Adamax Canada — 10 mg Lyophilized Vials
Nootropic Peptide
Also known as Adamantane-modified Semax analogue
Adamax is a synthetic peptide supplied for laboratory research, described by its originators as an adamantane-modified analogue of the ACTH(4-10) fragment peptide Semax.
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This product is intended strictly for laboratory research use within Canada. It is not approved by Health Canada for the diagnosis, treatment, cure, or prevention of any disease. Not for human or veterinary use.
By purchasing, you confirm the material will be used solely for lawful research purposes in accordance with applicable Canadian regulations.
Adamax is a synthetic peptide supplied for laboratory research, described by its originators as an adamantane-modified analogue of the ACTH(4-10) fragment peptide Semax.
No primary study of Adamax itself has been published. The experimental framing below describes the Semax scaffold it is derived from, not Adamax.
Third-party tested for purity, ID, quantity.
Coming Soon
The certificate of analysis for the 10mg lot is being finalised and will be published here as soon as the lab returns it.
Adamax is offered in the research market as a structural modification of N-acetyl Semax, with an adamantane group intended to alter stability and lipophilicity relative to the parent heptapeptide. The parent compound, Semax, is a synthetic analogue of the ACTH(4-10) fragment that has been characterized in Russian and international neuropharmacology research for effects on neurotrophin gene expression.
Because the adamantane-modified form has not itself been described in the peer-reviewed literature, its stability, receptor behaviour, and activity remain uncharacterized. Researchers should treat published Semax data as background on the scaffold rather than as evidence about Adamax.
Semax was developed from research on short ACTH fragments lacking hormonal activity, and has been studied for neurotrophic and cognitive endpoints since the 1980s. Structural work on the N-terminal region established that modification changes the expression of its nootropic profile.
Adamax emerged subsequently as a research-market modification of that scaffold. It has no published synthesis, characterization, or activity study of its own.
There is no compound-specific literature for Adamax. The references below characterize Semax, the ACTH(4-10) analogue scaffold from which Adamax is described as being derived, and cover neurotrophin gene expression, receptor binding, and behavioural endpoints in rodent models.
4 of the 4 areas below are addressed directly by a paper cited on this page.
Addressed on this page by Glazova 2021, Agapova 2007, Dolotov 2006. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
Addressed on this page by Agapova 2007, Dolotov 2006, Glazova 2005. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
Addressed on this page by Glazova 2005. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
Addressed on this page by Dolotov 2006, Glazova 2021. Each is linked to its source record in the references below, so what was measured — and in what system — can be read rather than taken on trust.
The references section of this page cites 4 primary papers published between 2005 and 2021 — a limited but non-trivial record. Every citation is linked to its PubMed or DOI record so it can be read rather than taken on trust, and the summaries above describe what those papers report rather than what the compound is claimed to do.
Worth noting when weighing that record: roughly 50% of the citations here list Glazova as lead author. A literature concentrated in one research group has not been independently replicated to the same degree as one drawn from many, and that is a real limitation on how far the findings can be generalised — regardless of how consistent the individual results look.
Adamax is frequently listed as a peptide by suppliers in this market. It is not one. The structure published on this page is the compound's actual chemistry, and research on it should be read against its own class rather than against peptide literature.
Research compounds attract claims that outrun their evidence. Below are the ones most often encountered for Adamax, set against what the papers cited on this page actually report. Where the record is thin or contested, that is stated rather than smoothed over.
Adamax is commonly described online in connection with sharper focus, better memory and improved mood. In the research literature the same compound is filed under ACTH(4-10) analogue pharmacology (parent scaffold), neurotrophin and BDNF gene-expression models and N-terminal modification structure-activity research.
The 4 papers cited on this page, published between 2005 and 2021 (3 in animal models) describe laboratory and animal work. None reports a controlled trial in humans. Findings in cell culture or in a rodent model describe what happened in that system; they do not establish that the same occurs in humans, and this compound is not approved for human use.
Presented as having independent scientific backing.
Around 50% of the papers cited here list Glazova as lead author. A literature concentrated in one research group has not been independently replicated to the degree its volume suggests, and that is a real limit on how far the findings generalise — however consistent the individual results appear.
Nothing above is a statement of what this material does. It is a summary of what has been published and what has not. Eppix Labs supplies research materials only and provides no dosing, administration or protocol guidance.
Every lot of Adamax is independently assayed before it is released, and the certificate for the lot shipped is published rather than summarised. Where a certificate for a current lot is not yet posted, the lot has not yet been released against it.
Researchers who buy Adamax in Canada through Eppix Labs receive a batch-labelled vial whose certificate is published against that lot code, so the material can be matched to its analysis rather than to a generic specification.
Adamax is supplied as lyophilized powder. It is not a peptide, and solvent behaviour follows from its own chemistry rather than from the aqueous-vehicle conventions that apply to peptide material — the published literature for this compound is the reference for solvent selection, not a general peptide protocol.
Dry storage below freezing and protection from light are the general controls. As with any lyophilized material, the powder frequently sits as a thin film at the base of the vial and is easy to mistake for an empty vial before inspection.
Vials may appear empty on arrival. Lyophilized material collects at the base of the vial and is often not visible until the vial is inspected under direct light.
Reconstitution materials are sourced separately. The reconstitution calculator on this site works out concentrations for a given volume, but it is an arithmetic tool for laboratory record-keeping and not a protocol.
No. Eppix Labs products are supplied exclusively for laboratory research. We do not provide dosing, administration, or usage guidance.
Each unit contains the labeled quantity of Adamax. Independent third-party analysis verifies purity, identity, and net content per batch.
The unit contains only the research compound. Any laboratory materials required for reconstitution or experimental procedures must be sourced separately.
Duration depends entirely on research design, storage conditions, and laboratory protocol.
Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus
PubMedSemax, synthetic ACTH(4-10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats
PubMedNeurotrophin gene expression in rat brain under the action of Semax, an analogue of ACTH 4-10
PubMedEffect of modification of the N-terminal region of molecule on the expression of neotropic effect of semax analogues
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