Research information only. PrecisePep is an educational library. It is not medical advice and is not intended to assist, encourage or enable self-administration. The compounds documented here are research chemicals — most are not approved for human use. Read the full disclaimer.
PrecisePep/Peptide Library/Selank
Neuro-Cognitive & Nootropic
Thr-Lys-Pro-Arg-Pro-Gly-Pro · tuftsin analogue · TP-7 · N-Acetyl Selank Amidate (NASA-Selank)
A tuftsin analogue registered in Russia as an anxiolytic — reported in domestic clinical work to match benzodiazepines for anxiety without sedation, dependence or withdrawal.
Selank is the calm half of the Russian nootropic pair. It is a synthetic analogue of tuftsin — an endogenous immunomodulatory tetrapeptide — extended with the same Pro-Gly-Pro stabilising tail used in Semax, and developed at the same Moscow institute. It is registered in Russia as an anxiolytic for generalised anxiety disorder and neurasthenia.
The interesting clinical claim, from Russian trial work, is that Selank produced anxiolytic effects comparable to classical benzodiazepines in generalised anxiety disorder — without sedation, without cognitive impairment, without dependence and without a withdrawal syndrome.[1][2] If that is accurate it is a genuinely unusual pharmacological profile. It has not been independently replicated to Western regulatory standards.
Mechanistically, Selank appears to work by modulating GABAergic gene expression and signalling rather than by directly agonising the benzodiazepine site — which would explain the absence of sedation and dependence.[3][4] It also raises BDNF and inhibits enkephalin degradation, overlapping with Semax at the neurotrophic level.
GABAergic modulation without direct receptor agonism. Selank alters expression of genes involved in GABAergic neurotransmission and enhances GABA_A-mediated inhibition allosterically rather than through the benzodiazepine binding site. This distinction is the mechanistic explanation for the reported absence of sedation, tolerance and withdrawal.[3][4]
Enkephalinase inhibition. Like Semax, Selank inhibits enzymes that degrade endogenous enkephalins, prolonging their action. This contributes to anxiolysis and mood stabilisation through the endogenous opioid system without exogenous opioid administration.
BDNF upregulation. Reported increases in BDNF expression, particularly in the hippocampus — shared with Semax and the basis for the nootropic rather than purely anxiolytic framing.
Serotonergic modulation. Reported effects on serotonin metabolism, relevant to the mood component of the profile.
Immunomodulation. Tuftsin, the parent peptide, is an immunostimulant; Selank retains some immune-modulating activity, reported as effects on interferon and cytokine balance. This is a genuine difference from Semax and is rarely discussed in community use.
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Russian clinical work in generalised anxiety disorder and neurasthenia reports efficacy comparable to classical benzodiazepine treatment, with the notable absence of sedation and cognitive impairment.
The defining claim. Unlike benzodiazepines, Selank is not reported to produce tolerance, physical dependence or a discontinuation syndrome.
Demonstrated changes in expression of genes involved in GABAergic neurotransmission in cell and animal models — the mechanistic substrate for the anxiolytic effect.
Selank potentiated the anxiolytic effect of diazepam in chronic mild stress models in rats, supporting an allosteric modulatory rather than direct agonist mechanism.
Reported efficacy in modelled withdrawal syndrome in rats with established alcohol motivation.
Easy to miss in the route study, and arguably the most useful single fact on this page. Selank was given to two mouse strains: BALB/c, which are naturally anxious with low exploratory activity, and C57BL/6, which are not. The anxiolytic and nootropic effects appeared only in the BALB/c mice. In the calm strain, neither route produced a measurable effect. If that carries to people, Selank normalises an elevated state rather than adding a felt effect on top of a normal one — which would make it close to inert in someone who is not anxious when they take it. That is a different proposition from a benzodiazepine, which does something noticeable regardless, and it is consistent both with the subtler than expected reports below and with the human evidence coming from diagnosed anxiety populations rather than healthy volunteers.
Review-level synthesis of the molecular aspects of Selank biological activity, describing the anxiolytic and nootropic mechanisms together.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Extrapolated from clinical anxiety-disorder populations to general stress management — the way it is almost universally used in the research community, and outside the evidenced population. The strain result above is the reason to take that caveat seriously rather than as boilerplate: in animals the effect was present in the anxious strain and absent in the calm one, so the gap between the studied population and the typical user may be the difference between an effect and none.
