Everything below concerns blood-brain barrier. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-04-11. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Typical purity report | 95% or higher by HPLC | Area percentage at 214 nm |
| Identity confirmation | Mass spectrometry | Electrospray or MALDI |
| Powder storage | -20 C, desiccated | Protect from light |
| Solution storage | 2-8 C short term | Freeze aliquots for longer |
| Quality document | Certificate of analysis | States method and value |
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.
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.
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.
Animal studies have examined behaviour in tests of anxiety, memory retention and stress response, and several report changes in neurotrophic or neurotransmitter-related markers. The human evidence base is much smaller, consisting mainly of short trials conducted in Russia with limited reporting in English-language journals. Sample sizes are modest and outcome measures vary between studies, so the findings are best described as preliminary. Independent replication under modern trial standards has not been widely reported.
==== ONRAB ==== ONRAB "Ultralite" (Artemis Technologies Inc., Guelph, Ontario, Canada) is an experimental adenovirus vaccine. ONRAB baits have been distributed by the United States Department of Agriculture (USDA) in select areas of the eastern United States under an experimental permit to target raccoons since 2011. ONRAB "Ultralite" baits consist of a blister pack with a coating matrix of vanilla flavor, green food coloring, vegetable oil and hydrogenated vegetable fat.
=== Agents of spontaneous missense mutation === Environmental mutagens, such as tobacco smoke or UV radiation, may be a cause of spontaneous missense mutations. Tobacco smoke has been implicated in transversion mutations in the K-ras gene, with a meta-analysis of lung carcinomas showing 25 tumours containing a G to T mutation causing an amino acid change from glycine to cysteine, and 11 tumours with a G to T mutation causing an amino acid change from glycine to valine. Similarly, numerous studies have shown ultraviolet light induces missense mutations in the p53 gene, which when unregulated, reduces the cell's ability to recognize DNA damage and engage in apoptosis, leading to cell proliferation and potential skin carcinogenesis.
Jan van Helmont began the research of the process in the mid-17th century when he carefully measured the mass of the soil a plant was using and the mass of the plant as it grew. After noticing that the soil mass changed very little, he hypothesized that the mass of the growing plant must come from the water, the only substance he added to the potted plant. His hypothesis was partially accurate – much of the gained mass comes from carbon dioxide as well as water. However, this was a signaling point to the idea that the bulk of a plant's biomass comes from the inputs of photosynthesis, not the soil itself. Joseph Priestley, a chemist and minister, discovered that when he isolated a volume of air under an inverted jar and burned a candle in it (which gave off CO2), the candle would burn out very quickly, much before it ran out of wax. He further discovered that a mouse could similarly "injure" air. He then showed that a plant could restore the air the candle and the mouse had "injured". In 1779, Jan Ingenhousz repeated Priestley's experiments. He discovered that it was the influence of sunlight on the plant that could cause it to revive a mouse in a matter of hours. In 1796, Jean Senebier, a Swiss pastor, botanist, and naturalist, demonstrated that green plants consume carbon dioxide and release oxygen under the influence of light. Soon afterward, Nicolas-Théodore de Saussure showed that the increase in mass of the plant as it grows could not be due only to uptake of CO2 but also to the incorporation of water.
Sources: en.wikipedia.org
==== Optic neuropathy ==== Some patients with copper deficiency have shown signs of vision and color loss. The vision is usually lost in the peripheral views of the eye. The bilateral vision loss is usually very gradual. An optical coherence tomography (OCT) shows some nerve fiber layer loss in most patients, suggesting the vision loss and color vision loss was secondary to optic neuropathy or neurodegeneration.
Other additions to ColdFusion 8 are built-in Ajax widgets, file archive manipulation (CFZIP), Microsoft Exchange server integration (CFEXCHANGE), image manipulation including automatic CAPTCHA generation (CFIMAGE), multi-threading, per-application settings, Atom and RSS feeds, reporting enhancements, stronger encryption libraries, array and structure improvements, improved database interaction, extensive performance improvements, PDF manipulation and merging capabilities (CFPDF), interactive debugging, embedded database support with Apache Derby, and a more ECMAScript compliant CFSCRIPT. For development of ColdFusion applications, several tools are available: primarily Adobe Dreamweaver CS4, Macromedia HomeSite 5.x, CFEclipse, Eclipse and others. "Tag updaters" are available for these applications to update their support for the new ColdFusion 8 features.
== Etymology == The name probably comes from a confusion between the Ricinus plant that produces it and another plant, the Vitex agnus-castus. An alternative etymology, though, suggests that it was used as a replacement for castoreum.
