Adamax

Dosing from the Literature

Published for focus: parent Semax's Russian nasal doses. Not published: any dose of Adamax itself.

The rows below are the parent’s Russian label doses. No dose of Adamax itself has been published, and no FDA-approved dose exists for either.

What It Is

Adamax is the community / vendor name most commonly used for N-Acetyl Semax Amidate (NASA) — a chemical derivative of the Russian ACTH-analog nootropic Semax. Semax itself (Met-Glu-His-Phe-Pro-Gly-Pro, MEHFPGP) is a seven-amino-acid peptide derived from the N-terminal region of adrenocorticotropic hormone (ACTH). It was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences and at Moscow State University, and has been marketed in Russia as Semaks (Семакс) since the 1990s for stroke, cognitive impairment, and asthenia.

Adamax modifies Semax at both ends. The N-terminal methionine is acetylated (Ac-Met...) to block aminopeptidase-mediated degradation; the C-terminal proline is amidated (...Pro-NH₂) to block carboxypeptidase cleavage. That the N-terminus is where the parent gets cut was measured in rat blood and serum: a bestatin-sensitive aminopeptidase clipped Semax’s N-terminal Met and Glu and accounted for a third to a half of the degrading activity (Potaman 1991, PMID 1851003). Parent Semax is already unusually stable because its C-terminal Pro-Gly-Pro motif is inherently resistant to most peptidases, but parent Semax still has a central nervous system duration of action measured in tens of minutes to a few hours. The double-blocked Adamax analog has been reported by Russian investigators and secondary reviewers to extend biochemical half-life and CNS exposure substantially. What has actually been published is the singly capped form: in vitro, N-acetyl Semax (Ac-Met-Glu-His-Phe-Pro-Gly-Pro) was almost untouched by leucine aminopeptidase even at 60 hours, while in rat blood plasma its concentration held only for the first 15 minutes and complete breakdown came about 30 minutes later than Semax’s (Shevchenko 2013, PMID 23652441, reported in Shevchenko 2019, DOI 10.1007/s11094-019-01960-x).

In the commercial nootropic hierarchy, the compound family is often described as: Semax → N-Acetyl Semax (single N-terminal blocked) → N-Acetyl Semax Amidate / Adamax (both ends blocked). Each modification is claimed by sellers to increase metabolic stability, duration of BDNF elevation, and in some cases BBB penetration. The published evidence supporting each successive analog is progressively thinner — Semax itself has decades of Russian clinical data, N-Acetyl Semax has a smaller preclinical database, and the doubly-blocked Adamax form has essentially only preclinical evidence with heavy reliance on analogical reasoning from the parent.

The name "Adamax" is a vendor-chosen trade name that overlaps with unrelated pharmaceutical products in other therapeutic areas. In the peptide / nootropic context, the name refers specifically to N-Acetyl Semax Amidate.

Mechanism of Action

Mechanistic work on Adamax is largely by-analogy to parent Semax with modest direct data. The mechanistic picture below reflects Semax-family biology as published by the Myasoedov / Grivennikov / Dolotov laboratories in Moscow plus a small number of Western citing reports.

• Hippocampal BDNF upregulation — A single 50 µg/kg dose of Semax raised BDNF protein about 1.4-fold and exon III BDNF mRNA about 3-fold in the rat hippocampus, alongside increased trkB phosphorylation (Dolotov et al., Brain Res 2006; PMID 16996037). The doubly-protected Adamax analog is reported in Russian preclinical work to achieve proportionally larger and longer-lasting BDNF elevation by virtue of its extended CNS exposure, though the comparative head-to-head human data does not exist.
• TrkB (BDNF's receptor — how brain growth signals reach neurons) / MAPK / ERK signaling — BDNF acts through TrkB receptor tyrosine kinase, activating the Ras-Raf-MEK-ERK and PI3K-Akt cascades that drive long-term potentiation (LTP), dendritic spine growth, and synaptic remodeling. Chronic ACTH-4-10 analog exposure in rodents increases markers of hippocampal plasticity.
• Enkephalinase inhibition — Semax and its analogs appear to inhibit enkephalin-degrading enzymes, indirectly potentiating endogenous opioid tone. This may underlie some of the reported analgesic / mood-modulating properties of the family. What was measured is broader than one enzyme: Semax and Selank each inhibited the enkephalin-degrading enzymes of human serum in a dose-dependent way, with IC50 values of 10 µM and 20 µM (Kost 2001, PMID 11443939).
• Melanocortin MC3 / MC4 receptor modulation — Because the parent ACTH(4-10) fragment retains melanocortin-system activity, Semax-family peptides engage MC3/MC4 receptors in the CNS. These receptors are involved in attention, motivation, and stress-reactive HPA-axis modulation. Effect on peripheral MC1/MC2 is attenuated.
• Dopaminergic (related to dopamine signaling) / serotonergic (related to serotonin signaling) tone — Preclinical Russian work has described Semax-induced modulation of striatal dopamine and cortical serotonin — effects broadly consistent with the compound's reported motivational and attentional properties.
• Neuroprotection in ischemia — In rats, six days of intranasal Semax after photoinduced ischemia of the prefrontal cortex decreased the volume of the cortical infarction and improved passive-avoidance retention (Romanova 2006, PMID 17603664); in incomplete global ischemia, Semax — but not its C-terminal tripeptide PGP — abated the manifestation of ischemic damage to nervous tissue (Stavchansky 2011, PMID 20617398). No published study tests the Adamax analog in either model.
• Dual-terminal protease resistance — Acetylation and amidation together confer resistance to both aminopeptidases and carboxypeptidases, the two major peptidase classes that limit peptide half-life in plasma and nasal mucosa. No study has measured the capped analog’s duration; this is the structural basis for the longer duration claim.
• Intranasal CNS delivery — Like parent Semax, Adamax is administered intranasally, taking advantage of direct olfactory and trigeminal nerve pathways that bypass the blood-brain barrier to some extent. Published ACTH(4-10) analog intranasal dosimetry shows CNS concentrations achievable at very low systemic exposure.

