The short version of Tuftsin analogue fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-06-24 and is reviewed periodically as new material appears.
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.
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.
Characterization of Selank in laboratory settings relies on standard peptide analytical techniques. Reverse-phase high-performance liquid chromatography separates the peptide from related impurities and degradation products, while mass spectrometry confirms molecular identity through accurate mass measurement. Amino acid analysis and peptide sequencing verify the primary structure when reference material is unavailable. Because Selank is a short chain, fragmentation-based analysis produces a diagnostic ion pattern that supports confident identification.
Peptide stability depends strongly on temperature, moisture, and pH. Lyophilized Selank is generally most stable when stored cold and dry, with freezer temperatures commonly used for long-term storage. In solution, the compound is susceptible to hydrolysis and to microbial growth if it is not handled aseptically. The C-terminal proline-rich extension appears to slow enzymatic cleavage relative to tuftsin, though quantitative degradation rates vary with the matrix and the conditions tested. Published stability data specific to Selank remain sparse.
| 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 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.
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.
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.
Selank is a synthetic heptapeptide developed in Russia. Its sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro, a seven-residue chain built around the natural tetrapeptide tuftsin. Researchers at the Institute of Molecular Genetics of the Russian Academy of Sciences first described the compound in the mid-1990s. The design combined the tuftsin core with an added Pro-Gly-Pro tail, a modification intended to extend the molecule's stability in biological fluids. Published work on the peptide has appeared mainly in Russian-language journals.
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.
== Ownership == The Nobel Institute places no restrictions on the ownership of the medal and the accompanying diploma and prize money once it has been awarded to the recipient. If the recipient chooses not to keep them, they may be sold, donated, or given away. The dedicatee cannot be changed and the prizes cannot be revoked.
Peppermint (Mentha × piperita) is a hybrid species of mint, a cross between watermint and spearmint. Indigenous to Europe and the Middle East, the plant is now widely spread and cultivated in many regions of the world. It is occasionally found in the wild with its parent species. Although the genus Mentha comprises more than 25 species, peppermint is the most widely used variant. While Western peppermint is derived from Mentha × piperita, Chinese peppermint, or bohe, is derived from the fresh leaves of M. haplocalyx. M. × piperita and M. haplocalyx are both recognised as plant sources of menthol and menthone, and are among the oldest herbs used for both culinary and medicinal products.
==== Remote monitoring ==== Spectrometers on earth-observation satellites allow monitoring of formaldehyde in the troposphere. Using ultraviolet–visible spectroscopy, instruments detect absorption features in sunlight reflected by the Earth and use differential optical absorption spectroscopy to calculate vertical column densities. Near-global maps of tropospheric HCHO with daily coverage and kilometer-scale spatial resolution come from the OMI instrument on Aura, the GOME-2 instrument on MetOp, and the newer TROPOMI sensor on Sentinel-5P. Regional maps with hourly coverage over North America are available from the TEMPO instrument on Intelsat 40e. The close coupling between isoprene and formaldehyde has been widely used in top-down approaches that derive regional and global isoprene emissions from satellite measurements of tropospheric formaldehyde columns. These studies provide important constraints on the magnitude and spatial pattern of biogenic isoprene emissions. Processes in the upper atmosphere contribute more than 80% of the total formaldehyde in the environment. Formaldehyde is an intermediate in the oxidation (or combustion) of methane and other carbon compounds from sources such as forest fires, automobile exhaust, and tobacco smoke. When produced in the atmosphere by the action of sunlight and oxygen on atmospheric methane and other hydrocarbons, it becomes part of smog. Formaldehyde has also been detected in outer space.
Sources: en.wikipedia.org
In 1977, the U. S. Navy realized that it needed a replacement for the Oerlikon 20 mm Mk 16 series of guns. In 1986, this requirement was satisfied with the introduction of the Mk 38 Mod 0 weapons system. A derivative of the M242 system, the Mk 38 consists of the M242 chain gun and the Mk 88 Mod 0 machine gun mount. It provides ships with defensive and offensive gunfire capability for the engagement of a variety of surface targets. Designed primarily as a close-range defensive measure, it provides protection against patrol boats, floating mines, and various shore-based targets.