The stated basis for the "always take them together" convention. Complementary mechanisms make this plausible; the combination has not been formally trialled.
Proposed on the basis of the GABAergic modulation and the diazepam-potentiation finding. This is a clinical decision with genuine risk — benzodiazepine tapering is medically supervised for good reason.
Reported effects on interferon balance suggest immune activity that community use ignores entirely. Direction and clinical relevance in healthy adults are unknown.
Indirect rather than sedative. Commonly claimed, not measured.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The characteristic report: calm without sedation or cognitive flattening. Distinct from how users describe benzodiazepines or alcohol, and consistent with the proposed mechanism.
Community consensus that Selank removes the edge and irritability Semax can produce.
Reported indirectly through reduced rumination rather than as sedation.
A frequent counter-report: Selank is often described as much less noticeable than Semax, with some users reporting no perceptible effect at all. There is a plausible reason for that, and it is not that the product was fake: in the two-strain study above the effect showed up only in animals that were anxious to start with. Someone taking it on a calm day may be the calm strain.
Consistently reported and consistent with the claimed absence of dependence.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Russian clinical work reports good tolerability with nasal irritation as the principal issue. Registration-supported but not subject to Western pharmacovigilance.
The most clinically significant safety claim, and the one that distinguishes it from the drug class it is compared against.
No regulatory safety assessment outside Russia, no long-term data in healthy adults, no independent adverse-event surveillance.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The diazepam-potentiation finding means additive effect with benzodiazepines, alcohol, gabapentinoids and z-drugs should be assumed. This is the most concrete interaction risk on this page and it has direct evidence behind it.
The tuftsin lineage implies immune activity. Chronic use in healthy adults has no characterisation of that dimension.
Suppressing anxiety symptoms without diagnosis removes the prompt to address a treatable condition.
Serotonergic modulation alongside prescribed antidepressants is uncharacterised.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most common complaint.
Occasionally reported, usually resolved by reducing the dose.
Infrequently reported.
Non-response is common enough to be worth stating plainly; Selank is subtler than Semax and a meaningful fraction of users report nothing.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
The Russian registered product is a 0.15% intranasal solution with defined dosing for anxiety indications over a defined treatment course.
This is the clearest route result for any compound in this library, and it argues against treating the two as interchangeable. Mice received 300 mcg/kg/day for five days, intraperitoneally or intranasally, with receptor binding measured afterwards. Intraperitoneal Selank raised GABA-receptor binding in the frontal cortex by 38% and left hippocampal NMDA receptors unchanged. Intranasal Selank raised NMDA-receptor binding by 23% and left GABA receptors unchanged. Same peptide, same dose, opposite receptor systems — which the authors attributed to differences in pharmacokinetics and biotransformation. Both routes were anxiolytic, but only in the BALB/c strain that begins anxious; neither route did anything measurable in C57BL/6 mice.
Clinical use is structured as defined treatment courses rather than continuous administration.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
All the clinical data was generated intranasally, and there is no human injection study. There is animal comparative data, and it does not support treating the routes as equivalent: at a matched dose the injected peptide engaged GABA receptors and the sprayed peptide engaged NMDA receptors.
Community protocols typically use the same microgram figure for both, which is convention rather than a dose-equivalence finding.
Some protocols divide the daily amount across morning and early afternoon. Reasonable given reported duration; unstudied.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The figure in the Gold Standard protocol: 500 mcg, one vial (about 20 days), then cycle off for an equal period, always taken with Semax.
The general community range.
Common practice, usually at the same 250—750 mcg used intranasally. The anxiolytic effect is reported by both routes in animals, so this is not baseless — but the receptor work above found them acting through different systems at the same dose, and no human study has used injection at all. Anyone reasoning that the injected version is the intranasal one with better absorption is assuming the part that was actually measured and found to differ.
The amidated analogue is reported as more potent and longer-acting; community doses are correspondingly lower. Conversion ratios are guesswork.
Some users dose only ahead of anticipated stress rather than continuously. Coherent with an anxiolytic that does not require steady-state accumulation.
| Form | Typical dose | Route | Timing |
|---|---|---|---|
| Selank | 250 – 750 mcg | Intranasal | Morning / early afternoon |
| Selank (Gold Standard) | 500 mcg | Intranasal | Never after 2pm |
| N-Acetyl Selank Amidate | 100 – 300 mcg | Intranasal | Morning |
| As-needed | 250 – 500 mcg | Intranasal | Ahead of stressor |
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Selank enhanced the anxiolytic effect of diazepam in rodent chronic mild stress models — direct evidence of interaction with the benzodiazepine class, relevant as both a synergy and a risk.
