Everything below concerns lyophilized powder. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-02-11. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. It was designed at the Institute of Molecular Genetics of the Russian Academy of Sciences as a structural analogue of tuftsin, a naturally occurring tetrapeptide fragment of the immunoglobulin heavy chain. The added Pro-Gly-Pro tail was intended to slow enzymatic degradation and extend biological activity. In Russia it is registered as an anxiolytic nasal preparation, while regulators elsewhere have not approved it for clinical use.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C33H57N11O9 | Free peptide form |
| Molecular mass | About 751.9 Da | Calculated average mass |
| Amino acid sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Single-letter form TKPRPGP |
| Structural basis | Tuftsin analogue | Extended version of a natural tetrapeptide |
| Development origin | Russian Academy of Sciences | Work carried out from the 1980s onward |
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.
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.
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.
Reverse-phase high-performance liquid chromatography with ultraviolet detection near 214 nanometres is the standard purity method. Mass spectrometry, typically electrospray ionisation, confirms identity through the expected mass-to-charge pattern. Amino acid analysis can verify composition independently. Chiral purity requires separate techniques such as derivatisation followed by chromatographic separation, and such data are rarely reported for research-grade material.
Quantification in biological matrices relies on liquid chromatography coupled to tandem mass spectrometry with stable-isotope internal standards. Low plasma concentrations and adsorption to container surfaces both complicate measurement. Solid-phase extraction is often needed to reduce matrix interference before injection. Reported limits of quantification differ widely between laboratories, which makes direct comparison of pharmacokinetic results difficult and limits meta-analysis.
Peptide bonds are vulnerable to protease attack, and Selank is no exception. Measured half-life in serum is short, on the order of minutes in several reports, which explains why intranasal administration is the common route described in the literature. Absorption across the nasal mucosa partially bypasses first-pass hepatic metabolism. Quantitative data on human bioavailability remain limited and are difficult to compare across studies.
Peptide bonds in selank are susceptible to hydrolysis under strongly acidic or basic conditions, and the terminal proline residues are vulnerable to exopeptidase activity in biological samples. Lyophilized powder stored dry at -20 °C typically remains stable for extended periods, whereas aqueous solutions degrade faster and may lose measurable purity within days to weeks depending on pH, temperature, and microbial load. Repeated freeze-thaw cycles promote aggregation and adsorption to container surfaces. For analytical work, solutions are usually prepared fresh, kept cold, and used within a single working day.
Handling follows standard practice for research peptides. Material is weighed in a low-humidity environment because the powder absorbs atmospheric moisture. Purity is reported as the percentage area of the main peak in a chromatogram, with specifications commonly set at 95 percent or higher; values below that threshold indicate the presence of truncated or modified species. Residual trifluoroacetate from purification is often present and may affect mass balance. Certificates of analysis should state the analytical method, the column and gradient used, and the lot-specific retention time so that results can be compared across suppliers.
The Theodor Bilharz Research Institute is located in Giza, Egypt. Theodor Bilharz was a German scientist who discovered, in autopsy material at Kasr El Aini Hospital, the causative agent of haematuria: Schistosoma worm, during his work in Egypt in 1851. The bilhariziasis disease was named after him.
== A scientific home in Pittsburgh == In a few short years, the Dean of the School of Medicine, himself a professor of Biochemistry, invited Hofmann to become Chairman of the Department. From the moment he took the position of Chairman of Biochemistry, it became clear that although he would always be a son of Switzerland, the United States offered him career opportunities he could never hope for in a small country like Switzerland. The US was to become his permanent home. The burgeoning field of peptide chemistry became his scientific focus and, in his own words, he fell in love with a molecule that was known to stimulate the adrenal cortex to produce the very steroids that had so fascinated him in Reichstein's laboratory. That molecule, not yet isolated, was ACTH and the love affair was lifelong. Despite detours into other areas, he kept returning to ACTH. In the last years before his death, he was developing methods to isolate the ACTH receptor.
