Selank

Selank is tuftsin, the immune tetrapeptide from IgG, with the same protective Pro-Gly-Pro tail used on Semax. Its best-documented action is inhibition of enkephalin-degrading enzymes, which prolongs endogenous enkephalin signalling - this is thought to account for the anxiolysis without the receptor occupancy and rebound of a benzodiazepine. Russian work also reports changes in GABA-A receptor subunit expression, altered serotonin metabolism, and modulation of IL-6 and interferon gene expression, the last reflecting its immune-peptide ancestry. It is not sedating and does not appear to impair memory formation, which is the whole clinical selling point against benzodiazepines.

Targets: Enkephalin-degrading enzymes, GABA-A receptor expression, Serotonergic system, IL-6 / interferon gene expression

• · Most people land at 300-500 mcg twice daily. Split each dose between nostrils.
• · Corresponds to the 0.15% solution used in the generalised anxiety trials - roughly 2-3 drops per nostril three times daily. This is around five times the typical grey-market dose and is where the actual human efficacy data sit.

Work out your exact syringe units →

• commonNasal irritation or dryness
• uncommonMild drowsiness or a heavy, relaxed feeling— Far less than a benzodiazepine, but real at clinical doses.
• uncommonEmotional flattening or reduced motivation— Mostly at the high clinical dose range; reverses on stopping.
• uncommonHeadache
• rareTransient dizziness

• Pregnancy and breastfeeding - no safety data.
• Do not use it as a substitute for tapering a benzodiazepine you are physically dependent on; it does not prevent withdrawal seizures.

• synergysemax — The standard Russian pair - Semax for drive, Selank to blunt the arousal it creates.
• redundantn-acetyl-selank-amidate — Same molecule with capped termini. Run one.
• synergyoxytocin — Both are used intranasally for social anxiety and both are non-sedating; commonly stacked, with no known conflict.

• · No bloodwork established.
• · Rate anxiety on something structured like a weekly GAD-7 rather than by feel - peptides that reduce arousal are easy to misjudge.

Registered prescription medicine in Russia. Unapproved research chemical in the US, UK and EU.

• Zozulya et al. 2008, comparative trial of Selank versus medazepam in generalised anxiety disorder (trial)
• Kolomin et al., Selank and gene-expression effects in brain and blood - review of the Russian literature (review)

The mechanism that actually has human evidence behind it is the enkephalin one, and it is more specific than the usual summary. In the Russian generalised anxiety trial the investigators measured enkephalin-degrading enzyme activity in patient blood and found it elevated in anxious patients in proportion to symptom severity; Selank treatment inhibited that enzyme activity and raised endogenous enkephalin levels, and the enkephalin change tracked the clinical improvement. That is an unusually clean mechanism-to-outcome chain for anything in this class, and it explains the clinical profile better than the GABA account does. If you prolong endogenous enkephalin signalling rather than occupying a receptor with an exogenous ligand, you get anxiolysis that follows the body's own release pattern - which is why it does not sedate, does not impair memory formation, does not produce tolerance on a two-week course, and does not generate a rebound when it stops. Every one of those properties is the opposite of a benzodiazepine, and all of them fall out of the same mechanistic difference. The GABA-A subunit expression changes and the IL-6 and interferon gene effects are real reported findings but sit at a different level of confidence - they are rodent gene-expression work from a single research lineage, and they are describing downstream consequences rather than the primary action. The tuftsin ancestry also means this is an immune peptide wearing a psychiatric hat, and the immunological effects are not incidental to it.

The dominant failure mode on Selank is under-dosing and concluding it does nothing. Grey-market protocols cluster at 300-600 mcg per day; the Russian trials that produced the actual efficacy evidence used 2700-3000 mcg per day divided into three doses. That is a five-fold gap, and a lot of people write Selank off having never taken a clinically meaningful amount of it. The second failure mode is the opposite: running the full clinical dose continuously for months and ending up flat and unmotivated. The Russian courses are 10-14 days, occasionally 30, and there is no data supporting continuous use beyond that. Third, and specific to this compound, is expecting a benzodiazepine. Selank does not produce a felt event. It removes an edge, and people watching for a distinct onset frequently miss a real effect. Fourth is misjudging what it is for - Selank is genuinely good at anticipatory and generalised anxiety and is not an acute panic abortive.

1. 300 mcgDays 1-3 — One intranasal dose, split between nostrils. Selank is forgiving enough that this step is about confirming tolerability rather than finding trouble.
2. 600 mcgDays 4-10 — 300 mcg twice daily. This is where most grey-market users settle - and it is roughly a fifth of the dose the clinical trials used.
3. 1.5 mgWeek 2-3 — 500 mcg three times daily. If 600 mcg/day did nothing, this is the honest next step rather than concluding the compound is inert.
4. 2.7 mgWeek 3 onward, clinical range — 900 mcg three times daily, approximating the 0.15% solution used in the Russian generalised anxiety trials. This is where the actual human efficacy evidence sits. Expect some flatness and mild drowsiness at this level.

• Enkephalin-degrading enzymes (enkephalinases) — Inhibition demonstrated in human plasma in the generalised anxiety trial; no Ki has been published

  Prolongs endogenous Leu- and Met-enkephalin signalling. Measured enkephalin rises in treated patients tracked their clinical improvement, which is the strongest mechanistic link this compound has.

• GABA-A receptor subunit expression — Not a binding interaction - Selank does not occupy the benzodiazepine site

  Altered subunit expression reported in rodent brain. This is why Selank does not sedate and does not produce benzodiazepine-type dependence: it is not sitting on the receptor.

• Serotonergic system — Not quantified

  Altered serotonin metabolism in rodent brain; the plausible substrate for the antidepressant-like effect that accumulates over one to two weeks rather than acutely.

