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Evidence graded using the PeptideScholar A-D system.
Adamax is a modified, more lipophilic analog of Semax in which the N-terminal acetyl group is replaced with an adamantane moiety. Semax itself is a synthetic fragment of adrenocorticotropic hormone (ACTH(4-7)) with a C-terminal Pro-Gly-Pro tripeptide. The adamantane modification is claimed to increase blood-brain barrier penetration and extend half-life. There are zero published studies on Adamax specifically — all evidence is extrapolated from Semax research.
Mechanism is extrapolated from Semax: Semax increases brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) expression, modulates dopaminergic and serotonergic systems, and upregulates neuroprotective gene expression. The adamantane group (also found in memantine, an NMDA antagonist for Alzheimer's) may confer additional membrane affinity and CNS penetration, but this claim is unverified for Adamax.
This content is for informational purposes only and does not constitute medical advice.
The dosing information above is sourced from published research literature and clinical trials. These are not recommendations. Individual responses vary. Always consult a healthcare provider before considering any peptide-based therapy.
Adamax is not FDA-approved. Always consult a licensed healthcare provider before considering any peptide.
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BMC Genomics, 2014
Semax significantly altered gene expression in rat brain following ischemia, upregulating neuroprotective and vascular remodeling genes
Neurochem Res, 2005
Semax increased dopamine and serotonin turnover in rodent brain regions, providing mechanistic basis for nootropic effects
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No claims of therapeutic efficacy are made for substances that are not FDA-approved for the discussed indications. Research citations reflect published findings and do not imply endorsement.