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.
Updated 2026-04-27. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
| 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 |
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.
Regulatory status differs sharply by region. Selank holds a Russian marketing authorization, where it is supplied mainly as nasal drops, while authorities elsewhere have not approved it for medical use. Material sold internationally is therefore usually labeled as a research chemical rather than a medicine. Peer-reviewed publications come predominantly from Russian laboratories, and sample sizes are generally small. Whether the compound produces comparable effects under independent, well-controlled replication remains an open question that the broader literature has not settled.
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.
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.
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.
Tuftsin, the parent structure, is a naturally occurring immunomodulatory tetrapeptide released from the Fc region of immunoglobulin G by spleen enzymes. Selank extends this four-residue sequence with three additional amino acids. The stated rationale is that the added tail slows enzymatic breakdown and may influence receptor interactions. How the full heptapeptide behaves at the molecular level is not firmly established, and proposed mechanisms often involve indirect modulation of neurotransmitter or immune signaling rather than a single defined target.
Selank is a hydrophilic peptide and dissolves readily in water and in aqueous buffers. The lyophilised powder is typically a white to off-white solid. Because short peptides are prone to hydrolysis and oxidation, handling benefits from limiting exposure to heat, moisture and strong light. Working solutions are commonly prepared in sterile water or saline, and repeated freeze-thaw cycles are avoided to reduce aggregation and loss of activity. These practices reflect general laboratory convention rather than published stability specifications.
Dry powder is normally held at -20 degrees Celsius or lower, in a sealed container with desiccant and protection from light. Reconstituted solutions are usually kept at 2 to 8 degrees Celsius for short periods and frozen for longer ones. Proline residues at several positions are generally associated with some resistance to peptidase attack, but chemical stability still declines at neutral to alkaline pH and at elevated temperature. Exact shelf-life figures are product-specific and are not standardised across suppliers.
=== Extraction and phase transfer using droplet microfluidics === Liquid-liquid extraction is a method used to separate an analyte from a complex mixture; with this method compounds separate based on their relative solubility in different immiscible liquid phases. To overcome some of the disadvantages associated with common bench top methods such as the shake-flask method, Microfluidic liquid-liquid extraction methods have been employed. Microfluidic droplet-based systems have demonstrated the capability to manipulate discrete volumes of fluids in immiscible phases with low Reynolds numbers. and laminar flow regimes. Microscale methods reduce time required, reduce sample and reagent volume, and allow for automation and integration. In some studies, the performance of droplet-based microfluidic extraction compares closely with the shake-flask method. A study which compared the shake-flask and microfluidic liquid-Liquid extrication methods for 26 compounds and found a close correlation between the values obtained (R2= 0.994). It has also been demonstrated that microfluidic liquid-liquid extraction devices can be integrated with other instruments for detection of the extracted analytes. For example, microfluidic extraction could be used to extract an analyte initially in an aqueous phase such as cocaine in saliva then interfaced with on-chip IR spectroscopy for detection.
=== Intermediates in various pathways === In cellular respiration Citric acid cycle: Through a series of chemical reactions, stored energy is released through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins into adenosine triphosphate (ATP) and carbon dioxide. β-oxidation: Acetyl-CoA is produced by the breakdown of both carbohydrates (by glycolysis) and lipids (by β-oxidation). It then enters the citric acid cycle in the mitochondrion by combining with oxaloacetate to form citrate. Cytosolic fatty acid synthesis (FAS): When the insulin concentration in the blood is high, and that of glucagon is low (i.e. after meals), the acetyl-CoA produced by glycolysis condenses as normal with oxaloacetate to form citrate in the mitochondrion. However, instead of continuing through the citric acid cycle to be converted to carbon dioxide and water, the citrate is removed from the mitochondrion into the cytoplasm. There it is cleaved by ATP citrate lyase into acetyl-CoA and oxaloacetate. The oxaloacetate is returned to the mitochondrion as malate (and then converted back into oxaloacetate to transfer more acetyl-CoA out of the mitochondrion). This cytosolic acetyl-CoA can then be used to synthesize fatty acids through carboxylation by acetyl-CoA carboxylase into malonyl CoA, the first committed step in the synthesis of fatty acids. This conversion occurs primarily in the liver, adipose tissue and lactating mammary glands, where the fatty acids are combined with glycerol to form triglycerides, the major fuel reservoir of most animals.
In the "Documents of the First (Founding) Congress of the CLP(USNA), the preamble to the Party Program stated "Basing ourselves on the ‘Communist Manifesto’ and the ‘Program of the Communist International,’ the Marxist-Leninists of the USNA set out to rally the revolutionary working class around the following program.” In the program is the germ of the future analysis of the Party: "The trend toward shifting the economic base from mechanics to electronics has not only increased the reserve army of unemployed but also created a huge qualitatively new army of permanently unemployed, especially amongst national minority proletarians.”
