A practical reference on lyophilization: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-04-25 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.
Purity assessment relies mainly on reverse-phase high-performance liquid chromatography with ultraviolet detection. Because the peptide lacks a strong chromophore, detection often uses backbone absorbance near 214 nm. Identity is confirmed by mass spectrometry, typically electrospray ionization or matrix-assisted laser desorption, comparing the measured mass against the expected value. Amino acid analysis can verify composition after acid hydrolysis. Diastereomer content and residual counterions are reported less often, although both can influence biological assays.
Lyophilized material is generally stable for extended periods when kept dry at or below minus twenty degrees Celsius. Working solutions are less stable, and common practice is to aliquot and freeze them so that repeated freeze-thaw cycles are avoided. Aqueous solutions are sensitive to pH extremes and to microbial growth, so short-term storage at refrigerator temperature is typical. Oxidation and hydrolysis are the principal degradation routes. Reconstitution with sterile water or a mild buffer is standard, and solutions should be protected from light.
| 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 |
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.
Regulatory status differs sharply by region. Selank holds a Russian marketing authorization, where it is supplied mainly as nasal drops, while authorities elsewhere have not approved it for medical use. Material sold internationally is therefore usually labeled as a research chemical rather than a medicine. Peer-reviewed publications come predominantly from Russian laboratories, and sample sizes are generally small. Whether the compound produces comparable effects under independent, well-controlled replication remains an open question that the broader literature has not settled.
Selank is a synthetic heptapeptide developed in Russia as a structural analogue of tuftsin, a naturally occurring immunomodulatory tetrapeptide. Its sequence, Thr-Lys-Pro-Arg-Pro-Gly-Pro, keeps the tuftsin core at the N-terminus and appends a Pro-Gly-Pro tail. Researchers at the Institute of Molecular Genetics in Moscow synthesized the compound during the 1990s while searching for peptides with combined anxiolytic and immunomodulatory activity. The added tail was intended to resist enzymatic cleavage and prolong the molecule's presence in circulation.
The compound has a calculated molecular weight near 751.9 daltons and carries a net positive charge at physiological pH because of its arginine residue. It dissolves freely in water and in common aqueous buffers, and typically appears as a white or off-white lyophilized powder. The amide backbone makes the molecule susceptible to peptidases, which limits oral use and favors intranasal or parenteral routes. Nomenclature in the literature varies: the substance is also described by the sequence abbreviation TP-7 and by a Russian trade designation.
=== 1951–1953: DNA structure === In 1951 and 1952, together with William Cochran and Vladimir Vand, Crick assisted in the development of a mathematical theory of X-ray diffraction by a helical molecule. This theoretical result matched well with X-ray data for proteins that contain sequences of amino acids in the alpha helix conformation. Helical diffraction theory turned out to also be useful for understanding the structure of DNA. Late in 1951, Crick started working with James Watson at Cavendish Laboratory at the University of Cambridge, England. Using "Photo 51" (the X-ray diffraction results of Rosalind Franklin and her graduate student Raymond Gosling of King's College London, given to them by Gosling and Franklin's colleague Wilkins), Watson and Crick together developed a model for a helical structure of DNA, which they published in 1953. For this and subsequent work they were jointly awarded the Nobel Prize in Physiology or Medicine in 1962 with Wilkins. When Watson came to Cambridge, Crick was a 35-year-old graduate student (due to his work during WWII) and Watson was only 23, but had already obtained a PhD. They shared an interest in the fundamental problem of learning how genetic information might be stored in molecular form. Watson and Crick talked endlessly about DNA and the idea that it might be possible to guess a good molecular model of its structure. A key piece of experimentally-derived information came from X-ray diffraction images that had been obtained by Franklin, and Gosling.
