Intranasal route 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 2026-07-11. 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.
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.
Naming conventions place Selank in the same research family as Semax, another Russian-developed peptide investigated for cognitive effects. The two compounds share a lineage but differ in sequence and in the biological systems proposed as their targets. Semax descends from ACTH fragments, whereas Selank descends from tuftsin. Publications sometimes identify Selank by its full peptide sequence or by laboratory codes rather than one uniform trade name. Because replication outside Russia is limited, reports on its properties are best read alongside the study design and the purity of the material tested.
| 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 |
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.
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.
Purity assessment relies mainly on reverse-phase high-performance liquid chromatography with ultraviolet detection. Because the peptide lacks a strong chromophore, detection often uses backbone absorbance near 214 nm. Identity is confirmed by mass spectrometry, typically electrospray ionization or matrix-assisted laser desorption, comparing the measured mass against the expected value. Amino acid analysis can verify composition after acid hydrolysis. Diastereomer content and residual counterions are reported less often, although both can influence biological assays.
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.
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.
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.
=== Examples === As enzymes have evolved to bind their substrates tightly, and most reversible inhibitors bind in the active site of enzymes, it is unsurprising that some of these inhibitors are strikingly similar in structure to the substrates of their targets. Inhibitors of dihydrofolate reductase (DHFR) are prominent examples. Other examples of these substrate mimics are the protease inhibitors, a therapeutically effective class of antiretroviral drugs used to treat HIV/AIDS. The structure of ritonavir, a peptidomimetic (peptide mimic) protease inhibitor containing three peptide bonds, as shown in the "competitive inhibition" figure above. As this drug resembles the peptide that is the substrate of the HIV protease, it competes with the substrate in the enzyme's active site. Enzyme inhibitors are often designed to mimic the transition state or intermediate of an enzyme-catalysed reaction. This ensures that the inhibitor exploits the transition state stabilising effect of the enzyme, resulting in a better binding affinity (lower Ki) than substrate-based designs. An example of such a transition state inhibitor is the antiviral drug oseltamivir; this drug mimics the planar nature of the ring oxonium ion in the reaction of the viral enzyme neuraminidase. However, not all inhibitors are based on the structures of substrates. For example, the structure of another HIV protease inhibitor tipranavir is not based on a peptide and has no obvious structural similarity to a protein substrate.
17α-Hydroxyprogesterone (17α-OHP), also known as 17-OH progesterone (17-OHP), or hydroxyprogesterone (OHP), is an endogenous progestogen steroid hormone related to progesterone. It is also a chemical intermediate in the biosynthesis of many other endogenous steroids, including androgens, estrogens, glucocorticoids, and mineralocorticoids, as well as neurosteroids.
A gene is a sequence of DNA that contains genetic information and can influence the phenotype of an organism. Within a gene, the sequence of bases along a DNA strand defines a messenger RNA sequence, which then defines one or more protein sequences. The relationship between the nucleotide sequences of genes and the amino-acid sequences of proteins is determined by the rules of translation, known collectively as the genetic code. The genetic code consists of three-letter 'words' called codons formed from a sequence of three nucleotides (e.g., ACT, CAG, TTT). In transcription, the codons of a gene are copied into messenger RNA by RNA polymerase. This RNA copy is then decoded by a ribosome that reads the RNA sequence by base-pairing the messenger RNA to transfer RNA, which carries amino acids. Since there are 4 bases in 3-letter combinations, there are 64 possible codons (43 combinations). These encode the twenty standard amino acids, giving most amino acids more than one possible codon. There are also three 'stop' or 'nonsense' codons signifying the end of the coding region; these are the TAG, TAA, and TGA codons, (UAG, UAA, and UGA on the mRNA).
=== Civil === Potential targets in internet sabotage include all aspects of the Internet from the backbones of the web, to the internet service providers, to the varying types of data communication mediums and network equipment. This would include: web servers, enterprise information systems, client server systems, communication links, network equipment, and the desktops and laptops in businesses and homes. Electrical grids, financial networks, and telecommunications systems are also deemed vulnerable, especially due to current trends in computerization and automation.
Sources: en.wikipedia.org
Unlike previous elections, healthcare reform played a much more minor role in the 2024 presidential election. Harris stated that she no longer supported a single-payer healthcare system as she had in 2020. Instead, she said she intended to protect and expand items legislated during the Obama and Biden administrations. She said she would "maintain and grow" the Affordable Care Act, while Trump said that he would replace it with his own healthcare plan. Harris also supported limiting yearly out-of-pocket drug costs for seniors, and expanding the $35 cap on insulin for seniors on Medicare to younger individuals in the program as well. Generally, both candidates supported using the government to rein in prescription drug costs. Trump suggested he was open to cutting entitlement programs, such as Social Security and Medicare, part of an effort to "[cut] waste" as described by his campaign. During his first term, several budget proposals did suggest cuts to the programs. Additionally, Vance and Speaker of the House Mike Johnson suggested cuts to the ACA, including around pre-existing conditions, were part of Trump's plan. After Robert F. Kennedy Jr. dropped out of the race and endorsed Trump, Kennedy advocated for his "Make America Healthy Again" agenda, pledging to combat the upward trend in chronic disease patients, with Trump saying Kennedy would "go wild" regarding policy on food and medicines.
=== EC 1.7.99 With other acceptors === EC 1.7.99.1: hydroxylamine reductase EC 1.7.99.2: deleted: reaction may have been due to the combined action of EC 1.7.99.6 nitrous-oxide reductase and EC 1.7.99.7 nitric-oxide reductase EC 1.7.99.3: Now included with EC 1.7.2.1, nitrite reductase (NO-forming) EC 1.7.99.4: Now EC 1.7.1.1, nitrate reductase (NADH), EC 1.7.1.2, nitrate reductase [NAD(P)H], EC 1.7.1.3, nitrate reductase (NADPH), EC 1.7.5.1, nitrate reductase (quinone), EC 1.7.7.2, nitrate reductase (ferredoxin) and EC 1.9.6.1, nitrate reductase (cytochrome) EC 1.7.99.5: Now included with EC 1.5.1.20, methylenetetrahydrofolate reductase [NAD(P)H] EC 1.7.99.6: Now EC 1.7.2.4 nitrous-oxide reductase EC 1.7.99.7: Now EC 1.7.2.5 nitric oxide reductase (cytochrome c) EC 1.7.99.8: hydroxylamine oxidoreductase EC 1.7.99.8: Now classified as EC 1.7.2.8, hydrazine dehydrogenase
=== Vinylic selenides === Vinylic selenides are organoselenium compounds that play a role in organic synthesis, especially in the development of convenient stereoselective routes to functionalized alkenes. Although various methods are mentioned for the preparation of vinylic selenides, a more useful procedure has centered on the nucleophilic or electrophilic organoselenium addition to terminal or internal alkynes. For example, the nucleophilic addition of selenophenol to alkynes affords, preferentially, the Z-vinylic selenides after longer reaction times at room temperature. The reaction is faster at a high temperature; however, the mixture of Z- and E-vinylic selenides was obtained in an almost 1:1 ratio. On the other hand, the adducts depend on the nature of the substituents at the triple bond. Conversely, vinylic selenides can be prepared by palladium-catalyzed hydroselenation of alkynes to afford the Markovnikov adduct in good yields. There are some limitations associated with the methodologies to prepare vinylic selenides illustrated above; the procedures described employ diorganoyl diselenides or selenophenol as starting materials, which are volatile and unstable and have an unpleasant odor. Also, the preparation of these compounds is complex.
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.
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.