The short version of ACTH(4–10) fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2025-11-18 and is reviewed periodically as new material appears.
The compound was developed in the 1980s at the Institute of Molecular Genetics in Moscow, where it emerged from research on short ACTH fragments and their effects on the central nervous system. Russian pharmaceutical listings describe it as a nootropic and neuroprotective agent, most often formulated as nasal drops. It is not a marketed medicine in the United States or the European Union, and no pharmacopoeial monograph covers it. Consequently, most published clinical experience with the substance originates from a small number of research centres, mainly in Russia and neighbouring countries.
Pharmacological accounts link semax to melanocortin signalling and to modulation of neurotrophic factor expression, particularly brain-derived neurotrophic factor and nerve growth factor. Much of this evidence comes from rodent studies using intranasal delivery, a route chosen because it allows peptides to reach the central nervous system with limited systemic exposure. Whether the same mechanisms operate in humans at comparable magnitude remains an open question. The precise receptor or receptors responsible for the reported behavioural and neuroprotective effects have not been conclusively identified.
Solid semax is typically supplied as a lyophilised powder that is hygroscopic and sensitive to moisture, light, and repeated temperature cycling. Long-term storage of the dry peptide is generally recommended at approximately -20 degrees Celsius, while shorter working periods may use refrigeration at 2 to 8 degrees Celsius. Vials should remain tightly closed and desiccated when brought to room temperature, because condensation can damage the material before it is weighed. Dividing a batch into aliquots is preferable to thawing one container repeatedly.
Dissolution is normally performed in water, phosphate-buffered saline, or normal saline, since the peptide is freely soluble in aqueous media and is rarely handled with strong organic solvents. Solution pH should be kept near neutral, because extreme acidity or alkalinity accelerates backbone hydrolysis and encourages oxidation of the methionine side chain. Once dissolved, the material is less stable than the dry powder and is commonly divided into single-use portions and frozen. Buffers containing primary amines, such as Tris, are often avoided because of possible side reactions.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C37H51N9O10S | Free acid form of the heptapeptide; depends on terminal groups |
| Molecular mass | About 813.9 g/mol | Average mass used for mass spectrometry confirmation |
| Appearance | White to off-white solid | Supplied as a lyophilised powder; hygroscopic |
| Solubility class | Freely soluble in aqueous media | Water, saline, and phosphate buffers; limited organic solubility |
| Typical storage temperature | -20 degrees Celsius | Long term and dry; short working periods may use 2 to 8 degrees Celsius |
Semax is a synthetic peptide created in the Soviet Union during the early 1980s by researchers working in Moscow. It was built from the short adrenocorticotropic hormone fragment known as ACTH(4-10), and the chain was then extended with three additional amino acids. The resulting molecule was named semax and entered clinical use in Russia in 1994. It is generally described as a nootropic and neuroprotective agent rather than as a hormone analogue.
The parent fragment ACTH(4-10) carries the sequence Met-Glu-His-Phe-Arg-Trp-Gly. Semax replaces the arginine and tryptophan positions with a proline-glycine-proline tail, giving Met-Glu-His-Phe-Pro-Gly-Pro. That change removes residues associated with adrenal stimulation, so the peptide does not drive cortisol release the way full ACTH does. This distinction shapes how the compound is grouped in the literature, where it sits with neuropeptides and peptide neuromodulators rather than with corticosteroids.
Regulatory status varies sharply by country. Semax is registered for medical use in Russia, where it appears in formularies as a nasal solution, and it also holds registration in a small number of neighbouring states. It has no approval from the United States Food and Drug Administration or the European Medicines Agency, and it is not a scheduled controlled substance in most jurisdictions. Elsewhere it circulates mainly as laboratory material, so purity documentation comes from suppliers rather than from a national pharmacopoeia.
The mechanisms attributed to semax are inferred from animal and cell studies rather than traced to one confirmed target. The most frequently cited pathway involves increased expression of brain-derived neurotrophic factor and nerve growth factor in hippocampal and cortical tissue. Some work points to engagement of melanocortin receptors, particularly MC4, which the parent ACTH fragment can activate. Effects on dopaminergic and serotonergic signalling have also been reported. No single account explains all observed results, and the relative weight of each pathway remains unsettled.
Published studies examine a fairly narrow set of endpoints. Rodent experiments commonly measure maze learning, infarct volume after induced ischemia, and tissue levels of neurotrophic factors. Clinical reports from Russian centres describe attention, memory and recovery scores in patients after stroke or transient ischemic attack. Most of those human studies are small and few have been repeated by independent groups. Outcome measures differ between studies, which limits direct comparison.
Laboratory work points toward modulation of neurotrophic signaling, particularly expression of brain-derived neurotrophic factor and nerve growth factor in hippocampal tissue. Studies also describe effects on monoamine turnover, inflammatory mediators, and oxidative markers. These observations come mainly from animal models and cultured cells, so the causal chain in humans is not firmly established. Whether the reported molecular changes translate into measurable clinical benefit is an open question. Reviews generally present the mechanism as plausible rather than demonstrated.
Clinical evidence consists largely of small trials with modest sample sizes, often without independent replication. Reported endpoints include cognitive scores, recovery after stroke, and visual function, but study designs vary widely and few trials meet contemporary reporting standards. Systematic reviewers have noted a high risk of bias in several of these reports. No large multicenter trial conducted outside Russia has been published. The compound is therefore best described as investigational in most jurisdictions, with its clinical role still unresolved.
