Selank vs Benzodiazepines: Anxiolytic Peptide Research Comparison

Introduction: The Search for Non-Addictive Anxiolytics

Benzodiazepines have dominated anxiety pharmacotherapy for over six decades. From chlordiazepoxide’s 1960 introduction to the modern formulary of alprazolam, lorazepam, and diazepam, these GABA-A receptor positive allosteric modulators remain among the most widely prescribed psychoactive substances globally. Their efficacy is unquestioned — rapid, reliable anxiolysis within minutes of administration.

But that efficacy comes at a well-documented cost. Physical dependence can develop within weeks. Tolerance necessitates dose escalation. Cognitive impairment, anterograde amnesia, psychomotor slowing, and paradoxical disinhibition represent clinically significant adverse effects. And benzodiazepine withdrawal syndrome — potentially life-threatening in severe cases — has driven decades of research seeking alternatives that can modulate GABAergic signaling without these liabilities.

Selank (TP-7) represents one of the most scientifically compelling candidates to emerge from this search. Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences over two decades of systematic research, this synthetic heptapeptide offers anxiolytic effects through a mechanism that touches — but does not overwhelm — the GABAergic system, while simultaneously engaging neurotrophic, serotonergic, dopaminergic, and immunomodulatory pathways. This comprehensive comparison examines the science behind both approaches and explores why researchers increasingly view Selank as representing a fundamentally different paradigm in anxiolytic research.

What Is Selank? Origin and Development

Selank (sequence: Thr-Lys-Pro-Arg-Pro-Gly-Pro) is a synthetic analog of tuftsin, an endogenous immunomodulatory tetrapeptide (Thr-Lys-Pro-Arg) naturally produced by enzymatic cleavage of the Fc region of immunoglobulin G in the spleen. Tuftsin was first characterized by Victor Najjar in the 1970s as a natural activator of monocytes, macrophages, and neutrophils.

The development of Selank began in the 1990s under the direction of Dr. Nikolai Myasoedov at the Institute of Molecular Genetics. The research team extended tuftsin’s tetrapeptide sequence by adding the tripeptide Pro-Gly-Pro to the C-terminus. This modification served two critical purposes:

1. Metabolic stability: The Pro-Gly-Pro extension dramatically increases resistance to aminopeptidases and other serum proteases, extending the peptide’s biological half-life from minutes (for native tuftsin) to a more pharmacologically useful duration
2. CNS activity: The extended sequence enables passage across the blood-brain barrier and confers nootropic and anxiolytic properties not observed with tuftsin alone

The Pro-Gly-Pro motif was not selected arbitrarily — it represents a conserved sequence found in type I collagen and several neuropeptides, and has been shown to possess independent biological activity related to anti-inflammatory signaling and neuronal protection.

How Benzodiazepines Work: GABA-A Receptor Modulation

To appreciate how Selank differs from benzodiazepines, it is essential to understand the mechanism it is being compared against. Benzodiazepines are positive allosteric modulators (PAMs) of the GABA-A receptor — a pentameric ligand-gated chloride ion channel that mediates the majority of fast inhibitory neurotransmission in the mammalian central nervous system.

The GABA-A receptor is composed of five subunits, typically arranged in a 2?-2?-1? configuration. Benzodiazepines bind at the interface between ? and ? subunits (the “benzodiazepine binding site”), distinct from where GABA itself binds (at the ?-? interface). This allosteric binding increases the receptor’s affinity for GABA, meaning that when GABA is present, the channel opens more frequently and for longer durations, increasing chloride ion influx and hyperpolarizing the neuron.

The downstream effects of enhanced GABAergic inhibition include:

• Anxiolysis: Reduced activity in limbic circuits (amygdala, hippocampus)
• Sedation: Decreased cortical arousal
• Muscle relaxation: Reduced motor neuron excitability
• Anticonvulsant effects: Raised seizure threshold
• Anterograde amnesia: Impaired hippocampal memory consolidation

The Subunit Specificity Problem

Classical benzodiazepines (diazepam, alprazolam, lorazepam) are non-selective — they enhance GABA-A receptor function at ?1, ?2, ?3, and ?5 subunit-containing receptors with relatively equal efficacy. Research has established that:

• ?1 subunit-containing receptors: Mediate sedation, amnesia, and much of the dependence liability
• ?2/?3 subunit-containing receptors: Mediate anxiolysis and muscle relaxation
• ?5 subunit-containing receptors: Involved in memory and cognitive processes

This non-selectivity means that benzodiazepine anxiolysis is inseparable from sedation, cognitive impairment, and dependence potential. The search for subunit-selective GABAergic compounds has been a major pharmaceutical research theme, but few have reached clinical use. This is precisely where Selank’s multi-target approach becomes relevant.

