The short version of freeze-thaw fits in a sentence. The long version — which is the one that helps — is below.
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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.
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.
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 |
|---|---|---|
| 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 |
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.
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.
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 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.
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.
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.
== Mechanism == As previously mentioned, BCKDC's primary function in mammals is to catalyze an irreversible step in the catabolism of branched-chain amino acids. However BCKDC has a relatively broad specificity, also oxidizing 4-methylthio-2-oxobutyrate and 2-oxobutyrate at comparable rates and with similar Km values as for its branched-chain amino acid substrates. The BCKDC will also oxidize pyruvate, but at such a slow rate this side reaction has very little physiological significance. The reaction mechanism is as follows. Please note that any of several branched-chain α-ketoacids could have been used as a starting material; for this example, α-ketoisovalerate was arbitrarily chosen as the BCKDC substrate.
== Achievements == Lee is best known for his research in capillary separations and mass spectrometry detection. He is an author or co-author of over 550 scientific publications. Among the scientific awards that he has received for his achievements in research and professional activities are the M.S. Tswett Chromatography Medal (1984), the Keene P. Dimick Chromatography Award (1988), the American Chemical Society Award in Chromatography (1988), the Russian Tswett Chromatography Medal (1992), the Martin Gold Medal (1996), the Latin-American Chromatography Congress Medal (1998), the M.J.E. Golay Award (1998), the American Chemical Society Award in Chemical Instrumentation (1998), an honorary doctorate from Uppsala University in Sweden (1998), the Dal Nogare Award (1999), the Eastern Analytical Symposium Award for Achievements in Separation Science (1999), the California Separation Science Society Award (2005), the Pittsburgh Analytical Chemistry Award (2008), R&D 100 Awards (1993, 2008), Eastern Analytical Symposium Award for Outstanding Achievements in the Fields of Analytical Chemistry (2008), the American Chemical Society Award in Separations Science and Technology (2012), and the LC/GC Europe Lifetime Achievement Award (2014). He is also an entrepreneur and has been involved in transferring technology from his university research laboratory to the private sector.
== Side effects == Adverse events are generally caused by incorrect dosing. Long-term suppression of TSH values below normal values frequently causes cardiac side effects and contributes to decreases in bone mineral density (low TSH levels are also well known to contribute to osteoporosis). Too high a dose of levothyroxine causes hyperthyroidism. Overdose can result in heart palpitations, abdominal pain, nausea, anxiety, confusion, agitation, insomnia, weight loss, and increased appetite. Acute massive overdose may be life-threatening; treatment should be symptomatic and supportive. Massive overdose can be associated with increased sympathetic activity, thus may require treatment with beta blockers. The effects of overdosing appear 6 hours to 11 days after ingestion.
Sources: en.wikipedia.org
PCP is well known for its primary action on the NMDA receptor, an ionotropic glutamate receptor. As such, PCP is a non-competitive NMDA receptor antagonist. The role of NMDAR antagonism in the effect of PCP, ketamine, and related dissociative agents was first published in the early 1980s by David Lodge and colleagues. Other NMDA receptor antagonists include ketamine, tiletamine, dextromethorphan, nitrous oxide, and dizocilpine (MK-801). Research also indicates that PCP inhibits nicotinic acetylcholine receptors (nAChRs) among other mechanisms. Analogues of PCP exhibit varying potency at nACh receptors and NMDA receptors. Findings demonstrate that presynaptic nAChRs and NMDA receptor interactions influence the postsynaptic maturation of glutamatergic synapses and consequently impact synaptic development and plasticity in the brain. These effects can lead to inhibition of excitatory glutamate activity in certain brain regions such as the hippocampus and cerebellum thus potentially leading to memory loss as one of the effects of prolonged use. Acute effects on the cerebellum manifest as changes in blood pressure, breathing rate, pulse rate, and loss of muscular coordination during intoxication. PCP, like ketamine, also acts as a potent dopamine D2High receptor partial agonist in rat brain homogenate and has affinity for the human cloned D2High receptor. This activity may be associated with some of the other more psychotic features of PCP intoxication, which is evidenced by the successful use of D2 receptor antagonists (such as haloperidol) in the treatment of PCP psychosis.
Co-developed and co-marketed with Bayer, sorafenib—sold under the trade name Nexavar—is a drug approved in the United States for the treatment of advanced renal cell carcinoma (kidney cancer) in 2005, and for the treatment of inoperable hepatocellular carcinoma, the most common form of liver cancer, in 2007. Sorafenib has also been evaluated in other types of cancer, including thyroid (as a treatment of last resort) and breast (in comparison to capecitabine). In July 2014, the company announced the phase III failure of a Sorafenib-Capecitabine combination trial. The drug combination failed to increase progression free survival of patients with advanced breast cancer.
Drug inactivation or modification: for example, enzymatic deactivation of penicillin G in some penicillin-resistant bacteria through the production of β-lactamases. Drugs may also be chemically modified through the addition of functional groups by transferase enzymes. For example, acetylation, phosphorylation, or adenylation are resistance mechanisms to aminoglycosides. Acetylation is the most common and can affect a number of drug classes. Alteration of target- or binding site: for example, alteration of PBP—the binding target site of penicillins—in MRSA and other penicillin-resistant bacteria. Another protective mechanism found among bacterial species is ribosomal protection proteins. These proteins protect the bacterial cell from antibiotics that target the cell's ribosomes to inhibit protein synthesis. The mechanism involves the binding of the ribosomal protection proteins to the ribosomes of the bacterial cell, which in turn changes its conformational shape. This allows the ribosomes to continue synthesizing proteins essential to the cell while preventing antibiotics from binding to the ribosome to inhibit protein synthesis. Alteration of metabolic pathway: for example, some sulfonamide-resistant bacteria do not require para-aminobenzoic acid (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides, instead, like mammalian cells, they turn to using preformed folic acid. Reduced drug accumulation: by decreasing drug permeability or increasing active efflux (pumping out) of the drugs across the cell surface.
=== Fight Song === In 2009, Santa Fe College adopted a fight song. "Saints Forever" was performed for the first time on Tuesday, April 21, 2009, between softball games in Gainesville. The song was a collaboration between Chris Sharp, the college's director of bands, and Ryan B. Leverone, a Santa Fe College student.
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.
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.