Systems-level analysis has examined both peptides in parallel, describing complementary rather than overlapping network effects.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The canonical pairing: activation and drive from Semax, calm and stress-resilience from Selank, with overlapping BDNF and enkephalinase mechanisms underneath. The most coherent nootropic combination in circulation.
Reduced anxiety and improved sleep onset supporting the nocturnal GH pulse. Indirect and speculative.
Alcohol, benzodiazepines, gabapentinoids and z-drugs should be assumed additive on the basis of the diazepam finding. This is the interaction most likely to matter in practice.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The near-universal community convention.
Reported alongside caffeine and prescribed stimulants. Uncharacterised interaction with the latter.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Defined intranasal dosing over a set course for generalised anxiety disorder and neurasthenia, as specified in the Russian registered product information.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Mirrors the registered clinical structure and limits total exposure in the absence of long-term data.
Aligns both peptides to the same window and avoids the sleep disruption reported with late Semax dosing.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
500 mcg daily, never after 2pm, always with Semax. One vial is about 20 days; cycle off for the same period.
Grouped with Semax in the neuro-cognitive and endocrine axis category.
Selank is sold on one comparison: that it works like a benzodiazepine without the dependence. There is a real trial behind that comparison and it is worth reading carefully, because what it actually established is narrower than what gets claimed — and one of the gaps is dangerous.
Selank is not approved outside Russia and has no Western trial evidence. The Russian clinical work is small, largely untranslated, and unreplicated elsewhere. The most-cited study compared Selank against medazepam — a benzodiazepine — in generalised anxiety disorder and neurasthenia, in roughly sixty patients split between arms.
Pathophysiology
GAD is persistent, excessive worry with physical symptoms, and it responds to both psychological and pharmacological treatment. Benzodiazepines work quickly and are limited by tolerance, dependence and cognitive effects with sustained use.
Mechanistic rationale
A published Russian trial compared Selank with medazepam in patients with GAD and neurasthenia and reported comparable anxiolytic effect, with Selank additionally showing antiasthenic and mildly activating effects the benzodiazepine did not. An active-comparator design is a harder test than placebo, which makes this a more interesting result than most in this library. It is also one small study, in one country, unreplicated.
Community reports
The most consistently positive category of reporting for this compound. Users describe reduced anxiety without sedation or cognitive dulling, which matches the trial description and is also exactly what someone expecting a non-sedating anxiolytic would report.
Components carrying the argument: Tuftsin analogue — GABAergic and monoaminergic modulation
Pathophysiology
Benzodiazepines are used for far more than generalised anxiety: acute panic, status epilepticus, seizure prophylaxis, alcohol withdrawal, procedural sedation, muscle spasm.
Mechanistic rationale
The trial compared the two agents in GAD and neurasthenia only. It did not establish equivalence for acute panic, for seizure control, for alcohol withdrawal, or for any other benzodiazepine indication. "Works like a benzodiazepine without the dependence" compresses a narrow finding into a broad claim, and the compression is where the danger lives.
Community reports
The claim circulates in the broad form almost universally. Very few people repeating it have read what the trial compared.
Components carrying the argument: A scope limitation, not a mechanism
Pathophysiology
Alcohol withdrawal can produce seizures and delirium tremens, and delirium tremens carries a meaningful mortality even when treated. Benzodiazepine withdrawal can likewise produce seizures. In both, benzodiazepines are the treatment because they are cross-tolerant with the GABAergic system that is in acute deficit.
Mechanistic rationale
Selank has no anticonvulsant evidence and is not cross-tolerant with anything. Substituting it for a benzodiazepine during withdrawal removes seizure protection from someone who needs it. This is the one place in this library where an unproven compound replacing a proven one could plausibly kill a person within days rather than costing them time. Withdrawal from alcohol or benzodiazepines is a medically supervised process, and dose tapering is not something to improvise.
Community reports
Selank is discussed in community spaces as a way to come off benzodiazepines. That discussion is the reason this entry exists and is written this bluntly.
Components carrying the argument: Absence of anticonvulsant and cross-tolerant activity
Pathophysiology
Asthenia — persistent fatigue and reduced capacity for effort — overlaps heavily with depression and with anxiety disorders, and it is poorly served by sedating anxiolytics.