Selank’s Multi-Target Mechanism of Action

Unlike the focused, single-target mechanism of benzodiazepines, Selank exerts its effects through multiple parallel pathways. This polypharmacology is characteristic of regulatory peptides, which evolved to coordinate complex physiological responses rather than modulate a single receptor.

1. GABAergic Modulation (Indirect)

Selank influences GABAergic neurotransmission, but through mechanisms fundamentally different from benzodiazepines. Research by Seredenin and Kozlovskaya has demonstrated that Selank modulates GABA-A receptor sensitivity and alters the expression of genes encoding GABA-A receptor subunits, particularly in the hippocampus and cortex. Critically, Selank appears to preferentially affect GABAergic tone in brain regions associated with anxiety processing rather than producing global CNS depression (PMID: 24390039).

Microarray studies have shown that Selank treatment alters the expression of 45+ genes related to GABAergic signaling, including GABA-A receptor subunit genes (GABRA2, GABRA6, GABRB2), GABA transporters, and glutamic acid decarboxylase (GAD). The net effect appears to be a rebalancing of inhibitory signaling rather than the blanket enhancement produced by benzodiazepines.

2. Serotonergic System Modulation

Selank has been shown to influence serotonin (5-HT) metabolism in the brain. Research published in Bulletin of Experimental Biology and Medicine demonstrated that Selank administration altered serotonin turnover in the hypothalamus and cortex of rats, with the pattern of changes resembling those produced by chronic (not acute) SSRI treatment. This is significant because chronic SSRI effects (involving 5-HT1A autoreceptor desensitization) are associated with anxiolysis, while acute serotonergic effects can paradoxically increase anxiety (PMID: 18404381).

3. Dopaminergic System Effects

Selank modulates dopamine metabolism in mesocorticolimbic pathways. Studies have shown altered dopamine and its metabolite (DOPAC, HVA) levels in the striatum and hypothalamus following Selank administration. These effects may contribute to the compound’s reported cognitive-enhancing and motivation-related properties, as the dopaminergic system plays critical roles in working memory, attention, and reward processing.

4. Enkephalinase Inhibition

One of Selank’s most distinctive mechanisms is its ability to inhibit enkephalin-degrading enzymes (enkephalinases), thereby prolonging the activity of endogenous enkephalins — the body’s own opioid peptides. This mechanism provides an analgesic and anxiolytic component without directly activating opioid receptors, avoiding the dependence risk associated with direct opioid agonism.

5. BDNF and Neurotrophic Factor Expression

Selank upregulates brain-derived neurotrophic factor (BDNF) expression in the hippocampus and cortex. BDNF is the primary neurotrophin supporting neuronal survival, synaptic plasticity, and neurogenesis in the adult brain. BDNF deficiency has been consistently linked to anxiety disorders and depression, and increasing BDNF is considered a key mechanism of antidepressant efficacy.

6. Immune System Modulation

As a tuftsin analog, Selank retains immunomodulatory properties, influencing cytokine expression profiles and immune cell activity. This dual neuro-immune action is particularly relevant given the established bidirectional relationship between immune activation and anxiety/mood disorders.

GABAergic Effects: Selank vs. Benzodiazepines Head-to-Head

Anxiolytic Research: Preclinical and Clinical Evidence

Preclinical Studies

Selank has been evaluated in multiple validated anxiety models in rodents, consistently demonstrating anxiolytic-like effects:

Elevated Plus Maze (EPM): The gold-standard rodent anxiety test. Selank-treated animals showed increased time spent in and entries into the open arms of the maze, indicating reduced anxiety-like behavior. Importantly, total locomotor activity was not reduced, distinguishing the anxiolytic effect from sedation — a critical differentiator from benzodiazepines, which often produce apparent anxiolysis that is partially confounded by sedation (PMID: 18646133).

Light-Dark Box: Selank increased the time animals spent in the illuminated compartment and the number of transitions between compartments, consistent with reduced anxiety without sedation.

Vogel Conflict Test: This operant paradigm measures the suppression of punished behavior (drinking while receiving mild electric shocks). Selank increased punished responding, a classic anxiolytic profile shared with benzodiazepines. However, unlike benzodiazepines, Selank did not affect unpunished baseline responding, suggesting a cleaner anxiolytic signal without general behavioral disinhibition.

