Adamax

Also known as: Semax analog (unpublished structure)

Evidence: Anecdotal

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Overview

Adamantane-modified analog of the ACTH(4-7) peptide Semax, intended for greater lipophilicity and brain uptake; almost no published research exists.

Adamax is a research analog of the Russian nootropic peptide Semax (ACTH 4-7 Pro-Gly-Pro) modified with an adamantane group intended to increase lipophilicity and blood-brain-barrier penetration. Unlike Semax itself, Adamax has essentially no peer-reviewed literature of its own; reported cognitive and neuroprotective effects are extrapolated from Semax research and community reports.

Benefits

Extrapolated from Semax research: memory, focus and neuroprotection; no published human or animal data on Adamax itself

Dosing reference

Research dose
100 to 500 mcg daily (vendor/community range, no published human dose)
Range
100 to 500 mcg, 1x daily
Reconstitution
2 mL bacteriostatic water
Common vial sizes
5 mg

Routes in circulation are intranasal and subcutaneous, both community convention. No published study has administered this compound, so there is no pharmacokinetic basis for any dose or interval. Parent-compound work used intranasal Semax in rats (Dolotov et al., 2006).

Mechanism

No mechanism has been published for Adamax itself; nothing in PubMed or PubChem describes the compound. Everything stated about it is extrapolated from Semax, the ACTH(4-7)-Pro-Gly-Pro heptapeptide. In rats, Semax raised BDNF and trkB expression in the hippocampus within hours of a single intranasal dose (Dolotov et al., 2006) and changed NGF and BDNF transcript levels in hippocampus, frontal cortex and retina (Shadrina et al., 2010). Transcriptome work after middle cerebral artery occlusion in rats found Semax altered immune and vascular gene sets (Filippenkov et al., 2020). Whether an adamantane or acetyl modification preserves any of this is untested.

Evidence

Anecdotal: no peer-reviewed data

  • No study of Adamax exists in PubMed under that name or any resolvable synonym (search run 2026-10-05)
  • Parent compound Semax raised hippocampal BDNF and trkB mRNA in rats after intranasal dosing (Dolotov et al., 2006)
  • Semax changed NGF and BDNF expression in rat hippocampus, frontal cortex and retina, with different time courses per region (Shadrina et al., 2010)
  • Semax altered immune and vascular gene expression after cerebral ischaemia-reperfusion in rats (Filippenkov et al., 2020)
  • Russian clinical reports of Semax in ischaemic stroke exist but are open-label and single-country (Gusev et al., 2018)
  • Human-trial status: no trial, no pharmacokinetics and no safety study of Adamax in any species; the parent peptide's approvals and trials are Russian and do not transfer to this analog

References

Side effects

No published human safety data; everything reported about it is extrapolated from Semax. Anecdotal reports mention headache, overstimulation, and irritability. The photosensitivity warning that circulates with this compound is unsourced.

Storage

Storage
Refrigerate 2-8°C (36-46°F)
Lyophilized
2+ years at room temp, 3+ years refrigerated
Reconstituted
28-30 days refrigerated

Pharmacology

Half-life
Not established in any species; no pharmacokinetic study of this compound exists
Bioavailability
Not measured. No bioavailability data exist for this compound by any route.

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