Everything below concerns Selank. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-01-04. Numbers and descriptions here follow the published literature rather than marketing material.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, frequently abbreviated as TKPRPGP. It was designed as a structural analogue of tuftsin, a naturally occurring tetrapeptide released by enzymatic cleavage of the immunoglobulin heavy chain. The two additional proline residues at the C-terminal end extend the parent chain and change how the molecule behaves in solution. The free peptide has a calculated molecular mass of approximately 751.9 g/mol and is generally supplied as a lyophilised white to off-white powder.
Development work on the compound began in the 1980s and 1990s at the Institute of Molecular Genetics in Moscow, within the same research programme that produced the peptide Semax. Early investigators sought a tuftsin derivative with improved resistance to enzymatic breakdown and with activity in the central nervous system after peripheral administration. Most of the primary literature from this period was published in Russian, a factor that still shapes how easily the findings can be checked by outside groups.
Naming for this compound is not fully standardised in English sources. The spelling Selanc appears in some transliterations, and catalogue entries may instead list the peptide sequence itself as the identifier. Reference material sometimes groups it with other short synthetic peptides studied for behavioural effects, which can create confusion when citations are compared. Distinguishing the exact sequence from related tuftsin analogues is therefore a practical first step when reviewing any dataset or specification sheet.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic heptapeptide | Tuftsin analogue |
| Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Single-letter form: TKPRPGP |
| Molecular formula | C33H57N11O9 | Calculated for the free peptide |
| Molecular weight | About 751.9 g/mol | Derived from the sequence |
| Appearance | White to off-white powder | Typical lyophilised form |
Measuring peptide exposure inside the brain is technically difficult. Selank is degraded rapidly in plasma, and assays must separate intact peptide from fragments, which favors targeted mass spectrometry over immunoassays alone. Reported half-lives are short, on the order of minutes, so effects observed hours later are attributed to downstream signaling rather than to the parent compound. Blood-brain barrier permeability is debated and rarely quantified directly. Gaps include absent dose-response characterization, inconsistent reporting of purity, and almost no pharmacokinetic data from human participants.
Selank is studied chiefly as an animal-model anxiolytic with proposed secondary effects on memory and immune signaling. Reported mechanisms include modulation of the GABA-A receptor complex, inhibition of enkephalin-degrading enzymes, and shifts in monoamine turnover within limbic structures. Some experiments describe increased expression of brain-derived neurotrophic factor in the hippocampus after repeated dosing. No single molecular target has been confirmed, and the peptide does not bind any receptor with the selectivity typical of a conventional small-molecule drug. Mechanism therefore remains a set of hypotheses rather than an established pathway.
Laboratory work relies on standard behavioral paradigms. Rodents are tested in the elevated plus maze, open field, and passive avoidance tasks, with outcomes compared against diazepam or vehicle controls. Intranasal dosing is used most often because it bypasses first-pass metabolism, though intraperitoneal and intravenous routes also appear in published protocols. Biochemical endpoints include tissue BDNF concentrations, cytokine levels, and monoamine metabolites. Human data are limited to small Russian trials reporting reduced anxiety scores; most were not prospectively registered, and few employed independent outcome assessment.
Reported activity for Selank centers on anxiolytic and nootropic effects. Russian clinical reports describe use in anxiety and in cognitive or attention-related complaints. Most of this evidence comes from studies conducted by the same research groups that developed the peptide. Independent replication in other countries remains limited, and no major Western regulatory agency has approved the compound for any indication. The gap between local reports and external verification is a recurring point in discussions of the peptide.
Tuftsin, the parent structure, is a naturally occurring immunomodulatory tetrapeptide released from the Fc region of immunoglobulin G by spleen enzymes. Selank extends this four-residue sequence with three additional amino acids. The stated rationale is that the added tail slows enzymatic breakdown and may influence receptor interactions. How the full heptapeptide behaves at the molecular level is not firmly established, and proposed mechanisms often involve indirect modulation of neurotransmitter or immune signaling rather than a single defined target.
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As a hormone, adrenaline acts on nearly all body tissues by binding to adrenergic receptors. Its effects on various tissues depend on the type of tissue and expression of specific forms of adrenergic receptors. For example, high levels of adrenaline cause smooth muscle relaxation in the airways but causes contraction of the smooth muscle that lines most arterioles. Adrenaline is a nonselective agonist of all adrenergic receptors, including the major subtypes α1, α2, β1, β2, and β3. Adrenaline's binding to these receptors triggers a number of metabolic changes. Binding to α-adrenergic receptors inhibits insulin secretion by the pancreas, stimulates glycogenolysis in the liver and muscle, and stimulates glycolysis and inhibits insulin-mediated glycogenesis in muscle. β adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland, and increased lipolysis by adipose tissue. Together, these effects increase blood glucose and fatty acids, providing substrates for energy production within cells throughout the body. Binding of β adrenergic receptor also increases the production of cyclic AMP. Adrenaline causes liver cells to release glucose into the blood, acting through both alpha and beta-adrenergic receptors to stimulate glycogenolysis. Adrenaline binds to β2 receptors on liver cells, which changes conformation and helps Gs, a heterotrimeric G protein, exchange GDP to GTP. This trimeric G protein dissociates to Gs alpha and Gs beta/gamma subunits.
