This is a working overview of Intranasal route, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-05-13 and is reviewed periodically as new material appears.
Proposed mechanisms center on modulation of the GABA system, but no single molecular target has been confirmed. Rodent studies report changes in GABA-A receptor expression and in the turnover of serotonin, dopamine, and norepinephrine in several brain regions. Increases in brain-derived neurotrophic factor and its receptor have also been described after repeated administration. These findings come largely from animal models, and the degree to which they describe human neurochemistry remains an open question. The mechanism is best characterized as multi-system and not fully resolved.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Route studied | Intranasal | Predominant route in published reports |
| Circulation stability | Short, minutes scale | Peptidases cleave it; the tail slows the process |
| Analytical method | RP-HPLC with mass spectrometry | Used for identity and purity assessment |
| Reported outcome domains | Anxiety and cognitive measures | Derived from small, mostly regional trials |
| Regulatory status | Marketed in Russia | Availability outside that market is limited |
Identity and purity of selank are established with reversed-phase high-performance liquid chromatography coupled to mass spectrometry. The peptide elutes from C18 columns with acetonitrile gradients in water containing trifluoroacetic acid or formic acid, and detection is usually performed by ultraviolet absorbance near 214 nm. Electrospray ionization in positive mode gives a doubly protonated ion near m/z 377, consistent with a mass of about 752 Da. Amino acid analysis or tandem mass spectrometry of fragment ions confirms the sequence. Because the molecule has no aromatic residues, it lacks a usable 280 nm chromophore, so low-wavelength detection or mass spectrometry is required.
Peptide bonds in selank are susceptible to hydrolysis under strongly acidic or basic conditions, and the terminal proline residues are vulnerable to exopeptidase activity in biological samples. Lyophilized powder stored dry at -20 °C typically remains stable for extended periods, whereas aqueous solutions degrade faster and may lose measurable purity within days to weeks depending on pH, temperature, and microbial load. Repeated freeze-thaw cycles promote aggregation and adsorption to container surfaces. For analytical work, solutions are usually prepared fresh, kept cold, and used within a single working day.
Handling follows standard practice for research peptides. Material is weighed in a low-humidity environment because the powder absorbs atmospheric moisture. Purity is reported as the percentage area of the main peak in a chromatogram, with specifications commonly set at 95 percent or higher; values below that threshold indicate the presence of truncated or modified species. Residual trifluoroacetate from purification is often present and may affect mass balance. Certificates of analysis should state the analytical method, the column and gradient used, and the lot-specific retention time so that results can be compared across suppliers.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. It was designed as a stabilized analogue of tuftsin, a naturally occurring tetrapeptide fragment derived from the immunoglobulin heavy chain. The additional Pro-Gly-Pro segment at the carboxyl terminus is intended to slow enzymatic cleavage. The compound is usually described in the literature as a synthetic peptide with anxiolytic and cognitive-related activity, a label that reflects a research context rather than an approved therapeutic category.
Most published work on selank originates from a small number of research groups in the Russian Federation. A large share of that record appears in Russian-language journals, which limits access for readers who rely on English-indexed databases. Independent replication by laboratories outside the original research network is sparse in publicly available sources. This concentration of origin and language is a frequently noted feature when the compound is summarized in broader reviews of synthetic peptides.
Reported pharmacological effects center on reduced anxiety-like behavior in animal models and on measures of memory and learning. Proposed contributing mechanisms include modulation of GABAergic signaling, shifts in monoamine turnover, and changes in the activity of enzymes that degrade neuropeptides. Effects on the expression of genes linked to neuroplasticity have also been described. No single molecular target is widely accepted, and whether the behavioral findings arise from one pathway or several remains an open question.
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.
In the dominant post-war narrative of West Germany, the Nazi regime was characterised as having been a 'criminal' state, illegal and illegitimate from the outset; while the Weimar Republic was characterised as having been a 'failed' state, whose inherent institutional and constitutional flaws had been exploited by Hitler in his illegal seizure of dictatorial powers. Consequently, following the death of Hitler in 1945 and the subsequent capitulation of the German Armed Forces, the national political, judicial, administrative, and constitutional instruments of both Nazi Germany and the Weimar Republic were understood as entirely defunct, such that a new West Germany could be established in a condition of constitutional nullity. Nevertheless, the new West Germany asserted its fundamental continuity with the 'overall' German state that was held to have embodied the unified German people since the Frankfurt Parliament of 1848, and which from 1871 had been represented within the German Reich; albeit that this overall state had become effectively dormant long before 8 May 1945. In 1949 with the continuation and aggravation of the Cold War (for example, the Berlin Airlift of 1948–49), the two German states that had originated in the Western Allied and the Soviet Zones respectively became known internationally as West Germany and East Germany. Commonly known in English as East Germany, the former Soviet occupation zone in Germany, eventually became the German Democratic Republic or GDR.
