The short version of Enkephalinase fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-05-24 and is reviewed periodically as new material appears.
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.
Outside its country of origin the compound is generally handled as a research chemical rather than an approved medicine. No regulatory approval from the United States Food and Drug Administration or the European Medicines Agency has been granted for human use. Identity and purity are normally checked by reverse-phase high-performance liquid chromatography, with mass spectrometry used to confirm the molecular mass. Lyophilised material is stored cold and desiccated, and repeated freeze-thaw cycles are avoided.
Published work on this peptide almost always uses intranasal delivery, with drops or a spray applied to the nasal mucosa. Some animal experiments have used subcutaneous or intraperitoneal injection, and a smaller number have compared routes directly. Oral administration is not a focus of the literature, because short peptides of this size are broken down by digestive enzymes and cross intestinal barriers poorly. How much of an intranasal dose reaches the bloodstream intact in humans remains an open question.
| 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 |
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.
Quality assessment of Selank samples typically combines purity determination with identity confirmation and counter-ion analysis. Purity is usually reported as a percentage by chromatographic area, with values above 95 percent often quoted for research-grade material. Water content and residual solvents are checked in lyophilized batches because they affect both stability and accurate mass determination. A reported purity figure does not by itself establish that a sample is the intended sequence, so orthogonal methods are needed to rule out sequence isomers or truncation products.
Characterization of Selank in laboratory settings relies on standard peptide analytical techniques. Reverse-phase high-performance liquid chromatography separates the peptide from related impurities and degradation products, while mass spectrometry confirms molecular identity through accurate mass measurement. Amino acid analysis and peptide sequencing verify the primary structure when reference material is unavailable. Because Selank is a short chain, fragmentation-based analysis produces a diagnostic ion pattern that supports confident identification.
Peptide stability depends strongly on temperature, moisture, and pH. Lyophilized Selank is generally most stable when stored cold and dry, with freezer temperatures commonly used for long-term storage. In solution, the compound is susceptible to hydrolysis and to microbial growth if it is not handled aseptically. The C-terminal proline-rich extension appears to slow enzymatic cleavage relative to tuftsin, though quantitative degradation rates vary with the matrix and the conditions tested. Published stability data specific to Selank remain sparse.
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.
After returning from the DL, Helton played only 6 games before announcing that he would have season-ending hip surgery in order to prepare for the 2013 season. Helton was healthier in 2013, playing in 124 games, while hitting 15 home runs with 61 RBIs. On September 14, 2013, Helton announced that he would be retiring at the conclusion of the 2013 season. On September 25, before his last game at Coors Field, Helton was honored by the Rockies in a pre-game ceremony. In the game, Helton hit a home run and drove in three runs versus the Boston Red Sox. On August 17, 2014, the Rockies retired Helton's number 17 before a game at Coors Field. He was the first Rockies player to have his number retired in the franchise's history.
Mubadala Investment Company PJSC (Arabic: شركة مبادلة للاستثمار), or simply Mubadala, is a state-owned global investment firm that acts as one of the sovereign wealth funds of the government of Abu Dhabi. The company was established in 2017 when then-named Mubadala Development Company (now Mamoura Diversified Global Holding) and the International Petroleum Investment Company (IPIC) merged. Headquartered in Abu Dhabi, Mubadala also has offices in London, Rio de Janeiro, New York, San Francisco and Beijing.
In broiler chickens, the use of lithium ascorbate from the 14th to the 42nd day of cultivation in the amount of 1, 5, 10 mg/kg of body weight increased the total protein in blood serum due to the increase in the globulin fraction, which indicates an increase in the protective functions of the body of chicken and is one of reasons for higher livestock safety (P<0.05). Lithium ascorbate was tested as a cerebroprotective agent in the model of ischemic stroke. The effect of lithium ascorbate was studied on a model of chronic alcohol intoxication, in which deviant behavior of animals is combined with irreversible degenerative changes in the liver and central nervous system (including demyelination of nerves). Lithium ascorbate at doses of 5, 10 and 30 mg/kg normalized behavioral responses in the open field and elevated plus maze tests. An increase in the dose of lithium ascorbate (10 mg/kg, 30 mg/kg) did not lead to a significant improvement in the studied parameters of the condition. Histological analysis showed that the use of lithium ascorbate minimized the level of ischemic damage to neurocytes to the level of a reversible state and contributed to the preservation of the myelin sheaths of nerves.
