anxiolytic is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2025-08-15. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic heptapeptide | Tuftsin analogue with a C-terminal Pro-Gly-Pro tail |
| Amino acid sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Abbreviated TKPRPGP in most catalogues |
| Molecular mass | About 752 Da | Value for the free peptide |
| Solubility | Freely soluble in water | Aqueous solutions are kept cold and used promptly |
| Typical storage | -20 °C, dry, protected from light | Applies to the lyophilised powder before reconstitution |
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.
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.
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.
== Effect of viruses == MHC class I molecules are loaded with peptides generated from the degradation of ubiquitinated cytosolic proteins in proteasomes. As viruses induce cellular expression of viral proteins, some of these products are tagged for degradation, with the resulting peptide fragments entering the endoplasmic reticulum and binding to MHC I molecules. It is in this way, the MHC class I-dependent pathway of antigen presentation, that the virus infected cells signal T-cells that abnormal proteins are being produced as a result of infection. The fate of the virus-infected cell is almost always induction of apoptosis through cell-mediated immunity, reducing the risk of infecting neighboring cells. As an evolutionary response to this method of immune surveillance, many viruses are able to down-regulate or otherwise prevent the presentation of MHC class I molecules on the cell surface. In contrast to cytotoxic T lymphocytes, natural killer (NK) cells are normally inactivated upon recognizing MHC I molecules on the surface of cells. Therefore, in the absence of MHC I molecules, NK cells are activated and recognize the cell as aberrant, suggesting that it may be infected by viruses attempting to evade immune destruction. Several human cancers also show down-regulation of MHC I, giving transformed cells the same survival advantage of being able to avoid normal immune surveillance designed to destroy any infected or transformed cells.
=== Depapillation === In some diseases, there can be depapillation of the tongue, where the lingual papillae are lost, leaving a smooth, red and possibly sore area. Examples of depapillating oral conditions include geographic tongue, median rhomboid glossitis and other types of glossitis. The term glossitis, particularly atrophic glossitis is often used synonymously with depapillation. Where the entire dorsal surface of the tongue has lost its papillae, this is sometimes termed "bald tongue". Nutritional deficiencies of iron, folic acid, and B vitamins may cause depapillation of the tongue.
=== Synthesis === 4-AcO-DMT can be obtained by acetylation of psilocin under alkaline or strongly acidic conditions. It is, therefore, a synthetic compound. 4-AcO-DMT is more resistant than psilocin to oxidation under basic conditions due to its acetoxy group. It is not as difficult as psilocybin to synthesize.
=== Timing === Newborn babies usually breastfeed 8 to 12 times every 24 hours, and they typically express hunger cues every one to three hours for the first two to four weeks of their lives. A newborn has a small stomach capacity, approximately 20 mL. The amount of breast milk that is produced is timed to meet the infant's needs in that the first milk, colostrum, is concentrated but produced in only very small amounts, gradually increasing in volume to meet the expanding size of the infant's stomach capacity. Cluster feeding may occur for several months, whereby infants will feed very frequently (every 30 minutes to 1 hour), usually associated with developmental milestones. Many newborns typically feed for 10 to 15 minutes on each breast; however, feeds may last up to 45 minutes, depending on the infant's alertness and efficiency. Nutritive sucking follows a slow, rhythmic pattern, with one to two sucks per swallow. Non-nutritive sucking is a faster-paced sucking pattern with few swallows. This swallow pattern is often observed at the beginning or the end of a feed. At the beginning of the feed, this pattern triggers milk letdown, while at the end of the feed, this may signal that the infant is tired or becoming relaxed with a slower milk velocity.
Sources: en.wikipedia.org
Aspartate transaminase (AST) or aspartate aminotransferase, also known as AspAT/ASAT/AAT or (serum) glutamic oxaloacetic transaminase (GOT, SGOT), is a pyridoxal phosphate (PLP)-dependent transaminase enzyme (EC 2.6.1.1) that was first described by Arthur Karmen and colleagues in 1954. AST catalyzes the reversible transfer of an α-amino group between aspartate and glutamate and, as such, is an important enzyme in amino acid metabolism. AST is found in the liver, heart, skeletal muscle, kidneys, brain, red blood cells and gall bladder. Serum AST level, serum ALT (alanine transaminase) level, and their ratio (AST/ALT ratio) are commonly measured clinically as biomarkers for liver health. The tests are part of blood panels. The half-life of total AST in the circulation approximates 17 hours and, on average, 87 hours for mitochondrial AST. Aminotransferase is cleared by sinusoidal cells in the liver.