The first application of barrier membranes in the mouth occurred in 1982 in the context of regeneration of periodontal tissues via GTR, as an alternative to resective surgical procedures to reduce pocket depths. A barrier membrane is utilized in the GBR technique to cover the bone defect and create a secluded space, which prevents the connective tissue from growing into the space and facilitates the growth priority of bone tissue. An added benefit of the membrane is that it provides protection of the wound from mechanical disruption and salivary contamination. Barrier membrane criteria should be as follows:
Zearalenone (ZEN), also known as RAL and F-2 mycotoxin, is a potent estrogenic metabolite produced by some Fusarium and Gibberella species. Specifically, the Gibberella zeae, the fungal species where zearalenone was initially detected, in its asexual/anamorph stage is known as Fusarium graminearum. Several Fusarium species produce toxic substances of considerable concern to livestock and poultry producers, namely deoxynivalenol, T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) and zearalenone. Particularly, ZEN is produced by Fusarium graminearum, Fusarium culmorum, Fusarium cerealis, Fusarium equiseti, Fusarium verticillioides, and Fusarium incarnatum. Zearalenone is the primary toxin that binds to estrogen receptors, causing infertility, abortion or other breeding problems, especially in swine. Often, ZEN is detected together with deoxynivalenol in contaminated samples and its toxicity needs to be considered in combination with the presence of other toxins. Zearalenone is heat-stable and is found worldwide in a number of cereal crops, such as maize, barley, oats, wheat, rice, and sorghum. Its production increases when the climate is warm with air humidity at or above twenty percent. The environmental pH plays also a role in the toxin's production. When temperatures fall to 15 °C, alkaline soils still support ZEN production. At the preferred Fusarium temperature, which ranges between 25 °C and 30 °C, neutral pH results in the greatest toxin production.
Sources: en.wikipedia.org
Before the 1960s, abstinence-based detox was the only option for opioid addicts in the United States and produced high relapse rates. However, in 1965, clinicians at Rockefeller University published a report in the Journal of the American Medical Association of the successful treatment of 22 men addicted to heroin with the use of orally administered methadone. In September 1969, the first methadone maintenance treatment program was created in Washington, D.C. by Robert DuPont, M.D, that oversaw 25 parolees. Currently methadone must be provided through opioid treatment programs (OTP) in the United States and can not be prescribed in office settings. Although not required by regulation at this time in the United States, people are usually encouraged to attempt other types of treatment methods before entering methadone treatment programs. Since its use began in the 1960s, methadone is still the preferred choice of treatment at the clinics, and is often part of other protocols. The National Institute on Drug Abuse (NIDA) provides the protocol of how to treat addiction with recommended options including medication assisted treatment, cognitive behavioral therapy (CBT), and medical withdrawal management. Other than methadone, newer medications with fewer side effects including buprenorphine and naltrexone have been introduced, relieve drug cravings, block opioid effects, and avoid physical dependence. CBT is an individualized treatment plan that allow therapists to explore patterns of maladaptive substance use to help generate alternative behavior skills.
In May 2016, a study published in the journal Nature determined that HNK, specifically (2S,6S;2R,6R)-HNK, is responsible for the antidepressant-like effects of ketamine in mice; administration of (2R,6R)-HNK demonstrated ketamine-type antidepressant-like effects, and preventing the metabolic conversion of ketamine into HNK blocked the antidepressant-like effects of the parent compound. As (2R,6R)-HNK, unlike ketamine, does not antagonize the NMDA receptor to a clinically relevant degree, and produces no dissociative or euphoric effects, it has consequently been concluded that the antidepressant effects of ketamine may in fact not be mediated via the NMDA receptor. This is tentative, as confirmation that the findings translate to humans is still needed, but it is notable that published human data show a positive association between the antidepressant responses of ketamine and plasma (2S,6S;2R,6R)-HNK levels. In accordance with the notion that the NMDA receptor is not responsible for the antidepressant effects of ketamine, dizocilpine (MK-801), which binds to and blocks the same site on the NMDA receptor that ketamine does, lacks antidepressant-like effects. Moreover, the findings would explain why other NMDA receptor antagonists such as memantine, lanicemine, and traxoprodil have thus far failed to demonstrate ketamine-like antidepressant effects in human clinical trials. Instead of acting via blockade of the NMDA receptor, (2R,6R)-HNK increases activation of the AMPA receptor via a currently unknown/uncertain mechanism.
Chemical information and Biochemical information. The chemical information includes more than 2,700 metabolite structures with detailed metabolite descriptions, extensive chemical classifications, synthesis information and observed/calculated chemical properties. It also contains nearly 5,000 NMR, GC-MS and LC-MS spectra from more than 600 different metabolites. The biochemical information includes >1,600 protein (and DNA) sequences and >3,100 biochemical reactions that are linked to these metabolite entries. The ECMDB supports many different types of online queries including text searches, chemical structure searches, sequence similarity searches and spectral similarity searches. This makes it particularly useful for metabolomic researchers who are studying E. coli as a model organism. Secondary electrospray ionization (SESI-MS) can discriminate between eleven E. Coli strains thanks to the volatile organic compound profiling.
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 most common approach combines reverse-phase liquid chromatography with mass spectrometry. Chromatography separates the components while mass spectrometry confirms the molecular mass. Peptide sequencing or tandem mass analysis can further verify the amino acid order.