Adamax 10mg

Product status information

Chemical reagent intended exclusively for laboratory tests (Research Use Only). It is not a medicinal product, dietary supplement or food. It is not intended for use on humans or animals. Sales only to registered research units and laboratories.

Native Semax degrades in serum within minutes – the heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) is one of the best described neuropharmacological tools of the Russian school of regulatory peptides, but its short half-life limits the window of observation in many research protocols. Adamax is the trade name under which Pro-Body delivers the peptide chemistry answer to this limitation – the neuropeptide of the line Endogenic, described by the manufacturer as a modified, stabilized analogue of Semax (“improved version of Semax”).

Adamax inherits the pharmacophore core of Semax, but carries a terminal modification that increases proteolytic resistance – which in research models translates into longer durability of the peptide in solution and tissue. Adamax is delivered as vial with lyophilisate, 10 mg of peptide — dry, lyophilized form for independent reconstitution by the researcher. The vial format does not determine the route of administration or working concentration: the researcher selects the solvent and its volume according to the parameters of the planned experiment, and the lyophilisate retains the longest storage stability among the peptide forms.

In the literature on the Semax family, the intranasal route remains the dominant route of administration – native Semax is registered in the Russian Federation as nasal drops and spray, and intranasal administration of regulatory peptides is standard in preclinical protocols examining nose-to-brain transport; this context is described below as literature background, not as a format for this reagent. The relationship of Adamax to Semax is analogous to the relationship ADALANK to Selank: in both cases we have a stabilized modification of the native peptide of the Russian school family, redesigned for longer proteolytic stability.

In terms of its pharmacological profile, Adamax – as an analogue of Semax – refers to the mechanisms of the native base compound: strong induction of BDNF and NGF in the hippocampus and cortex, an ACTH(4-7) analogue profile devoid of corticotropic activity, modulation of dopaminergic and serotonergic transmission, inhibition of enkephalinases and neuroprotective activity in ischemia models. Within a category peptides for brain function it is located on the side of the nootropic-neuroprotective axis. Purity verified by HPLC ≥98%, identity confirmed by mass spectrometry, COA available for each batch.

Regulatory status

Adamax is not registered as a medicine in the EU or USA. Native Semax is registered as a medicinal product only in the Russian Federation – the modified analogue Adamax does not have such registration in any jurisdiction. Communication of the product as an “over-the-counter nootropic”, “concentration peptide” or “memory booster” is contrary to the Research Use Only framework.

Semax was born from a simple observation: the ACTH(4-10) fragment – a seven-amino-acid fragment of the adrenocorticotropic hormone – has an effect on memory and learning in animal models, but is devoid of hormonal activity (does not stimulate the secretion of corticosteroids). The problem was instability: the ACTH fragment was rapidly proteolytically degraded. The team at the Institute of Molecular Genetics in Moscow rebuilt this molecule, shortening it to the ACTH(4-7) fragment — Met-Glu-His-Phe — and adding the C-terminal tripeptide Pro-Gly-Pro.

Semax (MEHFPGP) was created: a peptide that retains the neurotropic profile of the ACTH fragment, but is clearly more stable due to the presence of proline residues that hinder the action of peptidases.

Pro-Gly-Pro serves as a chemical stabilizer here – peptide bonds involving proline are resistant to most endopeptidases. This is the same design logic used in the related Selank (also finished with Pro-Gly-Pro). Adamax goes a step further in the same strategy: it adds a terminal modification (capping) to proline stabilization, closing another gate for peptidases attacking free end groups. This is the standard method of regulatory peptide chemistry – extending the shelf life without changing the core responsible for binding to molecular targets.

Adamax is a synthetic neuropeptide from the Endogenic line – a stabilized, modified derivative of Semax, an analogue of the ACTH(4-7) fragment extended with Pro-Gly-Pro. It is supplied as a lyophilized vial, requiring reconstitution before use.

• Trade name: Adamax (Pro-Body, Endogenic line)
• Manufacturer’s description: modified/stabilized Semax analogue (“improved version of Semax”)
• Base Core: Semax (Met-Glu-His-Phe-Pro-Gly-Pro, MEHFPGP) — ACTH(4-7) analogue with the attached tripeptide Pro-Gly-Pro
• Nature of modification: terminal modification increasing proteolytic resistance and extending half-life (probably N-terminal acetylation or other terminal capping); the manufacturer does not reveal the full sequence
• Chemical class: modified regulatory neuropeptide; a synthetic analogue of the ACTH(4-7) fragment with the Pro-Gly-Pro tripeptide attached
• Supplied form: vial with lyophilisate (lyophilized powder), 10 mg of peptide; for independent reconstitution; pharmaceutical grade ≥98% HPLC

