Selank

Selank is a synthetic seven-amino-acid chain (Thr-Lys-Pro-Arg-Pro-Gly-Pro, or TKPRPGP) built from tuftsin, a natural immune peptide, with a Pro-Gly-Pro tail added to make it resist breakdown ¹. It is best understood as a peptide anxiolytic with a secondary nootropic component and stress-protective activity ⁵.

It was discovered at Moscow State University in the regulatory-peptide program led by I.P. Ashmarin, the same program that produced Semax ¹. Selank is registered in Russia as a prescription anxiolytic nasal-drop product, while in the US and EU it circulates as an unregulated research peptide and has turned up in seized preparations ²⁵.

What the research supports, by strength of evidence:

Studied use	Evidence	Confidence
Generalized anxiety and anxiety-spectrum disorders	Comparative human RCTs 5	Moderate–high
Neurasthenia, asthenia, post-stress fatigue	Human trials 6	Moderate
Post-COVID brain fog and fatigue	Single 64-patient trial 8	Moderate, single study
Adjustment disorder	30-patient trial 9	Low–moderate
Cognitive and memory enhancement	Human fMRI 10; animal studies 17	Low–moderate
Alcohol or opioid withdrawal support	Animal models 15	Low

Most human evidence comes from one Russian research network, with total published enrollment under about 300 people across indications, and much of it is published only in Russian ⁵. Preclinical support is broader and unusually consistent on the core claims: anxiolysis without sedation, lowered stress hormones, and engagement of the body's natural opioid-like enkephalin system ¹⁸.

Selank calms overactive stress signaling through two converging systems: GABA, the brain's main inhibitory brake, and enkephalins, the body's natural opioid-like peptides ¹².

GABA-A positive allosteric modulation. GABA is the neurotransmitter that quiets excited nerve circuits, and benzodiazepines like diazepam work by boosting it at their own binding site. Selank also boosts GABA binding, but as a positive allosteric modulator at a different, partially overlapping site, and it alters rather than adds to diazepam's effect ¹². In rat brain slices, Selank strengthens inhibitory currents in neurons of the hippocampus, a memory center ²⁸, and in living mice it changed the expression of 45 GABA-related genes within an hour ²⁷.

Enkephalinase inhibition. Enkephalins are the body's built-in stress-dampening opioid peptides, and enzymes called enkephalinases clear them quickly. Selank inhibits those enzymes with an IC50 of roughly 15–20 µM, more potently than the classic inhibitors bacitracin and puromycin, which lengthens the half-life of leu-enkephalin in blood ¹³. This is considered the core anxiolytic mechanism: patients with generalized anxiety disorder show an abnormally short enkephalin half-life that normalizes with treatment ²⁹, and mice whose enkephalinase activity does not respond to Selank show no behavioral response ³⁰. The opioid blocker naloxone cancels Selank's effects in animal models, confirming the enkephalin system is a required part of the response, even though Selank does not itself bind opioid receptors ³³.

Supporting levers. Route changes the receptor signature: in mice, intraperitoneal dosing raised cortical GABA-A binding by 38%, while intranasal dosing raised hippocampal NMDA receptor binding by 23%, matching the more anxiolytic versus more nootropic profiles of each route ²⁴. Selank also normalizes stress-elevated corticosterone ¹⁸, regulates BDNF, a protein that supports neuron growth and memory, in the hippocampus ³⁷, tunes inflammation-related genes ³⁸, and its antiviral activity against influenza appears to work through interferon-alpha, an antiviral immune signal ²³.

Effects start fast: resting-state brain connectivity changed within 5–20 minutes of a single injection in healthy volunteers ¹⁰, and the anxiolytic benefit outlasted the last dose by about a week in the phenazepam-comparator trial ⁵.

Anxiolysis without sedation. Across two comparative trials, Selank matched the benzodiazepines phenazepam and medazepam for anxiety relief in generalized anxiety disorder and neurasthenia while avoiding sedation, muscle relaxation, and cognitive dulling ⁵. The effect lasted about one week after the final dose, with no rebound or withdrawal symptoms reported ⁵.

Fatigue and post-stress recovery. In anxiety trials, Selank added antiasthenic (anti-fatigue) and mildly psychostimulant effects that the benzodiazepine comparator lacked ⁶. In a 64-patient post-COVID trial, 30 days of intranasal Selank improved asthenia, mental performance, anxiety, and depressive symptoms against a neuroprotective complex alone ⁸. A 30-patient adjustment-disorder trial found meaningful symptom-score reductions after a 2-week course ⁹.

