tuftsin 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.
Updated 2026-08-01. Numbers and descriptions here follow the published literature rather than marketing material.
Selank is a synthetic heptapeptide developed in Russia. Its sequence is Thr-Lys-Pro-Arg-Pro-Gly-Pro, a seven-residue chain built around the natural tetrapeptide tuftsin. Researchers at the Institute of Molecular Genetics of the Russian Academy of Sciences first described the compound in the mid-1990s. The design combined the tuftsin core with an added Pro-Gly-Pro tail, a modification intended to extend the molecule's stability in biological fluids. Published work on the peptide has appeared mainly in Russian-language journals.
Reported activity for Selank centers on anxiolytic and nootropic effects. Russian clinical reports describe use in anxiety and in cognitive or attention-related complaints. Most of this evidence comes from studies conducted by the same research groups that developed the peptide. Independent replication in other countries remains limited, and no major Western regulatory agency has approved the compound for any indication. The gap between local reports and external verification is a recurring point in discussions of the peptide.
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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic heptapeptide | Modeled on tuftsin |
| Amino acid sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Seven residues |
| Approximate molecular mass | Around 750 Da | Depends on counter-ion and hydration |
| Common forms | Lyophilized powder | Also described as aqueous solution |
| Primary origin of research | Russian laboratories | Mid-1990s onward |
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.
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.
== Occurrence == It arises via the action of urocanase on urocanic acid. Hydrolysis of the heterocycle to the glutamic acid derivative is catalyzed by imidazolonepropionate hydrolase. Microbial production of imidazol-4-one-5-propionic acid in the human gut has been shown to affect insulin signaling, which is relevant to type II diabetes. Imidazole propionate has been causally implicated in atherosclerosis and Parkinson’s disease, primarily by triggering inflammation. Streptococcus mutans, known for its role in dental caries, has been identified as a contributor to elevated ImP levels through the urdA gene, which is involved in the conversion of urocanate to ImP.
== Causes == The cause of the scarring in UIP may be known (less commonly) or unknown (more commonly). Since the medical term for conditions of unknown cause is "idiopathic", the clinical term for UIP of unknown cause is idiopathic pulmonary fibrosis (IPF). Examples of known causes of UIP include connective tissue diseases (primarily rheumatoid arthritis), drug toxicity, chronic hypersensitivity pneumonitis, asbestosis and Hermansky–Pudlak syndrome.
In the example of a snake bite, the use of anti-venom halts the spread of toxins whilst receiving antibiotics to impede infection. Even after the initial cause of the necrosis has been halted, the necrotic tissue will remain in the body. The body's immune response to apoptosis, which involves the automatic breaking down and recycling of cellular material, is not triggered by necrotic cell death due to the apoptotic pathway being disabled.
Sources: en.wikipedia.org
The Levey–Jennings chart differs from the Shewhart individuals control chart because the standard deviation (σ, "sigma") is estimated. The Levey–Jennings chart uses the long-term (i.e., population) estimate of sigma whereas the Shewhart chart uses the short-term (i.e., within the rational subgroup) estimate.
=== Pharmacodynamics === Similarly to ketamine, norketamine acts as a noncompetitive NMDA receptor antagonist (Ki = 1.7 μM and 13 μM for (S)-(+)-norketamine and (R)-(–)-norketamine, respectively). Also, similarly again to ketamine, norketamine binds to the μ- and κ-opioid receptors. Relative to ketamine, norketamine is much more potent as an antagonist of the α7-nicotinic acetylcholine receptor, and produces rapid antidepressant effects in animal models which have been reported to correlate with its activity at this receptor. However, norketamine is about 1/5 as potent as ketamine as an antidepressant in mice as per the forced swim test, and this seems also to be in accordance with its 3–5-fold reduced comparative potency in vivo as an NMDA receptor antagonist. Norketamine's metabolites, dehydronorketamine (DHNK) and hydroxynorketamine (HNK), are far less or negligibly active as NMDA receptor antagonists in comparison, but retain activity as potent antagonists of the α7-nicotinic acetylcholine receptor. In 2024, norketamine was discovered to act as a highly potent positive allosteric modulator of the opioid receptors, including of the μ-opioid receptor (MOR). It shares this action with ketamine and hydroxynorketamine (HNK). They are all active in this action at very low concentrations, for instance 1 nM. Ketamine, norketamine, and HNK can potentiate the effects of endogenous opioids like met-enkephalin and exogenous opioids like morphine.
Absorption is the journey of a drug travelling from the site of administration to the site of action. The drug travels by some route of administration (oral, topical-dermal, etc.) in a chosen dosage form (e.g., tablets, capsules, or in solution). Absorption by some other routes, such as intravenous therapy, intramuscular injection, enteral nutrition, is even more straightforward and there is less variability in absorption and bioavailability is often near 100%. Intravascular administration does not involve absorption, and there is no loss of drug. The fastest route of absorption is inhalation. Absorption is a primary focus in drug development and medicinal chemistry, since a drug must be absorbed before any medicinal effects can occur. Moreover, the drug's pharmacokinetic profile can be easily and significantly changed by adjusting factors that affect absorption.
Indocyanine green is an FDA-approved photothermal agent that is primarily used in imaging techniques, but also displays anticancer and antimicrobial activity through photothermal therapy (PTT) treatments. Photothermal agents are active against diseased cells by accumulating in or around target cells, then converting light energy directly to heat, killing the target through heat-related damage. PTT has a low level of selectivity beyond the accumulation stage, in which it tends to preferentially accumulate within diseased and bacterial cells. This increases broadband antibiotic activity and decreases the likelihood of resistance development, but also raises the impact on human cells. Human cells experience irreversible damage in the range of 46-60 °C, which is below temperatures reached by some photothermal agents during photothermal therapy. Human cell viability may be maintained through low temperature PTT (≤ 45 °C), which is typically only possible in combination with an additional antibiotic or photodynamic activity.
Sources: en.wikipedia.org
Selank is a synthetic peptide made of seven amino acids. It is modeled on tuftsin, a natural tetrapeptide, with an added three-residue tail. It is not a small-molecule drug.
It originates from research in Russia, associated with the Institute of Molecular Genetics of the Russian Academy of Sciences. The first descriptions date to the mid-1990s. Most published studies come from Russian laboratories.
No, Selank itself does not occur naturally. Its backbone is based on tuftsin, which is produced in the body, but the seven-residue version is a synthetic construct. It is supplied as a manufactured peptide.
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.