peptidase raises a handful of sensible questions. This page answers them in order, starting with the fundamentals and moving to applications.
This page was last updated on 2026-01-30 and is reviewed periodically as new material appears.
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.
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 |
|---|---|---|
| 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 |
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.
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.
The primary structure of Selank is Thr-Lys-Pro-Arg-Pro-Gly-Pro, corresponding to the molecular formula C33H57N11O9 and a monoisotopic mass of roughly 751.9 daltons. The N-terminal threonine and the arginine residue in the fourth position are shared with tuftsin, which carries the sequence Thr-Lys-Pro-Arg. The three additional residues at the C-terminus, Pro-Gly-Pro, extend the chain and are associated with greater resistance to enzymatic degradation. This extension also separates Selank from the shorter parent peptide.
Naming conventions place Selank in the same research family as Semax, another Russian-developed peptide investigated for cognitive effects. The two compounds share a lineage but differ in sequence and in the biological systems proposed as their targets. Semax descends from ACTH fragments, whereas Selank descends from tuftsin. Publications sometimes identify Selank by its full peptide sequence or by laboratory codes rather than one uniform trade name. Because replication outside Russia is limited, reports on its properties are best read alongside the study design and the purity of the material tested.
PCP is well known for its primary action on the NMDA receptor, an ionotropic glutamate receptor. As such, PCP is a non-competitive NMDA receptor antagonist. The role of NMDAR antagonism in the effect of PCP, ketamine, and related dissociative agents was first published in the early 1980s by David Lodge and colleagues. Other NMDA receptor antagonists include ketamine, tiletamine, dextromethorphan, nitrous oxide, and dizocilpine (MK-801). Research also indicates that PCP inhibits nicotinic acetylcholine receptors (nAChRs) among other mechanisms. Analogues of PCP exhibit varying potency at nACh receptors and NMDA receptors. Findings demonstrate that presynaptic nAChRs and NMDA receptor interactions influence the postsynaptic maturation of glutamatergic synapses and consequently impact synaptic development and plasticity in the brain. These effects can lead to inhibition of excitatory glutamate activity in certain brain regions such as the hippocampus and cerebellum thus potentially leading to memory loss as one of the effects of prolonged use. Acute effects on the cerebellum manifest as changes in blood pressure, breathing rate, pulse rate, and loss of muscular coordination during intoxication. PCP, like ketamine, also acts as a potent dopamine D2High receptor partial agonist in rat brain homogenate and has affinity for the human cloned D2High receptor. This activity may be associated with some of the other more psychotic features of PCP intoxication, which is evidenced by the successful use of D2 receptor antagonists (such as haloperidol) in the treatment of PCP psychosis.
After a median follow-up of 40 months, the trial demonstrated a statistically significant improvement in IDFS in patients who received trastuzumab emtansine compared with those who received trastuzumab (HR 0.50; 95% CI: 0.39, 0.64; p<0.0001). Overall survival data were not mature at the time of the IDFS analysis.
== Taxidermists == Carl Akeley (1864–1926), the father of modern taxidermy Jean-Baptiste Bécœur (1718–1777), French ornithologist, taxidermist, and inventor of arsenical soap Harry Ferris Brazenor (1863–1948), 19th-century British taxidermist James Dickinson, MBE (1959–), retired British taxidermist, known for his restorations of existing specimens John Edmonstone (c. 1790-?), British-Guyanese taxidermist who taught Charles Darwin the art of taxidermy in 1825 William Temple Hornaday (1854–1937), American zoologist, conservationist, and taxidermist who was the first director of the Bronx Zoo Martha Maxwell (1831–1881), American naturalist, taxidermist, and artist who was the first female naturalist to obtain and taxidermy her own specimens Charles Johnson Maynard (1845–1929), American naturalist, ornithologist, and taxidermist who discovered many new species and authored many notable publications Charles Willson Peale (1741–1827), American painter, Revolutionary War veteran, inventor, naturalist, and polymath who organized the first U.S.
