This is a working overview of intranasal delivery, written for readers who want more than a one-paragraph summary but less than a textbook.
Reviewed 2026-01-02. Anything still debated is marked as such rather than presented as settled.
The mechanisms attributed to semax are inferred from animal and cell studies rather than traced to one confirmed target. The most frequently cited pathway involves increased expression of brain-derived neurotrophic factor and nerve growth factor in hippocampal and cortical tissue. Some work points to engagement of melanocortin receptors, particularly MC4, which the parent ACTH fragment can activate. Effects on dopaminergic and serotonergic signalling have also been reported. No single account explains all observed results, and the relative weight of each pathway remains unsettled.
Published studies examine a fairly narrow set of endpoints. Rodent experiments commonly measure maze learning, infarct volume after induced ischemia, and tissue levels of neurotrophic factors. Clinical reports from Russian centres describe attention, memory and recovery scores in patients after stroke or transient ischemic attack. Most of those human studies are small and few have been repeated by independent groups. Outcome measures differ between studies, which limits direct comparison.
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.
| Property | Value | Notes |
|---|---|---|
| Appearance | White to off-white powder | Lyophilized solid from research suppliers |
| Solubility | Freely soluble in water | Also dissolves in aqueous buffers; solutions are used fresh |
| Typical storage temperature | -20 °C for lyophilized powder | Short-term transport at 2-8 °C is common |
| Common analytical method | Reverse-phase HPLC | Paired with mass spectrometry for identity confirmation |
| Common synonyms | ACTH(4-10) analogue; MEHFPGP | N-terminal methionine retained in the chain |
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.
Material sold for laboratory use varies widely in stated purity and documentation. A certificate of analysis should list the analytical method, the column and detector used, and the observed purity value. Independent verification by an outside laboratory is the practical way to confirm identity when documentation is absent or internally inconsistent. Regulatory status differs by country, and a product legal in one jurisdiction may be unapproved or controlled in another.
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.
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.
Glutamate dehydrogenase (NAD(P)+) (EC 1.4.1.3, glutamic dehydrogenase, glutamate dehydrogenase [NAD(P)+]) is an enzyme with systematic name L-glutamate:NAD(P)+ oxidoreductase (deaminating). This enzyme is a type of glutamate dehydrogenase that is distinguished from other types by being able to use either NAD+/NADH or NADP+/NADPH as a cofactor. It is found in the mitochondria of humans encoded by the genes GLUD1 and GLUD2. It catalyses the following chemical reaction
The Ministry of Education is officially responsible for education in Somalia, and oversees the nation's primary, secondary, technical and vocational schools, as well as primary and technical teacher training and non-formal education. About 15% of the government's budget is allocated toward education.
=== Preparation === Harvested chilies may be used fresh, or dried, typically on the ground in hot countries, to make a variety of products. Drying enables chilies grown in temperate regions to be used in winter. For home use, chilies can be dried by threading them with cotton and hanging them up in a warm dry place to dry.
Sources: en.wikipedia.org
===== Low hourly pay ===== Resident salaries are relatively low compared to those of other healthcare workers, especially when considering hourly compensation. According to the American Medical Association, on average, residents earned approximately US$15 to US$20 per hour, when converting their salaries against an 80-hour work week in 2020.
=== Peripherally restricted === Peripherally acting μ-opioid receptor antagonists are used mainly in the treatment of opioid-induced constipation. These are designed to specifically inhibit certain opioid receptors in the gastrointestinal tract and with limited ability to cross the blood–brain barrier. Therefore, they do not affect the analgesic effects of opioids within the central nervous system.
Transdermal selegiline does not cause sexual dysfunction and may improve certain domains of sexual function, for instance sexual interest, maintaining interest during sex, and sexual satisfaction. These benefits were apparent in women but not in men. The lack of sexual dysfunction with transdermal selegiline is in contrast to many other antidepressants, such as the selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs), which are associated with high rates of sexual dysfunction. Transdermal selegiline patches have been underutilized in the treatment of depression compared to other antidepressants. A variety of factors contributing to this underutilization have been identified. One major factor is the very high cost of transdermal selegiline, which is often not covered by insurance and frequently proves to be prohibitive. Conversely, other widely available antidepressants are much cheaper in comparison.
The two substrates of this enzyme are L-arogenic acid (shown as its conjugate base arogenate) and oxidised nicotinamide adenine dinucleotide (NAD+). Its products are L-tyrosine, reduced NADH, and carbon dioxide. This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-CH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is L-arogenate:NAD+ oxidoreductase (decarboxylating). Other names in common use include arogenic dehydrogenase (ambiguous), cyclohexadienyl dehydrogenase, pretyrosine dehydrogenase (ambiguous), and L-arogenate:NAD+ oxidoreductase. This enzyme participates in phenylalanine, tyrosine and tryptophan biosynthesis and novobiocin biosynthesis.
Sources: en.wikipedia.org
SPECIAL obtains spatial localization from only a single dimension with pre-excitation inversion pulses (cycled on and off every other repetition time [TR]), making it a two-cycle sequence. The use of the preinversion pulse to remove one refocusing pulse (as compared with PRESS) is what allows SPECIAL to achieve a short TE, reaching a minimum of 2.2 msec on a preclinical scanner in rat brain while being able to recover the full signal and as low as 6 msec on a clinical 3T scanner. The largest drawback of SPECIAL and SPECIAL-sLASER is that they are two-cycle schemes, and systematic variations between cycles will manifest in their difference spectrum. Lipid contamination is a particularly large problem with SPECIAL and similar sequences. The state-of-the-art localization sequence is sLASER, which utilizes two pairs of adiabatic refocusing pulses. This has recently been recommended by consensus. The first is through OVS, which will reduce the contamination of lipid signals that originate from outside the voxel, although this comes at the cost of an increase in SAR. The second is not to set the amplitude of the pre-excitation inversion pulse to zero every other TR, but instead to shift the location of this ISIS plane such that the excited volume for the off condition is outside the object. This has been shown to greatly reduce lipid contamination, speculated to have arisen from the interaction between the RF pulse and lipid compartments due to incomplete relaxation, magnetization transfer, or the homonuclear Overhauser effect, although the exact mechanism remains unknown.
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"Classical" brown fat is found in highly vascularized deposits in somewhat consistent anatomical locations, such as between the shoulder blades, surrounding the kidneys, the neck, and supraclavicular area, and along the spinal cord. This is the smaller of the two types and has numerous small lipid droplets. Beige fat is the adrenergically inducible cell type that is dispersed throughout adipose tissue. It has greater variability in lipid droplet size and a greater proportion of mitochondria to lipid droplets than white fat, giving it a light brown appearance. In mouse and human organoid models, EPAC1 (exchange proteins directly activated by cAMP) was reported to preferentially increase the production of beige fat relative to WAT.
Sources: en.wikipedia.org
It consists mainly of animal experiments and small clinical reports, with much of the clinical material published in Russian-language journals. Large independent trials are scarce. Separating reliable effects from chance findings is consequently difficult.
A fraction of an intranasal dose is thought to reach the central nervous system, and this route is favoured partly for that reason. The proportion is not well characterized. Direct measurement in humans remains difficult with current methods.
Raised BDNF and NGF expression has been reported across several animal studies, which makes the signal fairly consistent. Whether the same change occurs in humans at usable doses is not established. It is best treated as a working hypothesis rather than a confirmed clinical mechanism.
It originated at the Institute of Molecular Genetics in Moscow during the 1980s. The work was carried out by a Russian research group that specialized in peptide neuropharmacology.