The short version of heptapeptide fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-09-20 and is reviewed periodically as new material appears.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Route studied | Intranasal | Predominant route in published reports |
| Circulation stability | Short, minutes scale | Peptidases cleave it; the tail slows the process |
| Analytical method | RP-HPLC with mass spectrometry | Used for identity and purity assessment |
| Reported outcome domains | Anxiety and cognitive measures | Derived from small, mostly regional trials |
| Regulatory status | Marketed in Russia | Availability outside that market is limited |
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.
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.
Proposed mechanisms centre on the GABAergic system. Animal and tissue studies report changes in GABA-A receptor expression and reduced activity of GABA transaminase, the enzyme that degrades GABA. Effects on monoamine turnover, including serotonin and dopamine pathways, are also described, and a separate line of work links the peptide to increased expression of brain-derived neurotrophic factor in hippocampal tissue. Most of these findings come from rodent models and cell preparations. How the individual observations combine into a single coherent mode of action is not settled.
Pharmacokinetic data are sparse and largely derived from animal work. After intranasal administration the peptide appears in plasma within minutes, and reported half-lives are short, on the order of minutes to tens of minutes. Degradation proceeds through ordinary proteolytic cleavage into constituent amino acids and smaller fragments. Direct evidence that intact Selank reaches brain tissue in meaningful amounts is limited, and the extent of blood-brain barrier penetration is debated. Some authors argue that fragments, not the parent peptide, carry much of the observed activity.
Published clinical work is concentrated in Russian-language journals and generally involves small samples without independent replication. Systematic reviews in English note the shortage of randomised, placebo-controlled trials and the difficulty of verifying methods from translated reports. Outcome measures vary between studies, which complicates pooling of results. Interest in the compound as a cognitive or anxiolytic agent therefore rests on a thinner evidence base than the volume of citations suggests. Replication in well-powered trials with preregistered endpoints would be needed before firm conclusions about efficacy can be drawn.
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The Purple Book, formally titled Compendium of Macromolecular Terminology and Nomenclature, contains the nomenclature of polymers. The first edition was first published in 1991. The second and latest edition was published in December 2008 and is also available for download.
== Pharmacology == 6-MAM occurs as a metabolite of heroin. Once it has passed first-pass metabolism, 6-MAM is then metabolized into morphine or excreted in urine. Heroin is rapidly metabolized by esterase enzymes in the brain and has an extremely short half-life. It has also relatively weak affinity to μ-opioid receptors because the 3-hydroxy group, essential for effective binding to the receptor, is masked by the acetyl group. Therefore, heroin acts as a prodrug, serving as a lipophilic transporter for the systemic delivery of morphine, which actively binds with μ-opioid receptors.
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The Earl S. Richardson Library's is the main academic information resource center on the campus. Constructed in 2008, the building covers approximately 222,517 square feet. The library's holding constitutes over 500,000 volumes, and access to over 1 million e-books and 5,000 periodical titles. There are 167 online databases that are subscribed to the Library. Reading and studying spaces are provided with wired and wireless access to databases for research. One such collection in the volumes includes books on Africa, with an emphasis on sub-Saharan Africa. The African-American collection includes papers and memorabilia of such persons as Emmett Jay Scott, secretary to Booker T. Washington. The Forbush Collection is composed of materials associated with the Quakers and slavery. The Martin D. Jenkins Collection was acquired in 1980.
== Legal status == Difenoxin is a Schedule I drug by itself in the US; the combination with atropine is in the less-restrictive category Schedule IV on account of the adulterant (the practice of making opioids more easily available by including an abuse-deterring adulterating agent is standard practice in the United States). Pure difenoxin, in Schedule I, has a quota of 50 grammes, and an ACSCN of 9168. The combination of difenoxin and atropine, in Schedule IV, has the DEA ACSCN of 9167 and being in Schedule IV is not assigned an aggregate annual manufacturing quota.
