This is a working overview of nasal formulation, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-08-01. Anything still debated is marked as such rather than presented as settled.
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.
研究兴趣主要集中在神经营养因子相关的路径上，包括脑源性神经营养因子与神经生长因子的表达变化。部分实验报告称在特定条件下观察到这些因子的水平上升，但具体信号通路和剂量依赖关系仍未完全厘清。多数公开数据来自细胞模型和动物实验，人体对照研究数量有限。因此，该化合物的作用机制在文献中属于活跃讨论，而非已经确立的定论。
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。
| 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 |
Laboratory work points toward modulation of neurotrophic signaling, particularly expression of brain-derived neurotrophic factor and nerve growth factor in hippocampal tissue. Studies also describe effects on monoamine turnover, inflammatory mediators, and oxidative markers. These observations come mainly from animal models and cultured cells, so the causal chain in humans is not firmly established. Whether the reported molecular changes translate into measurable clinical benefit is an open question. Reviews generally present the mechanism as plausible rather than demonstrated.
Clinical evidence consists largely of small trials with modest sample sizes, often without independent replication. Reported endpoints include cognitive scores, recovery after stroke, and visual function, but study designs vary widely and few trials meet contemporary reporting standards. Systematic reviewers have noted a high risk of bias in several of these reports. No large multicenter trial conducted outside Russia has been published. The compound is therefore best described as investigational in most jurisdictions, with its clinical role still unresolved.
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.
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.
=== Mechanism of action === Codeine is an opiate and an agonist of the μ-opioid receptor (MOR). It acts on the central nervous system to have an analgesic effect. It is metabolised in the liver to produce morphine which is ten times more potent against the MOR. Opioid receptors are G protein-coupled receptors that positively and negatively regulate synaptic transmission through downstream signalling. Binding of codeine or morphine to the μ-opioid receptor results in hyperpolarization of the neuron leading to the inhibition of the release of nociceptive neurotransmitters, causing an analgesic effect and increased pain tolerance due to reduced neuronal excitability.
Bicalutamide more than blocks the effects of the increased testosterone levels that it induces in men, which is evidenced by its dose-dependent antiandrogenic effects (e.g., PSA decreases) and by the fact that monotherapy with the drug is about as effective as GnRH analogue therapy in the treatment of prostate cancer. However, in contrast, the effects of the elevated estrogen levels remain unopposed by bicalutamide, and this is importantly involved in the feminizing side effects (e.g., gynecomastia) of the drug in men. Testosterone levels decline with age in men and younger men have higher testosterone levels on average than older men. Men with prostate cancer treated with bicalutamide are relatively elderly. The increases in testosterone levels with NSAAs like flutamide and bicalutamide may result in greater absolute levels of testosterone and estradiol in younger men than in older men. In one study that administered flutamide, free testosterone levels in young men increased from about 26 pg/mL at baseline to about 34 pg/mL with flutamide (+31%) and in elderly men from about 16 pg/mL at baseline to about 21 pg/mL (+31%) with flutamide. Hence, free testosterone levels with flutamide were approximately 1.6-fold higher in young men than in elderly men in this study. In the case of estradiol, total estradiol levels in young men increased from about 26 pg/mL at baseline to about 45 pg/mL with flutamide (+73%) and in elderly men changed from about 31 pg/mL to about 30 pg/mL (–3%).
is the number of constituent antiquarks. Beta decay just changes neutron to proton or, in the case of positive beta decay (electron capture) proton to neutron so the number of individual quarks doesn't change. It is only the baryon flavor that changes, here labelled as the isospin. Up and down quarks have total isospin
Nuclear warfare and weapons are staple elements of speculative fiction. The War Game by Peter Watkins is a docudrama depicting a hypothetical nuclear attack on Britain. Fail Safe, directed by Sidney Lumet, is a 1964 Cold War techno-thriller presenting a dramatization of an unintended nuclear escalation triggered by a mechanical failure.
Florey's portrait appeared on the Australian fifty-dollar note for 22 years between 1973 and 1995. The note also depicted the Sir William Dunn School of Pathology, Penicillin notatum, mice used in penicillin experiments, colonies of mould inhibiting bacterial growth on a Petri dish, and Heatley's assay method. The street of Florey Drive and suburb of Florey in the Australian Capital Territory, the Florey Institute of Neuroscience and Mental Health at the University of Melbourne, Victoria, the Florey Unit of the Royal Berkshire Hospital in Reading, Berkshire, the Florey Institute for Host–Pathogen Interactions at the University of Sheffield, and a lecture theatre in the University of Adelaide's medical school are named after him. The Electoral district of Florey, a single-member electoral district for the South Australian House of Assembly, is also named after him. It was estimated that the development of penicillin saved over 80 million lives.
Sources: en.wikipedia.org
Prior to this, there had been failed synthesis attempts in 1986–87 at the Joint Institute for Nuclear Research in Dubna (then in the Soviet Union) and in 1990 at the GSI. A 1995 attempt at the Lawrence Berkeley National Laboratory resulted in signs suggesting but not pointing conclusively at the discovery of a new isotope 267Ds formed in the bombardment of 209Bi with 59Co, and a similarly inconclusive 1994 attempt at the JINR showed signs of 273Ds being produced from 244Pu and 34S. Each team proposed its own name for element 110: the American team proposed hahnium after Otto Hahn in an attempt to resolve the controversy of naming element 105 (which they had long been suggesting this name for), the Russian team proposed becquerelium after Henri Becquerel, and the German team proposed darmstadtium after Darmstadt, the location of their institute. The IUPAC/IUPAP Joint Working Party (JWP) recognised the GSI team as discoverers in their 2001 report, giving them the right to suggest a name for the element.
== Application == As of 2022, there is limited quality evidence for the use of lactoferrin medicinally. For example, while there is evidence for its role in the treatment of conditions such as inflammatory bowel disease and for anti-microbial activity, there is not yet enough quality data to understand lactoferrin's bioavailability (such as through the digestive system) and more research needs to be done to understand the difference between various sources of lactoferrin (such as human vs. bovine forms).
=== Medical === The primary therapeutic use of nicotine is treating nicotine dependence to eliminate smoking and the damage it does to health. Nicotine itself is not a standalone cessation tool; its efficacy in smoking cessation relies on nicotine replacement therapy (NRT) delivery systems, which vary formulations (e.g., transdermal patches and lozenges for steady release versus oral gum, inhalers, and nasal sprays for acute relief) to control and modify how much nicotine is delivered and absorbed, and to mimic tobacco pharmacokinetics without harmful byproducts. A 2018 Cochrane Collaboration review found high-quality evidence that all current forms of nicotine replacement therapy (gum, patch, lozenges, inhaler, and nasal spray) increase the chances of successfully quitting smoking by 50–60%, regardless of setting. Combining nicotine patch use with a faster acting nicotine replacement, like gum or spray, improves the odds of treatment success. In contrast to recreational nicotine products, which have been designed to maximize the likelihood of addiction, nicotine replacement products (NRTs) are designed to minimize addictiveness. The more quickly a dose of nicotine is delivered and absorbed, the higher the addiction risk.
== Prognosis == Venous ulcers are costly to treat, and there is a significant chance that they will recur after healing; one study found that up to 48% of venous ulcers had recurred by the fifth year after healing. However, treatment with local anaesthetic endovenous techniques suggests a reduction of this high recurrence rate is possible. Without proper care, the ulcer may get infected, leading to cellulitis or gangrene and eventually may need amputation of the part of the limb in the future. Some topical drugs used to treat venous ulcer may cause venous eczema.
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.
不是。Semax 是完全人工合成的七肽，自然界中没有对应的已知肽段。它的设计灵感来自促肾上腺皮质激素片段 ACTH(4-10)，但序列经过了替换和延长。