Everything below concerns Pro-Gly-Pro. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-01-20. Numbers and descriptions here follow the published literature rather than marketing material.
The primary structure of Selank is Thr-Lys-Pro-Arg-Pro-Gly-Pro, corresponding to the molecular formula C33H57N11O9 and a monoisotopic mass of roughly 751.9 daltons. The N-terminal threonine and the arginine residue in the fourth position are shared with tuftsin, which carries the sequence Thr-Lys-Pro-Arg. The three additional residues at the C-terminus, Pro-Gly-Pro, extend the chain and are associated with greater resistance to enzymatic degradation. This extension also separates Selank from the shorter parent peptide.
Naming conventions place Selank in the same research family as Semax, another Russian-developed peptide investigated for cognitive effects. The two compounds share a lineage but differ in sequence and in the biological systems proposed as their targets. Semax descends from ACTH fragments, whereas Selank descends from tuftsin. Publications sometimes identify Selank by its full peptide sequence or by laboratory codes rather than one uniform trade name. Because replication outside Russia is limited, reports on its properties are best read alongside the study design and the purity of the material tested.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular class | Synthetic heptapeptide | Stabilized analog of tuftsin |
| Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Single-letter form: TKPRPGP |
| Molecular formula | C33H57N11O9 | Monoisotopic mass about 751.9 Da |
| Appearance | White to off-white powder | Typically supplied as lyophilized solid |
| Solubility | Freely soluble in water | Also soluble in common polar solvents |
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.
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.
Proposed mechanisms centre on modulation of the GABAergic system, with reports of altered expression of genes related to GABA-A receptor subunits and changed monoamine turnover. Some studies describe inhibition of enkephalinase, the enzyme that degrades endogenous enkephalins, which may prolong opioid peptide signalling. Effects on brain-derived neurotrophic factor and on cytokine expression have also been reported. These findings come largely from animal models and small human studies, and the precise primary target remains unresolved.
Published clinical evidence is limited. Most controlled trials were conducted in Russia, enrolled modest numbers of participants, and appeared in Russian-language journals, which restricts independent verification. Reported outcomes include lower anxiety scores, improved attention and memory measures, and changes in fatigue ratings. Reviews written in English note methodological limitations such as small samples and inconsistent endpoints. Whether the compound produces clinically meaningful benefit relative to established anxiolytics is therefore an open question rather than an established finding.
=== Fusexin === The fusexin family consists of eukaryotic HAP2/GCS1, eukaryotic EFF-1, viral "class II", and haloarchaeal Fsx1. They all share a common fold and fuse membranes. In an unrooted phylogenetic tree from 2021, HAP2/GCS1 and EFF-1/AFF-1 occupy two ends of the tree, the middle being occupied by viral sequences; this suggests that they may have been acquired separately. The latest structure-based unrooted phylogenetic tree of Brukman et al. (2022), which takes into account the newly-discovered archaeal sequences, shows that Fsx1 groups with HAP2/GCS1, and that they are separated from EFF-1 by a number of viral sequences. Based on where the root is placed, a number of different hypotheses regarding the history of these families – their horizontal transfer and vertical inheritance – can be generated. Older comparisons excluding archaeal sequences would strongly favor an interpretation where HAP2/GCS1 is acquired from a virus, but the grouping of Fsx1 with HAP2/GCS1 has allowed the possibility of a much more ancient source.
The hypodermis, otherwise known as the subcutaneous layer, is a layer beneath the skin. It invaginates into the dermis and is attached to the latter, immediately above it, by collagen and elastin fibers. It is essentially composed of a type of cell known as adipocytes, which are specialized in accumulating and storing fats. These cells are grouped together in lobules separated by connective tissue. The hypodermis acts as an energy reserve. The fats contained in the adipocytes can be put back into circulation, via the venous route, during intense effort or when there is a lack of energy-providing substances, and are then transformed into energy. The hypodermis participates, passively at least, in thermoregulation since fat is a heat insulator.
