A practical reference on Selank: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
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.
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 developed in Russia during the 1990s. Researchers at the Institute of Molecular Genetics of the Russian Academy of Sciences designed it as a stabilized analog of tuftsin, a naturally occurring immunomodulatory tetrapeptide. The compound has been studied primarily for its reported anxiolytic and nootropic effects. It remains largely unknown in Western pharmacology and is not approved as a medicine by major regulators such as the FDA or the EMA.
| 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 |
Regulatory status differs sharply by region. Selank holds a Russian marketing authorization, where it is supplied mainly as nasal drops, while authorities elsewhere have not approved it for medical use. Material sold internationally is therefore usually labeled as a research chemical rather than a medicine. Peer-reviewed publications come predominantly from Russian laboratories, and sample sizes are generally small. Whether the compound produces comparable effects under independent, well-controlled replication remains an open question that the broader literature has not settled.
Selank is a synthetic heptapeptide developed in Russia as a structural analogue of tuftsin, a naturally occurring immunomodulatory tetrapeptide. Its sequence, Thr-Lys-Pro-Arg-Pro-Gly-Pro, keeps the tuftsin core at the N-terminus and appends a Pro-Gly-Pro tail. Researchers at the Institute of Molecular Genetics in Moscow synthesized the compound during the 1990s while searching for peptides with combined anxiolytic and immunomodulatory activity. The added tail was intended to resist enzymatic cleavage and prolong the molecule's presence in circulation.
The compound has a calculated molecular weight near 751.9 daltons and carries a net positive charge at physiological pH because of its arginine residue. It dissolves freely in water and in common aqueous buffers, and typically appears as a white or off-white lyophilized powder. The amide backbone makes the molecule susceptible to peptidases, which limits oral use and favors intranasal or parenteral routes. Nomenclature in the literature varies: the substance is also described by the sequence abbreviation TP-7 and by a Russian trade designation.
Regulatory treatment varies by jurisdiction. In Russia the compound is a registered prescription product, while in the European Union and the United States it is generally handled as a research chemical without a marketing authorization. Suppliers therefore operate outside pharmaceutical oversight, and buyers rely on supplier documentation for purity and identity claims. Chain of custody and third-party testing are the main verification tools. Analysts note that the absence of a pharmacopoeial monograph for research-grade material limits standardization across vendors.
Purity assessment relies mainly on reverse-phase high-performance liquid chromatography with ultraviolet detection. Because the peptide lacks a strong chromophore, detection often uses backbone absorbance near 214 nm. Identity is confirmed by mass spectrometry, typically electrospray ionization or matrix-assisted laser desorption, comparing the measured mass against the expected value. Amino acid analysis can verify composition after acid hydrolysis. Diastereomer content and residual counterions are reported less often, although both can influence biological assays.
Lyophilized material is generally stable for extended periods when kept dry at or below minus twenty degrees Celsius. Working solutions are less stable, and common practice is to aliquot and freeze them so that repeated freeze-thaw cycles are avoided. Aqueous solutions are sensitive to pH extremes and to microbial growth, so short-term storage at refrigerator temperature is typical. Oxidation and hydrolysis are the principal degradation routes. Reconstitution with sterile water or a mild buffer is standard, and solutions should be protected from light.
Clinical evidence comes mainly from small studies conducted in Russia, several of which were open-label or lacked robust blinding. Reported outcomes include lower anxiety scores, changes in attention measures, and effects on asthenic states following illness. Sample sizes are typically in the tens of participants, and independent replication outside the region is scarce. Reviews published in English generally note the limited methodological quality of the underlying trials. Whether the compound produces clinically meaningful effects under rigorous conditions remains unresolved.
Proposed mechanisms center on modulation of the GABA system, but no single molecular target has been confirmed. Rodent studies report changes in GABA-A receptor expression and in the turnover of serotonin, dopamine, and norepinephrine in several brain regions. Increases in brain-derived neurotrophic factor and its receptor have also been described after repeated administration. These findings come largely from animal models, and the degree to which they describe human neurochemistry remains an open question. The mechanism is best characterized as multi-system and not fully resolved.
