The short version of TKPRPGP fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-10-09 and is reviewed periodically as new material appears.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C33H57N11O9 | Free peptide form |
| Molecular mass | About 751.9 Da | Calculated average mass |
| Amino acid sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Single-letter form TKPRPGP |
| Structural basis | Tuftsin analogue | Extended version of a natural tetrapeptide |
| Development origin | Russian Academy of Sciences | Work carried out from the 1980s onward |
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.
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.
=== Gut and Brain === Signal peptide (1-20) Glicentin (21–89) Oxyntomodulin (OXY or OXM, 53–89) – A further cleavage of Glicentin Glucagon-like peptide 1 (GLP-1, 92–128) – first seven residues further cleaved Glucagon-like peptide 2 (GLP-2, 146–178)
Ropinirole acts as a D2, D3, and D4 dopamine receptor agonist with highest affinity for D3, which are mostly found in the limbic areas. It is weakly active at the 5-HT2, and α2 receptors and is said to have virtually no affinity for the 5-HT1, GABA, mAChRs, α1-, and β-adrenoreceptors. It is a potent agonist of the 5-HT2B receptor, but shows biased agonism at this receptor and does not appear to pose a risk of cardiac valvulopathy. The comprehensive receptor interactions of ropinirole have been described. Ropinirole produces marked hypolocomotion at lower doses (1–50 mg/kg i.p.) and causes hyperlocomotion at higher doses (100 mg/kg i.p.) in rodents. The former effect is thought to be mediated by activation of inhibitory presynaptic dopamine autoreceptors and reduced dopamine release, while the latter action is thought to be due to stimulation of postsynaptic dopamine receptors. Activation of postsynaptic dopamine D2 receptors is thought to be involved in the antiparkinsonian effects of dopamine D2 receptor agonists like ropinrole.
=== 1951 === January 4: Chinese soldiers capture Seoul. March 14: United Nations forces recapture Seoul during Operation Ripper. By the end of March, they have reached the 38th Parallel, and formed a defensive line across the Korean Peninsula. March 29: Julius and Ethel Rosenberg are convicted of espionage for their role in passing atomic secrets to the Soviets during and after World War II; they were executed on June 19, 1953. April 11: U.S. President Harry S. Truman fires Douglas MacArthur from command of US forces in Korea due to him demanding nuclear weapons to be used on the enemy. April 18: The European Coal and Steel Community is formed by the Treaty of Paris. April 23: American journalist William N. Oatis is arrested in Czechoslovakia for alleged espionage. May 23: The Seventeen Point Agreement is signed between Tibet and the People's Republic of China, formally annexing Tibet into China itself. September 1: Australia, New Zealand, and the United States sign the ANZUS Treaty. This compels the three countries to cooperate on matters of defense and security in the Pacific. October 10: President Harry S. Truman signs the Mutual Security Act, announcing to the world, and its communist powers in particular, that the U.S. was prepared to provide military aid to "free peoples". November 14: President Harry Truman asks Congress for U.S. military and economic aid for the communist nation of Yugoslavia. December 12: The International Authority for the Ruhr lifts part of the remaining restrictions on German industrial production and on production capacity.
Sources: en.wikipedia.org
==== Core ==== There is some dispute about the origin of the fluorescent chromophore core. Originally, it was widely thought to be synthesized by the pvcABCD operon, as deletion of portions of the pvcC and pvcD genes disrupts pyoverdine production. Like other aspects of pyoverdine biosynthesis, the regulation of the pvcABCD is iron-dependent, and the loss of these genes' activity resulted in pyoverdine disruption. A separate report suggests that pvcABCD may be responsible for the synthesis of paerucumarin (a pseudoverdine-related molecule) instead, and claims that loss of activity in the locus has no effect on pyoverdine production. In addition, some fluorescent Pseudomonads lack apparent homologs of these genes, further calling into question whether this is the function of these genes. This is consistent with reports that pvdL combines coenzyme A to a myristic acid moiety, then adds a glutamate, D-tyrosine, and L-2,4-diaminobutyric acid (DAB). An alternate biosynthetic pathway suggests that pvdL incorporates glutamate, 2,4,5-trihydroxyphenylalanine and L-2,4-diaminobutyric acid instead. This latter is supported by the identification of incorporation of a radiolabeled tyrosine into either pyoverdine or pseudoverdine. This discrepancy remains unresolved.
== History == ITGA1 was first identified in 1986 as a Very Late Antigen-1 (VLA-1), a surface protein expressed on activated T lymphocytes. Later studies demonstrated that VLA-1 corresponds to the α1 integrin subunit, which pairs with the β1 integrin subunit to fom the α1β1 heterodimer, a receptor for collagen and laminin. During the early 1990s, cloning of the human ITGA1 gene enabled detailed characterization of its structure and tissue distribution. Structural studies later identified the α1 subunit as one of the integrins containing an inserted von Willebrand factor A domain responsible for collagen recognition. More recent research has expanded the biological significance of ITGA1 beyond cell adhesion to include roles in mechanotransduction, immune regulation, fibrosis, and cancer, leading to growing interest in ITGA1 as a potential therapeutic target.
== Chemistry == Mirtazapine is a tetracyclic piperazinoazepine; mianserin was developed by the same team of organic chemists and mirtazapine differs from it via the addition of a nitrogen atom in one of the rings. It is a racemic mixture of enantiomers. The (S)-(+)-enantiomer is known as esmirtazapine. Analogues of mirtazapine include mianserin, setiptiline, and aptazapine.
Sources: en.wikipedia.org
It is a seven-amino-acid peptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro, produced by chemical synthesis rather than extracted from biological tissue. Its design is based on tuftsin, a natural immunomodulatory tetrapeptide. The C-terminal Pro-Gly-Pro segment is a common stabilising motif in short regulatory peptides.
The core four residues correspond to tuftsin, which occurs naturally as part of immunoglobulin G. The full seven-residue sequence, however, is not a known endogenous peptide. It is a laboratory-designed analogue intended to combine tuftsin-like activity with greater resistance to breakdown.
No single receptor has been confirmed as the primary target. Reports describe involvement of the GABAergic system, interference with enkephalin degradation, and shifts in neurotrophic factor expression. Because these observations come from different models and assays, they have not yet been integrated into one accepted mechanism.
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.