Semax 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 2026-04-28. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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 compound is registered in Russia as a pharmaceutical product, most commonly formulated as a nasal solution, and has been used in that setting since the 1990s. Outside that jurisdiction it is generally handled as a research chemical rather than an approved medicine. Regulatory status therefore differs sharply between countries, and material sold internationally may not correspond to the Russian pharmaceutical formulation. Documentation with commercial samples is typically limited to a certificate of analysis covering purity and identity, not clinical status or local legal classification.
Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. It corresponds to the ACTH(4-7) fragment extended at the C-terminus by a Pro-Gly-Pro tripeptide, an addition intended to slow enzymatic breakdown. The molecular formula is C37H51N9O10S and the molecular mass is approximately 814 daltons. In the literature it is often described as an ACTH(4-10) analog, although that label reflects a naming convention as much as a precise structural relationship. The compound was developed in Russia and remains most closely associated with that research tradition.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C37H51N9O10S | Calculated for the free peptide |
| Molar mass | 813.9 g/mol | Anhydrous free base |
| Peptide class | Synthetic heptapeptide | ACTH(4-10) analogue |
| Parent fragment | ACTH(4-10) | Adrenocorticotropic hormone segment |
| Developmental origin | Institute of Molecular Genetics, Moscow | Work began in the 1980s |
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。
各国监管态度分化明显。俄罗斯按处方药管理，部分东欧国家留有使用记录；欧盟与美国未批准其作为药物上市，市面流通品通常标注为研究用化学品。身份差异意味着标示含量、纯度与无菌性缺少统一核查。体育领域还牵涉反兴奋剂名录，跨境携带则受目的地药品法规约束。
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。
Regulatory status differs sharply between jurisdictions. In Russia the peptide is registered as a prescription nasal preparation, while agencies such as the United States Food and Drug Administration have not approved it for any indication. Products sold elsewhere are typically labeled for laboratory research only, and such labels shift responsibility for safe handling to the purchaser. Because the same name covers pharmaceutical-grade nasal drops and bulk research powder, identity and purity documentation becomes the main practical concern when comparing sources.
Semax is a synthetic seven-amino-acid peptide whose sequence extends the ACTH(4-10) fragment with a C-terminal proline-glycine-proline tripeptide. The commonly cited sequence is Met-Glu-His-Phe-Pro-Gly-Pro, giving a molecular formula near C37H51N9O10S and a molecular weight close to 813.9 g/mol. It belongs to the broader class of synthetic ACTH fragments studied for central nervous system effects rather than for adrenal steroid stimulation. In practice the material appears as a lyophilized white powder for laboratory work or as a dilute saline solution in clinical settings.
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 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.
Later generations of the molecule include an N-acetylated form and an amidated form, both marketed online alongside the parent peptide. These variants differ in terminal chemistry and stability, and they are frequently discussed in the same breath even though they have not been compared in controlled trials. Supply outside formal healthcare systems comes largely from laboratories that synthesize peptides to order. Purity and identity of these materials vary widely, and no single body oversees the international trade.
Semax is a synthetic heptapeptide developed in the Soviet Union during the 1980s by researchers at the Institute of Molecular Genetics in Moscow. It was designed as a truncated analog of adrenocorticotropic hormone, retaining only the fragment spanning residues four through ten. Investigators sought a peptide that would preserve the cognitive effects associated with ACTH while eliminating the hormonal stimulation of the adrenal cortex. The compound entered clinical use in Russia during the following decade.
Russian regulatory authorities approved the peptide for nasal administration, and it remains listed in the national pharmacopoeia under several trade names. Documented indications include acute ischemic stroke, transient ischemic attacks, traumatic brain injury, and certain ophthalmological and neurological conditions. Physicians also prescribe it for cognitive complaints in older patients, although the evidence base for that use is thinner. Outside Russia and a few neighboring states, the substance is not an approved medicine and is sold instead as a research chemical.
