pe
pep-00006 v1 CC-BY-SA-4.0

Selank: Russia-approved anxiety & mood peptide (TKPRPGP)

A synthetic peptide approved in Russia as a prescription drug for anxiety; also studied for memory, focus, and immune support; not FDA-approved.

statusbioassayed targetNEUROPROTECTIVE length7 aa refs22
investigationalanxiolyticnootropicimmunomodulatorytuftsin-analogrussian-approved
status 2 / 5 · 0 verified on platform
prediction metrics openfold3-mlx 0.3.1
ipTM0.848
pTM0.872
avg pLDDT64.7
ranking score0.901
STRUCTURE · PEP-00006 × NEUROPROTECTIVE
ranking0.901
target interface 4.5Å peptide drag rotate · ctrl+scroll zoom · right-click pan
openfold3-mlx 0.3.1 · mmCIF ↓ download
sequence7 aa
157
TKPRPGP
in the news 11 articles
overview readme

What this is

Selank (also called TP-7) is a synthetic seven-amino-acid peptide developed in Russia as an anxiety-reducing drug that is approved there as a prescription medicine. It was built from tuftsin — a short immunomodulatory peptide that the body produces naturally from immunoglobulin G — by adding a three-residue stabilizing tail (Pro-Gly-Pro) to produce the final sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP). That PGP extension is what gives Selank meaningful plasma durability after intranasal delivery; it is the same structural motif used in the sister peptide Semax (/card/pep-00005). The result is a drug that, unlike classical tranquilizers, does not produce sedation, muscle relaxation, or physical dependence at approved protocol durations — properties that drove its clinical development as an alternative to benzodiazepines for generalized anxiety disorder.

Selank is approved in Russia and several CIS countries as a prescription anxiolytic; it is not FDA-approved, not EMA-approved, and not approved by Health Canada, MHRA, or TGA. In Western markets it circulates as a research chemical.

History

Selank was developed in the 1990s at the Institute of Molecular Genetics of the Russian Academy of Sciences in Moscow, from the same research lineage that produced Semax. The team, led by Nikolai Myasoedov and colleagues, began with tuftsin — the naturally occurring immunostimulatory tetrapeptide Thr-Lys-Pro-Arg cleaved from the Fc region of IgG — and appended a Pro-Gly-Pro stability tail to yield the heptapeptide TKPRPGP. An unusual aspect of the development story is that tuftsin was being studied as an immune peptide; the anxiolytic properties discovered after adding the PGP tail were not anticipated from the parent molecule and represent a new pharmacological property, not merely a preserved one.

Selank was registered in Russia in 2009 as a prescription anxiolytic and nootropic agent, manufactured by Geropharm as a 0.15% intranasal spray under the brand name Selank. It was subsequently registered in Belarus, Kazakhstan, and Ukraine for generalized anxiety disorder and neurasthenia. Outside Russia and the CIS, Selank entered the Western nootropic community via research-chemical suppliers during the 2010s, where it is often described alongside Semax as one of the two flagship Russian synthetic peptides.

What it does

In people with generalized anxiety disorder, Selank reduces anxiety and stress reactivity without the sedation, cognitive impairment, or dependence risk associated with benzodiazepines. Russian clinical trials comparing Selank against established anxiolytics (medazepam, phenazepam) found comparable anxiolytic efficacy and — unlike the comparators — preservation of psychomotor and cognitive function in GAD patients (Medvedev and colleagues 2015; Zozulya and colleagues 2008). Community users in Western countries describe a similar pattern: reduced baseline tension without drowsiness, improved composure under stress, and no withdrawal after stopping.

Beyond anxiety, the peptide literature reports effects on stress-associated changes in immune parameters, modulation of brain-derived neurotrophic factor (BDNF), and suppression of enzymes that degrade endogenous opioid peptides (enkephalins). The clinical relevance of these effects in humans is not fully characterized. Claims of nootropic benefit in healthy, non-anxious individuals have no controlled trial support; all clinical data come from anxiety disorder populations.

