Everything below concerns Heptapeptide. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-07-25. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
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, 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.
On 5 December 2001, a 2,000lb GPS-guided bomb landed among the Green Berets from ODA 574, killing 3 members and wounding the rest of the team, over 20 of Karzai's militia were also killed and Karzai himself slightly wounded. ODB 570 and ODA 524 were immediately dispatched by helicopter to assist with the wounded and to eventually replace the fallen operators of ODA 574. ODA 572 and a CIA Jawbreaker team (small group of CIA SAD ground branch operators) were dispatched to eastern Afghanistan where they recruited some 2,500 to 3,000 into the Afghan Militia Force to take part in the Battle of Tora Bora. On December 20, following the battle, ODA 561 were inserted into the White Mountains to support ODA 572 in conducting sensitive site exploitation of the caves and to assist with recovering DNA samples from terrorist bodies. Time reported that on 4 January 2002, Green Beret SFC Scott Neil jumped out the back of an MH-53 half a mile from a suspected al-Qaeda compound, 140 miles south of Kabul. With just one-hour on-scene time due to limited helicopter fuel, Neil rushed through AK-47 fire and overcame the al-Qaeda fighters; intelligence from the compound proved it to be an al-Qaeda way station, containing hundreds of fake passports to give terrorists new identities, and multiple computers, powered by car batteries and linked to satellite phones for internet connection.
Fluorescence microscopy using auramine O—a nucleic acid–binding fluorochrome—has largely replaced these techniques in clinical laboratories due to higher sensitivity, rapidity, and safety. Rhodamine, sometimes added as a secondary dye, contributes little to sensitivity but slightly enhances contrast.
n RCHNHC(O)OC(O) → [N(H)CH(R)CO)]n + n CO2 Poly-L-lysine has been prepared from N-carbobenzyloxy-α-N-carboxy-L-lysine anhydride, followed by deprotection with phosphonium iodide. Peptide synthesis from NCAs does not require protection of the amino acid functional groups. N-Substituted NCAs, such as sulfenamide derivatives have also been examined. The ring-opening polymerization of NCAs is catalyzed by metal catalysts. The polymerization of NCA’s have been considered as a prebiotic route to polypeptides. NCAs can also be used to form amides and lactams by reaction of carboxylic acids and isocyanates.
=== Dependence and withdrawal === Tolerance to phenibut easily develops with repeated use, leading to dependence. Withdrawal symptoms may occur upon discontinuation, and, in recreational users taking high doses, have been reported to include severe rebound anxiety, insomnia, aggression, irritability, agitation, visual and auditory hallucinations, seizures and acute psychosis. Baclofen has successfully been used for treatment of phenibut dependence.
Sources: en.wikipedia.org
===== Social interaction ===== One of the most researched aspects of social interaction in which serotonin is involved is aggression. Aggression is regulated by the 5-HT system, as serotonin levels can both induce or inhibit aggressive behaviors, as seen in mice (see section on Mice) and crabs. While this is widely accepted, it is unknown if serotonin interacts directly or indirectly with parts of the brain influencing aggression and other behaviors. Studies of serotonin levels show that they drastically increase and decrease during social interactions, and they generally correlate with inhibiting or inciting aggressive behavior. The exact mechanism of serotonin influencing social behaviors is unknown, as pathways in the 5-HT system in various vertebrates can differ greatly.
=== DNA repair === Exposure of the earthworm Eisenia fetida to ionizing radiation induced DNA strand breaks and oxidized DNA bases. These DNA damages could then be repaired in somatic and spermatogenic cells. Earthworm testis cells are also capable of repairing hydrogen peroxide induced oxidative DNA adducts.
=== MALDI-TOF === The same research group that developed COLD-PCR and used it to compare the sensitivity of regular PCR for genotyping with direct Sanger sequencing, RFLP, and pyrosequencing, also ran a similar study using MALDI-TOF as a downstream application for detecting mutations. Their results indicated that COLD-PCR could enrich mutation sequences from a mixture of DNA by 10–100 fold and that mutations with an initial prevalence of 0.1–0.5% would be detectable. Compared to the 5–10% low-level detection rate expected with traditional PCR.
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.