=== Depression === Mirtazapine is primarily used for major depressive disorder and other mood disorders. Onset of action appears faster than some selective serotonin reuptake inhibitors and similar to tricyclic antidepressants. In 2010, the National Institute for Health and Care Excellence recommended generic selective serotonin reuptake inhibitors as first-line choices, as they are "equally effective as other antidepressants and have a favourable risk–benefit ratio." For mirtazapine, it found "no difference between mirtazapine and other antidepressants on any efficacy measure, although in terms of achieving remission mirtazapine appears to have a statistical though not clinical advantage. In addition, mirtazapine has a statistical advantage over selective serotonin reuptake inhibitors in terms of reducing symptoms of depression, but the difference is not clinically significant. However, there is strong evidence that patients taking mirtazapine are less likely to leave treatment early because of side effects, although this is not the case for patients reporting side effects or leaving treatment early for any reason." A 2011 Cochrane review comparing mirtazapine to other antidepressants found that while it appeared to have a faster onset in people for whom it worked (measured at two weeks), its efficacy was about the same as other antidepressants after six weeks' use.
==== Paid leave while on Family and Medical Leave Act leave ==== The temporary tax credit for employers who give paid leave to an employee while they are on Family and Medical Leave Act leave has been made permanent. In order to qualify for the tax credit, the employer must pay the employee at least 50% of the employee's usual wages. The amount of the tax credit used to be equal to 12.5% of eligible wages paid to an eligible employee, but it now increases by 0.25% for each percentage point paid above the 50% threshold, up to a maximum credit of 25%. In order to be eligible for the tax credit, the employee must have worked at least six months for the employer, which is up from 12 months previously. Paid family and medical leave that is required under state or local law is now eligible for the tax credit, as are employer-paid amounts for qualifying paid leave insurance policies.
=== Graphic content === In June 2021, TikTok made an apology after a shock video, showing a girl dancing which then cuts to a graphic scene of a man being beheaded by a saw, went viral. The video has been put on TikTok's blacklist, which detects it before being uploaded. TikTok has previously worked to remove graphic content from its platform, including a suicide video that circulated in September 2020, which had appeared among the recommended clips of TikTok's For You section.
=== Category:EC 1.6 (act on NADH or NADPH) === Category:EC 1.6.1 (with NAD+ or NADP+ as acceptor) Category:EC 1.6.2 (with a cytochrome as acceptor) Category:EC 1.6.3 (with oxygen as acceptor) Category:EC 1.6.4 now Category:EC 1.8.1 Category:EC 1.6.5 (with a quinone or similar compound as acceptor) NADH dehydrogenase EC 1.6.5.3 Category:EC 1.6.6 (with a nitrogenous group as acceptor) Category:EC 1.6.7 now Category:EC 1.18.1 Category:EC 1.6.8 now Category:EC 1.5.1 Category:EC 1.6.99 (with other acceptors)
When bacterial cells run out of nutrients, they enter stationary phase and downregulate protein synthesis. Several processes mediate this transition. For instance, in E. coli, 70S ribosomes form 90S dimers upon binding with a small 6.5 kDa protein, ribosome modulation factor RMF. These intermediate ribosome dimers can subsequently bind a hibernation promotion factor (the 10.8 kDa protein, HPF) molecule to form a mature 100S ribosomal particle, in which the dimerization interface is made by the two 30S subunits of the two participating ribosomes. The ribosome dimers represent a hibernation state and are translationally inactive. A third protein that can bind to ribosomes when E. coli cells enter the stationary phase is YfiA (previously known as RaiA). HPF and YfiA are structurally similar, and both proteins can bind to the catalytic A- and P-sites of the ribosome. RMF blocks ribosome binding to mRNA by preventing interaction of the messenger with 16S rRNA. When bound to the ribosomes the C-terminal tail of E. coli YfiA interferes with the binding of RMF, thus preventing dimerization and resulting in the formation of translationally inactive monomeric 70S ribosomes.
