Everything below concerns Selank. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Last reviewed on 2026-04-19. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| 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 |
Outside its country of origin the compound is generally handled as a research chemical rather than an approved medicine. No regulatory approval from the United States Food and Drug Administration or the European Medicines Agency has been granted for human use. Identity and purity are normally checked by reverse-phase high-performance liquid chromatography, with mass spectrometry used to confirm the molecular mass. Lyophilised material is stored cold and desiccated, and repeated freeze-thaw cycles are avoided.
Published work on this peptide almost always uses intranasal delivery, with drops or a spray applied to the nasal mucosa. Some animal experiments have used subcutaneous or intraperitoneal injection, and a smaller number have compared routes directly. Oral administration is not a focus of the literature, because short peptides of this size are broken down by digestive enzymes and cross intestinal barriers poorly. How much of an intranasal dose reaches the bloodstream intact in humans remains an open question.
Selank is not a naturally occurring peptide and has no known endogenous counterpart in human physiology. Russian-language sources frequently call it TP-7, while English-language sources use the name Selank almost exclusively. Database indexing is uneven, partly because early reports appeared in regional journals that are not widely cataloged. Some summaries describe the material as a tuftsin analog and others as a synthetic heptapeptide; the labels overlap rather than conflict. Citing the primary sequence resolves ambiguity more reliably than the research or trade name alone.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, written TKPRPGP in one-letter notation. Its structure consists of the immunomodulatory tetrapeptide tuftsin, Thr-Lys-Pro-Arg, extended at the carboxyl terminus by a Pro-Gly-Pro segment. The molecular formula is commonly given as C33H57N11O9, corresponding to a monoisotopic mass near 751.4 Da and an average molecular mass near 751.9 Da. All seven residues are proteinogenic amino acids, and the molecule carries no modified side chains or non-natural linkages.
The compound was designed at the Institute of Molecular Genetics of the Russian Academy of Sciences during the 1980s and 1990s. The stated design goal was to retain the immunomodulatory and central nervous system activity attributed to tuftsin while improving resistance to enzymatic breakdown. Adding a proline-rich tail to the short parent peptide was a deliberate strategy, because proline residues restrict the conformations available to many peptidases. The same laboratory produced Semax, an ACTH fragment analog, and both compounds were developed in parallel as short, enzymatically stabilized peptides intended for intranasal use.
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.
Quality assessment of Selank samples typically combines purity determination with identity confirmation and counter-ion analysis. Purity is usually reported as a percentage by chromatographic area, with values above 95 percent often quoted for research-grade material. Water content and residual solvents are checked in lyophilized batches because they affect both stability and accurate mass determination. A reported purity figure does not by itself establish that a sample is the intended sequence, so orthogonal methods are needed to rule out sequence isomers or truncation products.
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.
Axonotmesis are a range of peripheral nerve injuries that are considered more severe than Neurapraxia and less severe than Neurotmesis. Axonotmesis involves loss of relative axon continuity and myelin covering, but preservation of the connective tissue framework (including encapsulating tissue, the epineurium and perineurium). Since connective tissue framework is preserved then axonal regeneration is possible, but recovery is slower. Other characteristics:
Mathematical and computational models are essential for understanding the action potential, and offer predictions that may be tested against experimental data, providing a stringent test of a theory. The most important and accurate of the early neural models is the Hodgkin–Huxley model, which describes the action potential by a coupled set of four ordinary differential equations (ODEs). Although the Hodgkin–Huxley model may be a simplification with few limitations compared to the realistic nervous membrane as it exists in nature, its complexity has inspired several even-more-simplified models, such as the Morris–Lecar model and the FitzHugh–Nagumo model, both of which have only two coupled ODEs. The properties of the Hodgkin–Huxley and FitzHugh–Nagumo models and their relatives, such as the Bonhoeffer–Van der Pol model, have been well-studied within mathematics, computation and electronics. However the simple models of generator potential and action potential fail to accurately reproduce the near threshold neural spike rate and spike shape, specifically for the mechanoreceptors like the Pacinian corpuscle. More modern research has focused on larger and more integrated systems; by joining action-potential models with models of other parts of the nervous system (such as dendrites and synapses), researchers can study neural computation and simple reflexes, such as escape reflexes and others controlled by central pattern generators.