Pharmacokinetic data are limited. Like most short peptides, Selank is vulnerable to plasma and tissue peptidases, and its measured half-life in circulation is short, on a minutes scale. The Pro-Gly-Pro tail slows this degradation but does not eliminate it. Intranasal administration is the route described in most reports, with absorption through the nasal mucosa and a hypothesized path into the central nervous system that avoids the blood-brain barrier. Direct measurements of human brain exposure are unavailable, so distribution claims rest on inference from animal work.
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.
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.
== Synthesis and Post-translational Modification == Proinsulin is synthesized on membrane associated ribosomes found on the rough endoplasmic reticulum, where it is folded and its disulfide bonds are oxidized. It is then transported to the Golgi apparatus where it is packaged into secretory vesicles, and where it is processed by a series of proteases to form mature insulin. Mature insulin has 35 fewer amino acids; 4 are removed altogether, and the remaining 31 form the C-peptide. The C-peptide is abstracted from the center of the proinsulin sequence; the two other ends (the B chain and A chain) remain connected by disulfide bonds. The post translational modification of proinsulin to mature insulin only occurs in the beta cells of the pancreatic islets. When proinsulin is transported through the Golgi apparatus the C-peptide is cleaved. This cleavage occurs with the aid of two endoproteases. Type I endoproteases, PC1 and PC3, disrupt the C peptide-B chain connection. PC2, a type II endoprotease, cleaves the C peptide-A chain bond. The resulting molecule, now mature insulin, is stored as a hexamer in secretory vesicles and is stabilized with
== Reference ranges == General guidelines for diagnosing prolactin excess (hyperprolactinemia) define the upper threshold of normal prolactin at 25 μg/L for women and 20 μg/L for men. Similarly, guidelines for diagnosing prolactin deficiency (hypoprolactinemia) are defined as prolactin levels below 3 μg/L in women and 5 μg/L in men. However, different assays and methods for measuring prolactin are employed by different laboratories and as such the serum reference range for prolactin is often determined by the laboratory performing the measurement. Furthermore, prolactin levels vary according to factors as age, sex, menstrual cycle stage and pregnancy. The circumstances surrounding a given prolactin measurement (assay, patient condition, etc.) must therefore be considered before the measurement can be accurately interpreted. The following chart illustrates the variations seen in normal prolactin measurements across different populations. Prolactin values were obtained from specific control groups of varying sizes using the IMMULITE assay.
Yohimbine is a substance found in the bark of yohim trees in West Africa. It was traditionally used in West African cultures, in which the bark would be boiled and the resulting water drunk until it increased sexual desire. It is also found in over-the-counter health products. Yohimbine is an indole alkaloid and is an adrenoceptor antagonist. Known adverse effects include nausea, anxiety, irregular heartbeats, and restlessness.
=== Estonian === Sünnipäevanädalalõpupeopärastlõunaväsimatus meaning "afternoon untiredness of a weekend birthday party" which is 43 letters. 31 lettered word of uusaastaöövastuvõtuhommikuidüll [uːsɑːstaøːvastuvɤtuhomikuidyl] meaning "morning idyll after the new year". There is also the 25 letter long word of põllumajandusministeerium which is "Ministry of Agriculture". The word kuulilennuteetunneliluuk meaning "the hatch a bullet flies out of when exiting a tunnel" is 24 letters long and a palindrome. It could be one of the longest palindromes.
