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Last reviewed on 2026-04-16. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
The primary structure of Selank is Thr-Lys-Pro-Arg-Pro-Gly-Pro, corresponding to the molecular formula C33H57N11O9 and a monoisotopic mass of roughly 751.9 daltons. The N-terminal threonine and the arginine residue in the fourth position are shared with tuftsin, which carries the sequence Thr-Lys-Pro-Arg. The three additional residues at the C-terminus, Pro-Gly-Pro, extend the chain and are associated with greater resistance to enzymatic degradation. This extension also separates Selank from the shorter parent peptide.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular class | Synthetic heptapeptide | Stabilized analog of tuftsin |
| Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Single-letter form: TKPRPGP |
| Molecular formula | C33H57N11O9 | Monoisotopic mass about 751.9 Da |
| Appearance | White to off-white powder | Typically supplied as lyophilized solid |
| Solubility | Freely soluble in water | Also soluble in common polar solvents |
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.
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.
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.
Natriuretic peptide receptor B (NPR2), also known as atrionatriuretic peptide receptor B and formerly as guanylate cyclase B, is an atrial natriuretic peptide receptor which in humans is encoded by the NPR2 gene. A mutation in the NPR2 gene can result in achondroplasia and disproportionate dwarfism with short limbs.
Acute intermittent porphyria Adrenoleukodystrophy (Schilder's disease) Alkaptonuria Aminolevulinic acid dehydratase deficiency porphyria (Doss porphyria, plumboporphyria) B-mannosidase deficiency Carotenosis Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy syndrome (CADASIL syndrome) Cerebrotendinous xanthomatosis Citrullinemia Congenital erythropoietic porphyria (Gunther's disease) Diabetic bulla (bullosis diabeticorum, bullous eruption of diabetes mellitus) Diabetic cheiroarthropathy Diabetic dermopathy (shin spots) Dystrophic calcinosis cutis Eruptive xanthoma Erythropoietic protoporphyria Fabry disease (Anderson–Fabry disease, angiokeratoma corporis diffusum) Familial alpha-lipoprotein deficiency (Tangier disease) Familial amyloid polyneuropathy Familial apoprotein CII deficiency Familial combined hyperlipidemia (multiple-type hyperlipoproteinemia) Familial defective apolipoprotein B-100 Familial dysbetalipoproteinemia (broad beta disease, remnant removal disease) Familial hypertriglyceridemia Farber disease (fibrocytic dysmucopolysaccharidosis, lipogranulomatosis) Fucosidosis Gaucher's disease Gout (podagra, urate crystal arthropathy, urate deposition disease) Hartnup disease (pellagra-like dermatosis) Hemodialysis-associated amyloidosis Hepatoerythropoietic porphyria Hereditary coproporphyria Hereditary gelsolin amyloidosis Heredofamilial amyloidosis Hunter syndrome Hurler syndrome (gargoylism, mucopolysaccharidosis type I) Hurler–Scheie syndrome (mucopolysaccharidosis type I H-S) Hyaluronidase deficiency (mucopolysaccharidosis type IX) Iatrogenic calcinosis cutis Idiopathic scrotal calcinosis (idiopathic calcified nodules of the scrotum) Lafora disease Lesch–Nyhan syndrome (juvenile gout) Lichen amyloidosis Limited joint mobility Lipoid proteinosis (hyalinosis cutis et mucosae, Urbach–Wiethe disease) Lipoprotein lipase deficiency (chylomicronemia, chylomicronemia syndrome) Macular amyloidosis Maroteaux–Lamy syndrome (mucopolysaccharidosis type VI) Medication-induced hyperlipoproteinemia Metastatic calcinosis cutis Milia-like calcinosis Morquio's disease (mucopolysaccharidosis type IV) Necrobiosis lipoidica (necrobiosis lipoidica diabeticorum) Niemann–Pick disease Nodular amyloidosis Nodular xanthoma Normolipoproteinemic xanthomatosis Obstructive liver disease (xanthomatous biliary cirrhosis) Ochronosis Osteoma cutis Palmar xanthoma Phenylketonuria Phytosterolemia (sitosterolemia) Porphyria cutanea tarda Primary cutaneous amyloidosis Primary systemic amyloidosis Prolidase deficiency Pseudoporphyria (pseudoporphyria cutanea tarda) Sanfilippo syndrome Scheie syndrome (mucopolysaccharidosis type I S) Secondary cutaneous amyloidosis Secondary systemic amyloidosis Sialidosis Sly syndrome (mucopolysaccharidosis type VII) Subepidermal calcified nodule (solitary congenital nodular calcification, Winer's nodular calcinosis) Transient erythroporphyria of infancy (purpuric phototherapy-induced eruption) Traumatic calcinosis cutis Tuberoeruptive xanthoma (tuberous xanthoma) Tumoral calcinosis Variegate porphyria (mixed hepatic porphyria, mixed porphyria, South African genetic porphyria, South African porphyria) Verruciform xanthoma Waxy skin Wilson's disease (hepatolenticular degeneration) Xanthelasma palpebrarum (xanthelasma) Xanthoma diabeticorum Xanthoma planum (plane xanthoma) Xanthoma striatum palmare Xanthoma tendinosum (tendinous xanthoma) Xanthoma tuberosum
