Intranasal route comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Updated 2025-11-19. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Selank is studied chiefly as an animal-model anxiolytic with proposed secondary effects on memory and immune signaling. Reported mechanisms include modulation of the GABA-A receptor complex, inhibition of enkephalin-degrading enzymes, and shifts in monoamine turnover within limbic structures. Some experiments describe increased expression of brain-derived neurotrophic factor in the hippocampus after repeated dosing. No single molecular target has been confirmed, and the peptide does not bind any receptor with the selectivity typical of a conventional small-molecule drug. Mechanism therefore remains a set of hypotheses rather than an established pathway.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Principal proposed target | GABA-A receptor complex | Hypothesis derived mainly from animal pharmacology |
| Common behavioral assay | Elevated plus maze | Rodent test for anxiety-like behavior |
| Reported molecular marker | Hippocampal BDNF expression | Measured by immunoassay or mRNA quantification |
| Typical dosing route | Intranasal | Chosen to reduce first-pass metabolism |
| Reported plasma half-life | Minutes | Based on limited peptide stability data |
Naming for this compound is not fully standardised in English sources. The spelling Selanc appears in some transliterations, and catalogue entries may instead list the peptide sequence itself as the identifier. Reference material sometimes groups it with other short synthetic peptides studied for behavioural effects, which can create confusion when citations are compared. Distinguishing the exact sequence from related tuftsin analogues is therefore a practical first step when reviewing any dataset or specification sheet.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, frequently abbreviated as TKPRPGP. It was designed as a structural analogue of tuftsin, a naturally occurring tetrapeptide released by enzymatic cleavage of the immunoglobulin heavy chain. The two additional proline residues at the C-terminal end extend the parent chain and change how the molecule behaves in solution. The free peptide has a calculated molecular mass of approximately 751.9 g/mol and is generally supplied as a lyophilised white to off-white powder.
Development work on the compound began in the 1980s and 1990s at the Institute of Molecular Genetics in Moscow, within the same research programme that produced the peptide Semax. Early investigators sought a tuftsin derivative with improved resistance to enzymatic breakdown and with activity in the central nervous system after peripheral administration. Most of the primary literature from this period was published in Russian, a factor that still shapes how easily the findings can be checked by outside groups.
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.
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.
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.
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.
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.
The New South Wales Corps, later known as the 102d Regiment of Foot, and lastly as the 100th Regiment of Foot, was a formation of the British Army organised in 1789 in England to relieve the New South Wales Marine Corps, which had accompanied the First Fleet to New South Wales. In Australia, the New South Wales Corps gained notoriety for its trade in rum and mutinous behaviour. Reconstituted as the 102d Regiment of Foot, it was transferred to Bermuda and Nova Scotia, before taking part in the Chesapeake campaign of the War of 1812. Reconstituted for the second time after the war as the 100th Regiment of Foot, it was disbanded in 1818.
== Function == The main biological function of metallothioneins is to maintain homeostasis of the essential metals zinc and copper, but metallothioneins also protect against metal toxicity and oxidative stress.
However, Waley also testified that majority rule was not desirable immediately. Talks aimed at easing the differences between Rhodesia and the United Kingdom were carried out aboard Royal Navy vessels once in December 1966 and again in October 1968. Both efforts failed to achieve agreement, although Harold Wilson added a sixth principle to the five he had previously enunciated: "it would be necessary to ensure that, regardless of race, there was no oppression of the majority by the minority or of [any] minority by the majority." Rhodesian resolve stiffened following a failure to reach a new settlement, with more radical elements of the Rhodesian Front calling for a republican constitution. During a two-proposition referendum held in 1969, the proposal for severing all remaining ties to the British Crown passed by a majority of 61,130 votes to 14,327. Rhodesia declared itself a republic on 2 March 1970. Under the new constitution, a president served as ceremonial head of state, with the prime minister nominally reporting to him. Some in the Rhodesian government had hoped in vain that the declaration of a republic would finally prompt other nations to grant recognition.
There is agreement in the research community that tau contributes strongly to dementia in Alzheimer's disease. Tauopathy occurs in over 30 diseases in addition to Alzheimer's disease. In addition, mutations of the gene for tau (MAPT) cause neurodegenerative disorders known as primary tauopathies, but these diseases occur in the absence of Aβ proteopathy. Current evidence thus favors abnormal Aβ as the prime mover of Alzheimer's disease. However, the Aβ hypothesis and tau hypothesis are not mutually exclusive, in that abnormalities of Aβ initiate the disease and tauopathy is required for its complete expression.
== Pathology == One of the important manifestations of acute rheumatic fever, Sydenham's chorea is believed to be caused by an autoimmune response following infection by group A β-hemolytic streptococci. Two cross-reactive streptococcal antigens have been identified, the M protein and N-acetyl-beta-D-glucosamine, whereby infection leads to autoantibodies being produced against host tissues (molecular mimicry) causing a variety of streptococcal related diseases including Sydenham's chorea but also rheumatic heart disease and nephritic syndrome. Autoantibodies against basal ganglia proteins have been found in Sydenham's chorea but these are non-specific. Dopamine receptor autoantibodies have been reported to correlate with clinical symptoms. Whether these antibodies represent an epiphenomenon or are pathogenic, remains to be proven.
Sources: en.wikipedia.org
== Further reading == Bernard D, Prasanth KV, Tripathi V, Colasse S, Nakamura T, Xuan Z, Zhang MQ, Sedel F, Jourdren L, Coulpier F, Triller A, Spector DL, Bessis A (2010). "A long nuclear-retained non-coding RNA regulates synaptogenesis by modulating gene expression". EMBO J. 29 (18): 3082–3093. doi:10.1038/emboj.2010.199. PMC 2944070. PMID 20729808. Tano K, Mizuno R, Okada T, Rakwal R, Shibato J, Masuo Y, Ijiri K, Akimitsu N (2010). "MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes". FEBS Lett. 584 (22): 4575–4580. Bibcode:2010FEBSL.584.4575T. doi:10.1016/j.febslet.2010.10.008. PMID 20937273. S2CID 207575862.
==== Release ==== The decision to release Olofsson came after a negotiation on conditional release in Belgium at the end of May 2018. On 30 July 2018, Olofsson landed at Landvetter Airport outside Gothenburg, Sweden as a free man.
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Sources: en.wikipedia.org
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.
Behavioral endpoints include time spent in open arms of the elevated plus maze and avoidance latencies. Biochemical endpoints include BDNF concentration, cytokine levels, and monoamine metabolite ratios in brain tissue.
Most published studies are small, originate from a limited number of laboratories, and lack independent replication. Dose-response relationships, measured brain exposure, and long-term outcomes are not well characterized.
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.