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Adamax is a synthetic heptapeptide analog of Semax (itself an ACTH(4-7) fragment derivative) bearing an adamantane-type N-terminal modification intended to increase lipophilicity and resistance to enzymatic degradation. It is offered strictly for laboratory research and is studied in the context of neurotrophic and neuroplasticity signaling.
Adamax is a research peptide belonging to the Semax family, which derives from a fragment of adrenocorticotropic hormone (ACTH 4-10). Semax itself is the heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro, and Adamax is described in supplier and secondary literature as a Semax analog carrying an adamantane-type N-terminal modification designed to raise lipophilicity and slow enzymatic breakdown.
Because Adamax is a proprietary analog rather than a peptide with an established regulatory monograph, it does not have a verified PubChem entry, and its exact structure is reported inconsistently across sources. The scientific rationale for the compound is extrapolated from the comparatively larger body of published work on the parent peptide Semax.
All information here is compiled from published literature on Semax and from secondary descriptions of the analog. Adamax is intended for research use only and is not a drug, supplement, or medical product.
Semax-family peptides are studied for their reported ability to modulate brain-derived neurotrophic factor (BDNF) and its receptor TrkB, and to influence the dopaminergic and serotonergic systems in animal models. Published work on Semax reports increased BDNF and trkB mRNA expression in the rat hippocampus following administration.
The adamantane modification attributed to Adamax is proposed, on chemical grounds, to increase membrane permeability and metabolic stability relative to unmodified Semax. Direct mechanistic data specific to Adamax itself is limited in the peer-reviewed literature.
Reporting only — not guidance. Dolotov et al. (2006, J Histochem Cytochem) administered Semax to rats and reported increased BDNF immunoreactivity and trkB mRNA in the hippocampus, characterizing a neurotrophic response in a rodent model.
Medvedeva et al. (2014, J Neural Transm) applied Semax in a rat model of experimental ischemic stroke and used transcriptome profiling to describe changes in gene expression associated with inflammation and vascular processes. These are descriptions of published animal experiments involving the parent peptide; they are not protocols for use.
Combinations examined in the research literature. Descriptive only — not a recommendation to combine compounds.