A practical reference on tuftsin: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
Reviewed 2025-11-06. Anything still debated is marked as such rather than presented as settled.
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.
Regulatory treatment varies by jurisdiction. In Russia the compound is a registered prescription product, while in the European Union and the United States it is generally handled as a research chemical without a marketing authorization. Suppliers therefore operate outside pharmaceutical oversight, and buyers rely on supplier documentation for purity and identity claims. Chain of custody and third-party testing are the main verification tools. Analysts note that the absence of a pharmacopoeial monograph for research-grade material limits standardization across vendors.
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.
| 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.
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.
Peptide stability depends strongly on temperature, moisture, and pH. Lyophilized Selank is generally most stable when stored cold and dry, with freezer temperatures commonly used for long-term storage. In solution, the compound is susceptible to hydrolysis and to microbial growth if it is not handled aseptically. The C-terminal proline-rich extension appears to slow enzymatic cleavage relative to tuftsin, though quantitative degradation rates vary with the matrix and the conditions tested. Published stability data specific to Selank remain sparse.
Quality assessment of Selank samples typically combines purity determination with identity confirmation and counter-ion analysis. Purity is usually reported as a percentage by chromatographic area, with values above 95 percent often quoted for research-grade material. Water content and residual solvents are checked in lyophilized batches because they affect both stability and accurate mass determination. A reported purity figure does not by itself establish that a sample is the intended sequence, so orthogonal methods are needed to rule out sequence isomers or truncation products.
Characterization of Selank in laboratory settings relies on standard peptide analytical techniques. Reverse-phase high-performance liquid chromatography separates the peptide from related impurities and degradation products, while mass spectrometry confirms molecular identity through accurate mass measurement. Amino acid analysis and peptide sequencing verify the primary structure when reference material is unavailable. Because Selank is a short chain, fragmentation-based analysis produces a diagnostic ion pattern that supports confident identification.
Preotact contains recombinant human parathyroid hormone which is identical to the full-length native 84-amino acid polypeptide. Physiological actions of parathyroid hormone include stimulation of bone formation by direct effects on bone forming cells (osteoblasts) indirectly increasing the intestinal absorption of calcium and increasing the tubular reabsorption of calcium and excretion of phosphate by the kidney.
=== No development reported === ACH-36 – undefined mechanism of action [22] Alprazolam sublingual – GABAA receptor positive allosteric modulator and benzodiazepine [23] Antalarmin (CP-154526) – corticotropin-releasing hormone (CRH) inhibitor [24] Buspirone controlled release (Buspirone ER) – serotonin 5-HT1A receptor partial agonist and other actions [25] BW-723C86 – serotonin 5-HT2B and 5-HT2C receptor agonist [26] Cannabidiol dry powder inhalation (RLS-103) – cannabinoid receptor modulator and other actions [27] Darigabat (CVL-865; PF-06372865; PF-6372865) – GABAA receptor positive allosteric modulator [28] Divaplon (RU-32698) – GABAA receptor positive allosteric modulator and nonbenzodiazepine/imidazolpyrimidine [29] Fananserin (RP-62203) – serotonin 5-HT2A receptor antagonist and dopamine D4 receptor antagonist [30] FR260010 (FR-260010) – serotonin 5-HT2C receptor antagonist [31] [32] GSK-588045 (GSK588045) – serotonin 5-HT1A, 5-HT1B, and 5-HT1D receptor antagonist [33] GSK-1360707 – serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI) [34] GT-001 – GABAA receptor positive allosteric modulator [35] Guanfacine extended release (Connexyn; Intuniv; Intuniv XR; S-877503; SHP-503; SPD-503) – α2-adrenergic receptor agonist [36] Itriglumide (CR-2945) – cholecystokinin B (CCKB) receptor antagonist [37] Lohocla-201 (Kindolor) – various actions [38] LY-293284 – serotonin 5-HT1A receptor agonist [39] NMRA-511 (BTRX-323511; NMRA-323511) – vasopressin V1A receptor antagonist [40] Paroxetine (Aropax; BRL-29060; Deroxat; Divarius; FG-7051; Frosinor; Motivan; NNC-207051; Paxil; Seroxat; SI-211103; Tagonis) – selective serotonin reuptake inhibitor (SSRI) [41] Psilocybin (MYCO-001; MYCO-003) – non-selective serotonin receptor agonist and psychedelic hallucinogen [42] PT-00114 (PT100114) – corticotropin-releasing hormone (CRH) inhibitor [43] Research programme: allosteric modulators - Addex Therapeutics – various actions [44] Research programme: AMPA receptor agonists - RespireRx (ampakines; CX compounds) – AMPA receptor agonists and brain-derived neurotrophic factor (BDNF) stimulants [45] Research programme: anxiety and neurological disorder therapeutics - AstraZeneca – various actions [46] Research programme: cannabis-based therapeutics - Skye Bioscience – cannabinoid receptor agonists [47] Research programme: neuropeptide S receptor modulators - Pfizer (WYE-198232) – neuropeptide receptor agonists [48] Research programme: oxytocin receptor agonist - Wyeth – oxytocin receptor agonists [49] RGH-618 – metabotropic glutamate mGlu5 receptor negative allosteric modulator [50] Riluzole (PK-26124; Rilutek; RP-54274) – various actions [51] Risperidone (JNJ-410397-AAA; R-64766; R064766; Risperdal; Risperdal Consta; Risperdal Depot) – atypical antipsychotic (non-selective monoamine receptor modulator) [52] Saripidem (SL-850274) – GABAA receptor positive allosteric modulator and nonbenzodiazepine/imidazopyridine [53] SB-242084 (SB242084) – serotonin 5-HT2C receptor antagonist [54] SRX-246 (API-246) – vasopressin V1A receptor antagonist [55] SYT-510 – anandamide reuptake inhibitor [56] Tebideutorexant (JNJ-3215; JNJ-61393215; Orexin-1) – orexin OX1 receptor antagonist [57] WAY-100135 – serotonin 5-HT1A receptor antagonist [58] Ziprasidone (CP-88059-01; CP-88059-1; Geodon; ME-2112; RQ-00000003; Zeldox) – atypical antipsychotic (non-selective monoamine receptor modulator) [59]