Table of physicochemical characteristics

Adamax – as an analogue of Semax – probably works through several parallel neurobiological pathways. The following mechanisms have been documented for native Semax in preclinical models; transferring them to a modified analogue remains the subject of research. Pharmacological profile described for the Semax family in research models:

1. Strong induction of BDNF and NGF (neurotrophic factors) — the best described and most characteristic mechanism. Semax in rat models increases the expression of BDNF (brain neurotrophic factor) and NGF (nerve growth factor) in the hippocampus and cortex, along with the activation of their TrkA and TrkB receptors (Dolotov et al. 2006). This is a probable basis for the influence on synaptic plasticity, neurogenesis and neuronal survival. The neurotrophic profile of Semax is clearly stronger than that of the related Selank – this is the difference that distinguishes the nootropic-neuroprotective axis from the anxiolytic axis
2. ACTH(4-7) analogue without corticotropic activity — Met-Glu-His-Phe core comes from melanocortin, but Semax does not stimulate the secretion of cortisol or corticosterone. The neurotropic activity of the ACTH fragment has been separated from its hormonal function – the peptide acts at the level of the central nervous system, not at the level of the hypothalamic-pituitary-adrenal axis. This is an important feature of profile security in research models
3. Modulation of dopaminergic and serotonergic transmission — Semax in animal models affects the dopamine system (including in the structures of the striatum and prefrontal cortex) and the serotonergic system, which is related to the observed pro-cognitive profile and the impact on motivation and mood in behavioral tests. Modulation of monoamines is a probable co-mechanism of nootropic action
4. Inhibition of enkephalinases — Semax inhibits the activity of enkephalin-degrading enzymes in serum and brain tissue (Kost et al. 2001), which increases the concentration of endogenous Met- and Leu-enkephalins in synapses. Prolonged activity of endogenous opioid peptides likely contributes to neuroprotective and mood-stabilizing effects
5. Neuroprotection in ischemia models — in models of cerebral ischemia (experimental stroke, hypoxia), Semax reduces the area of ​​damage and affects neuronal survival markers and the inflammatory response (Medvedeva et al. 2014). This is the basis for the most widely researched direction of applications of native Semax in Russian experimental neurology

The intranasal route dominates the Semax family in the literature and is the most frequently chosen variant of administration in preclinical protocols for this group of peptides. The vial format does not determine the route of administration – the researcher selects it in the experimental methodology – but the following context explains why the intranasal route is so important in this family.

Reagents supplied directly in a form prepared for this route are collected in the catalog as spray peptides. Most regulatory peptides do not cross the blood-brain barrier (BBB) ​​well when administered peripherally – they are too large and too polar. Intranasal administration offers an alternative delivery route to the central nervous system (CNS), partially bypassing the BBB. Two parallel nose-to-brain transport pathways have been described in research models:

• Olfactory pathway (olfactory) — a peptide applied to the olfactory epithelium in the upper part of the nasal cavity can be transported along the olfactory nerves directly to the olfactory bulb and further to the structures of the forebrain, bypassing the systemic circulation
• Trigeminal nerve pathway — the endings of the trigeminal nerve innervating the nasal mucosa constitute a second route of transport to the brain stem and further structures of the CNS

In research models, intranasal administration of regulatory peptides demonstrates nose-to-brain transport, achieving higher concentrations in brain structures at lower total doses than systemic administration. For the Semax family, the intranasal route is preferred in preclinical protocols for this very reason – the short half-life of the peptide in the blood makes direct transport to the CNS, bypassing the systemic circulation, particularly important.

SCIENTIFIC PERSPECTIVE

Native Semax has a precedent for intranasal administration in humans – it is registered in the Russian Federation as a nasal solution (drops/spray), and research on the neuropeptide has been conducted in experimental neurology, among others. in ischemic conditions and reduced hypoxia tolerance (Kaplan et al.

1992). Fair distinction: this precedent is for native Semax (MEHFPGP), not a modified Adamax analogue. Data from native Semax in the form of nasal drops are not fully portable on a modified molecule – the terminal modification changes the lipophilicity, charge and kinetics of transport through the nasal epithelium. The nose-to-brain profile for Adamax requires separate characterization.