=== Toxicity === In rodents and primates, sufficiently high doses of amphetamine cause dopaminergic neurotoxicity, or damage to dopamine neurons, which is characterized by dopamine terminal degeneration and reduced transporter and receptor function. There is no evidence that amphetamine is directly neurotoxic in humans. However, large doses of amphetamine may indirectly cause dopaminergic neurotoxicity as a result of hyperpyrexia, the excessive formation of reactive oxygen species, and increased autoxidation of dopamine. Animal models of neurotoxicity from high-dose amphetamine exposure indicate that the occurrence of hyperpyrexia (i.e., core body temperature ≥ 40 °C) is necessary for the development of amphetamine-induced neurotoxicity. Prolonged elevations of brain temperature above 40 °C likely promote the development of amphetamine-induced neurotoxicity in laboratory animals by facilitating the production of reactive oxygen species, disrupting cellular protein function, and transiently increasing blood–brain barrier permeability.
In molecular biology, protein fold classes are broad categories of protein tertiary structure topology. They describe groups of proteins that share similar amino acid and secondary structure proportions. Each class contains multiple, independent protein superfamilies (i.e. are not necessarily evolutionarily related to one another).
Sources: en.wikipedia.org
However at this time, using spider silk to grow artificial skin in mass quantities is not practical because of the tedious process of harvesting spider silk. Australian researchers are currently searching for a new, innovative way to produce artificial skin. This would produce artificial skin more quickly and in a more efficient way. The skin produced would only be 1 millimeter thick and would only be used to rebuild the epidermis. They can also make the skin 1.5 millimetres thick, which would allow the dermis to repair itself if needed. This would require bone marrow from a donation or from the patient's body. The bone marrow would be used as a "seed", and would be placed in the grafts to mimic the dermis. This has been tested on animals and has been proven to work with animal skin. Professor Maitz said, "In Australia, someone with a full-thickness burn to up to 80 per cent of their body surface area has every prospect of surviving the injury... However their quality of life remains questionable as we're unable, at present, to replace the burned skin with normal skin...We're committed to ensuring the pain of survival is worth it, by developing a living skin equivalent."
Second-harmonic imaging microscopy (SHIM) is based on a nonlinear optical effect known as second-harmonic generation (SHG). SHIM has been established as a viable microscope imaging contrast mechanism for visualization of cell and tissue structure and function. A second-harmonic microscope obtains contrasts from variations in a specimen's ability to generate second-harmonic light from the incident light while a conventional optical microscope obtains its contrast by detecting variations in optical density, path length, or refractive index of the specimen. SHG requires intense laser light passing through a material with a noncentrosymmetric molecular structure, either inherent or induced externally, for example by an electric field. Second-harmonic light emerging from an SHG material is exactly half the wavelength (frequency doubled) of the light entering the material. While two-photon-excited fluorescence (TPEF) is also a two photon process, TPEF loses some energy during the relaxation of the excited state, while SHG is energy conserving. Typically, an inorganic crystal is used to produce SHG light such as lithium niobate (LiNbO3), potassium titanyl phosphate (KTP = KTiOPO4), or lithium triborate (LBO = LiB3O5). Though SHG requires a material to have specific molecular orientation in order for the incident light to be frequency doubled, some biological materials can be highly polarizable, and assemble into fairly ordered, large noncentrosymmetric structures.
The term reticulin was coined in 1892 by M. Siegfried. Today, the term reticulin or reticular fiber is restricted to referring to fibers composed of type III collagen. However, during the pre-molecular era, there was confusion in the use of the term reticulin, which was used to describe two structures:
=== Negative selection and the role of the thymus === The elimination of self-reactive T cells occurs primarily through a mechanism known as "negative selection" within the thymus, an organ responsible for the maturation of T cells. This process serves as a key line of defense against autoimmunity. If these protective mechanisms fail, a pool of self-reactive cells can become functional within the immune system, contributing to the development of autoimmune diseases.
== Tissue == Bone is not uniformly solid, but consists of a flexible matrix (about 30%) and bound minerals (about 70%), which are intricately woven and continuously remodeled by a group of specialized bone cells. Their unique composition and design allows bones to be relatively hard and strong, while remaining lightweight. Bone matrix is 90 to 95% composed of elastic collagen fibers, also known as ossein, and the remainder is ground substance. The elasticity of collagen improves fracture resistance. The matrix is hardened by the binding of inorganic mineral salt, calcium phosphate, in a chemical arrangement known as bone mineral, a form of calcium apatite. It is the mineralisation that gives bones rigidity. Within any single bone, the tissue is woven into two main patterns: cortical and cancellous bone, each with distinct appearances and characteristics. Bone is actively constructed and remodeled throughout life by specialized bone cells known as osteoblasts and osteoclasts.
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.
Most published work uses intranasal application, either as drops or as a nasal spray. Injection routes appear in a smaller set of animal experiments. Oral use is uncommon in the literature because peptide breakdown and poor absorption limit this route.