If you have been reading about Selank 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.
Updated 2025-08-17. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Lyophilized selank is normally supplied as a dry powder and is considered stable for extended periods when kept cold and dry. Moisture uptake is the main practical threat, because absorbed water promotes both hydrolysis and aggregation in the solid state. Vials are usually warmed to room temperature before opening so that condensation does not form on the powder. Supplier documentation commonly specifies -20 °C for routine storage, with -80 °C used for material intended to be archived for years.
Once dissolved, the peptide is markedly less stable than the dry powder. Aqueous solutions are subject to backbone hydrolysis and to microbial growth when they are handled without sterile technique. Buffered solutions near neutral pH are common for short-term laboratory work, while acidic conditions are sometimes used to improve solubility. Analytical laboratories generally prepare working solutions fresh rather than storing them, and a residual water film left in a reopened vial can seed degradation even when the container appears dry.
Reversed-phase high-performance liquid chromatography is the standard technique for estimating peptide purity. The result is a peak-area percentage, which describes how much of the detected material elutes as the main peak in one run. Mass spectrometry confirms the molecular mass and can reveal truncated, adducted, or otherwise modified species. Amino acid analysis or tandem mass spectrometry can address sequence fidelity when identity is in doubt. None of these measurements, taken alone, establishes that a sample is fit for any specific purpose.
| Property | Value | Notes |
|---|---|---|
| Peptide sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Seven residues; tuftsin plus a Pro-Gly-Pro tail |
| Molecular formula | C33H57N11O9 | Commonly reported value for the free peptide |
| Monoisotopic mass | Roughly 751.4 Da | Average molecular mass near 751.9 Da |
| Appearance | White to off-white powder | Typically supplied as a lyophilized solid |
| Solubility class | Freely soluble in water | Also dissolves in saline and other polar solvents |
Reverse-phase high-performance liquid chromatography with ultraviolet detection near 214 nanometres is the standard purity method. Mass spectrometry, typically electrospray ionisation, confirms identity through the expected mass-to-charge pattern. Amino acid analysis can verify composition independently. Chiral purity requires separate techniques such as derivatisation followed by chromatographic separation, and such data are rarely reported for research-grade material.
Quantification in biological matrices relies on liquid chromatography coupled to tandem mass spectrometry with stable-isotope internal standards. Low plasma concentrations and adsorption to container surfaces both complicate measurement. Solid-phase extraction is often needed to reduce matrix interference before injection. Reported limits of quantification differ widely between laboratories, which makes direct comparison of pharmacokinetic results difficult and limits meta-analysis.
Peptide bonds are vulnerable to protease attack, and Selank is no exception. Measured half-life in serum is short, on the order of minutes in several reports, which explains why intranasal administration is the common route described in the literature. Absorption across the nasal mucosa partially bypasses first-pass hepatic metabolism. Quantitative data on human bioavailability remain limited and are difficult to compare across studies.
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.
Religious affiliation in West Germany decreased from the 1960s onward. Religious affiliation declined faster among Protestants than among Catholics, causing the Roman Catholic Church to overtake the EKD as the largest denomination in the country during the 1970s.
==== MeSH D12.776.556.579.374 – nonheme iron proteins ==== MeSH D12.776.556.579.374.187 – hemerythrin MeSH D12.776.556.579.374.281 – inositol oxygenase MeSH D12.776.556.579.374.375 – iron-sulfur proteins MeSH D12.776.556.579.374.375.025 – adrenodoxin MeSH D12.776.556.579.374.375.150 – ferredoxin-nitrite reductase MeSH D12.776.556.579.374.375.275 – ferredoxins MeSH D12.776.556.579.374.375.275.450 – molybdoferredoxin MeSH D12.776.556.579.374.375.275.725 – rubredoxins MeSH D12.776.556.579.374.375.637 – iron regulatory protein 1 MeSH D12.776.556.579.374.375.818 – iron regulatory protein 2 MeSH D12.776.556.579.374.375.863 – electron transport complex i MeSH D12.776.556.579.374.375.863.500 – nadh dehydrogenase MeSH D12.776.556.579.374.375.909 – electron transport complex ii MeSH D12.776.556.579.374.375.909.500 – succinate dehydrogenase MeSH D12.776.556.579.374.375.954 – electron transport complex iii MeSH D12.776.556.579.374.375.977 – nitrate reductase (nad(p)h) MeSH D12.776.556.579.374.375.988 – nitrate reductase (nadph) MeSH D12.776.556.579.374.450 – lipoxygenase MeSH D12.776.556.579.374.450.025 – arachidonate lipoxygenases MeSH D12.776.556.579.374.450.025.020 – arachidonate 5-lipoxygenase MeSH D12.776.556.579.374.450.025.025 – arachidonate 12-lipoxygenase MeSH D12.776.556.579.374.450.025.030 – arachidonate 15-lipoxygenase MeSH D12.776.556.579.374.687 – retinal dehydrogenase MeSH D12.776.556.579.374.925 – tyrosine 3-monooxygenase
Moxidectin has a longer half-life than ivermectin and may eventually supplant ivermectin as it is a more potent microfilaricide, but there is a need for additional clinical trials, with long-term follow-up, to assess whether moxidectin is safe and effective for treatment of nematode infection in children and women of childbearing potential. There is tentative evidence that ivermectin kills bedbugs, as part of integrated pest management for bedbug infestations. However, such use may require a prolonged course of treatment which is of unclear safety.