== Structure and bonds == Conjugated proteins always have a prosthetic group that is highly associated with the polypeptide chain. Association can occur either through covalent bonding or strong noncovalent interactions like hydrogen bonding, ionic bonding, or coordination bonding. Depending on whether the prosthetic group is a carbohydrate or phosphate, covalent bonds would involve the formation of either glycoside linkage between the carbohydrate and amino acids or ester linkage between the phosphate residue and the protein.
=== Helmut Schmidt === Finance Minister Helmut Schmidt (SPD) formed a coalition and he served as Chancellor from 1974 to 1982. Hans-Dietrich Genscher, a leading FDP official, became Vice-Chancellor and Foreign Minister. Schmidt, a strong supporter of the European Community (EC) and the Atlantic alliance, emphasised his commitment to "the political unification of Europe in partnership with the USA". Mounting external problems forced Schmidt to concentrate on foreign policy and limited the domestic reforms that he could carry out. The USSR upgraded its intermediate-range missiles, which Schmidt complained was an unacceptable threat to the balance of nuclear power, because it increased the likelihood of political coercion and required a western response. NATO responded in the form of its twin-track policy. The domestic reverberations were serious inside the SPD, and undermined its coalition with the FDP. One of his major successes, in collaboration with French President Valéry Giscard d'Estaing, was the launching of the European Monetary System (EMS) in April 1978.
Sources: en.wikipedia.org
==== MeSH D12.776.377.715.548 – immunoglobulins ==== MeSH D12.776.377.715.548.114 – antibodies MeSH D12.776.377.715.548.114.071 – antibodies, anti-idiotypic MeSH D12.776.377.715.548.114.107 – antibodies, archaeal MeSH D12.776.377.715.548.114.125 – antibodies, bacterial MeSH D12.776.377.715.548.114.125.288 – antistreptolysin MeSH D12.776.377.715.548.114.134 – antibodies, bispecific MeSH D12.776.377.715.548.114.143 – antibodies, blocking MeSH D12.776.377.715.548.114.167 – antibodies, catalytic MeSH D12.776.377.715.548.114.179 – antibodies, fungal MeSH D12.776.377.715.548.114.185 – antibodies, helminth MeSH D12.776.377.715.548.114.191 – antibodies, heterophile MeSH D12.776.377.715.548.114.224 – antibodies, monoclonal MeSH D12.776.377.715.548.114.224.570 – muromonab-cd3 MeSH D12.776.377.715.548.114.240 – antibodies, neoplasm MeSH D12.776.377.715.548.114.248 – antibodies, phospho-specific MeSH D12.776.377.715.548.114.252 – antibodies, protozoan MeSH D12.776.377.715.548.114.254 – antibodies, viral MeSH D12.776.377.715.548.114.254.150 – deltaretrovirus antibodies MeSH D12.776.377.715.548.114.254.150.440 – hiv antibodies MeSH D12.776.377.715.548.114.254.150.500 – htlv-i antibodies MeSH D12.776.377.715.548.114.254.150.510 – htlv-ii antibodies MeSH D12.776.377.715.548.114.254.450 – hepatitis antibodies MeSH D12.776.377.715.548.114.254.450.251 – hepatitis a antibodies MeSH D12.776.377.715.548.114.254.450.504 – hepatitis b antibodies MeSH D12.776.377.715.548.114.254.450.510 – hepatitis c antibodies MeSH D12.776.377.715.548.114.257 – antigen-antibody complex MeSH D12.776.377.715.548.114.301 – antitoxins MeSH D12.776.377.715.548.114.301.138 – antivenins MeSH D12.776.377.715.548.114.301.268 – botulinum antitoxin MeSH D12.776.377.715.548.114.301.438 – diphtheria antitoxin MeSH D12.776.377.715.548.114.301.849 – tetanus antitoxin MeSH D12.776.377.715.548.114.323 – autoantibodies MeSH D12.776.377.715.548.114.323.190 – antibodies, antineutrophil cytoplasmic MeSH D12.776.377.715.548.114.323.204 – antibodies, antinuclear MeSH D12.776.377.715.548.114.323.210 – antibodies, antiphospholipid MeSH D12.776.377.715.548.114.323.210.100 – antibodies, anticardiolipin MeSH D12.776.377.715.548.114.323.210.600 – lupus coagulation inhibitor MeSH D12.776.377.715.548.114.323.300 – complement c3 nephritic factor MeSH D12.776.377.715.548.114.323.390 – immunoconglutinins MeSH D12.776.377.715.548.114.323.480 – immunoglobulins, thyroid-stimulating MeSH D12.776.377.715.548.114.323.480.500 – long-acting thyroid stimulator MeSH D12.776.377.715.548.114.323.732 – rheumatoid factor MeSH