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Selank

A synthetic heptapeptide that extends the tuftsin sequence with a C-terminal Pro-Gly-Pro tripeptide, studied in radioligand binding on isolated brain membranes, hippocampal slice electrophysiology, neuroblastoma gene panels and analytical identification work.

For in-vitro research only.Reviewed 2026-09-20

Key findings

  • In a neuroblastoma IMR-32 culture screened across 84 genes of the GABAergic and neurotransmission panel, the peptide alone produced no change in the measured mRNA levels, while combined exposures with GABA or with olanzapine gave different patterns. [1]
  • Radioligand work on isolated brain cell plasma membranes reported the peptide acting on tritiated GABA binding as a positive allosteric modulator, and its joint action with benzodiazepines was not additive. [2]
  • Applied to rat hippocampal slices the peptide raised the amplitude and discharge rate of spontaneous inhibitory postsynaptic currents in CA1 pyramidal neurons, with no significant concentration dependence across the range tested. [3]
  • Thromboelastography of whole blood placed the heptapeptide among arginine containing glyproline oligopeptides that shifted clotting parameters toward hypocoagulation, and it showed the strongest shift of the three tested sequences. [4]

Identity and structure

Sequence
Thr-Lys-Pro-Arg-Pro-Gly-Pro [2][4]
Origin
The tuftsin tetrapeptide extended at the C terminus by a Pro-Gly-Pro tripeptide, placing it in the glyproline family [2][4]
Identification method in cited work
Liquid chromatography with tandem mass spectrometry, validated in several matrices against the General European Official Medicines Control Laboratory network screening recommendation [5]
Form as supplied
Sterile lyophilized powder

Mechanism as studied

The binding evidence points to allosteric modulation rather than direct occupancy of the orthosteric site. On isolated brain cell plasma membranes the peptide changed tritiated GABA binding in a concentration dependent and subtype selective way, and it blocked the modulatory activity of diazepam and olanzapine, which the authors read as partly overlapping but non-identical binding sites. [2]

Slice electrophysiology is consistent with an effect on inhibitory transmission rather than on transcription. Spontaneous inhibitory postsynaptic currents in CA1 pyramidal neurons rose in amplitude and rate, in some neurons after a transient decrease, while the neuroblastoma panel found no mRNA change from the peptide alone. [3][1]

Research findings

In vitro
System
Neuroblastoma IMR-32 cell culture, with GABA, olanzapine and the combinations of each with the peptide tested alongside it
Measured
Expression of 84 genes of the GABAergic system and neurotransmission by quantitative PCR
Reported
No change was found in the mRNA levels of the studied genes under the peptide alone. GABA together with the peptide nearly abolished the expression changes GABA produced on its own, and the peptide together with olanzapine altered more genes than olanzapine alone. [1]
Ex vivo
System
Isolated plasma membranes from brain cells, with peptide purity confirmed by HPLC before use
Measured
Tritiated GABA binding by the radioligand receptor method, alone and jointly with benzodiazepines, diazepam and olanzapine, with membrane protein concentration determined for normalization
Reported
The peptide acted on tritiated GABA binding as a positive allosteric modulator. Its joint action with benzodiazepines was not cumulative and differed from either substance alone, and it blocked the modulatory activity of diazepam and olanzapine, which the authors interpret as binding sites that may partly overlap without being the same. [2]
Ex vivo
System
Rat hippocampal slices, CA1 pyramidal neurons
Measured
Amplitude and discharge rate of spontaneous inhibitory postsynaptic currents across a 1 to 8 µM concentration range
Reported
Amplitude and discharge rate increased, in some neurons after a transient decrease in the same activity, and the effect showed no significant concentration dependence across the range tested. [3]
Preclinical in vivo
System
Frontal cortex of rats sampled 1 h and 3 h after exposure to the peptide or to GABA
Measured
Expression of 84 neurotransmission genes including a major GABA receptor subunit, transporters, ion channels and dopamine and serotonin receptors, by real-time PCR
Reported
Expression of 45 genes changed significantly at 1 h and 22 genes at 3 h. The 1 h changes under the peptide correlated positively with those under GABA, which the authors read as a complex effect on nerve cells consistent with allosteric modulation of the GABAergic system. [6]
In vitro
System
Whole blood in thromboelastography, comparing the heptapeptide with His-Phe-Arg-Trp-Pro-Gly-Pro and with Pro-Gly-Pro at several concentrations
Measured
Thromboelastography parameters R, K, MA, S, TMA and J
Reported
All three glyproline oligopeptides moved the measured parameters toward hypocoagulation relative to control, and the heptapeptide showed the largest shift of the three. [4]
In vitro
System
Mouse embryonic stem cells and their derivatives, testing this peptide alongside Semax, thyroliberin, HLDF-6, Pro-Gly-Pro, Arg-Pro-Gly-Pro and Pro-Gly-Leu-Pro rather than this peptide alone
Measured
Proliferative activity, survival under serum deprivation, formation of neuronal precursors, differentiation into mature neurons and the proportion of GABA positive neurons
Reported
The peptide had an insignificant effect on differentiation into mature neurons and little effect on neuronal precursor formation. It lowered the proportion of GABA positive neurons by 61 percent relative to control, alongside 58 percent for thyroliberin and 87 percent for nerve growth factor in the same comparison. [7]
Analytical
System
Two seized pharmaceutical preparations and a panel of 10 polypeptides sold online, of which this peptide was one
Measured
Identity by a combined liquid chromatography tandem mass spectrometry method, validated in different matrices under ISO 17025
Reported
The seized preparations were identified as containing this heptapeptide and Semax. The authors note that neither peptide had completed a clinical trial and that the material circulates both as lyophilized powder and in ready-made preparations. [5]
Order Selank with the certificate for the lot that ships

