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.
Last reviewed on 2025-09-18. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
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.
| 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.
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.
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.
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.
Dexatrim has been on the market for more than 45 years. The brand was originally owned by Thompson Medical, which was acquired by Chattem in 1998. It is now part of Sanofi. Dexatrim formula has changed considerably over the years. In prior formulations, Dexatrim contained the decongestant phenylpropanolamine (PPA) and the amphetamine-like compound ephedra. A 2000 study by Yale University School of Medicine showed an increased risk of hemorrhagic stroke with taking PPA. A case of myocardial injury was also reported using Dexatrim (with PPA) at doses recommended for weight control. In 2000, following the request of the FDA to discontinue marketing drug products containing PPA, Dexatrim dropped PPA from its formula. In 2004, FDA banned a second Dexatrim ingredient, ephedra. Although ephedra showed some effectiveness for short-term weight loss, it was linked to raising blood pressure and increasing the risk of heart problems and stroke. In March 2014, Chattem sold Dexatrim to NVE Pharmaceuticals.
CCL7 is expressed in many types of cells, including stromal cells, keratinocytes, airway smooth muscle cells, parenchymal cells, fibroblasts and leukocytes and also in tumor cells. CCL7 mainly acts as a chemoattractant for several leukocytes, including monocytes, eosinophils, basophils, dendritic cells (DCs), neutrophils, NK cells and activated T lymphocytes. Thus, chemotactic factor CCL7 recruits leukocytes to infected tissues to mediate the immune response. Furthermore, CCL7 has an influence to diapedesis and extravasation of leukocytes. The positive effect of CCL7 is mainly observed in monocyte mobilization from bone marrow to blood circulation and in the recruitment of monocytes to sites of inflammation. It was also reported, that CCL7 can also induce neutrophil migration to the inflammatory site by increasing intracellular Ca2+ flux, which is more typical for the CXC chemokine family members. The speed of immune responses varies depending on the type of the cells. In epithelial cells, fibroblasts, and endothelial cells the response is immediate after the stimulation by proinflammatory cytokines as IL-1β and TNFα. In T lymphocytes the expression of CCL7 occurs after 3–5 days after the stimulation. CCL7 has been shown to interact with MMP2 by binding CCR2 receptor.
The formation of chain structures has a direct impact on the overall strength of the whole polymer; the longer a chain is, the more differing the effects amylopectin will have on starch's morphology. Packing of chains, inter block chain length (IB-CL), also correlates with the gelatinization temperature of starch granules. In tandem, the IB-CL will increase as the length of B chains increases, meaning that as the length of individual B chains increases, so does the blocks between connections with other chains. Finally, in general, the more densely packed the resulting molecule of amylopectin, the higher the strength of the starch gel as a whole unit. Starch utilizes the density-strength correlation of amylopectin as a measure of forming dense, strong bricks as a basis for the final starch configuration. Amylopectin in starch is formed into helices to compose hexagonal structures that will subsequently be differentiated into A (cereal) and B (high-amylose; tubular) type starch. Structurally, A is more compact, while B is looser, hence the higher concentration of amylose.
=== GamerGate === In 2014, Baldwin became associated with GamerGate after using the hashtag "#GamerGate" during the controversy. Sources differed on how to characterize his role in the hashtag's origin: Time wrote that Baldwin "coined" the term, The Washington Post reported that its origin was disputed and that Baldwin claimed credit for it, and The New Yorker described it as having been popularized by him. The New Yorker also reported that Baldwin linked to a video making an allegation about game developer Zoë Quinn that the magazine said had since been "proved false". In a 2014 interview with Vulture, Baldwin described GamerGate as focused on ethics in games journalism and argued that threats of violence should not be treated as inherent to the hashtag, calling it "a mistake to commingle the two". WIRED later described Baldwin as lending "high profile support" to the controversy, while the Columbia Journalism Review wrote that, in the absence of clear spokespeople for GamerGate, journalists sometimes interviewed "proxies like actor Adam Baldwin".
== External links == "Glimepiride mixture with pioglitazone hydrochloride". Drug Information Portal. U.S. National Library of Medicine. Archived from the original on 28 June 2019. "Glimepiride mixture with pioglitazone". Drug Information Portal. U.S. National Library of Medicine. Archived from the original on 28 June 2019.
Sources: en.wikipedia.org
Ser-Thr-Arg-Thr-Arg motif from one subunit and a His from the neighboring subunit both interact with the phosphate group of CP for binding. Binding the primary nitrogen of CP are residues Gln, Cys, and Arg. The carbonyl oxygen of CP is bound by residues Thr, Arg, and His.
== See also == Torricelli's law Coandă effect Euler equations – for the flow of an inviscid fluid Hydraulics – applied fluid mechanics for liquids Navier–Stokes equations – for the flow of a viscous fluid Teapot effect Terminology in fluid dynamics
== History and production == Its industrial production was developed in Italy by Antonio Carpenè in collaboration with Enrico Comboni. Originally it was separated directly from the red wine (in which it is present for approximately 1% of the total) by precipitating it with basic lead acetate and obtaining a dark blue substance. Today, enocyanin is obtained from the peels of black grapes rich in anthocyanins (Italian cultivars "Ancellotta", "Colorino", "Sangiovese", "Lambrusco") by extraction in acidified water (often with citric or tartaric acid) at medium temperature (30–50°C) so as not to degrade the anthocyanins, sometimes with the addition of food-grade ethanol to improve yield and conservation. After separating the solids (seeds, fibers, and spent peels) using pressure filters or centrifugation, the extract is purified using ion exchange resins or membrane filtration, concentrated under low-temperature vacuum to preserve thermolabile compounds, and, if necessary, transformed into a powder through freeze-drying or spray-drying. The final product is stabilized with natural antioxidants and packaged in dark, airtight containers, often under an inert atmosphere. Classified as E163, enocyanin is used in the winemaking industry as a color enhancer and in the food and cosmetic industries for its intense pigmentation, excellent color stability in acidic environments, and its natural origin based on the recovery of winemaking byproducts. The starting pomace must be fresh and free of sulfur dioxide or other additives that could interfere with the extraction process.
Ketoacidosis is a metabolic state caused by uncontrolled production of ketone bodies that cause a metabolic acidosis. While ketosis refers to any elevation of blood ketones, ketoacidosis is a specific pathologic condition that results in changes in blood pH and requires medical attention. The most common cause of ketoacidosis is diabetic ketoacidosis but it can also be caused by alcohol, medications, toxins, and rarely, starvation.
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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.