The separation of these two molecules is the most important substantive caveat of this description. Adamax (modified analogue) and native Semax (MEHFPGP) share a pharmacophore core but differ in their terminal modification, which has practical consequences:

• Proteolytic stability — the end modification blocks peptidases, so the analogue is designed to be more stable in solution and tissue than native Semax. This is the main intention of the modification and the point by which the manufacturer justifies the term “improved version of Semax”
• Pharmacokinetics of nasal transport — changing the charge and lipophilicity of the peptide end affects the kinetics of penetration through the olfactory epithelium. The nose-to-brain profile of native Semax does not translate 1:1 to the modified analogue
• Data portability — almost all documented literature (BDNF/NGF, neuroprotection, clinical precedent for intranasal administration) concerns native Semax. The Adamax profile is a working hypothesis derived from core similarity, not a set of independently confirmed observations
• Structural identity — the manufacturer does not disclose the full sequence or exact structure of the modification. Peptide sequence and mass confirmation by MS remain the only binding signals of identity – the label and trade name alone do not determine what terminal modification is in the package

The starting form for this family is the unmodified peptide available as Semax 50mg (MEHFPGP core, nootropic-neuroprotective axis) – the durability and kinetics of the modified analogue are compared to it. An analogous caution applies to the related Selank and its stabilized analogue Adalank: the precedent of intranasal administration of native Semax and native Selank (both registered in the Russian Federation as nasal formulations) is a strong argument for the logic of the intranasal route for the entire family, but is not evidence for modified forms. The Semax base data is a reference point, not a documented Adamax profile.

Adamax in the format of a lyophilized vial is used in research directions analogous to native Semax, with additional emphasis on characterizing the profile of the modified molecule. The lyophilized form allows you to select the solvent, working concentration and route of administration according to the methodology of a specific protocol:

• Neuroprotection models — experimental models of cerebral ischemia, hypoxia and neuronal damage; assessment of the effect of the analogue on the area of ​​damage, markers of neuronal survival and inflammatory response
• Research on neurotrophic factors — expression of BDNF and NGF and activation of Trk receptors in the hippocampus and cortex; comparison of the kinetics and induction strength of the modified analogue compared to native Semax
• Cognitive models — memory and learning tests (Morris water maze, passive avoidance, radial arm maze), especially in conditions of cognitive impairment caused by stress, ischemia or neurotoxins
• Nose-to-brain transport studies — comparative pharmacokinetics of intranasal versus systemic administration; characterization of the effect of terminal modification on transport through the olfactory epithelium and achieved concentrations in brain structures
• Models of monoaminergic transmission — influence on the dopamine and serotonergic systems in the structures of the striatum, prefrontal cortex and hippocampus; research on the basis of the procognitive profile
• Pharmacokinetic characterization of modifications — comparative assessment of the proteolytic stability and distribution profile of the modified form compared to native Semax; confirmation of structural identity by MS

Adamax is the trade name under which Pro-Body supplies a modified, stabilized analogue of Semax from the Endogenic line – a neuropeptide described by the manufacturer as an “improved version of Semax”, delivered as a lyophilized vial containing 10 mg of the peptide, for independent reconstitution by the researcher. Adamax inherits the core pharmacophore of Semax (MEHFPGP, an ACTH(4-7) analogue from Pro-Gly-Pro), but carries a terminal modification that increases proteolytic resistance and extends half-life – analogous to the relationship of Adalank to Selank.

The pharmacological profile derived from Semax includes strong induction of BDNF and NGF, a neurotrophic profile of the ACTH fragment without corticotropic activity, modulation of dopaminergic and serotonergic transmission, inhibition of enkephalinases, and neuroprotection in ischemia models – all documented for native Semax in rodent and in vitro models, with the need for separate validation for the modified analogue.

The intranasal route dominates in the literature of the Semax family and is associated with the nose-to-brain transport mechanism, but the vial format does not determine the route of administration – the solvent, working concentration and administration variant are selected by the researcher.

The exact sequence and structure of the modifications are not disclosed by the manufacturer – they are decided by the batch COA (sequence plus MS mass). HPLC purity ≥98%, MS confirmation (Q-TOF), COA for each batch. Regulatory status – Research Use Only. The broader background to this class of compounds is described in the guide nootropic substances — their classification and mechanisms of action.

1. Dolotov OV, Karpenko EA, Inozemtseva LS, Seredenina TS, Levitskaya NG, Rozyczka J, et al. (2006). Semax, an analogue of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. PubMed
2. Medvedeva EV, Dmitrieva VG, Povarova OV, Limborska SA, Skvortsova VI, Myasoedov NF, Dergunova LV (2014). The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. PubMed
3. Shadrina M, Kolomin T, Agapova T, Agniullin Y, Shram S, Slominsky P, et al. (2010). Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action. PubMed
4. Ashmarin IP, Nezavibatko VN, Myasoedov NF, Kamensky AA, Grivennikov IA, Ponomareva-Stepnaya MA, et al. (1997). A nootropic adrenocorticotropin analog 4-10-Semax (15 years of experience in its design and study). PubMed
5. Kaplan AYa, Koshelev VB, Nezavibatko VN, Ashmarin IP (1992). Increased resistance to hypoxia effected by the neuropeptide preparation Semax. PubMed
6. Kost NV, Sokolov OY, Gabaeva MV, Grivennikov IA, Andreeva LA, Myasoedov NF, Zozulya AA (2001). Semax and selank inhibit the enkephalin-degrading enzymes from human serum. PubMed