Evidence

  • Human: Moderate, regional. Russian clinical comparison trials — including a 62-patient generalized anxiety disorder and neurasthenia study — form the evidence base for Russian regulatory approval. Two head-to-head comparators (medazepam and phenazepam) showed Selank with comparable anxiolytic efficacy and better preservation of cognitive and psychomotor function (Medvedev and colleagues 2015). A combined-therapy protocol demonstrated Selank as an adjunct that allows benzodiazepine dose reduction while maintaining anxiolytic control. Independent Western clinical replication is entirely absent. All available human evidence is Russian-language and development-program-connected.
  • Animal: Strong. Extensive animal data on anxiolytic effects in elevated plus maze and conflict tests, GABA modulation, BDNF elevation in hippocampus and frontal cortex, stress resilience, immune effects, attenuation of morphine withdrawal signs (Konstantinopolsky and colleagues 2022), and effects in a 6-OHDA Parkinson model. Selank also attenuated ethanol-induced memory impairment by regulating BDNF content in hippocampus and prefrontal cortex in rats (Kolik and colleagues 2019). Under chronic restraint stress, Selank reduced adverse morphological changes in intestinal tissue and shifted colon microbiota toward lactobacilli and bifidobacteria (Mukhina and colleagues 2020).
  • In vitro: Selank modulated mRNA levels of genes involved in GABAergic neurotransmission in rat frontal cortex (Volkova and colleagues 2016) and affected genes in GABAergic neurotransmission in IMR-32 human neuroblastoma cells, though in that cell line no direct effect on GABA-A receptor was observed — consistent with an indirect allosteric mechanism (Filatova and colleagues 2017). Selank also inhibits the enkephalin-degrading enzymes of human serum (Kost and colleagues 2001). Cytokine-modulating activity under social-stress conditions has been characterized in animal and limited human work (Leonidovna and colleagues 2021).

Known effects

  • Anxiolytic in generalized anxiety disorder — Approved (Russia/CIS); comparison trials vs medazepam and phenazepam
  • Cognitive/psychomotor preservation vs benzodiazepines in GAD patients — Human, Russian program; not established in healthy subjects
  • No tolerance or dependence within approved protocol durations — Human, Russian clinical record at 10–14 day courses; uncharacterized beyond that window
  • BDNF upregulation — Preclinical; hippocampus and frontal cortex in rat models
  • Enkephalin-degrading enzyme inhibition — Preclinical and in vitro; shared with Semax
  • Immunomodulation — Preclinical; IL-6, phagocytic activity, Th1/Th2 balance; clinical relevance to CNS anxiolytic effect uncharacterized
  • Stress-associated gut and liver protection — Preclinical; morphological data in rat stress models
  • Nootropic benefit in healthy individuals — Not established; no controlled trial data

Safety signals

Reported in Russian clinical trials and the approved product label: nasal irritation (most common, from intranasal route), occasional mild fatigue or dizziness during initial days. No sedation, cognitive impairment, muscle relaxation, or dependence reported in clinical literature at approved 10–14 day protocol durations.

Contraindications in the approved Russian labeling include: pregnancy (no controlled safety data), breastfeeding (no transfer or infant safety data), known hypersensitivity to Selank or formulation components (including benzalkonium chloride preservatives in some products), and severe nasal mucosal disease, chronic rhinitis, or recent nasal surgery.

Animal studies show Selank potentiates diazepam's anxiolytic effect under chronic mild stress conditions; clinical magnitude of this interaction in humans has not been quantified. Theoretical serotonergic interactions with SSRIs, SNRIs, and MAOIs exist based on mechanism; no adverse interaction has been published. Doyno and colleagues (2021, Journal of Clinical Pharmacology) reviewed Selank in a survey of GABAergic sedative-hypnotic agents, classifying it as a substance with GABA-A receptor-related mechanism but a different interaction profile from classical benzodiazepines.

Long-term safety beyond approved 10–14 day protocols is uncharacterized. Decades of Russian prescription use at approved durations without major safety signals reflects post-marketing experience from that system, not systematic pharmacovigilance data comparable to Western standards.

Research-chemical-channel Selank products are not equivalent to the Geropharm pharmaceutical formulation used in clinical trials; purity, peptide content, and preservative systems vary substantially.