Benzodiazepine support. Added to phenazepam, Selank sped up the therapeutic response and reduced sedation, attention and memory problems, sleep prolongation, emotional indifference, and sexual dysfunction, both during treatment and after tranquilizer withdrawal ⁷.

Cognitive effects. In healthy volunteers, a single injection changed resting-state connectivity between the right amygdala and temporal cortex within 5–20 minutes ¹⁰. In rats, Selank stabilized memory traces for up to 30 days after a single consolidation-phase dose ³⁶ and normalized ethanol-induced BDNF disruption in the hippocampus and prefrontal cortex ¹⁷.

Stress protection. In 28-day restraint-stress rats, dosing before the stressor reduced serum corticosterone, with 750 mcg/kg producing anxiolysis and 250 mcg/kg an antidepressant-like effect ¹⁸. Selank also reversed stress-induced gut dysbiosis ¹⁹ and reduced ulcer area across three gastric-ulceration models ²⁰.

Withdrawal support. A single 0.3 mg/kg dose cut naloxone-precipitated morphine withdrawal severity by 39.6% in rats ¹⁵, and in alcohol-dependent rats the same dose eliminated withdrawal anxiety without changing alcohol consumption ¹⁶.

Immune and antiviral activity. As an add-on in 124 atopic dermatitis patients, Selank enhanced the anti-inflammatory effect of standard therapy and UV phototherapy, lowering IL-1β, IL-4, IL-10, IL-13, and IgE ¹¹. Preventive dosing suppressed influenza A replication in cell culture and mice via interferon-alpha induction ²³.

Nearly all published human Selank data use the intranasal route, typically as a 0.15% drop solution ⁸. Trial and community patterns differ mainly in dose and cycle length.

• Registered clinical regimen: 2–3 drops four times daily, about 0.6–1.0 mg total per day, for 14-day courses in anxiety trials ⁵ and 30 days in the post-COVID asthenia trial ⁸.
• Community intranasal protocol: 100–300 mcg per application, 1–2 times daily, usually in 2–4-week cycles (community protocol).
• Community subcutaneous protocol: weight-tiered daily dosing: 150–250 mcg below 59 kg, 200–350 mcg for 59–82 kg, and 300–500 mcg for 82–109 kg, often split morning and evening. No published subcutaneous human trials exist (community protocol).
• Pre-event anxiolysis: community protocols use 100–300 mcg intranasally about 15 minutes before an anticipated stressor, timing modeled on the animal literature, where Selank is given 15 minutes before stress exposure ¹⁸.

Route differences

Route shapes the effect profile in animals: intraperitoneal dosing raised cortical GABA-A binding by 38%, while intranasal dosing raised hippocampal NMDA binding by 23%, with the intranasal profile skewing more nootropic and the systemic profile more anxiolytic ²⁴. Human trials used intranasal administration exclusively ⁸, so intranasal is the route with direct human evidence; subcutaneous use is a community extrapolation from animal parenteral data.

Timing and cycling

The clinical asthenia regimen doses four times daily ⁸, and community protocols often split the daily dose: morning for focus and evening for anxiety, since Selank is mildly activating rather than sedating ⁶. The nootropic effect in animals is strongest when dosed during the memory-consolidation window after learning ³⁶, which researchers extrapolate to dosing shortly after study or practice rather than only beforehand.

Published courses run 2 weeks ⁹, 14 days ⁶, or 30 days ⁸, and the anxiolytic effect persisted about a week past the final dose ⁵, so intermittent scheduling retains coverage. Community protocols typically run 2–4 weeks on with 1–2 weeks off. Repeated animal dosing over 14–28 days stayed effective without tolerance, and no dependence or withdrawal syndrome appears in either the clinical or animal literature ⁵.

Selank is supplied lyophilized, meaning freeze-dried into powder; market surveillance has identified it both as powder for injection and as ready-made nasal sprays ²⁶. Bacteriostatic water is the standard diluent for research preparations, and sterile saline is acceptable for nasal use (community practice). Add the diluent slowly down the vial wall and swirl gently to dissolve, rather than shaking.

