Bromantan is not a peptide or a protein. Chemically, it is a synthetic small molecule based on the adamantane scaffold derived from adamantane. Scientific research on bromantan included fatigue-related symptoms, behavioral responses, and neurochemical signaling, rather than the properties of a compound composed of amino acids.
The scientific literature also includes the names bromantane and Ladasten. The chemical identity of the substance is relatively well established, but many broader claims regarding cognitive function, motivation, safety, and performance go beyond the findings of available human studies. 1 2
A thorough discussion requires a distinction between chemical identification and the strength of evidence regarding biological or clinical effects. The chemical database can confirm molecular identifiers, but does not prove clinical efficacy. Similarly, a favorable outcome of an animal experiment does not mean that an equivalent effect will occur in humans.
What is bromantan? Names, synonyms and identity
Differences in nomenclature are of practical importance when reviewing the literature. Publications indexed under the name Ladasten may belong to the history of research on the same substance, even if their title does not include the English name bromantane.
On the other hand, commercial offers using one of these names do not constitute scientific confirmation of identity. The chemical documentation, the description of the study, and the actual documentation of the analyzed sample must be considered separately.
Bromantane and bromantan are alternative spellings of the same chemically defined substance, and not the names of separate analogues. Ladasten is the name of a medicinal product or a development name widely used in Russian-speaking clinical literature.
In a study in rats, Ladasten was unequivocally identified as N-(2-adamantyl)-N-(para-bromophenyl)amine, which links the experimental name to a specific chemical structure. 1 3
The substance identification system maintained by the FDA contains bromantan under the identifier N1ILS53XWK.
This is an entry regarding the identity of the substance, not proof of the drug’s approval by the FDA. Regulatory databases can include substances for many reasons, including to track and standardize names.
The existence of the entry cannot be interpreted as a positive decision regarding the balance of benefits and risks. 4
The identity of the active substance should not be confused with the identity or quality of the finished product.
The tablet, oil preparation and research powder can be marketed under the name bromantan, while at the same time differing in composition and available evidence regarding their properties.
The study of one preparation does not confirm the authenticity of another or an equivalent exposure.
During the evaluation of the claim, the chemical substance, the formulation actually being tested, and the publication describing the result must be identified.
Searching exclusively for the term „bromantane peptide” may lead to the omission of relevant literature, while perpetuating a flawed molecular classification.
How is bromantan classified? Peptide, protein, mixture, or other substance?
It is worth distinguishing three levels of terminology.
The structural category informs us about the type of molecule we are dealing with. The pharmacological description indicates the effect studied under specific experimental conditions. Therapeutic indication, however, requires clinical evidence and an appropriate regulatory decision.
Moving from the first category to the third without confirmatory tests leads to misleading conclusions.
In structural chemistry, bromantan belongs to the family of small organic compounds derived from adamantane.
It has a cage-like carbon structure connected by an atom of nitrogen with a brominated aromatic group.
It does not consist of amino acid residues linked in a peptide chain and is not a protein. 1
Terms such as psychostimulant, anxiolytic substance, antistaminic agent or aktoprotector refer to the investigated functional effects, not to the chemical class of the molecule.
They therefore do not describe the same thing as molecular classification.
For example, the term „antistaminic” refers to studies concerning the weakening or symptoms associated with fatigue, while „adamantane derivative” describes the chemical structure.
In clinical literature, these functional terms appear in the context of specific research populations. 2 5
The term „nootropic” also appears in discussions about bromantane, especially outside of formal clinical trials.
However, it does not mean a standardized therapeutic indication, does not prove an improvement in cognitive function in healthy individuals, nor suggests the absence of adverse effects.
The claim regarding memory requires an appropriate end-point for evaluating memory. The claim regarding alertness requires an appropriate measurement of alertness.
None of these effects are automatically derived from the general label.
| Term | What does it mean |
|---|---|
| Derivative of adamantane | Structural relationship with the chemical skeleton of adamantane |
| A small molecule | Useful distinction between peptide chains and large proteins |
| Studies on anti-asthmatic activity | Analyzing symptoms related to fatigue or weakness |
| Psychostimulant or anxiolytic substance | Description of the effects studied in specific experiments |
| A product described as a nootropic | Marketing terminology requiring separate proofs |
| Peptide | Incorrect classification of bromantane |
The structure and composition of bromantane – what has been confirmed?
The summary pattern and the CAS number are useful for matching scientific documentation, but none of these identifiers confirms the quality of the commercial sample.