=== Pharmacokinetics === Following a single topical application of 10 g nadifloxacin 1% cream to normal human back skin, the highest plasma concentration was determined to be 107 ng/mL with an elimination half-life of 19.4 hours. Approximately 0.09% of the administered dose was excreted in the urine over 48 hours post- dosing. The plasma concentration reached a steady state on Day 5 of repeated administration study when nadifloxacin 1% cream was applied at 5 g twice daily to normal healthy individuals for a period of 7 days. The plasma concentration reached a peak of 4.1 ng/ml at 8 hours post-final dosing with an elimination half-life of 23.2 hours. The urinary excretion rate reached 0.16% on Day 7.
==== TAS1R1 + TAS1R3 ==== The TAS1R1 + TAS1R3 receptor is a G-protein-coupled receptor, much like the sweet and bitter receptors. It uses the same downstream signaling molecules, including G proteins beta-gamma, PLCB2 and IP3, to ultimately cause a release of calcium (Ca2+) from intracellular stores. Calcium activates a so-called transient-receptor-potential cation channel TRPM5 that leads to membrane depolarization and the consequent release of ATP across a channel of CALHM1 and CALHM3. The ATP released by the "Type II" cell is detected by P2X receptors on nearby afferent gustatory nerve fibers and P2Y receptors on adjacent taste cells. P2X appears to be indispensable for the transduction of umami, so this is probably the main route for umami signals. "Type III" cells, which directly connect to the nerve synapses, also respond to the released ATP by releasing neurotransmitters. One of these neurotransmitters, serotonin, regulates the release of ATP by the type II cells.
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Nitrogen has two stable isotopes: 14N and 15N. The first is much more common, making up 99.634% of natural nitrogen, and the second (which is slightly heavier) makes up the remaining 0.366%. This leads to an atomic weight of around 14.007 u. Both of these stable isotopes are produced in the CNO cycle in stars, but 14N is more common as its proton capture is the rate-limiting step. 14N is one of the five stable odd–odd nuclides (a nuclide having an odd number of protons and neutrons); the other four are 2H, 6Li, 10B, and 180mTa. The relative abundance of 14N and 15N is practically constant in the atmosphere but can vary elsewhere, due to natural isotopic fractionation from biological redox reactions and the evaporation of natural ammonia or nitric acid. Biologically mediated reactions (e.g., assimilation, nitrification, and denitrification) strongly control nitrogen dynamics in the soil. These reactions typically result in 15N enrichment of the substrate and depletion of the product. The heavy isotope 15N was first discovered by S. M. Naudé in 1929, and soon after heavy isotopes of the neighbouring elements oxygen and carbon were discovered. It presents one of the lowest thermal neutron capture cross-sections of all isotopes. It is frequently used in nuclear magnetic resonance (NMR) spectroscopy to determine the structures of nitrogen-containing molecules, due to its fractional nuclear spin of one-half, which offers advantages for NMR such as narrower line width.
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Applications of contact mechanics further extend into the micro- and nanotechnological realm. The original work in contact mechanics dates back to 1881 with the publication of the paper "On the contact of elastic solids" "Über die Berührung fester elastischer Körper" by Heinrich Hertz. Hertz attempted to understand how the optical properties of multiple, stacked lenses might change with the force holding them together. Hertzian contact stress refers to the localized stresses that develop as two curved surfaces come in contact and deform slightly under the imposed loads. This amount of deformation is dependent on the modulus of elasticity of the material in contact. It gives the contact stress as a function of the normal contact force, the radii of curvature of both bodies and the modulus of elasticity of both bodies. Hertzian contact stress forms the foundation for the equations for load bearing capabilities and fatigue life in bearings, gears, and any other bodies where two surfaces are in contact.
Sources: en.wikipedia.org
Reports describe effects on GABA-A receptor expression, monoamine turnover, and neurotrophic factor levels. These are proposed mechanisms drawn mainly from animal models. No single molecular target has been established.
Intranasal delivery is the route described in most published work. It is used because the peptide is degraded quickly once it reaches circulation. Direct evidence of brain penetration in humans is lacking.
Most trials are small, regionally concentrated, and often lack rigorous blinding or placebo control. Independent replication is limited. Reviews in English generally rate the evidence as preliminary.
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.