The short version of ACTH(4–10) fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-04-20 and is reviewed periodically as new material appears.
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.
| 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 |
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.
Terminology around the compound varies by source. It appears in catalogues and papers as Semax, as the heptapeptide ACTH(4-7)-Pro-Gly-Pro, and under various alphanumeric laboratory codes used by individual suppliers. These names refer to the same sequence but may imply different salt forms, purity grades, or counter-ions. Peptide databases usually list the free base mass, while product descriptions sometimes report acetate or trifluoroacetate salts with a different formula weight. Because naming conventions for research peptides are not standardised across vendors, checking the declared sequence and measured mass is more reliable than relying on a trade name alone.
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.
Semax is a synthetic heptapeptide whose sequence is Met-Glu-His-Phe-Pro-Gly-Pro. It was developed as a fragment analog of adrenocorticotropic hormone, modeled specifically on the ACTH(4-10) region. The first four residues reproduce that fragment, while a Pro-Gly-Pro tripeptide is appended at the C-terminus. Work on the compound originated in Russia, where it entered clinical use as an intranasal preparation. Its sequence places it among short regulatory peptides studied for effects on the central nervous system rather than on the adrenal axis.
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.
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.
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.
Semax is a synthetic heptapeptide whose sequence is Met-Glu-His-Phe-Pro-Gly-Pro. The first four residues correspond to the ACTH(4-10) fragment, while the terminal Pro-Gly-Pro extension was added to improve metabolic stability. Its molecular formula is C37H51N9O10S and its monoisotopic mass is approximately 813.9 Da. The compound is classified as a peptide research chemical and as a registered pharmaceutical product in Russia, but it does not hold marketing approval in the European Union or the United States. Naming conventions vary across supplier catalogs.
Development of the compound took place in the Soviet Union during the 1980s, largely through peptide research groups affiliated with the Shemyakin-Ovchinnikov Institute and Moscow State University. Investigators screened fragments of adrenocorticotropic hormone for activity on the central nervous system while attempting to separate cognitive effects from hormonal ones. The shortened sequence was selected because it retained behavioral activity in animal models without stimulating corticosteroid release. Early publications described the molecule as an ACTH(4-10) analog.
Published research on this peptide originates mainly from Russian laboratories, and the wider international literature is comparatively thin. Studies have used rodent models of stroke, hypoxia, and memory tasks, with a smaller number of human trials reported. Reported outcomes include changes in attention and memory measures, along with effects on neurotrophic factor expression in some experiments. Small sample sizes, inconsistent dosing protocols, and limited independent replication are widely noted limitations, so the strength of the clinical evidence remains an open question.
Mysore State, colloquially Old Mysore, was a political territory within the Dominion of India and the subsequent Republic of India from 1950 until 1956. The state was formed by renaming the Kingdom of Mysore, with Bangalore replacing Mysore as the state's capital when Parliament passed the States Reorganisation Act in 1956. Mysore State was considerably enlarged when it became a linguistically homogeneous Kannada-speaking state within the Republic of India by incorporating territories from Andhra, Bombay, Coorg, Hyderabad, and Madras States, as well as other petty fiefdoms. It was subsequently renamed Karnataka in 1973.
== Structure == The first 3D structure of hCTR1 was based on electron crystallography, revealing that hCTR1 has a homotrimeric channel-like architecture. It consists of three indentical monomers, the monomers oligomerize through their transmembrane regions, and a monomer of hCtr1 has these characteristics:
In 1950, a 21 SAS squadron was raised to fight in the Korean War. After three months of training in Britain, it was informed that the squadron would no longer be required in Korea and so it instead volunteered to fight in the Malayan Emergency. Upon arrival in Malaya, it came under the command of Mike "Mad Mike" Calvert who was forming a new unit called the Malayan Scouts (SAS). Calvert had already formed one squadron from 100 volunteers in the Far East, which became A Squadron; the 21 SAS squadron then became B Squadron; and after a recruitment visit to Rhodesia by Calvert, C Squadron was formed from 100 Rhodesian volunteers. The Rhodesians returned home after three years' service and were replaced by a New Zealand squadron. By this time the need for a regular army SAS regiment had been recognised; the 22 SAS Regiment was formally added to the army list in 1952 and has been based at Hereford since 1960. In 1959 the third regiment, the 23 SAS Regiment, was formed by renaming the Reserve Reconnaissance Unit, which had succeeded MI9 and whose members were experts in escape and evasion.
