Selank

What Is Selank?

Selank is a synthetic heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro, described in research as an analog of the endogenous immunomodulatory peptide tuftsin and studied mainly for anxiolytic activity. Its first four residues match tuftsin, and a C-terminal Pro-Gly-Pro tripeptide is added.^[1][2]

Published papers characterize Selank as a peptide anxiolytic and report that clinical studies have shown a spectrum of effects similar to that of classical benzodiazepines such as diazepam and phenazepam. That observation has driven much of the laboratory work on how Selank interacts with the GABA system.^[3][4]

Most of the indexed research consists of rat studies of stress, anxiety, memory and withdrawal, plus gene-expression experiments in rat brain and human neuroblastoma cells. A 2026 review of therapeutic peptides grouped Selank with other neuroactive peptides and noted a general lack of clinical trials for this class.^[5]

Chemical Structure and Molecular Identity

Selank is a linear seven-residue peptide, TKPRPGP, with a free N-terminal amine and a free C-terminal carboxylic acid. PubChem lists it under CID 11765600 with the molecular formula C33H57N11O9 and a molecular weight of 751.9 g/mol.

The Thr-Lys-Pro-Arg segment corresponds to tuftsin, and the Pro-Gly-Pro extension places Selank among the glyprolines; one rat study refers to it as a glyproline neuropeptide.^[6] Semax ends in the same Pro-Gly-Pro motif, and a 2006 study compared Selank, Semax and other glyprolines as regulatory proline-containing oligopeptides with effects on blood coagulation.^[7]

Key identifiers

• InChIKey: JTDTXGMXNXBGBZ-YVHUGQOKSA-N
• CAS number: 129954-34-3
• UNII: TS9JR8EP1G
• Synonyms: TP-7; Selanc; threonyl-lysyl-prolyl-arginyl-prolyl-glycyl-proline

With lysine and arginine side chains and three proline residues, Selank is basic and highly polar. PubChem’s computed XLogP of -6.1 and topological polar surface area of 322 are consistent with a water-soluble short peptide. Its formula contains no sulfur, which distinguishes it from methionine-containing Semax in elemental and mass spectrometric analysis.

Research History and Development

Selank was designed by extending the tuftsin sequence with Pro-Gly-Pro, and its research record centers on anxiety and stress models. The indexed literature runs from 2006 comparative work on proline-containing peptides to studies published in the 2020s.^[7][1]

Several lines of work stand out:

• GABAergic mechanism studies (2016 to 2017): gene-expression profiling in rat frontal cortex and in IMR-32 neuroblastoma cells, and a behavioral study combining Selank with diazepam.^[3][4][8]
• Stress models (2019 to 2021): chronic foot-shock stress with liver morphology, and male confrontation (“social”) stress with serum cytokines.^[9][6]
• Memory and dependence models (2019 to 2022): chronic ethanol exposure with hippocampal and cortical BDNF, and naloxone-precipitated morphine withdrawal.^[2][1]
• Human imaging (2020): a resting-state fMRI study in healthy participants comparing Selank, Semax and placebo.^[10]

Much of this work appears in Russian journals such as the Bulletin of Experimental Biology and Medicine and Doklady Biological Sciences, alongside papers in Frontiers in Pharmacology and Behavioural Neurology.^{[9][10][3][8]}

Mechanisms Studied in Research

The leading hypothesis in published studies is that Selank modulates the GABAergic system allosterically, with additional evidence pointing to BDNF and cytokine regulation. None of these mechanisms has been confirmed as primary.

GABAergic gene expression

In rat frontal cortex, real-time PCR of 84 neurotransmission genes found that 45 changed expression 1 hour after Selank or GABA administration and 22 after 3 hours, with a positive correlation between the changes produced by the two compounds. The authors concluded that one possible mechanism is allosteric modulation of the GABAergic system.^[3]

The hypothesis draws on how classical benzodiazepines work: they enhance the inhibitory effect of GABA through allosteric modulation of GABA-A receptors, and Selank’s reported anxiolytic profile resembles theirs.^[4] In human IMR-32 neuroblastoma cells, Selank alone did not change mRNA levels of the same gene panel. However, when combined with GABA it almost completely suppressed the expression changes GABA produced, and combined with olanzapine it altered more genes than olanzapine alone. The authors interpreted this as partial support for an effect on GABA’s interaction with GABA-A receptors.^[4]

BDNF and cytokines

In rats given ethanol as their only fluid for 30 weeks, Selank prevented the ethanol-induced increase in BDNF content in the hippocampus and frontal cortex, which the authors took as evidence of a neurotrophin-related mechanism.^[2] In a rat male-confrontation stress model, stress raised serum IL-1beta, IL-6 and TGF-beta1, and the authors reported that results in the Selank group indicated stress-protective activity.^[6]

Key Findings From Published Studies

Published findings on Selank come mostly from rat models of anxiety, stress, memory impairment and opioid withdrawal, with one small human imaging study. The table summarizes the main results.

Anxiety and withdrawal models

In the chronic mild stress study, a course of either test substance alone worsened anxiety measures in unstressed rats, but less so with Selank. Under chronic stress, anxiety values after combined Selank and diazepam did not differ from pre-stress values.^[8] In the morphine withdrawal model, Selank attenuated convulsive reactions, ptosis and posture disorders and raised the tactile sensitivity threshold ninefold, while being slightly less active than diazepam overall.^[1]

Memory and organ-level effects

In 9-month-old rats not exposed to ethanol, Selank produced a cognitive-stimulating effect in object recognition testing; in ethanol-exposed rats it prevented memory and attention deficits that developed during withdrawal.^[2] In the foot-shock model, stress caused hydropic degeneration, focal necrosis and altered nucleus-to-cytoplasm ratios in hepatocytes, and Selank reduced the intensity of these changes at all levels tested.^[9]

Human data

In 52 healthy participants, resting-state fMRI was recorded before and 5 and 20 minutes after Selank, Semax or placebo. The authors reported group differences in connectivity between the right amygdala and right temporal cortex regions, with both shared and peptide-specific effects.^[10]

Selank lacks sulfur and differs in mass from its capped analogs, so mass spectrometry on a certificate of analysis gives a clear identity check.

Regulatory and Research Status

Selank is not approved by the US Food and Drug Administration for any use and is studied in the United States as a research compound. Papers cite clinical studies comparing it with benzodiazepines, but those trials are not among the indexed abstracts reviewed for this page.^[3][4]

A 2026 review of therapeutic peptides stated that, although preclinical studies of neuroactive peptides including Selank are promising, clinical trials are lacking.^[5] The findings summarized here come mainly from rat models and one small imaging study, and should be read with that limitation in mind.

Selank is also distinct from N-acetyl Selank amidate, a modified analog with terminal capping groups. Published data on Selank do not automatically apply to that analog, and the two can be distinguished by mass spectrometry.