Two preparations bearing the same chemical name may differ in impurities, degradation products, concentration, and additional ingredients.
These differences are particularly important when comparing a historical clinical study with a preparation whose production and quality testing have not been documented.
According to the cited entry in PubChem, bromantan has a molecular formula of C₁₆H₂₀BrN and an approximate molecular mass of 306.24 g/mol.
The commonly given CAS number is 87913-26-6, and the compound identifier in the PubChem database is 4660557.
These identifiers help distinguish the molecule from products with similar names. 1
Bromantan does not have an amino acid sequence because its structure does not consist of residues linked by peptide bonds.
The compound containing the nitrogen atom is not a repeating amide backbone characteristic of peptides.
The question about the „peptide sequence of bromantane” therefore uses an incorrect way of describing the structure.
Even a well-described chemical structure of a compound does not specify the content of each specific sample.
Analytical studies would have to determine whether a given preparation contains the intended molecule, what its quantity is, and whether significant impurities or degradation products can be detected.
The compliance of the name or the nominal mass stated on the label is not sufficient.
Analytical purity, the actual content of the compound and the properties of the final formulation constitute separate parameters that must be documented independently.
A high percentage of chromatographic purity does not automatically determine the amount of active substance in the container or confirm its biological usefulness.
In the case of an oil-based preparation or another multi-component product, the carrier introduces additional formulation issues that the chemical formula of bromantane does not address on its own.
Scientific studies on bromantane – evidence in humans, animals and in the laboratory
Studies in people with asthenic disorders
These publications should be evaluated as a collection of studies with different methodological approaches, rather than being combined into a single aggregate assessment of effectiveness.
Randomized comparisons provide other information about the causal relationship than uncontrolled clinical observations.
Short follow-up after completion of treatment also does not answer all questions regarding the durability of the response or delayed adverse effects.
If only an indexed summary is available, it is better to point out the lack of methodological details than to draw unwarranted conclusions.
In a pilot phase 2 study published in 2006, Ladasten was evaluated in people diagnosed with psychogenic asthenic disorder.
The indexed English-language summary describes the results related to the stimulant effect and anxiety symptoms, but contains limited information allowing for an independent assessment of the sample size, the magnitude of the effects, and the risk of systematic error.
The publication confirms the conduct of clinical trials, but does not justify the provision of precise numerical results that are absent from the available description. 2
In 2009, researchers described a blinded, randomized, placebo-controlled comparison for neurasthenia.
The observation during treatment lasted 28 days, after which there was an additional week-long period with placebo.
The researchers reported greater improvement in the basic asthenic symptoms in the Ladasten group.
Short follow-up after completion of treatment is important for assessing withdrawal symptoms, but it cannot confirm that dependence or withdrawal symptoms are impossible with every exposure method. 5
A separate multicenter publication described the observations of 728 patients with asthenic disorders, who were included in the study at 28 centers in Russia.
Improvements in symptoms and a relatively small number of reported adverse reactions were described during a short follow-up period.
The indexed summary does not describe a parallel placebo group, therefore the reported rates of response should not be interpreted as effects of treatment adjusted for placebo. 6
In subsequent studies, the relationships between subjective patient reports, objective observations, personality-related parameters, and EEG characteristics and the response to the intervention under study were analyzed.
These experiments highlight the complexity of subjective responses to treatment.
However, they do not confirm the existence of a validated EEG test used to select bromantane treatment in routine practice. 7
Studies in animals and in the laboratory
Mechanistic studies allow for the measurement of changes that are difficult to directly observe in routine clinical studies, such as enzyme expression or electrical responses in tissue preparations.
This precision is valuable when formulating hypotheses.
At the same time, it narrows the interpretation of the results: observation in the hippocampus tissue of rats does not quantify the improvement in attention, work performance, or memory in humans.
Experiments on rats focused on enzymes involved in dopamine synthesis, neurochemical changes in specific brain regions, and the time of occurrence of the observed responses.
These are mechanistic observations obtained in an experimental system.
They cannot be directly translated into guaranteed increases in motivation, concentration, or productivity in people. 8
In an experimental study from 2007, neurochemical analyses in rats were combined with electrophysiological studies of hippocampal tissue.
The effect on the parameters related to tyrosine hydroxylase and the intensification of synaptic amplification were reported in a laboratory preparation.