== Bioequivalence issues == While the FDA maintains that approved generic drugs are equivalent to their branded counterparts, bioequivalence problems have been reported by physicians and patients for many drugs. Certain classes of drugs are suspected to be particularly problematic because of their chemistry. Some of these include chiral drugs, poorly absorbed drugs, and cytotoxic drugs. In addition, complex delivery mechanisms can cause bioequivalence variances. Physicians are cautioned to avoid switching patients from branded to generic, or between different generic manufacturers, when prescribing anti-epileptic drugs, warfarin, and levothyroxine. Major issues were raised in the verification of bioequivalence when multiple generic versions of FDA-approved generic drug were found not to be equivalent in efficacy and side effect profiles. In 2007, two providers of consumer information on nutritional products and supplements, ConsumerLab.com and The People's Pharmacy, released the results of comparative tests of different brands of bupropion. The People's Pharmacy received multiple reports of increased side effects and decreased efficacy of generic bupropion, which prompted it to ask ConsumerLab.com to test the products in question. The tests showed that some generic versions of Wellbutrin XL 300 mg didn't perform the same as the brand-name pill in laboratory tests. The FDA investigated these complaints and concluded that the generic version is equivalent to Wellbutrin XL in regard to bioavailability of bupropion and its main active metabolite hydroxybupropion.
In common with other nitriles, acetonitrile can be metabolised in microsomes, especially in the liver, to produce hydrogen cyanide, as was first shown by Pozzani et al. in 1959. The first step in this pathway is the oxidation of acetonitrile to glycolonitrile by an NADPH-dependent cytochrome P450 monooxygenase. The glycolonitrile then undergoes a spontaneous decomposition to give hydrogen cyanide and formaldehyde. Formaldehyde, a toxin and a carcinogen on its own, is further oxidized to formic acid, which is another source of toxicity. The metabolism of acetonitrile is much slower than that of other nitriles, which accounts for its relatively low toxicity. Hence, one hour after administration of a potentially lethal dose, the concentration of cyanide in the rat brain was 1/20 that for a propionitrile dose 60 times lower (see table). The relatively slow metabolism of acetonitrile to hydrogen cyanide allows more of the cyanide produced to be detoxified within the body to thiocyanate (the rhodanese pathway). It also allows more acetonitrile to be excreted unchanged before it is metabolised. The main pathways of excretion are by exhalation and in the urine.
Shunting inhibition has no direct effect on the membrane potential of the cell; however, it reduces the effect of any coincident synaptic input by reducing the electrical resistance of the cell's membrane. Shunting inhibition can "override" the excitatory effect of depolarising GABA, resulting in overall inhibition even if the membrane potential becomes less negative. It was thought that a developmental switch in the molecular machinery controlling the concentration of chloride inside the cell changes the functional role of GABA between neonatal and adult stages. As the brain develops into adulthood, GABA's role changes from excitatory to inhibitory.
Sources: en.wikipedia.org
==== Feud with outgoing Vice President Verónica Abad Rojas ==== Upon their inauguration in November 2023, both Noboa and Abad Rojas distanced themselves from each other, with Abad Rojas launching personal attacks against Noboa. She did not appear in the inaugural photo of the cabinet and subsequently was appointed ambassador to Israel. Shortly thereafter, she was ordered to move to Istanbul within three days. Abad Rojas called these decisions a "forced exile". In June 2024, Abad Rojas survived an impeachment attempt by the Noboa government due to legal issues. In November 2024, she was suspended from the vice presidency by the labor ministry for 150 days. Noboa named Secretary of National Planning Sariha Moya as acting vice president. Abad Rojas' suspension was lifted by a judge in December 2024, along with an order for the labor ministry to give her an apology for the suspension. According to Ecuador's electoral law, the president is required to take a leave of absence during the presidential campaign and appoint the elected vice-president to act as president temporarily. Noboa refused to appoint Abad Rojas as interim president during the election campaign. Instead, in January 2025, he appointed Cynthia Gellibert as vice president with temporary presidential responsibilities during the campaign. On 30 March 2025, Noboa caused controversy for ignoring the Constitutional Court and appointing Cynthia Gellibert by decree as vice president, suspending Abad Rojas once again.
Corneal neovascularization is a condition where new blood vessels invade into the cornea from the limbus. It is triggered when the balance between angiogenic and antiangiogenic factors are disrupted that otherwise maintain corneal transparency. The immature new blood vessels can lead to persistent inflammation and scarring, lipid exudation into the corneal tissues, and a reduction in corneal transparency, which can affect visual acuity.
Lance Henriksen at IMDb Lance Henriksen at the TCM Movie Database (archived) Lance Henriksen at the Internet Broadway Database Films in Review interview Archived September 9, 2018, at the Wayback Machine
== Production == Similar to other varieties of cheese, the process of making blue cheese consists of six standard steps. However, additional ingredients and processes are required to give this blue cheese its distinctive properties. To begin with, the commercial-scale production of blue cheese consists of two phases: the culturing of suitable spore-rich inocula and fermentation for maximum, typical flavor.
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.