If you have been reading about Semax 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.
Last reviewed on 2025-10-10. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
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.
Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. Its chain combines the first seven residues of corticotropin with a C-terminal proline-glycine-proline extension, a modification intended to slow enzymatic breakdown. The free peptide has a molecular mass near 813.9 daltons. It belongs to the class of ACTH-derived fragments studied for central nervous system activity rather than for adrenal steroid stimulation. This structural relationship to a natural hormone fragment is the usual starting point for describing the compound in the literature.
| 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 seven-amino-acid peptide whose sequence extends the ACTH(4-10) fragment with a C-terminal proline-glycine-proline tripeptide. The commonly cited sequence is Met-Glu-His-Phe-Pro-Gly-Pro, giving a molecular formula near C37H51N9O10S and a molecular weight close to 813.9 g/mol. It belongs to the broader class of synthetic ACTH fragments studied for central nervous system effects rather than for adrenal steroid stimulation. In practice the material appears as a lyophilized white powder for laboratory work or as a dilute saline solution in clinical settings.
Development is attributed to researchers at the Institute of Molecular Genetics in Moscow during the early 1980s, building on earlier Soviet work with ACTH fragments. Russian regulatory approval followed for intranasal use, and the compound has remained commercially available there for decades. Most published human data originate from Russian and, later, some Eastern European clinical reports, which are not always accessible in English translation. Outside that region the material is generally handled as a research chemical rather than a licensed medicine.
Regulatory status differs sharply between jurisdictions. In Russia the peptide is registered as a prescription nasal preparation, while agencies such as the United States Food and Drug Administration have not approved it for any indication. Products sold elsewhere are typically labeled for laboratory research only, and such labels shift responsibility for safe handling to the purchaser. Because the same name covers pharmaceutical-grade nasal drops and bulk research powder, identity and purity documentation becomes the main practical concern when comparing sources.
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.
All the Rh(III) halides are known. Synthesis of many rhodium complexes begin with RhCl3·3H2O, the hydrated trichloride, but RhCl3, the anhydrous form, is largely inert. Other rhodium(III) chlorides include sodium hexachlororhodate, Na3RhCl6, and pentaamminechlororhodium dichloride, [Rh(NH3)5Cl]Cl2. They are used in the recycling and purification of this very expensive metal. Heating a methanolic solution of hydrated rhodium trichloride with sodium acetate gives the blue-green rhodium(II) acetate, Rh2(O2CCH3)4, which features a Rh–Rh bond. This complex and related rhodium(II) trifluoroacetate have attracted attention as catalysts for cyclopropanation reactions. Heating treated with triphenylphosphine in ethanol, hydrated rhodium trichloride converts to RhCl(P(C6H5)3)3. This square planar complex, which is known as Wilkinson's catalyst, is a common and early example of a well-defined homogeneous catalyst for hydrogenation of alkenes.
=== Laboratory evaluation === Polycythemia is often initially identified on a complete blood count (CBC). The CBC is often repeated to evaluate for persistent polycythemia. If an etiology of polycythemia is unclear from history or physical, additional laboratory evaluation might include:
==== Levels of severity ==== The use of the body mass index in the diagnosis of eating disorders has been controversial, largely owing to its oversimplification of health and failure to take into account complicating factors such as body composition or the initial bodyweight of the patient prior to the onset of AN. As such, the DSM-5 does not have a strict BMI cutoff for the diagnosis of anorexia nervosa, but it nevertheless uses BMI to establish levels of severity, which it states as follows:
Sources: en.wikipedia.org
=== Credibility and validity of testimony === The credibility of individuals with personality disorders has been questioned at least since the 1960s. Two concerns are the incidence of dissociation episodes among people with BPD and the belief that lying is not uncommon in those diagnosed with the condition.
The defense along the Vistula took place from August 1944 until the renewed Soviet offensive in January 1945. By January 1945, the 4th Panzer Army was holding static defensive positions on Hitler's direct orders and during the lull in the fighting it had created a defensive zone in southern Poland. On 1 January 1945, the 4th Panzer Army, then under Army Group A, had a total strength of 133,474 men spread across seven infantry divisions (68th, 72nd, 88th, 168th, 291st, 304th, 342nd), two Panzergrenadier divisions (10th, 20th), two panzer divisions (16th, 17th), two autonomous brigades, an autonomous regiment and several autonomous artillery detachments. With its manpower, it was the largest single contributor to Army Group A's overall manpower of 400,556. Unknown to the Wehrmacht, the Soviet command planned to saturate the entire defensive zone with artillery bombardment. The Red Army began their Vistula–Oder Offensive on January 17, quickly encircling the LVI Panzer Corps and destroying half of all armoured forces concentrated with the 4th Panzer Army. The commander of the LVI Corps, General Johannes Block, was killed in action on 26 January. The remnants of the army retreated along the entire front before re-grouping on the western bank of the Oder River in February 1945. The Red Army halted its offensive in February 1945. The 3rd Panzer Army was tasked to halt the Soviets in the north, while the 9th Army was guarding against the Soviets in the centre.
In the proposed biosynthetic pathway, Scheme 1, L-Phe (1) is used as the starting material. It is converted into Cinnamic acid (2) via phenylalanine ammonia lyase (PAL). Then it is turned into p-Coumaric acid (3) with use of cinnamate 4-hydroxylase (C4H). 4-coumarate:CoA ligase (4CL) is then used to get p-Coumaroyl-CoA (5). P-Coumaroyl shikimate transferase (CST) is the enzyme that is responsible for the bonding of shikimic acid and p-Coumaroyl-CoA. The complexed (5) is then selectively oxidized at C3 by p-coumaroyl 5-O-shikimate 3'-hydroxylase (CS3'H) to alcohol. With another action of CST, shikimate is broken off from this intermediate, thereby yielding Caffeoyl-CoA (7). In order to get desired substitution pattern on the aromatic ring, caffeoyl-CoA O-methyltransferase (CCOMT) converts the hydroxyl group at C3 into methoxy as seen in Feruloyl-CoA (8). Up until this step, according to Ramirez-Ahumada et al., the enzyme activities are very active. It is speculated that some polyketide synthases (PKS) and reductases are involved in final synthesis of 6-Gingerol (10).
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 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.