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Sources: en.wikipedia.org
== Safety == Due to reclassification as UN0508, a class 1.3C explosive, hydroxybenzotriazole and its monohydrate crystal are no longer allowed to be transported by sea or air as per 49CFR (USDOT hazardous materials regulations). However, UNECE draft proposal ECE/TRANS/WP.15/AC.1/HAR/2009/1 has been circulated to UN delegates and, if implemented, would amend current regulations thus allowing for the monohydrate crystal to be shipped under the less-stringent code of UN3474 as a class 4.1 desensitized explosive. HOBt was demonstrated to not exhibit dermal corrosion or irritation but did exhibit eye irritation. The sensitization potential of HOBt was shown to be low (non-sensitizing at 1% in LLNA testing according to OECD 429).
=== Bleeding === SSRIs directly increase the risk of abnormal bleeding by lowering platelet serotonin levels, which are essential to platelet-driven hemostasis. SSRIs interact with anticoagulants, like warfarin, and antiplatelet drugs, like aspirin. This includes an increased risk of GI bleeding, and post operative bleeding. The relative risk of intracranial bleeding is increased, but the absolute risk is low. SSRIs are known to cause platelet dysfunction. This risk is greater in those who are also on anticoagulants, antiplatelet agents and NSAIDs (nonsteroidal anti-inflammatory drugs), as well as with the co-existence of underlying diseases such as cirrhosis of the liver or liver failure.
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AI's propensity to produce inaccurate content has led to an estimated global enterprise loss at over $67 million, though other research says the true impact is significant but not yet well-quantified. According to McKinsey’s State of AI 2024 survey, about 44% of organizations have experienced at least one negative consequence from GenAI, with inaccuracy and hallucination among the top cited risks. Numerous studies have found AI consistently creates inaccurate summaries that sound confidently correct. The New York Times defines slop as analogous to spam: "shoddy or unwanted A.I. content in social media, art, books, and ... in search results." Journalists have expressed concerns about the scale of low-quality generated content with respect to social media content moderation, the monetary incentives from social media companies to spread such content, false political messaging, spamming of scientific research paper submissions, increased time and effort to find higher quality or desired content on the Internet, the indexing of generated content by search engines, and on journalism itself. Studies have found that AI can create inaccurate claims, citations or summaries that sound confidently correct, a phenomenon called hallucination. A paper published by researchers at Amazon Web Services AI Labs found that over 57% of sentences from a sample of over 6 billion sentences from Common Crawl, a snapshot of web pages, were machine translated. Many of these automated translations were seen as lower quality, especially for sentences that were translated into at least three languages.
Sources: en.wikipedia.org
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.
It was developed in Russia, at the Institute of Molecular Genetics of the Russian Academy of Sciences, during the 1990s. Most published research originates from Russian institutions. Independent international replication remains limited.
Tuftsin is a natural tetrapeptide with the sequence Thr-Lys-Pro-Arg that participates in immune signaling. Selank extends that sequence with Pro-Gly-Pro at the C-terminus. The added residues are linked to greater resistance to enzymatic breakdown.
Selank is a synthetic seven-amino-acid peptide modeled on tuftsin, a fragment of the immunoglobulin G heavy chain. It was designed in Russia to combine anxiolytic and immunomodulatory properties in one molecule.