Selank

1. Overview

Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) is a synthetic heptapeptide developed in the late 1990s at the Institute of Molecular Genetics of the Russian Academy of Sciences, in collaboration with the V.V. Zakusov Research Institute of Pharmacology. It was designed by extending the naturally occurring immunomodulatory tetrapeptide tuftsin (Thr-Lys-Pro-Arg, a fragment of the human immunoglobulin G heavy chain) with a C-terminal Pro-Gly-Pro tripeptide to improve metabolic stability and duration of action [19].

Selank was registered by the Russian Federation Ministry of Health in 2009 and approved for medical use as an anxiolytic and nootropic drug, available as a 0.15% intranasal solution (trade name Selank). It is indicated for the treatment of generalized anxiety disorder (GAD) and neurasthenia in Russia and Ukraine [1]. Outside of Russia, selank has no regulatory approval from the FDA, EMA, or other major Western agencies and remains classified as a research compound.

The development of selank was led by Nikolai Myasoedov and colleagues, who sought to create a peptide with dual anxiolytic and immunomodulatory properties, retaining the immunoregulatory activity of tuftsin while gaining neurotropic effects through the Pro-Gly-Pro extension, a motif also found in the related peptide semax [5] [7].

Molecular Weight

~751.9 Da

Sequence

Thr-Lys-Pro-Arg-Pro-Gly-Pro (tuftsin + Pro-Gly-Pro)

Half-life

~2-3 minutes in plasma (effects persist longer)

Routes Studied

Intranasal (primary), subcutaneous, intraperitoneal

FDA Status

Not approved outside Russia; approved in Russia since 2009

CAS Number

129954-34-3

2. Mechanism of Action

Selank exerts its pharmacological effects through multiple converging mechanisms involving neurotransmitter systems, neurotrophic factors, endogenous opioid pathways, and immune regulation.

GABAergic Modulation

One of the primary anxiolytic mechanisms of selank involves modulation of the GABAergic system. Selank allosterically modulates GABA-A receptor activity, altering the affinity of endogenous ligands for the receptor without directly binding to the benzodiazepine site [5]. In a comprehensive gene expression study, Volkova et al. (2016) found that selank significantly altered expression of 45 of 84 examined neurotransmission-related genes in the rat frontal cortex at 1 hour post-administration, including GABA receptor subunits, transporters, and ion channels [5]. This GABAergic modulation is thought to underlie the anxiolytic effects that are clinically comparable to benzodiazepines but without sedation, tolerance, or dependence [1] [2].

Serotonergic Effects

Selank directly influences serotonin (5-HT) metabolism in multiple brain regions. Kozlovskii et al. (2010) demonstrated that a single injection of selank activated 5-HT metabolism in the hypothalamus and caudal brain stem for 30 minutes to 2 hours [12]. In rats with pharmacologically depleted serotonin (PCPA-pretreated), selank enhanced 5-HT metabolism in the brain stem within 30 minutes, suggesting a restorative action on the serotonergic system [10]. Narkevich et al. (2008) further showed that selank modulated serotonin and its metabolite 5-HIAA in a strain-dependent manner across hippocampus, hypothalamus, striatum, and frontal cortex [11].

BDNF and Neurotrophic Factor Upregulation

Selank increases expression of brain-derived neurotrophic factor (BDNF), a key mediator of synaptic plasticity, learning, and neuronal survival. Semenova et al. (2009) showed that intranasal selank at 250 and 500 mcg/kg elevated BDNF mRNA in the rat hippocampus at 3 hours and BDNF protein at 24 hours post-administration [8]. Volkova et al. (2019) demonstrated that selank prevented ethanol-induced memory impairment through regulation of BDNF content in the hippocampus and prefrontal cortex [9].