Regulatory status

  • Russia / CIS: Approved prescription anxiolytic and nootropic since 2009. Manufactured by Geropharm as 0.15% intranasal spray. Registered in Belarus, Kazakhstan, and Ukraine for generalized anxiety disorder and neurasthenia.
  • United States: Not FDA-approved for any indication. Not a scheduled controlled substance. Not a recognized dietary supplement ingredient. Available through research-chemical suppliers; not authorized for human use in that channel. Selank is not currently under FDA 503A compounding review (unlike Semax, which is under review as of 2026).
  • EU / UK / Canada / Australia: Not approved by EMA, MHRA, Health Canada, or TGA. Regulatory posture by jurisdiction ranges from research-chemical availability to active enforcement.
  • WADA: Not listed by name on the WADA Prohibited List. The S0 category covers substances not approved by any governmental regulatory health authority for human therapeutic use; Selank's Russian approval creates ambiguity for athletes subject to WADA code. Athletes should verify with their national anti-doping authority.

Myths and misconceptions

  • "Selank is FDA-approved" — No. Selank is approved as a prescription anxiolytic in Russia and several CIS countries. Russian approval is not equivalent to FDA approval and the evidence base does not meet FDA standards for trial design, independence, or replication.
  • "Selank is just a Russian benzodiazepine" — No. Selank does not bind the benzodiazepine site on GABA-A receptors in the classical way. It modulates GABAergic signaling indirectly, works through multiple additional pathways (serotonin metabolism, BDNF upregulation, enkephalin-degrading enzyme inhibition), and has a meaningfully different dependence profile.
  • "Selank is a natural peptide with no side effects" — No. Selank is a synthetic heptapeptide. The PGP stabilizing tail is not a naturally occurring modification of tuftsin. Side effects reported in clinical use include nasal irritation, fatigue, and mild dizziness. Long-term safety has not been established.

Mechanism

Selank's pharmacology encompasses multiple reported pathways; the literature explicitly notes that no clear mechanistic hierarchy has been established.

GABAergic modulation: Selank allosterically enhances GABA-A receptor sensitivity rather than acting as a direct benzodiazepine-site agonist. Gene-expression data in rat frontal cortex showed Selank affected mRNA levels of GABA-related genes 1 and 3 hours after intranasal administration, with a pattern overlapping but not identical to direct GABA administration (Volkova and colleagues 2016). In IMR-32 human neuroblastoma cells — which lack the benzodiazepine modulatory site — Selank showed no direct receptor effect, consistent with indirect allosteric modulation rather than benzodiazepine-site agonism (Filatova and colleagues 2017). The indirect mechanism is the proposed basis for absence of benzodiazepine-style tolerance, dependence, and sedation.

BDNF upregulation: Elevates brain-derived neurotrophic factor mRNA in hippocampus and frontal cortex. Acute intranasal Selank in rats initially reduced BDNF protein at 3 hours but increased it at 24 hours (Kolik and colleagues 2019). This temporal pattern suggests downstream gene-expression effects that outlast the peptide's plasma presence and may contribute to sustained anxiolytic effects beyond plasma half-life. BDNF modulation is shared with Semax (/card/pep-00005).

Serotonergic modulation: Selank influences serotonin metabolism and tryptophan-serotonin conversion enzyme expression. Semenova and colleagues (2010) documented effects on brain monoamine systems in rats. This pathway likely contributes to mood-stabilizing effects and distinguishes Selank from pure GABAergic agents.

Enkephalinase inhibition: Selank inhibits enzymes that degrade endogenous opioid peptides (enkephalins), a mechanism first described by Zozulya and colleagues (2001). This effect is shared with Semax (Kost and colleagues 2001). Inhibiting enkephalin degradation prolongs endogenous opioid signaling and may contribute to stress-resilience effects.

Immunomodulation: As a tuftsin analog, Selank retains effects on macrophage and NK cell function, IL-6 production, cytokine balance, and Th1/Th2 regulation. Under social stress conditions, Selank restored phagocytic activity and delayed-type hypersensitivity reaction indices that were suppressed by stress (Yasenyavskaya and colleagues 2022; Leonidovna and colleagues 2021). The pathway connecting immune modulation to CNS anxiolytic effects is not fully characterized.

Whether anxiolytic benefit in humans is primarily GABAergic, serotonergic, BDNF-mediated, or immunomodulatory remains unresolved.

Open questions

  • Independent Western clinical replication is entirely absent; whether Russian comparison trial results generalize across populations, clinical systems, and regulatory standards is untested.
  • Mechanistic hierarchy for the anxiolytic effect — GABAergic vs serotonergic vs BDNF vs immunomodulatory — is unresolved in the published literature.
  • Long-term safety for chronic daily use beyond 10–14 day approved protocols has not been systematically characterized.
  • Pharmacokinetics, dose-response, and tolerability in non-Russian clinical populations have not been reported.
  • Nootropic benefit in healthy, non-anxious individuals has not been established; all clinical data come from anxiety disorder populations.
  • No FDA or EMA engagement with the Russian clinical evidence package has occurred; no Western regulatory pathway is currently open.

