The short version of TKPRPGP fits in a sentence. The long version — which is the one that helps — is below.
Reviewed 2025-09-30. Anything still debated is marked as such rather than presented as settled.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Primary route studied | Intranasal | Also examined parenterally in animal work |
| Reported plasma half-life | Minutes to tens of minutes | Values vary widely between reports |
| Main model systems | Rodent behavioural and cell assays | Human trials are few and small |
| Principal proposed targets | GABA-A receptor, GABA transaminase | Monoamine and neurotrophic pathways also reported |
| Evidence grade | Preliminary | Limited independent replication |
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.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, written TKPRPGP in one-letter notation. Its structure consists of the immunomodulatory tetrapeptide tuftsin, Thr-Lys-Pro-Arg, extended at the carboxyl terminus by a Pro-Gly-Pro segment. The molecular formula is commonly given as C33H57N11O9, corresponding to a monoisotopic mass near 751.4 Da and an average molecular mass near 751.9 Da. All seven residues are proteinogenic amino acids, and the molecule carries no modified side chains or non-natural linkages.
The compound was designed at the Institute of Molecular Genetics of the Russian Academy of Sciences during the 1980s and 1990s. The stated design goal was to retain the immunomodulatory and central nervous system activity attributed to tuftsin while improving resistance to enzymatic breakdown. Adding a proline-rich tail to the short parent peptide was a deliberate strategy, because proline residues restrict the conformations available to many peptidases. The same laboratory produced Semax, an ACTH fragment analog, and both compounds were developed in parallel as short, enzymatically stabilized peptides intended for intranasal use.
Selank is not a naturally occurring peptide and has no known endogenous counterpart in human physiology. Russian-language sources frequently call it TP-7, while English-language sources use the name Selank almost exclusively. Database indexing is uneven, partly because early reports appeared in regional journals that are not widely cataloged. Some summaries describe the material as a tuftsin analog and others as a synthetic heptapeptide; the labels overlap rather than conflict. Citing the primary sequence resolves ambiguity more reliably than the research or trade name alone.
=== 241Am === Americium-241 is a candidate isotope with much greater availability than 238Pu. Though 241Am has a half-life of 432 years, which is about five times longer than that of 238Pu and could hypothetically power a device for centuries, missions with more than 10 years were not the subject of the research until 2019. The power density of 241Am is only one-fourth that of 238Pu, and 241Am produces more penetrating radiation through decay chain products than 238Pu and needs more shielding. Its shielding requirements in a RTG are the third lowest: only 238Pu and 210Po require less. With a current global shortage of 238Pu, 241Am is being studied as RTG fuel by ESA and in 2019, UK's National Nuclear Laboratory announced the generation of usable electricity. An advantage over 238Pu is that it is produced as nuclear waste and is nearly isotopically pure. Prototype designs of 241Am RTGs expect 2–2.2 We/kg for 5–50 We RTGs design but in practical testing dropped to 1.3–1.9 We/kg. Americium-241 is currently used in small quantities in household smoke detectors and thus its handling and properties are well-established. However, it decays to neptunium-237, the most chemically mobile among the actinides.
Cl−CH2CH2−OH + KOH → (CH2CH2)O + KCl + H2O Wurtz measured the boiling point of ethylene oxide as 13.5 °C (56.3 °F), slightly higher than the present value, and discovered the ability of ethylene oxide to react with acids and salts of metals. Wurtz mistakenly assumed that ethylene oxide has the properties of an organic base. This misconception persisted until 1896, when Georg Bredig found that ethylene oxide is not an electrolyte. That it differed from other ethers — particularly by its propensity to engage in the addition reactions typical of unsaturated compounds — had long been a matter of debate. The heterocyclic triangular structure of ethylene oxide was proposed by 1868 or earlier. Wurtz's 1859 synthesis long remained the only method of preparing ethylene oxide, despite numerous attempts, including by Wurtz himself, to produce ethylene oxide directly from ethylene. Only in 1931 did French chemist Theodore Lefort develop a method of direct oxidation of ethylene in the presence of silver catalyst. Since 1940, almost all industrial production of ethylene oxide has relied on this process. Sterilization by ethylene oxide for the preservation of spices was patented in 1938 by the American chemist Lloyd Hall. Ethylene oxide achieved industrial importance during World War I as a precursor to both the coolant ethylene glycol and the chemical weapon mustard gas.
=== Glucose metabolism === Phosphorylation of sugars is often the first stage in their catabolism. Phosphorylation allows cells to accumulate sugars because the phosphate group prevents the molecules from diffusing back across their transporter. Phosphorylation of glucose is a key reaction in sugar metabolism. The chemical equation for the conversion of D-glucose to D-glucose-6-phosphate in the first step of glycolysis is given by:
Listed below are the athletes who have achieved a 1,000 pounds (453.6 kilograms) or more deadlift, a feat which has been accomplished by only 40 men in history. It includes both strongman and powerlifting deadlifts performed using only the conventional stance. Sanctioned lifts during competitions and exhibitions, as well as unsanctioned lifts during training (with video proof) are included.
Sources: en.wikipedia.org
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Sources: en.wikipedia.org
Reports describe modulation of GABA signalling, changes in monoamine turnover and effects on neurotrophic factor expression. These observations come mainly from animal and cell studies. A single unifying mechanism has not been demonstrated.
The peptide enters plasma rapidly and is broken down by ordinary proteases into amino acids and shorter fragments. Reported half-lives are short. Whether meaningful amounts of the intact molecule reach the brain is an open question.
Most clinical reports are small, published in Russian and not independently replicated. English-language reviews highlight the absence of large randomised trials. Conclusions about efficacy should be treated as provisional.
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.