== History == The first monoamine oxidase inhibitor (MAOI), iproniazid, was discovered accidentally when developing the new antitubercular drug isoniazid. The drug was found to induce euphoria and improve the patient's appetite and sleep quality. The first tricyclic antidepressant, imipramine, was originally developed and studied to be an antihistamine alongside other first-generation antihistamines of the time, such as promethazine. TCAs can increase the level of norepinephrine and serotonin by inhibiting their reuptake transport proteins. The majority of TCAs exert greater effect on norepinephrine, which leads to side effects like drowsiness and memory loss. In order to be more effective on serotonin agonism and avoid anticholinergic and antihistaminergic side effects, selective serotonin reuptake inhibitors (SSRI) were researched and introduced to treat anxiety disorders. The first SSRI, fluoxetine (Prozac), was discovered in 1974 and approved by FDA in 1987. After that, other SSRIs like sertraline (Zoloft), paroxetine (Paxil), and escitalopram (Lexapro) have entered the market. The first serotonin norepinephrine reuptake inhibitor (SNRI), venlafaxine (Effexor), entered the market in 1993. SNRIs can target serotonin and norepinephrine transporters while avoiding imposing significant effects on other adrenergic (α1, α2, and β), histamine (H1), muscarinic, dopamine, or postsynaptic serotonin receptors.
Tensions between Portuguese and Brazilians increased and the Portuguese Cortes, guided by the new political regime imposed by the Liberal Revolution, tried to re-establish Brazil as a colony. The Brazilians refused to yield, and Prince Pedro decided to side with them, declaring the country's independence from Portugal on 7 September 1822. A month later, Prince Pedro was proclaimed the first Emperor of Brazil, with the royal title of Dom Pedro I, resulting in the founding of the Empire of Brazil. The Brazilian War of Independence, which had already begun along this process, spread through the northern, northeastern regions and in the Cisplatina province. The last Portuguese soldiers surrendered on 8 March 1824; Portugal officially recognized Brazilian independence on 29 August 1825. On 7 April 1831, worn down by years of administrative turmoil and political dissent with both liberals and conservatives, including an attempt of republican secession and unreconciled to the way that absolutists in Portugal had given in the succession of King John VI, Pedro I departed for Portugal to reclaim his daughter's crown after abdicating the Brazilian throne in favor of his five-year-old son and heir (Dom Pedro II).
Sources: en.wikipedia.org
Aluminium potassium sulfate: White Copper(II) sulfate: Blue Chromium(III) chloride: Green Nickel(II) sulfate: Green Iron(II) sulfate: Green Iron(III) chloride: Orange Cobalt(II) chloride: Purple Calcium chloride: White Zinc sulfate: White Manganese(II) chloride: Pink
=== August === 8 August – A helicopter crashes into the Tijuca National Park near Rio de Janeiro, killing four people including three Colombian nationals. 13 August – Eight illustrations by Henri Matisse that were stolen in a 2025 heist from the Mário de Andrade Library in São Paulo are recovered by police at a house in São Bernardo do Campo. 18 August – Petrobras announces the discovery of a petroleum field off the coast of Amapá. 19 August – A minibus collides with a truck near Ipiranga, Paraná, killing 23 people.
=== Pharmacokinetics === The oral activity of nandrolone has been studied. With oral administration of nandrolone in rodents, it had about one-tenth of the potency of subcutaneous injection of nandrolone. Nandrolone has very low affinity for human serum sex hormone-binding globulin (SHBG), about 5% of that of testosterone and 1% of that of DHT. It is metabolized by the enzyme 5α-reductase, among others. Nandrolone is less susceptible to metabolism by 5α-reductase and 17β-hydroxysteroid dehydrogenase than testosterone. This results in it being transformed less in so-called "androgenic" tissues like the skin, hair follicles, and prostate gland and in the kidneys, respectively. Metabolites of nandrolone include 5α-dihydronandrolone, 19-norandrosterone, and 19-noretiocholanolone, and these metabolites may be detected in urine. Single intramuscular injections of 100 mg nandrolone phenylpropionate or nandrolone decanoate have been found to produce an anabolic effect for 10 to 14 days and 20 to 25 days, respectively. Conversely, unesterified nandrolone has been used by intramuscular injection once daily.
