ADAMAX 10mg
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Buy Adamax 10mg — N-Acetyl Semax Amidate Research Peptide
Adamax is the N-acetyl amidate modified form of Semax – a synthetic heptapeptide derived from the ACTH(4-10) fragment. The name “Adamax” combines the N-Acetyl and Amidate modifications: N-terminal acetylation (N-Ac) replaces the free amino group at the N-terminus, while C-terminal amidation (NH2) replaces the free carboxyl group at the C-terminus. These two modifications together alter the compound’s enzymatic stability, charge profile, and receptor interaction characteristics compared to standard Semax, making Adamax a complementary research tool for studying ACTH-derived neuropeptide structure-activity relationships.
Adamax 10mg is independently tested to greater than 99% purity. All products are for laboratory research use only.
Structural Modifications vs Standard Semax
N-Terminal Acetylation
Acetylating the N-terminus neutralizes the free amino group, reducing susceptibility to aminopeptidase enzymes that cleave N-terminal residues. This modification is studied for its effects on membrane permeability and receptor binding kinetics — the neutralized N-terminus may alter how the peptide interacts with cellular membranes and target receptors compared to the free-amine form in Semax.
C-Terminal Amidation
Amidating the C-terminus replaces the free carboxyl group with an amide (-NH2), neutralizing the negative charge at that terminus. C-terminal amidation is one of the most common modifications in naturally occurring bioactive peptides and is studied for its effects on proteolytic stability (resistance to carboxypeptidases) and receptor recognition. Many endogenous neuropeptides are naturally C-terminally amidated — Adamax’s amidated form may provide a closer structural analog to naturally amidated neuropeptides in research models.
Research Applications
ACTH-derived peptide structure-activity relationship studies
Comparison of N-acetyl/amidate modifications on BDNF pathway modulation vs standard Semax
Proteolytic stability studies — acetylation/amidation vs standard free-termini
Receptor interaction studies — modified vs unmodified ACTH fragment binding
Neuropeptide modification research — studying how termini modifications affect bioactivity
Product Specifications
| Compound | Adamax (N-Acetyl Semax Amidate) |
| Also Known As | N-Ac-Semax-NH2, Acetylated Semax, Adamax |
| Parent Compound | Semax (Met-Glu-His-Phe-Pro-Gly-Pro) |
| Modifications | N-terminal acetylation + C-terminal amidation of Semax |
| Type | Modified synthetic heptapeptide - ACTH(4-10) analog |
| Molecular Formula | C39H53N9O10S (approximate, acetyl+amide modified) |
| Molecular Weight | ~855 g/mol (approximate) |
| Form | Lyophilized powder |
| Purity | >99% HPLC Verified - Batch COA Available |
| Available Size | 10mg |
| Storage | Lyophilized: -20°C | Reconstituted: 2-8°C, use within 28 days |
| Reconstitution | Bacteriostatic Water (BAC Water) |
| Intended Use | Research Use Only (RUO) |
Frequently Ask Questions
What is the difference between Adamax and Semax?
Semax is the standard heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro with free N-terminus and C-terminus. Adamax is N-acetylated at the N-terminus and amidated at the C-terminus - modifications that change charge distribution, enzymatic stability, and potentially receptor interaction profiles. Adamax is studied for how these structural modifications affect the biological activity profile of the Semax parent compound, making it a structure-activity research tool rather than simply a "stronger" or "weaker" version of Semax.
Should I use Adamax or Semax for my research?
This depends on your research question. Standard Semax is appropriate for studying baseline ACTH(4-10)-related BDNF upregulation and neuroprotective signaling. Adamax is appropriate for research specifically examining how N-acetyl/amidate terminal modifications affect peptide stability, receptor interaction, or pathway modulation compared to the parent compound. For comparative structure-activity studies, both compounds together provide the most research utility.