== Function == GPX1 is ubiquitously expressed in many tissues, where it protects cells from oxidative stress. Within cells, it localizes to the cytoplasm and mitochondria. As a glutathione peroxidase, GPx1 functions in the detoxification of hydrogen peroxide, specifically by catalyzing the reduction of hydrogen peroxide to water. The glutathione peroxidase also catalyzes the reduction of other organic hydroperoxides, such as lipid peroxides, to the corresponding alcohols. GPx1 typically uses glutathione (GSH) as the reductant, but when glutathione synthetase (GSS) is, as in brain mitochondria, γ-glutamylcysteine can serve as the reductant instead. The protein encoded by this gene protects from CD95-induced apoptosis in cultured breast cancer cells and inhibits 5-lipoxygenase in blood cells, and its overexpression delays endothelial cell death and increases resistance to toxic challenges, especially oxidative stress. This protein is one of only a few proteins known in higher vertebrates to contain selenocysteine, which occurs at the active site of glutathione peroxidase and is coded by the nonsense (stop) codon TGA.
==== MeSH E05.393.285 – cytogenetic analysis ==== MeSH E05.393.285.130 – chromosome banding MeSH E05.393.285.350 – in situ hybridization, fluorescence MeSH E05.393.285.350.125 – chromosome painting MeSH E05.393.285.350.125.800 – spectral karyotyping MeSH E05.393.285.475 – karyotyping MeSH E05.393.285.475.800 – spectral karyotyping MeSH E05.393.285.830 – sex determination (analysis)
Sources: en.wikipedia.org
== Medical uses == Vancomycin is indicated for the treatment of serious, life-threatening infections by Gram-positive bacteria of both aerobic and anaerobic types that are unresponsive to other antibiotics. The increasing emergence of vancomycin-resistant enterococci (VRE) has resulted in the development of guidelines for use by the Centers for Disease Control Hospital Infection Control Practices Advisory Committee. These guidelines restrict use of vancomycin to these indications:
The C-terminal domain has structural similarities to the serum protein hemopexin. It has a four-bladed β-propeller structure. β-Propeller structures provide a large flat surface that is thought to be involved in protein-protein interactions. This determines substrate specificity and is the site for interaction with TIMP's (tissue inhibitor of metalloproteinases). The hemopexin-like domain is absent in MMP-7, MMP-23, MMP-26, and the plant and nematode. The membrane-bound MMPs (MT-MMPs) are anchored to the plasma membrane via a transmembrane or a GPI-anchoring domain.
=== Channel 5 === In 2010, Willis replaced Melinda Messenger on the Channel 5 series Live from Studio Five, but she left after only two months to co-present Big Brother's Little Brother and was replaced by Jayne Middlemiss. In August 2011, she returned to the revived series, presenting the spin-off show Big Brother's Bit on the Side. On 13 March 2013, it was reported that Brian Dowling would be axed from Big Brother and be replaced by Willis with a source saying, 'Brian has been a great host but Emma is seen by channel chiefs as a true successor to Davina. They're talking to her now about taking over the role from the summer.' Her appointment as host was confirmed on 2 April 2013. On 13 June 2013, she began presenting the fourteenth series of Big Brother. As well as presenting the main Big Brother and celebrity series, she continued to host the spin-off show Bit on the Side, sharing the presenting duties with Rylan Clark. On 2 February 2015, it was announced that Willis was to present her final edition of Bit on the Side that night, and Clark would take over as the main presenter of the spin off show. Willis interrogated Winston McKenzie during his exit interview on Celebrity Big Brother over his controversial opinions. Willis has expressed personal pride on this moment in her career. On 30 March 2014, Willis presented the Mum of the Year Awards, with the highlights being shown on Channel 5 that same evening.
== Purpose == Without trichrome staining, discerning one feature from another can be extremely difficult. Smooth muscle tissue, for example, is hard to differentiate from collagen. A trichrome stain can colour the muscle tissue red, and the collagen fibres green or blue. Liver biopsies may have fine collagen fibres between the liver cells, and the amount of collagen may be estimated based on the staining method. Trichrome methods are now used for differentiating muscle from collagen, pituitary alpha cells from beta cells, fibrin from collagen, and mitochondria in fresh frozen muscle sections, among other applications. It helps in identifying increases in collagenous tissue (i.e., fibrotic changes) such as in liver cirrhosis and distinguishing tumours arising from muscle cells and fibroblasts.
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.
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.