== Disadvantages == The primary disadvantage of in vitro experimental studies is that it may be challenging to extrapolate from the results of in vitro work back to the biology of the intact organism. Investigators doing in vitro work must be careful to avoid over-interpretation of their results, which can lead to erroneous conclusions about organismal and systems biology. For example, scientists developing a new viral drug to treat an infection with a pathogenic virus (e.g., HIV-1) may find that a candidate drug functions to prevent viral replication in an in vitro setting (typically cell culture). However, before this drug is used in the clinic, it must progress through a series of in vivo trials to determine if it is safe and effective in intact organisms (typically small animals, primates, and humans in succession). Typically, most candidate drugs that are effective in vitro prove to be ineffective in vivo because of issues associated with delivery of the drug to the affected tissues, toxicity towards essential parts of the organism that were not represented in the initial in vitro studies, or other issues.
Sources: en.wikipedia.org
Psilocybin, also known as 4-phosphoryloxy-N,N-dimethyltryptamine (4-PO-DMT), is a naturally occurring tryptamine alkaloid and investigational drug found in more than 200 species of mushrooms, with hallucinogenic and serotonergic effects. Effects include euphoria, changes in perception, a distorted sense of time, and perceived spiritual experiences. Psilocin is the metabolite of psilocybin. The compound psilocybin itself is biologically inactive but quickly converted by the body to psilocin. Psilocybin is transformed into psilocin by dephosphorylation mediated via phosphatase enzymes. Psilocin is chemically related to the neurotransmitter serotonin and acts as a non-selective agonist of the serotonin receptors. Activation of one serotonin receptor, the serotonin 5-HT2A receptor, is specifically responsible for the hallucinogenic effects of psilocin and other serotonergic psychedelics. Psilocybin is usually taken orally. By this route, its onset is about 20 to 50 minutes, peak effects occur in about 1 to 2 hours, and its duration is about 4 to 6 hours. Psilocybin mushrooms were used ritualistically in pre-Columbian Mexico, but claims of their widespread ancient use are largely exaggerated and shaped by modern idealization and ideology. In 1958, the Swiss chemist Albert Hofmann isolated psilocybin and psilocin from the mushroom Psilocybe mexicana. His employer, Sandoz, marketed and sold pure psilocybin to physicians and clinicians worldwide for use in psychedelic therapy.
The major pathways of human exposure to MNPs are inhalation, ingestion and dermal contact, with bioaccumulation varying based on particle size, composition, and physicochemical characteristics. Research suggests that MNPs above 150 μm typically remain confined to tissues and do not enter systemic circulation, whereas particles below 200 nm can breach cellular and tissue barriers, potentially reaching the bloodstream and other organs. This diversity in bioaccumulation pathways underscores the widespread yet nuanced risks of MNP exposure to human health. These findings collectively suggest that MNPs may accumulate in multiple organ systems depending on the exposure route, potentially leading to long-term health consequences as their presence in human tissues builds up over time.
MHC Class II molecules are a class of major histocompatibility complex (MHC) molecules normally found only on professional antigen-presenting cells such as dendritic cells, macrophages, some endothelial cells, thymic epithelial cells, and B cells. These cells are important in initiating immune responses. Antigens presented by MHC class II molecules are exogenous, originating from extracellular proteins rather than cytosolic and endogenous sources like those presented by MHC class I. The loading of a MHC class II molecule occurs by phagocytosis. Extracellular proteins are endocytosed into a phagosome, which subsequently fuses with a lysosome to create a phagolysosome. Within the phagolysosome, lysosomal enzymes degrade the proteins into peptide fragments. These fragments are then loaded into the peptide-binding groove of the MHC class II molecule. Once loaded, the MHC class II-peptide complexes are transported to the plasma membrane via vesicular transport, where they present the antigens to the extracellular environment. In humans, the MHC class II protein complex is encoded by the human leukocyte antigen gene complex (HLA). Class II HLAs are composed of the classical HLA-DP, HLA-DQ, and HLA-DR and non-classical HLA-DM and HLA-DO MHC molecules.