The result regarding synaptic plasticity helps to form hypotheses about neuronal mechanisms, but it is not a clinical memory test. 3
An appropriate summary of the evidence should therefore take into account their different levels of importance.
There are studies involving humans, but they focus on specific populations defined by symptoms and include a relatively limited database of publications.
Animal studies and laboratory experiments provide a mechanistic context, leaving many contemporary consumer claims unresolved.
The mechanisms of action of bromantane studied scientifically
It is also necessary to distinguish between changes in the mechanisms responsible for the synthesis of neurotransmitters and the confirmed clinical effect.
For example, increased enzyme expression does not necessarily mean a proportional increase in the release of a neurotransmitter in every area of the brain.
The relationship between molecular measurements and behavior involves additional regulatory, temporal, and compensatory processes that a single experiment does not explain.
A significant part of mechanistic literature concerns the pathways related to dopamine production and signaling.
Hydroxylase of tyrosine participates in the conversion of tyrosine leading to the synthesis of dopamine, while decarboxylase of aromatic L-amino acids takes part in the later stage.
In studies in rats, changes in the expression of these enzymes and in regional parameters related to dopamine were reported.
These effects depend on the type of tissue, the time point, and the experimental conditions. 8
The observation of these should not be simplified into the claim that bromantan is a direct agonist of dopamine receptors.
The study of preparations derived from rats did not show a direct effect on the analyzed D1, D2 and D3 receptors, while indicating effects regarding the biosynthesis, release and transport of dopamine under the tested conditions.
The results support a more cautious description than the statement that the substance „activates dopamine receptors”. 9
Experiments on the hippocampus also included protein synthesis and processes sensitive to dopamine, related to synaptic enhancement.
Pharmacological interruption of the experimental effect may indicate a pathway that requires further investigation, but it does not prove that the same pathway is responsible for every clinical response.
The mechanism may be biologically plausible, although it has not yet been fully confirmed in humans. 3
Claims of lasting restoration of normal dopamine levels, repair of the brain, or the creation of a lifelong improvement in cognitive function require evidence beyond these experiments.
To justify such statements, researchers would need appropriate measurements in humans, lasting results, and a convincing consideration of alternative explanations.
The cited studies do not support such broad conclusions.
Limitations of scientific evidence regarding bromantane
The differences between the formulations create an additional evidentiary gap.
A significant portion of the named clinical trials concerns Ladasten used under certain conditions.
Transferring these results to any powder, oil preparation, or other commercial form would be unreasonable without evidence of comparable exposure and product quality.
The same caution applies when the seller uses research terminology to suggest regulatory approval.
The interpretation of clinical literature requires special attention to the methodological design, the availability of results, and the completeness of the reporting.
Some available summaries are short, and some publications come from overlapping research communities.
The number of publications should not be equated with the number of independent studies that confirm them.
A large uncontrolled study and a smaller randomized study answer different questions.
Another important limitation is the number of diagnostic populations represented in the publications.
Neurasthenia and asthenic disorders are not equivalent to all causes of fatigue, depression, ADHD, or problems with concentration.
Improvement in a specific scale of symptoms does not confirm the treatment of another disease or an improvement in cognitive functions in healthy people.
Any statement regarding tolerance or safety should take into account the duration of the participants' observation and the types of adverse reactions that were actively evaluated.
Short-term studies can identify frequent events and direct tolerance, but provide less information about rare effects, long-term exposure, pregnancy, interactions, or improper use.
The absence of a reported event is particularly difficult to interpret when the surveillance methods and the number of people subject to observation are unclear.
The favorable formulations used by the authors of the original studies should therefore be distinguished from the comprehensive safety conclusion. 6
The prohibition on use in sports is a separate regulatory issue from chemical identity and medical effectiveness.
The WADA list of substances and methods banned for 2026 lists bromantan in category S6.A, which includes non-specific stimulants prohibited during competitions.
This classification does not confirm a specific clinical benefit and should not be confused with the decision on the marketing authorization of the drug that applies in all countries. 10
Frequently asked questions about bromantan
1. Does bromantan mean a specific substance?
Yes. Bromantan identifies a specific small molecule with established chemical identifiers and a defined structure. However, this does not guarantee that every product using this name contains the same verified material or formulation. The identity of the substance must be distinguished from the confirmation of the authenticity of a specific sample. 4 Chemical identifiers allow databases and publications to be combined, but verification of a single batch requires appropriate analytical documentation. Differentiation is particularly important when a product uses a known synonym without indicating the source of production.
