This is a working overview of Selank, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2025-09-24 and is reviewed periodically as new material appears.
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.
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.
Solubility behavior is a practical concern for handling. Selank dissolves readily in water and in common aqueous buffers, which simplifies preparation of working solutions. The choice of solvent, ionic strength, and pH can influence aggregation over time, particularly at higher concentrations. Aqueous solutions are typically sterile-filtered before use. Because stability depends on several variables, storage and handling notes should be treated as general guidance rather than fixed rules, and specific values are best confirmed against a certificate of analysis for each batch.
Characterization of Selank in a laboratory setting relies on standard peptide methods. Reverse-phase high-performance liquid chromatography separates the target from related impurities and provides a purity figure, commonly reported as 95 percent or higher. Mass spectrometry, typically electrospray ionization or matrix-assisted laser desorption, confirms the molecular mass and helps detect truncation or modification. Amino acid analysis can verify composition when a sequence-level check is needed. These techniques together establish identity and purity for a given lot.
Lyophilized Selank, the dry powder form, is generally stored frozen at minus 20 degrees Celsius or colder for long-term keeping. The solid is hygroscopic and should stay sealed, dry, and protected from light. Once dissolved, the peptide is less stable and is usually held refrigerated at 2 to 8 degrees Celsius for short periods. Repeated freezing and thawing is avoided because it can promote aggregation and loss of activity. Buffers and pH choice also affect how long a solution remains usable.
| 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 |
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.
Selank is a synthetic heptapeptide developed in Russia during the 1990s. Researchers at the Institute of Molecular Genetics of the Russian Academy of Sciences designed it as a stabilized analog of tuftsin, a naturally occurring immunomodulatory tetrapeptide. The compound has been studied primarily for its reported anxiolytic and nootropic effects. It remains largely unknown in Western pharmacology and is not approved as a medicine by major regulators such as the FDA or the EMA.
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 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.
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.
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.
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.
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.
=== Category:EC 3.4 (act on peptide bonds - Peptidase) === Category:EC 3.4.11 Alanine aminopeptidase Category:EC 3.4.15 Angiotensin converting enzyme Category:EC 3.4.21 Serine protease Chymotrypsin (EC 3.4.21.1) Trypsin (EC 3.4.21.4) Thrombin (EC 3.4.21.5) Factor X (EC 3.4.21.6) Plasmin (EC 3.4.21.7) Acrosin (EC 3.4.21.10) Factor VII (EC 3.4.21.21) Factor IX (EC 3.4.21.22) Prolyl oligopeptidase (EC 3.4.21.26) Factor XI (EC 3.4.21.27) Elastase (EC 3.4.21.37) Factor XII (EC 3.4.21.38) Proteinase K (EC 3.4.21.64) Tissue plasminogen activator (EC 3.4.21.68) Protein C (EC 3.4.21.69) Category:EC 3.4.22 Separase (EC 3.4.22.49) Category:EC 3.4.23 Pepsin (EC 3.4.23.1) Rennet (EC 3.4.23.4) Renin (EC 3.4.23.15) Trypsinogen (EC 3.4.23.18) and (20/21/23/24/26) Plasmepsin (EC 3.4.23.39) Category:EC 3.4.24 Matrix metalloproteinase (EC 3.4.24.7) Category:EC 3.4.25 Metalloendopeptidase
Carrasco had previously been Castillo's Interior Minister during the Bellido cabinet. On 19 November, Presidential Secretary Bruno Pacheco resigned. Pacheco claimed to be innocent, and said he was resigning to stop the smear campaign against the president.
RSH + Cl–S–C(=O)–Cl → RS–S–C(=O)–Cl + HClThese reagents are useful for the derivatization of biological thiols. Methoxycarbonylsulfenyl chloride, a related reagent derived from the above chemistry, is used in solid-phase peptide synthesis for selective disulfide bond formation via conversion of the acetamidomethyl (Acm) cysteine protecting group to thiol-labile S-alkylsulfenyl thiocarbonate (carbomethylsulfenyl, Scm) protecting group.
== Overdose == CPA is relatively safe in acute overdose. It is used at very high doses of up to 300 mg/day by mouth and 700 mg per week by intramuscular injection. For comparison, the dose of CPA used in birth control pills is 2 mg/day. There have been no deaths associated with CPA overdose. There are no specific antidotes for CPA overdose, and treatment should be symptom-based. Gastric lavage can be used in the event of oral overdose within the last 2 to 3 hours.
=== Pharmacodynamics === DPIA is a norepinephrine transporter inhibitor with an IC₅₀ value of 3.1 µM, as well as a dopamine transporter inhibitor with a potency approximately 13 times weaker than that of amphetamine, but 7 times more potent than amphetamine in inhibiting the serotonin transporter, although, unlike amphetamine, DPIA does not exhibit monoamine-releasing activity. It exhibits moderate affinity for 5-HT1A serotonin receptors (Ki = 3.5 µM) and for alpha-1A-adrenoreceptors (Ki = 0.12 µM), and binds to alpha-2A-adrenoreceptors and TAAR1. In experiments on rodents, DPIA produced the same central effects and toxicity as amphetamine, but was less potent. Interestingly, unlike amphetamine, DPIA caused a reduction in heart rate and blood pressure (exhibiting cardiodepressant properties).