Sources: en.wikipedia.org
{\displaystyle {\begin{array}{l}{}\\{\ce {^{238}_{92}U->[\alpha ][4.463\times 10^{9}\ {\ce {y}}]{^{234}_{90}Th}->[\beta ^{-}][24.11\ {\ce {d}}]{^{234\!m}_{91}Pa}}}{\begin{Bmatrix}{\ce {->[0.16\%][1.16\ {\ce {min}}]{^{234}_{91}Pa}->[\beta ^{-}][6.70\ {\ce {h}}]}}\\{\ce {->[99.84\%\ \beta ^{-}][1.16\ {\ce {min}}]}}\end{Bmatrix}}{\ce {^{234}_{92}U->[\alpha ][2.455\times 10^{5}\ {\ce {y}}]{^{230}_{90}Th}->[\alpha ][7.54\times 10^{4}\ {\ce {y}}]{^{226}_{88}Ra}->[\alpha ][1600\ {\ce {y}}]{^{222}_{86}Rn}}}\\{\ce {^{222}_{86}Rn->[\alpha ][3.8235\ {\ce {d}}]{^{218}_{84}Po}->[\alpha ][3.097\ {\ce {min}}]{^{214}_{82}Pb}->[\beta ^{-}][27.06\ {\ce {min}}]{^{214}_{83}Bi}->[\beta ^{-}][19.9\ {\ce {min}}]{^{214}_{84}Po}->[\alpha ][164.3\ \mu {\ce {s}}]{^{210}_{82}Pb}->[\beta ^{-}][22.2\ {\ce {y}}]{^{210}_{83}Bi}->[\beta ^{-}][5.012\ {\ce {d}}]{^{210}_{84}Po}->[\alpha ][138.376\ {\ce {d}}]{^{206}_{82}Pb}}}\end{array}}}
== Engineering and computer science == Renewable energy target Renewable energy technology Resolution enhancement technology, image processing technology used to manipulate dot characteristics ret, return from subroutine instruction in the x86 assembly language Registered engineering technologist, former certification in Alberta, Canada Rehabilitation engineering technologist, a role in rehabilitation engineering Ret, a measurement of the resistance to evaporative heat loss
== Activity and stability == Pepsin is most active in acidic environments between pH 1.5 to 2.5. Accordingly, its primary site of synthesis and activity is in the stomach (pH 1.5 to 2). In humans the concentration of pepsin in the stomach reaches 0.5 – 1 mg/mL. Pepsin is inactive at pH 6.5 and above; however, pepsin is not fully denatured or irreversibly inactivated until pH 8.0. Therefore, pepsin in solutions of up to pH 8.0 can be reactivated upon re-acidification. The stability of pepsin at high pH has significant implications on disease attributed to laryngopharyngeal reflux. Pepsin remains in the larynx following a gastric reflux event. At the mean pH of the laryngopharynx (pH = 6.8) pepsin would be inactive but could be reactivated upon subsequent acid reflux events resulting in damage to local tissues. Pepsin exhibits a broad cleavage specificity. Pepsin will digest up to 20% of ingested amide bonds. Residues in the P1 and P1' positions are most important in determining cleavage probability. Generally, hydrophobic amino acids at P1 and P1' positions increase cleavage probability. Phenylalanine, leucine and methionine at the P1 position, and phenylalanine, tryptophan and tyrosine at the P1' position result in the highest cleavage probability. Cleavage is disfavoured by positively charged amino acids histidine, lysine and arginine at the P1 position.
==== P-51 introduction ==== The P-51 Mustang was a solution to the need for an effective bomber escort. It used a common, reliable engine and had internal space for a larger-than-average fuel load. With external fuel tanks, it could accompany the bombers from England to Germany and back. By the time the Pointblank offensive resumed in early 1944, matters had changed. Bomber escort defenses were initially layered, using the shorter-range P-38s and P-47s to escort the bombers during the initial stages of the raid before handing over to the P-51s when they were forced to turn for home. This provided continuous coverage during the raid. The Mustang was so clearly superior to earlier US designs that the 8th Air Force began to steadily switch its fighter groups to the Mustang, first swapping arriving P-47 groups to the 9th Air Force in exchange for those that were using P-51s, then gradually converting its Thunderbolt and Lightning groups. By the end of 1944, 14 of its 15 groups flew Mustangs.
Sources: en.wikipedia.org
Purity is usually reported as an HPLC area percentage, most often measured at 214 nm. Identity is confirmed separately by mass spectrometry. A certificate of analysis should state both the method and the observed value.
Dry powder is kept frozen, desiccated, and shielded from light. Dissolved material is aliquoted and frozen to limit freeze-thaw cycles. Short-term refrigerated storage is common for working solutions.
Russia registers it as a prescription nasal product. Most other markets classify it as a research chemical with no approved medical use. Oversight of purity and labeling is consequently minimal in those markets.
Selank is a synthetic peptide made of seven amino acids. It is modeled on tuftsin, a natural tetrapeptide, with an added three-residue tail. It is not a small-molecule drug.