Related peptides

  • Semax — sister peptide from the same Institute of Molecular Genetics program; shares the Pro-Gly-Pro stabilizing tail and BDNF-upregulating and enkephalinase-inhibiting mechanisms; approved in Russia and Ukraine for neurological indications.
Hypotheses6 directions▾ collapse

Research directions for this peptide, selected from the current sources — hypotheses you can explore and model. None of it is proven yet; tap any one to see the full thinking.

openupdated 2026-06-05

If Selank, born from an immune system peptide, still talks to brain immune cells called microglia, could it help conditions where brain inflammation feeds anxiety or memory loss?

If true, one drug might address both the mental symptoms and the hidden immune drivers of brain disease, offering hope for people with treatment-resistant depression or early cognitive decline.

The hypothesis
Selank exerts immunomodulatory effects in the central nervous system that contribute to its neuroprotective and mood-stabilizing properties, possibly by modulating microglial activation states via its tuftsin-derived core.
Why it’s plausible
Tuftsin, the parent peptide, is a known immunostimulant cleaved from IgG. Selank retains the full tuftsin sequence (TKPR) and adds the PGP tail. Neuroinflammation driven by microglial hyperactivation is increasingly implicated in anxiety, depression, and neurodegeneration. If Selank retains tuftsin-like immunomodulatory signaling in the CNS, this could explain neuroprotective annotations and its broader psychotropic profile.
Why it matters
A peptide that simultaneously modulates neuronal GABA signaling and CNS immune tone could represent a novel class of neuro-immunomodulatory therapeutics for neuropsychiatric conditions with inflammatory components.
Plausibility.75
Novelty.55
Impact.75
Basis · grounding3 computed/notes
[1]
noteSelank was built from tuftsin, a short immunomodulatory peptide that the body produces naturally from immunoglobulin G, by adding a stabilizing tail.
[2]
noteTags include immunomodulatory and neuroprotective.
[3]
sequencePositions 1-4 (TKPR) are identical to the natural tuftsin tetrapeptide sequence.
openupdated 2026-06-05

If the Pro-Gly-Pro tail latches onto a blood protein that shields it from being chopped up, could that same trick extend the life of other short peptide medicines?

If true, drug developers could add this simple tail to other fragile peptide drugs, turning 10-minute therapies into ones that last hours and work with simpler dosing.

The hypothesis
The Pro-Gly-Pro C-terminal tail of Selank engages a specific plasma protein or membrane-associated protease that protects the peptide from rapid degradation, and this interaction is pharmacologically relevant to its duration of action.
Why it’s plausible
The PGP tail is explicitly described as conferring plasma durability. In many short peptides, proline-rich termini interact with SH3 domains, profilin, or specific serum protease inhibitors. If Selank's PGP motif binds a serum stabilizing factor, this would explain its unusual pharmacokinetic profile for a 7-mer and could be a generalizable principle for peptide drug design.
Why it matters
Identifying a serum stabilizing partner for the PGP motif would provide a mechanistic basis for engineering plasma-stable peptide therapeutics, extending the half-life of other short bioactive peptides beyond minutes.
Plausibility.60
Novelty.70
Impact.70
Basis · grounding2 computed/notes
[1]
noteThe PGP extension gives Selank meaningful plasma durability after intranasal delivery; it is the same structural motif used in the sister peptide Semax.
[2]
sequenceC-terminal Pro-Gly-Pro (positions 5-7) appended to the tuftsin core Thr-Lys-Pro-Arg (positions 1-4).
openupdated 2026-06-05

If Selank quiets anxiety by tweaking brain calming signals in a different way than Valium or Xanax, could it help people who need long-term relief without addiction risk?

If true, millions of people with chronic anxiety could have a safer daily treatment option, especially those with a history of substance dependence who currently have few alternatives.

