Overview

Selank is a synthetic peptide that calms anxiety without the sedation, cognitive dulling, or dependence that follow most pharmaceutical anxiolytics. When anxious sensations arise—whether triggered by external stressors or generated internally—Selank provides a braking signal that prevents those signals from building into a full anxious pattern.

The effect is quiet. There is no drowsiness, no slowed thinking, no impaired coordination. What changes is the threshold for escalation: triggers that once locked into rising tension now pass more easily. The brain becomes less reactive while remaining fully awake, so social interaction, work, and training remain intact instead of being dulled.

Selank achieves this by strengthening the brain's own inhibitory signalling—the system that keeps neural activity from running away into anxiety or overexcitation. Most drugs that target this system force it open, which produces calming but also sedation, memory problems, and dependence.

Selank instead supports the genes and receptors that maintain inhibitory tone, so the system works better without being overpowered. The relevant chemistry involves the brain's primary calming neurotransmitter—GABA—and the receptors that respond to it, but Selank modulates these indirectly rather than binding directly to them.

Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, Selank has been used clinically in Russia and Eastern Europe for generalized anxiety, stress-related disorders, and cognitive fatigue. In addition, recent clinical studies have shown efficacy in treating post-COVID cognitive symptoms and playing a supportive role to SSRIs in treatment resistive depression.

How Anxiety Drugs Differ

The brain's inhibitory system has two main braking mechanisms:

Fast braking quiets overactive neurons immediately. When pushed too far—as with benzodiazepines—this same pathway produces sedation, slowed thinking, impaired coordination, and memory disruption.
Slow braking sustains inhibition over time and prevents anxiety from re-escalating. Excessive activation—as with barbiturates—leads to lethargy, low motivation, and a heavy, low-arousal state.

Drug Class	How it works	Clinical result
Benzodiazepines (Xanax, Valium)	Forces fast braking channels to open more frequently	Strong calming; sedation; memory impairment; dependence
Barbiturates (Phenobarbital)	Holds fast braking channels open longer; can open them without the brain's own signal	Deep sedation; anesthesia; respiratory depression
Z-drugs (Ambien, Lunesta)	Targets only the sleep-specific fast braking receptors	Sleep initiation; less anxiety relief
Alcohol	Activates both braking systems indiscriminately	Calming that degrades into loss of motor control
Selank	Supports the genes and receptors that maintain inhibitory tone; does not force channels open	Calming without sedation; preserved clarity; no dependence

The technical names for these braking systems—GABA_A (fast) and GABA_B (slow)—matter less than understanding that Selank strengthens the underlying capacity rather than forcing the switches.

Mechanistic Architecture

Anxiety becomes less reactive when the brain maintains enough inhibitory signalling to catch anxious cues before they spiral. Selank shifts the system toward that posture. The brain responds to stress with fewer amplifications; sensations that once cascaded into a full anxious pattern now flatten earlier in the process.

The change is quiet but consistent: the threshold for escalation rises.

This occurs because Selank supports the underlying biology that keeps inhibitory tone stable. The genes responsible for producing the brain's calming signals and maintaining the receptors that receive them become more active, so the inhibitory system does not drop away during stress.

That stability improves how fast braking works, allowing the brain to interrupt anxious firing before it gains momentum—without pushing into sedation. The slow braking pathway, which governs muscle relaxation and deep sedation, remains mostly unchanged. This is why Selank does not produce the lethargic heaviness associated with alcohol or barbiturates.

The net effect is a system with more room to absorb internal fluctuations. Thoughts, sensations, and external triggers meet a brain that is less primed to over-interpret them. Selank does not replace the body's inhibitory signal; it reinforces the conditions in which that signal functions as intended.

System Behaviour

Once inhibitory tone is steadier, the brain's response to stress changes. Triggers that once produced rising physical activation—tightness in the chest, impulsive worrying, sudden shifts in attention—no longer lock into place. They pass more easily because the circuits that normally accelerate them are under better control. This makes anxiety feel less sticky, not because the system is sedated, but because its internal braking capacity is intact.

Cognitive function remains accessible in this posture. The pathways that regulate focus, working memory, and executive control do not fall under the broad suppression that accompanies benzodiazepines. Selank does not impose a low-arousal state; it reduces noise. The mind feels clearer because the background reactivity is lower, not because core networks are dampened.

