If you have been reading about Heptapeptide 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 2026-06-10. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Development work on the compound began in the 1980s and 1990s at the Institute of Molecular Genetics in Moscow, within the same research programme that produced the peptide Semax. Early investigators sought a tuftsin derivative with improved resistance to enzymatic breakdown and with activity in the central nervous system after peripheral administration. Most of the primary literature from this period was published in Russian, a factor that still shapes how easily the findings can be checked by outside groups.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic heptapeptide | Tuftsin analogue |
| Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Single-letter form: TKPRPGP |
| Molecular formula | C33H57N11O9 | Calculated for the free peptide |
| Molecular weight | About 751.9 g/mol | Derived from the sequence |
| Appearance | White to off-white powder | Typical lyophilised form |
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.
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.
Proposed mechanisms centre on modulation of the GABAergic system, with reports of altered expression of genes related to GABA-A receptor subunits and changed monoamine turnover. Some studies describe inhibition of enkephalinase, the enzyme that degrades endogenous enkephalins, which may prolong opioid peptide signalling. Effects on brain-derived neurotrophic factor and on cytokine expression have also been reported. These findings come largely from animal models and small human studies, and the precise primary target remains unresolved.
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.
While no other government actively supported the Boer cause, individuals from several countries volunteered and formed Foreign Volunteer Units. These primarily came from Europe, particularly the Netherlands, Germany and Sweden-Norway. Other countries such as France, Italy, Ireland (then part of the United Kingdom), and restive areas of the Russian Empire, including Congress Poland and Georgia, also formed smaller volunteer corps. Finns fought in the Scandinavian Corps. Two volunteers, George Henri Anne-Marie Victor de Villebois-Mareuil of France and Yevgeny Maximov of Russia, became veggeneraals (fighting generals) of the South African Republic.
=== Mechanical ventilation === Isolated mechanical forces may not adequately explain ventilator induced lung injury (VILI). The damage is affected by the interaction of these forces and the pre-existing state of the lung tissues, and dynamic changes in alveolar structure may be involved. Factors such as plateau pressure and positive end-expiratory pressure (PEEP) alone do not adequately predict injury. Cyclic deformation of lung tissue may play a large part in the cause of VILI, and contributory factors probably include tidal volume, positive end-expiratory pressure and respiratory rate. There is no protocol guaranteed to avoid all risk in all applications.
The medication is used to treat clear cell renal cell carcinoma, the most common histological subtype. The treatment phase is continuing treatment beyond three months. The patient has been issued an authority prescription for pazopanib. The patient must have stable or responding disease according to the Response Evaluation Criteria In Solid Tumours (RECIST). This treatment must be the sole tyrosine kinase inhibitor subsidised for this condition. Pazopanib has also demonstrated initial therapeutic properties in patients with aggressive fibromatosis (desmoid tumor), ovarian and non-small cell lung cancer. However, plans to apply to the EMA for a variation to include advanced ovarian cancer have been withdrawn and a license will not be sought in any country.
Other experiments show that a single miRNA may repress the production of hundreds of proteins, but that this repression often is relatively mild (less than 2-fold). The effects of miRNA dysregulation of gene expression seem to be important in cancer. For instance, in gastrointestinal cancers, nine miRNAs have been identified as epigenetically altered and effective in down regulating DNA repair enzymes. The let-7 family of miRNAs provides a well-characterized example of miRNA dysregulation in cancer. Let-7-5p isoforms are among the most consistently downregulated miRNAs in hepatocellular carcinoma and several other malignancies, and their suppression is associated with upregulation of oncogenes including c-MYC, CDK6, and the RNA-binding protein LIN28B, as well as efflux ATP-binding cassette (ABC) transporters that govern multidrug resistance. Loss of let-7 activity establishes a self-reinforcing circuit, as LIN28B actively suppresses let-7 maturation, further sustaining the expression of let-7 target genes and contributing to a chemotherapy-resistant phenotype. Reintroduction of depleted tumor-suppressive miRNAs has therefore been explored as a strategy to restore natural post-transcriptional regulation of oncogenic targets and resensitize resistant cancer cells to treatment.
Sources: en.wikipedia.org
Over the next 11 years, she discovered that females only had the X chromosome and males had both X and Y chromosomes. She was able to conclude that sex is a chromosomal factor and is determined by the male. In 1911, Thomas Hunt Morgan argued that genes are on chromosomes, based on observations of a sex-linked white eye mutation in fruit flies. In 1913, his student Alfred Sturtevant used the phenomenon of genetic linkage to show that genes are arranged linearly on the chromosome.