Sources: en.wikipedia.org
Chinese small-leaf-type tea was introduced into India in 1836 by the British in an attempt to break the Chinese monopoly on tea. In 1841, Archibald Campbell brought seeds of Chinese tea from the Kumaun region and experimented with planting tea in Darjeeling. The Alubari tea garden was opened in 1856, and Darjeeling tea began to be produced. In 1848, Robert Fortune was sent by the East India Company on a mission to China to bring the tea plant back to Great Britain. He began his journey in high secrecy as his mission occurred in the lull between the First Opium War and the Second Opium War. The Chinese tea plants he brought back were introduced to the Himalayas, though most did not survive. The British had discovered that a different variety of tea was endemic to Assam and the northeast region of India, which was then hybridized with Chinese small-leaf-type tea. Using Chinese planting and cultivation techniques, the British colonial government established a tea industry by offering land in Assam to any European who agreed to cultivate it for export. Tea was originally consumed only by Anglo-Indians; however, it became widely consumed in India in the 1950s because of a successful advertising campaign by the India Tea Board. The British introduced tea industry to Sri Lanka (then Ceylon) in 1867.
=== Disease association === Genetic activation of NRF2 has been implicated in the development of de novo tumors, as well as in the progression of atherosclerosis by increasing plasma cholesterol levels and hepatic cholesterol content. It has been suggested that these pro-atherogenic effects may outweigh the protective benefits of NRF2-mediated antioxidant induction.
This elevation leads to increased brain-derived neurotrophic factor (BDNF) levels, which in turn enhance dendritic branching and spine density in neurons of the nucleus accumbens and prefrontal cortex, potentially persisting for weeks after drug cessation. In transgenic mice engineered to express ΔFosB in the nucleus accumbens and dorsal striatum, heightened behavioral sensitization to cocaine has been observed. These mice self-administer cocaine at lower doses and display a greater propensity for relapse after withdrawal ΔFosB also enhances sensitivity to reward by upregulating the AMPA receptor subunit GluR2 and downregulating the expression of dynorphin. Cocaine use has also been shown to increase DNA damage in the brains of rodents. During subsequent DNA repair, enduring alterations in chromatin structure may arise, such as DNA methylation and methylation or acetylation of histones at the repair loci. These modifications may result in lasting epigenetic "scars", which are believed to contribute to the persistent epigenetic changes observed in cocaine addiction.
== External links == FML – Functional Materials Laboratory of the ETH Zürich Properties and use of magnetic nanoparticle clusters (magnetic nanobeads) Magnetic nanoparticles target human cancer cells Magnetic Nanoparticles Remove Ovarian Cancer Cells from the Abdominal Cavity Wiedwald, U. and Ziemann, P. (Ed.): Properties and applications of magnetic nanoparticles, Thematic Series in the Open Access Beilstein Journal of Nanotechnology. Effects of surfactant on the structural and magnetic properties of hydrothermally synthesized NiFe2O4 nanoparticles
Sources: en.wikipedia.org
It is a seven-amino-acid peptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro, produced by chemical synthesis rather than extracted from biological tissue. Its design is based on tuftsin, a natural immunomodulatory tetrapeptide. The C-terminal Pro-Gly-Pro segment is a common stabilising motif in short regulatory peptides.
The core four residues correspond to tuftsin, which occurs naturally as part of immunoglobulin G. The full seven-residue sequence, however, is not a known endogenous peptide. It is a laboratory-designed analogue intended to combine tuftsin-like activity with greater resistance to breakdown.
No single receptor has been confirmed as the primary target. Reports describe involvement of the GABAergic system, interference with enkephalin degradation, and shifts in neurotrophic factor expression. Because these observations come from different models and assays, they have not yet been integrated into one accepted mechanism.
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.