intranasal delivery comes up often in conversation and rarely with the context attached. Here we lay out the basics in order, then work through the practical considerations.
Last reviewed on 2025-09-01. Where a claim depends on a specific study, the study is described rather than over-claimed.
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.
Proposed mechanisms center on neurotrophic signaling rather than on classical melanocortin receptor activation. Rodent experiments have reported shifts in the expression of brain-derived neurotrophic factor and nerve growth factor after administration, together with changes in the associated receptor systems. Several authors argue that the peptide acts largely through its degradation products and their interaction with peptidergic pathways, but this remains a hypothesis rather than a settled finding. No single molecular target has been identified in a way that the field broadly accepts.
Published research covers ischemic stroke, traumatic brain injury, cognitive impairment, optic nerve conditions and attention-related measures. Much of the human evidence comes from small trials conducted in one country, which limits how far the results generalize. Animal models supply the larger share of the data, and effects seen in rodents do not transfer automatically to people. Reviews have noted that methodological reporting is often incomplete, making it difficult to pool results or compare treatment schedules across studies.
Pharmacokinetic accounts emphasize rapid breakdown. After intravenous dosing the intact peptide disappears from blood within minutes, and nasal delivery produces low but measurable concentrations. Metabolites rather than the parent molecule may account for part of the observed activity, although the relative contribution is unresolved. Dosing in the literature varies widely and no optimal schedule has been agreed. These gaps are regularly cited as a reason the findings have not produced broad clinical adoption beyond the original research setting.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C37H51N9O10S | Free acid form of the heptapeptide; depends on terminal groups |
| Molecular mass | About 813.9 g/mol | Average mass used for mass spectrometry confirmation |
| Appearance | White to off-white solid | Supplied as a lyophilised powder; hygroscopic |
| Solubility class | Freely soluble in aqueous media | Water, saline, and phosphate buffers; limited organic solubility |
| Typical storage temperature | -20 degrees Celsius | Long term and dry; short working periods may use 2 to 8 degrees Celsius |
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.
Identity and purity of semax are established with reversed-phase high-performance liquid chromatography coupled to ultraviolet detection, usually at 214 nanometres. Mass spectrometry, most often electrospray ionisation in positive mode, confirms the molecular mass and reveals truncated sequences. Amino acid analysis and peptide mapping after enzymatic digestion provide additional structural confirmation. Laboratories typically report purity as the percentage area of the main peak, a figure that does not capture isomeric or oxidised variants unless the method resolves them.
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.
It has been long observed that the licking of their wounds by dogs might be beneficial. Indeed, a dog's saliva is bactericidal against the bacteria Escherichia coli and Streptococcus canis, although not against coagulase-positive Staphylococcus or Pseudomonas aeruginosa. Wound licking is also important in other animals. Removal of the salivary glands of mice and rats slows wound healing, and communal licking of wounds among rodents accelerates wound healing. Communal licking is common in several primate species. In macaques, hair surrounding a wound and any dirt is removed, and the wound is licked, healing without infection. An Elizabethan collar may be used on pet animals to prevent them from biting an injury or excessively licking it, which can cause a lick granuloma. These lesions are often infected by pathogenic bacteria such as Staphylococcus intermedius. Horses that lick wounds may become infected by a stomach parasite, Habronema, a type of nematode worm. The rabies virus may be transmitted between animals, such as the kudu antelopes by wound licking of wounds with residual infectious saliva.
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Sources: en.wikipedia.org
== History == DOBU was first described in the literature by Alexander Shulgin in 1970. Subsequently, it was described in greater detail by Shulgin in his book PiHKAL (Phenethylamines I Have Known and Loved) in 1991.
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=== Legal === This technique is also used for detection of illicit drugs in various samples. The most common method of drug detection has been an immunoassay. This method is much more convenient. However, convenience comes at the cost of specificity and coverage of a wide range of drugs, therefore, HPLC has been used as well as an alternative method. As HPLC is a method of determining (and possibly increasing) purity, using HPLC alone in evaluating concentrations of drugs was somewhat insufficient. Therefore, HPLC in this context is often performed in conjunction with mass spectrometry. Using liquid chromatography-mass spectrometry (LC-MS) instead of gas chromatography-mass spectrometry (GC-MS) circumvents the necessity for derivitizing with acetylating or alkylation agents, which can be a burdensome extra step. LC-MS has been used to detect a variety of agents like doping agents, drug metabolites, glucuronide conjugates, amphetamines, opioids, cocaine, BZDs, ketamine, LSD, cannabis, and pesticides. Performing HPLC in conjunction with mass spectrometry reduces the absolute need for standardizing HPLC experimental runs.
Sources: en.wikipedia.org
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.
It appears in Russian pharmaceutical listings as a nasal formulation, but it is not an authorised medicine in the United States or the European Union. Outside those markets it is normally encountered as a research chemical rather than a prescription product.
Laboratory and animal work points to melanocortin signalling and changes in neurotrophic factor levels, especially brain-derived neurotrophic factor. The exact receptor targets and the degree to which these findings transfer to humans are still unresolved.
The main proposal is modulation of neurotrophic factors such as brain-derived neurotrophic factor, supported largely by animal experiments. Receptor-level targets have not been firmly established. Most reviews describe the mechanism as only partially characterized.