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Adamax

Cognitive & Neurological · ['Adamax', 'Adamantyl-Semax analog', 'N-adamantyl Semax derivative']

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.

🔬 Research use only — not for human or veterinary use. K4 Elite does not provide dosing instructions.
Research Level
Emerging Research
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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.

  • BDNF / TrkB signaling: Studies of the parent peptide Semax report upregulation of BDNF and trkB expression in rodent hippocampus (Dolotov et al., 2006).
  • Neuroprotection in ischemia models: Semax has been examined in experimental cerebral ischemia and stroke models for effects on neuronal survival and gene expression (Medvedeva et al., 2014).
  • Cognition and learning in animals: ACTH(4-10)-derived peptides have been studied for effects on attention and memory-related behavior in rodents.
  • Peptide stability chemistry: Adamantane conjugation is a general medicinal-chemistry strategy studied for improving lipophilicity and enzymatic resistance of peptides.
  • Neuroinflammation and gene expression: Transcriptomic studies of Semax report modulation of inflammation- and vascular-related gene sets in ischemic brain tissue.
📋 How published studies were conducted — a research reference summarizing study designs from the literature. This is not usage, dosing, or administration guidance. K4 Elite does not provide dosing instructions; determining any research protocol is the sole responsibility of the qualified researcher.

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.

SemaxNeutral
Structurally related parent peptide; comparative research context only.
Selank / AdalankCompatible
Studied within overlapping cognitive-research literature; no established combined-use data.
BDNF pathway modulatorsSynergistic
Mechanistic overlap on BDNF/TrkB in animal models; interaction not clinically characterized.
Stimulant nootropicsCaution
No controlled interaction data; combined effects on neurological signaling are uncharacterized.
  1. Dolotov OV et al. Semax, an ACTH(4-10) analogue, increases BDNF in rat hippocampus. J Histochem Cytochem 2006
  2. Medvedeva EV et al. Effects of Semax on the transcriptome of ischemic rat brain. J Neural Transm 2014
  3. Shevchenko KV et al. Pharmacokinetics of Semax and its metabolism. Doklady Biol Sci
Is Adamax approved for human use?
No. Adamax is a research compound with no regulatory approval. It is intended for laboratory research use only and is not a drug, supplement, or medical product.
How does Adamax relate to Semax?
Adamax is described as a Semax analog carrying an adamantane-type modification intended to increase lipophilicity and enzymatic stability. Most published mechanistic data pertains to the parent peptide Semax.
Does Adamax have a PubChem entry?
No verified PubChem CID was found for Adamax as a distinct compound, so no molecular identifiers are listed here. We do not publish fabricated identifiers.
What has been studied about this compound?
Published research on the Semax family reports effects on BDNF/TrkB signaling and neuroprotection in rodent models. Data specific to the Adamax analog itself is limited.
Can you tell me a dose?
No. This reference is for research context only and does not provide human or veterinary dosing, routes, or administration guidance.
Disclaimer: This profile summarizes published preclinical and laboratory research for reference only. It is not medical advice and makes no claim of safety or efficacy in humans. Determining any research protocol is the sole responsibility of the qualified researcher. Products are sold strictly for in-vitro research and have not been evaluated by the FDA.