Adamax is an experimental synthetic peptide discussed in the context of Semax and other peptides studied in neurobiology. It is most commonly presented as a modified analog of Semax, developed to alter the stability of the molecule and its potential impact on its interactions with the signaling pathways of the nervous system. However, these assumptions should not be equated with proven pharmacological properties. Direct, controlled studies determining the effects of Adamax in humans are still unavailable or very limited.
The name Adamax often appears in discussions about nootropic peptides, nootropic agents, neurotrophic signaling, and peptide chemistry. However, many claims regarding its activity are based on the extrapolation of results from studies on Semax, P21, compounds containing adamantan, or other molecules. These are related areas of research, but the evidence obtained from them cannot be treated interchangeably.
The article presents the described structure and classification of Adamax, the proposed biological mechanisms, the studies that form the basis of these hypotheses, the available formulations, safety issues, regulatory issues, and limitations of the information published online. The text does not contain instructions for use or recommendations regarding the use of Adamax in humans.
What is the Adamax peptide?
Adamax is described as a chemically modified derivative of Semax, a synthetic heptapeptide associated with the fragment of the adrenocorticotropic hormone (ACTH). The amino acid sequence of Semax is Met–Glu–His–Phe–Pro–Gly–Pro, abbreviated as MEHFPGP. Adamax represents an attempt to modify this structure through modifications of the peptide chain ends and the introduction of a structural element associated with adamantan.
The sequence often given in descriptions of Adamax is Ac-MEHFPGPAG-NH₂. In this notation, „Ac” stands for the acetylated amino end, while „NH₂” indicates the amidated carboxyl end. The additional amino acid residues distinguish the presented sequence from the unmodified Semax. However, the sequence notation itself does not specify the position of the adamantan group or the way it is chemically attached. To accurately determine which compound the given source or supplier is describing, a complete structural formula or verified analytical characterization would be needed.
This distinction is important because the product descriptions are not uniform. The source materials indicate molecular masses ranging from approximately 984–1032 g/mol. However, different values may correspond to different representations of the structure or preparations. Without a clearly defined chemical structure, the entire range should not be considered to be a confirmed molecular property of a single substance.
Adamax is sometimes classified as a nootropic peptide, modified neuropeptide, or peptide analog containing adamantan. It is a synthetic compound, not a peptide that is known to naturally occur in human tissues. Some descriptions also classify it as a cell penetrating peptide. Such a classification would require direct studies confirming Adamax’s penetration into cells under strictly defined conditions.
Adamax is often offered in research material catalogs as a white, lyophilized powder. Information about solubility in dimethylsulfoxide (DMSO) and controlled storage conditions also appears in the suppliers' descriptions. This information does not replace studies confirming the identity, purity, stability, and solubility of a specific batch. The properties measured for acetylated Semax cannot be automatically attributed to Adamax [2, 3].
Adamax is not a commonly approved medicinal product. The source materials mention restrictions and regulatory classifications in individual countries, including New Zealand. However, the cited scientific publications do not independently confirm all such claims. The legal status should be checked in the current regulations of the respective country, and not determined solely based on the designation „for research purposes”.
The original material mentioned the illustration of the chemical structure and the Wikipedia page. The most important structural distinction is that the often-given sequence Ac-MEHFPGPAG-NH₂ describes the peptide residues with chain-end modifications, whereas the claimed attachment of the adamantan group requires a separate, unambiguous representation of the structure.
The source material did not contain an established structural scheme that could be independently verified.
Adamax as a nootropic peptide
The term „nootropic” is widely used to refer to compounds discussed in the context of learning, memory, attention, and other cognitive functions. In the case of Adamax, it primarily refers to the research interest and classification encountered online, rather than to proven improvements in cognitive abilities.
Adamax is classified in this category primarily due to its structural similarity to Semax. In studies of Semax and its derivatives, the neurobiological pathways, peptide stability, and responses to experimental tissue damage were analyzed. For example, studies on N-terminal acetylation concerned changes in resistance to proteolytic degradation and the ability to coordinate metal ions [2, 3]. They provide scientific justification for modifying peptide structures, but do not prove that Adamax works the same or more effectively than Semax.
