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For research use only. Not for human consumption.

SELANK 10MG research vial, 3rd Rock Compounds

Front label

Cognitive | Research use only

SELANK 10MG

Selank (TP-7) is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro) derived from the endogenous tetrapeptide tuftsin, a natural fragment of the heavy chain of human immunoglobulin G (IgG).

$55

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Quantity

SELANK 10MG

1 vial · $55

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  • Shipping 2–4 business days

Identifiers

CAS number
129954-34-3
Molecular formula
C₃₃H₅₇N₁₁O₉
Molecular weight
751.887 Da
Sequence
TKPRPGP

Mechanism of Action

Dual Mechanism: GABA-A Modulation + Enkephalinase Inhibition

Selank possesses a unique dual mechanism of action distinguishing it from classical anxiolytics:

1. GABA-A Receptor Positive Allosteric Modulation

Selank acts as a positive allosteric modulator (PAM) of the GABA-A receptor. Its binding site is distinct from the classical benzodiazepine site, though partial overlap may exist.[8] This modulation enhances the affinity of the receptor for GABA, increasing inhibitory neurotransmission without producing sedation, amnesia, or muscle relaxation.[5]

Selank administration significantly alters mRNA levels of GABA receptor subunits — Gabrb3, Gabre (epsilon), and Gabrq (theta) — as well as the GABA transporter Slc6a13 (GAT-2) in the frontal cortex. Dramatically, Gabre and Gabrq decreased approximately 20-fold at 1 hour, while Hcrt (orexin/hypocretin) decreased 25-fold then surged 128-fold by 3 hours.[9] This orexin rebound is hypothesized to explain the absence of sedation typical of benzodiazepines.

2. Enkephalinase Inhibition

Selank competitively inhibits enzymes responsible for the degradation of enkephalins (endogenous opioid peptides), including aminopeptidases, carboxypeptidase H, and angiotensin-converting enzyme (ACE). The inhibitory effect has an IC50 of approximately 15–20 μM in human serum assays.[10] This extends the half-life of Leu-enkephalin, potentiating the body's natural stress-limiting and analgesic pathways.[11]

BDNF/TrkB Signaling

Selank rapidly elevates expression of Brain-Derived Neurotrophic Factor (BDNF) and its receptor TrkB. An increase in Bdnf mRNA is observed in the hippocampus as early as 90 minutes, with protein levels increasing by 24 hours.[12]

Monoamine Neurotransmitter Modulation

Selank induces region-specific changes in monoamine metabolism:

  • Serotonin: Increased 5-HIAA (metabolite) in hypothalamus and brainstem within 30 minutes to 2 hours[13]
  • Norepinephrine: Increased in the hypothalamus[13]
  • Dopamine: Strain-dependent — decreased metabolites in high-anxiety (BALB/c) mice, increased in low-anxiety (C57BL/6) mice[13]

Immunomodulation

Selank modulates IL-6 expression, normalizes the Th1/Th2 cytokine balance, and induces interferon-alpha (IFN-α) secretion.[14]

Receptor Selectivity

Importantly, radioreceptor assays show that Selank does not directly displace ligands from benzodiazepine, dopamine (D2), serotonin (5-HT2), or opioid (μ, δ) receptors. Its effects on these systems are downstream or allosteric.[8] However, the opioid antagonist naloxone blocks Selank's anxiolytic effects, confirming the enkephalin system's involvement.[15]

Preclinical Research Findings

In laboratory research, Selank is investigated in multiple experimental paradigms:

  1. Anxiety and Generalized Anxiety Models — Registered in the Russian Federation for research related to generalized anxiety disorders and neurasthenia. Experimental readouts demonstrate anxiolytic effects comparable to benzodiazepines without sedation, dependence, or withdrawal.[5][6]
  2. Cognitive Enhancement / Nootropic Paradigms — Studied for effects on memory consolidation and learning. A single injection increased memory trace stability for up to 30 days via serotonin metabolism activation.[13]
  3. Alcohol Withdrawal Models — Eliminated withdrawal-induced anxiety (EPM open arm time p<0.01), prevented mechanical allodynia, and regulated BDNF content in hippocampus and prefrontal cortex.[16]
  4. Opioid Withdrawal Models — Reduced mean morphine withdrawal index by 39.6%, significantly attenuating convulsive reactions, ptosis, and posture disorders (p<0.0001). Increased tactile sensitivity threshold 9-fold.[17]
  5. Immunomodulation and Antiviral Activity — Demonstrated antiviral effects against Influenza A (H3N2) both in vivo and in vitro. Induced IFN-α secretion and normalized Th1/Th2 cytokine balance.[14]
  6. Gene Expression Modulation — Administration altered expression of 45 genes at 1 hour in frontal cortex, including GABAergic receptor subunits and orexin/hypocretin (128-fold rebound at 3 hours).[9]
  7. Gastric Protection Models — Exhibited protective effects against stress- and ethanol-induced gastric mucosal injury, increasing mucosal resistance to ulcerogenic factors.[2]
  8. Gut Microbiota and Stress — Prevented stress-induced decreases in obligate microflora, reduced corticosterone levels, and attenuated colon wall pathomorphological changes.[18]
  9. BDNF/TrkB Signaling Investigation — Investigated for its capacity to up-regulate hippocampal Bdnf transcription and TrkB-receptor expression as a potential mechanism for memory-trace persistence beyond the compound's plasma residence time.[12][20]
  10. Cytokine Network Profiling — Examined for selective IL-6 suppression and Th1/Th2 normalization in stress-loaded animal models, situating it within a broader research interest in peptide-mediated neuroimmune crosstalk.[14][23]

Comparative Research Context

Within the regulatory-peptide research literature, Selank is most often paired with Semax for comparative GABAergic versus melanocortinergic CNS pharmacology, with DSIP for divergent stress-axis modulation, and with oxytocin for anxiolytic activity through non-benzodiazepine receptor systems. These cross-comparisons inform research designs investigating the molecular boundary between sedating and nonsedating anxiolytic mechanisms.[2]

Safety Profile

Findings summarised above derive from in-vitro and animal studies. No safety profile for human use is established or implied, and none is offered here.

Handle as a laboratory reagent: avoid inhalation and contact, reconstitute under aseptic conditions, and observe the storage conditions below.

For research use only. Not for human consumption.

Shipping and Storage

  • Supplied as lyophilised powder in a sealed vial.
  • Store at 2–8°C (36–46°F). Protect from light.
  • Same-day fulfilment on orders before 2pm; shipping 2–4 business days.
  • For research use only. Not for human consumption.