D12.776.377.715.548.114.345 – binding sites, antibody MeSH D12.776.377.715.548.114.345.180 – complementarity determining regions MeSH D12.776.377.715.548.114.525 – hemolysins MeSH D12.776.377.715.548.114.573 – immune sera MeSH D12.776.377.715.548.114.573.203 – antilymphocyte serum MeSH D12.776.377.715.548.114.580 – immunoconjugates MeSH D12.776.377.715.548.114.580.450 – immunotoxins MeSH D12.776.377.715.548.114.606 – immunoglobulin allotypes MeSH D12.776.377.715.548.114.606.586 – immunoglobulin gm allotypes MeSH D12.776.377.715.548.114.606.587 – immunoglobulin km allotypes MeSH D12.776.377.715.548.114.619 – immunoglobulin isotypes MeSH D12.776.377.715.548.114.619.026 – immunoglobulin a MeSH D12.776.377.715.548.114.619.026.030 – immunoglobulin a, secretory MeSH D12.776.377.715.548.114.619.026.030.500 – secretory component MeSH D12.776.377.715.548.114.619.026.515 – immunoglobulin alpha-chains MeSH D12.776.377.715.548.114.619.251 – immunoglobulin d MeSH D12.776.377.715.548.114.619.251.500 – immunoglobulin delta-chains MeSH D12.776.377.715.548.114.619.312 – immunoglobulin e MeSH D12.776.377.715.548.114.619.312.500 – immunoglobulin epsilon-chains MeSH D12.776.377.715.548.114.619.393 – immunoglobulin g MeSH D12.776.377.715.548.114.619.393.522 – immunoglobulin gamma-chains MeSH D12.776.377.715.548.114.619.393.522.400 – immunoglobulin gm allotypes MeSH D12.776.377.715.548.114.619.393.550 – long-acting thyroid stimulator MeSH D12.776.377.715.548.114.619.393.570 – muromonab-cd3 MeSH D12.776.377.715.548.114.619.393.700 – rho(d) immune globulin MeSH D12.776.377.715.548.114.619.574 – immunoglobulin m MeSH D12.776.377.715.548.114.619.574.500 – immunoglobulin mu-chains MeSH D12.776.377.715.548.114.632 – immunoglobulins, intravenous MeSH D12.776.377.715.548.114.648 – immunoglobulins, thyroid-stimulating MeSH D12.776.377.715.548.114.656 – insulin antibodies MeSH D12.776.377.715.548.114.664 – isoantibodies MeSH D12.776.377.715.548.114.715 – oligoclonal bands MeSH D12.776.377.715.548.114.767 – opsonin proteins MeSH D12.776.377.715.548.114.820 – plantibodies MeSH D12.776.377.715.548.114.837 – precipitins MeSH D12.776.377.715.548.114.890 – reagins MeSH D12.776.377.715.548.397 – gamma-globulins MeSH D12.776.377.715.548.397.500 – tuftsin MeSH D12.776.377.715.548.538 – immunoglobulin constant regions MeSH D12.776.377.715.548.538.249 – immunoglobulin fab fragments MeSH D12.776.377.715.548.538.500 – immunoglobulin fc fragments MeSH D12.776.377.715.548.538.500.249 – cd4 immunoadhesins MeSH D12.776.377.715.548.680 – immunoglobulin fragments MeSH D12.776.377.715.548.680.650 – immunoglobulin fab fragments MeSH D12.776.377.715.548.680.650.500 – immunoglobulin variable region MeSH D12.776.377.715.548.680.650.500.180 – complementarity determining regions MeSH D12.776.377.715.548.680.650.500.590 – immunoglobulin joining region MeSH D12.776.377.715.548.680.650.750 – tuftsin MeSH D12.776.377.715.548.680.660 – immunoglobulin fc fragments MeSH D12.776.377.715.548.680.660.249 – cd4 immunoadhesins MeSH D12.776.377.715.548.680.660.500 – immunoglobulin constant regions MeSH D12.776.377.715.548.680.745 – immunoglobulin idiotypes MeSH D12.776.377.715.548.705 – immunoglobulin subunits MeSH D12.776.377.715.548.705.500 – immunoglobulin heavy chains MeSH D12.776.377.715.548.705.500.350 – immunoglobulin alpha-chains MeSH D12.776.377.715.548.705.500.360 – immunoglobulin delta-chains MeSH D12.776.377.715.548.705.500.370 – immunoglobulin epsilon-chains MeSH D12.776.377.715.548.705.500.380 – immunoglobulin gamma-chains MeSH D12.776.377.715.548.705.500.380.500 – immunoglobulin gm allotypes MeSH D12.776.377.715.548.705.500.500 – immunoglobulin mu-chains MeSH D12.776.377.715.548.705.625 – immunoglobulin j-chains MeSH D12.776.377.715.548.705.750 – immunoglobulin light chains MeSH D12.776.377.715.548.705.750.530 – immunoglobulin kappa-chains MeSH D12.776.377.715.548.705.750.530.500 – immunoglobulin km allotypes MeSH D12.776.377.715.548.705.750.550 – immunoglobulin lambda-chains MeSH D12.776.377.715.548.705.875 – secretory component MeSH D12.776.377.715.548.797 – immunoglobulin variable region MeSH D12.776.377.715.548.797.180 – complementarity determining regions MeSH D12.776.377.715.548.797.570 – immunoglobulin fab fragments MeSH D12.776.377.715.548.797.590 – immunoglobulin joining region MeSH D12.776.377.715.548.900 – paraproteins MeSH D12.776.377.715.548.900.120 – bence jones protein MeSH D12.776.377.715.548.900.225 – cryoglobulins MeSH D12.776.377.715.548.900.500 – myeloma proteins MeSH D12.776.377.715.548.900.700 – pyroglobulins MeSH D12.776.377.715.548.950 – receptors, antigen, b-cell MeSH D12.776.377.715.548.950.500 – antigens, cd79
