A practical reference on 合成七肽: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-07-16 and is reviewed periodically as new material appears.
Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. It is described in the literature as an analogue of the ACTH(4–10) fragment, a short N-terminal portion of adrenocorticotropic hormone that retains some neurotropic activity without the full hormonal effects of the parent peptide. The molecule carries a methionine residue at the N-terminus and two proline residues near the C-terminus, features that shape both its interactions with receptor systems and its chemical stability. The free peptide corresponds to the formula C37H51N9O10S and a molecular mass near 813.9 Da.
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.
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.
| 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 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。
Semax 是一种人工合成的七肽，氨基酸序列为 Met-Glu-His-Phe-Pro-Gly-Pro，单字母缩写记作 MEHFPGP。它被归类为促肾上腺皮质激素片段 ACTH(4-10) 的结构类似物，但并不天然存在于生物体内。母体片段 ACTH(4-10) 的序列为 Met-Glu-His-Phe-Arg-Trp-Gly，Semax 替换了中间两个残基，并在羧基端延长了 Pro-Gly-Pro 三肽。这种延长被普遍认为能提升分子对肽酶的耐受性。
该化合物于二十世纪八十年代在俄罗斯被开发，相关工作由俄罗斯科学院分子遗传学研究所的研究团队主导。开发目标并非复制 ACTH 的完整激素活性，而是寻找保留其神经作用方向、同时去除促肾上腺皮质激素释放效应的短肽片段。研究记录显示，这一方向促成了多个相关短肽的合成与筛选，而 Semax 是其中被研究最广泛的一个。当地文献常以 Семакс 这一名称指代它。
== History == In the 19th century, the mass-to-charge ratios of some ions were measured by electrochemical methods. The first attempt to measure the mass-to-charge ratio of cathode ray particles, assuming them to be ions, was made in 1884-1890 by German-born British physicist Arthur Schuster. He put an upper limit of 10^10 coul/kg, but even that resulted in much greater value than expected, so little credence was given to his calculations at the time. In 1897, the mass-to-charge ratio of the electron was first measured by J. J. Thomson. By doing this, he showed that the electron was in fact a particle with a mass and a charge, and that its mass-to-charge ratio was much smaller than that of the hydrogen ion H+. In 1898, Wilhelm Wien separated ions (canal rays) according to their mass-to-charge ratio with an ion optical device with superimposed electric and magnetic fields (Wien filter). In 1901 Walter Kaufman measured the increase of electromagnetic mass of fast electrons (Kaufmann–Bucherer–Neumann experiments), or relativistic mass increase in modern terms. In 1913, Thomson measured the mass-to-charge ratio of ions with an instrument he called a parabola spectrograph. Today, an instrument that measures the mass-to-charge ratio of charged particles is called a mass spectrometer.
A 1995 study found that daily consumption of water treated with 4 tablets containing tetraglycine hydroperiodide reduced the uptake of radioactive iodine in human subjects to a mean of 1.1 percent, from a baseline mean of 16 percent, after a week of treatment. At 90 days of daily treatment, uptake was further reduced to a mean of 0.5 percent. However, unlike KI, tetraglycine hydroperiodide is not recommended by the WHO for this purpose. Iodine should be allowed at least 30 minutes to kill Giardia.
=== Allergic asthma reactions === Asthma may be atopic (i.e., symptoms triggered by allergens) or non-atopic (i.e., symptoms triggered by non-allergenic factors such as cold air). The studies reported here relate to allergen-induced asthma. Mice fed a diet that lowers their SC-FAs levels and then given intranasal injections of dust mite extract developed dust mite allergy asthma reactions to the injections. Their respiratory tract airways had increased numbers of eosinophils and goblet cells as well as excessive levels of mucus; their lung tissue levels of interleukin-4, interleukin-5, interleukin-13, and interleukin-17A and serum immunoglobulin E levels were elevated; and their airway resistance response to a bronchial challenge test was high. In contrast, mice fed a diet that increased their SC-FAs levels developed less of these responses to the extract. Furthermore, mice on the SC-FA lowering diet that were given propionic acid also had far less of these responses to the mite extract. And, Ffar3 (but not Ffar2) gene knockout mice on the low SF-FA diet did not show rises in their lung airway eosinophil levels in response to the mite extract (this was the only parameter of asthma reported in the knockout studies). These finding implicate propionic acid and FFAR3 in the suppression of asthma allergic reactions to mite extract in mice. A second study investigated the effects that an inulin-rich diet (which raises bodily SC-FA levels) feed to rats had on their offsprings' development of asthma. Pregnant rats were feed a normal or inulin-rich diet for 1 week.
Sources: en.wikipedia.org
== Significance == Among bark and ambrosia beetle pests that disperse various fungi, the degree to which the beetle and its symbiont are each responsible for causing host damage varies from system to system – for example, Harringtonia lauricola represents a true pathogen of Lauraceae vectored by Xyleborus glabratus, but others merely facilitate the mass accumulation of beetles on wood. A. roeperi and the symbionts of most other Xylosandrus fall into the latter category. As previously mentioned, X. crassiusculus is highly attracted to ethanol produced by stressed trees, in which they can kill twigs, branches, and saplings; this makes them of particular concern in settings such as nurseries and orchards, where the protrusion of noodle-like extrusions of beetle frass can be a diagnostic feature for this and other Xylosandrus. The potential for damage necessitates management techniques such as ensuring the growth of vigorous, unstressed stands by allowing more space between individual trees, keeping track of soil water content, selecting plants well-adapted to the climate, pruning infested twigs, monitoring beetle populations with ethanol-based lures, designating trap trees or logs, and applying insecticides (for example, through direct injection) [28]. Novel methods such as entomopathogenic or mycopathogenic microorganisms remain under exploration [29]. Ecologically, though biologists may be concerned about the downstream impact of beetle attacks on native plants such as oaks, cedars, maples, elms, redbud, magnolia, etc.
To avoid this, freshly prepared samples as well as complementary analysis methods are used for confident nuclear materials characterization. The decay of nuclear samples makes rapid analysis methods highly desirable.
== Definition == The term "niacin" was originally coined from "nicotinic acid vitamin", with the goal of distancing the nutrient B3 from the drug nicotine in tobacco. As a result, it originally referred to the nutritional entity of vitamin B3. However, in American English, the term has also come to mean "nicotinic acid" in the context of high-dose use as a prescription medicine. In other varieties of English, the medicine is only ever called "nicotinic acid". The term "nicotinic acid" unambiguously refers to the substance and the prescription medicine containing it, which treats elevated cholesterol and triglycerides. When used as a drug, daily doses range from 500 to 3,000 mg/day. High-dose nicotinamide does not have this medicinal effect.
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.
It originated at the Institute of Molecular Genetics in Moscow during the 1980s. The work was carried out by a Russian research group that specialized in peptide neuropharmacology.