Enkephalinase Inhibition

Selank dose-dependently inhibits the enzymatic hydrolysis of enkephalins in human serum with an IC50 of approximately 15-20 microM, making it more potent than classical peptidase inhibitors bacitracin and puromycin [19]. By preserving endogenous enkephalin levels, selank may enhance opioidergic tone, contributing to its anxiolytic and mood-stabilizing properties. Notably, only the heptapeptide and its pentapeptide fragments showed this inhibitory effect; smaller fragments did not [19].

Dopaminergic Modulation

Selank also modulates dopamine metabolism. Narkevich et al. (2008) reported that selank (0.3 mg/kg) increased norepinephrine levels in the hypothalamus and produced strain-dependent changes in dopamine metabolites (DOPAC, HVA) in the frontal cortex and hippocampus [11]. Semenova et al. (2008) showed that selank corrected integrative brain activity and biogenic amine levels in rats with antenatal hypoxia-induced neurological dysfunction [21].

Gene Expression Effects

The impact of selank on gene expression is remarkably broad. Kolomin et al. (2013) used cDNA microarray analysis and found that a single selank dose altered mRNA levels of 36 genes by more than 2-fold in the rat hippocampus, while course administration changed 20 genes [7]. Most of these genes encoded membrane-associated proteins involved in ion homeostasis, directly relevant to learning and memory processes [7]. The in vitro confirmation came from Kolomin et al. (2017), who showed that selank modulated GABAergic neurotransmission gene expression in human IMR-32 neuroblastoma cells [6].

3. Pharmacokinetics

Intranasal Absorption and Bioavailability

Selank is administered almost exclusively via the intranasal route, which exploits the direct nose-to-brain transport pathway. The nasal mucosa provides a large absorptive surface area with high vascularity, and the olfactory epithelium enables direct access to the CNS by bypassing the blood-brain barrier (BBB) through transcellular transport along olfactory and trigeminal nerve pathways [8] [4]. Intranasal bioavailability of selank is estimated at approximately 92.8% based on pharmacokinetic studies in animal models, which is exceptionally high for a peptide drug and reflects both the efficiency of nasal mucosal absorption and the stabilizing effect of the Pro-Gly-Pro C-terminal extension [8].

Half-life and Metabolic Stability

The plasma half-life of selank is approximately 2-3 minutes, which is notably longer than the half-life of the parent peptide tuftsin (approximately 20-30 seconds in plasma). This 5-10 fold improvement in metabolic stability is directly attributable to the C-terminal Pro-Gly-Pro extension, which confers resistance to degradation by carboxypeptidases and aminopeptidases that rapidly cleave tuftsin [19] [7]. Despite the short plasma half-life, the pharmacodynamic effects of selank persist substantially longer than the peptide's presence in circulation, with anxiolytic effects lasting several hours after a single dose and gene expression changes detectable at 1-24 hours post-administration [5] [7].

Selank is metabolized primarily by carboxypeptidases and aminopeptidases present in blood plasma and tissues. The degradation pathway produces several bioactive fragments, including the tuftsin core sequence (Thr-Lys-Pro-Arg) and the Pro-Gly-Pro tripeptide, both of which retain independent biological activity [18] [19].

Blood-Brain Barrier Penetration

Evidence for selank's CNS penetration comes from multiple lines of investigation. The 2020 fMRI study by Ershov et al. provided direct evidence in humans, demonstrating altered functional connectivity between the right amygdala and temporal cortex regions within 20 minutes of intranasal administration [4]. In animal studies, intranasal selank produces measurable changes in neurotransmitter levels (serotonin, dopamine, norepinephrine) across hippocampus, hypothalamus, striatum, and frontal cortex [11] [12], and alters gene expression in the hippocampus and frontal cortex [5] [7], confirming significant CNS distribution after intranasal delivery. Semenova et al. (2009) demonstrated that intranasal selank elevated BDNF mRNA in the hippocampus at 3 hours and BDNF protein at 24 hours, indicating sustained CNS bioavailability after a single intranasal dose [8].

