Everything below concerns TP-7. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-06-26. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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 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.
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic heptapeptide | Analog of the tetrapeptide tuftsin |
| Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro | Reported consistently across pharmacopoeial descriptions |
| Appearance | White to off-white lyophilized powder | Typical form of research-grade material |
| Solubility | Freely soluble in water | Aqueous buffers; poor in nonpolar solvents |
| Typical storage temperature | -20 degrees Celsius | Lyophilized powder; protect from moisture |
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.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. Its four N-terminal residues reproduce tuftsin, a tetrapeptide fragment of the immunoglobulin heavy chain, while the C-terminal Pro-Gly-Pro extension is a synthetic addition. The peptide has a molecular mass near 752 daltons and carries a net positive charge at physiological pH because of the arginine and lysine side chains. Published indexes list it under the name Selank and the sequence abbreviation TKPRPGP. Solid-phase peptide synthesis is the standard production route for research quantities.
Development took place at the Institute of Molecular Genetics of the Russian Academy of Sciences, where a series of short peptides were designed in the 1980s and 1990s. Selank was selected from variants of tuftsin that showed resistance to plasma peptidases. Russian regulatory approval covers it as an anxiolytic agent given intranasally. Outside that market the compound is normally handled as a research chemical rather than a medicine, and no widely recognised international pharmacopoeial monograph exists. The name Selank is a coined trade designation rather than a systematic chemical name.
== Uses == Hydroquinone has a variety of uses principally associated with its action as a reducing agent that is soluble in water. It is a major component in most black and white photographic developers for film and paper, where, with the compound metol, it reduces silver halides to elemental silver. There are various other uses associated with its reducing power. As a polymerisation inhibitor, exploiting its antioxidant properties, hydroquinone prevents polymerization of acrylic acid, methyl methacrylate, cyanoacrylate, and other monomers that are susceptible to radical-initiated polymerization. By acting as a free radical scavenger, hydroquinone serves to prolong the shelf life of light-sensitive resins such as preceramic polymers. Hydroquinone can lose a hydrogen cation from both hydroxyl groups to form a diphenolate ion. The disodium diphenolate salt of hydroquinone is used as an alternating comonomer unit in the production of the polymer PEEK.
=== RNA editing and the genome === Octopuses, like other coleoid cephalopods but unlike more basal cephalopods or other molluscs, are capable of greater RNA editing, changing the nucleic acid sequence of the primary transcript of RNA molecules, than any other organisms. Much editing is done in the nervous system, particularly for excitability and neuronal morphology. Coleoids rely mostly on ADAR enzymes for RNA editing, which requires large, double-stranded RNA structures. The many editing sites are conserved in the coleoid genome and the mutation rates for the sites are hampered. Hence, greater transcriptome plasticity has come at the cost of slower genome evolution. The genome of octopuses has also gone through several chromosomal fusions and rearrangements, unlike that of their closest relative the vampire squid, whose chromosomal structure is more basal and squid-like. The octopus genome is unremarkably bilaterian except for large developments of two gene families: protocadherins, which regulate the development of neurons; and the C2H2 zinc-finger transcription factors. Many novel genes in both cephalopods generally and octopus specifically manifest in the animals' skin, suckers, and nervous system.