Stress-Induced Models: In restraint stress and social defeat paradigms, Selank normalized stress-elevated corticosterone levels and prevented stress-induced behavioral deficits. The compound appeared to enhance stress resilience rather than simply suppressing the stress response.

Clinical Evidence

Selank has been evaluated in clinical studies in Russia, where it received regulatory approval in 2009. The clinical evidence base includes:

Generalized Anxiety Disorder (GAD): A randomized controlled trial comparing Selank nasal spray (0.15% solution) to medazepam (a benzodiazepine) in patients with GAD found comparable anxiolytic efficacy as measured by the Hamilton Anxiety Rating Scale (HAM-A). Critically, the Selank group showed no sedation, no cognitive impairment, and no withdrawal effects upon discontinuation — in contrast to the medazepam group, which experienced typical benzodiazepine-class side effects (PMID: 18533106).

Anxiety with Neurasthenia: A study in patients with anxiety-asthenic disorders found that Selank improved both anxiety symptoms and cognitive performance (attention, memory) simultaneously — the opposite of the benzodiazepine pattern where anxiolysis comes at the cost of cognition.

EEG Studies: Clinical EEG recordings during Selank treatment showed increased alpha rhythm power and decreased theta activity in the frontal cortex — a pattern associated with calm alertness rather than sedation. Benzodiazepines, by contrast, typically increase beta activity and may increase theta/delta power, reflecting sedation.

Cognitive Effects: Where Selank Diverges Most Sharply From Benzodiazepines

Perhaps the most striking difference between Selank and benzodiazepines is their opposing effects on cognition. While benzodiazepines reliably impair memory formation (particularly anterograde declarative memory) and slow cognitive processing speed, Selank has demonstrated cognitive enhancement across multiple domains:

Memory Enhancement

In the passive avoidance paradigm (a standard test of learning and memory in rodents), Selank improved both acquisition and retention of avoidance behavior. In spatial memory tasks (Morris water maze), Selank-treated animals showed faster learning curves and better probe trial performance compared to controls. These effects are attributed to Selank’s upregulation of BDNF and modulation of hippocampal neurotransmitter systems.

Attention and Processing Speed

Clinical studies using psychometric batteries showed improved attention, concentration, and information processing speed in Selank-treated subjects. This is particularly relevant for the anxiety population, where attentional biases and cognitive impairment are core features of the disorder.

Neuroprotection

Beyond acute cognitive enhancement, Selank has shown neuroprotective properties in ischemia and neurotoxicity models. Its ability to upregulate BDNF, modulate inflammatory cytokines, and stabilize enkephalin levels may contribute to protection against neuronal damage from excitotoxicity and oxidative stress. This positions Selank in a fundamentally different category from benzodiazepines, where chronic use has been associated with increased risk of cognitive decline and potentially dementia (though this association remains debated).

For researchers interested in cognitive-enhancing peptides, Semax (a related regulatory peptide derived from ACTH 4-10) offers complementary nootropic properties through BDNF upregulation and neurovascular mechanisms.

BDNF, Neuroplasticity, and the Neurotrophic Advantage

Selank’s effect on brain-derived neurotrophic factor (BDNF) represents one of its most mechanistically important properties. BDNF is the primary neurotrophin in the adult brain, essential for:

• Synaptic plasticity (the basis of learning and memory)
• Adult hippocampal neurogenesis
• Neuronal survival and dendritic arborization
• Long-term potentiation (LTP) — the cellular substrate of memory formation
• Stress resilience and mood regulation

Research has demonstrated that Selank administration increases BDNF mRNA expression in the hippocampus and frontal cortex of rodents by 40–60% compared to vehicle-treated controls. This upregulation occurs within hours of administration and persists for at least 24 hours after a single dose (PMID: 19340573).

The contrast with benzodiazepines is stark. Chronic benzodiazepine treatment has been shown to decrease BDNF expression in the hippocampus in multiple studies. This BDNF suppression may underlie the cognitive impairment observed with chronic benzodiazepine use and could theoretically contribute to the structural brain changes (hippocampal volume reduction) reported in some neuroimaging studies of long-term benzodiazepine users.

“Selank is among the few known compounds that simultaneously produce anxiolytic effects while enhancing cognitive function — a combination that is pharmacologically opposite to the benzodiazepine profile and theoretically superior for anxiety disorders where cognitive impairment is a core feature.”

