Semax comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Last reviewed on 2026-08-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Clinical reports describe use in ischaemic stroke, transient ischaemic attack, optic nerve conditions, and cognitive complaints, but most of these studies are small and were conducted in a single region. Systematic reviews have generally described the evidence base as limited in size and variable in methodological quality. Randomised controlled data suitable for international regulatory assessment are scarce. As a result, major treatment guidelines outside Russia do not include the peptide, and interest in it remains largely research-driven rather than routine clinical.
Semax is a synthetic heptapeptide whose sequence is Met-Glu-His-Phe-Pro-Gly-Pro. It was developed as a fragment analog of adrenocorticotropic hormone, modeled specifically on the ACTH(4-10) region. The first four residues reproduce that fragment, while a Pro-Gly-Pro tripeptide is appended at the C-terminus. Work on the compound originated in Russia, where it entered clinical use as an intranasal preparation. Its sequence places it among short regulatory peptides studied for effects on the central nervous system rather than on the adrenal axis.
The C-terminal Pro-Gly-Pro extension is not incidental. Proline-rich tails are known to resist several common peptidases, and the published literature attributes the longer half-life of Semax, relative to unmodified ACTH fragments, to this feature. The modification also removes the melanocyte-stimulating and corticosteroidogenic activity that characterizes longer ACTH-derived sequences. Because the molecule is small and hydrophilic, it is typically formulated as an aqueous solution for intranasal or parenteral delivery. Acetylation or amidation at the termini appears in closely related research peptides and shifts the mass by a fixed increment.
Reported pharmacological work centers on neurotrophic signaling, including changes in BDNF and NGF expression in hippocampal tissue in animal models. Human data come largely from studies conducted in Russia, and how well those results generalize to other populations remains an open question. Regulatory status differs sharply by jurisdiction: Semax is a registered prescription medicine in Russia, while it holds no approved marketing status in the United States or the European Union. Outside such jurisdictions it is generally handled as a research chemical, which affects both documentation and quality expectations.
| 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.
Semax 是人工设计的七肽，序列为 Met-Glu-His-Phe-Pro-Gly-Pro，骨架取自促肾上腺皮质激素片段 ACTH(4-10)。它于二十世纪八十年代在苏联的分子遗传学研究机构内合成。设计目标是保留该片段与注意力和记忆相关的活性，同时剔除促皮质激素释放等内分泌作用。此后俄罗斯将其登记为药品并进入临床使用。
当时的短肽研究普遍关注能否穿越血脑屏障、在低剂量下产生中枢效应，Semax 属于这一路线。鼻内给药是其主要使用方式，俄语文献报道的适应症涵盖缺血性卒中、短暂性脑缺血发作、认知功能减退以及视神经病变。这些研究大多发表在当地期刊上，样本规模与终点设置同西方试验惯例存在差异，国际同行对其临床证据的强度看法不一。
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.
Scientific literature on semax is unevenly distributed. A substantial share of published work originates from a small number of laboratories in Russia, while independent replication elsewhere is limited. Human data consist mostly of small trials with short follow-up, and several reported outcomes rely on subjective rating scales. Questions about how much intact peptide reaches the central nervous system after nasal administration, and how long it persists there, are still unresolved. The compound is best described as an active research subject rather than a settled pharmacological agent.
Dow AgroSciences – poultry vaccine against Newcastle disease virus (first PMP to be approved for marketing by the USDA Center for Veterinary Biologics Dow never intended to market the vaccine. "'Dow Agrosciences used the animal vaccine as an example to completely run through the process. A new platform needs to be approved, which can be difficult when authorities get in contact with it for the first time', explains the plant physiologist Stefan Schillberg, head of the Molecular Biology Division at the Fraunhofer Institute for Molecular Biology and Applied Ecology Aachen." Fraunhofer Institute for Molecular Biology and Applied Ecology, with sites in Germany, the US, and Chile is the lead institute of the Pharma Planta consortium of 33 partner organizations from 12 European countries and South Africa, funded by the European Commission. Pharma Planta is developing systems for plant production of proteins in greenhouses in the European regulatory framework. It is collaborating on biosimilars with Plantform and PharmaPraxis (see below). Genzyme – antithrombin III in goat milk GTC Biotherapeutics – ATryn (recombinant human antithrombin) in goat milk Icon Genetics produces therapeutics in transiently infected Nicotiana benthamiana (relative of tobacco) plants in greenhouses in Halle, Germany or in fields. First product is a vaccine for a cancer, non-Hodgkin's lymphoma. Iowa State University – immunogenic protein from E. coli bacteria in pollen-free corn as a potential vaccine against E.