Another frequently discussed topic is the brain-derived neurotrophic factor (BDNF). BDNF is involved in the development and survival of neurons and synaptic plasticity. Its main signaling receptor, TrkB, is involved in the responses of specific populations of neurons to neurotrophic signals. Since these pathways are important for memory and learning, they often appear in hypothetical explanations for possible activity of Adamas.
However, the source material does not present direct evidence that Adamax increases BDNF levels, sensitizes TrkB receptors, or causes a measurable improvement in cognitive function. Results regarding BDNF biology or the influence of other peptides on neurogenesis should not be presented as results from experiments with Adamax [4–6, 9].
Adamax is also discussed in the context of dopamine, acetylcholine, glutamate, and gamma-aminobutyric acid (GABA). The systems of these neurotransmitters are involved in the regulation of motivation, attention, learning, and neuronal activity. Their importance for cognitive processes explains why they appear in discussions about experimental neuropeptides. However, it does not confirm that Adamax directly affects any of these systems.
Comparisons with P21 and other neurotrophic peptides are also of an intermediate nature. In studies of specific peptides derived from CNTF or containing adamantan moieties, changes in neurogenesis, synaptic parameters, and learning were observed in animal models [4–6]. These results apply to specific compounds studied. They do not confirm the analogous properties of Adamax simply because some structural features or research concepts are similar.
Adamax can therefore best be described as an experimental peptide structurally related to Semax, discussed in nootropic studies, whose effect on cognitive functions has not been confirmed in controlled human studies.
How does Adamax work? Proposed mechanisms and gaps in scientific evidence
The mechanism of action of Adamax has not been established based on a sufficiently developed set of direct, controlled studies. A significant portion of the available explanations are based on hypotheses regarding molecule design, known neurotrophic pathway biology, and results from studies on related but distinct compounds.
BDNF and neuronal plasticity
BDNF is a signaling protein involved in the maintenance of neurons, activity-dependent adaptation, and synaptic changes. It is particularly important in studies of learning and memory because synapses must adapt to experiences and changes in the activity of neuronal networks.
Some descriptions suggest that Adamax may influence BDNF-related signaling. However, this remains a hypothesis until it is confirmed by experiments directly measuring BDNF production or release, its interactions with receptors, or further activation of signaling pathways following exposure to chemically-verified Adamax.
The increase in BDNF levels observed after the administration of Semax or another peptide does not indicate that the same effect occurs after the administration of Adamax. Structural modifications can alter the stability, binding, distribution, and metabolism of the compound in a way that is difficult to predict solely based on sequence similarity.
TrkB receptor signaling
The TRkB is one of the main receptors of BDNF and is involved in pathways important for neuron survival and synaptic regulation. In this context, the hippocampus, the area of the brain involved in learning and memory processes, is often mentioned.
Internet explanations sometimes include claims that Adamax increases the sensitivity of TrkB receptors. However, the source material does not indicate any direct, controlled experiments confirming this effect. Therefore, these claims should be presented as a proposed mechanism rather than as an observed effect.
Demonstrating TrkB modulation would require studies that distinguish the direct effect on the receptor from secondary changes in BDNF signaling and other cellular pathways.
Dopamine, glutamate, GABA and acetylcholine
Dopaminergic pathways are involved in the regulation of motivation, reinforcement processes, and selected aspects of information processing. Glutamicergic signaling plays a key role in excitatory nerve transmission and synaptic plasticity. The GABAergic system provides important inhibitory regulation, while acetylcholine participates in attention and memory processes.
Because these systems interact with each other, scientists often analyze them during studies of compounds that may affect neuronal signaling. Adamax is often mentioned in articles explaining and discussions on the internet.
However, the source material does not present measurements specific to Adamax that would show changes in neurotransmitter release, receptor activity, or the functioning of neuronal networks. These dependencies should be treated as research questions rather than confirmed mechanisms of action.
Structural modifications, lipophilicity and stability
The proposed structure of Adamax includes modifications to the peptide chain ends and an element associated with adamantan. In medical chemistry, acetylation, amidation, and the introduction of lipophilic groups can in some cases alter the stability of the peptide, solubility, susceptibility to enzymatic action, or distribution in the body.
Studies on acetylated Semax have analyzed resistance to proteolysis and other biochemical properties [2, 3]. These results confirm the general principle that even small structural changes can affect the peptide’s behavior. However, they do not prove that Adamax remains longer in the human body, reaches the brain more effectively, or exhibits greater activity than Semax.
Adamantan is a rigid hydrocarbon skeleton found in some biologically active compounds. However, the clinical properties of adamantan cannot be attributed to the Adamax preparations solely because the structures associated with adamantan appear in the descriptions of both substances [7, 8]. The common chemical motif does not imply an identical mechanism of action.
Pathways related to stress response
Semax stems from the research on peptides derived from ACTH. This led to hypotheses regarding possible connections between modified peptides and stress signaling, including the hypothalamic-pituitary-adrenal axis.
The presented material does not provide direct evidence that Adamax regulates this axis, increases stress tolerance, or improves cognitive functions under stress conditions. These are still hypotheses that require appropriately designed experiments.
Figure 2. Proposed mechanisms of action of Adamax
The scheme, consistent with the current state of scientific evidence, should present Adamax as the center of several unconfirmed research hypotheses: BDNF/TrkB signaling, neurotransmitter pathways, peptide stability, and potential distribution to the tissues of the nervous system.
Arrows in such a diagram should be clearly marked as hypothetical, and not represent established causal-consequential relationships.
The source material mentioned this scene, but the image that could have been preserved in the translation was not included.
The context of the research and the scientific basis
Understanding Adamas requires a clear distinction between studies conducted directly on this substance and those concerning Semax, other modified peptides, or small molecules containing adamantan.
Semax and its acetylated derivatives
Semax has a history of research related to the chemistry of peptides derived from ACTH and experimental neurobiology. Early work analyzed ACTH fragments and their analogs for memory-related parameters [1]. Later studies examined how modifications such as acetylation of the N-terminus affect Semax stability and molecular interactions [2, 3].
These publications help explain why scientists may consider modifying the Semax sequence. However, the result regarding Semax or acetylated Semax is not evidence of identical activity in Adamax. During the interpretation of the results, the exact molecular identity of the substance under study is crucial.
P21 and other neurotrophic peptides
Studies on neurotrophic peptides and fragments derived from CNTF have observed changes in neurogenesis in the hippocampus, synaptic parameters, and memory-related tasks in mice [4, 5]. In another study, neurotrophic peptides containing adamantan were analyzed in animal models of learning and neuronal plasticity [6].
These experiments are relevant to the broader concept of designing modified peptides for neurobiological research. However, they do not prove that Adamax itself improves memory, increases neurogenesis, or reproduces the effects obtained for specific compounds being studied.
Amantadine and the structure of adamantane
Amantadine is a well-known small molecule drug whose chemical structure contains the adamantane skeleton. Its neurological applications have been studied in clinical trials, including in the recovery process after severe traumatic brain injury [7, 8].
The association with Adamax is limited, however, to the context of designing the chemical structure. Adamax is a different substance and cannot be inferred from clinical data regarding amantadine for its effects. The similarity of one structural fragment does not imply comparable pharmacokinetics, receptor interactions, efficacy, or safety.
What do the available evidence actually confirm?
The cited literature confirms three more limited observations: modified peptides associated with ACTH have been the subject of scientific research, chain-end modifications can affect the properties of certain peptide compounds, and some distinct neurotrophic peptides have produced measurable effects in animal models.
However, it does not confirm that Adamax has a defined mechanism of action, achieves clinically relevant concentrations in the brain, produces validated cognitive effects, or has an acceptable long-term safety profile in humans.
Are there any scientific studies regarding Adamax?
Direct scientific evidence regarding Adamas specifically is limited. The source material is largely based on studies of Semax, acetylated Semax, peptide compounds related to P21, and amantadine.
These works provide the context for the proposed molecular design strategies, but do not replace the direct experiments with Adamax.
The lack of robust clinical studies in humans is therefore one of the main limitations, not a minor gap in a well-established body of evidence.
Dosage of Adamax and available characters – educational context
Adamax appears in research material catalogs as lyophilized powder, sometimes packaged in small vials labeled with quantities such as 10 mg. Some suppliers also describe liquid solutions and preparations in the form of a nasal spray.
These are forms of product presentation, and not evidence of the existence of approved pharmaceutical formulations.
The term „dosage” often appears in searches for Adamas, but there is no medically approved or clinically verified standard of dosage for humans. The numerical information circulating on the internet is usually based on descriptions from suppliers or anecdotal reports, rather than on official dosage guidelines.
Claims that Adamax works in smaller amounts than Semax due to greater stability should be treated with caution. Even if a specific modification improves stability in a specific experiment, it does not indicate greater biological activity or longer duration of action in humans.
Such conclusions would require direct comparative pharmacokinetic and pharmacodynamic studies.
Similarly, information about storage and solubility depends on the exact chemical identity and formulation. General mentions of cooling, freezing, or solubility in DMSO should not be taken as verified specifications of any product described as Adamax.
The most important educational distinction concerns the amount of substance given on the label of the research material and the dose confirmed in clinical studies. In the case of Adamax, the latter was not determined.
Safety, adverse reactions and limitations of the studies
The safety profile of Adamas in humans has not been sufficiently studied. The source material does not indicate large, controlled studies evaluating adverse effects, the effects of prolonged exposure, interactions with medications, or potential for dependence.
Anecdotal reports sometimes mention headaches, anxiety, sleep disturbances, and changes in the subjectively perceived arousal. However, these observations have not been collected in a systematic or independently verified manner. Therefore, they do not allow for determining the frequency, severity, or causes of adverse effects.
Some reports also suggest that Adamax is generally well tolerated or has little potential for addiction. These claims remain unconfirmed without adequate safety and addiction risk studies. The absence of documented problems is not evidence of the substance's safety.
The risk associated with a specific formulation may also differ from the risk resulting from the action of the peptide molecule itself. The product identity, impurities, concentration, excipients, and microbiological quality are separate issues that require evaluation.
The supplier's designation „exclusively for research purposes” does not confirm these properties or the product's suitability for human use.
Regulatory restrictions or cases of product recalls described in public materials may indicate that the competent authorities consider the product to be subject to specific regulations. However, they do not in themselves prove either clinical harm or therapeutic benefits.
Claims regarding individual countries require an up-to-date verification by the relevant regulatory authorities.
The most important safety finding remains uncertainty. The available evidence is insufficient to reliably characterize the risk associated with Adamax, especially during prolonged exposure.
Public discussions and mentions on the internet
Adamax often appears on forums related to peptides, in communities interested in nootropics, on blogs, and in personal experience reports.
These discussions usually focus on the subjectively perceived alertness, motivation, mood, concentration, or comparisons with Semax.
Some people describe stronger or longer-lasting subjective effects, while others report discomfort, anxiety, or excessive arousal.
These relationships are not controlled experiments. They usually lack a confirmed identity of the relationship, consistent measurement methods, blinded comparisons, and systematic observation.
Expectations, the placebo effect, differences in health status, and simultaneous exposure to other substances can all influence subjective experiences.
Therefore, a positive or negative opinion does not allow determining the pharmacological mechanism of Adamax or its safety profile.
Public discussions are useful for identifying the most common questions and areas of interest. However, they do not constitute a reliable substitute for laboratory characteristics, pharmacokinetic studies, or controlled clinical trials in humans.
Adamax's place in the studies on peptides
Adamax should be best viewed as a proposed modified neuropeptide belonging to a broader area of peptide design.
Scientists analyze structural modifications such as chain end protection, amino acid attachment, and the introduction of non-peptide groups, because they can alter the chemical and biological properties of molecules.
The closest reference point in terms of structure is Semax.
Selank and P21 appear in related discussions about neuropeptides because they have also been studied in the context of neurobiology. However, these compounds differ in their sequence, research history, and the range of available evidence.
The results of their studies should not be combined as if they were about a single class of substances with identical properties.
A separate article Adamax vs Semax it helps to distinguish structural similarities from differences in the degree of advancement of research.
Meanwhile, the material Adamax Spray – Adamax spray for effective results discusses issues related to the formulation and reporting of peptide data.
Neither a structural comparison nor a discussion of the composition of the preparation confirms the clinical effectiveness of Adamax.
The most important conclusion is that rational molecular design allows for formulating hypotheses that can be tested in experiments. However, it does not guarantee that the new compound will be more effective than its predecessor or safe for humans.
Conclusions
Adamax is an experimental synthetic peptide most commonly described as a modified Semax analog. According to available descriptions, its design includes modifications to the chain ends and a structural element related to adamantan. The goal of these modifications is to investigate the possibility of achieving different stability and potential interactions with neurobiological pathways.
These characteristics explain why Adamax appears in discussions about BDNF, TrkB signaling, neurotransmitters, and the delivery of peptides.
However, most of these associations remain hypothetical. Direct evidence regarding the unambiguous molecular identity of the compound in commercial descriptions, its mechanism of action, human pharmacokinetics, and its effects on cognitive functions and long-term safety are limited.
Studies of Semax and its acetylated derivatives show that modifications of peptides can affect selected biochemical properties.
Studies of peptides related to P21 and other neurotrophic compounds indicate that certain experimental molecules can affect neuronal parameters in animal models.
Meanwhile, studies of amantadine provide context regarding the structure of adamantane.
However, none of these results should be taken as direct evidence of Adamax's activity.
Adamax therefore remains an unresolved research issue and not a proven nootropic, cognitive enhancement agent or treatment method.
Its scientific significance stems from the questions it raises regarding the relationship between the structure of a peptide and its biological behavior.
Drawing reliable conclusions will require a thorough chemical characterization of the compound and rigorous experimental and clinical studies.
Frequently asked questions about Adamax (FAQ)
Peptyd Adamax składa się z czterech aminokwasów: kwasu glutaminowego, alaniny, lizyny i metioniny.
Adamax is described as a synthetic peptide structurally related to Semax, with a frequently reported Ac-MEHFPGPAG-NH₂ sequence. This record indicates an acetylated N-terminus and an amidated C-terminus, as well as differences in amino acid composition compared to Semax. Some descriptions also mention a structural element containing adamantan. However, the peptide sequence itself does not specify the way this group is attached. Therefore, confirmation of the exact identity of the compound in question requires a complete structural formula and appropriate analytical characteristics.
Is Adamax the same as Semax?
No. Adamax is described as a modified analog of Semax, not an identical molecule. Semax is a heptapeptide with the sequence MEHFPGP, whereas the descriptions of Adamax include modifications of the chain ends and additional structural elements. These differences may affect chemical properties, but they do not indicate greater stability, biological activity, or more effective cognitive effects. The results obtained for Semax should not be automatically attributed to Adamax.
Is Adamax a medicine or a dietary supplement?
Adamax is usually described as an experimental research compound rather than an approved drug or recognized ingredient in dietary supplements. Regulatory classification depends on the country, the declared intended use, and applicable regulations. The designation „for research purposes” in itself does not determine legal status or confirm pharmaceutical quality. The source material does not provide evidence for the broad approval of Adamax for medical use.
Is Adamax available in a spray form?
Yes. Some research material suppliers offer Adamax in the form of a liquid spray for reporting or a solution intended for oral administration. This term describes the formulation and delivery system, not the approved treatment method. There are no standardized data on the absorption, delivery efficacy, and safety of Adamax oral spray in humans. The composition and quality of products may also vary between suppliers.
Does Adamax have proven long-term effects?
No. The long-term effects of Adamas have not been reliably established in large, controlled human studies. Both the potential long-term benefits and the long-term risks remain uncertain. The results of studies on Semax or other peptides do not fill this gap, because even compounds with similar structures can behave differently in biological systems.
Why is Adamax considered an experimental substance?
Adamax is an experimental substance because direct evidence regarding its mechanism of action, pharmacokinetics, efficacy, and safety is insufficient. A significant portion of the publications cited in discussions about Adamax concerns other compounds, including Semax, acetylated Semax, and other neurotrophic peptides. The lack of a well-established clinical evidence base prevents drawing reliable conclusions about its use in humans.
Jest Adamax legalny?
The legal status of Adamax may vary between countries and depend on whether the product is offered as a medicine, a dietary supplement, or a chemical for research. The source material mentions restrictions in some countries, but these claims require confirmation in current regulatory documents. The availability of the product does not mean that it has been legally approved for human use. Similarly, the regulatory classification is not evidence of clinical efficacy.
Is Adamax designed to improve athletic performance?
No. Adamax is not a recognized or approved substance intended to improve athletic performance. References to endurance, recovery, and mental performance occasionally appear in online discussions, but the evidence presented does not include controlled studies demonstrating such effects for Adamax. Claims regarding sports benefits should therefore be considered unconfirmed.
Is Adamax a proven means of improving cognitive functions?
No. Adamax should not be considered a proven means of improving cognitive functions. Its proposed links with learning, attention, and memory result primarily from structural considerations, indirect studies, and anecdotal reports. No controlled human studies demonstrating repeated cognitive benefits have been established. Scientific interest does not equate to clinical confirmation.
In what forms does Adamax appear?
Adamax is most commonly described as a white, lyophilized powder, sometimes packaged in small test vials. It may also be available as a liquid solution or a nasal spray. These descriptions refer to the physical form, not the verified pharmaceutical formulations. Products sold under the same name may differ in chemical identity, purity, concentration, stability, and the content of excipients.
Does Adamax cause side effects?
The adverse reaction profile of Adamax has not been reliably characterized. Anecdotal reports mention headaches, restlessness, changes in sleep patterns, and perceived agitation. However, these observations have not been confirmed in systematic, controlled studies. Without reliable safety data, it is not possible to determine either the frequency of these effects or their causal relationship with Adamax.
Is the use of Adamax safe?
The safety of Adamas in humans has not been established. There is a lack of sufficient controlled clinical data regarding adverse effects, interactions, potential for dependence, and long-term exposure. An additional limitation may be the uncertainty regarding the quality of the formulations and the product identity. Claims of good tolerability published online do not replace clinical safety assessment.
Can Adamax improve memory and concentration?
There is no solid clinical evidence showing that Adamax improves memory or concentration in humans. These claims are mainly based on its connections with Semax, hypotheses regarding neurotrophic pathways, and personal relationships. Studies demonstrating the effect of other peptides on memory do not show that Adamax produces the same effects.
Is Adamax addictive?
The addictive potential of Adamas has not been adequately studied. The lack of well-documented cases of addiction does not prove that the substance cannot cause dependence. Determining such a risk would require appropriate experimental and clinical studies, including a systematic assessment of behavior and physiological responses.
What place does Adamax hold in the research on peptides?
Adamax belongs to the broader field of research into chemically modified neuropeptides and experimental peptide design. It is most often compared to Semax, while compounds such as Selank and P21 provide additional scientific context. However, their mechanisms and the range of available evidence are not identical. Adamax remains a compound in the research phase and not a recognized clinical intervention.
Is Adamax intended for use in humans?
Suppliers of research materials often label Adamax as a substance intended solely for laboratory use, not for human consumption or administration. These designations reflect the lack of a determined clinical approval and should not be interpreted as evidence of quality or safety. The source material does not provide grounds for treating Adamax as a validated drug intended for human administration.
Will future studies allow us to better understand the effects of Adamax?
Further research can help clarify Adamax’s molecular identity, its stability, biological targets, distribution, safety, and potential effects. These studies should begin with a precise chemical characterization of the material and direct experiments on this particular compound. Subsequently, controlled human studies would be needed before it is possible to formulate valid clinical conclusions. Until such evidence is available, the proposed benefits of Adamax remain unconfirmed.
Disclaimer
This article is for educational and scientific information purposes only. It presents an experimental peptide, the associated molecular studies, and the limitations of the available scientific evidence. It does not constitute medical advice, does not recommend the use of Adamax, nor specifies the dosage, methods of administration, or treatment protocols. The results of laboratory tests and animal studies regarding other compounds, descriptions from suppliers, and individual user reports do not constitute evidence of the safety or efficacy of Adamax in humans.
References
The references below are retained from the supplied manuscript. Their numbering and formatting were inconsistent in the source, and some entries provide background on related compounds rather than direct evidence from Adamax. They have not been independently verified or renumbered to match every inline citation.
- Ponomareva-Stepnaya, M. A., Achfeeva, L. Y., Maksimova, L. A. Synthesis and investigation of fragments of ACTH and their analogues—memory stimulators. Pharmaceutical Chemistry Journal, 1981, 15(10), 720–725. https://link.springer.com/article/10.1007/BF00765384
- Shevchenko, K. V., Nagaev, I. Y., Andreeva, L. A., Shevchenko, V. P., Myasoedov, N. F. Stability of Semax acetyl to proteolysis in various biological media. Doklady Biological Sciences, 2013, 449(1), 110–112. https://pubmed.ncbi.nlm.nih.gov/23652441/
- Magrì, A., Tabbì, G., Giuffrida, A., Pappalardo, G., Satriano, C., Naletova, I., Nicoletti, V. G., Attanasio, F. Influence of N-terminus acetylation of Semax on metal coordination and biological properties. Journal of Inorganic Biochemistry, 2016, 164, 59–69. https://doi.org/10.1016/j.jinorgbio.2016.08.013
- Chohan, M. O., Li, B., Blanchard, J., Tung, Y.-C., Heaney, A. T., Rabe, A., Iqbal, K., Grundke-Iqbal, I. Enhancement of dentate gyrus neurogenesis, dendritic and synaptic plasticity, and memory by a neurotrophic peptide. Neurobiology of Ageing, 2011, 32(8), 1420–1434. https://pubmed.ncbi.nlm.nih.gov/19767127/
- Blanchard, J., Chohan, M. O., Li, B., Liu, F., Iqbal, K., Grundke-Iqbal, I. Beneficial effect of a CNTF tetrapeptide on adult hippocampal neurogenesis and spatial memory in mice. Journal of Alzheimer’s Disease, 2010, 21(4), 1185–1195. https://pubmed.ncbi.nlm.nih.gov/20952820/
- Li, B., Wanka, L., Blanchard, J., Liu, F., Chohan, M. O., Iqbal, K., Grundke-Iqbal, I. Neurotrophic peptides including adamantane improve learning, memory, neurogenesis and synaptic plasticity in mice. FEBS Letters, 2010, 584(15), 3359–3365. https://doi.org/10.1016/j.febslet.2010.06.025
- Giacino, J. T., Whyte, J., Bagiella, E., Kalmar, K., Childs, N., Khademi, A., et al. Placebo-controlled trial of amantadine for severe traumatic brain injury. New England Journal of Medicine, 2012, 366(9), 819–826. https://doi.org/10.1056/NEJMoa1102609
- Morrow, K., Choi, S., Young, K., Haidar, M., Boduch, C., Bourgeois, J. A. Amantadine for the treatment of childhood and adolescent psychiatric symptoms. Baylor University Medical Center Proceedings, 2021, 34(5), 566–570. https://pubmed.ncbi.nlm.nih.gov/34456474/
- Baazaoui, N., Iqbal, K. A novel therapeutic approach to treat Alzheimer’s disease by neurotrophic support during synaptic compensation. Journal of Alzheimer’s Disease, 2018, 62(3), 1211–1218. https://pubmed.ncbi.nlm.nih.gov/29562539/
- Li, B., Yamamori, H., Tatebayashi, Y., Shafit-Zagardo, B., Tanimukai, H., Chen, S., Iqbal, K., Grundke-Iqbal, I. Failure of neuronal maturation in Alzheimer's disease dentate gyrus. Journal of Neuropathology & Experimental Neurology, 2008, 67(1), 78–84. https://pubmed.ncbi.nlm.nih.gov/18091557/
- Jin, K., Peel, A. L., Mao, X. O., Xie, L., Cottrell, B. A., Henshall, D. C., Greenberg, D. A. Increased hippocampal neurogenesis in Alzheimer’s disease. Proceedings of the National Academy of Sciences, 2004, 101(1), 343–347. https://pubmed.ncbi.nlm.nih.gov/14660786/
- Government of the Russian Federation. Directive No. 2738-r, dated 10 December 2018. Moscow, Russian Federation. The original manuscript supplied a malformed website address (
https//:russianpeptide.com/); the document has not been independently authenticated.