The Immunomodulatory Dimension: What Benzodiazepines Can’t Do

As a tuftsin analog, Selank inherits and extends the immunomodulatory properties of its parent peptide. This immune component is increasingly recognized as relevant to anxiety disorders, given the robust bidirectional links between immune activation and psychiatric symptoms.

Cytokine Modulation

Selank has been shown to modulate the expression of pro-inflammatory (IL-1?, IL-6, TNF-?) and anti-inflammatory (IL-10) cytokines. The pattern is generally normalizing rather than purely suppressive or stimulatory — Selank appears to rebalance cytokine profiles toward homeostasis. In gene expression studies, Selank altered the expression of 36 genes related to immune signaling within 1 hour of administration, with effects persisting at 24 hours (PMID: 25446800).

The Neuroinflammation-Anxiety Connection

Elevated pro-inflammatory cytokines have been consistently found in anxiety disorders, and peripheral inflammation can drive central neuroinflammation through multiple pathways (vagal afferents, circumventricular organs, cytokine transport across the BBB). By modulating peripheral immune signaling, Selank may address an upstream driver of anxiety that benzodiazepines completely ignore.

Clinical Relevance for Virus-Associated Anxiety

Several studies have investigated Selank’s antiviral properties, particularly against influenza viruses. The peptide has demonstrated interferon-stimulating activity and enhanced innate antiviral defense mechanisms. For researchers studying the intersection of viral infection, immune activation, and neuropsychiatric symptoms, Selank represents a uniquely multifunctional tool.

Other peptides with immunomodulatory properties relevant to neuroimmune research include BPC-157 (cytoprotective, anti-inflammatory) and TB-500 (Thymosin Beta-4) (tissue repair, immune modulation).

Tolerance, Dependence, and Withdrawal: The Critical Difference

The tolerance and dependence profile is arguably the most clinically significant point of comparison between Selank and benzodiazepines.

Benzodiazepine Tolerance and Dependence

Benzodiazepine tolerance develops through well-characterized molecular mechanisms:

• Receptor internalization: Chronic GABA-A receptor potentiation leads to compensatory receptor endocytosis, reducing the number of surface receptors
• Subunit composition changes: Prolonged benzodiazepine exposure alters GABA-A receptor subunit expression, shifting toward configurations less sensitive to benzodiazepine modulation
• Glutamatergic upregulation: Chronic inhibitory enhancement triggers compensatory excitatory adaptations, including NMDA receptor upregulation
• Intracellular signaling changes: Alterations in protein kinase C (PKC) activity, CREB phosphorylation, and gene expression profiles

Physical dependence can develop within 2–4 weeks of daily benzodiazepine use, and withdrawal symptoms (ranging from rebound anxiety and insomnia to seizures and delirium) can persist for weeks to months after discontinuation. The severity and duration of withdrawal depend on the specific benzodiazepine, dose, duration of use, and rate of taper.

Selank: No Tolerance or Dependence Observed

In contrast, published preclinical and clinical studies have not identified tolerance development, physical dependence, or withdrawal effects with Selank. Several factors likely contribute to this favorable profile:

• Indirect GABA modulation: Because Selank modulates GABAergic signaling through gene expression changes rather than direct receptor binding, it does not trigger the same compensatory receptor downregulation that drives benzodiazepine tolerance
• Multi-target mechanism: The distributed pharmacology (GABA + serotonin + dopamine + enkephalin + BDNF + immune) means no single system bears the full allostatic load, reducing the pressure for compensatory adaptation at any one target
• Physiological rather than pharmacological enhancement: Selank appears to restore and optimize existing signaling rather than forcing supraphysiological activation, resulting in less homeostatic disruption
• BDNF upregulation: The neurotrophic support provided by BDNF may actively counteract the neuroplastic changes (synaptic weakening, neuronal shrinkage) associated with dependence development

Enkephalinase Inhibition and Endogenous Opioid Modulation

One of Selank’s less-discussed but mechanistically important properties is its inhibition of enkephalin-degrading enzymes. Enkephalins (Met-enkephalin and Leu-enkephalin) are endogenous pentapeptides that activate delta and mu opioid receptors, contributing to pain modulation, stress responses, and emotional regulation.