References

  1. [1]Kolomin TA, Shadrina M, Slominsky P, Limborska SA, Myasoedov NF. A New Generation of Drugs: Synthetic Peptides Based on Natural Regulatory Peptides. Neuroscience & Medicine. 2013;4(4):223–252. DOI →
  2. [2]Vyunova TV, Andreeva LA, Shevchenko KV, Myasoedov NF. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein & Peptide Letters. 2018;25(10):914–923.
  3. [3]Medvedev VE, Tereshchenko ON, Kost NV, et al. Optimization of the treatment of anxiety disorders with selank. Zhurnal Nevrologii i Psikhiatrii. 2015;115(6):33–40. PubMed →
  4. [4]U.S. Food and Drug Administration. Bulk Drug Substances Used in Compounding Under Section 503B. FDA Compounding Database. 2023. fda.gov →
  5. [5]Zozulya AA, Neznamov GG, Syunyakov TS, et al. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia. Zhurnal Nevropatologii i Psikhiatrii. 2008;108(4):38–48.
  6. [6]Kozlovskii II, Danchev ND. The optimizing action of the synthetic peptide Selank on a conditioned active avoidance reflex in rats. Neuroscience and Behavioral Physiology. 2003;33(7):639–643.
  7. [7]Kolomin TA, Agapova T, Agniullin YV, et al. Changes in the Transcription Profile of the Hippocampus in Response to Administration of the Tuftsin Analog Selank. Neuroscience and Behavioral Physiology. 2014;44(8):849–855. DOI →
  8. [8]V'yunova TV, Andreeva LA, Shevchenko KV, et al. Peptide regulation of specific ligand-receptor interactions of GABA with the plasma membranes of nerve cells. Neurochemical Journal. 2014;8(4):259–264. DOI →
  9. [9]Volkova A, Shadrina M, Kolomin T, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Frontiers in Pharmacology. 2016;7:31.
  10. [10]Kost NV, Sokolov OY, Gabaeva MV, et al. Semax and Selank Inhibit the Enkephalin-Degrading Enzymes of Human Serum. Russian Journal of Bioorganic Chemistry. 2001;27(3):180–183. DOI →
  11. [11]Zozulya AA, Kost NV, Sokolov OY, et al. The Inhibitory Effect of Selank on Enkephalin-Degrading Enzymes as a Possible Mechanism of Its Anxiolytic Activity. Bull Exp Biol Med. 2001;131(4):315–317.
  12. [12]Inozemtseva LS, Karpenko EA, Dolotov OV, et al. Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo. Doklady Biological Sciences. 2008;421:241–243.
  13. [13]Narkevich VB, Kudrin VS, Klodt PM, et al. Effects of Selank on monoamine neurotransmitters in the brain of BALB/c and C57BL/6 mice. Bull Exp Biol Med. 2008;145(1):68–71.
  14. [14]Uchakina ON, Uchakin PN, Miasoedov NF, et al. Immunomodulatory effects of selank in patients with anxiety-asthenic disorders. Zhurnal Nevrologii i Psikhiatrii. 2008;108(5):71–75. PubMed →
  15. [15]Kozlovskii II, Andreeva LA, Kozlovskaya MM. The role of the endogenous opioid system in the anxiolytic action of Selank. Bull Exp Biol Med. 2012;153(5):728–730.
  16. [16]Kolik LG, Nadorova AV, Kozlovskaya MM. Efficacy of Peptide Anxiolytic Selank during Modeling of Withdrawal Syndrome in Rats with Stable Alcoholic Motivation. Bull Exp Biol Med. 2014;157(1):61–65.
  17. [17]Konstantinopolsky MA, Kolik LG, Chernyakova IV. Selank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats. Bull Exp Biol Med. 2022;173(6):730–733.
  18. [18]Mukhina AY, et al. Effects of Selank on intestinal microbiota and stress-induced changes. Russian Journal of Physiology. 2019/2020.
  19. [19]Kasian A, Kolomin T, Andreeva L, et al. Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats. Behavioural Neurology. 2017;2017:5091027.
  20. [20]Kolik LG, Nadorova AV, Antipova TA, Durnev AD. Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content. Bull Exp Biol Med. 2019;167(5):641–644.
  21. [21]Medvedev VE, Tereshchenko ON, Israelian AI, et al. A comparison of the anxiolytic effect and tolerability of selank and phenazepam. Zhurnal Nevrologii i Psikhiatrii. 2014;114(7):17–22.
  22. [22]Semenova TP, Kozlovskii II, Zakharova NM, Kozlovskaya MM. Experimental optimization of learning and memory processes by selank. Eksperimental'naia i Klinicheskaia Farmakologiia. 2010;73(8):2–5. PubMed →
  23. [23]Filatova E, Kasian A, Kolomin T, et al. GABA, Selank, and Olanzapine Affect the Expression of Genes Involved in GABAergic Neurotransmission in IMR-32 Cells. Frontiers in Pharmacology. 2017;8:89.
  24. [24]Kolomin TA, Shadrina M, Andreeva LA, et al. Expression of inflammation-related genes in mouse spleen under tuftsin analog Selank. Regulatory Peptides. 2011;170(1-3):18–23.
  25. [25]Andreeva LA, Nagaev IY, Mezentseva MV, et al. Antiviral properties of structural fragments of the peptide Selank. Doklady Biological Sciences. 2010;431:79–82.

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