Adamax
Also known as: Semax analog (unpublished structure)
Evidence: Anecdotal
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
- Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Dolotov OV, Karpenko EA, Inozemtseva LS, et al., Brain Research, 2006
- Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action. Shadrina M, Kolomin T, Agapova T, et al., Journal of Molecular Neuroscience, 2010
- The heptapeptide SEMAX stimulates BDNF expression in different areas of the rat brain in vivo. Dolotov OV, Seredenina TS, Levitskaya NG, et al., Doklady Biological Sciences, 2003
- Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats. Filippenkov IB, Stavchansky VV, Denisova AE, et al., Genes, 2020
- The efficacy of semax in the tretament of patients at different stages of ischemic stroke. Gusev EI, Martynov MY, Kostenko EV, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2018
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.