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Adamax

Studied for attention and working memory, recovery after brain injury or stroke and mood and stress resilience. A Semax-family peptide sold on the nootropic gray market since the 2010s, with no published chemistry, pharmacology or clinical literature under that name.

categorycognitive
clinical evidencenone
community adoptionniche
uses graded4
sources8
last reviewed24 Aug 2026
compound file

The answer, first. A Semax-family peptide sold on the nootropic gray market since the 2010s, with no published chemistry, pharmacology or clinical literature under that name. The strongest evidence is for attention and working memory, graded D — animal or mechanism only. Nothing has been published on Adamax.

The claim rides on Semax, whose only placebo-controlled healthy-volunteer study measured brain networks rather than cognition 4. Every other use — recovery after brain injury or stroke, mood and stress resilience, longer duration than Semax — grade D or E: animal or mechanism data with no controlled human outcome.

What it is used for

Every use graded on its own evidence, not the compound as a whole. 4 outcomes, ranked by what the human record supports.

#outcome · human · animal · gradewhat the best evidence actually shows
01Attention and working memoryno trial · no study of Adamaxgrade DNothing has been published on Adamax. The claim rides on Semax, whose only placebo-controlled healthy-volunteer study measured brain networks rather than cognition 4.
02Recovery after brain injury or strokeno trial · no study of Adamaxgrade DNo Adamax study exists in any species. Semax has Russian open-label stroke trials, none of them blinded 1. That record belongs to a different molecule.
03Mood and stress resilienceno trial · no study of Adamaxgrade DNo Adamax data. Semax showed antidepressant-like and antistress effects in male rats under chronic unpredictable stress 3. A rat result on the parent compound is not evidence for this one.
04Longer duration than Semaxno trial · no study of Adamaxgrade DThe selling point is the modification, not an outcome. No half-life, brain concentration or duration has been measured for Adamax in any species. Semax degrades rapidly on rat brain membranes 5.
gradewhat it means
ARegulatory approval, or multiple adequately-powered trials agreeing with each other
BAt least one well-powered human randomised trial, with the direction replicated
CSmall or open-label human trials only
DAnimal or mechanism data only, with no controlled human outcome
EA claim the human trials have already killed

How it works

The proposed mechanism, in three steps. A mechanism is a reason to run a trial, never a substitute for one.

1targetNo target has been published for Adamax. The parent Semax binds saturable sites on rat basal forebrain membranes, Kd 2.4 nM 25.
2signalBy extrapolation only: intranasal Semax raised BDNF protein in rat basal forebrain within 3 hours 2. Adamax has never been tested.
3effectNo measured effect of Adamax in any model. Every step above is the parent compound's record, not this molecule's 123.

What it does not do

Claims the current record does not support. Worth knowing before you set expectations.

not supported by the evidence

How it is used

What published protocols administered, and what the community reports doing. Descriptive on both counts, and never a recommendation.

routeIntranasal, following the Semax convention. No published protocol exists for this compound.
formatNasal solution or lyophilised powder from research-chemical vendors.
published dosesNone. No human or animal dosing study of Adamax has been published. Semax protocols run 0.015 to 0.050 mg/kg intranasally in the developers' work 6 and 12 mg/day in a motor neuron disease series 7. Those describe a different molecule.
human pharmacokineticsNo pharmacokinetic data published for Adamax in humans or animals.
reported conventionsAs reported on nootropics forums and vendor threads, 2018 to 2026: intranasal doses described as a fraction of a Semax dose. Taken on single days rather than in courses, on the belief that it lasts longer. Convention, not guidance.
commonly paired withSemax

This site does not publish protocols to follow. The doses above are what studies administered or what users report, stated as facts about the literature and the market. How protocols are structured, mixing and storage and the reconstitution calculator cover the arithmetic.

What to expect

Where a trial measured it, the trial. Where only the community reports it, that is said out loud.

onsetNo trial has measured anything about Adamax, so there is no onset to report. As reported: a same-day effect, described by users who are also comparing against Semax from memory.
most common reportAs reported: a stimulant-like focus shift, sometimes with irritability, in a very small reporting base.
adverse effectsNo adverse-event data exist for this compound at any dose. As reported: headache, irritability and nasal irritation, the same cluster reported for Semax and not separable from it.
the stop signalNo published stop criterion, because nothing has been published. As reported: users stop on irritability or on a headache that follows the dose.

