Semax is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Last reviewed on 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
Selank is studied chiefly as an animal-model anxiolytic with proposed secondary effects on memory and immune signaling. Reported mechanisms include modulation of the GABA-A receptor complex, inhibition of enkephalin-degrading enzymes, and shifts in monoamine turnover within limbic structures. Some experiments describe increased expression of brain-derived neurotrophic factor in the hippocampus after repeated dosing. No single molecular target has been confirmed, and the peptide does not bind any receptor with the selectivity typical of a conventional small-molecule drug. Mechanism therefore remains a set of hypotheses rather than an established pathway.
Laboratory work relies on standard behavioral paradigms. Rodents are tested in the elevated plus maze, open field, and passive avoidance tasks, with outcomes compared against diazepam or vehicle controls. Intranasal dosing is used most often because it bypasses first-pass metabolism, though intraperitoneal and intravenous routes also appear in published protocols. Biochemical endpoints include tissue BDNF concentrations, cytokine levels, and monoamine metabolites. Human data are limited to small Russian trials reporting reduced anxiety scores; most were not prospectively registered, and few employed independent outcome assessment.
Measuring peptide exposure inside the brain is technically difficult. Selank is degraded rapidly in plasma, and assays must separate intact peptide from fragments, which favors targeted mass spectrometry over immunoassays alone. Reported half-lives are short, on the order of minutes, so effects observed hours later are attributed to downstream signaling rather than to the parent compound. Blood-brain barrier permeability is debated and rarely quantified directly. Gaps include absent dose-response characterization, inconsistent reporting of purity, and almost no pharmacokinetic data from human participants.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Principal proposed target | GABA-A receptor complex | Hypothesis derived mainly from animal pharmacology |
| Common behavioral assay | Elevated plus maze | Rodent test for anxiety-like behavior |
| Reported molecular marker | Hippocampal BDNF expression | Measured by immunoassay or mRNA quantification |
| Typical dosing route | Intranasal | Chosen to reduce first-pass metabolism |
| Reported plasma half-life | Minutes | Based on limited peptide stability data |
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.
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.
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.
== Autism == William Shaw became focused on autism in 1993, and has claimed that acetaminophen may be a major cause of autism. Nevertheless, as of 2017, there still was no good evidence to claim that acetaminophen caused autism. Shaw has also alleged without credible scientific evidence that yeast infections cause autism. He was accused of "exploit[ing] the parents' understandable and desperate search for a cause of their children's autism". Shaw has endorsed dangerous and discredited chelation treatments for autism.
== Sequence == The amino acid sequence (44 long) of human GHRH is: HO - Tyr - Ala - Asp - Ala - Ile - Phe - Thr - Asn - Ser - Tyr - Arg - Lys - Val - Leu - Gly - Gln - Leu - Ser - Ala - Arg - Lys - Leu - Leu - Gln - Asp - Ile - Met - Ser - Arg - Gln - Gln - Gly - Glu - Ser - Asn - Gln - Glu - Arg - Gly - Ala - Arg - Ala - Arg - Leu - NH2
=== 1960s–1980s === For several petty crimes, sixteen-year-old Olofsson was placed in a behavioural institution for young offenders in 1963. Olofsson and two other boys escaped from the institution in August 1965 and entered the country estate of Swedish Prime Minister Tage Erlander at Harpsund, where they stole grapes, cucumbers, and tomatoes from the greenhouse. They fled when the gardener discovered them. Three months later, Olofsson assaulted two police officers in Eskilstuna. On 4 February 1966, he was sentenced to three years in prison; this was his third sentence and his first real prison sentence. In late 1966, he made his first escape from the prison at Tidaholm. On 29 July 1966, police officers Ragnar Sandahl and Lennart Mathiasson responded to a burglary at a bicycle shop at Skjutsaregatan in Nyköping. Sandahl was shot and killed by Gunnar Norgren. The other burglar was Olofsson, who became a nationally known criminal. Norgren was arrested on 16 August that year in an apartment at Utåkersgatan 4 in Kålltorp, Gothenburg, and later confessed to the murder. The apartment belonged to a boyfriend of Olofsson's sister. Norgren gave up after the police fired several shots through the door to the apartment. Olofsson had escaped from the apartment before police entered and managed to elude them for two weeks but was eventually arrested on 25 August in Grimmaredsskogen in Västra Frölunda. Via telephone tapping, the police found out that Olofsson and his 20-year-old girlfriend were to meet at a special mountain hill in Grimmaredsskogen.