Tissue Distribution

Following intranasal administration, selank achieves therapeutically relevant concentrations in multiple CNS regions. The monoamine studies by Narkevich et al. (2008) showed measurable effects in the hippocampus, hypothalamus, striatum, and frontal cortex [11]. Gene expression profiling revealed that selank reached the hippocampus in sufficient concentrations to alter mRNA levels of 36 genes (more than 2-fold change) after a single dose [7], and 45 of 84 neurotransmission-related genes in the frontal cortex [5]. Peripheral tissue distribution is evidenced by immunomodulatory effects in spleen tissue, where selank modulated inflammation-related gene expression at 6 and 24 hours post-administration [14] [15].

4. Researched Applications

Anxiolytic Effects

The most clinically validated application of selank is in the treatment of anxiety disorders. In an open-label trial, Zozulya et al. (2008) compared selank to medazepam (a benzodiazepine) in 62 patients with GAD and neurasthenia, finding equivalent anxiolytic efficacy with additional antiasthenic and psychostimulant benefits unique to selank [1]. Medvedev et al. (2014) compared selank to phenazepam in 60 patients with anxiety and somatoform disorders, reporting that selank's anxiolytic effects persisted for one week after cessation of treatment, with superior quality-of-life outcomes [2]. Critically, selank demonstrated no sedation, muscle relaxation, tolerance, or withdrawal syndrome across these clinical studies [1] [2] [3].

In a follow-up study, Medvedev et al. (2015) showed that combining selank with phenazepam reduced the benzodiazepine's side effects, including sedation, memory impairment, and sexual disturbances, compared to phenazepam monotherapy [3].

Nootropic and Cognitive Effects

Selank demonstrates consistent nootropic properties in animal models. Kozlovskii et al. (2010) established that selank enhanced memory trace stability for up to 30 days when administered during the consolidation phase of learning [12]. Semenova et al. (2008) showed that selank at 300 mcg/kg restored cognitive processes (learning, memory, and attention) that were impaired by chronic catecholaminergic system disruption during early development [20]. Volkova et al. (2019) further demonstrated protection against ethanol-induced memory impairment through BDNF-mediated mechanisms [9].

The first neuroimaging evidence of selank's central effects in humans was provided by Ershov et al. (2020) in a functional connectomics study of 52 healthy participants. Resting-state fMRI revealed that intranasal selank altered functional connectivity between the right amygdala and regions in the temporal cortex within 20 minutes of administration [4].

Antidepressant-like Effects

Kozlovskii et al. (2008) evaluated selank in animal models of depression using WAG/Rij rats, Wistar rats, and BALB/c mice, demonstrating antidepressant-like effects in both genetically-based and situation-provoked depressive behavioral paradigms [22].

Immunomodulatory Effects

As a tuftsin analog, selank retains significant immunomodulatory activity. Uchakina et al. (2008) demonstrated that selank treatment in patients with anxiety-asthenic disorders normalized Th1/Th2 cytokine balance, restored CD4+/CD8+ T-cell ratios, and enhanced suppressed NK cell activity [13]. In vitro, selank at 10^-7 M completely suppressed IL-6 gene expression in peripheral blood cells of depressed patients but not healthy controls, indicating selective immune modulation [13].

Andreeva et al. (2011) showed that selank modulated expression of inflammation-related genes in mouse spleen, including chemokines, cytokines, and their receptors [14]. A subsequent study (Andreeva et al., 2014) demonstrated that selank caused a rapid 3-fold decrease in complement C3 mRNA within 30 minutes and wave-like alterations in caspase-1 and IL-2 receptor gamma gene expression [15].