Cereulide 2-methyl-5-HT Alpha-Methyltryptamine Bufotenin Chlorophenylbiguanide Ibogaine Phenylbiguanide Quipazine RS-56812 – Potent and selective 5-HT3 partial agonist, 1000× selectivity over other serotonin receptors SR-57227 Varenicline YM-31636 S 21007 (SAR c.f. CGS-12066A)
Sources: en.wikipedia.org
Pillsbury's Executive Vice President of Restaurant Operations Norman E. Brinker was tasked with turning the brand around, and strengthening its position against its main rival, McDonald's. One of his initiatives was a new advertising campaign featuring a series of attack ads against its major competitors. This campaign started a competitive period between Burger King, McDonald's, and top burger chains known as the Burger wars. Brinker left Burger King in 1984, to take over Dallas-based gourmet burger chain Chili's. Smith and Brinker's efforts were initially effective, but after their respective departures, Pillsbury relaxed or discarded many of their changes and scaled back on construction of new locations. These actions stalled corporate growth and sales declined again, eventually resulting in a damaging fiscal slump for Burger King and Pillsbury. Poor operation and ineffectual leadership continued to bog down the company for many years. Pillsbury was eventually acquired by the British entertainment conglomerate Grand Metropolitan in 1989. Initially, Grand Met attempted to bring the chain to profitability under newly minted CEO Barry Gibbons; the changes he initiated during his two-year tenure had mixed results, as successful new product introductions and tie-ins with The Walt Disney Company were offset by continuing image problems and ineffectual advertising programs. Additionally, Gibbons sold off several of the company's assets in an attempt to profit from their sale and laid off many of its staff members.
==== Output ==== After an incident particle has fused with a parent nucleus, if the excitation energy is sufficient, the nucleus breaks into fragments. This is called scission, and occurs at about 10−20 seconds. The fragments can emit prompt neutrons at between 10−18 and 10−15 seconds. At about 10−11 seconds, the fragments can emit gamma rays. At 10−3 seconds β decay, β-delayed neutrons, and gamma rays are emitted from the decay products. Typical fission events release about two hundred million eV (200 MeV) of energy for each fission event. The exact isotope which is fissioned, and whether or not it is fissionable or fissile, has only a small impact on the amount of energy released. This can be easily seen by examining the curve of binding energy (image below), and noting that the average binding energy of the actinide nuclides beginning with uranium is around 7.6 MeV per nucleon. Looking further left on the curve of binding energy, where the fission products cluster, it is easily observed that the binding energy of the fission products tends to center around 8.5 MeV per nucleon. Thus, in any fission event of an isotope in the actinide mass range, roughly 0.9 MeV are released per nucleon of the starting element. The fission of 235U by a slow neutron yields nearly identical energy to the fission of 238U by a fast neutron. This energy release profile holds for thorium and the various minor actinides as well.