Mechanistic rationale
The reported antiasthenic and mildly activating profile is the genuinely distinctive claim for this compound, because it is the opposite of what a benzodiazepine does. If it holds, the population it would suit is people whose anxiety comes with fatigue rather than agitation. Selank has effects on serotonergic and BDNF signalling in preclinical work, which supports the direction without establishing it.
Community reports
Users frequently describe it as clarifying rather than blunting — consistent with the trial description of the profile.
Components carrying the argument: Serotonergic and BDNF effects
Pathophysiology
Anxiety is a common driver of sleep-onset insomnia, and treating the anxiety often improves the sleep without acting on sleep directly.
Mechanistic rationale
Any improvement here is most plausibly downstream of reduced anxiety rather than a hypnotic effect — which is a meaningful difference, because a non-sedating anxiolytic will not help sleep maintenance or a circadian problem.
Community reports
Improved sleep onset is commonly reported; sleep maintenance much less so, which fits the reading above.
Components carrying the argument: Anxiolysis, not sedation
Pathophysiology
Selank is a synthetic analogue of tuftsin, an endogenous immunomodulatory tetrapeptide derived from immunoglobulin G that stimulates phagocytosis.
Mechanistic rationale
The parent molecule is an immune peptide, and Selank has reported effects on interleukin expression in preclinical work. Shifting immune signalling in an unspecified direction is not obviously desirable, particularly in anyone with an autoimmune condition, and it is not something anyone using this compound for anxiety is monitoring.
Community reports
Almost never raised. Included because the immunological ancestry of the molecule is a real fact about it and is routinely omitted.
Components carrying the argument: Tuftsin-derived immunomodulation
| Question | Position |
|---|---|
| Approved anywhere? | Russia only; no Western approval or trial |
| The key trial | vs medazepam in GAD and neurasthenia, ~60 patients |
| What it showed | Comparable anxiolysis, plus antiasthenic and activating effects |
| What it did not show | Equivalence for panic, seizures, withdrawal or sedation |
| Alcohol / benzo withdrawal | Do not substitute — no anticonvulsant activity |
| Sleep | Onset, via anxiolysis — not a hypnotic |
| Origin | Tuftsin analogue — an immune peptide |
For anxiety disorders: cognitive behavioural therapy has the strongest evidence of any intervention and its benefit persists after treatment ends, which medication’s does not. SSRIs and SNRIs are first-line pharmacotherapy. Exercise has a real effect size. Benzodiazepines work quickly and are appropriate short-term, with the dependence risk being the reason for the time limit rather than a reason to avoid them entirely.
For alcohol or benzodiazepine withdrawal: this is a medical process. Benzodiazepine tapering or substitution under supervision, thiamine to prevent Wernicke encephalopathy, and inpatient management where the withdrawal is severe or there is a seizure history. Naltrexone and acamprosate for relapse prevention afterwards.
For insomnia: cognitive behavioural therapy for insomnia is first-line and outperforms hypnotics at follow-up. Screening for obstructive sleep apnoea and restless legs matters — both are common, both are missed, both are treatable.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Supplied lyophilised, commonly 5 or 10 mg per vial, or as a pre-made intranasal spray. Transfer to a nasal spray bottle for intranasal use introduces sterility and dose-accuracy considerations.
Lyophilised: refrigerated or frozen. Reconstituted: 2–8 °C.
Commonly 5 mg and 10 mg lyophilised vials; 0.15% intranasal solution in registered form.
The Pro-Gly-Pro tail confers resistance to enzymatic degradation, as with Semax.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Registered medicine in the Russian Federation as an anxiolytic for generalised anxiety disorder and neurasthenia. Not approved by the FDA, EMA or MHRA.
Western supply is research-chemical grade. The amidated analogue (N-Acetyl Selank Amidate) has no registration anywhere.
Regulatory and trial claims re-checked against primary sources on 20 August 2026. Checked: the medazepam comparison trial in GAD; the intranasal versus intraperitoneal receptor-binding comparison and the absence of any human injection study. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
Athletes subject to WADA, USADA, UKAD, NCAA or military testing should assume any peptide is prohibited unless they have verified otherwise against the current WADA Prohibited List. Several classes here (growth-hormone secretagogues, TB-4 analogues, metabolic modulators) are explicitly named. Check the current list — it is republished annually.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