{\displaystyle {\begin{array}{lll}\Delta G_{\text{bind}}=-RT\ln K_{\text{d}}\\[1.3ex]K_{\text{d}}={\dfrac {[{\text{Ligand}}][{\text{Receptor}}]}{[{\text{Complex}}]}}\\[1.3ex]\Delta G_{\text{bind}}=\Delta G_{\text{desolvation}}+\Delta G_{\text{motion}}+\Delta G_{\text{configuration}}+\Delta G_{\text{interaction}}\end{array}}}
Competition between RNA may have favored the emergence of cooperation between different RNA chains, opening the way for the formation of the first protocell. Eventually, RNA chains developed with catalytic properties that help amino acids bind together (a process called peptide-bonding). These amino acids could then assist with RNA synthesis, giving those RNA chains that could serve as ribozymes the selective advantage. The ability to catalyze one step in protein synthesis, aminoacylation of RNA, has been demonstrated in a short (five-nucleotide) segment of RNA. In 2014, a group of researchers managed to produce all four components of RNA by simulating an asteroid impact in primordial conditions. In March 2015, NASA scientists reported that, for the first time, complex DNA and RNA organic compounds of life, including uracil, cytosine, and thymine, have been formed in the laboratory under conditions found only in outer space, using starting chemicals, like pyrimidine, found in meteorites. Pyrimidine, like polycyclic aromatic hydrocarbons (PAHs), may have been formed in red giant stars or in interstellar dust and gas clouds, according to the scientists. That same month, researchers were able to produce over 50 aminoacids in a laboratory setting by using only hydrogen sulfide, hydrogen cyanide (presumably produced after outer space meteorites reacted with atmospheric nitrogen) and ultraviolet light.
Sources: en.wikipedia.org
He is currently a professor of ophthalmology at the University of Geneva, an adjunct clinical professor of ophthalmology at the Keck School of Medicine, University of Southern California, a research group leader of the Ocular Cell Biology Group at the Center for Applied Biotechnology and Molecular Medicine at the University of Zurich, a visiting professor at the University of Wenzhou, China, a research professor of ophthalmology at the NYU Grossman School of Medicine, and medical director of the ELZA Institute.
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==== Attenuated ==== The idea of wildlife vaccination was conceived during the 1960s, and modified-live rabies viruses were used for the experimental oral vaccination of carnivores by the 1970s. Development of an oral immunization for wildlife began in the United States with laboratory trials using the live, attenuated Evelyn-Rokitnicki-Abelseth (ERA) vaccine, derived from the Street Alabama Dufferin (SAD) strain. The first ORV field trial using the live attenuated vaccine to immunize foxes occurred in Switzerland during 1978. Modified live virus vaccines may use strains such as SAG2 and SAD B19..
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A familiar example of the opposite, a shear thinning fluid, or pseudoplastic fluid, is wall paint: The paint should flow readily off the brush when it is being applied to a surface but not drip excessively. Note that all thixotropic fluids are extremely shear thinning, but they are significantly time dependent, whereas the colloidal "shear thinning" fluids respond instantaneously to changes in shear rate. Thus, to avoid confusion, the latter classification is more clearly termed pseudoplastic. Another example of a shear thinning fluid is blood. This application is highly favoured within the body, as it allows the viscosity of blood to decrease with increased shear strain rate.
Sources: en.wikipedia.org
The sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro, commonly written as TKPRPGP. It shares the first four residues with tuftsin and carries three prolines in the chain. The proline-rich tail is the main structural feature that separates it from the parent tetrapeptide.
Selank is a synthetic analogue built on the tuftsin tetrapeptide Thr-Lys-Pro-Arg. Extra proline residues were added to the C-terminus during design work. That modification is intended to make the peptide less vulnerable to rapid enzymatic degradation.
Transliteration from Russian produces variant spellings such as Selanc. Many suppliers avoid the trade-style name entirely and list the peptide sequence. Comparing sequences rather than names is the reliable way to confirm two entries describe the same molecule.
Selank is a seven-amino-acid peptide built from the tuftsin sequence plus a Pro-Gly-Pro tail. It is produced by chemical synthesis rather than extracted from a natural source. The free peptide is usually supplied as a lyophilised powder or in an aqueous formulation.