Research chemical raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
Reviewed 2025-12-02. Anything still debated is marked as such rather than presented as settled.
Reported pharmacological effects center on reduced anxiety-like behavior in animal models and on measures of memory and learning. Proposed contributing mechanisms include modulation of GABAergic signaling, shifts in monoamine turnover, and changes in the activity of enzymes that degrade neuropeptides. Effects on the expression of genes linked to neuroplasticity have also been described. No single molecular target is widely accepted, and whether the behavioral findings arise from one pathway or several remains an open question.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. It was designed as a stabilized analogue of tuftsin, a naturally occurring tetrapeptide fragment derived from the immunoglobulin heavy chain. The additional Pro-Gly-Pro segment at the carboxyl terminus is intended to slow enzymatic cleavage. The compound is usually described in the literature as a synthetic peptide with anxiolytic and cognitive-related activity, a label that reflects a research context rather than an approved therapeutic category.
Most published work on selank originates from a small number of research groups in the Russian Federation. A large share of that record appears in Russian-language journals, which limits access for readers who rely on English-indexed databases. Independent replication by laboratories outside the original research network is sparse in publicly available sources. This concentration of origin and language is a frequently noted feature when the compound is summarized in broader reviews of synthetic peptides.
Published clinical work is concentrated in Russian-language journals and generally involves small samples without independent replication. Systematic reviews in English note the shortage of randomised, placebo-controlled trials and the difficulty of verifying methods from translated reports. Outcome measures vary between studies, which complicates pooling of results. Interest in the compound as a cognitive or anxiolytic agent therefore rests on a thinner evidence base than the volume of citations suggests. Replication in well-powered trials with preregistered endpoints would be needed before firm conclusions about efficacy can be drawn.
Proposed mechanisms centre on the GABAergic system. Animal and tissue studies report changes in GABA-A receptor expression and reduced activity of GABA transaminase, the enzyme that degrades GABA. Effects on monoamine turnover, including serotonin and dopamine pathways, are also described, and a separate line of work links the peptide to increased expression of brain-derived neurotrophic factor in hippocampal tissue. Most of these findings come from rodent models and cell preparations. How the individual observations combine into a single coherent mode of action is not settled.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C33H57N11O9 | Derived from the seven-residue sequence |
| Molecular weight | About 751.9 g/mol | Average mass; the monoisotopic value is slightly lower |
| Residue count | Seven amino acids | Thr-Lys-Pro-Arg-Pro-Gly-Pro |
| Parent compound | Tuftsin (Thr-Lys-Pro-Arg) | Selank extends tuftsin at the C-terminus |
| Compound class | Synthetic short peptide | Studied in a research setting; not a licensed drug in most markets |
Development took place at the Institute of Molecular Genetics of the Russian Academy of Sciences, where a series of short peptides were designed in the 1980s and 1990s. Selank was selected from variants of tuftsin that showed resistance to plasma peptidases. Russian regulatory approval covers it as an anxiolytic agent given intranasally. Outside that market the compound is normally handled as a research chemical rather than a medicine, and no widely recognised international pharmacopoeial monograph exists. The name Selank is a coined trade designation rather than a systematic chemical name.
Enzymatic stability motivates the extra three residues at the carboxyl end. Native tuftsin is cleaved quickly by circulating aminopeptidases and carboxypeptidases, which limits its duration of action and its usefulness as a tool compound. Extending the chain with proline-rich segments is a common design tactic because proline constrains the backbone and slows proteolysis. The same Pro-Gly-Pro motif appears in other Russian-developed peptides of the era. Whether the full seven-residue chain is required for activity, or whether it acts mainly as a prodrug releasing tuftsin, remains unresolved.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. Its four N-terminal residues reproduce tuftsin, a tetrapeptide fragment of the immunoglobulin heavy chain, while the C-terminal Pro-Gly-Pro extension is a synthetic addition. The peptide has a molecular mass near 752 daltons and carries a net positive charge at physiological pH because of the arginine and lysine side chains. Published indexes list it under the name Selank and the sequence abbreviation TKPRPGP. Solid-phase peptide synthesis is the standard production route for research quantities.
Identity and purity are usually assessed by reversed-phase high-performance liquid chromatography, with mass spectrometry used to confirm molecular mass and sequence information. Amino acid analysis and peptide mapping may supplement these methods. Certified reference standards are scarce, and many commercial lots are sold as research chemicals without a pharmacopoeial monograph. Regulatory treatment differs by country: Selank is a registered prescription medicine in Russia, while in the European Union and the United States it is not an approved drug and may fall under research-chemical or unapproved-product frameworks.
Selank is a hydrophilic peptide and dissolves readily in water and in aqueous buffers. The lyophilised powder is typically a white to off-white solid. Because short peptides are prone to hydrolysis and oxidation, handling benefits from limiting exposure to heat, moisture and strong light. Working solutions are commonly prepared in sterile water or saline, and repeated freeze-thaw cycles are avoided to reduce aggregation and loss of activity. These practices reflect general laboratory convention rather than published stability specifications.
The pituitary gland is divided into three lobes: the anterior pituitary, the intermediate pituitary lobe, and the posterior pituitary. The hypothalamus controls the anterior pituitary's hormone secretion by sending releasing factors, called tropic hormones, down the hypothalamo-hypophysial portal system. For example, thyrotropin-releasing hormone released by the hypothalamus in to the portal system stimulates the secretion of thyroid-stimulating hormone by the anterior pituitary. The posterior pituitary is directly innervated by the hypothalamus; the hormones oxytocin and vasopressin are synthesized by neuroendocrine cells in the hypothalamus and stored at the nerve endings in the posterior pituitary. They are secreted directly into systemic circulation by the hypothalamic neurons.
Both carboxamides and aldoximes can be dehydrated using aluminum chloride and sodium iodide in acetonitrile. Likewise, both classes can be dehydrated with oxalyl chloride and catalytic dimethyl sulfoxide in a reaction analogous to the Swern oxidation. Conversion to nitriles under catalysis by heptavalent rhenium species (perrhenic acid or trimethylsilyl perrhenate) is effective for both amides and aldoximes; the water formed can be removed by azeotropic distillation. The conversion of aldehydes to nitriles via aldoximes is a popular laboratory route. Aldehydes react readily with hydroxylamine salts, sometimes at temperatures as low as ambient, to give aldoximes. These can be dehydrated to nitriles by simple heating, although a wide range of reagents may assist with this, including triethylamine/sulfur dioxide, zeolites, or sulfuryl chloride. The related hydroxylamine-O-sulfonic acid reacts similarly.
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Despite these promising findings, translation into clinical applications in humans remains limited, and further research is required to evaluate the safety, efficacy, and feasibility of therapeutic strategies inspired by this model.
== History == Hohhot Baita Airport was opened on 1 October 1958. When it first opened to air traffic, it had only one dirt runway, three single‑story buildings, and five tents. The taxiway and apron were simple, and the runway measured 1,500 meters in length and 100 meters in width. In the mid-1980s and 1990s, it underwent two expansions and in June 2007 a new terminal was constructed. The new terminal covers an area of 54,499 square metres (586,620 sq ft) with 11 parking jetways and is capable of handling three million passengers each year. Its runway was also lengthened and its widened to accommodate jumbo jets such as the Airbus A380. It served as one of the diversion airports for air traffic during the 2008 Summer Olympics. With the rapid expansion of the city, Baita Airport is now surrounded by urban area and has no more room to expand to accommodate growing traffic. The Hohhot Shengle International Airport is being constructed in Horinger County which will replace Baita Airport and Baita is set to be closed once the new airport opened.
Sources: en.wikipedia.org
== Display == While some of the tablets are being preserved for future study, some will be displayed in a museum exhibit entitled "London Mithraeum" located on the first two floors of the Bloomberg European Headquarters, which opened in November 2017.
== Biology / Functions == IRAP functions depend on the cell type and extracellular environment. For example, in adipocytes and muscle cells, IRAP is a major component of Glut4storage vesicles (GSV) and regulates GSV trafficking in response to insulin receptor signaling. Alteration of IRAP recruitment at the cell surface, as observed in type 2 diabetes, impairs glucose uptake by blocking the glucose transporter type 4 (Glut4) trafficking at the cell membrane. This evidence underlies a central function of the aminopeptidase in this disease. IRAP cleaves several hormones, vasoactive peptides, and neuropeptides such as oxytocin, somatostatin, cholecystokinin, angiotensin III (Ang), Lys-bradykinin, arginin vasopressin, Met-and Leu-enkephalin, neurokinin A, and dynorphin A. Most of them have primary functions in the development of neurological disorders, including schizophrenia and memory disorders. Furthermore, an alteration in neuropeptide levels, due to IRAP deregulation, seems to be one of the mechanisms affecting learning and cognition processes, highlighting a fundamental function of IRAP also in memory disorders. In the brain, IRAP is the major receptor of Ang IV, an essential component of the renin-angiotensin system which has been shown to have a neuroprotective effect. This evidence has prompted research on developing analogues with high IRAP selectivity, that show potential in memory enhancement, vascular regulation, and anticonvulsive/antiepileptogenic effects.
==== Androgen receptor ==== Although it functions as an endogenous precursor to more potent androgens such as testosterone and DHT, DHEA has been found to possess some degree of androgenic activity in its own right, acting as a low affinity (Ki = 1 μM), weak partial agonist of the androgen receptor (AR). However, its intrinsic activity at the receptor is quite weak, and on account of that, due to competition for binding with full agonists like testosterone, it can actually behave more like an antagonist depending on circulating testosterone and dihydrotestosterone (DHT) levels, and hence, like an antiandrogen. However, its affinity for the receptor is very low, and for that reason, is unlikely to be of much significance under normal circumstances.
Paul J. Flory – Facts. NobelPrize.org. Nobel Media AB 2019. Wed. 19 Jun 2019. <The Nobel Prize in Chemistry 1974> Somsen, Geert. Paul J Flory. Encyclopædia Britannica. June 15, 2019. Paul J. Flory | Nobel Prize-Winning American Chemist | Britannica Paul John Flory. Stanford Chemistry. [1] Archived August 9, 2022, at the Wayback Machine.
Sources: en.wikipedia.org
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, designed as a metabolically stabilized analogue of the endogenous tetrapeptide tuftsin. It has been studied mainly against anxiety-related and cognitive endpoints rather than as an approved medicine in most jurisdictions.
Tuftsin contains four residues, while selank carries an additional Pro-Gly-Pro segment at the carboxyl end. That extension is intended to reduce enzymatic cleavage. Comparative pharmacokinetic data in humans remain limited.
No single receptor target is widely accepted as the definitive mediator of the reported effects. Proposed contributors include GABAergic modulation, shifts in monoamine turnover, and altered neuropeptide degradation. The mechanism is treated in the literature as unresolved.
Reports describe modulation of GABA signalling, changes in monoamine turnover and effects on neurotrophic factor expression. These observations come mainly from animal and cell studies. A single unifying mechanism has not been demonstrated.