2. What do the available studies on bromantane confirm?
Studies confirm that bromantane has been studied in humans with aphasias and in animal and laboratory experiments regarding neuronal mechanisms. The evidence does not support all the claimed claims about memory, motivation, or performance in healthy individuals. Conclusions must remain linked to the population actually studied and the result. 5 3 The most justified interpretation refers to specific populations: the symptoms of asthenia were studied, whereas claims regarding healthy users require a different evidence base. The design of the study and the availability of numerical results also influence the certainty of the interpretation of the reported effect.
3. Is bromantan a peptide or a protein?
No. It is an organic compound derived from adamantane, not an amino acid chain. Placing it alongside peptides in the catalog does not change its chemistry. Molecular classification should be based on a confirmed structure, not on a commercial category chosen by the seller. 1 Peptides contain amino acid residues linked by characteristic bonds, whereas bromantan has an organic backbone associated with adamantan. Its presence in the peptide catalog therefore constitutes a classification error rather than a new biochemical discovery.
4. Are bromantan and bromantane different compounds?
No. These are alternative names for the same compound. Searching for both entries can improve the discovery of scientific publications, especially in the case of different transliterations. However, matching the name is only the first step. Before comparing the results, it is also necessary to check the formulation and research methods. 4 Transliteration and regional naming practices explain why more than one spelling appears in the literature. Researchers should compare molecular identifiers before accepting publications with different titles as evidence regarding separate substances.
5. Is Ladasten a substance that is not associated with bromantan?
No. Ladasten is the name used for bromantane in much of the clinical and experimental literature. The original publication in the field of neuropharmacology unequivocally links this name with the chemical identity of the adamantane derivative compound. It should not be considered a separate analog simply because the studies use a different name. 3 This correlation is important when tracking older Russian-language publications and later mechanistic studies. However, the common name of the drug does not guarantee that the different formulations or research protocols were identical.
6. Does the anti-asthmatic effect prove an improvement in cognitive function?
No. Reducing fatigue-related symptoms and improving cognitive function are different outcomes. To justify a claim about memory or attention, the study must use appropriate cognitive measures, rather than relying on a general relationship of better well-being. Improvement in symptoms may be meaningful without confirming a broader effect enhancing cognitive functions. 2 Fatigue, attention, memory, and daily functioning should be measured using tools appropriate for each outcome. Improvements in the scale of asthenia cannot be transformed into a quantitative increase in learning ability or concentration without direct tests.
7. Does the mechanism related to dopamine evidence greater motivation?
No. Neurochemical measurements do not directly measure motivation, and behavioral consequences depend on the conditions and the individual. The results of studies in rats provide hypotheses for further research in humans, not a predictable psychological effect. A credible claim about motivation requires direct evidence in humans with appropriate control groups. 8 The result regarding enzyme expression is an indirect biological observation, not a measure of motivation. Even repeated neurochemical changes leave questions about the timing of the effect, its regional specificity in the brain, and its significance for human behavior.
8. Is bromantan a direct agonist of dopamine receptors?
The receptor study cited does not support such a simple description. In preparations derived from rats, no direct effect on the studied subtypes of dopamine receptors was shown, although other dopamine-related effects were reported. These results should not be interpreted as ruling out all possible receptor interactions. 9 The observation concerns the tested receptor subtypes and experimental conditions. It is more precise to describe the research hypothesis related to dopamine than to unconditionally attribute the substance to a receptor agonist mechanism.
9. Do experiments on memory in animals confirm the improvement of memory in humans?
No. Laboratory measurements such as synaptic potentiation are not the same as information retention in everyday life. Transferring the results requires human studies and evidence that the potential improvement is significant and repeatable. Interest in the mechanism alone is not sufficient to confirm a clinical effect on memory. 3 Experimental potentiation is one of the possible indicators of neuronal plasticity, but it does not replace validated memory assessment. Translational studies would have to demonstrate reproducible cognitive outcomes in a relevant human population.
10. Does a large observational study prove effectiveness?
Not in itself. A large trial allows for a more accurate description of the observed experiences, but it does not eliminate the placebo effect, the changes that occur over time, or selection bias. The multi-center publication on Ladasten provides information, but its results should not be presented as if they come from a large controlled placebo comparison. 6 Without an appropriate control group, changes may reflect expectations, regression to the mean, parallel care, or natural variability. A large number of participants can increase the precision of the observations, leaving the question of the causal relationship unresolved.
