Peptide Registry

Adamax

Price range: $49.00 through $79.00

  • Contents: Adamax (N-Acetyl Semax-Adamantane; Ac-MEHFPGP-Adamantyl)
  • Form: Lyophilized powder
  • Purity: >99%
Quantity Discount Price
1 - 3 - -
4 - 7 10% -
8 + 18% -
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Description

Adamax is a synthetic heptapeptide built on the Semax backbone, itself derived from the ACTH(4-10) fragment Met-Glu-His-Phe-Pro-Gly-Pro,  with two structural modifications engineered to address the primary pharmacokinetic limitations of the parent compound. N-terminal acetylation blocks aminopeptidase-mediated degradation at the peptide’s most vulnerable cleavage point. A C-terminal adamantane moiety, the same rigid hydrophobic carbon cage used in P-21 and in established CNS drugs memantine and amantadine, increases lipophilicity and passive diffusion across lipid bilayers, including the blood-brain barrier. Together, these modifications extend metabolic stability and broaden the compound’s potential distribution profile relative to unmodified Semax. Therefore, Adamax is studied in nootropic peptide CNS research models where the modification profile itself, rather than simply the parent sequence, is the experimental variable of interest.

Chemical Information

  • Chemical Name: N-Acetyl Semax-Adamantane
  • Sequence: Ac-Met-Glu-His-Phe-Pro-Gly-Pro-Adamantyl
  • Compound Class: Synthetic ACTH(4-10)-derived heptapeptide analog
  • Molecular Weight: ~1,050 g/mol (calculated; verify against lot COA)
  • Parent Compound: Semax (Met-Glu-His-Phe-Pro-Gly-Pro; ACTH 4-10 fragment)
  • Modifications: N-terminal acetylation; C-terminal adamantane conjugation
  • Production: Solid-phase peptide synthesis (SPPS)

Applications

  • Preclinical studies examining how C-terminal adamantane conjugation affects metabolic stability and CNS distribution relative to unmodified Semax. The modification profile is a research variable independent of the parent sequence’s biological activity
  • BDNF expression and TrkB pathway research in neural cell models. Mechanistic context derives from the Semax parent compound literature. However, Adamax-specific data remains limited, and researchers should treat parent compound findings as hypothesis-generating rather than directly applicable
  • Structure-activity relationship studies comparing adamantane-conjugated versus terminally amidated Semax analogs. Adamax (adamantane) and N-Acetyl Semax Amidate (amidation) address the same pharmacokinetic problem through different chemical strategies, making them useful in comparative SAR designs
  • Melanocortin receptor interaction studies in neural tissue models. ACTH(4-10)-derived sequences engage melanocortin receptor pathways; the adamantane modification’s effect on receptor binding affinity relative to unmodified Semax is itself a tractable research question
  • Peptide-membrane interaction studies examining how adamantane conjugation affects lipid bilayer partitioning in CNS model systems

Storage and Handling

Store as lyophilized powder under refrigeration at 2–8°C for routine storage, or at -20°C for long-term stability. Protect from heat, moisture, and direct light. Reconstitute immediately before use. Avoid repeated freeze-thaw cycles to preserve compound integrity. The adamantane moiety increases hydrophobicity relative to unmodified Semax. Verify solubility behavior in the target buffer system before preparing working solutions.

Compliance Notice

Adamax is for laboratory research use only. It is not for human or veterinary use and carries no therapeutic, diagnostic, or clinical indication. This product has not been evaluated by the FDA. By purchasing this product, the buyer confirms it will be used exclusively for controlled in vitro research by qualified personnel following appropriate institutional safety procedures.

Frequently Asked Questions

What is Adamax?

Adamax (N-Acetyl Semax-Adamantane) is a synthetic heptapeptide analog of Semax, the ACTH(4-10)-derived research peptide. It carries two structural modifications. N-terminal acetylation to reduce aminopeptidase-mediated degradation, and a C-terminal adamantane group to increase lipophilicity and passive BBB diffusion. Researchers use it in CNS neuropeptide studies where the modification profile and its pharmacokinetic consequences are experimental variables alongside the underlying Semax sequence biology.

How does Adamax differ from N-Acetyl Semax Amidate?

Both are stability-optimized Semax analogs addressing the same pharmacokinetic limitation — rapid proteolytic clearance — through different C-terminal chemistry. N-Acetyl Semax Amidate replaces the C-terminal carboxyl group with an amide, blocking carboxypeptidase access. Adamax conjugates an adamantane group at the C-terminus. This blocks degradation while simultaneously increasing lipophilicity through the hydrophobic carbon cage structure. The adamantane modification predicts greater BBB permeability enhancement than amidation alone, though direct comparative permeability data for these two analogs in the same experimental system have not been published.

Does Adamax have its own published research literature?

No. Essentially no dedicated published research exists for Adamax specifically. Its mechanistic rationale derives entirely from the Semax parent compound literature and established medicinal chemistry principles around adamantane conjugation. Researchers should treat Semax findings as hypothesis-generating context rather than directly applicable data, and validate Adamax behavior independently in their experimental system before drawing mechanistic conclusions.