Xi's first marriage was to Ke Lingling, the daughter of Ke Hua, China's ambassador to the United Kingdom in the early 1980s. They divorced within a few years. The two were said to fight "almost every day," and after the divorce, Ke moved to the UK. In 1987, Xi married famed folk singer Peng Liyuan. Xi and Peng were introduced by friends as many Chinese couples were in the 1980s. Peng had gained fame in the 1980s and remained far better known in China than Xi until the latter emerged as a likely successor in the late 2000s. The couple frequently lived apart due largely to their separate professional lives. Peng has played a much more visible role as China's "first lady" compared to her predecessors; for example, Peng hosted U.S. First Lady Michelle Obama on her high-profile visit to China in March 2014. Xi and Peng have a daughter named Xi Mingze, who graduated from Harvard University in the spring of 2015. While at Harvard, she used a pseudonym and studied Psychology and English. Xi's family has a home in Jade Spring Hill, a garden and residential area in north-western Beijing run by the CMC. In June 2012, Bloomberg News reported that members of Xi's extended family including his sister Qi Qiaoqiao have substantial business interests, although there was no evidence he had intervened to assist them. The Bloomberg News website was blocked in mainland China in response to the article about his family's wealth and the sales of Bloomberg Terminals in China slowed, while access to the files of Qinchuan Dadi, which was Qi's investment vehicle, was shut down.
=== Direct-to-consumer === Direct-to-consumer tests are regulated as medical devices, although they are not necessarily reviewed by the FDA. 23andMe direct-to-consumer genetic tests were originally offered as LDTs, but the FDA challenged that and forced the company to submit the test for approval as a class II medical device.
== Medical uses == Atenolol is used for a number of conditions including hyperthyroidism, hypertension, angina, long QT syndrome, acute myocardial infarction, supraventricular tachycardia, ventricular tachycardia, essential tremor (ET), and the symptoms of alcohol withdrawal. The role for β-blockers in general in hypertension was downgraded in June 2006 in the United Kingdom, and later in the United States, as they are less appropriate than other agents such as ACE inhibitors, calcium channel blockers, thiazide diuretics and angiotensin receptor blockers, particularly in the elderly. Atenolol has been used to treat anxiety disorders, such as generalized anxiety disorder and social anxiety disorder. It is thought that beta blockers do not directly treat psychological symptoms of anxiety, but can help control physical symptoms such as palpitations, and this may interfere with a positive feedback loop to indirectly reduce psychological anxiety. A 2025 systematic review and meta-analysis that included atenolol found widespread prescription of beta blockers for treatment anxiety disorders, but found no evidence of a beneficial effect relative to placebo or benzodiazepines in people with social phobia or panic disorder. However, the quality of evidence, including both numbers of studies and patients as well as quality and risk of bias of those studies, was limited.
Sources: en.wikipedia.org
=== Cancer risk === Sirolimus may increase an individual's risk for contracting skin cancers from exposure to sunlight or UV radiation, and risk of developing lymphoma. In studies, the skin cancer risk under sirolimus was lower than under other immunosuppressants such as azathioprine and calcineurin inhibitors, and lower than under placebo.
Informed consent approaches include conversations between the medical provider and person seeking care on the details of risks and outcomes, current understandings of scientific research, and how the provider can best assist the person in making decisions. Local standards of care exist in many countries, with most local standards being based on the WPATH standards, with some minor exceptions.
Off California, white sharks will eat cabezons, white seabasses, lingcod, halibut, leopard sharks, smooth-hounds, spiny dogfishes, school sharks, stingrays, bat rays, and skates. In the Mediterranean, they consume Atlantic bluefin tunas, bullet tunas, Atlantic bonitos, swordfishes, blue sharks, shortfin makos, and stingrays. An ocean sunfish was also recorded in a white shark's stomach. Off the northeastern US, juveniles commonly eat bottom-dwelling fish like hake, while off South Africa, they often prey on dusky sharks. The remains of an adult whale shark were found in a white shark, though whether this was active hunting or scavenging could not be determined. They are also recorded to consume cephalopods, as evidenced by beaks found in their stomachs. Off South Africa, white sharks under 2.5 m (8.2 ft) were found with remains of coastal and bottom-dwelling species like certain octopus species, as well as species of the genera Sepia and Loligo, while larger sharks seem to prefer more open-ocean species like those of the genera Ancistrocheirus, Octopoteuthis, Lycoteuthis, Ornithoteuthis, Chiroteuthis, and Argonauta. Near Guadalupe, white sharks have been documented with scars that appear to have been caused by neon flying squids, jumbo squids, and giant squids. Both fish and cephalopods may be important food sources at the White Shark Café. Other animals recorded as prey include sea turtles.
== Signs and symptoms == Yaws primarily occurs in children, most frequently in those aged 6–10. Yaws is classified as primary, secondary, and tertiary; this can be clinically useful, but infected patients often have a mix of stages. Within 9–90 days (but usually about 21 days) of infection, a painless but distinctive "mother yaw" nodule appears. Initially reddened and inflamed, it may become a papilloma, which can then become an ulcer, possibly with a yellow crust. Mother yaws are most commonly found on the legs and ankles, and are rarely found on the genitals (unlike syphilis). The mother yaw enlarges and becomes warty in appearance. Nearby "daughter yaws" may also appear simultaneously. This primary stage resolves completely, with scarring, within 3–6 months. The scar is often pigmented.