==== CYP17A1 inhibition ==== Flutamide and hydroxyflutamide have been found in vitro to inhibit CYP17A1 (17α-hydroxylase/17,20-lyase), an enzyme which is required for the biosynthesis of androgens. In accordance, flutamide has been found to slightly but significantly lower androgen levels in GnRH analogue-treated male prostate cancer patients and women with polycystic ovary syndrome. In a directly comparative study of flutamide monotherapy (375 mg once daily) versus bicalutamide monotherapy (80 mg once daily) in Japanese men with prostate cancer, after 24 weeks of treatment flutamide decreased dehydroepiandrosterone (DHEA) levels by about 44% while bicalutamide increased them by about 4%. As such, flutamide is a weak inhibitor of androgen biosynthesis. However, the clinical significance of this action may be limited when flutamide is given without a GnRH analogue to non-castrated men, as the medication markedly elevates testosterone levels into the high normal male range via prevention of AR activation-mediated negative feedback on the hypothalamic–pituitary–gonadal axis in this context.
== Nomenclature == 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 ribitol:NAD+ 2-oxidoreductase. Other names in common use include adonitol dehydrogenase, ribitol dehydrogenase A (wild type), ribitol dehydrogenase B (mutant enzyme with different properties), and ribitol dehydrogenase D (mutant enzyme with different properties).
== Comparison to other assays == While the colloidal gold assay is the most sensitive in-solution colorimetric protein assay, it may be equally sensitive or surpassed in sensitivity by fluorescent protein assays such as the CBQCA, FQ, NanoOrange, Quant-iT, and EZQ assays.
Sources: en.wikipedia.org
== Contaminant classes == Contaminants of emerging concern (CEC) can be broadly classed into several categories of chemicals such as pharmaceuticals and personal care products, cyanotoxins, nanoparticles, and flame retardants, among others. However, these classifications are constantly changing as new contaminants (or effects) are discovered and emerging contaminants from past years become less of a priority. These contaminants can generally be categorized as truly "new" contaminants that have only recently been discovered and researched, contaminants that were known about but their environmental effects were not fully understood, or "old" contaminants that have new information arising regarding their risks.
=== Aortic insufficiency === Aortic insufficiency (AI) occurs in half to two-thirds of ascending AD, and the diastolic heart murmur of aortic insufficiency is audible in about 32% of proximal dissections. The intensity (loudness) of the murmur depends on the blood pressure and may be inaudible in the event of low blood pressure. Multiple causes exist for AI in the setting of ascending AD. The dissection may dilate the annulus of the aortic valve, preventing the leaflets of the valve from coapting. The dissection may extend into the aortic root and detach the aortic valve leaflets. Alternatively, following an extensive intimal tear, the intimal flap may prolapse into the left ventricular outflow tract, causing intimal intussusception into the aortic valve, thereby preventing proper valve closure.
However, action potentials may end prematurely in certain places where the safety factor is low, even in unmyelinated neurons; a common example is the branch point of an axon, where it divides into two axons. Some diseases degrade myelin and impair saltatory conduction, reducing the conduction velocity of action potentials. The most well-known of these is multiple sclerosis, in which the breakdown of myelin impairs coordinated movement.
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.
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.