== External links == PDB: 1RIE - X-ray structure of Rieske protein (water-soluble fragment) of the bovine mitochondrial cytochrome bc1 complex PDB: 1RFS - X-ray structure of Rieske protein (water-soluble fragment) of the spinach chloroplast cytochrome b6 fcomplex PDB: 1FQT - X-ray structure of Rieske-type ferredoxin associated with biphenyl dioxygenase from Burkholderia cepacia PDB: 1G8J - X-ray structure of Rieske subunit of arsenite oxidase from Alcaligenes faecalis PDB: 2I7F - X-ray structure of the Sphingomonas yanoikuyae B1 Rieske ferredoxin PDB: 2QPZ - X-ray structure of the Pseudomonas Naphthalene 1,2-dioxygenase Rieske ferredoxin InterPro: IPR005806 - InterPro entry for Rieske [2Fe-2S] region
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Jeremy Randall Knowles (28 April 1935 – 3 April 2008) was a professor of chemistry at Harvard University who served as dean of the Harvard University faculty of arts and sciences (FAS) from 1991 to 2002. He joined Harvard in 1974, received many awards for his research, and remained at Harvard until his death, leaving the faculty for a decade to serve as Dean. Knowles died on 3 April 2008 at his home. In 2006, he was selected by incoming interim president Derek Bok to return to his position as Dean of the Faculty of Arts and Sciences on an interim basis, replacing William C. Kirby.
Sources: en.wikipedia.org
== Performing with the Grateful Dead == In early 1970, Lagin initiated a correspondence with Jerry Garcia after seeing the Grateful Dead at the Boston Tea Party in 1969. In May 1970, he helped facilitate a concert and free live outdoor performance featuring the band at MIT that coincided with the Kent State shootings. That summer, Lagin, at Garcia's invitation, visited San Francisco and contributed piano to "Candyman" during the American Beauty album sessions, played in several jams, and started what would become close friendships with Garcia, bassist Phil Lesh, and David Crosby. From 1970 to 1975, Lagin contributed Hammond B3 organ, electric piano, and clavichord to material of his choice (primarily—but not exclusively—songs with long instrumental passages) at several Grateful Dead concerts. His first performances with the Grateful Dead were on November 5 and November 8, 1970 at the Capitol Theater in Port Chester, New York; his first complete concert was at Boston University's Sargent Gym on November 21, 1970. During many 1974 Grateful Dead concerts over several tours, including Europe, he performed a middle set of electronic music, including parts of his composition Seastones, on computer-controlled analog synthesizers with Phil Lesh on electronically processed bass. Some sets included Jerry Garcia playing guitar filtered through effects processors and Bill Kreutzmann on drums; these sets occasionally segued into the final Grateful Dead set, with Lagin performing with the Dead, including an appearance in The Grateful Dead Movie.
=== Neutral phase === If the temperature variation from climatology is within 0.5 °C (0.9 °F), ENSO conditions are described as neutral. Neutral conditions are the transition between warm and cold phases of ENSO. Sea surface temperatures (by definition), tropical precipitation, and wind patterns are near average conditions during this phase. Close to half of all years are within neutral periods. During the neutral ENSO phase, other climate anomalies/patterns such as the sign of the North Atlantic Oscillation or the Pacific–North American teleconnection pattern exert more influence.
The gamma decay from a metastable state is referred to as isomeric transition (IT), or internal transition, though it resembles shorter-lived "prompt" gamma decays in all external aspects with the exception of the longer life. This is generally associated with a high nuclear spin change, or "forbiddenness", which would be required in gamma emission to reach the ground state; this is even more true of beta decays. A low transition energy both slows the transition rate and makes it more likely that only highly forbidden decays are available, so most long-lived isomers have a relatively low excitation energy above the ground state (in the extreme case of thorium-229m, low excitation alone causes the measurably long life). In 210m83Bi, the forbiddenness of available beta and gamma decays is so high that alpha decay is observed exclusively, though even that is slower than for the ground state. For most lighter isomers including 180m73Ta, alpha decay is not practically available, but others are not quite so forbidden as those two. The first nuclear isomer and decay-daughter system (uranium X2/uranium Z, now known as 234m91Pa/23491Pa) was discovered by Otto Hahn in 1921. Metastable isomers can be produced through any nuclear reaction, including radioactive decay, neutron capture, nuclear fission, and bombardment by accelerated charged particles. A nucleus produced this way generally starts its existence in an excited state that loses its excess energy through the emission of one or more gamma rays or conversion electrons.
Sources: en.wikipedia.org
It is described as a synthetic analogue of the ACTH(4–10) fragment, a short segment of adrenocorticotropic hormone. Its sequence differs from that fragment and includes two proline residues, which influence stability and behaviour in solution.
It appears in Russian pharmaceutical listings as a nasal formulation, but it is not an authorised medicine in the United States or the European Union. Outside those markets it is normally encountered as a research chemical rather than a prescription product.
Laboratory and animal work points to melanocortin signalling and changes in neurotrophic factor levels, especially brain-derived neurotrophic factor. The exact receptor targets and the degree to which these findings transfer to humans are still unresolved.
Dry powder is usually kept at about -20 degrees Celsius for long-term storage and at 2 to 8 degrees Celsius for short working periods. Containers should stay sealed and protected from light and moisture to limit degradation.