Antiviral Activity

Selank demonstrates antiviral properties mediated through immune modulation. Zhuikova et al. (2009) showed that selank completely suppressed influenza A/H3N2 viral reproduction in vitro when applied 24 hours before viral inoculation, outperforming recombinant interferon-alpha [17]. Myasoedov et al. (2010) expanded these findings, demonstrating broad antiviral activity of selank and its fragments against influenza A (H3N2, H5N1), influenza B, herpes simplex viruses 1 and 2, and cytomegalovirus [18]. The antiviral mechanism appears to operate through modulation of the Th1/Th2/Treg cytokine balance and induction of interferon-alpha expression [17].

5. Clinical Evidence Summary

Clinical evidence for selank derives primarily from Russian clinical studies. Three clinical trials have evaluated selank in anxiety disorders. Zozulya et al. (2008) compared selank to medazepam in 62 patients with GAD and neurasthenia [1]. Medvedev et al. (2014) compared selank to phenazepam in 60 patients with anxiety and somatoform disorders [2]. Medvedev et al. (2015) evaluated combined selank-phenazepam therapy versus phenazepam monotherapy in 70 patients [3]. All three studies reported anxiolytic efficacy comparable to benzodiazepines with a more favorable side effect profile.

The 2020 functional connectomics study by Ershov et al. represents the only published study using neuroimaging to assess selank's effects in healthy human participants, providing objective evidence of central nervous system activity [4].

It should be noted that these trials were conducted in Russian clinical settings and published predominantly in Russian-language journals. They were generally completed before the widespread adoption of international trial reporting standards (CONSORT). Independent replication by non-Russian research groups has not been published, and no trials registered on ClinicalTrials.gov have been identified. The overall evidence level is considered preliminary despite the drug's regulatory approval in Russia.

6. Dosing in Published Research

The following doses have been used in published research. These are not recommendations and should not be interpreted as therapeutic guidance.

The commercially available Russian formulation (Selank 0.15%) delivers approximately 75 mcg per drop. The standard clinical protocol involves 2-3 drops per nostril, 3 times daily for 10-14 days [1] [2]. In animal studies, doses of 100-500 mcg/kg administered intranasally or intraperitoneally have been used [5] [8] [12].

7. Dose-Response Relationships

Anxiolytic Dose Range

The clinically studied anxiolytic dose range for intranasal selank spans 75 to 500 mcg per administration. The approved Russian formulation (0.15% solution) delivers approximately 75 mcg per drop, with the standard clinical dosing protocol of 2-3 drops per nostril, 3 times daily yielding a total daily dose of approximately 250-450 mcg [1] [2]. The Russian clinical trials by Zozulya et al. (2008) and Medvedev et al. (2014) used this standardized dosing protocol over 14-day treatment courses, establishing it as the optimal dose for the treatment of generalized anxiety disorder and neurasthenia [1] [2].

Gene Expression Changes at Different Doses

The gene expression profile of selank is dose- and time-dependent. Kolomin et al. (2013) demonstrated that a single selank dose altered mRNA levels of 36 genes by more than 2-fold in the rat hippocampus, with these genes predominantly encoding membrane-associated proteins involved in ion homeostasis, learning, and memory [7]. In contrast, course administration (repeated daily dosing) changed the expression of 20 genes, suggesting that chronic exposure produces a distinct but partially overlapping transcriptomic signature compared to acute dosing [7]. At the systems level, Volkova et al. (2016) showed that selank altered 45 of 84 neurotransmission genes in the frontal cortex at a dose of 300 mcg/kg, with particularly pronounced effects on GABA receptor subunits (GABRA2, GABRB1, GABRG1), serotonin receptors (HTR3A), and dopamine receptors (DRD1) [5].

Onset of Action

Selank demonstrates a rapid onset of central effects. The fMRI study by Ershov et al. (2020) detected altered functional connectivity between the amygdala and temporal cortex within 20 minutes of intranasal administration in healthy volunteers [4]. In animal studies, serotonin metabolism changes in the hypothalamus and brain stem were observed within 30 minutes of administration [10] [12], and complement C3 mRNA decreased 3-fold within 30 minutes in peripheral tissue [15]. The BDNF response follows a more delayed time course, with mRNA elevation at 3 hours and protein elevation at 24 hours [8].