In three terms over the next six years, Mizell gained a reputation as a conservative. He opposed the Blue Ridge Power Project, introducing a House Bill in 1974 to add the New River to the National Wild and Scenic Rivers System. Though the bill was unsuccessful at the time, it became law in 1976. Mizell, however, lost his seat to Stephen L. Neal in 1974, also losing to the Democrat when he ran against him in 1976. Presidents Gerald Ford, Ronald Reagan, and George H. W. Bush each appointed him to Assistant Secretary positions within their administrations. After suffering a heart attack in 1998, Mizell died in 1999.
Sources: en.wikipedia.org
Wnt comprises a diverse family of secreted lipid-modified signaling glycoproteins that are 350–400 amino acids in length. The lipid modification of all Wnts is palmitoleoylation of a single totally conserved cysteine residue. Palmitoleoylation is necessary because it is required for Wnt to bind to its carrier protein Wntless (WLS) so it can be transported to the plasma membrane for secretion and it allows the Wnt protein to bind its receptor Frizzled Wnt proteins also undergo glycosylation, which attaches a carbohydrate in order to ensure proper secretion. In Wnt signaling, these proteins act as ligands to activate the different Wnt pathways via paracrine and autocrine routes. These proteins are highly conserved across species. They can be found in mice, humans, Xenopus, zebrafish, Drosophila and many others.
On 24 July 1967, shortly before midnight, President Lyndon B. Johnson ordered the US military to occupy Detroit. At 1:10 a.m., 4,700 paratroopers of the 82nd and 101st Airborne Divisions, under the command of Lieutenant General John L. Throckmorton, arrived in Detroit and began working in the streets, coordinating refuse removal, tracing persons who had disappeared in the confusion, and carrying out routine military functions, such as the establishment of mobile patrols, guard posts, and roadblocks. Rioting peaked in high intensity. The 82nd worked alongside the 101st to secure east of Woodward, while the National Guard took land west of Woodward. "Incidents" began to decline as paratroopers constantly patrolled the perimeter with M16 rifles, M60 machine guns, and M48 tanks, while the police began making arrests on those violating curfew regulations or who were caught looting. On 27 July, with a sense of normalcy returned to the city, in part due to the presence of Army and National Guard troops, and the riot was officially declared over. The Army began to scale down to return to their normal duties, relinquishing control to local authorities. Although Army paratroopers exercised some restraint on firepower due to being racially integrated, as well as their combat experience in Vietnam (as opposed to the mainly white and inexperienced National Guard troops), the 82nd was directly responsible for at least one death.
=== Post-settlement activity === In 1991, the local Bhopal authorities charged Anderson, who had retired in 1986, with manslaughter, a crime that carries a maximum penalty of 10 years in prison. He was declared a fugitive from justice by the Chief Judicial Magistrate of Bhopal on 1 February 1992 for failing to appear at the court hearings in a culpable homicide case in which he was named the chief defendant. Orders were passed to the Government of India to press for an extradition from the United States. The United States declined to extradite him citing a lack of evidence. The U.S. Supreme Court refused to hear an appeal of the decision of the lower federal courts in October 1993 against allowing victims of the Bhopal disaster to seek damages in a U.S. court. In 2004, the Indian Supreme Court ordered the Indian government to release any remaining settlement funds to victims. And in September 2006, the Welfare Commission for Bhopal Gas Victims announced that all original compensation claims and revised petitions had been "cleared". In 2006, the U.S. Court of Appeals for the Second Circuit in New York City upheld the dismissal of remaining claims in the case of Bano v. Union Carbide Corporation. This move blocked plaintiffs' motions for class certification and claims for property damages and remediation.
=== Potential for toxicity === Preliminary research indicates that prolonged exposure to high doses of THC may interfere with chromosomal stability, which may be hereditary as a factor affecting cell instability and cancer risk. The carcinogenicity of THC in the studied populations of so-called "heavy users" remains dubious due to various confounding variables, most significantly concurrent tobacco use.
==== Other specialty chemical industries ==== Apart from life sciences, specialty chemicals —and therefore their active ingredients, commodities or fine chemicals, as the case may be — are used ubiquitously in both industrial applications, such as biocides and corrosion inhibitors in cooling water towers, and consumer applications, such as personal care and household products. The active ingredients extend from high-price low-volume fine chemicals, used for liquid crystal displays, to large-volume/low-price amino acids used as feed additives.
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.
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.