Everything below concerns melanocortin signalling. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-06-10. Numbers and descriptions here follow the published literature rather than marketing material.
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.
Pharmacokinetic accounts emphasize rapid breakdown. After intravenous dosing the intact peptide disappears from blood within minutes, and nasal delivery produces low but measurable concentrations. Metabolites rather than the parent molecule may account for part of the observed activity, although the relative contribution is unresolved. Dosing in the literature varies widely and no optimal schedule has been agreed. These gaps are regularly cited as a reason the findings have not produced broad clinical adoption beyond the original research setting.
| 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 with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. Its design combines the ACTH(4-7) core fragment with a C-terminal Pro-Gly-Pro extension, a modification intended to improve stability and prolong activity. The molecule is hydrophilic, carries no lipid chains or glycosylation, and has a theoretical mass just over 810 daltons in its free form. All seven residues are proteinogenic amino acids, so no non-natural building blocks appear in the backbone. A free N-terminal methionine and C-terminal proline define the unmodified parent peptide.
The compound was developed during the 1980s at the Institute of Molecular Genetics in Moscow as part of research on fragments of adrenocorticotropic hormone. Early work examined short ACTH-derived sequences that retained neurotrophic effects while lacking the endocrine activity of the full hormone. Semax entered clinical use in Russia during the 1990s, where it received registration for several neurological indications. Outside that region it remained primarily a laboratory research material rather than an approved therapeutic. English-language literature on it grew more slowly and frequently cited the original Russian studies.
Identity and purity of semax are established with reversed-phase high-performance liquid chromatography coupled to ultraviolet detection, usually at 214 nanometres. Mass spectrometry, most often electrospray ionisation in positive mode, confirms the molecular mass and reveals truncated sequences. Amino acid analysis and peptide mapping after enzymatic digestion provide additional structural confirmation. Laboratories typically report purity as the percentage area of the main peak, a figure that does not capture isomeric or oxidised variants unless the method resolves them.
The peptide is prone to several degradation pathways. Oxidation of the methionine residue produces a sulfoxide that elutes close to the parent peak in many chromatographic systems. Hydrolysis of peptide bonds and deamidation of susceptible residues in related sequences also reduce purity over time. Lyophilised material kept dry at minus twenty degrees Celsius and shielded from light is the most stable form commonly described in laboratory practice.
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.
多数实验室与市售的 Semax 以冻干粉形式提供。冻干粉通常建议保存在 -20 °C 或更低温度下，同时避免光照与反复升温。短期运输有时采用冷藏条件，但长期保存仍以冷冻为主。分包操作应尽量减少开盖次数，以降低吸湿和微生物污染的风险。开封后若未一次用完，建议在干燥环境中密封并尽快放回低温储存。
溶液状态的稳定性明显低于冻干粉。肽类在水溶液中可能经历水解、氧化与聚集，其中甲硫氨酸和天冬酰胺等残基常是敏感位点。Semax 含有甲硫氨酸，因此氧化风险相对突出。工作液一般主张现配现用，或冷藏并在数日内用尽。缓冲液种类、pH 和离子强度都会影响降解速率，而关于最佳条件的公开数据并不统一。
常规纯度与身份确认依赖反相高效液相色谱，并辅以质谱测定分子量。氨基酸组成分析可用于验证序列构成，肽图分析则能进一步定位修饰或降解产物。杂质谱通常关注缺失序列肽、截短片段和氧化产物。不同方法的检出限并不相同，因此各实验室报告的纯度数值不宜直接横向比较。
==== MeSH D13.570.583 – purine nucleosides ==== MeSH D13.570.583.138 – adenosine MeSH D13.570.583.138.025 – adenosine-5'-(n-ethylcarboxamide) MeSH D13.570.583.138.240 – s-adenosylhomocysteine MeSH D13.570.583.138.264 – s-adenosylmethionine MeSH D13.570.583.138.300 – 2-chloroadenosine MeSH D13.570.583.138.300.200 – cladribine MeSH D13.570.583.138.325 – deoxyadenosines MeSH D13.570.583.138.325.075 – cladribine MeSH D13.570.583.138.325.105 – dideoxyadenosine MeSH D13.570.583.138.325.800 – puromycin aminonucleoside MeSH D13.570.583.138.500 – isopentenyladenosine MeSH D13.570.583.138.630 – phenylisopropyladenosine MeSH D13.570.583.138.711 – puromycin MeSH D13.570.583.138.711.650 – puromycin aminonucleoside MeSH D13.570.583.138.900 – vidarabine MeSH D13.570.583.454 – guanosine MeSH D13.570.583.454.240 – deoxyguanosine MeSH D13.570.583.454.500 – nucleoside q MeSH D13.570.583.616 – inosine MeSH D13.570.583.616.130 – didanosine MeSH D13.570.583.616.450 – inosine pranobex MeSH D13.570.583.616.900 – thioinosine MeSH D13.570.583.616.900.500 – methylthioinosine MeSH D13.570.583.910 – tubercidin
== Further reading == Budd, A. (2012). "Introduction to genome biology: features, processes, and structures". Evolutionary Genomics. Methods in Molecular Biology. Vol. 855. pp. 3–4. doi:10.1007/978-1-61779-582-4_1. ISBN 978-1-61779-581-7. PMID 22407704.
By further optimizing the CNTs and CNT fibers, CNT fibers with improved electrical properties could be developed. CNT-based yarns are suitable for applications in energy and electrochemical water treatment when coated with an ion-exchange membrane. Also, CNT-based yarns could replace copper as a winding material. Pyrhönen et al. (2015) have built a motor using CNT winding.
Sources: en.wikipedia.org
== Drug interactions == Some of the important clinical interactions of probenecid include those with captopril, indomethacin, ketoprofen, ketorolac, naproxen, cephalosporins, quinolones, penicillins, methotrexate, zidovudine, ganciclovir, lorazepam, and aciclovir. In all these interactions, the excretion of these drugs is reduced due to probenecid, which in turn can lead to increased concentrations of these.
== Toxicity == Studies carried out on the toxicity of convulxin show that symptoms are a function of the dose. The effects of the toxin stand out through the sudden and brief duration of the symptoms after exposure. In mice, low doses (5 μg/animal) administered intravenously (I.V) elicited tachypnea, followed by apnea, within 20 seconds. The ED50 for brief duration apnea was determined to be 180 μg/kg. Higher doses (10 μg/animal) evoked intense convulsive crisis, and usually ended with the death of the animal. LD50 was determined to be 524 μg/kg. Intraperitoneal (I.P.) administration of up to 200 μg/animal proved to be ineffective. In cats, I.V. injections of 100 μg/kg showed respiratory disturbances, miosis, salivation, abdominal cramps, nystagmus, loss of equilibrium, convulsions and sometimes a brief phase of hypotonia. The ED50 dose for convulsions is 80 μg/kg. The majority of animals recovered within 30 minutes. In dogs, the effect of convulxin showed two stages. After I.V. injection of 100-125 μg/kg they became excited, barked and exhibited loss of equilibrium, respiratory disturbances, nystagmus, urination, defecation and vomiting. After recovery, two out of five animals had intermittent crisis of clonic convulsions that appeared after 24 hours and lasted until their death. The other three dogs showed periods of vivid agitation alternating with torpor. While the lethal dose in humans is not yet known, what has been discovered is that the level of toxic effects depends on the origin of the snake. As for a cure, so far a polyvalent snake antivenom is being used.
The Cantley lab also was one of a few labs that nearly simultaneously identified LKB1 as a regulator of AMPK that also serves to regulate TORC1. For the discovery of PI-3-Kinase and its role in cancer metabolism, Cantley was one of eleven recipients of the inaugural Breakthrough Prize in Life Sciences, "the world's richest academic prize for medicine and biology. The prize, which carries a $3 million cash award, recognizes excellence in research aimed at curing intractable diseases and human life." The fundamental and far-reaching nature of the discovery of PI-3-kinase, together with Cantley's role in mapping the upstream regulation of PI-3-kinase and the downstream signaling pathways, have led to speculation that Cantley is a likely candidate for the Nobel prize in Medicine or Physiology. The growing evidence for a primary role for PI-3-kinase in cancer and its critical role in insulin signaling have served to strengthen the significance of this fundamentally important discovery. The first drug targeting the PI-3-kinase pathway as a treatment for cancer – Idelalisib (PI3K Delta inhibitor) – was approved by the FDA as a treatment for leukemia and two types of lymphoma in July 2014. Other drugs are currently in clinical development.
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 main proposal is modulation of neurotrophic factors such as brain-derived neurotrophic factor, supported largely by animal experiments. Receptor-level targets have not been firmly established. Most reviews describe the mechanism as only partially characterized.