Duration of Anxiolytic Effect

A distinctive feature of selank compared to benzodiazepines is the persistence of its therapeutic effects beyond the period of active administration. Medvedev et al. (2014) demonstrated that selank's anxiolytic effects persisted for one week after cessation of the 14-day treatment course, which is in marked contrast to benzodiazepines where anxiolytic effects cease immediately upon discontinuation and may be followed by rebound anxiety and withdrawal [2]. This sustained effect likely reflects selank's mechanism through gene expression modulation and BDNF upregulation rather than direct receptor agonism, fundamentally altering neuronal signaling pathways rather than simply occupying receptor binding sites [5] [7] [8].

8. Safety and Side Effects

Published clinical data from Russian trials consistently report a favorable safety profile for selank. In the three clinical studies involving a combined total of approximately 192 patients, selank was well tolerated with no serious adverse events reported [1] [2] [3]. These studies represent the Phase II/III clinical data supporting selank's regulatory approval in Russia in 2009, and the safety database, while modest by Western regulatory standards, demonstrates a consistent absence of the serious adverse events characteristic of conventional anxiolytics.

Comparison with Benzodiazepines

A principal advantage of selank over conventional benzodiazepine anxiolytics is the absence of characteristic benzodiazepine side effects. Across all three clinical trials, selank produced no sedation, no muscle relaxation, no amnesia or cognitive impairment, no tolerance development, and no withdrawal syndrome [1] [2] [3]. This stands in sharp contrast to benzodiazepines such as phenazepam and medazepam, which produce dose-dependent sedation in 30-50% of patients, clinically significant memory impairment, psychomotor slowing, physical dependence with chronic use, and potentially dangerous withdrawal syndromes upon discontinuation [2] [3].

When combined with phenazepam, selank reduced the incidence of benzodiazepine-associated adverse effects including cognitive impairment, excessive sedation, asthenia, and sexual dysfunction compared to phenazepam monotherapy [3]. This suggests selank may have a protective or counterbalancing effect against benzodiazepine-induced neurological depression.

Reported Side Effects

The most commonly reported side effects are mild and transient, including nasal irritation following intranasal administration, occasional headaches, and rare drowsiness [2]. No cardiovascular, hepatic, or renal toxicity has been reported at therapeutic doses.

Adverse Event Profile Summary

The complete adverse event profile from Russian clinical trials can be summarized as follows: selank demonstrated no sedation (vs. 30-50% with benzodiazepines), no cognitive impairment (vs. clinically significant amnesia with benzodiazepines), no psychomotor impairment (vs. dose-dependent coordination deficits with benzodiazepines), no tolerance or dose escalation requirement over the 14-day treatment courses (vs. rapid tolerance development with benzodiazepines), no withdrawal symptoms upon cessation (vs. potentially severe withdrawal with benzodiazepines including seizure risk), and no abuse potential or dependence liability [1] [2] [3]. Additionally, selank produced no cardiovascular effects, no hepatotoxicity, no weight gain, and no sexual dysfunction, which are common concerns with SSRIs and other first-line anxiolytics [2].

Safety Concerns

The U.S. FDA has raised concerns about potential immunogenicity of compounded peptide preparations containing selank, noting the theoretical risk of immune response against the peptide. This concern is rooted in the general principle that exogenous peptides may be recognized by the immune system and elicit antibody formation. However, this concern must be contextualized: selank is a seven-amino-acid peptide with a molecular weight of only 751.9 Da, well below the typical immunogenic threshold of 5,000-10,000 Da for most peptides. Furthermore, selank is composed entirely of the endogenous tuftsin sequence plus a Pro-Gly-Pro motif, both of which are naturally present in the human body [13]. The clinical immunomodulatory data from Uchakina et al. (2008) demonstrate that selank's immune effects are modulatory and normalizing rather than stimulatory, with restoration of dysregulated immune parameters toward physiological baselines rather than immune activation [13].