Approval and status

What regulators and sport bodies have actually said, separately from what the evidence shows.

approvalNever approved anywhere. Not a registered medicine in any country.
FDANo FDA approval and no US drug product. Sold as a research chemical.
sport [WADA]Not named on the Prohibited List. The S0 catch-all covers unapproved substances.
sold asresearch chemical

Check the vial

The grade above describes a molecule studied under controlled conditions. It says nothing about the powder in a particular vial.

That gap is the one part of this market a reader can actually close. How to read a certificate of analysis covers the five measures in five minutes, and the 2026 audit grades vendors on the documents they publish against a rubric printed in full.

Questions we get

What is Adamax used for?

It is sold as a longer-acting Semax for attention, focus and mood. Nothing supports that under this name. A PubMed search for Adamax returns no study of the peptide in any species.

The only case for it is anecdote plus extrapolation from Semax, whose own human record is Russian, open-label and unblinded 14.

How is Adamax used?

Descriptively, from the market rather than the literature, because no protocol has been published. Vendors sell a nasal solution or a powder and the convention follows Semax at a lower volume.

For comparison, Semax protocols run 0.015 to 0.050 mg/kg intranasally in the developers' work 6 and 12 mg/day in a clinical series 7. Those describe a different molecule.

How long does Adamax take to work?

No study has measured anything about this compound, including whether it does anything at all, so there is no onset. Even the parent record is thin.

The one placebo-controlled study of Semax in healthy adults detected a resting brain-network difference 5 to 20 minutes after a dose 4. That is not an effect a person would notice.

Is Adamax an approved drug?

No, and it carries the only none rating on our clinical evidence axis. That is not a harsh grade, it is a literal one: there is no published study of Adamax in humans, in animals or in cells.

Vendors do not even agree on its structure. On our index it is graded none on clinical evidence and niche on community adoption.

How do I know what is actually in a vial of Adamax?

You do not, unless a certificate of analysis for that specific lot says so. A certificate worth trusting covers five measures: identity, purity, measured net content, endotoxin and a microbial screen.

It names the lab that ran them and carries an accession number you can verify with that lab. Most certificates on this market cover one to three of the five. Purity alone is one number, not a quality programme.

References

  1. Gusev EI, Martynov MY, Kostenko EV, et al. [The efficacy of semax in the treatment of patients at different stages of ischemic stroke]. Zh Nevrol Psikhiatr Im S S Korsakova. 2018. PMID 29798983
  2. Dolotov OV, Karpenko EA, Seredenina TS, et al. Semax, an analogue of adrenocorticotropin 4-10, binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. J Neurochem. 2006. PMID 16635254
  3. Inozemtseva LS, Yatsenko KA, Glazova NY, et al. Antidepressant-like and antistress effects of the ACTH 4-10 synthetic analogs Semax and Melanotan II on male rats in a model of chronic unpredictable stress. Eur J Pharmacol. 2024. PMID 39442746
  4. Lebedeva IS, Panikratova YR, Sokolov OY, et al. Effects of Semax on the Default Mode Network of the Brain. Bull Exp Biol Med. 2018. PMID 30225715
  5. Dolotov OV, Zolotarev YA, Dorokhova EM, et al. [The binding of Semax, ACTH 4-10 heptapeptide, to plasma membranes of the rat forebrain basal nuclei and its biodegradation]. Bioorg Khim. 2004. PMID 15344653
  6. Asmarin IP, Nezavibat'ko VN, Miasoedov NF, et al. [A nootropic adrenocorticotropin analog 4-10-semax, 15 years experience in its design and study]. Zh Vyssh Nerv Deiat Im I P Pavlova. 1997. PMID 9173745
  7. Serdiuk AV, Levitskii GN, Miasoedov NF, et al. [The study of chronic partial denervation and quality of life in patients with motor neuron disease treated with semax]. Zh Nevrol Psikhiatr Im S S Korsakova. 2007. PMID 18379501
  8. Filippenkov IB, Stavchansky VV, Denisova AE, et al. Novel Insights into the Protective Properties of ACTH 4-7 PGP, Semax, Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats. Genes. 2020. PMID 32580520

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