Sources: en.wikipedia.org
=== Brain localization and biochemistry === Delta waves can arise either in the thalamus or in the cortex. When associated with the thalamus, they are thought to arise in coordination with the reticular formation. In the cortex, the suprachiasmatic nuclei have been shown to regulate delta waves, as lesions to this area have been shown to cause disruptions in delta wave activity. In addition, delta waves show a lateralization, with right hemisphere dominance during sleep. Delta waves have been shown to be mediated in part by T-type calcium channels. During delta wave sleep, neurons are globally inhibited by gamma-aminobutyric acid (GABA). Delta activity stimulates the release of several hormones, including growth hormone releasing hormone GHRH and prolactin (PRL). GHRH is released from the hypothalamus, which in turn stimulates release of growth hormone (GH) from the pituitary. The secretion of (PRL), which is closely related to (GH), is also regulated by the pituitary. The release of thyroid stimulating hormone (TSH), is decreased in response to delta-wave signaling.
Some cats will have completed the shedding period by the time the test is run, leading to false-negative results. Electron microscopy, virus isolation and seroconversion can also be used to document active or recent infection. Leukopenia on a complete blood count (nadir 50–3,000 WBC/μL) supports a diagnosis of FPLV. In an unvaccinated cat, the presence of antibodies against FPV indicates that the cat either has the disease or has had the disease in the past. Elevated IgM titers (1:10 or greater) indicate active infection and if clinical signs are obvious (diarrhea, panleukopenia) the prognosis is poor. Elevated IgG titers (1:100 or greater) in a cat with clinical signs indicates a better prognosis. Differential diagnoses include salmonellosis, enteric toxins, feline immunodeficiency virus (FIV), feline leukemia virus (FeLV), cryptosporidiosis, pancreatitis, septicaemia with acute endotoxemia, toxoplasmosis, peritonitis, and lymphoma.
== External links == FSL Constructs: A Simple Method for Modifying Cell/Virion Surfaces with a Range of Biological Markers Without Affecting their Viability – Journal of Visualised Experiments (JOVE) free video article [1] kodecyte.org - the academic resource for Kode Technology
=== Mechanism of action === Plecanatide works as a laxative by drawing water in to the gastrointestinal tract thereby softening stool and encouraging its natural passage. Similar to its endogenous counterpart, plecanatide activates guanylate cyclase-C on endothelial cells within the gastrointestinal tract. The activation of guanylate cyclase-C catalyses the production of the second messenger guanosine 3’,5’-cyclic monophosphate (cGMP) which leads to the protein kinase A (PKA) and protein kinase G II (PKGII)-mediated phosphorylation of the cystic fibrosis transmembrane conductance regulator (CFTR) protein. CFTR is an anion channel and upon activation it will secrete negatively charged ions, particularly chloride (Cl−) and bicarbonate (HCO3−) in to the GI tract lumen. This disruption to the electrochemical gradient is in part rectified by the passive secretion of positively charged sodium ions in to the lumen and water follows by osmosis. Plecanatide is also known to have an anti-nociceptive effect in animal models, however the exact mechanism of action is not yet fully elucidated. It has been suggested that this may be in part to the anti-inflammatory action of guanylate cyclase-C by its inhibition of pro-inflammatory cytokines, or through the inhibition of associated sensory neurons.
Sources: en.wikipedia.org
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.
It is registered for clinical use in Russia and a few other countries, typically as a nasal drop formulation. It does not hold approval from the United States Food and Drug Administration or the European Medicines Agency. Outside those markets it is generally handled as a research chemical.
The compound was developed in Moscow and the earliest studies were conducted there, so the primary literature is largely in Russian-language journals. Translation and indexing have been incomplete, which limits access for outside researchers. Independent groups have since published some work, but the total volume remains modest.
It is registered as a pharmaceutical product in Russia, where it is typically supplied as a nasal solution. In most other countries it is not an approved drug and is traded as a research chemical instead. Approval status depends entirely on the jurisdiction involved.