Long-term Safety Data

Long-term safety data beyond 14-day treatment courses are limited in the published literature. The Russian prescribing information recommends treatment courses of 10-14 days with 1-3 week breaks between courses, and clinical experience in Russia since the 2009 approval has not generated post-marketing safety signals requiring label changes or market withdrawal. However, systematic long-term safety studies with extended follow-up periods have not been published in peer-reviewed journals. The recommended course-based dosing pattern (10-14 days on, 1-3 weeks off) may inherently mitigate long-term exposure risks [1] [2].

Limitations

Safety in pregnancy, lactation, pediatric populations, and patients with significant organ impairment has not been systematically studied. The absence of Western regulatory review means that manufacturing quality standards for research-grade selank are variable, and peptide purity, sterility, and stability may differ substantially between suppliers outside of the regulated Russian pharmaceutical supply chain.

February 2026 U.S. Compounding Update: On February 27, 2026, HHS Secretary Robert F. Kennedy Jr. announced that selank would be among approximately 14 peptides moved from FDA Category 2 back to Category 1, restoring legal access through licensed U.S. compounding pharmacies with a physician's prescription. This reclassification does not constitute FDA approval. The FDA's formal updated list had not been published at the time of this update.

9. Comparative Effectiveness

Selank vs. Benzodiazepines

The clinical comparison between selank and benzodiazepines is the most well-documented in the literature. Zozulya et al. (2008) demonstrated that selank was comparable in anxiolytic efficacy to medazepam in GAD patients, with the additional benefits of antiasthenic and psychostimulant effects not observed with the benzodiazepine [1]. Medvedev et al. (2014) found comparable anxiolytic efficacy between selank and phenazepam, with selank producing superior quality-of-life outcomes and anxiolytic effects that persisted for one week after treatment cessation [2]. Crucially, selank achieves this equivalent anxiolytic efficacy without the sedation, cognitive impairment, tolerance, dependence, or withdrawal that are intrinsic pharmacological properties of benzodiazepines [1] [2] [3]. Selank also lacks the abuse potential and respiratory depression risk associated with benzodiazepines, making it fundamentally safer in overdose scenarios. The 2017 study by Kasian et al. further showed that selank can enhance benzodiazepine efficacy under chronic stress while reducing benzodiazepine side effects, suggesting potential utility as an adjunct to allow benzodiazepine dose reduction [16].

Selank vs. SSRIs

While no direct head-to-head clinical trials comparing selank with SSRIs have been published, the pharmacological profiles can be compared based on available data. SSRIs require 2-6 weeks for onset of anxiolytic effect due to the need for serotonergic system adaptation, whereas selank demonstrates central effects within 20 minutes of intranasal administration [4] and meaningful anxiolytic effects within the first days of treatment [1] [2]. SSRIs commonly produce side effects including sexual dysfunction (30-70% incidence), weight gain, emotional blunting, gastrointestinal disturbance, and discontinuation syndrome, none of which have been reported with selank [2]. However, SSRIs have a far larger evidence base from multiple large-scale randomized controlled trials conducted internationally, whereas selank's clinical evidence is limited to Russian studies with relatively small sample sizes.

Selank vs. Phenibut

Phenibut (beta-phenyl-GABA) is another Russian-developed anxiolytic that acts as a GABA-B agonist and, at higher doses, a GABA-A agonist. Unlike selank, phenibut produces dose-dependent sedation, has significant abuse and dependence potential, produces tolerance with chronic use, and can cause a severe withdrawal syndrome including psychosis and seizures. Selank's mechanism through allosteric GABA-A modulation and gene expression changes rather than direct GABA receptor agonism fundamentally distinguishes it from phenibut's pharmacology and eliminates the dependence liability [1] [5].