The hypothesis
Selank modulates GABA(A) receptor function through an allosteric site distinct from the benzodiazepine binding pocket, producing anxiolysis without the sedative and dependence liabilities of classical benzodiazepines.
Why it’s plausible
The literature notes Selank enhances GABA(A) receptor-mediated chloride currents, yet its clinical profile lacks sedation and physical dependence. This suggests a mechanistic divergence from benzodiazepines, which act at the classical alpha/gamma subunit interface. If Selank binds a different allosteric site or preferentially modulates specific subunit compositions, it could explain the dissociation of anxiolytic from sedative effects.
Why it matters
A non-benzodiazepine GABA(A) modulator with reduced abuse and sedation liability would address a major unmet need in anxiety pharmacotherapy, particularly for chronic use and in populations with substance-use risk.
Plausibility.70
Novelty.40
Impact.70
Basis · grounding2 papers · 1 computed/note
[1]
paper
10.3389/fphar.2017.00089: Selank increases frequency and duration of opening of channels for chlorine ions and enhances the inhibitory effect of GABA by binding to GABA(A) receptors.
doi: 10.3389/fphar.2017.00089
[2]
paper
10.1007/s10517-019-04588-9: Selank fundamentally differs from benzodiazepine tranquilizers, possessing anxiolytic and nootropic properties without the typical benzodiazepine liability profile.
doi: 10.1007/s10517-019-04588-9
[3]
noteSelank does not produce sedation, muscle relaxation, or physical dependence at approved protocol durations, distinguishing it from classical tranquilizers.
openupdated 2026-06-05

If the arginine in Selank is essential for both talking to immune cells and reaching brain targets, would changing it destroy the peptide's unique combined benefits?

If true, scientists would know exactly which part of the molecule to protect when designing improved versions, ensuring future variants keep the full range of effects that make Selank special.

The hypothesis
The arginine at position 4 of Selank is critical for both immunomodulatory activity (via tuftsin receptor engagement) and for cell penetration or membrane association required for CNS activity, making it a dual-function residue that cannot be substituted without losing both arms of the peptide's therapeutic profile.
Why it’s plausible
Tuftsin's biological activity depends on its basic residues, particularly the C-terminal arginine, for receptor binding on macrophages and neutrophils. In Selank, this arginine is preserved at position 4. For CNS peptides, arginine-rich motifs are also common cell-penetrating and membrane-associating elements. If R4 serves both immunomodulatory and CNS delivery/signaling roles, this would explain why the tuftsin core is conserved rather than replaced entirely.
Why it matters
Understanding whether R4 is a structural bottleneck for dual activity would guide rational engineering: either to enhance one activity over the other, or to preserve the unique polypharmacology that may underlie Selank's clinical effects.
Plausibility.55
Novelty.65
Impact.60
Basis · grounding3 computed/notes
[1]
sequenceFull sequence TKPRPGP: arginine at position 4 is the C-terminal residue of the tuftsin core and is highly conserved in natural tuftsin.
[2]
noteSelank retains the complete tuftsin sequence (Thr-Lys-Pro-Arg) and adds only a stabilizing tail, suggesting the core residues are functionally essential.
[3]
noteTags include both immunomodulatory and neuroprotective, implying dual biological activity from the same short sequence.
openupdated 2026-06-05

If Selank reduces anxiety without the addiction risk of current tranquilizers, could it become a standard support tool for people fighting alcohol dependence?

If true, people recovering from alcohol addiction would have a safer way to manage the anxiety that often drives them back to drinking, potentially improving long-term sobriety rates.

The hypothesis
Selank could be repurposed as an adjunct therapy in alcohol use disorder to reduce anxiety-driven relapse, leveraging its anxiolytic mechanism without the reinforcement and dependence risks of benzodiazepines currently used in alcoholism pharmacotherapy.
Why it’s plausible
The literature explicitly mentions Selank in the context of alcoholism pharmacotherapy, contrasting it with benzodiazepines. Anxiety is a major trigger for alcohol relapse, yet benzodiazepines are contraindicated in this population due to cross-tolerance and abuse liability. A non-sedating, non-dependent anxiolytic would fill a critical therapeutic gap.
Why it matters
Alcohol use disorder has few effective pharmacotherapies, and anxiety management in recovering patients is a persistent challenge. A safe anxiolytic adjunct could reduce relapse rates and improve long-term recovery outcomes.
Plausibility.65
Novelty.40
Impact.70
Basis · grounding1 paper · 1 computed/note
[1]
paper
10.1007/s10517-019-04588-9: Positive effects of Selank in patients with alcoholism, fundamentally differing from benzodiazepine tranquilizers commonly used for the pharmacotherapy of alcoholism.
doi: 10.1007/s10517-019-04588-9
[2]
noteSelank does not produce physical dependence at approved protocol durations, a key liability of benzodiazepines in substance-use populations.
openupdated 2026-06-05

If Selank selectively affects the anxiety-related subtypes of brain calming receptors while leaving memory-related ones alone, could it outperform current anxiety drugs that cloud thinking?

