbacks and concerns
- The only published human RCT (Zozulia 2008) enrolled 62 patients over 14 days — far too small and short to characterise efficacy or safety for a psychiatric indication; no independent Phase 3 trial exists.
- All human trial data come from the same Russian institutes (Institute of Molecular Genetics and others) that developed and commercialised Selank; no independent replication by unaffiliated groups has been published in English-language literature.
- Registered only in Russia for specific anxiety indications; not approved by the FDA, EMA, or any equivalent regulator. Sold outside Russia exclusively as a research chemical.
- The intranasal route used in trials depends on correct nasal mucosal absorption — DIY intranasal administration of grey-market peptide solutions has no verified bioavailability data outside the clinical setting.
- Long-term effects on the GABAergic system, HPA axis, and BDNF signalling from chronic use are unknown; interactions with prescribed anxiolytics or antidepressants have not been studied.
- Peptide purity and concentration in commercially sourced Selank solutions are unverified; the nasal spray used in the Zozulia trial was a pharmaceutical-grade 0.15% formulation manufactured under GMP conditions.
Doses used in research
The following reflects what scientists actually administered in published studies; it is not a recommendation for human use.
- Zozulia 2008 Phase 2 GAD trial (Zh Nevrol Psikhiatr Im S S Korsakova): Selank 0.15% nasal spray, 2 drops per nostril 3 times daily (total ~2100 µg/day) for 14 days in patients with generalised anxiety disorder.
- Rodent anxiolytic studies (Semenova et al., multiple publications 2000s): Selank 100–600 µg/kg intraperitoneally or intranasally in rats and mice, single or repeated administration, in open-field, elevated-plus-maze, and stress models.
- Rodent BDNF / neurotrophic studies (Inozemtseva et al.): Selank 300 µg/kg IP daily for 5–14 days in rats, with hippocampal and cortical tissue collected for BDNF and mRNA analysis.
These doses are from published research only. No safe or effective dose has been established for human use of Selank outside the Russian clinical programme, and Selank is not approved for human use by the FDA, EMA, or equivalent regulators.
Safety and limitations
In animal studies, Selank has a clean acute safety profile: no lethal dose has been established, it does not impair motor coordination at anxiolytic doses, and no withdrawal or tolerance has been observed in chronic dosing experiments. Russian clinical researchers report good tolerability in patients. However, all human safety data derive from small trials run by the same groups that developed the compound — these are not independent regulatory assessments, and a 62-patient, 14-day trial is far too small to characterise a medicine's safety profile.
The "no benzodiazepine side effects" claim is plausible given Selank's distinct GABAergic profile in animal models — less sedation, less motor impairment, no conditioned-place-preference — but it originates from the developers themselves and needs independent replication before it can be treated as established. Whether the rodent advantage translates to humans is unknown.
Intranasal administration (the approved Russian route) delivers drug directly to the brain by bypassing hepatic first-pass metabolism; subcutaneous injection — the route common in grey-market use — has different and incompletely characterised pharmacokinetics in humans. Products sold online as "Selank" carry no guarantees of purity, sterility, or correct sequence. Self-administration is not supported by any independent clinical evidence.
Sources
- Zozulia A.A. et al. "[Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia]." Zh Nevrol Psikhiatr Im S S Korsakova, 2008;108(4):25–34. PubMed 18454096
- Uchakina O.N. et al. "[Immunomodulatory effects of selank in patients with anxiety-asthenic disorders]." Zh Nevrol Psikhiatr Im S S Korsakova, 2008;108(5):71–5. PubMed 18577961
- Kolomin T. et al. "Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission." Frontiers in Pharmacology, 2016. PubMed 26924987
- Semenova T.P. et al. "[Comparison of the effects of selank and tuftsin on the metabolism of serotonin in the brain of rats pretreated with PCPA]." Eksperimental'naia i klinicheskaia farmakologiia, 2009;72(4):6–8. PubMed 19803361
- Kolpakov V.G. et al. "Efficacy of peptide anxiolytic selank during modeling of withdrawal syndrome in rats with stable alcoholic motivation." Bulletin of Experimental Biology and Medicine, 2014;157(2):202–4. PubMed 24913576
- Inozemtsev A.N. et al. "Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats." Neurochemical Journal, 2016. PubMed 28280289
Related products & further reading
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Peptide Protocols Vol. 1 — Dr. William Seeds
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