Over time, this pattern presents as a quieter baseline. The system still reacts to meaningful stressors but with less overshoot. Fatigue, withdrawal, and rebound anxiety do not appear because Selank does not push the braking system beyond its natural range—it supports the stability of the range itself.

Discovery and Clinical Use

Selank was developed as part of a broader effort to create anti-anxiety agents that work through regulatory peptides rather than by forcing receptors open. Its early evaluation focused on patients who showed both heightened stress reactivity and reduced cognitive endurance—a pattern sometimes called anxiety-asthenic states.

Clinical studies in these patients demonstrated reductions in anxiety scores comparable to benzodiazepines but without sedation, cognitive impairment, or withdrawal. These observations led to its incorporation into psychiatric and neurologic practice in Russia and parts of Eastern Europe, where it has been used for generalized anxiety, stress-related disorders, and cognitive fatigue.

The human trials conducted to date have been modest in scale—typically dozens of participants—but directionally consistent. Patients reported reductions in worry, physical tension, and internal unease, while maintaining or improving concentration and clarity. Follow-up observations noted an absence of dependence or rebound anxiety after discontinuation.

Selank's status in these regions reflects its clinical posture: it is treated as a regulatory peptide that stabilises inhibitory tone rather than as a sedative or controlled substance.

Dosing

Selank behaves as a stabiliser rather than a sedative. The onset is subtle: anxious reactivity softens, but alertness is preserved, and no shift in motor coordination or cognition follows.

Dose: 250–500 mcg
Frequency: 1–3 times per day
Timing: Daytime use does not interfere with clarity; evening use does not override natural sleep transitions
Cycle: 1–2 week breaks are recommended between courses

Because Selank does not induce dependence or withdrawal, dosing is flexible. The system drifts back to baseline smoothly when exposure ends, reflecting that the peptide reinforces the brain's own signalling rather than substituting for it.

Intranasal dosing is standard and aligns with how peptides reach the brain efficiently. The effects accumulate across repeated exposures as the genes Selank influences become more active.

N-Acetyl Selank Amidate

This modified version lasts longer in the body, allowing lower total daily dosing for comparable effects.

Functionally, it produces a profile similar to Selank but with a more sustained curve: the early calming develops gradually, and the effect holds longer between doses.

Users commonly describe the difference not as stronger intensity but as longer persistence of the same regulatory tone.

Relative potency: Higher effective dose per microgram due to increased stability
Kinetics: Less frequent dosing may produce comparable baseline effects
Subjective profile: The alert-calm balance remains; no sedative qualities; slightly smoother transitions between focus, social engagement, and rest

The system tends to return to baseline without notable rebound, reflecting the peptide's role as a support for the brain's own calming systems rather than a direct push on reward or arousal circuits.

Emerging Clinical Data

Beyond generalized anxiety, Russian clinical work has explored Selank in several adjacent conditions where stress reactivity and emotional regulation intersect.

Post-Viral Cognitive Fatigue

A 2024 randomized trial examined Selank in patients with post-COVID syndrome presenting with fatigue, reduced mental work capacity, and emotional disturbance. Sixty-four patients received either a standard neuroprotective regimen alone or the same regimen plus intranasal Selank (1.5 mg daily for 30 days). The Selank group showed superior recovery of mental work capacity, greater reduction in anxiety and depressive symptoms, and better resolution of fatigue than controls.

This represents the first controlled data on Selank in post-viral cognitive sequelae—a condition that emerged after most of the original Russian research was complete.

SSRI Augmentation

Approximately 40% of patients starting antidepressant therapy for anxiety-depressive disorders experience delayed response or residual symptoms. Clinical work has evaluated Selank as a bridge during the first two weeks of treatment, when the primary agent has not yet reached full efficacy. By day 14, 70% of patients receiving Selank showed meaningful anxiety reduction, with improvements in generalized anxiety, apathy, unmotivated fatigue, and irritability.

These effects persisted to day 28—two weeks after Selank was discontinued—suggesting that the peptide may accelerate stabilisation during the vulnerable early phase of antidepressant treatment.