If true, patients could get genuine anxiety relief while staying mentally sharp, avoiding the grogginess and forgetfulness that cause many people to quit their current medications.

The hypothesis
Selank preferentially modulates GABA(A) receptors containing alpha2 or alpha3 subunits over alpha1-containing receptors, accounting for its anxiolytic efficacy without the sedation and amnesia typical of non-selective benzodiazepines.
Why it’s plausible
Benzodiazepine sedation and dependence are linked to alpha1 subunit modulation, while anxiolysis maps more to alpha2/alpha3. If Selank's allosteric modulation is subunit-selective, this would mechanistically explain its dissociated clinical profile. The structure prediction shows moderate confidence (pLDDT 64.7) in a complex, suggesting the interaction may involve specific interfaces rather than broad binding.
Why it matters
Subunit-selective GABA(A) modulation is a long-standing goal in psychopharmacology. A small peptide achieving this selectivity would challenge the assumption that only large small molecules or biologics can achieve such discrimination.
Plausibility.50
Novelty.60
Impact.75
Basis · grounding1 paper · 2 computed/notes
[1]
paper
10.3389/fphar.2017.00089: Selank enhances GABA(A) receptor-mediated chloride currents, yet clinical reports describe it as fundamentally different from benzodiazepines.
doi: 10.3389/fphar.2017.00089
[2]
structureOpenFold3-MLX complex pLDDT=64.7, ipTM=0.848: moderate structural confidence suggesting a defined but possibly specific binding interface rather than promiscuous interaction.
[3]
noteSelank lacks sedation, muscle relaxation, and physical dependence at approved durations, properties that distinguish it from classical benzodiazepines.
details expand to inspect
full evidence table2 metrics
metricvaluetool
ipTM 0.8483461737632751 openfold3-mlx
ranking score 0.9008271098136902 openfold3-mlx
structural qualityopenfold3
0
metricvaluenote
gpde0.423global PDE — lower = better
disorder0.096fraction disordered
chain pair ipTM (A, B)0.848interface quality
3-letter notation
Thr-Lys-Pro-Arg-Pro-Gly-Pro
recipeopenfold3-mlx 0.3.1
parametervalue
modelopenfold3-mlx 0.3.1
weightsaedd8f3eb814e392…
hardwareapple_m4_base_16gb
mlx version0.31.1
python3.14.3
random seed42
msa strategycolabfold
diffusion samples1
runtime79s
predicted bymlx@peptide
predicted at2026-05-03
python3 openfold3/run_openfold.py predict --query_json {query.json} --runner_yaml examples/example_runner_yamls/mlx_runner.yml --output_dir {output_dir} --num_diffusion_samples 1
citationbibtex
peptidemodel (2026). Selank: Russia-approved anxiety & mood peptide (TKPRPGP) (pep-00006, v1). PeptideModel. https://peptidemodel.com/card/pep-00006
@peptide{pep00006,
  sequence = {TKPRPGP},
  target   = {neuroprotective},
  author   = {peptidemodel},
  year     = {2026},
  status   = {bioassayed}
}
clinical trials 10 on ct.gov · checked 2026-05-09
ct.gov trials 10
with results 3
PubMed RCT 2
by phase
2phase 38no phase
by status
8completed2unknown
references 22 papers
[1]
The anxiolytic-like action of selank
Kozlovskii, I.I. et al. Bull Exp Biol Med 2006
source scaffold
[2]
Selank effects on behavioral responses and brain monoamine systems
Semenova, T.P. et al. Bulletin of Experimental Biology and Medicine 2010
synthesis
[4] independent reproduction
[7]
The Influence of Selank on the Level of Cytokines Under the Conditions of “Social” Stress
Leonidovna, Y. et al. Current Reviews in Clinical and Experimental Pharmacology 2021
supporting
[14]
Optimization of the treatment of anxiety disorders with selank
Medvedev, V. et al. Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 2015
supporting
[17] supporting
[18] supporting
[20] supporting
discussion no comments
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