Selank
Also known as: Selanc, TP-7, Thr-Lys-Pro-Arg-Pro-Gly-Pro
4 notable studies · 4 references
TLDR
Selank is a synthetic tuftsin-derived heptapeptide studied primarily for anxiety and neuroregulation, with human clinical research suggesting anxiolytic activity and extensive mechanistic and animal evidence involving GABA, enkephalins, monoamines, and gene expression, but modern independently replicated human evidence remains limited.
Research Supports
- Studied for anxiolytic activity, including Russian clinical research in anxiety-related disorders
- Investigated for GABA receptor modulation, possibly as a positive allosteric modulator
- Examined for effects on enkephalin-degrading enzymes and endogenous opioid signaling
- Studied in animal models of learning, memory, and attention
- Investigated for changes in hippocampal gene expression
Observations Reported in Research
- Dose-dependently inhibited enkephalin-degrading enzymes in plasma (Kost et al., 2001)
- Both Selank and Semax inhibited enkephalin-degrading enzymes in human serum (Kost et al., 2001)
- Modified radiolabeled GABA binding consistent with positive allosteric modulation (2018)
- Altered expression of 36 genes by more than twofold after a single dose, and 20 after repeated dosing, in rat hippocampus (2014)
These are brief summaries of what the referenced research examined or reported — not conclusions about safety or effectiveness, and not medical advice. See Notable Studies and Sources & References below for the full context and citations.
At a Glance
Classification: Synthetic heptapeptide; tuftsin analogue; glyproline peptide; experimental anxiolytic/neuropeptide
Selank is a synthetic seven-amino-acid peptide: Thr-Lys-Pro-Arg-Pro-Gly-Pro. It was developed from tuftsin, an endogenous immunomodulatory tetrapeptide with the sequence Thr-Lys-Pro-Arg. Researchers added the glyproline sequence Pro-Gly-Pro, producing Selank. It is primarily associated with research involving anxiety, stress responses, GABA signaling, enkephalins, learning and memory, neurotransmitter regulation, gene expression, and immune-neural interactions. Selank has a far more substantial Russian research history than its status as a Western “research peptide” might suggest. Much of the human clinical literature is older, Russian-language, difficult to independently evaluate, and not comparable with the large multinational regulatory programs used to establish modern psychiatric medications. “Selank has no human research” is wrong. But “Selank is a clinically proven replacement for benzodiazepines” goes much too far.
What Is Selank?
Selank is a synthetic analogue of the endogenous peptide tuftsin. Tuftsin corresponds to the sequence Thr-Lys-Pro-Arg. Selank extends that sequence with Pro-Gly-Pro, producing Thr-Lys-Pro-Arg-Pro-Gly-Pro. The glyproline portion was incorporated partly to influence peptide stability and biological activity. Selank was developed primarily as an anxiolytic peptide and has subsequently been investigated for effects on cognition, neurotransmitter systems, gene expression, and immune function. Its pharmacology does not resemble a simple benzodiazepine-like direct receptor agonist. Research suggests more complex modulation of several neural systems.
What Are Researchers Studying?
Anxiety
Anxiety is Selank's defining research area. Russian clinical-development literature describes anxiolytic effects in people with anxiety-related disorders, while animal models have repeatedly reported reduced anxiety-like behavior. The peptide has often been investigated as a potential anxiolytic that might avoid some problems associated with conventional sedatives. The quality and international reproducibility of the human evidence remain major limitations. Human anxiolytic research exists, but modern high-quality confirmatory evidence is limited.
GABA signaling
One proposed Selank mechanism involves the GABAergic system. Research has reported that Selank can modify binding involving GABA receptors and may act as a positive allosteric modulator in experimental systems. This could potentially contribute to anxiolytic effects. It does not mean Selank is simply a peptide benzodiazepine. Its molecular effects appear broader and considerably less well characterized.
Enkephalins and endogenous opioid signaling
Selank has been shown experimentally to inhibit enzymes responsible for breaking down enkephalins, endogenous opioid peptides involved in pain, stress, reward, and emotional regulation. One study found dose-dependent inhibition of plasma enkephalin hydrolysis. Related research found both Selank and Semax inhibited enkephalin-degrading enzymes in human serum. This provides another possible mechanism for Selank's behavioral effects. It does not establish that Selank acts like a conventional opioid.
Learning and memory
Selank has been investigated in animal models of learning, memory formation, attention, cognitive impairment, and stress-related cognitive disruption. In rats exposed to antenatal hypoxia, Selank improved several measures of attention and learning while altering serotonin and noradrenaline balance. Other experiments reported protective effects in pharmacologically induced memory impairment. These are interesting preclinical findings, but evidence that Selank improves cognition in healthy humans remains much weaker.
Gene expression
One of the more unusual Selank research areas involves changes in gene transcription. A rat hippocampus study found that a single administration altered expression of 36 genes by more than twofold, while repeated administration altered 20 genes by more than twofold. Many affected genes encoded membrane-associated proteins. This has led researchers to propose that some longer-lasting Selank effects may involve changes in transcription rather than only immediate receptor signaling. Gene-expression change ≠ demonstrated cognitive enhancement.