Calcium carbonate is widely used medicinally as an inexpensive dietary calcium supplement or gastric antacid (such as Tums and Eno). It may be used as a phosphate binder for the treatment of hyperphosphatemia (primarily in patients with chronic kidney failure). It is used in the pharmaceutical industry as an inert filler for tablets and other pharmaceuticals. Calcium carbonate is used in the production of calcium oxide as well as toothpaste and has seen a resurgence as a food preservative and color retainer, when used in or with products such as organic apples. Calcium carbonate is used therapeutically as phosphate binder in patients on maintenance haemodialysis. It is the most common form of phosphate binder prescribed, particularly in non-dialysis chronic kidney disease. Calcium carbonate is the most commonly used phosphate binder, but clinicians are increasingly prescribing the more expensive, non-calcium-based phosphate binders, particularly sevelamer. Excess calcium from supplements, fortified food, and high-calcium diets can cause milk-alkali syndrome, which has serious toxicity and can be fatal. In 1915, Bertram Sippy introduced the "Sippy regimen" of hourly ingestion of milk and cream, and the gradual addition of eggs and cooked cereal, for 10 days, combined with alkaline powders, which provided symptomatic relief for peptic ulcer disease. Over the next several decades, the Sippy regimen resulted in kidney failure, alkalosis, and hypercalcaemia, mostly in men with peptic ulcer disease.
==== Fistula formation and gallstone ileus ==== The inflammation of cholecystitis can lead to adhesions between the gallbladder and other parts of the gastrointestinal tract, most commonly the duodenum. These adhesions can lead to the formation of direct connections between the gallbladder and gastrointestinal tract, called fistulas. With these direct connections, gallstones can pass from the gallbladder to the intestines. Gallstones can get trapped in the gastrointestinal tract, most commonly at the connection between the small and large intestines (ileocecal valve). When a gallstone gets trapped, it can lead to an intestinal obstruction, called gallstone ileus, leading to abdominal pain, vomiting, constipation, and abdominal distension.
Sources: en.wikipedia.org
On 5 December 2001, a 2,000lb GPS-guided bomb landed among the Green Berets from ODA 574, killing 3 members and wounding the rest of the team, over 20 of Karzai's militia were also killed and Karzai himself slightly wounded. ODB 570 and ODA 524 were immediately dispatched by helicopter to assist with the wounded and to eventually replace the fallen operators of ODA 574. ODA 572 and a CIA Jawbreaker team (small group of CIA SAD ground branch operators) were dispatched to eastern Afghanistan where they recruited some 2,500 to 3,000 into the Afghan Militia Force to take part in the Battle of Tora Bora. On December 20, following the battle, ODA 561 were inserted into the White Mountains to support ODA 572 in conducting sensitive site exploitation of the caves and to assist with recovering DNA samples from terrorist bodies. Time reported that on 4 January 2002, Green Beret SFC Scott Neil jumped out the back of an MH-53 half a mile from a suspected al-Qaeda compound, 140 miles south of Kabul. With just one-hour on-scene time due to limited helicopter fuel, Neil rushed through AK-47 fire and overcame the al-Qaeda fighters; intelligence from the compound proved it to be an al-Qaeda way station, containing hundreds of fake passports to give terrorists new identities, and multiple computers, powered by car batteries and linked to satellite phones for internet connection.
=== Sources === Ellis, Richard; McCosker, John E. (1991). Great White Shark. Stanford University Press. ISBN 0-8047-2529-2. Klimley, A. Peter; Ainley, David G., eds. (1996). Great White Sharks: The Biology of Carcharodon carcharias. Academic Press. ISBN 0-12-415031-4. Civard-Racinais, Alexandrine (2012). Great White Shark: Myth and Reality. Firefly. ISBN 978-1-77085-102-3. Domeier, Michael L., ed. (2012). Global Perspectives on the Biology and Life History of the White Shark. CRC Press. ISBN 978-1-4398-4840-1. Skomal, Greg (2023). The Great White Shark Handbook. Cider Mill Press. ISBN 978-1-60433-771-6.
=== Rhinopharyngitis mutilans === Rhinopharyngitis mutilans, also known as gangosa, is a destructive ulcerative condition that usually originates about the soft palate and spreads into the hard palate, nasopharynx, and nose, resulting in mutilating cicatrices, and outward to the face, eroding intervening bone, cartilage, and soft tissues. It occurs in the late stages of yaws, usually 5 to 10 years after the first symptoms of infection. This is now rare. Very rarely, yaws may cause bone spurs in the upper jaw near the nose (gondou); gondou was rare even when yaws was a common disease.
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.
The sequence is Met-Glu-His-Phe-Pro-Gly-Pro, a seven-residue peptide. The first four residues correspond to the ACTH(4-10) fragment, and Pro-Gly-Pro is added at the C-terminus. N-acetylated versions also appear in the literature and differ in mass.