The peptide itself tolerates routine handling: the C-terminal Pro-Gly-Pro tail is what gives glyproline-family peptides their resistance to breakdown, and the family's stability is described as comparable to mainstream pharmaceutical preparations ⁴². Once in solution, the peptide is gradually metabolized into the fragments TKPRP, TKP, RP, and GP, with intact Selank still measurable in brain tissue after intranasal administration ⁴¹.

Storage follows standard lyophilized-peptide practice (community protocol):

• Unreconstituted vials keep best frozen at −20°C for long-term storage, or refrigerated at 2–8°C for up to several months if protected from light and moisture.
• A reconstituted vial prepared with bacteriostatic water is stored refrigerated at 2–8°C and used within roughly 14–30 days.
• Freezing reconstituted solutions is avoided; discard any solution that turns turbid, contains particles, or discolors.

The interactive calculator below handles the dilution arithmetic: enter the vial size, diluent volume, and target dose to see the corresponding measured volume. One sourcing note: Selank sold outside regulatory channels carries no identity verification by any regulator, and control laboratories have confirmed open availability of unapproved preparations, so third-party testing is standard practice for research use ²⁶.

Human interaction data are limited to small Russian trials; animal work fills in the mechanistic gaps ⁵.

• Benzodiazepines: the best-documented interaction. In mice, Selank enhanced diazepam's and mezapam's anxiolysis while blocking their sedative and motor-suppressant effects ¹⁴, and under chronic stress the diazepam + Selank combination restored anxiety measures to baseline better than either drug alone ⁴⁴. In a human add-on trial, Selank plus phenazepam produced a faster response and fewer benzodiazepine side effects, with benefits continuing after tranquilizer withdrawal ⁷.
• Opioids: Selank inhibits the enzymes that degrade enkephalins, so it engages opioid-system machinery ¹³. It potentiated morphine analgesia in rodents, raising the maximum possible effect from 9% to 29.9%, without producing analgesia on its own ³¹, and a single dose reduced morphine-withdrawal severity by 39.6% ¹⁵. Conversely, the opioid blockers naloxone and naltrexone blunt Selank's anxiolysis ³³.
• Alcohol: in mice, Selank blocked ethanol-induced hyperlocomotion and behavioral sensitization, eliminated withdrawal anxiety in alcohol-dependent rats, and prevented ethanol-induced memory impairment and BDNF disruption, all without changing how much alcohol the animals consumed ¹⁶.
• Antipsychotics and dopaminergics: Selank suppressed apomorphine-induced activation comparably to olanzapine, without binding dopamine D2 receptors directly, and naloxone reversed the effect ³⁴. In a Parkinsonism model, it reduced anxiety without worsening motor behavior ⁵⁴.
• SSRIs: one clinical report describes Selank potentiating SSRI antidepressants in anxiety and depressive disorders, though the evidence is limited ⁵³.
• Blood thinners: in thromboelastography, a lab assay of how blood clots, Selank shifted clotting parameters toward reduced clotting, the strongest such effect among the glyprolines tested ²¹. No human bleeding data exist, but this argues against combining with anticoagulants or antiplatelets and for caution around surgery ²¹.
• Hepatotoxic drug regimens: in rats, Selank added to isoniazid plus rifampicin restored liver biochemistry and histology, outperforming the reference hepatoprotectors Essentiale and Mexidol ⁵².

Selank is most often researched alone. Its best-documented combination is a benzodiazepine adjunct rather than a peptide stack ⁷, but community stacking practice exists and rests on mechanistic reasoning rather than trials (community protocol).

• Selank plus diazepam or phenazepam is the combination with the most evidence: anxiolysis is enhanced and the benzodiazepine's sedative and memory side effects are reduced, in rodents and in a human add-on trial ⁷. This supports Selank's role as a benzodiazepine-sparing adjunct.
• Semax is Selank's sibling in the Ashmarin program ¹, and both inhibit enkephalin-degrading enzymes ²⁹. Community practice is to alternate them rather than stack, since they share the enkephalinase pathway.
• Noopept and Semax converge with Selank on the NMDA glycine site after intranasal dosing, so practitioners generally run one neuroactive peptide at a time ³⁵.
• BPC-157, TB-500, and GHK-Cu act on tissue-repair and blood-vessel-growth axes with no documented conflicts, which is why they appear in combination protocols with Selank for stress-plus-repair goals (community protocol).
• Growth-hormone secretagogues such as ipamorelin and CJC-1295 share no identified pathway with Selank, and no interaction is expected (practitioner consensus).
• GABAergic botanicals such as valerian, passionflower, or phenibut carry a theoretical central-nervous-system depressant load when combined with any GABA-acting agent, although Selank itself counters rather than potentiates sedation in rodents ¹⁴.