Masters had also done the same to buy himself a property. Several titles, including Accountancy Age and Computing were sold to the rival company VNU in 1980. The transaction raised £17m, half of which went to Heseltine, but in Crick's view was a bad move for Haymarket. During Heseltine's second period out of office (1986–1990), Masters threatened to resign if Heseltine returned to Haymarket, but once again he became a consultant on £100,000 per annum.
Serine/threonine protein kinases (EC 2.7.11.-) phosphorylate the OH group of serine or threonine (which have similar side chains). Activity of these protein kinases can be regulated by specific events (e.g., DNA damage), as well as numerous chemical signals, including cAMP/cGMP, diacylglycerol, and Ca2+/calmodulin. One very important group of protein kinases are the MAP kinases (acronym from: "mitogen-activated protein kinases"). Important subgroups are the kinases of the ERK subfamily, typically activated by mitogenic signals, and the stress-activated protein kinases JNK and p38. While MAP kinases are serine/threonine-specific, they are activated by combined phosphorylation on serine/threonine and tyrosine residues. Activity of MAP kinases is restricted by a number of protein phosphatases, which remove the phosphate groups that are added to specific serine or threonine residues of the kinase and are required to maintain the kinase in an active conformation.
Sources: en.wikipedia.org
internal carotid the supratrochlear artery to the midline forehead. The supratrochlear artery is a branch of the ophthalmic branch of the internal carotid artery. the supraorbital artery to the lateral forehead and scalp as far up as the vertex. The supraorbital artery is a branch of the ophthalmic branch of the internal carotid artery. external carotid the superficial temporal artery gives off frontal and parietal branches to supply much of the scalp the occipital artery which runs posteriorly to supply much of the posterior aspect of the scalp the posterior auricular artery, a branch of the external carotid artery, ascends behind the auricle to supply the scalp above and behind the auricle. Because the walls of the blood vessels are firmly attached to the fibrous tissue of the superficial fascial layer, cut ends of vessels here do not readily retract; even a small scalp wound may bleed profusely. Venous drainage The veins of the scalp accompany the arteries and thus have similar names, e.g. Supratrochlear and supraorbital veins, which unite at the medial angle of the eye, and form the angular vein, which further continues as the facial vein. The superficial temporal vein descends in front of the tragus, enters the parotid gland, and then joins the maxillary vein to form the retromandibular vein. The anterior part of it unites with the facial vein to form the common facial vein, which drains into jugular vein, and ultimately to the subclavian vein. The occipital vein terminates to the sub-occipital plexus.
== Signs and symptoms == As with other cerebral creatine deficiency syndromes, individuals affected with AGAT deficiency are intellectually disabled and can have seizures. They can often have muscle weakness. These symptoms are caused by the lack of creatine in skeletal muscles and in the brain. AGAT deficiency was first identified in 2000, in a pair of sisters aged 4 and 6. Both sisters had severe intellectual disability.
dehydrogenase, glyceraldehyde phosphate (nicotinamide adenine dinucleotide phosphate) (phosphorylating) GAPDH glyceraldehyde phosphate dehydrogenase (nicotinamide adenine dinucleotide phosphate) (phosphorylating) glyceraldehyde-3-phosphate dehydrogenase (NADP) (phosphorylating) NADP-dependent glyceraldehyde phosphate dehydrogenase NADP-glyceraldehyde phosphate dehydrogenase NADP-glyceraldehyde-3-phosphate dehydrogenase NADP-triose phosphate dehydrogenase triosephosphate dehydrogenase (NADP)
Sources: en.wikipedia.org
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.
Tuftsin is a natural tetrapeptide derived from the Fc portion of immunoglobulin G. Selank retains that tetrapeptide at its N-terminus and adds three residues to improve resistance to enzymatic breakdown. The relationship is structural, and the two molecules are not interchangeable in experimental work.
It holds a product registration in Russia for intranasal use as an anxiolytic. Registrations of that kind are not automatically accepted by regulators elsewhere. In most other countries it is treated as an unapproved substance or a research material.
Intranasal administration predominates in both animal and human research because it avoids hepatic first-pass metabolism. Injectable and intraperitoneal routes appear in animal work mainly for comparison.