By inhibiting enkephalinase (also known as neprilysin/CD10 and aminopeptidase N/CD13), Selank prolongs the activity of endogenously produced enkephalins without introducing exogenous opioid receptor ligands. This “turning up the volume” on the body’s own opioid system provides several advantages:

• Anxiolytic and mild analgesic effects mediated by delta opioid receptors
• No risk of respiratory depression (a major concern with exogenous opioid agonists)
• Self-limiting effect — the enhancement is bounded by natural enkephalin production rates
• Preservation of physiological opioid receptor regulation (no forced supramaximal activation)

This mechanism is particularly interesting because delta opioid receptor activation has been independently shown to produce anxiolytic effects in preclinical models without the sedation, euphoria, or dependence liability associated with mu opioid receptor activation.

Pharmacokinetics and Administration Routes

Selank’s pharmacokinetic profile reflects its peptide nature, with important implications for research design:

Intranasal Administration

The primary administration route for Selank in both research and clinical settings is intranasal delivery. This route offers several advantages for peptide administration:

• Bypasses first-pass hepatic metabolism
• Provides relatively direct access to the CNS via the olfactory epithelium and trigeminal nerve pathways
• Non-invasive, enabling repeated dosing without injection stress (critical for behavioral studies)
• Rapid absorption with peak brain concentrations achieved within minutes

Metabolic Stability

The Pro-Gly-Pro C-terminal extension significantly improves Selank’s resistance to proteolytic degradation compared to native tuftsin. While specific half-life data varies by study, the extended sequence provides a biologically useful duration of action sufficient for once or twice-daily intranasal dosing in clinical protocols.

Blood-Brain Barrier Penetration

Selank has been demonstrated to cross the blood-brain barrier following intranasal administration. Brain distribution studies using radiolabeled Selank showed accumulation in the hippocampus, cortex, hypothalamus, and other structures relevant to its anxiolytic and cognitive effects.

Russian Regulatory History and Clinical Use

Selank was approved by the Russian Ministry of Health in 2009 as a nasal spray formulation for the treatment of generalized anxiety disorder and neurasthenia. The approval was based on Phase I–III clinical trials conducted at multiple Russian medical centers.

Key milestones in Selank’s regulatory history:

• 1990s: Development at the Institute of Molecular Genetics, Russian Academy of Sciences
• Early 2000s: Extensive preclinical pharmacology and toxicology studies
• 2005–2008: Phase I–III clinical trials for anxiety disorders
• 2009: Approval as an anxiolytic nasal spray (0.15% solution)
• Ongoing: Post-marketing surveillance and additional clinical investigations

It is important to note that Selank has not been evaluated by the FDA, EMA, or other Western regulatory agencies, and the Russian clinical trial data has not been subjected to the same level of independent scrutiny that characterizes major Western regulatory approvals. Much of the clinical literature is published in Russian-language journals, limiting accessibility for the international research community. However, the breadth and consistency of the preclinical data from international laboratories provides independent support for Selank’s pharmacological properties.

Research Protocols and Dosing in Published Studies

Preclinical Dosing

• Rodent studies (intranasal): 100–300 ?g/kg, typically administered 15–30 minutes before behavioral testing
• Rodent studies (intraperitoneal): 100–500 ?g/kg for pharmacokinetic and mechanistic studies
• In vitro neuronal cultures: 0.1–10 ?M concentration range for gene expression and neuroprotection studies

Clinical Dosing (Russian Trials)

• Formulation: 0.15% nasal spray solution (approximately 75 ?g per spray)
• Typical protocol: 2–3 sprays per nostril, 2–3 times daily
• Duration: 14-day treatment courses in most published protocols
• Total daily dose: Approximately 450–900 ?g/day intranasally

Research Design Considerations

Researchers designing studies with Selank should consider several practical factors:

• Storage: Reconstituted peptide solutions should be stored at 2–8°C and used within the validated stability period
• Vehicle: Standard peptide vehicles (sterile saline, phosphate-buffered saline) are appropriate
• Timing: For acute anxiolytic effects, administer 15–30 minutes before behavioral assessment; for gene expression studies, allow 1–24 hours depending on the target
• Controls: Include vehicle control and, where relevant, a positive control (benzodiazepine such as diazepam 1 mg/kg) for comparison

Related Peptides: Semax, Tuftsin, and the Regulatory Peptide Family

Selank exists within a family of regulatory peptides developed through similar design principles — taking endogenous peptide sequences and modifying them for enhanced stability and specific pharmacological properties.

Semax (ACTH 4-10 + Pro-Gly-Pro)

Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is Selank’s sister compound, derived from the ACTH (4-10) fragment with the same Pro-Gly-Pro stabilizing extension. While Selank is primarily anxiolytic with nootropic properties, Semax is primarily nootropic with mild anxiolytic effects. Semax’s mechanisms include BDNF upregulation, melanocortin receptor modulation, and neurovascular effects. The two peptides are sometimes used in combination in Russian clinical practice for conditions involving both anxiety and cognitive impairment.

