nasal drops 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 2025-11-14. Numbers and descriptions here follow the published literature rather than marketing material.
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.
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.
纯度评估以反相高效液相色谱为主，通过主峰面积百分比给出粗略结果，再配合电喷雾质谱核对分子量。氨基酸分析可验证组成比例，手性色谱或毛细管电泳用于检查残基构型。常见杂质包括缺失序列的短肽、氧化产物与二聚体。由于多数市售品不附带完整检验报告，独立第三方检测常被用来核实标称值。
从分子层面看，Semax 是线性七肽，没有二硫键、糖基或脂链修饰，N 端为游离氨基，C 端为游离羧基。分子含组氨酸与谷氨酸侧链，因此在水和甲醇等极性溶剂中溶解良好，在非极性溶剂中溶解有限。计算分子量约为 814 Da，与其质子化离子的质荷比吻合，可用于质谱确认。
| Property | Value | Notes |
|---|---|---|
| Chemical class | Synthetic heptapeptide | Analogue of the ACTH(4-10) fragment |
| Amino acid sequence | Met-Glu-His-Phe-Pro-Gly-Pro | Single-letter form MEHFPGP |
| Molecular formula | C37H51N9O10S | Free peptide, nominal mass near 814 Da |
| First registration | 1994, Russia | Nasal formulation for neurological indications |
| Typical purity grade | 95% or higher by HPLC | Research material; higher grades used as reference standards |
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 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.
Proposed mechanisms center on neurotrophic signaling rather than on classical melanocortin receptor activation. Rodent experiments have reported shifts in the expression of brain-derived neurotrophic factor and nerve growth factor after administration, together with changes in the associated receptor systems. Several authors argue that the peptide acts largely through its degradation products and their interaction with peptidergic pathways, but this remains a hypothesis rather than a settled finding. No single molecular target has been identified in a way that the field broadly accepts.
Published research covers ischemic stroke, traumatic brain injury, cognitive impairment, optic nerve conditions and attention-related measures. Much of the human evidence comes from small trials conducted in one country, which limits how far the results generalize. Animal models supply the larger share of the data, and effects seen in rodents do not transfer automatically to people. Reviews have noted that methodological reporting is often incomplete, making it difficult to pool results or compare treatment schedules across studies.
History of cancer Unexplained weight loss Immunosuppression Urinary infection Intravenous drug use Prolonged use of corticosteroids Back pain not improved with conservative management History of significant trauma Minor fall or heavy lift in a potentially osteoporotic or elderly individual Acute onset of urinary retention, overflow incontinence, loss of anal sphincter tone, or fecal incontinence Saddle anesthesia Global or progressive motor weakness in the lower limbs Being over the age of 50 or under the age of 25
== G == Gabriel ethylenimine method Gabriel synthesis Gabriel–Colman rearrangement, Gabriel isoquinoline synthesis Gallagher–Hollander degradation Gassman indole synthesis Gastaldi synthesis Gattermann aldehyde synthesis Gattermann Koch reaction Gattermann reaction Geminal halide hydrolysis Gewald reaction Gibbs phthalic anhydride process Gilman reagent Glaser coupling Glycol cleavage Goldberg reaction Gomberg–Bachmann reaction Gomberg–Bachmann–Hey reaction Gomberg radical reaction Gould–Jacobs reaction Graebe–Ullmann synthesis Grignard degradation Griesbaum coozonolysis Grignard reaction Grob fragmentation Grubbs' catalyst in Olefin metathesis Grundmann aldehyde synthesis Gryszkiewicz–Trochimowski and McCombie method Guareschi–Thorpe condensation Guerbet reaction Gutknecht pyrazine synthesis
== In popular culture == The fictional character Dexter Morgan uses Etorphine M-99 to capture and sedate his victims in the television series, Dexter, although this was retroactively changed to ketamine in the sequel series, Dexter: New Blood, only for etorphine to return in the succeeding series, Dexter: Original Sin and Dexter: Resurrection. In the film The Meg etorphine is used to neutralise the first megalodon. The fictional character Katherine Dutta uses etorphine to murder her victims in the television series Lewis, Lewis: Down Among the Fearful. In an Agatha Raisin book, a fictional veterinarian is murdered with the Immobilon he planned to use to sedate a horse for an operation.
Brazil ranked 52nd in the Global Innovation Index in 2025, up from 66th in 2019. Among the most renowned Brazilian inventors are priests Bartolomeu de Gusmão, Landell de Moura and Francisco João de Azevedo, besides Alberto Santos-Dumont, Evaristo Conrado Engelberg, Manuel Dias de Abreu, Andreas Pavel and Nélio José Nicolai. Brazilian science is represented by the likes of César Lattes (Brazilian physicist Pathfinder of Pi Meson), Mário Schenberg (considered the greatest theoretical physicist of Brazil), José Leite Lopes (the only Brazilian physicist holder of the UNESCO Science Prize), Artur Avila (the first Latin American winner of the Fields Medal), and Fritz Müller (pioneer in factual support of the theory of evolution by Charles Darwin).