Sources: en.wikipedia.org
Perforated peptic ulcer Acute pancreatitis Liver abscess Pneumonia Myocardial ischemia Hiatal hernia Biliary colic Choledocholithiasis Cholangitis Appendicitis Colitis Acute peptic ulcer exacerbation Amoebic liver abscess Acute intestinal obstruction Kidney stone Biliary ascariasis
At this point, there was a sudden burst of element formation (first deuterium, which immediately fused into helium). However, very soon thereafter, at twenty minutes after the Big Bang, the Universe became too cool for any further nuclear fusion or nucleosynthesis. At this point, the elemental abundances were nearly fixed, changing only as some of the radioactive products of Big Bang nucleosynthesis (such as tritium) decayed. The deuterium bottleneck in the formation of helium, together with the lack of stable ways for helium to combine with hydrogen or with itself (no stable nucleus has a mass number of 5 or 8) meant that an insignificant amount of carbon, or any elements heavier than carbon, formed in the Big Bang. These elements thus required formation in stars. At the same time, the failure of much nucleogenesis during the Big Bang ensured that there would be plenty of hydrogen in the later universe available to form long-lived stars, such as the Sun.
=== Pharmacodynamics === Flmodafinil is a selective dopamine reuptake inhibitor (DRI). Its affinity (Ki) for the DAT is 4,090 nM. At the serotonin transporter (SERT), its affinity (Ki) was 48,700 nM (12-fold lower than for the DAT), and it had negligible affinity for the sigma σ1 receptor (Ki > 100,000 nM). The drug has been found to block the dopamine transporter (DAT) by 83%, to a greater extent than methylphenidate without unfavorable concomitant adrenergic effects. The drug is an atypical DRI similarly to modafinil. The affinities for the DAT of flmodafinil's enantiomers and modafinil have also been studied. The affinities (Ki) were 5,480 nM for armodafinil ((R)-modafinil), 2,970 nM for (S)-(+)-flmodafinil (JBG1-048), and 4,830 nM for (R)-(–)-flmodafinil (JBG1-049). Their affinities for the SERT and σ1 receptor have also been reported. Similarly to modafinil, (S)-(+)-flmodafinil and (R)-(–)-flmodafinil increase dopamine levels in the nucleus accumbens in animals. They have been found to increase dopamine levels by up to 150 to 200% of baseline at the highest assessed dose. These increases are much smaller than those elicited by amphetamine or cocaine. In a study comparing the wake-promoting effects of flmodafinil and modafinil, flmodafinil was found to maintain wakefulness over a significantly longer timeframe than modafinil. While the administration of neither compound resulted in sleep rebound, flmodafinil perturbed sleep architecture to a lesser degree than modafinil.
Sources: en.wikipedia.org
The sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro, written TKPRPGP in one-letter code. It combines the tetrapeptide tuftsin with a carboxyl-terminal Pro-Gly-Pro extension. This full sequence identifies the molecule more precisely than the research name.
No peptide with this exact sequence has been identified as an endogenous substance. It is a laboratory-designed analog of tuftsin, a naturally occurring immunomodulatory tetrapeptide. The Pro-Gly-Pro extension has no known natural source.
Proline introduces conformational constraints that make a peptide less accessible to common peptidases. This is a standard stabilization strategy in peptide design. The added residues also increase the distance between the active tuftsin portion and typical cleavage sites.
Sealed, desiccated storage at -20 °C or colder is the standard recommendation for research-grade material. Vials should reach room temperature before they are opened, which limits condensation. Repeated temperature cycling is discouraged.