Serotonin and noradrenaline
Animal studies have reported effects involving serotonergic and noradrenergic systems. In rats exposed to prenatal hypoxia, Selank altered brain serotonin and noradrenaline measures alongside behavioral changes. This suggests that Selank's pharmacology may extend beyond GABA.
Immune-neural signaling
Because Selank is derived from tuftsin, which itself has immunological activity, researchers have also investigated possible immune effects. This makes Selank interesting as part of the broader field examining communication between immune signaling, neuropeptides, and brain function. The evidence remains primarily mechanistic and preclinical.
How Does It Work?
There is no single established Selank mechanism. Current hypotheses include: GABAergic modulation: Experimental evidence suggests modulation of GABA receptor binding. Enkephalin preservation: Selank inhibits enzymes that degrade endogenous enkephalins. Monoamine regulation: Animal experiments suggest effects involving serotonin and noradrenaline. Gene-expression changes: Selank alters hippocampal transcription in animal models. Immune signaling: Its structural relationship to tuftsin provides a plausible connection to immune-neural regulation. Selank’s anxiolytic effects cannot currently be reduced confidently to one receptor or neurotransmitter.
What Does the Research Show?
Human research
Human research exists, particularly from Russia and the former Soviet research ecosystem. Clinical literature describes Selank in anxiety and related neuropsychiatric conditions, and some publications characterize it as having completed advanced clinical evaluation in Russia. A 2008 paper described Selank as having completed Phase III clinical testing as a selective anxiolytic. Evidence-quality limitations: many reports are Russian-language; some are difficult to access in full; sample sizes are often modest; trial reporting frequently predates modern CONSORT standards; independent international replication is limited; there are few large contemporary multicenter trials. Human evidence exists. Confidence should remain below that assigned to established FDA/EMA psychiatric drugs.
Animal research
Animal studies have examined anxiety-like behavior, depression-like behavior, learning, memory, attention, prenatal hypoxia, neurotransmitters, stroke models, gastric injury, and immune signaling. In rats exposed to antenatal hypoxia, Selank improved sensory attention and learning alongside normalization of serotonergic/noradrenergic balance. Other rodent studies investigated depression-like behavior.
In-vitro research
Laboratory studies have examined GABA receptor binding, enkephalin-degrading enzymes, peptidases, blood coagulation, and gene-expression mechanisms. Both Selank and Semax inhibited enkephalin-degrading enzymes in human serum. Experimental work has also found anticoagulant activity among glyproline peptides including Selank. The clinical significance of that observation is uncertain.
Notable Studies
The Inhibitory Effect of Selank on Enkephalin-Degrading Enzymes as a Possible Mechanism of Its Anxiolytic Activity
in-vitroSelank dose-dependently inhibited enzymatic degradation of enkephalins in plasma, suggesting preservation of endogenous opioid peptides as one possible mechanism contributing to its behavioral effects.
Limitations: Enzyme inhibition in vitro does not establish that this mechanism explains clinical anxiolytic effects in humans.
View publication →Semax and Selank Inhibit the Enkephalin-Degrading Enzymes from Human Serum
in-vitroBoth Selank and Semax produced dose-dependent inhibition of enzymes involved in enkephalin degradation.
Limitations: Human serum was used experimentally, but this was not a clinical administration study in humans.
View publication →Peptide-Based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity
in-vitroResearchers examined GABA-related mechanisms and reported that Selank modified radiolabeled GABA binding in a manner consistent with positive allosteric modulation.
Limitations: Receptor-binding experiments do not establish comparative clinical efficacy or safety versus established anxiolytics.
View publication →Transcriptome Alteration in Hippocampus Under the Treatment of Tuftsin Analog Selank
animalResearchers examined hippocampal gene expression following single and repeated Selank administration. Thirty-six genes changed by more than twofold following a single exposure and 20 following repeated administration.
Limitations: Gene-expression changes in rat hippocampus do not establish improved cognition, reduced anxiety, or therapeutic benefit in humans.
View publication →What We Still Don't Know
Effect size for anxiety in modern randomized human trials Comparative efficacy versus SSRIs, SNRIs, buspirone, or benzodiazepines Long-term human safety Dependence and withdrawal characteristics Human pharmacokinetics Optimal route of administration Actual CNS exposure after different administration routes Dose-response relationships in humans Whether cognitive effects translate to healthy people Which proposed mechanism matters most Clinical significance of gene-expression effects Clinical significance of anticoagulant findings Whether Russian clinical findings reproduce in independent international trials Whether commercially sold research Selank is chemically equivalent to material used in published studies
Related Compounds
Recent publications
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Sources & References
- The Inhibitory Effect of Selank on Enkephalin-Degrading Enzymes as a Possible Mechanism of Its Anxiolytic Activity.
- Semax and Selank Inhibit the Enkephalin-Degrading Enzymes from Human Serum.
- Peptide-Based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity.
- Transcriptome Alteration in Hippocampus Under the Treatment of Tuftsin Analog Selank.
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