This is a working overview of Neurotrophic signalling, 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.
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 with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. It was derived from the ACTH(4-10) fragment, a short segment of adrenocorticotropic hormone that lacks the hormonal activity associated with the full-length peptide. Researchers at the Institute of Molecular Genetics in Moscow developed the compound during the 1980s. It has been registered as a pharmaceutical product in Russia and several neighbouring countries, where it is supplied as a nasal solution, and it is also sold internationally as a research chemical.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular class | Synthetic heptapeptide | Analog of an ACTH fragment |
| Amino acid length | Seven residues | Met-Glu-His-Phe-Pro-Gly-Pro |
| Origin | Moscow, 1980s | Institute of Molecular Genetics |
| Approved regions | Russia and some neighboring states | Not cleared in Western markets |
| Common trade names | Multiple national brands | Sold as a nasal formulation |
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.
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.
当时的短肽研究普遍关注能否穿越血脑屏障、在低剂量下产生中枢效应，Semax 属于这一路线。鼻内给药是其主要使用方式，俄语文献报道的适应症涵盖缺血性卒中、短暂性脑缺血发作、认知功能减退以及视神经病变。这些研究大多发表在当地期刊上，样本规模与终点设置同西方试验惯例存在差异，国际同行对其临床证据的强度看法不一。
各国监管态度分化明显。俄罗斯按处方药管理，部分东欧国家留有使用记录；欧盟与美国未批准其作为药物上市，市面流通品通常标注为研究用化学品。身份差异意味着标示含量、纯度与无菌性缺少统一核查。体育领域还牵涉反兴奋剂名录，跨境携带则受目的地药品法规约束。
=== Familia Rotary/R100 === In July 1968 Mazda added a Familia Rotary model to the range, offered in both two-door coupé and four-door saloon variants. Saloon models were given an additional "SS" nameplate. The Familia Rotary was powered by a 982 cc 10A Wankel rotary engine and the coupé version was sold outside Japan as the "Mazda R100". After an April 1970 update (known colloquially in Australia as the Series 2) it was known as the "Familia Presto Rotary" in Japan as the Presto nameplate was added into the entire Familia range. Power was rated at just 100 PS (74 kW) due to a small carburetor (thus the "R100" name). The rotary engined R100 has a unique front end design, with a more prominent pointed bonnet, grille, and bumper. The rear also gained its own design with twin round tail lights, which became for a time a signature design element for the rotary engined versions of Mazda's cars. Inside, the cars were more sumptuously appointed with plusher seats and chrome plated accents, full sized interior door trim panels, a floor mounted handbrake lever, and a unique cockpit styled dashboard with full instrumentation. Mazda referred to this dashboard as the "T-Dash", and fitted it to top spec piston engined variants of the Familia on the Japanese market as well as the rotary models.
Once a sequence has been isolated, it must be inserted into a vector. The easiest way to do this is to cut the vector DNA using restriction enzymes; if the same enzymes were used to isolate the target sequence, then the same "overhang" sequences will be created on each end allowing for hybridization. Once the target gene has hybridized to the vector DNA, they can be joined using a DNA ligase. An alternative strategy uses recombination between homologous sites on the target gene and the vector sequence, eliminating the need for restriction enzymes.
Physical side effects included pupil dilation, tingling, trembling, numbness, sweating, lightheadedness, athetosis, slight nausea, and increased heart rate and blood pressure. In addition to parenteral DMT, Shulgin described the effects of oral DMT plus harmaline or in some cases Peganum harmala seeds in TiHKAL. The effects were reported to include closed-eye imagery such as colors, infinitely repeated and wavy sheets of patterns, and kaleidoscopic images, visual changes like brighter colors and patterns and distortions, music enhancement, time distortion, clarity, insights, intoxication, emotional changes, feeling alive and excited, depression, despair, and feeling psychotic. Other effects included difficulty focusing on thoughts, short-term memory disruption, feeling cold, nausea, gait impairment or difficulty walking, and an afterglow. The preceding effects are variably due to both DMT and harmaline, with harmaline also producing its own hallucinogenic effects at sufficiently doses, for instance 150 mg or more.