=== Discontinued === 2-BUMP – monoamine oxidase B (MAO-B) inhibitor [238] A-77636 – dopamine D1 receptor agonist [239] Acamprosate/baclofen (PXT-864) – combination of acamprosate (various actions) and baclofen (GABAB receptor agonist) [240] Adrogolide (ABT-431; DAS-431; A-86929 O,O′-diacetate) – dopamine D1 receptor agonist (prodrug of A-86929) [241] AP-001 – various actions [242] Apomorphine inhalation (VR-004; VR-040; VR-400) – non-selective dopamine receptor agonist and other actions [243] Apomorphine intranasal – non-selective dopamine receptor agonist and other actions [244] Apomorphine subcutaneous (ND-0701) – non-selective dopamine receptor agonist and other actions [245] Apomorphine transdermal patch – non-selective dopamine receptor agonist and other actions [246] Arimoclomol (BRX-345; Miplyffa; OR-01; OR-04) – undefined mechanism of action [247] Arundic acid (Arocyte Injection; Cereact Capsule; MK-0724; ONO-2506; Proglia) – various actions [248] Atomoxetine (LY-139603; Strattera; Tomoxetine) – norepinephrine reuptake inhibitor (NRI) [249] AVE-8112 (AVE8112; AVE-8112A) – phosphodiesterase PDE4 inhibitor [250] AX-201 (AX201) – nerve growth factor (NGF) stimulant [251] Bifeprunox (DU-127090) – serotonin 5-HT1A receptor agonist and dopamine D2 receptor agonist [252] BP-897 – dopamine D3 receptor agonist [253] Carbidopa/levodopa (AP-09004; AP-CD/LD) – combination of carbidopa (aromatic L-amino acid decarboxylase (AAAD) inhibitor) and levodopa (dopamine precursor) [254] CEP-1347 (KT-7515) – mitogen-activated protein kinase inhibitor and mixed-lineage kinase inhibitor [255] CERE-120 (AAV-NRTN; AAV-NTN; AAV2-neurturin; AAV2-NTN; neurturin gene therapy) – gene therapy, nerve tissue protein modulator, and neurturin agonist [256] Cinpanemab (BIIB-054) – monoclonal antibody against α-synuclein [257] CVXL-0107 – glutamate release inhibitor [258] Dactolisib (BEZ-235; NVP-BEZ-235; NVP-BEZ235-ANA; NVP-BEZ235-NX; RTB-101) – 1-phosphatidylinositol 3 kinase inhibitor and mTOR inhibitor [259] Davunetide intranasal (AL-108; NAP; NAPVSIPQ) – various actions [260] Dihydrexidine (DAR-0100) – dopamine D1 receptor agonist [261] Dihydrexidine (IP-202) – dopamine D1 and D5 receptor agonist [262] DNS-7801 – undefined mechanism of action [263] Embryonic neural cell therapy-Parkinson's Disease - CellFactors (Parkinson's disease cell therapy) – dopaminergic cell replacement [264] Emlenoflast (inzomelid; IZD-174; MCC-7840) – NLR family pyrin domain containing 3 (NLRP3) inhibitor [265] Entacapone (Comtan; Comtess; OR-611) – catechol O-methyltransferase (COMT) inhibitor [266] Ethyl eicosapentaenoic acid (AMR-101; Ethyl-EPA; LAX-101; Miraxion; Vascepa; Vazkepa) – various actions [267] Etrabamine (14-839JL; JL-14839) – dopamine D2 receptor agonist [268] Ezaladcigene resoparvovec (AAV-AADC; AV-201; GZ-404477; NBIb-1817) – gene transference and aromatic-L-amino-acid decarboxylase (AAAD) replacement [269] Fipamezole (BVF-025; JP-1730) – α2-adrenergic receptor antagonist [270] Florbenazine F18 (18F-DTBZ; 18F-AV-133; 18F-FP-dihydrotatetrabenazine; AV-133) – vesticular monoamine transporter 2 (VMAT2) inhibitor and radiopharmaceutical – diagnosis [271] Foliglurax (PXT-2331; PXT002331) – metabotropic glutamate mGlu4 receptor positive allosteric modulator [272] FRM-0334 (EVP-0334) – class I and class II histone deacetylase inhibitor [273] GYKI-52895 – dopamine reuptake inhibitor (DRI) [274] Levetiracetam (Keppra; L-059; SIB-S1; UCB-059; UCB-22059; UCB-L059) – synaptic vesicle glycoprotein 2A (SV2A) modulator [275] Lu-AA47070 (LU-AA-47070) – adenosine A2A receptor antagonist [276] Methylthioninium chloride (MTC; methylene blue; TRx-0014; TRx-014) – various actions [277] Naxagolide (L-647339) – dopamine D2 and D3 receptor agonist [278] Nebicapone (BIA-3202) – catechol O-methyltransferase (COMT) inhibitor [279] Nitecapone (OR-462) – catechol O-methyltransferase (COMT) inhibitor Nitisinone (NTBC; Orfadin; SC-0735; SYN-118) – 4-hydroxyphenylpyruvate dioxygenase inhibitor and dopamine release stimulant [280] NPT-088 (NPT088) – immunoglobulin fusion general amyloid interaction motif (GAIM) based dimer [281] NPT-189 (NPT189) – immunoglobulin fusion protein [282] NW-1048 – monoamine oxidase B (MAO-B) inhibitor [283] NYX-458 – ionotropic glutamate NMDA receptor positive allosteric modulator [284] ODM-103 – catechol O-methyltransferase (COMT) inhibitor [285] Omigapil (CGP-3466; SNT-317; TCH-346) – glyceraldehyde 3 phosphate dehydrogenase (GAPDH) inhibitor [286] OPM-201 (S-221237) – leucine-rich repeat kinase 2 (LRRK2) inhibitor [287] OSU-6162 (OSU6162; PNU-9639; PNU-96391; PNU-96391A) – serotonin 5-HT2A receptor partial agonist (non-hallucinogenic), dopamine D2 receptor partial agonist, and sigma σ1 receptor ligand (so-called "monoaminergic stabilizer") [288] Paliroden (SR-57667; SR-57667B) – nerve growth factor (NGF) stimulant [289] Pardoprunox (SLV-308; SME-308) – dopamine D2 and D3 receptor partial agonist, serotonin 5-HT1A receptor full agonist, and other actions [290] Parkinson's disease gene therapy - Oxford BioMedica (AXO Lenti PD; OXB-101; OXB-102; ProSavin) – gene transference [291] Pegipanermin (DN-TNF; INB-03; LIVNate™; Quellor™; soluble tumour necrosis factor inhibitor; XENP1595; XENP345; XPro 1595; XPro595; XProTM) – tumour necrosis factor alpha (TNFα) inhibitor and immunostimulant [292] PF-06412562 (CVL-562) – dopamine D1 and D5 receptor partial agonist [293] Piclozotan (SUN-4057; SUN-N-4057) – serotonin 5-HT1A receptor agonist – dyskinesia in Parkinson's disease [294] Preclamol ((–)-3-PPP) – dopamine D2 receptor partial agonist [295] Preladenant (MK-3814; privadenant; SCH-420814) – adenosine A2A receptor antagonist [296] Proxison – synthetic flavonoid-based antioxidant [297] Quinelorane (LY-163502) – dopamine D2 receptor agonist [298] Raseglurant (ADX-10059) – metabotropic glutamate mGlu5 receptor negative allosteric modulator [299] Razpipadon (CVL-871; PF-6669571; PF-06669571; PW-0464) – dopamine D1 receptor agonist [300] Renzapride (ATL-1251; AZM-112; BRL-24924) – serotonin 5-HT3 receptor antagonist and serotonin 5-HT4 receptor agonist [301] Research programme: Alzheimer's and Parkinson's disease diagnostic agents - Bayer HealthCare Pharmaceuticals/TauRx – undefined mechanism of action – diagnosis [302] Research programme: AMC therapeutics - Animuscure – undefined mechanism of action [303] Research programme: Ig fusion GAIM dimers - Proclara Biosciences (NPT-288; NPT-007; NPT-014; NPT-289) – various actions [304] Research programme: Parkinson's disease therapeutics - Araclon Biotech (AB-03) – undefined mechanism of action [305] Research programme: Parkinson's disease therapies - Neose/Neuronyx – undefined mechanism of action [306] Research programme: Parkinson's disease therapies - Proteome Systems (EUK-418) – free radical scavenger and oxygen radical scavenger [307] Research programme: Parkinson's disease therapeutics - TauRx Therapeutics (G2 PD; TRx 018) – synuclein inhibitor [308] Research programme: protein aggregation inhibitors - Proclara Biosciences (NPT-001; NPT-002) – various actions [309] Riluzole (PK-26124; Rilutek; RP-54274) – various actions [310] Ropinirole implant – dopamine D2, D3, and D4 receptor agonist [311] Sarsasapogenin (Cogane; JNX-1001; PYM-50028; Smilagenin) – various actions [312] Sipagladenant (KW-6356) – adenosine A2A receptor antagonist [313] SPD-474 – undefined mechanism of action [314] Sumanirole (PNU-95666; U-95666) – dopamine D2 receptor agonist [315] TAK-065 – undefined mechanism of action [316] TAK-071 – muscarinic acetylcholine M1 receptor positive allosteric modulator [317] Tc 99m TRODAT-1 – single-photon emission-computed tomography (SPECT) enhancer – diagnosis [318] Terguride (Dironyl; Mysalfon; SH-406; Teluron; transdihydrolisuride; VUFB-6638; ZK-31224) – dopamine D2 receptor agonist and other actions [319] Tozadenant (A2a-(3); RO4494351; SYN-115) – adenosine A2A receptor antagonist [320] Utreloxastat (EPI-857; PTC-857) – 15-lipoxygenase (15-LOX/ALOX15) inhibitor [321] Vipadenant (BG-14; BIIB-014; BIIB14; CEB-4520; V-2006; VER-11135; VER-A00-11; VER-A00049; VER-ADO-49; VR-2006) – adenosine A2A receptor antagonist [322] [323]