==== MeSH D12.776.220.525.475 – myosins ==== MeSH D12.776.220.525.475.100 – myosin heavy chains MeSH D12.776.220.525.475.200 – myosin light chains MeSH D12.776.220.525.475.300 – myosin subfragments MeSH D12.776.220.525.475.470 – myosin type i MeSH D12.776.220.525.475.475 – myosin type ii MeSH D12.776.220.525.475.475.124 – cardiac myosins MeSH D12.776.220.525.475.475.124.249 – atrial myosins MeSH D12.776.220.525.475.475.124.500 – ventricular myosins MeSH D12.776.220.525.475.475.249 – nonmuscle myosin type iia MeSH D12.776.220.525.475.475.500 – nonmuscle myosin type iib MeSH D12.776.220.525.475.475.750 – skeletal muscle myosins MeSH D12.776.220.525.475.475.875 – smooth muscle myosins MeSH D12.776.220.525.475.612 – myosin type iii MeSH D12.776.220.525.475.681 – myosin type iv MeSH D12.776.220.525.475.750 – myosin type v
== History == Finasteride was the first 5-ARI to be introduced for medical use. It was marketed for the treatment of BPH in 1992 and was subsequently approved for the treatment of pattern hair loss in 1997. Epristeride was the second 5-ARI to be introduced and was marketed for the treatment of BPH in China in 2000. Dutasteride was approved for the treatment of BPH in 2001 and was subsequently approved for pattern hair loss in South Korea in 2009 and in Japan in 2015. The patent protection on finasteride and dutasteride has expired and both drugs are available as generic medications.
=== Other lymphomas and squamous-cell carcinoma === In September 2022, the FDA announced new information regarding other types of cancers related to breast implants, based on medical device reports (MDRs) of cases of patients with squamous-cell carcinoma or various lymphomas found in the scar tissue around breast implants. The agency reported 10 MDRs about squamous-sell carcinoma found in the capsule scar tissue and 12 MDRs about various lymphomas also in the scar tissue around the breast implants. These new cases do not overlap with cases of BIA-ALCL. SCC and other lymphomas have been found in smooth-surface and textured implants as well as silicone-gel-filled and saline-filled implants. Patients who reported symptoms specified swelling, pain, lumps, and changes to their skin. As of 2022, neither the incidence rate nor prevalence is known.
Sources: en.wikipedia.org
Another meta-analysis, which included only RCTs, found that 25 mg was the most effective dose, relative to lower doses like 10 mg and 0.215 mg/kg body weight (~15 mg for a 70-kg person). A third meta-analysis found that half of psilocybin's maximal antidepressant effect occurred with a dose of about 10 mg per 70 kg body weight, while 95% of the maximal effect occurred at a dose of about 41 mg per 70 kg body weight, and that higher doses might especially be better for treatment-resistant depression. The risk of adverse effects was also greater with higher doses. A 2025 network meta-analysis of RCTs of psilocybin for depression found that it did not significantly improve depression scores relative to placebo on day 2 post-dose but did improve them day 8 and day 15 post-dose. Depressive symptoms were improved only slightly more with psilocybin than with placebo. Another 2024 meta-analysis found that depressive symptoms were improved on days 2, 14, and 42, with similar effect sizes. In the previously described dose-ranging Phase II trial of psilocybin for depression, the time to median depressive event after administration of psilocybin was 92 to 189 days for 25 mg, 43 to 83 days for 10 mg, and 21 to 62 days for 1 mg, depending on the analysis. Repeated dosing of psilocybin is being explored for maximization and maintenance of depressive symptom improvement, with preliminary effectiveness observed.
=== Cosmetics === Some sucrose esters, such as sucrose distearate, sucrose dilaurate, sucrose palmitate, etc. are added in cosmetics products as an emulsifier. Some have a function in skin conditioning and emollient. Cosmetics products that might have sucrose esters as an ingredient includes eyelash products, hair treatments, oil gels, skin products and deodorants.
°C), which aligns well with modeled results of methane formation temperature and yield. However, some thermogenic methane samples have clumped-isotope temperatures that are unrealistically high. Possible explanations for exceedingly high clumped isotope temperatures include natural gas migration after formation, mixing effect, and kinetic isotope effect of secondary cracking.
Sources: en.wikipedia.org
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.
Intranasal delivery is the route described in most published work. It is used because the peptide is degraded quickly once it reaches circulation. Direct evidence of brain penetration in humans is lacking.
Most trials are small, regionally concentrated, and often lack rigorous blinding or placebo control. Independent replication is limited. Reviews in English generally rate the evidence as preliminary.
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.