ACTH(4–10) is one of those subjects where the details matter more than the headlines. This page pulls together the background, the mechanisms, and the practical points readers ask about most.
Updated 2026-06-22. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. It was derived from the ACTH(4-10) fragment, a short segment of adrenocorticotropic hormone that lacks the hormonal activity associated with the full-length peptide. Researchers at the Institute of Molecular Genetics in Moscow developed the compound during the 1980s. It has been registered as a pharmaceutical product in Russia and several neighbouring countries, where it is supplied as a nasal solution, and it is also sold internationally as a research chemical.
The proposed mechanism centres on neurotrophic signalling rather than direct receptor activation. Semax is reported to increase expression of brain-derived neurotrophic factor and nerve growth factor in several brain regions, and to shift the balance between excitatory and inhibitory neurotransmitter systems. Interaction with melanocortin receptors has been suggested because of the parent ACTH fragment. Many of these findings come from rodent studies, and the extent to which they translate to human physiology remains an open question.
| 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 heptapeptide whose sequence is Met-Glu-His-Phe-Pro-Gly-Pro. The first four residues correspond to the ACTH(4-10) fragment, while the terminal Pro-Gly-Pro extension was added to improve metabolic stability. Its molecular formula is C37H51N9O10S and its monoisotopic mass is approximately 813.9 Da. The compound is classified as a peptide research chemical and as a registered pharmaceutical product in Russia, but it does not hold marketing approval in the European Union or the United States. Naming conventions vary across supplier catalogs.
Development of the compound took place in the Soviet Union during the 1980s, largely through peptide research groups affiliated with the Shemyakin-Ovchinnikov Institute and Moscow State University. Investigators screened fragments of adrenocorticotropic hormone for activity on the central nervous system while attempting to separate cognitive effects from hormonal ones. The shortened sequence was selected because it retained behavioral activity in animal models without stimulating corticosteroid release. Early publications described the molecule as an ACTH(4-10) analog.
Published research on this peptide originates mainly from Russian laboratories, and the wider international literature is comparatively thin. Studies have used rodent models of stroke, hypoxia, and memory tasks, with a smaller number of human trials reported. Reported outcomes include changes in attention and memory measures, along with effects on neurotrophic factor expression in some experiments. Small sample sizes, inconsistent dosing protocols, and limited independent replication are widely noted limitations, so the strength of the clinical evidence remains an open question.
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== Career and research == In 1933 the Ochoas returned to Madrid where he began to study glycolysis in heart muscle. Within two years, he was offered the directorship of the Physiology Section in a newly created Institute for Medical Research at the University of Madrid Medical School. Unfortunately the appointment was made just as the Spanish Civil War erupted. Ochoa decided that trying to perform research in such an environment would destroy forever his "chances of becoming a scientist." Thus, "after much thought, my wife and I decided to leave Spain." In September 1936 they began what he later called the "wander years" as they traveled from Spain to Germany, to England, and ultimately to the United States within a span of four years. Ochoa left Spain and returned to Meyerhof's Kaiser Wilhelm Institute for Biology now relocated in Heidelberg, where Ochoa found a profoundly changed research focus. During his 1930 visit the laboratory work was "classical physiology," which Ochoa described as "one could see muscles twitching everywhere". By 1936 Meyerhof's laboratory had become one of the world's foremost biochemical facilities focused on processes such as glycolysis and fermentation. Rather than studying muscles "twitch," the lab was now purifying and characterizing the enzymes involved in muscle action and those involved in yeast fermentation.
Sources: en.wikipedia.org
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== History == Tentatively called "radium F", polonium was discovered by Marie and Pierre Curie in July 1898, and was named after Marie Curie's native land of Poland (Latin: Polonia). Poland at the time was under Russian, German, and Austro-Hungarian partition, and did not exist as an independent country. It was Curie's hope that naming the element after her native land would publicize its lack of independence. Polonium may be the first element named to highlight a political controversy. This element was the first one discovered by the Curies while they were investigating the cause of pitchblende radioactivity. Pitchblende, after removal of the radioactive elements uranium and thorium, was more radioactive than the uranium and thorium combined. This spurred the Curies to search for additional radioactive elements. They first separated out polonium from pitchblende in July 1898, and five months later, also isolated radium. German scientist Willy Marckwald successfully isolated 3 milligrams of polonium in 1902, though at the time he believed it was a new element, which he dubbed "radio-tellurium", and it was not until 1905 that it was demonstrated to be the same as polonium. In the United States, polonium was produced as part of the Manhattan Project's Dayton Project during World War II. Polonium and beryllium were the key ingredients of the 'Urchin' initiator at the center of the bomb's spherical pit. 'Urchin' initiated the nuclear chain reaction at the moment of prompt-criticality to ensure that the weapon did not fizzle. 'Urchin' was used in early U.S.
== External links == Anatomy Atlases – Microscopic Anatomy, plate 01.05 Histology image: 22201loa – Histology Learning System at Boston University - "Ultrastructure of the Cell: chief cells and enteroendocrine cell" Histology image: 11304loa – Histology Learning System at Boston University - "Digestive System: Alimentary Canal: fundic stomach, gastric glands, base" "chief cell" at Dorland's Medical Dictionary Nosek, Thomas M. "Section 6/6ch4/s6ch4_8". Essentials of Human Physiology. Archived from the original on 2016-03-24.
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.
Semax is based on the ACTH(4-10) fragment, a seven-amino-acid segment of adrenocorticotropic hormone. The synthetic peptide retains the core sequence while removing regions associated with endocrine activity. This modification is intended to isolate effects on the nervous system.