Sources: en.wikipedia.org
=== Bradycardia or AV block === Unless a pacemaker is present, beta blockers can severely depress conduction in the AV node, resulting in a reduction of heart rate and cardiac output. One should be very cautious with the use of beta blockers in tachycardia patients with Wolff-Parkinson-White Syndrome, as it can result in life-threatening arrhythmia in certain patients. By slowing the conduction through the AV node, preferential conduction through the accessory pathway is favored. If the patient happens to develop atrial flutter, this could lead to a 1:1 conduction with very fast ventricular rate, or worse, ventricular fibrillation in the case of atrial fibrillation.
PKPD modeling (pharmacokinetic pharmacodynamic modeling) (alternatively abbreviated as PK/PD or PK-PD modeling) is a technique that combines the two classical pharmacologic disciplines of pharmacokinetics and pharmacodynamics. It integrates a pharmacokinetic and a pharmacodynamic model component into one set of mathematical expressions that allows the description of the time course of effect intensity in response to administration of a drug dose. PKPD modeling is related to the field of pharmacometrics. Central to PKPD models is the concentration-effect or exposure-response relationship. A variety of PKPD modeling approaches exist to describe exposure-response relationships. PKPD relationships can be described by simple equations such as linear model, Emax model or sigmoid Emax model. However, if a delay is observed between the drug administration and the drug effect, a temporal dissociation needs to be taken into account and more complex models exist:
== Education and early career == LeBlanc received his bachelor's degree in biology from the University of Massachusetts Dartmouth in 1975, followed by a Master's in Biology from Bridgewater State University in 1981. Following his Bachelor's, he started his professional career as an Aquatic Toxicologist at EG&G Bionomics in Wareham, Massachusetts in 1975, a position he held for five years. Subsequently, in 1980, he was appointed as the Director of Toxicology and held that position until 1983. He then joined the University of South Florida in Tampa in 1983 as a Research Associate and received his Ph.D. in biology in 1986. From 1986 to 1989 he served as a Research Fellow in the Department of Biological Chemistry & Molecular Pharmacology and Dana-Farber Cancer Institute at Harvard Medical School where he completed his post-doctoral training.
Sources: en.wikipedia.org
Network analysis seeks to understand the relationships within biological networks such as metabolic or protein–protein interaction networks. Although biological networks can be constructed from a single type of molecule or entity (such as genes), network biology often attempts to integrate many different data types, such as proteins, small molecules, gene expression data, and others, which are all connected physically, functionally, or both. Systems biology involves the use of computer simulations of cellular subsystems (such as the networks of metabolites and enzymes that comprise metabolism, signal transduction pathways and gene regulatory networks) to both analyze and visualize the complex connections of these cellular processes. Artificial life or virtual evolution attempts to understand evolutionary processes via the computer simulation of simple (artificial) life forms.
The fission of one atom of uranium-235 releases 202.5 MeV (3.24×10−11 J) inside the reactor. That corresponds to 19.54 TJ/mol, or 83.14 TJ/kg. Another 8.8 MeV escapes the reactor as anti-neutrinos. When 23592U nuclei are bombarded with neutrons, one of the many fission reactions that it can undergo is the following (shown in the adjacent image):
The first long-acting analogue, insulin glargine, was approved in 2000. Insulin aspart, insulin glulisine, and insulin detemir were all approved by 2005. The second wave of insulin analogues, which include insulin degludec and insulin icodec, started in the 2010s. Insulin analogues are on the World Health Organization's List of Essential Medicines.
== Discovery of optical activity == In 1843, Louis Pasteur discovered optical activity in paratartaric, or racemic, acid found in grape wine. He separated two enantiomer crystals that rotated polarized light in opposite directions.
Sources: en.wikipedia.org
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.
It is registered as a medicine in Russia and has been used clinically there for decades. No regulatory agency in Western Europe or North America has approved it for any indication.
Semax corresponds to the four-to-ten fragment of adrenocorticotropic hormone. Because it omits the first three residues, it lacks the adrenal-stimulating action of the full hormone.
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.