Sources: en.wikipedia.org
A 2017 systematic review and meta-analysis of suvorexant for the treatment of insomnia found that the medication significantly increased the rate of somnolence by 3.5-fold, daytime sleepiness/sedation by 3.1-fold, fatigue by 2.1-fold, abnormal dreams by 2.1-fold, and dry mouth by 2.0-fold. Conversely, suvorexant did not significantly differ from placebo in the rates of any other assessed adverse effects. This included back pain, diarrhea, dizziness, falls, headache, car accidents/traffic violations, nasopharyngitis, nausea, potential drug misuse, suicidal ideation, complex sleep behaviors, hypnagogic or hypnopompic hallucinations, and sleep paralysis. The overall risk of any adverse event was increased 1.07-fold while discontinuation due to adverse events was unchanged (RRTooltip relative risk=0.93, 95% CITooltip confidence interval 0.60 to 1.44). Tolerance, dependence, withdrawal, and rebound effects do not appear to occur with suvorexant in the treatment of insomnia at studied doses. In three-month clinical studies, no rebound insomnia as assessed by measures of sleep onset or maintenance was observed with discontinuation of suvorexant at doses of 15 to 40 mg. Similarly, no withdrawal effects were observed with discontinuation of suvorexant at these doses. However, in other reports, some tolerance as assessed by diminishing somnolence and rebound insomnia upon discontinuation has been noted. The orexin neuropeptides augment the signaling of the mesolimbic dopamine reward pathway and are thought to potentiate hedonic tone.
== External links == Histology at utmb.edu Histology image: 36_02 at the University of Oklahoma Health Sciences Center - "ureter" Histology image: 37_02 at the University of Oklahoma Health Sciences Center - "urinary bladder" Anatomy Atlases – Microscopic Anatomy, plate 02.24 - "Transitional Epithelium", Ureter Histology at KUMC urinary-renal16 "ureter" www.urothelium.com is an online resource for information about Human Urothelium and the "Biomimetic Urothelium" Archived 2011-02-01 at the Wayback Machine Urothelium at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Histology at qmul.ac.uk Archived 2011-07-21 at the Wayback Machine Diagram at umich.edu Archived 2006-09-10 at the Wayback Machine Histology at wisc.edu Archived 2008-06-10 at the Wayback Machine
Light sources such as fluorescent lamps, high-intensity discharge lamps and LED lamps have higher luminous efficiency. These devices produce light by luminescence. Their light has bands of characteristic wavelengths, without the "tail" of invisible infrared emissions, instead of the continuous spectrum produced by a thermal source. By careful selection of fluorescent phosphor coatings or filters which modify the spectral distribution, the spectrum emitted can be tuned to mimic the appearance of incandescent sources, or other different color temperatures of white light. When used for tasks sensitive to color, such as motion picture lighting, these sources may require particular techniques to duplicate the appearance of incandescent lighting. Metamerism describes the effect of different light spectrum distributions on the perception of color.
Tautomerism – A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base, resulting in incorrect base pairing during replication. Theoretical results suggest that proton tunneling is an important factor in the spontaneous creation of GC tautomers. Depurination – Loss of a purine base (A or G) to form an apurinic site (AP site). Deamination – Hydrolysis changes a normal base to an atypical base containing a keto group in place of the original amine group. Examples include C → U and A → HX (hypoxanthine), which can be corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be detected as a mutation because thymine is a normal DNA base. Slipped strand mispairing – Denaturation of the new strand from the template during replication, followed by renaturation in a different spot ("slipping"). This can lead to insertions or deletions.
== Applications == One of the largest volume uses for ICP-MS is in the medical and forensic field, specifically, toxicology. A physician may order a metal assay for a number of reasons, such as suspicion of heavy metal poisoning, metabolic concerns, and even hepatological issues. Depending on the specific parameters unique to each patient's diagnostic plan, samples collected for analysis can range from whole blood, urine, plasma, serum, to even packed red blood cells. Another primary use for this instrument lies in the environmental field. Such applications include water testing for municipalities or private individuals all the way to soil, water and other material analysis for industrial purposes. In recent years, industrial and biological monitoring has presented another major need for metal analysis via ICP-MS. Individuals working in factories where exposure to metals is likely and unavoidable, such as a battery factory, are required by their employer to have their blood or urine analyzed for metal toxicity on a regular basis. This monitoring has become a mandatory practice implemented by the U.S. Occupational Safety and Health Administration, in an effort to protect workers from their work environment and ensure proper rotation of work duties (i.e. rotating employees from a high exposure position to a low exposure position). ICP-MS is also used widely in the geochemistry field for radiometric dating, in which it is used to analyze relative abundance of different isotopes, in particular uranium and lead.