Sources: en.wikipedia.org
The human body's rate of iron absorption appears to respond to a variety of interdependent factors, including total iron stores, the extent to which the bone marrow is producing new red blood cells, the concentration of hemoglobin in the blood, and the oxygen content of the blood. The body also absorbs less iron during times of inflammation, in order to deprive bacteria of iron. Recent discoveries demonstrate that hepcidin regulation of ferroportin is responsible for the syndrome of anemia of chronic disease.
Reports from clinicians based at other Italian institutions detailed significantly fewer leucotomy operations. Experimental modifications of Moniz's operation were introduced with little delay by Italian medical practitioners. Most notably, in 1937 Amarro Fiamberti, the medical director of a psychiatric institution in Varese, first devised the transorbital procedure whereby the frontal lobes were accessed through the eye sockets. Fiamberti's method was to puncture the thin layer of orbital bone at the top of the socket and then inject alcohol or formalin into the white matter of the frontal lobes through this aperture. Using this method, while sometimes substituting a leucotome for a hypodermic needle, it is estimated that he leucotomised about 100 patients in the period up to the outbreak of World War II. Fiamberti's innovation of Moniz's method would later prove inspirational for Walter Freeman's development of transorbital lobotomy.
A hydrated ion is one kind of a complex ion (or simply a complex), a species formed between a central metal ion and one or more surrounding ligands, molecules or ions that contain at least one lone pair of electrons. If all the ligands are monodentate, then the number of donor atoms equals the number of ligands. For example, the cobalt(II) hexahydrate ion or the hexaaquacobalt(II) ion [Co(H2O)6]2+ is a hydrated-complex ion that consists of six water molecules attached to a metal ion Co. The oxidation state and the coordination number reflect the number of bonds formed between the metal ion and the ligands in the complex ion. However, the coordination number of Pt(en)22+ is 4 (rather than 2) since it has two bidentate ligands, which contain four donor atoms in total. Any donor atom will give a pair of electrons. There are some donor atoms or groups which can offer more than one pair of electrons. Such are called bidentate (offers two pairs of electrons) or polydentate (offers more than two pairs of electrons). In some cases an atom or a group offers a pair of electrons to two similar or different central metal atoms or acceptors—by division of the electron pair—into a three-center two-electron bond. These are called bridging ligands.
Sources: en.wikipedia.org
Selank is a synthetic seven-amino-acid peptide modeled on tuftsin, a fragment of the immunoglobulin G heavy chain. It was designed in Russia to combine anxiolytic and immunomodulatory properties in one molecule.
The first four residues of Selank reproduce the tuftsin sequence Thr-Lys-Pro-Arg. A Pro-Gly-Pro extension at the C-terminus was added to slow enzymatic breakdown and extend residence time.
It holds marketing authorization in Russia, where nasal drop formulations are sold. No equivalent approval exists in the European Union, the United States, or most other countries.
Selank is a synthetic heptapeptide designed as a stabilized analog of the natural tetrapeptide tuftsin. It has been investigated mainly for anxiolytic and cognitive effects. It is not an approved pharmaceutical in most countries.