Russia

Selank is registered in the Russian Federation as a prescription peptide anxiolytic delivered as nasal drops ¹⁴. Phase II clinical results were reported by 2005 ³, and by 2008 the molecule was described as having completed Phase III testing toward registration as a selective anxiolytic ⁴.

United States

Selank has no FDA approval for any indication and no completed Western registration trials ²⁵. A 2021 US clinical pharmacology review classifies it as a poorly studied Russian drug that is, in the review's words, inexplicably sold to US consumers as a dietary supplement, and it flags the unevaluated abuse potential of a GABA-acting agent on the open market ²⁵. Synthetic peptides do not meet the statutory definition of a dietary ingredient, so US supplement marketing is legally questionable, though no FDA warning letter naming Selank is documented in the literature (practitioner consensus). Selank is not scheduled under the US Controlled Substances Act (practitioner consensus).

Europe and elsewhere

No EMA marketing authorization exists, and the UK (MHRA) and Australia (TGA) grant no national authorization, with personal importation sitting outside recognized regulatory pathways (practitioner consensus). Belgian official medicines-control laboratories seized preparations containing Selank and Semax in 2017–2018 and built LC-MS/MS screening methods specifically for such gray-market cognitive-enhancing peptides, evidence of active EU enforcement interest ²⁶.

Sport

The available literature documents no WADA determination and no athlete sanction involving Selank (practitioner consensus). WADA's S0 category covers substances lacking governmental therapeutic approval in any jurisdiction; because Selank is a registered medicine in Russia, it falls outside a strict S0 reading, but that does not bind future List revisions, and athletes subject to testing should re-verify the annual list (practitioner consensus).

Across every published human series, Selank's adverse-event record is sparse. In comparative trials versus phenazepam and medazepam, it matched benzodiazepine anxiolysis while producing no sedation, muscle relaxation, or memory impairment; instead a mild activating and antiasthenic effect appeared ⁵. The 124-patient atopic dermatitis series, the 64-patient post-COVID trial, the 30-patient adjustment-disorder trial, and the 52-volunteer fMRI study all reported no adverse events ⁸.

Community users report transient and mild effects: fatigue or sleepiness in the first one to two days, mild headache, lightheadedness after injection, nasal stinging or postnasal drip with intranasal use, and vivid dreams when dosed in the evening (community protocol).

Blood thinning. In a thromboelastography assay, Selank shifted clotting toward reduced clotting more strongly than other glyprolines ²¹, and glyprolines as a class inhibit primary and plasma hemostasis ⁵⁰. No human bleeding event appears in any trial, but this grounds caution for bleeding disorders, anticoagulant or antiplatelet use, and the period around surgery ²¹.

Blood pressure. In anesthetized cats, a massive IV bolus caused a transient 32% drop in arterial pressure for 1–3 minutes while raising cerebral blood flow 24% ⁵¹. Human trials report no blood-pressure events; brief lightheadedness after the first injections is plausible and usually transient (practitioner consensus).

Abuse potential is formally unstudied. The 2021 US review argues that a GABA-acting compound sold as a supplement should undergo abuse-liability testing before open consumer access ²⁵. Against this, Russian trials report no dependence, withdrawal, or rebound anxiety, and the anxiolytic effect fades over about a week after the last dose without a taper ⁵.

Pregnancy and lactation have no human data. A stem-cell assay showed no general toxicity, but high concentrations reduced the proportion of GABA-producing neurons that developed in vitro, so developmental effects are not ruled out ²².

Immune shifts. Selank is not immunologically inert: it lowered IL-1β, IL-4, IL-10, IL-13, and IgE in the dermatitis cohort ¹¹, and it suppresses influenza replication via interferon-alpha induction ²³. That is therapeutic in context but argues for caution with immunosuppressants or checkpoint inhibitors until studied.

The largest open questions: no safety data beyond 30 days, the longest published course ⁸; no human drug-interaction trials ²⁵; and no in-vivo human coagulation studies ²¹.