The precise reason why there are only four nucleotides is debated, but there are several unused possibilities. Furthermore, adenine is not the most stable choice for base pairing: in Cyanophage S-2L, diaminopurine (DAP) is used instead of adenine. Diaminopurine basepairs perfectly with thymine as it is identical to adenine but has an amine group at position 2 forming 3 intramolecular hydrogen bonds, eliminating the major difference between the two types of basepairs (weak A-T vs strong C-G). This improved stability affects protein-binding interactions that rely on those differences. Other combination include:
Sources: en.wikipedia.org
That fall, Jacob and Monod coined the name "messenger RNA" and developed the first theoretical framework to explain its function. In February 1961, James Watson revealed that his Harvard-based research group had been right behind them with a series of experiments whose results pointed in roughly the same direction. Brenner and the others agreed to Watson's request to delay publication of their research findings. As a result, the Brenner and Watson articles were published simultaneously in the same issue of Nature in May 1961, while that same month, Jacob and Monod published their theoretical framework for mRNA in the Journal of Molecular Biology.
Genetic factors, along with socio-environmental (e.g., psychosocial) factors, have been established as significant contributors to addiction vulnerability. Addiction is substantially heritable. Twin and adoption studies estimate the heritability of alcohol use disorder at approximately 50%, with comparable estimates across other substances. This risk is polygenic: it reflects the combined small effects of many common variants rather than any single gene. Genome-wide association studies (GWAS) are used to examine genetic associations with dependence, addiction, and drug use, and have begun to map this architecture, and distinguish loci associated with a broad general liability to addiction across substances from loci conferring risk for a specific drug. Individual common variants each contribute only a small increment of risk, so genetic vulnerability is best understood as an aggregate rather than as the effect of any identified gene.
=== Myelosuppression === Proliferating cells, such as tumour cells, are more sensitive to alkylating agents, rendering these drugs useful for chemotherapy. However, alike drugs of this class, thiotepa is nonselective, which often results in its most important side effect: myelosuppression, the decreased activity of bone marrow. In turn, this can lead to leukopenia, thrombocytopenia, infection, and anemia. These side effects are often the most severe between 15 and 20 days following low dose treatment. Bone marrow has a high turn-over in the production of blood cells, which can be analogously inhibited by alkylating agents. This toxicity is dose-dependent and can be anticipated on. However, even a low dose can lead to life-threatening situations. Higher, and, therefore, more therapeutically effective, doses of thiotepa have successfully been applied by the autologous transplantation of bone marrow. In these high-dose therapies, the dose can be as much as a hundred times greater than that of conventional therapy. Despite the use of bone marrow transplantation, complications from the therapy can be fatal. Monoalkylation of DNA leads to mispairing of bases and, if not repaired, can reside in the DNA sequence. Mutated DNA that does not undergo cell death can find its way into daughter cells and potentially cause genetic disorders such as cancer. As a result of cell mutation in the bone marrow, chemotherapies with alkylating agents are known to cause acute myeloid leukaemia (AML) and myelodysplastic syndrome (MDS).
Sources: en.wikipedia.org
Intranasal administration predominates in both animal and human research because it avoids hepatic first-pass metabolism. Injectable and intraperitoneal routes appear in animal work mainly for comparison.
Behavioral endpoints include time spent in open arms of the elevated plus maze and avoidance latencies. Biochemical endpoints include BDNF concentration, cytokine levels, and monoamine metabolite ratios in brain tissue.
Most published studies are small, originate from a limited number of laboratories, and lack independent replication. Dose-response relationships, measured brain exposure, and long-term outcomes are not well characterized.
Selank is a seven-amino-acid peptide built from the tuftsin sequence plus a Pro-Gly-Pro tail. It is produced by chemical synthesis rather than extracted from a natural source. The free peptide is usually supplied as a lyophilised powder or in an aqueous formulation.