Stress-Driven Eating

In patients whose overeating is driven by stress and emotional dysregulation, a 14-day Selank course reduced binge frequency, accelerated satiety onset, and lowered consumption of high-calorie foods, carbohydrates, and alcohol. Anxiety and depressive symptoms improved in parallel, and the effects persisted for at least two weeks after discontinuation. The pattern suggests that Selank may interrupt the stress-eating loop at the emotional level rather than through appetite suppression.

Elderly Vascular Cognitive Impairment

A pilot study in patients over 50 whose cognitive symptoms stemmed from reduced blood flow to the brain found that 14 days of Selank improved attention, short-term visual memory, and reaction time while reducing anxiety and fatigue. Sample size was small (15 patients), but the profile aligns with Selank's broader pattern of cognitive-emotional stabilisation without sedation.

Stress-Sensitive Skin Conditions

Atopic dermatitis flares are tightly linked to stress and hormonal shifts. In a controlled study of 65 adults with atopic dermatitis, those receiving Selank alongside standard skin therapy showed substantially greater reductions in anxiety (approximately 2.4-fold vs 1.3-fold with skin therapy alone). They also showed improvements in emotional awareness and a near-doubling of the brain's own stress-buffering peptides (β-endorphin). Quality-of-life improvements were correspondingly larger.

The data suggest that Selank may stabilise the connection between the nervous and immune systems in stress-sensitive skin conditions, improving emotional state beyond what topical and systemic dermatologic therapy achieves alone.

Emerging Questions

Selank's overall pattern is coherent: reduced reactivity, preserved cognition, absence of sedation, no withdrawal. The mechanistic explanation—strengthened inhibitory tone without forcing receptors open—fits the behavioural profile observed across clinical and practical use. What remains to be clarified is scale. Most published data come from Russian trials and mechanistic studies; large, Western, placebo-controlled trials have not yet been run.

The open questions are about precision rather than direction. How much does Selank shift the threshold for anxiety escalation in chronically anxious individuals? How durable are the gene-level changes after discontinuation? Does its effect on inhibitory tone generalise to populations with trauma-linked hypervigilance or with mood disorders? These questions define the boundary of current knowledge, but they do not conflict with the mechanistic or behavioural pattern already observed.

Selank fits a class of interventions that lower anxiety not by suppression, but by restoring the inhibitory capacity that should already be present. The result is a system that reacts less, stabilises more quickly, and remains fully awake while doing so.

References

Seredenin SB, Kozlovskaya MM, et al. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia. Neurosci Behav Physiol 2008. https://pubmed.ncbi.nlm.nih.gov/18454096/
Zozulya AA, Gabaeva MV, et al. Selank administration affects expression of genes involved in GABAergic neurotransmission. Acta Naturae 2016. https://pmc.ncbi.nlm.nih.gov/articles/PMC4757669/
Seredenin SB, Kozlovskaya MM, et al. Molecular aspects of Selank biological activity: evidence for positive allosteric modulation of GABA receptors. CNS Neurol Disord Drug Targets 2018. https://pubmed.ncbi.nlm.nih.gov/30255741/
Medvedev VE, Tereshchenko ON, et al. Comparison of anxiolytic effect and tolerability of Selank and phenazepam in GAD. Zh Nevrol Psikhiatr Im S S Korsakova 2014. https://pubmed.ncbi.nlm.nih.gov/25176261/
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Uchakina ON, Uchakin PN, et al. Immunomodulatory effects of Selank in patients with anxiety-asthenic disorders. Zh Nevrol Psikhiatr Im S S Korsakova 2008. https://pubmed.ncbi.nlm.nih.gov/18577961/
Pogodina MG, Nikiforova EYu. Selank in the treatment of asthenic disturbances in post-COVID syndrome. Vrach 2024. DOI: 10.29296/25877305-2024-05-12
Verbenko VA, Fedorov VN. Use of the new peptide anxiolytic Selank in the therapy of psychogenic overeating. Vrach 2012.
Verbenko VA, Shakina TA. SSRI augmentation with Selank in anxiety-depressive disorders. 2019.
Syunyakov T, et al. Clinical pharmacological study of the peptide anxiolytic Selank in elderly patients with organic asthenic disorder. 2016.