== Playing career == Because the population of Duttlenheim was short in numbers, it proved difficult to field a team of 11 players of equal ages; Wenger did not play for FC Duttlenheim until the age of 12. Claude Wenger, a teammate of Arsène's, noted his lack of pace as a player, which he made up for with his "ability to guard the ball, [seeming] to have a complete vision of the pitch and having an influence among his team-mates", according to Marcel Brandner, the president of FC Duttlenheim. As a young teenager, he was called Petit; the nickname ceased when he had a growth spurt and broke into FC Duttlenheim's first team, aged 16. The team did not have a coach to prepare the players tactically, rather a person who supervised training sessions. Wenger took it upon himself to manage the side, with Claude stating "Arsène wasn't the captain and yet he was. It was 'You do this, you do that, you do this, you do that.' He was the leader".
Sources: en.wikipedia.org
== Spectroscopy == Both the fluorescence excitation and emission spectrums of wild-type EosFP are shifted ~65 nm to the right upon excitation toward the red end of the spectrum. This spectral change is caused by an extension of the chromophore accompanied by a break in the peptide backbone between Phe-61 and His-62 in an irreversible mechanism. The presence of a crisp isosbestic point at 432 nm also suggests an interconversion between two species. An absorption peak at 280 nm is visible due to aromatic amino acids which transfer their excitation energy to the green chromophore. The quantum yield of the green-emitting form of Eos is 0.7. In the red shifted species, there are pronounced vibronic sidebands separate from the main peak at 533 nm and 629 nm in the excitation spectrum and emission spectrum respectively. There is another peak in the red excitation spectrum at 502 nm likely due to FRET excitation of the red fluorophore. The quantum yield of the red-emitting form is 0.55. EosFPs variants show almost no difference in spectroscopic properties, therefore, it is likely that the structural modifications which arise from separation of interfaces have little to no effect on the structure of the fluorophore-binding site.
For the first time the SADF began losing aircraft in numbers, indicating the contested extent of the Angolan skies. The SADF's declining air supremacy forced a number of operational changes. South African pilots exercised a standoff bombing capacity of twenty kilometres and timed their raids so they were out of range before FAPLA MiGs could be scrambled to intercept them. The necessity of avoiding prolonged aerial contact was partly dictated by fuel considerations: the SADF Mirage F1AZ and F1CZ fighters launched from distant bases in South West Africa, which meant they had barely enough fuel for three minutes of combat once they reached Cuito Cuanavale. The impact on ground operations was more consequential. FAPLA MiGs flew reconnaissance missions in search of the G5 and G6 howitzers, forcing the South African artillery crews to resort to increasingly elaborate camouflage and take the precaution of carrying out their bombardments after dark. Owing to the increase in losses and damage due to UNITA's US-supplied Stinger missiles, however, MiG pilots had to adopt contingencies of their own to reduce the vulnerability of their aircraft. Cuban and Angolan warplanes were forced to drop bombs from higher altitudes, greatly reducing their accuracy. FAPLA airfields were also monitored by South African forward artillery observers, who called in bombardments to destroy aircraft while they were exposed on the runway and preparing to take off.
== Neurochemical mechanisms == Existing experimental methods have provided enough evidence to suggest that variations in synaptic serotonin, noradrenaline, and dopamine are significant drivers of central nervous system fatigue. An increased synaptic dopamine concentration in the CNS is strongly ergogenic (promotes exercise performance). Paradoxically, however, direct dopamine agonists such as bromocriptine and pramipexole have caused opposite, pro-fatigue effects in healthy humans.
Sources: en.wikipedia.org
Selank is a synthetic heptapeptide designed as a stabilized analog of the natural tetrapeptide tuftsin. It has been investigated mainly for anxiolytic and cognitive effects. It is not an approved pharmaceutical in most countries.
It was developed in Russia, at the Institute of Molecular Genetics of the Russian Academy of Sciences, during the 1990s. Most published research originates from Russian institutions. Independent international replication remains limited.
Tuftsin is a natural tetrapeptide with the sequence Thr-Lys-Pro-Arg that participates in immune signaling. Selank extends that sequence with Pro-Gly-Pro at the C-terminus. The added residues are linked to greater resistance to enzymatic breakdown.
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.