11. Has it been shown that bromantan cannot cause withdrawal symptoms?
No. A short study in which no withdrawal syndrome was reported cannot confirm that withdrawal symptoms are impossible after prolonged or different exposure. The 2009 study provides limited post-treatment observation, not a universal guarantee. The safety description should maintain this distinction. 5 The length of observation and the size of the population studied limit the significance of any negative result. Long-term exposure, other preparations, and less selective users may be associated with questions that a short study did not analyze.
12. Can the EEG model determine who will benefit?
The available EEG study does not confirm the validated clinical guideline for patient selection. It analyzed the relationships between patient characteristics and responses, including responses to placebo. Transforming such associations into a useful decision-making tool would require prospective validation and evidence that the tool improves outcomes. 7 The association observed during the exploratory analysis may help in designing a subsequent study. Before clinical use, the proposed EEG marker would require previously established thresholds, independent validation, and confirmation of predictive value.
13. Does the substance identifier in the FDA database mean FDA approval?
No. The substance identifier serves to standardize the chemical identity and is not an authorization to place the drug on the market for a specific use. Approval requires separate regulatory documentation for the specific product. Therefore, the listing of bromantan in the registry should be cited as the source of information about the identity, not as proof of approval. 4 An identification entry can exist even when the finished drug has not been approved for sale. Registration of the substance and the authorization of the product for sale address fundamentally different regulatory questions.
14. Is bromantan allowed during competitions in accordance with WADA regulations?
No. The WADA list for 2026 lists bromantan as a banned stimulant during competitions. This statement applies to specific anti-doping regulations and the given year, not to a general legal request regarding the possession or prescription of substances. The rules should be checked independently of product advertisements. 10 Anti-doping restrictions relate to participation in accordance with the relevant sports regulations. They should not be equated with the status of drug approval, the authenticity of the product, or evidence of performance improvement.
15. Do the studies of the tablets confirm the properties of the oil product?
Not automatically. Different formulations can alter the exposure, stability, and significance of the remaining ingredients. Evidence regarding the investigated product does not confirm the equivalence of an unverified product bearing the same substance name. Such a comparison would require analytical and clinical information regarding the specific formulation. Changes in the carrier and composition of the product can affect properties that were not evaluated in the original clinical studies for the alternative product. Without adequate evidence of the comparability of the test results for the tablets, it is not possible to generalize to a separate oil product.
16. Does good short-term tolerance prove long-term safety?
No. Short periods of observation provide limited information about rare events and repeated or prolonged exposure. The reported tolerance in a multicenter study should be interpreted in the context of the actual observation time. A broader safety conclusion requires more extensive surveillance and appropriate long-term data. 6 Detecting frequent short-term events and rare long-term harms requires different numbers of trials and observation periods. The reassuring results of a short study cannot establish a complete safety profile for all potential users and types of exposure.
17. What makes the claim regarding bromantane scientifically credible?
A credible claim identifies the study design, population, comparator, and measured outcome, then explains the uncertainty. It does not transform the mechanism observed in rats into a guarantee of effect in humans, nor does it relate improved symptoms to universal claims about cognitive functions. The ability to trace information back to the original study is more useful than the general label „nootropic.” Value claims are detailed enough to be tested in a study, and cautious enough to reflect their limitations. Statements that omit the population, comparator, and endpoint are particularly prone to exaggeration.
Applications
The most reliable interpretation of literature does not consist either in rejecting the reported studies or in exaggerating their significance.
The chemical identity of bromantane has been determined; specific clinical observations have been reported in populations with asthenic symptoms, and dopamine-related mechanisms have been experimentally analyzed.
Claims about broad improvements in cognitive function, universal safety, or the equivalence of products produced in different ways remain separate questions that require direct evidence.
Bromantan is a chemically defined small molecule that is not a peptide. Available evidence includes limited clinical literature involving humans, as well as a broader set of laboratory and animal studies.
A reliable description separates the confirmed chemical structure from proposed mechanisms, and clinical claims that have not been sufficiently studied.
The results of studies on asthenic symptoms should not be generalized to all purposes related to cognitive functions or performance.
The article provides an overview of the evidence, not a protocol of treatment or an assessment of the product offered by any vendor.
Educational and medical warnings regarding safety and regulations
The article is purely educational and scientifically informative. It summarizes the identity of bromantane as well as the scope and limitations of the published studies. It does not constitute medical advice, diagnosis, therapeutic recommendations, or instructions for self-experimentation. It does not include instructions for dosage, administration, formulation preparation, or purchase.
