ADAMAX (also written Adamax) is an unapproved synthetic peptide sold online as a “nootropic,” meaning a cognitive enhancer. It is marketed as a modified version of Semax, a short fragment-based analog of adrenocorticotropic hormone (ACTH), with an adamantane group added to the end of the chain.
The most important fact is that no published study of any kind, human or animal, has tested ADAMAX itself. We could not find a peer-reviewed paper, patent, PubChem entry or drug label for it. Its only appearance in an official document is a 2025 submission from New Zealand’s medicines regulator, which named it as a peptide being intercepted at the border and proposed classifying it as a prescription medicine (Medsafe, 2025).
This page summarizes what regulators and the research on its two parent molecules report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Class | Unapproved synthetic peptide; described as an ACTH analog |
| Parent molecules | Semax (an ACTH(4–10) analog) and the adamantane end group of the research compound P021 |
| Approval | Not approved as a medicine by any regulator we could find |
| Human data | None published |
| Animal data | None published for ADAMAX itself |
| Half-life | Not measured; no pharmacokinetic data exist |
| PubChem entry | None (no record found under the name) |
| New Zealand | Named by Medsafe in a 2025 proposal to make ACTH analogs prescription medicines |
| WADA status | Not named; unapproved substances fall under S0 (prohibited at all times) |
What it is
The Semax backbone
Semax is a seven-amino-acid peptide, Met-Glu-His-Phe-Pro-Gly-Pro, developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. It corresponds to the ACTH(4–7) sequence followed by Pro-Gly-Pro, and is referred to in the literature as an ACTH(4–10) analog (Shevchenko et al., Bioorg Khim 2006). PubChem lists its formula as C₃₇H₅₁N₉O₁₀S, molecular weight 813.9 g/mol (PubChem).
The library has a separate page on Semax, and on Selank, a different peptide derived from tuftsin that Medsafe grouped separately (Medsafe, 2025).
The adamantane end group from P021
Adamantane is a rigid, cage-shaped hydrocarbon. Researchers at the New York State Institute for Basic Research added an adamantane-containing residue to a short peptide derived from ciliary neurotrophic factor (CNTF), creating a compound called P021 (also P21), Ac-DGGL-[adamantyl residue]-NH₂ (Li et al., FEBS Lett 2010). The group’s stated aim was to improve passage across the blood-brain barrier (Kazim and Iqbal, Mol Neurodegener 2016). PubChem’s structure for P021 shows that this end group is a 3-carbamoyl-1-adamantyl amide (PubChem).
What ADAMAX is said to be
Sellers describe ADAMAX as Semax with two changes taken from P021: an acetyl group on the starting (N-terminal) end and the adamantane-containing amide on the far (C-terminal) end. No peer-reviewed paper or chemical registry entry confirms that structure, so no formula or molecular weight is given here.
No peer-reviewed or regulatory source confirms this structure, and nobody has published analytical testing of products sold under the name. What is in a given vial is therefore unknown.
| Molecule | What it is | Published research |
|---|---|---|
| Semax | ACTH(4–7) + Pro-Gly-Pro heptapeptide | See the Semax page |
| P021 | CNTF-derived peptide with an adamantane end group | Mouse and rat studies only |
| ADAMAX | Semax with P021-style end modifications (as marketed) | None |
How it works in the body
There are no pharmacokinetic or mechanism studies of ADAMAX. The claims made for it, such as longer duration of action, better brain entry and raised brain-derived neurotrophic factor (BDNF, a protein that supports nerve cell growth and survival), are borrowed from research on its parent molecules. None of that research tested the combined molecule.
What the parent-molecule studies show:
- Semax is broken down quickly. In rats given tritium-labeled Semax into the nose (50 µg/kg), 0.093% of the dose per gram was found in the brain at 2 minutes. The peptide underwent rapid enzymatic breakdown, and the fragment Pro-Gly-Pro dominated in samples (Shevchenko et al., Bioorg Khim 2006).
- Cells clip both ends of Semax. In rat brain cell cultures and membranes, the main breakdown steps were removal of the first two (Met-Glu) and last two (Gly-Pro) amino acids (Zolotarev et al., Amino Acids 2006). These are the ends that ADAMAX’s added groups would cover, which is the rationale for the design. Whether it actually slows breakdown has not been tested.
- Semax raised BDNF in rat brain. A 2003 rat study reported increased BDNF expression in several brain areas (Dolotov et al., Dokl Biol Sci 2003).
- P021 was stable and long-lived in preclinical testing. Its developers reported a plasma half-life of over 3 hours, over 95% stability in artificial intestinal fluid for 2 hours, and blood-brain barrier permeability (Kazim and Iqbal, Mol Neurodegener 2016).
These properties belong to different molecules. A peptide built from parts of both cannot be assumed to share them.
Regulatory status
New Zealand
In June 2025, Medsafe told the Medicines Classification Committee that its enforcement team had intercepted 56 parcels containing peptides or SARMs between 1 April and 19 May 2025. Because many of these peptides were unscheduled, Medsafe had no legal grounds to seize them and released them with a high-risk medicine letter (Medsafe, 2025).
Medsafe proposed a group entry classifying all ACTH analogs as prescription medicines. It named “Adamax and Semax” as examples, describing them as peptide products marketed as cognitive enhancers. It also noted that there is limited clinical research on ACTH analogs and little known about their side effects or long-term effects.
At its July 2025 meeting the committee deferred a decision pending more information on possible unintended effects, for example in cosmetics. In a later note, the secretariat reported that cosmetics bodies raised no issues and that Medsafe recommends classifying the peptides as prescription medicines (MCC 74th meeting minutes).
Sport
ADAMAX is not named on the WADA list. Class S0 prohibits at all times any pharmacological substance not covered elsewhere on the list that has no current approval by a government health authority for human therapeutic use, explicitly including designer drugs (WADA 2026 Prohibited List). An unapproved peptide like ADAMAX fits that description.
United States
We found no FDA approval or application for ADAMAX. It is not named among the controlled anabolic steroids in Schedule III (21 CFR 1308.13).
What the research shows
There is no research on ADAMAX. No randomized trial, observational study, case report or animal experiment using the compound has been published.
The parent compound P021 has been studied only in rodents. Examples:
- In normal adult mice, P021 given outside the brain improved learning and memory and increased the formation of new neurons in the hippocampus (Li et al., FEBS Lett 2010).
- In 22- to 24-month-old rats, oral P021 reduced age-related decline in learning and memory and raised BDNF (Bolognin et al., Neurobiol Aging 2014).
- In a mouse model of Alzheimer’s disease, 12 months of oral P021 reduced abnormal tau and soluble amyloid-β and improved cognition (Kazim et al., Neurobiol Dis 2014).
None of these studies used ADAMAX, and none were in humans. For the Semax evidence base, see the Semax page.
Side effects and risks
Unknown safety profile
Because ADAMAX has never been studied, its side effects, toxicity, interactions and long-term effects are unknown. Medsafe’s submission stated the general concern directly: the quality, efficacy and interactions of these imported peptide products are unknown (Medsafe, 2025).
Product identity and quality
ADAMAX is sold only through unregulated “research chemical” channels. No pharmacopeial standard, reference material or published analysis exists. Buyers have no independent way to confirm the identity, dose, purity or sterility of a product.
Borrowed claims
Claims about BDNF, neurogenesis or improved brain entry come from rat and mouse studies of Semax and P021. Results in rodents often do not carry over to people, and results for one molecule do not transfer automatically to a structurally different one.
Key takeaways
- A marketed Semax derivative. ADAMAX is sold as Semax with an acetyl group and an adamantane end group borrowed from the research peptide P021.
- No studies at all. No human or animal study of ADAMAX has been published, and no peer-reviewed source documents its structure.
- Claims are borrowed. Effects on BDNF, neurogenesis and brain entry come from rodent research on its parent molecules, not on ADAMAX.
- No pharmacokinetic data. Its half-life, absorption and breakdown have never been measured.
- Regulators are moving to restrict it. New Zealand’s Medsafe named it in a 2025 proposal to classify ACTH analogs as prescription medicines, and WADA’s S0 class prohibits unapproved substances like it in sport.
Sources
- Medsafe. Classification of unscheduled peptides: submission to the Medicines Classification Committee. June 2025. Medsafe.
- Medicines Classification Committee. Minutes of the 74th meeting, 23 July 2025, item 5.7 Peptide groups. Medsafe.
- World Anti-Doping Agency. The 2026 Prohibited List: International Standard. WADA.
- Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.
- National Center for Biotechnology Information. Semax, PubChem CID 9811102. PubChem.
- National Center for Biotechnology Information. P021, PubChem CID 56599151. PubChem.
- Shevchenko KV, Nagaev IIu, Alfeeva LIu, et al. Kinetics of Semax penetration into the brain and blood of rats after its intranasal administration [in Russian]. Bioorg Khim. 2006;32(1):64–70. PubMed.
- Zolotarev YA, Dolotov OV, Inozemtseva LS, et al. Degradation of the ACTH(4-10) analog Semax in the presence of rat basal forebrain cell cultures and plasma membranes. Amino Acids. 2006;30(4):403–408. PubMed.
- Dolotov OV, Seredenina TS, Levitskaya NG, et al. The heptapeptide SEMAX stimulates BDNF expression in different areas of the rat brain in vivo. Dokl Biol Sci. 2003;391:292–295. PubMed.
- Li B, Wanka L, Blanchard J, et al. Neurotrophic peptides incorporating adamantane improve learning and memory, promote neurogenesis and synaptic plasticity in mice. FEBS Lett. 2010;584(15):3359–3365. PubMed.
- Kazim SF, Iqbal K. Neurotrophic factor small-molecule mimetics mediated neuroregeneration and synaptic repair: emerging therapeutic modality for Alzheimer’s disease. Mol Neurodegener. 2016;11(1):50. PubMed.
- Bolognin S, Buffelli M, Puoliväli J, Iqbal K. Rescue of cognitive-aging by administration of a neurogenic and/or neurotrophic compound. Neurobiol Aging. 2014;35(9):2134–2146. PubMed.
- Kazim SF, Blanchard J, Dai CL, et al. Disease modifying effect of chronic oral treatment with a neurotrophic peptidergic compound in a triple transgenic mouse model of Alzheimer’s disease. Neurobiol Dis. 2014;71:110–130. PubMed.