Handling for in-vitro work

Purity check in cited work
Peptide purity was confirmed by HPLC before the membrane binding experiments [2]
Storage
Lyophilized at -20 °C, dark and dry; reconstituted aliquots kept cold and used promptly

Open questions

  • The null result in IMR-32 cells and the binding result on isolated membranes are not in conflict, but the cited work does not identify which cell type carries the modulated site.
  • The site that distinguishes this peptide from diazepam and olanzapine is inferred from competition, not resolved structurally, in the cited work.
  • Whether the slice electrophysiology result reproduces in a human derived neuronal preparation is not addressed by the cited studies.
  • Evidence for this peptide alone does not characterize a mixture that also contains Semax.

A clinical literature on this sequence exists and concerns finished formulations; it is out of scope for a research material profile.

Lot records

Check the record for the exact material you order. A published paper and a batch certificate answer different questions.

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References

  1. 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.

    PubMed 28293190 · doi:10.3389/fphar.2017.00089

  2. Vyunova TV, Andreeva L, Shevchenko K, et al. Peptide-based Anxiolytics: The Molecular Aspects of Heptapeptide Selank Biological Activity. Protein and peptide letters. 2018.

    PubMed 30255741 · doi:10.2174/0929866525666180925144642

  3. Povarov IS, Kondratenko RV, Derevyagin VI, et al. Effect of Selank on Spontaneous Synaptic Activity of Rat Hippocampal CA1 Neurons. Bulletin of experimental biology and medicine. 2017.

    PubMed 28361410 · doi:10.1007/s10517-017-3676-3

  4. Rogozinskaya EY, Lyapina MG Anticoagulant Effects of Arginine-Containing Peptides of the Glyproline Family (His-Phe-Arg-Trp-Pro-Gly-Pro and Thr-Lys-Pro-Arg-Pro-Gly-Pro) Revealed by Thromboelastography. Bulletin of experimental biology and medicine. 2017.

    PubMed 29181670 · doi:10.1007/s10517-017-3950-4

  5. Vanhee C, Francotte A, Janvier S, et al. The occurrence of putative cognitive enhancing research peptides in seized pharmaceutical preparations: An incentive for controlling agencies to prepare for future encounters of the kind. Drug testing and analysis. 2020.

    PubMed 31667971 · doi:10.1002/dta.2717

  6. Volkova A, Shadrina M, Kolomin T, et al. Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission. Frontiers in pharmacology. 2016.

    PubMed 26924987 · doi:10.3389/fphar.2016.00031

  7. Kobylyanskii AG, Zolotarev YA, Andreeva LA, et al. Studying the Toxic Effects of Some Biologically Active Peptides on the Model of Mouse Embryonic Stem Cells. Bulletin of experimental biology and medicine. 2017.

    PubMed 29063333 · doi:10.1007/s10517-017-3891-y

Publication records fetched from PubMed on 2026-09-20. Profile text reviewed 2026-09-20.