Chloral hydrate had some other important advantages that kept it in use for five decades despite the existence of more advanced barbiturates. It was the safest available sedative until the middle of the twentieth century, and thus was particularly favored for children. It also left patients much more refreshed after a deep sleep than more recently invented sedatives. Its frequency of use made it an early and regular feature in The Merck Manual. Chloral hydrate was also a significant object of study in various early pharmacological experiments. In 1875, Claude Bernard tried to determine if chloral hydrate exerted its action through a metabolic conversion to chloroform. This was not only the first attempt to determine whether different drugs were converted to the same metabolite in the body but also the first to measure the concentration of a particular pharmaceutical in the blood. The results were inconclusive. In 1899 and 1901 Hans Horst Meyer and Ernest Overton respectively made the major discovery that the general anaesthetic action of a drug was strongly correlated to its lipid solubility. However, chloral hydrate was quite polar but nonetheless a potent hypnotic. Overton was unable to explain this mystery. Thus, chloral hydrate remained one of the major and persistent exceptions to this breakthrough discovery in pharmacology. This anomaly was eventually resolved in 1948, when Claude Bernard's experiment was repeated.
A 2004 essay on the relation between car colour and safety stated that no previous studies had been scientifically conclusive. Since then, a Swedish study found that pink cars are involved in the fewest and black cars are involved in the most crashes (Land transport NZ 2005). In Auckland New Zealand, a study found that there was a significantly lower rate of serious injury in silver cars, with higher rates in brown, black, and green cars. The Vehicle Colour Study, conducted by Monash University Accident Research Centre (MUARC) and published in 2007, analysed 855,258 crashes that occurring between 1987 and 2004 in the Australian states of Victoria and Western Australia that resulted in injury or in a vehicle being towed away. The study analysed risk by light condition. It found that in daylight, black cars were 12% more likely than white to be involved in a collision, followed by grey cars at 11%, silver cars at 10%, and red and blue cars at 7%, with no other colours found to be significantly more or less risky than white. At dawn or dusk, the risk ratio for black cars jumped to 47% more likely than white, and that for silver cars to 15%. In the hours of darkness, only red and silver cars were found to be significantly more risky than white, by 10% and 8% respectively.
Sources: en.wikipedia.org
==== Unstructured ==== An unstructured repository may simply be a stack of tapes, DVD-Rs or external HDDs with minimal information about what was backed up and when. This method is the easiest to implement, but unlikely to achieve a high level of recoverability as it lacks automation.
Kennedy, Jr., Dan Olmsted, and David Kirby, as evidence that autistic children lack sufficient glutathione to remove mercury from their bodies and are therefore more susceptible to the toxicity of mercury in vaccines. However, James herself has cautioned against such conclusions, saying they are an overstatement of what her research actually shows; with specific regard to Kirby's claims, she said, "I'm afraid Mr. Kirby is overstating our conclusions -- which did not mention mercury. We simply showed for the first time that children with autism have lower levels of the major intracellular antioxidant, glutathione, which incidentally happens to be the major mechanism for mercury elimination from the body." On March 27, 2012, the Jane Botsford Johnson Foundation awarded a $1.2 million research grant to Arkansas Children's Hospital to fund research into autism biomarkers; this research was to be led by James. At the time the grant was being awarded, Johnson herself said that "Jill James' work at ACHRI holds great promise for the future of autism therapy and prevention."
== Structure == Encoded by the fusA gene on the str operon, EF-G is made up of 704 amino acids that form 5 domains, labeled Domain I through Domain V. Domain I may be referred to as the G-domain or as Domain I(G), since it binds to and hydrolyzes guanosine triphosphate (GTP). Domain I also helps EF-G bind to the ribosome, and contains the N-terminal of the polypeptide chain. Domain IV is important for translocation, as it undergoes a significant conformational change and enters the A site on the 30S ribosomal subunit, pushing the mRNA and tRNA molecules from the A site to the P site. The five domains may be also separated into two super-domains. Super-domain I consists of Domains I and II, and super-domain II consists of Domains III - IV. Throughout translocation, super-domain I will remain relatively unchanged, as it is responsible for binding tightly to the ribosome. However, super-domain II will undergo a large rotational motion from the pre-translocational (PRE) state to the post-translocational (POST) state. Super-domain I is similar to the corresponding sections of EF-Tu. Super-domain II in the POST state mimics the tRNA molecule of the EF-Tu • GTP • aa-tRNA ternary complex.