Tuftsin (Thr-Lys-Pro-Arg)

Selank’s parent peptide, tuftsin, is a naturally occurring immunostimulatory tetrapeptide. While tuftsin itself has limited CNS activity due to rapid proteolytic degradation and poor BBB penetration, understanding its immunological functions helps explain Selank’s dual neuro-immune pharmacology.

BPC-157

BPC-157 (Body Protection Compound-157) is another peptide with multimodal mechanisms, including GABAergic modulation, dopaminergic system regulation, and potent cytoprotective effects. While not primarily an anxiolytic, BPC-157 has shown anxiolytic-like effects in preclinical models and shares with Selank the characteristic of producing beneficial effects through multiple parallel pathways rather than a single-target mechanism.

GHK-Cu

GHK-Cu (copper peptide) is a tripeptide with wound-healing and anti-inflammatory properties that also modulates gene expression related to tissue remodeling and neuroprotection. While mechanistically distinct from Selank, it illustrates the broader principle that short peptide sequences can exert powerful and multifaceted biological effects.

Frequently Asked Questions

References

1. Seredenin SB, Kozlovskaya MM. Anxiolytic activity of selank. Bull Exp Biol Med. 2014;157(1):43-46. PMID: 24390039
2. Zozulya AA, Sizov SV, Kost NV, et al. Effect of selank on the level of enkephalin-degrading enzymes. Bull Exp Biol Med. 2008;145(4):454-456. PMID: 18646133
3. Kozlovskii II, Danchev ND. Optimizing effect of selank on the conditioned active avoidance reflex in rats. Bull Exp Biol Med. 2003;135(1):44-46. PMID: 12717508
4. Medvedev VE, Tereshchenko ON, Kost NV, et al. Optimization of therapy of anxiety disorders with selank. Zh Nevrol Psikhiatr Im S S Korsakova. 2015;115(6):33-40. PMID: 18533106
5. Uchakina ON, Uchakin PN, Miasoedov NF, et al. Immunomodulatory effects of selank in patients with anxiety-asthenic disorders. Zh Nevrol Psikhiatr. 2008;108(5):71-75. PMID: 18404381
6. Inozemtseva LS, Karpenko EA, Dolotov OV, et al. Intranasal administration of the peptide selank regulates BDNF expression in the rat hippocampus in vivo. Dokl Biol Sci. 2008;421(1):241-243. PMID: 19340573
7. Kolomin T, Morozova M, Volkova A, et al. Transcriptomic analysis of the effects of selank on gene expression in the rat hippocampus. Bull Exp Biol Med. 2014;158(2):257-260. PMID: 25446800
8. Grigoriev VV, Ivanova TA, Kustova EA, et al. Selank modulates GABA-A receptor subunit gene expression in the hippocampus. Bull Exp Biol Med. 2015;160(2):234-237.
9. Najjar VA, Nishioka K. “Tuftsin”: a natural phagocytosis stimulating peptide. Nature. 1970;228(5272):672-673. PMID: 5472497
10. Kozlov SV, Mezentseva MV, Myasoedov NF, et al. Selank and its metabolites maintain the homeostasis of the immune status in conditions associated with the influenza virus. Russ J Bioorg Chem. 2002;28(1):33-36.
11. Kasian A, Kolomin T, Kolyvanova T, et al. Peptide selank enhances the effect of diazepam in the elevated plus-maze test. Bull Exp Biol Med. 2013;156(1):57-59.
12. Volkova A, Shadrina M, Kolomin T, et al. Selank administration affects the expression of genes related to GABAergic neurotransmission in the frontal cortex. Bull Exp Biol Med. 2016;160(5):662-665.
13. Ershov FI, Uchakin PN, Uchakina ON, et al. Antiviral activity of immunomodulatory peptide selank in experimental and clinical studies. Bull Exp Biol Med. 2010;149(1):1-4.
14. Seredenin SB, Voronina TA. Neuroreceptor mechanisms of selank anxiolytic action. Ross Fiziol Zh Im I M Sechenova. 2009;95(11):1180-1188.
15. Narkevich VB, Kudrin VS, Klodt PM, et al. Effects of selank on serotonin metabolism in the brain of rats. Bull Exp Biol Med. 2008;145(5):605-607.

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