• Tuftsin receptor / immune signalling (IL-6, interferon gene expression) — Not quantified in humans

  Modulation of IL-6 and interferon gene expression in brain and blood. Inherited from its tuftsin parent structure; largely ignored by consumers and probably shouldn't be.

• Selank versus medazepam in generalised anxiety disorder and neurasthenia (Zozulya et al., Russian State Research Centre) Comparative clinical trial · 2 weeks · 2008

  Anxiolytic efficacy against the benzodiazepine medazepam. Anxiolytic effects were comparable between the two, with Selank additionally showing antiasthenic and mild psychostimulant effects that medazepam did not. The investigators also measured enkephalin-degrading enzyme activity, found it elevated in proportion to symptom severity at baseline, and showed Selank treatment raised enkephalin levels alongside clinical improvement. Small, Russian-language, never independently replicated.

20-30 minutes to noticeable anxiolysis after an intranasal dose, though it is a subtraction rather than an addition and is easy to miss. A single dose is useful for roughly 4-8 hours by subjective report, with rodent behavioural effects reported considerably longer than plasma presence would predict. Sleep-onset benefits, where they occur, show up within the first few nights. The antidepressant-like and antiasthenic effects that the Russian trial documented accumulate over 7-14 days - this is the timescale the clinical data actually describes. Full courses in the trials ran 14 days, with assessment at the end. There is no rebound or discontinuation syndrome on stopping, which is one of the more useful things about it.

Selank is the least conflict-prone compound in this class and stacks with almost anything without a mechanistic argument against it. The Semax pairing is the standard and works because the two are genuinely opposed on arousal - dose Semax in the morning and Selank when the edge appears, typically early afternoon, rather than fixing a schedule in advance. Oxytocin plus Selank is a reasonable social-anxiety combination since neither sedates and the receptor systems do not overlap, though both are intranasal and you will be irritating the same mucosa twice. Selank pairs well with Noopept specifically because it blunts the irritability that is Noopept's main failure mode. The one combination to think about is any opioid or opioid-adjacent compound: Selank works by prolonging endogenous enkephalin signalling, and while there is no documented interaction, stacking it with something else acting on that system has no data behind it. Do not use Selank as the anxiolytic arm of a benzodiazepine taper - it does not prevent withdrawal seizures and treating it as a substitute is the one genuinely dangerous mistake available here.

Against a benzodiazepine, which is the comparison that matters: the Russian trial found comparable anxiolysis to medazepam without sedation, without cognitive impairment, without tolerance over the course and without withdrawal. That is a genuinely favourable profile, and it comes from one small unblinded Russian study that nobody has replicated. Treat it as promising rather than proven, and do not extrapolate it to severe anxiety disorders. Against buspirone or an SSRI, the honest positioning is that those have large replicated Western trial programmes and Selank has one Russian study, but Selank works within days rather than weeks and has no sexual side effects, no emotional blunting at normal doses and no discontinuation syndrome. Against N-Acetyl Selank Amidate: same molecule capped, longer duration, roughly a third to a half the dose, and no evidence of its own whatsoever - the parent at least has the human trial. Against Semax: opposite direction on arousal, and the two are designed to be used together rather than chosen between. Of everything in this class, Selank has the best ratio of evidence to risk, which says as much about the class as about Selank.

$20–$120/month. A 30 mg vial runs roughly 40-70 USD. At a typical 600 mcg/day that is 50 days of use and about 25-40 USD per month. At the clinical 2700-3000 mcg/day it is 10 days per vial and 120-200 USD per month, which is the hidden cost of dosing it properly. Russian pharmacy 0.15% solution is often the cheaper route to clinical dosing where it can be obtained.

• ?No human pharmacokinetic study of Selank has been published. Half-life, bioavailability, volume of distribution, protein binding and clearance are all unmeasured in people.
• ?Participant numbers in the Zozulya comparative trial were not stated in the abstract I could access and I did not resolve them.
• ?Whether intranasal delivery achieves meaningfully different brain exposure than subcutaneous has never been compared.
• ?The GABA-A subunit expression findings come from a single Russian research lineage and have not been independently replicated.
• ?No enkephalinase inhibition constant has been published, so the potency of the primary mechanism is unquantified.
• ?The Pro-Gly-Pro tail is independently active on brain transcription in the Semax literature, and how much of Selank's effect is attributable to that shared fragment rather than to the tuftsin core is unresolved.
• ?Nothing is known about continuous use beyond about 30 days. The emotional flattening reported at high doses over long periods has no published characterisation.
• ?The immune effects inherited from tuftsin are documented at the gene-expression level and their clinical significance in a healthy user is entirely unknown.

• Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia Zozulya AA, Neznamov GG, Siuniakov TS, Kost NV, Gabaeva MV, Sokolov OY, Serebryakova EV, Siranchieva OA, Andryushenko AV, Telesheva ES, Siuniakov SA, Smulevich AB, Myasoedov NF, Seredenin SB, Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2008 · PMID 18454096

  The single most important human study on Selank. Comparable anxiolysis to medazepam without sedation, plus the enkephalin mechanism measured in the same patients. Everything credible said about Selank traces here.

• Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation Zolotarev YA, Dadayan AK, Dolotov OV, Kozik VS, Kost NV, Sokolov OY, Dorokhova EM, Meshavkin VK, Inozemtseva LS, Gabaeva MV, Andreeva LA, Alfeeva LI, Grivennikov IA, Zozulya AA, Myasoedov NF, Bioorganicheskaia Khimiia, 2006 · PMID 16637290

  The tritium-labelling methodology behind what little distribution and degradation data exists for Selank and its relatives. Read it for the method rather than for a clean PK number.