== Deficiency == Plasma vitamin C is the most widely applied test for vitamin C status. Adequate levels are defined as near 50 μmol/L. Hypovitaminosis of vitamin C is defined as less than 23 μmol/L, and deficiency as less than 11.4 μmol/L. For people 20 years of age or above, data from the US 2017–18 National Health and Nutrition Examination Survey showed mean serum concentrations of 53.4 μmol/L. Deficiency was reported in 5.9% of people. Globally, vitamin C deficiency is common in low and middle-income countries, and not uncommon in high income countries. In the latter, prevalence is higher in males than in females. Plasma levels are considered saturated at about 65 μmol/L, achieved by intakes of 100 to 200 mg/day, which are well above the recommended intakes. Even higher oral intake does not further raise plasma nor tissue concentrations because absorption efficiency decreases and any excess that is absorbed is excreted in urine.
There are several pressure-lowering medication groups that could be used in lowering the IOP, usually eyedrops. The choice of medication usually depends on the dose, duration, and side effects of each medication. However, in general, prostaglandin analogues are the first-line treatment for glaucoma. Prostaglandin analogues, such as latanoprost, bimatoprost, and travoprost, reduce the IOP by increasing the aqueous fluid outflow through the draining angle. It is usually prescribed once daily at night. The systemic side effects of this class are minimal. However, they can cause local side effects, including redness of the conjunctiva, a change in the iris color, and eyelash elongation. Several other classes of medications could be used as a second-line in case of treatment failure or presence of contraindications to prostaglandin analogues. These include:
Sources: en.wikipedia.org
=== Potential degradation by sonication === Wang et al. reported that aqueous solutions of poloxamer 188 (Pluronic F-68) and poloxamer 407 (Pluronic F-127) sonicated in the presence or absence of multi-walled carbon nanotubes (MWNTs) can became highly toxic to cultured cells. Moreover, toxicity correlated with the sonolytic degradation of the polymers.
The lack of a separate chromosome 17 probe on the same section is an issue with regards to acceptance of CISH. As of June 2011 Roche has obtained FDA approval for the INFORM HER2 Dual ISH DNA Probe cocktail developed by Ventana Medical Systems. The DDISH (Dual-chromagen/Dual-hapten In-situ hybridization) cocktail uses both HER2 and Chromosome 17 hybridization probes for chromagenic visualization on the same tissue section. The detection can be achieved by using a combination of ultraView SISH(silver in-situ hybridization) and ultraView Red ISH for deposition of distinct chromgenic precipitates at the site of DNP or DIG labeled probes.
=== Malaysian and Singaporean === Malays from Malaysia, using the Malay dialect similar to Indonesian, use the word kicap for soy sauce. Kicap is traditionally of two types: kicap lemak (lit "fat/rich soy sauce") and kicap cair. Kicap lemak is similar to Indonesian kecap manis but with very much less sugar, while kicap cair is the Malaysian equivalent of kecap asin.
=== Volatiles === Cultivars of G. globosa vary in the identity of floral volatiles but the volatile compounds of nonanal, decanal, geranyl acetone, and 4,8,12-tetradecatrienal, 5,9,13-trimethyl, were commonly detected by chromatography-mass spectrometry analysis. The cultivar ‘Fireworks’ has a high abundance of volatile esters such as geranyl propionate, geranyl isovalerate, benzyl isovalerate, and benzyl tiglate. The floral volatile emission of this cultivar of G. globosa was found to exhibit a diurnal pattern independent of light. Emission of floral volatiles can be regulated by phytohormone and defense signaling molecules. Experimentally, the ethylene inhibitor silver thiosulphate increased volatile emission of molecules derived from the terpenoid pathway. Defense signaling molecules can have temporal effects on floral volatile emission such as increased emission after four hours and reduced emission of volatiles after 24 hours in time studies analyzed with chromatography-mass spectrometry.
== History == Calcitriol was first identified in 1971 by Michael F. Holick working in the laboratory of Hector DeLuca, and also by Tony Norman and colleagues. Calcitriol was approved for medical use in the United States in 1978.
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.
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.