From late May 1900, the first successes of the Boer guerrilla strategy were at Lindley (where 500 Yeomanry surrendered), and at Heilbron (where a large convoy and its escort were captured) and other skirmishes resulting in 1,500 British casualties in less than ten days. In December 1900, De la Rey and Christiaan Beyers attacked and mauled a British brigade at Nooitgedacht, inflicting 650 casualties. As a result, the British, led by Lord Kitchener, mounted extensive searches for Christiaan de Wet, but without success. However, Boer raids on British army camps and other targets were sporadic and poorly planned, and the nature of the Boer guerrilla war itself had no long-term objectives, with the exception to harass the British. This led to a disorganised pattern of scattered engagements between the British and Boers.
==== MeSH D12.125.067 – amino acids, acidic ==== MeSH D12.125.067.500 – aspartic acid MeSH D12.125.067.500.150 – d-aspartic acid MeSH D12.125.067.500.275 – isoaspartic acid MeSH D12.125.067.500.400 – n-methylaspartate MeSH D12.125.067.500.700 – potassium magnesium aspartate MeSH D12.125.067.750 – glutamic acid MeSH D12.125.067.750.150 – 1-carboxyglutamic acid MeSH D12.125.067.750.400 – glutamates MeSH D12.125.067.750.400.700 – polyglutamic acid MeSH D12.125.067.750.400.800 – sodium glutamate MeSH D12.125.067.750.700 – pyrrolidonecarboxylic acid
Sources: en.wikipedia.org
=== Aroma === Aroma compounds giving B. edulis mushrooms their characteristic fragrance include some 100 components, such as esters and fatty acids. In a study of aroma compounds, 1-octen-3-one was the most prevalent chemical detected in raw mushrooms, with pyrazines having increased aroma effect and elevated content after drying.
== Pathophysiology == Since envenomation is completely voluntary, all venomous snakes are capable of biting without injecting venom into a person. Snakes may deliver such a "dry bite" rather than waste their venom on a creature too large for them to eat, a behaviour called venom metering. However, the percentage of dry bites varies among species: 80 percent of bites inflicted by sea snakes, which are normally timid, do not result in envenomation, whereas for pit viper bites the number is closer to 25 percent. Furthermore, some snake genera, such as rattlesnakes, can internally regulate the amount of venom they inject. There is a wide variance in the composition of venoms from one species of venomous snake to another. Some venoms may have their greatest effect on a victim's respiration or circulatory system. Others may damage or destroy tissues. This variance has imparted to the venom of each species a distinct chemistry. Sometimes antivenins have to be developed for individual species. For this reason, standard therapeutic measures will not work in all cases. Some dry bites may also be the result of imprecise timing on the snake's part, as venom may be prematurely released before the fangs have penetrated the person. Even without venom, some snakes, particularly large constrictors such as those belonging to the Boidae and Pythonidae families, can deliver damaging bites; large specimens often cause severe lacerations, or the snake itself pulls away, causing the flesh to be torn by the needle-sharp recurved teeth embedded in the person.
== History and background == GFS was designed by Michael C. Giddings (University of North Carolina, Chapel Hill) et al., and released in 2003. Giddings expanded the algorithms for GFS from earlier ideas. Two papers were published in 1993 explaining the techniques used to identify proteins in sequence databases. These methods determined the mass of peptides using mass spectrometry, and then used the mass to search protein databases to identify the proteins In 1999 a more complex program was released called Mascot that integrated three types of protein/database searches: peptide molecular weights, tandem mass spectrometry from one or more peptide, and combination mass data with amino acid sequence. The fallback with this widely used program is that it is unable to detect alternative splice sites that are not currently annotated, and it not usually able to find proteins that have not been annotated. Giddings built upon these sources to create GFS which would compare peptide mass data to entire genomes to identify the proteins. Giddings system is able to find new annotations of genes that have not been found, such as undocumented genes and undocumented alternative splice sites.
Sources: en.wikipedia.org
The sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro, commonly written as TKPRPGP. It shares the first four residues with tuftsin and carries three prolines in the chain. The proline-rich tail is the main structural feature that separates it from the parent tetrapeptide.
Selank is a synthetic analogue built on the tuftsin tetrapeptide Thr-Lys-Pro-Arg. Extra proline residues were added to the C-terminus during design work. That modification is intended to make the peptide less vulnerable to rapid enzymatic degradation.
Transliteration from Russian produces variant spellings such as Selanc. Many suppliers avoid the trade-style name entirely and list the peptide sequence. Comparing sequences rather than names is the reliable way to confirm two entries describe the same molecule.
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.