Sources: en.wikipedia.org
=== Geelong: 2005–2008 === At the start of 2006, he moved out of his Werribee home and moved to Geelong to live with teammates Corey Enright and Henry Playfair, with whom he would later go on to start a personal training organisation. He then set his sights on playing a senior game for Geelong and, after playing in the team that had earlier won the pre-season cup, he was selected to play in round 5. Only minutes into his debut, on 29 April against the Sydney Swans, he broke his arm and only played eight games for the year. After a solid pre-season, he played the first five games of 2007 before being omitted and then broke his wrist while playing for the Geelong VFL side on 8 July 2007. As a result, Prismall was unable to play for several weeks but recovered in time to play finals for the VFL side. In 2008, Prismall played in 11 home and away games and was selected to play in the qualifying final against St Kilda on 7 September 2008, which was to be his 25th game and finals debut. However, midway through the first quarter, he was stretchered off and did not return after landing awkwardly and badly injuring his right knee. It was later confirmed that he would have to undergo a full knee reconstruction after scans revealed a ruptured anterior cruciate ligament. After the 2008 season, Prismall declined the new two-year contract offered to him by Geelong and asked the club to be traded to get a better chance of playing more regularly in the AFL. On the final day of trade week, he was traded to the Essendon Football Club for national draft pick number 39.
Bupropion is an aminoketone that belongs to the class of substituted cathinones and the more general class of substituted phenethylamines. It is also known structurally as 3-chloro-N-tert-butyl-β-keto-α-methylphenethylamine, 3-chloro-N-tert-butyl-β-ketoamphetamine, or 3-chloro-N-tert-butylcathinone. The clinically used bupropion is racemic, which is a mixture of two enantiomers: S-bupropion and R-bupropion. Although the optical isomers of bupropion can be separated, they rapidly racemize under physiological conditions. Bupropion is a small-molecule compound with the molecular formula C13H18ClNO and a molecular weight of 239.74 g/mol. It is a highly lipophilic compound, with an experimental log P of 3.6. Pharmaceutically, bupropion is used mainly as the hydrochloride salt but also to a lesser extent as the hydrobromide salt. There have been reported cases of false-positive urine amphetamine tests in persons taking bupropion.
Uterine prolapse occurs when there is a disruption to any of the structures mentioned above that help hold the uterus in place. Weakening of the levator ani muscles can occur during vaginal childbirth, in which portions of the muscle can detach from the bony pelvis, or through age-related changes to musculature, and this can lead to a loss of support for the uterus. Pregnancy, vaginal childbirth, or injury can also stretch and weaken the uterosacral ligaments, leading to poor suspension or positioning of the uterus so that it is no longer supported by pelvic floor muscles. Problems with the vaginal wall, such as trauma or loss of smooth muscle support in the wall, can lead to the uterus collapsing downward due to a loss of support. When the uterus prolapses, it also drags the upper portion of the vagina (the apical vagina) along with it due to its anatomic relationship with the apical vagina. Additionally, the pelvic musculature and connective tissues are estrogen sensitive and respond to changes in estrogen level. Estrogen deficiency, which can occur during menopause, can affect the production of collagen that is needed to build connective tissue that makes up ligaments and fascia, which can contribute to uterine prolapse. This is also a reason that connective tissue disorders can predispose certain people to uterine prolapse.
==== Metabolism ==== Fospropofol is metabolized in the liver by alkaline phosphatases to propofol, formaldehyde, and phosphate. The hepatic metabolism of this prodrug to an active metabolite means that peak plasma levels of propofol after the administration of a bolus of fospropofol are lower than for an equipotent dose of propofol and also that its clinical effect is more sustained. These features can be desirable for endoscopic procedures such as esophagogastroduodenoscopy, colonoscopy, bronchoscopy, as well as for some surgical procedures done under local or regional anesthesia. Propofol is further metabolised to propofol glucuronide (34.8%) and quinol glucuronide. Formaldehyde is a known carcinogen but label information states that serum formaldehyde levels are similar to background levels. No long term studies have been done on the cancer risks. The parent drug has a terminal elimination half-life of 0.88+/-0.08 hours, which is non-renal.
=== Lactogenesis I and other changes in pregnancy === Changes in pregnancy, starting around 16 weeks gestational age, prepare the breast for lactation. These changes, collectively known as Lactogenesis I, are directed by hormones produced by the placenta and the brain, namely estrogen, progesterone, prolactin, which gradually increase throughout the pregnancy, and result in the structural development of the alveolar (milk-producing) tissue and the production of colostrum. While prolactin is the predominant hormone in milk production, progesterone, which is at high levels during pregnancy, blocks the prolactin receptors in the breast, thus inhibiting milk from "coming in" during pregnancy.
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.
Reverse-phase HPLC is the usual method and gives a percentage purity value. Mass spectrometry then confirms the molecular mass. Together they provide a basic identity and purity profile for a lot.