=== Dietary === The effects of eating habits on childhood obesity are difficult to determine. A three-year randomized controlled study of 1,704 third-grade children which provided two healthy meals a day in combination with an exercise program and dietary counselling failed to show a significant reduction in percentage body fat when compared to a control group. This was partly due to the fact that even though the children believed they were eating less, their actual calorie consumption did not decrease with the intervention. At the same time observed energy expenditure remained similar between the groups. This occurred even though dietary fat intake decreased from 34% to 27%. A second study of 5,106 children showed similar results. Even though the children ate an improved diet there was no effect found on BMI. Why these studies did not bring about the desired effect of curbing childhood obesity has been attributed to the interventions being insufficient. Changes were made primarily in the school environment while it is felt that they must occur in the home, the community, and the school simultaneously to have a significant effect. A Cochrane review of a lower fat diet in children (30% or less of total energy) to prevent obesity found the existing evidence of very low to moderate quality, and firm conclusions could not be made. Calorie-rich drinks and foods are readily available to children. Consumption of sugar-laden soft drinks may contribute to childhood obesity.
Sources: en.wikipedia.org
==== Other factors ==== Oxytocin reaches lactotrophs via portal vessels and fulfils the criteria of a prolactin-releasing factor during suckling. Serotonin mediates the nocturnal prolactin surge and suckling-induced prolactin release via 5-HT1A and 5-HT2 receptors. Other reported stimulatory factors include neurotensin, angiotensin II, and galanin. Prolactin-releasing peptide (PrRP), despite its name, does not appear to function as a classical hypophysiotropic releasing factor in vivo.
In a systematic review of published evidence, the United States Preventive Services Task Force in 2017 concluded that there was uncertainty about the accuracy or clinical utility of all potential screening tools for OSA, and recommended that evidence is insufficient to assess the balance of benefits and harms of screening for OSA in asymptomatic adults. The diagnosis of OSA syndrome is made when the patient shows recurrent episodes of partial or complete collapse of the upper airway during sleep resulting in apneas or hypopneas, respectively. Criteria defining an apnea or a hypopnea vary. The American Academy of Sleep Medicine (AASM) defines apnea as a reduction in airflow of ≥ 90% lasting at least 10 seconds. A hypopnea is defined as a reduction in airflow of ≥ 30% lasting at least 10 seconds and associated with a ≥ 4% decrease in pulse oxygenation, or as a ≥ 30% reduction in airflow lasting at least 10 seconds and associated either with a ≥ 3% decrease in pulse oxygenation or with an arousal. To define the severity of the condition, the Apnea-Hypopnea Index (AHI) or the Respiratory Disturbance Index (RDI) are used. While the AHI measures the mean number of apneas and hypopneas per hour of sleep, the RDI adds to this measure the respiratory effort-related arousals (RERAs). The OSA syndrome is thus diagnosed if the AHI is > 5 episodes per hour and results in daytime sleepiness and fatigue or when the RDI is ≥ 15 independently of the symptoms.
Over the following week, the secondary buds branch into tertiary buds, about ten on each side. From the sixth week to the sixteenth week, the major elements of the lungs appear except the alveoli. From week 16 to week 26, the bronchi enlarge and lung tissue becomes highly vascularised. Bronchioles and alveolar ducts also develop. By week 26, the terminal bronchioles have formed which branch into two respiratory bronchioles. During the period covering the 26th week until birth the important blood–air barrier is established. Specialised type I alveolar cells where gas exchange will take place, together with the type II alveolar cells that secrete pulmonary surfactant, appear. The surfactant reduces the surface tension at the air-alveolar surface which allows expansion of the alveolar sacs. The alveolar sacs contain the primitive alveoli that form at the end of the alveolar ducts, and their appearance around the seventh month marks the point at which limited respiration would be possible, and the premature baby could survive.
== Clinical Significance == In diseases related to the cartilage, the territorial matrix undergoes structural and material changes, leading to degradation of the joints, like in the case of osteoarthritis. Osteoarthritis occurs when the proteoglycans and collagen fibers degrade and become disorganized. Consequently, the decreased mechanical support makes chondrocytes more vulnerable to damage. Matrix-degrading enzymes including matrix metalloproteinases (MMPs) target the region which can accelerate cartilage degradation. Attempts to restore a functional territorial matrix is a particular area of interest in tissue engineering and cartilage repair, since its structure significantly contributes to optimal mechanical and biochemical behavior. Studies on biomimetic proteoglycans, which mimic the natural existing component of the ECM, and their effect on neighboring cartilage regions have shown promising results for strengthening cartilage with osteoarthritis. Additionally, biomaterials designed to mimic native composition and mechanical properties of cartilage, especially those with synthetic proteoglycans or collagen, have shown experimental promise. In combination with these structures, the durability of engineering cartilage may be enhanced by regenerating the territorial matrix and could improve integration with native tissue.
Sources: en.wikipedia.org
Registered medical products are most often 0.1% nasal drops. Research suppliers ship lyophilized powder, usually in milligram quantities, which is dissolved before use. The active peptide is the same in both cases; presentation and excipients differ.
No. The peptide is synthetic, although it is modelled on a fragment of a naturally occurring hormone. ACTH(4-10) is generated when ACTH is cleaved, but the Pro-Gly-Pro extension is not a known endogenous sequence. It is therefore a designed analogue rather than a natural metabolite.
The label reflects reported effects on attention, memory and recovery after neurological injury in regional clinical reports. Those reports are mostly small and have not been widely replicated outside the region. The classification is descriptive and does not imply a single defined mechanism.
电喷雾或基质辅助激光解吸电离质谱是常用手段，测得的质子化离子质荷比可换算为分子量。结果与理论值落在合理误差内，才支持结构一致的判断。