==== Apoptosis inhibition ==== Sendai virus P gene encodes a nested set of proteins (C', C, Y1 and Y2), which are named to collectively as the C proteins (see the section "Genome structure" below). C proteins of SeV are able to suppress apoptosis. The antiapoptotic activity of the C proteins supports SeV infection in the host cells.
Sources: en.wikipedia.org
==== Wound healing ==== High dose aspirin treatment (which inhibits cyclooxygenases-1 and -2 to block their production of 12-HHT), thromboxane synthase knockout, and BLT2 receptor knockout, but not TXA2 receptor knockout, impair keratinocyte-based re-epithelialization and thereby closure of experimentally induced wounds in mice. A synthetic BLT2 receptor agonist accelerates wound closure not only in this mouse model but also in the db/db mouse model of obesity, diabetes, and dyslipidemia due to leptin receptor deficiency. 12-HHT accumulated in the wounds of the former mouse model. Companion studies using an in vitro scratch test assay indicated that 12-HHT stimulated human and mouse keratinocyte migration by a BLT2 receptor-dependent mechanism that involved the production of tumor necrosis factor α and metalloproteinases. These results indicate that the 12-HHT/BLT2 receptor axis is a critical contributor to wound healing in mice and possibly humans. The axis operates by recruiting the movement of keratinocytes to close the wound. This mechanism may underlie the suppression of wound healing that accompanies the high dose intake of aspirin and, based on mouse studies, other non-steroidal anti-inflammatory agents (NSAIDs) in humans. Synthetic BLT2 agonists may be useful for speeding the healing of chronic ulcerative wounds, particularly in patients with, for example diabetics, that have impaired wound healing.
The three substrates of this enzyme are L-aspartic acid, water, and oxidised nicotinamide adenine dinucleotide (NAD+}. Its products are oxaloacetic acid, ammonia, reduced NADH, and a proton. Nicotinamide adenine dinucleotide phosphate can be used as an alternative cofactor. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-NH2 group of donors with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is L-aspartate:NAD(P)+ oxidoreductase (deaminating). Other names in common use include NAD-dependent aspartate dehydrogenase, NADH2-dependent aspartate dehydrogenase, and NADP+-dependent aspartate dehydrogenase. This enzyme participates in nicotinate and nicotinamide metabolism.
== Other epitope-tag combinations == The principle of tandem-affinity purification of multiprotein complexes is not limited to the combination of CBP and Protein A tags used in the original work by Rigaut et al. (1999). For example, the combination of FLAG- and HA-tags has been used since 2000 by the group of Nakatani to purify numerous protein complexes from mammalian cells. Many other tag combinations have been proposed since the TAP principle was published.
== Research == Valko's 1986 study compared the efficacy of microwave irradiation as a sample preparation method for chromatography with traditional approaches. This research highlighted its exceptional time and energy efficiency, particularly suited for rapid extractions in large sample series. In 1997, she invented the Chromatographic Hydrophobicity Index (CHI) based on reversed-phase HPLC retention times, offering a high-throughput approach for physicochemical profiling in drug design, demonstrating strong correlations with acetonitrile distribution and octanol/water partition coefficients. Her collaborative effort with GSK colleagues in 2003 outlined the development and validation of a rapid gradient HPLC method for determining Human Serum Albumin (HSA) binding of discovery compounds. In 2011, she proposed a novel approach, using calibrated HPLC retention times on biomimetic stationary phases to develop mechanistic models. This approach enabled estimating in vivo unbound volume of distribution (V(du)) and fraction unbound in tissue (f(ut)) during lead optimization, aiding consideration of in vitro potency and estimated in vivo pharmacokinetic distribution of compounds. In the same year, she explored the optimization of drug properties in drug discovery, introducing the drug efficiency index (DEI) as a marker of in vivo efficacy. Moreover, her 2015 study explored developing and optimizing a high-throughput assay for directly measuring intracellular compound concentration in HeLa cells.
=== Vaccines === When pseudouridine is used in place of uridine in synthetic mRNA, the modified mRNA molecule arouses less response from Toll-like receptors, a part of the human immune system that would otherwise identify the mRNA as unwelcome. This makes pseudouridine useful in mRNA vaccines, including the mRNA COVID-19 vaccines. This property of pseudouridine was discovered by Katalin Karikó and Drew Weissman in 2005, for which they shared the 2023 Nobel Prize in Physiology or Medicine. N1-Methylpseudouridine provides even less innate immune response than Ψ, as well as improving translation capacity. Both Pfizer-BioNTech and Moderna mRNA vaccines therefore use N1-Methylpseudouridine rather than Ψ.
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.
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.