The results of the studies involving humans discussed here come from specific populations and research projects. They should not be interpreted as evidence of the efficacy of bromantane in ADHD, depression, improved memory, productivity, athletic performance, or in other conditions not confirmed in these studies. Animal experiments, enzymatic measurements, and electrophysiological results do not demonstrate equivalent clinical effects in humans.
Safety and regulatory status are separate issues from molecular identity. Entry in a chemical database, publication, analysis certificate, or description of a commercial product do not confirm drug approval, pharmaceutical equivalence, long-term safety, or suitability for human use. Regulations vary among jurisdictions and may change. The article also describes the ban on bromantane use during competitions in accordance with the WADA list for 2026. Current sports regulations should be checked in the applicable official documentation.
In this review, neither the authenticity was confirmed nor any product originating from an external supplier was evaluated. Individuals with health-related questions should consult with appropriately qualified medical personnel, rather than using the article as the basis for therapeutic decisions. The references were retained from the original article and were not independently re-verified during this editorial process.
References
- National Center for Biotechnology Information. (n.d.). PubChem compound summary for CID 4660557, Bromantan. Retrieved October 23, 2026. https://pubchem.ncbi.nlm.nih.gov/compound/4660557
- Siuniakov, S. A., Grishin, S. A., Teleshova, E. S., Neznamov, G. G., & Seredenin, S. B. (2006). [Pilot clinical trial of ladasten]. Experimental and clinical pharmacology, 69(4), 10–15. https://pubmed.ncbi.nlm.nih.gov/16995430/
- Mikhaylova, M., Vakhitova, J. V., Yamidanov, R. S., Salimgareeva, M. K. h., Seredenin, S. B., & Behnisch, T. (2007). The effects of ladasten on dopaminergic neurotransmission and hippocampal synaptic plasticity in rats. Neuropharmacology, 53(5), 601–608. https://doi.org/10.1016/j.neuropharm.2007.07.001
- U.S. Food and Drug Administration. (n.d.). Bromantane: N1ILS53XWK [Substance identity record]. Retrieved October 23, 2026. https://precision.fda.gov/ginas/app/ui/substances/N1ILS53XWK
- Neznamov, G. G., Siuniakov, S. A., Teleshova, S. E., Chumakov, D. V., Reutova, M. A., Siuniakov, T. S., Mametova, L. E., Dorofeeva, O. A., & Grishin, S. A. (2009). [Ladasten, the new drug with psychostimulant and anxiolytic actions in the treatment of neurasthenia (results of the comparative clinical study with placebo)]. Journal of Neurology and Psychiatry named after S.S. Korsakov, 109(5), 20–26. https://pubmed.ncbi.nlm.nih.gov/19491814/
- Voznesenskaia, T. G., Fokina, N. M., & Iakhno, N. N. (2010). [Treatment of asthenic disorders in patients with psychoautonomic syndrome: results of a multicenter study on efficacy and safety of ladasten]. Journal of Neurology and Psychiatry named S.S. Korsakov, 110(5 Pt 1), 17–26. https://pubmed.ncbi.nlm.nih.gov/21322821/
- Neznamov, G. G., Bochkarev, V. K., Reutova, M. A., Shabanova, A. A., & Siuniakov, S. A. (2012). [Self-evaluated Ladasten versus placebo effect by neurasthenia patients with different EEG alpha rhythm types]. Experimental and clinical pharmacology, 75(5), 7–13. https://pubmed.ncbi.nlm.nih.gov/22834121/
- Vakhitova, I. u. V., Iamidanov, R. S., & Seredinin, S. B. (2004). [Ladasten induces the expression of genes regulating dopamine biosynthesis in various structures of rat brain]. Experimental and Clinical Pharmacology, 67(4), 7-11. https://pubmed.ncbi.nlm.nih.gov/15500036/
- Zimin, I. A., Abaimov, D. A., Budygin, E. A., Zolotarev, I. u. A., & Kovalev, G. I. (2010). [Role of the brain dopaminergic and serotoninergic systems in psychopharmacological effects of ladasten and sydnocarb]. Experimental and Clinical Pharmacology, 73(2), 2–5. https://pubmed.ncbi.nlm.nih.gov/20369592/
- World Anti-Doping Agency. (2025). The 2026 prohibited list: International standard of the World Anti-Doping Code. https://www.wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf