If you have been reading about ACTH analog and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Updated 2026-04-06. Numbers and descriptions here follow the published literature rather than marketing material.
Development took place during the 1980s at institutes of the Russian Academy of Sciences, where peptide fragments of ACTH were screened for cognitive and neuroprotective effects. The compound received regulatory approval in Russia as a nasal preparation, marketed for conditions such as ischemic stroke, transient ischemic attacks, and optic nerve disorders. Registration in other countries has not followed. Most published clinical reports originate from a small number of Russian research groups, and independent replication outside that setting remains limited. The regulatory status therefore differs sharply between Russia and the rest of the world.
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.
Identity and purity are confirmed with reversed-phase high-performance liquid chromatography, typically monitored at 214 nanometres where the peptide bond absorbs. Mass spectrometry, either electrospray or MALDI-TOF, verifies molecular mass against the theoretical value and detects truncation or adduct formation. Amino acid analysis and peptide mapping provide additional confirmation when required. The most frequently reported impurities are deletion sequences from incomplete coupling, methionine sulfoxide from oxidation, and dimeric species formed through non-covalent aggregation. Impurity profiles depend strongly on the synthesis and purification route chosen by the producer.
Published research has focused mainly on neurological and cognitive endpoints in animal models, with proposed mechanisms involving brain-derived neurotrophic factor and related signalling pathways. A substantial share of the human data originates from a limited number of research groups, and independent replication in other countries remains sparse. Regulatory status reflects that distribution: the peptide is registered as a medicine in Russia and appears in some neighbouring markets, while elsewhere it is handled as a research chemical without approved therapeutic labelling. Questions about dose-response relationships, long-term effects, and comparability across studies are still open.
Lyophilised powder is normally kept at -20 °C in a desiccated container, with some suppliers recommending -80 °C for long-term archival storage. Repeated freeze-thaw cycles are the most common cause of avoidable loss, so aliquoting before freezing reduces variability between working sessions. Dissolved peptide is far less stable than the dry solid and is usually prepared fresh or held briefly at 4 °C. Aqueous solutions support both hydrolysis of the backbone and oxidation of the N-terminal methionine, and these two routes dominate degradation under ordinary laboratory conditions.
| Property | Value | Notes |
|---|---|---|
| Sequence | Met-Glu-His-Phe-Pro-Gly-Pro | Heptapeptide; ACTH(4-10) analog extended at C-terminus |
| Molecular mass | ~813.9 Da | Free peptide, unmodified |
| Appearance | White to off-white powder | Typical lyophilized solid |
| Solubility | Soluble in water and saline | Also soluble in common aqueous buffers |
| Storage (solid) | -20 °C, desiccated | Protect from moisture and repeated thawing |
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.
稳定性主要由水解与氧化两条路径支配。肽键在中性或弱酸性条件下相对稳定，遇到强碱或长时间高温则明显断裂；甲硫氨酸侧链容易被氧化成亚砜，使主峰前移并拉低实际含量。金属离子、光照和反复冻融会进一步促进降解或聚集。冻干粉在低温避光条件下可存放较长时间，配制后的水溶液通常需要冷藏并尽快用完。
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。
Flattened squamous cells are more resistant to both abrasion and infection. The permeability of the epithelium allows for an effective response from the immune system since antibodies and other immune components can easily reach the surface. The vaginal epithelium differs from the similar tissue of the skin. The epidermis of the skin is relatively resistant to water because it contains high levels of lipids. The vaginal epithelium contains lower levels of lipids. This allows the passage of water and water-soluble substances through the tissue. Keratinization happens when the epithelium is exposed to the dry external atmosphere. In abnormal circumstances, such as in pelvic organ prolapse, the mucosa may be exposed to air, becoming dry and keratinized.
First, the ancient tanners would soak the skins in water to clean and soften them. Then they would pound and scour the skin to remove any remaining flesh and fat. Hair was removed by soaking the skin in urine, painting it with an alkaline lime mixture, or simply allowing the skin to putrefy for several months then dipping it in a salt solution. After the hair was loosened, the tanners scraped it off with a knife. Once the hair was removed, the tanners would "bate" (soften) the material by pounding dung into the skin, or soaking the skin in a solution of animal brains. Bating was a fermentative process that relied on enzymes produced by bacteria found in the dung. Among the kinds of dung commonly used were those of dogs or pigeons. Historically the actual tanning process used vegetable tanning. In some variations of the process, cedar oil, alum, or tannin was applied to the skin as a tanning agent. As the skin was stretched, it would lose moisture and absorb the agent. Following the adoption in medicine of soaking gut sutures in a chromium (III) solution after 1840, it was discovered that this method could also be used with leather and thus was adopted by tanners.
Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. A complementary model has recently been described where the many elements of wound healing are more clearly delineated. The importance of this new model becomes more apparent through its utility in the fields of regenerative medicine and tissue engineering (see Research and development section below). In this construct, the process of wound healing is divided into two major phases: the early phase and the cellular phase: Electrospun nanofiber-based wound dressings have attracted increasing attention because their porous architecture and high surface-area-to-volume ratio can mimic the extracellular matrix, thereby supporting cell adhesion, proliferation, and tissue regeneration. The early phase, which begins immediately following skin injury, involves cascading molecular and cellular events leading to hemostasis and formation of an early, makeshift extracellular matrix that provides structural staging for cellular attachment and subsequent cellular proliferation. The cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer. Subdivisions of the cellular phase are:
=== Filler injections === Filler injections of collagen can be used to raise atrophic scars to the level of surrounding skin. Risks vary based upon the filler used, and can include further disfigurement and allergic reaction.
Sources: en.wikipedia.org
Thus, iodine-131 is increasingly less employed in small doses in medical use (especially in children), but increasingly is used only in large and maximal treatment doses, as a way of killing targeted tissues (i.e. therapeutic use). Iodine-131 can be "seen" by nuclear medicine imaging techniques (e.g., gamma cameras) whenever it is given for therapeutic use, since it is a strong emitter of gamma radiation. However, since the beta radiation causes tissue damage without contributing to any ability to see or "image" the isotope, other less-damaging radioisotopes of iodine such as iodine-123 (see isotopes of iodine) are preferred in situations when only imaging is wanted. The isotope 131I is still occasionally used for purely diagnostic (i.e., imaging) work, due to its low expense compared to other iodine radioisotopes. No increase in thyroid cancer has been seen from the small medical imaging doses of 131I. The low-cost availability of 131I, in turn, is due to the relative ease of creating 131I by neutron bombardment of natural tellurium in a nuclear reactor, then separating 131I out by various simple methods (i.e., heating to drive off the volatile iodine). By contrast, other iodine radioisotopes are usually created by far more expensive techniques, starting with cyclotron radiation of capsules of pressurized xenon gas. Iodine-131 is also one of the most commonly used gamma-emitting radioactive industrial tracer.
== Parallel evolution of cardiotonic steroid resistance in vertebrates == Several studies have detailed the evolution of cardiotonic steroid resistance of the alpha-subunit gene family of Na/K-ATPase (ATP1A) in vertebrates via amino acid substitutions most often located in the first extracellular loop domain. Amino acid substitutions conferring cardiotonic steroid resistance have evolved independently many times in all major groups of tetrapods. ATP1A1 has been duplicated in some groups of frogs and neofunctionlised duplicates carry the same cardiotonic steroid resistance substitutions (Q111R and N122D) found in mice, rats and other muroids.
However, with more recent advances in disease specific therapies, survival in 2010 was 86%, 69%, and 61% at 1, 3 and 5 years respectively. Signs and symptoms may be initially non-specific and may lead to a delay in appropriate diagnosis. Early symptoms include breathlessness (dyspnea). Other symptoms include fatigue, lightheadedness or fainting and chest pain. Late findings include swelling of the extremities, edema and ascites (which are signs of right heart failure). Lower estimates regarding the prevalence of PAH are 15 cases per million adults with idiopathic PAH being 5.9 cases per million, with other estimates being 25 cases per 1 million people. In Europe, the prevalence ranges from 15 to 60 cases per year. More than half of PAH is believed to be idiopathic, drug induced or heritable. Disease specific therapy involves targeting the various aberrant pathways involved in the disease. PDE5 inhibitors are used which cause dilation of blood vessels. Riociguat also causes vasodilation. Endothelin receptor antagonists cause vasodilation as well by blocking the action of the potent vasoconstrictor endothelin-1. Prostacyclins and prostacyclin agonists also cause vasodilation and also inhibit platelet aggregation. In disease that is refractory to medical therapy, an atrial septostomy may be used palliatively or as a bridge to lung transplantation.
== Cause == Beriberi is often caused by eating a diet with a very high proportion of calorie-rich white rice (common in Asia) or cassava root (common in sub-Saharan Africa), without much if any thiamine-containing animal products or vegetables. It may also be caused by shortcomings other than inadequate intake – diseases or operations on the digestive tract, alcoholism, dialysis or genetic deficiencies. All those causes mainly affect the central nervous system, and provoke the development of Wernicke's encephalopathy. Wernicke's disease is one of the most prevalent neurological or neuropsychiatric diseases. In autopsy series, features of Wernicke lesions are observed in approximately 2% of general cases. Medical record research shows that about 85% had not been diagnosed, although only 19% would be asymptomatic. In children, only 58% were diagnosed. In alcohol abusers, autopsy series showed neurological damages at rates of 12.5% or more. Mortality caused by Wernicke's disease reaches 17% of diseases, which means 3.4/1000 or about 25 million contemporaries. The number of people with Wernicke's disease may be even higher, considering that early stages may have dysfunctions prior to the production of observable lesions at necropsy. In addition, uncounted numbers of people can experience fetal damage and subsequent diseases.
Using one of the above definitions, dinosaurs can be generally described as archosaurs with hind limbs held erect beneath the body. Other prehistoric animals, including pterosaurs, mosasaurs, ichthyosaurs, plesiosaurs, and Dimetrodon, while often popularly conceived of as dinosaurs, are not taxonomically classified as dinosaurs. Pterosaurs are distantly related to dinosaurs, being members of the clade Ornithodira. The other groups mentioned are, like dinosaurs and pterosaurs, members of Sauropsida (the reptile and bird clade), except Dimetrodon (which is a synapsid). None of them had the erect hind limb posture characteristic of true dinosaurs. Dinosaurs were the dominant terrestrial vertebrates of the Mesozoic Era, especially the Jurassic and Cretaceous periods. Other groups of animals were restricted in size and niches; mammals, for example, rarely exceeded the size of a domestic cat and were generally rodent-sized carnivores of small prey. Dinosaurs have always been recognized as an extremely varied group: over 900 non-avian dinosaur genera have been confidently identified (2018) with 1,124 species (2016). Estimates put the total number of dinosaur genera preserved in the fossil record at 1850, nearly 75% still undiscovered, and the number that ever existed (in or out of the fossil record) at 3,400. A 2016 estimate put the number of dinosaur species living in the Mesozoic at 1,543–2,468, compared to the number of modern-day birds (avian dinosaurs) at 10,806 species.
Sources: en.wikipedia.org
Mass analyzers separate the ions according to their mass-to-charge ratio. There are many types of mass analyzers, using either static or dynamic fields, magnetic or electric fields. Each analyzer type has its strengths and weaknesses. Many mass spectrometers use two or more mass analyzers for tandem mass spectrometry (MS/MS). In addition to the more common mass analyzers listed below, there are others designed for special situations.
He consulted the weather records for 1928, and found that, as in 1966, there was a heat wave in mid-August followed by nine days of cold weather starting on 28 August that greatly favoured the growth of the mould.
=== EC 2.4.99: Transferring Other Glycosyl Groups === EC 2.4.99.1: β-galactoside α-(2,6)-sialyltransferase EC 2.4.99.2: β-D-galactosyl-(1→3)-N-acetyl-β-D-galactosaminide α-2,3-sialyltransferase EC 2.4.99.3: α-N-acetylgalactosaminide α-2,6-sialyltransferase EC 2.4.99.4: β-galactoside α-2,3-sialyltransferase EC 2.4.99.5: galactosyldiacylglycerol α-2,3-sialyltransferase EC 2.4.99.6: N-acetyllactosaminide α-2,3-sialyltransferase EC 2.4.99.7: α-N-acetylneuraminyl-2,3-β-galactosyl-1,3-N-acetylgalactosaminide 6-α-sialyltransferase EC 2.4.99.8: α-N-acetylneuraminate α-2,8-sialyltransferase EC 2.4.99.9: lactosylceramide α-2,3-sialyltransferase EC 2.4.99.10: Now included in EC 2.4.99.6, N-acetyllactosaminide α-2,3-sialyltransferase EC 2.4.99.11: Now included with EC 2.4.99.1,β-galactoside α-(2,6)-sialyltransferase EC 2.4.99.12: lipid IVA 3-deoxy-D-manno-octulosonic acid transferase EC 2.4.99.13: (Kdo)-lipid IVA3-deoxy-D-manno-octulosonic acid transferase EC 2.4.99.14: (Kdo)2-lipid IVA (2-8) 3-deoxy-D-manno-octulosonic acid transferase EC 2.4.99.15: (Kdo)3-lipid IVA (2-4) 3-deoxy-D-manno-octulosonic acid transferase EC 2.4.99.16: starch synthase (maltosyl-transferring) EC 2.4.99.17: S-adenosylmethionine:tRNA ribosyltransferase-isomerase EC 2.4.99.18: dolichyl-diphosphooligosaccharide—protein glycotransferase EC 2.4.99.19: undecaprenyl-diphosphooligosaccharide—protein glycotransferase EC 2.4.99.20: 2′-phospho-ADP-ribosyl cyclase/2′-phospho-cyclic-ADP-ribose transferase EC 2.4.99.21: dolichyl-phosphooligosaccharide-protein glycotransferase EC 2.4.99.22: N-acetylglucosaminide α-(2,6)-sialyltransferase
== Background == The Government of India and UNESCO signed a Memorandum of Understanding (MoU) on 14 July 2006 to establish RCB. The centre is now recognized as a "Category II Centre" by "the principles and guidelines for the establishment and functioning of UNESCO Institutes and Centres". Following approval from the Union Cabinet, the centre became operational from its interim campus at Gurgaon, Haryana from 20 April 2009.
Sources: en.wikipedia.org
Semax is a synthetic seven-amino-acid peptide derived from a fragment of corticotropin. It is used in Russia as a nasal preparation, while elsewhere it is studied as a research compound. It is not approved as a medicine in most countries.
Its sequence corresponds to the 4-10 region of corticotropin extended by three residues. This fragment lacks the region responsible for adrenal steroid release, so it is explored for neural rather than hormonal effects. The relationship explains the compound's classification among ACTH-derived peptides.
It holds approval in Russia for several neurological indications as a nasal spray or drop formulation. Regulatory agencies in the United States and the European Union have not approved it. Products sold elsewhere are generally labeled for research use only.
Reversed-phase HPLC gives the main purity figure, most often with UV detection near 214 nanometres. Mass spectrometry then confirms the molecular mass. Together the two methods distinguish a correct sequence from a closely related impurity.