=== Differentiation from pituitary pars intermedia dysfunction === EMS shares similarities to pituitary pars intermedia dysfunction (also known as equine Cushing's disease), which also causes regional adiposity, laminitis, and sometimes insulin resistance. Treatment and management differ between the conditions, making it important to distinguish between the two. However, both diseases may occur simultaneously; horses with EMS may develop PPID.
Sources: en.wikipedia.org
Without interactions between the compounds there would be no enthalpy of mixing and the entropy of mixing would be ideal. The ideal entropy of mixing of multiple pure compounds is always positive (the term -T∙ΔS is negative) and ΔG would be negative for all compositions, causing complete miscibility. Therefore, the fact that miscibility gaps are observed can only be explained by interaction. In the case of polymer solutions, polymer-polymer, solvent-solvent and polymer-solvent interactions have to be taken into account. A model for the phenomenological description of polymer phase diagrams was developed by Flory and Huggins (see Flory–Huggins solution theory). The resulting equation for the change of Gibbs energy consists of a term for the entropy of mixing for polymers and an interaction parameter that describes the sum of all interactions.
Converts human Glu-plasminogen to plasmin by cleaving the Arg560-Val peptide bond that is also hydrolysed by the mammalian u-plasminogen activator and t-plasminogen activator. Also cleaves arginyl bonds in other proteins. This enzyme is isolated from the bacterium Yersinia pestis that causes plague. Y. pestis carries a 9.5-kb plasmid, pPCP1, that encodes the plasminogen activator. Pla is a critical virulence factor for plague. In bubonic plague, Pla promotes the invasion of Y. pestis from subcutaneous sites of inoculation into the lymphatic system and deeper tissues. In contrast, Pla is important for bacterial growth in the lung during pneumonic plague but it is not required for dissemination to other tissues. It is found in the outer membrane of gram-negative bacteria, and it functions as a surface protease and an adhesin. It has suggested that the fate of Y.pestis infection of the lung is decided extremely early during infection, and that Pla plays a dual role to tilt the balance in favor of the pathogen. In the initial stages of infection, Pla inhibits the activation of complement system and neutrophil-mediated killing such as phagocytosis and degranulation with its proteolytic activity. In addition, with its adhesin function, it suppresses the neutrophil influx, and facilitates type three secretion system (T3SS) to deliver multiple toxic Yersinia effector proteins Yops directly into target cells to inhibit the cytokine signalling.
{\displaystyle {\begin{aligned}\nabla \varphi &=\left({\frac {\partial \varphi }{\partial x}},\,{\frac {\partial \varphi }{\partial y}}\right)^{\mathsf {T}},\\[5pt]\nabla \times \varphi &=\left({\frac {\partial \varphi }{\partial y}},\,-{\frac {\partial \varphi }{\partial x}}\right)^{\mathsf {T}}.\end{aligned}}}
Despite initial resistance from American cattle ranchers, who believed the white hair of a freeze brand could be dyed to confuse ownership, the technique has since become a popular means of marking animals for identification worldwide.
For protein expression and purification in bacteria it is recommended that protein induction and cell harvesting should be done at specific OD600 (usually at the end of the log phase, OD600 = 0.4). OD600 is preferable to UV spectroscopy when measuring the growth over time of a cell population because at this wavelength, the cells will not be killed as they would under too much UV radiation. UV radiation has also been shown to cause small to medium-sized mutations in bacteria, potentially altering or destroying genes of interest.
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.
Purity is usually reported as an HPLC area percentage, most often measured at 214 nm. Identity is confirmed separately by mass spectrometry. A certificate of analysis should state both the method and the observed value.