If you have been reading about Tuftsin and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Last reviewed on 2025-09-13. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| 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.
He attributed beriberi to the high levels of starch in rice being toxic. He believed that the toxicity was countered in a compound present in the rice polishings. An associate, Gerrit Grijns, correctly interpreted the connection between excessive consumption of polished rice and beriberi in 1901: He concluded that rice contains an essential nutrient in the outer layers of the grain that is removed by polishing. Eijkman was eventually awarded the Nobel Prize in Physiology and Medicine in 1929, because his observations led to the discovery of vitamins. In 1910, a Japanese agricultural chemist of Tokyo Imperial University, Umetaro Suzuki, isolated a water-soluble thiamine compound from rice bran, which he named aberic acid. (He later renamed it Orizanin.) He described the compound as not only an anti-beriberi factor, but also as being essential to human nutrition; however, this finding failed to gain publicity outside of Japan, because a claim that the compound was a new finding was omitted in translation of his publication from Japanese to German. In 1911 a Polish biochemist Casimir Funk isolated the antineuritic substance from rice bran (the modern thiamine) that he called a "vitamine" (on account of its containing an amino group). However, Funk did not completely characterize its chemical structure. Dutch chemists, Barend Coenraad Petrus Jansen and his closest collaborator Willem Frederik Donath, went on to isolate and crystallize the active agent in 1926, whose structure was determined by Robert Runnels Williams, in 1934.
==== On Natural Amino Acids ==== Rh-catalyzed Trp and Cys alkylation Using in situ generated RhII-carbenoid by activation of vinyl-substituted diazo compounds with Rh2(OAc)4, tryptophans and cysteines were shown to be selectively alkylated in aqueous media. However, this method is limited to surface tryptophans and cysteines possibly because of steric constraints.
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Prostaglandins are found in most tissues and organs. They are produced by almost all nucleated cells. They are autocrine and paracrine lipid mediators that act upon platelets, endothelium, uterine and mast cells. They are synthesized in the cell from the fatty acid arachidonic acid. Arachidonic acid is created from diacylglycerol via phospholipase-A2, then brought to either the cyclooxygenase pathway or the lipoxygenase pathway. The cyclooxygenase pathway produces thromboxane, prostacyclin and prostaglandin D, E and F. Alternatively, the lipoxygenase enzyme pathway is active in leukocytes and in macrophages and synthesizes leukotrienes.
Sources: en.wikipedia.org
Angelicin synthase is a cytochrome P450 protein containing heme, isolated from parsnip. It uses molecular oxygen for the oxidation and requires a partner cytochrome P450 reductase for functional expression. This uses nicotinamide adenine dinucleotide phosphate.
== History == Urea was first obtained by Herman Boerhaave in 1727 from evaporates of urine. The discovery is also attributed to the French chemist Hilaire Rouelle as well as William Cruickshank. In 1773, Hilaire Rouelle obtained crystals containing urea by evaporating human urine and treating the concentrate with alcohol. This method was aided by Carl Wilhelm Scheele's discovery that crystals precipitated when urine was treated by concentrated nitric acid. Uremic frost was first described in 1856 by the Austrian physician Anton Drasche. Uremic frost has become rare since the advent of dialysis. It is the classical pre-dialysis era description of crystallized urea deposits over the skin of patients with prolonged kidney failure and severe uremia.
=== Ethanol fuel === Fermentation is the main source of ethanol in the production of ethanol fuel. Common crops such as sugar cane, potato, cassava, and maize are fermented by yeast to produce ethanol which is further processed to become fuel.
The two substrates of this enzyme are D-xylose and oxidised nicotinamide adenine dinucleotide phosphate (NADP+). Its products are D-xylono-1,5-lactone, reduced NADPH, and a proton. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is D-xylose:NADP+ 1-oxidoreductase. Other names in common use include D-xylose (nicotinamide adenine dinucleotide phosphate), dehydrogenase, D-xylose-NADP+ dehydrogenase, D-xylose:NADP+ oxidoreductase, and D-xylose 1-dehydrogenase (NADP+).
=== Defects === There are two kinds of defects: Equilibrium defects, and Non-Equilibrium defects. Self-assembled structures contain defects. Dislocations caused during the assembling of nanomaterials can majorly affect the final structure and in general defects are never completely avoidable. Current research on defects is focused on controlling defect density.[23] In most cases, the thermodynamic driving force for self-assembly is provided by weak intermolecular interactions and is usually of the same order of magnitude as the entropy term. In order for a self-assembling system to reach the minimum free energy configuration, there has to be enough thermal energy to allow the mass transport of the self-assembling molecules. For defect formation, the free energy of single defect formation is given by:
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.