Selank vs. Semax

While both are synthetic heptapeptides from the same research institute sharing the Pro-Gly-Pro C-terminal motif, selank and semax have distinct parent peptides and primary clinical profiles. Semax is derived from ACTH(4-10), acts primarily through melanocortin receptor interactions, and is classified as a nootropic/neuroprotective agent approved for stroke and cognitive disorders. Selank is derived from tuftsin, acts primarily through GABAergic modulation and serotonin metabolism, and is classified as an anxiolytic. Selank retains substantially stronger immunomodulatory properties from its tuftsin heritage, including antiviral activity and cytokine modulation [13] [17], effects not attributed to semax. A detailed comparison is provided in section 10 below.

Selank vs. N-Acetyl Selank (NASA)

N-Acetyl Selank Amidate (commonly abbreviated NASA or NA-Selank) is a modified version of selank featuring an N-terminal acetyl group and C-terminal amide cap. These modifications are designed to further enhance metabolic stability by protecting against both aminopeptidases (N-terminal acetylation) and carboxypeptidases (C-terminal amidation), theoretically extending the already-improved half-life of selank beyond the parent compound's 2-3 minutes. N-Acetyl Selank has not been studied in clinical trials and has no regulatory approval in any jurisdiction. The pharmacological comparison is based entirely on theoretical considerations of peptide stability and limited preclinical observations. Users should note that the clinical efficacy and safety data established for selank in Russian trials cannot be directly extrapolated to N-Acetyl Selank, as the structural modifications may alter receptor binding affinity, tissue distribution, and metabolic pathway profiles.

10. Comparison with Semax

Selank and semax are both synthetic heptapeptides developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, and both share the C-terminal Pro-Gly-Pro stabilizing motif. However, they differ significantly in their parent molecules, primary mechanisms, and clinical applications.

Semax is derived from ACTH(4-10) (Met-Glu-His-Phe-Pro-Gly-Pro) and is classified primarily as a nootropic and neuroprotective agent, with approval in Russia for stroke and cognitive disorders. Selank is derived from tuftsin (Thr-Lys-Pro-Arg-Pro-Gly-Pro) and is classified primarily as an anxiolytic with nootropic properties.

Mechanistically, semax acts primarily through melanocortin receptor interactions and robust BDNF upregulation, while selank operates principally through GABAergic modulation, serotonin metabolism, and enkephalinase inhibition. Selank retains stronger immunomodulatory properties from its tuftsin heritage. The 2017 study by Kasian et al. showed that selank enhanced the anxiolytic effect of diazepam under chronic stress conditions, a property not reported for semax [16].

11. Related Peptides

See also: Semax, Epithalon, Thymosin Alpha-1

12. References

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2. [2] Medvedev VE, Tereshchenko ON, Israelian AYu, Chobanu IK, Kost NV, Sokolov OYu, Myasoedov NF, Zozulya AA (2014). A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders. Zh Nevrol Psikhiatr Im S S Korsakova. PubMed
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6. [6] Kolomin T, Volkova A, Shadrina M, Andreeva L, Slominsky P, Limborska S, Myasoedov N (2017). GABA, selank, and olanzapine affect the expression of genes involved in GABAergic neurotransmission in IMR-32 cells. Front Pharmacol. DOI PubMed
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9. [9] Volkova A, Shadrina M, Kolomin T, Andreeva L, Limborska S, Myasoedov N, Slominsky P (2019). Selank, peptide analogue of tuftsin, protects against ethanol-induced memory impairment by regulating of BDNF content in the hippocampus and prefrontal cortex in rats. Bull Exp Biol Med. DOI PubMed
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17. [17] Zhuikova SE, Simonova MA, Mezentseva MV, Kolobov AA, Lesnova EI, Grigorieva IV, Zuikov AV, Myasoedov NF, Ershov FI (2009). Antiviral activity of immunomodulator selank in experimental influenza infection. Vopr Virusol. PubMed
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