What the Research Shows

• Parent Semax clinical base — Parent Semax is approved in Russia (registered 1996–1997) for ischemic stroke, transient ischemic attack, cognitive impairment, and optic nerve disorders. Russian-language randomized trials in these indications form the clinical backbone of the Semax family. Independent Western replication is limited.
• BDNF elevation (preclinical) — Semax increases hippocampal BDNF mRNA and protein in rats (Dolotov et al., 2006). No study read for this page tested the capped analogs in the same assays.
• Cognitive testing (preclinical) — Rodent learning and memory tasks (Morris water maze, passive avoidance, radial arm maze) show improved acquisition and retention with Semax-family peptides. No study read for this page tested the capped analogs or with less-frequent dosing.
• Stroke models — MCAO models in rats and gerbils demonstrate reduced infarct volume, preserved CA1 neurons, and improved functional outcomes. This preclinical stroke signal is the basis for the parent compound's Russian clinical stroke indication.
• Anxiolytic / anti-depressant signal — Forced-swim, elevated-plus-maze, and open-field tests in rodents show anxiolytic-like and antidepressant-like effects. Russian clinical reports extend this to human asthenia and post-stroke depression.
• Optic nerve / retinal preservation — Russian ophthalmology trials report benefit in optic nerve atrophy and vascular retinopathy; the peptide was given intranasally, as nasal drops or by endonasal electrophoresis, not as an eye drop.
• Addiction / withdrawal — Some Russian work has explored Semax-family effects on opioid withdrawal severity — coherent with the enkephalinase inhibition mechanism.
• Head-to-head Adamax vs Semax — Formal head-to-head clinical comparisons do not exist. Pharmacokinetic comparison data is limited to preclinical analogs of analogs, not to the specific NASA compound sold as Adamax. The one published study of an acetylated Semax tested chemistry rather than behavior: N-terminal acetylation changed the copper(II) complex the peptide forms, and the acetylated peptide did not protect SH-SY5Y neuroblastoma cells from copper-induced toxicity, which the authors read as the free N-terminal amine doing that work (Magrì 2016, PMID 27586814).

Human Data

There is no published Western human clinical trial of Adamax (N-Acetyl Semax Amidate) as such. The parent Semax compound has decades of Russian clinical use and multiple Russian-language RCTs for stroke, post-stroke cognitive recovery, asthenia, and optic nerve disorders; those are the human evidence base on which Adamax claims rest.

• Parent Semax — Russian stroke trials — Two Russian studies of intranasal Semax added to standard care report faster recovery — one against 80 patients on conventional therapy, one comparing patients given semax with patients not given it. Neither was placebo-controlled. These are published primarily in Russian journals with limited independent verification. The largest published series ran 110 patients after ischemic stroke on 6,000 mcg/day in two 10-day courses against patients not given it, and reports higher plasma BDNF and faster Barthel-index recovery (Gusev 2018, PMID 29798983).
• Parent Semax — asthenia / cognitive fog — Smaller Russian trials in neurasthenia and post-viral cognitive impairment report benefit on subjective and neuropsychological endpoints.
• Parent Semax — ophthalmology — No published study gave it as an eye drop. The optic-nerve study gave it intranasally — one group nasal drops, one endonasal electrophoresis, one control — alongside standard neurotrophic and anti-inflammatory therapy, and reports improved visual acuity, a wider total visual field and better color vision (Polunin 2000, PMID 10741256).
• N-Acetyl Semax / Adamax — no published human trials — ClinicalTrials.gov shows no registered Western trial. The Russian State Registry of Medicines lists approved Semax products (nasal drops) but does not separately register Adamax.
• Community use — Nootropic community reports describe subjective cognitive stimulation, improved focus, reduced mental fatigue, and occasional mild restlessness / insomnia when dosed late in the day. These are uncontrolled anecdotes, not clinical evidence.

Reconstitution & Storage

Adamax is sold as powder in vials and as premixed nasal spray. No label or guideline read for this page gives a storage condition or shelf life for either. The table is arithmetic only: what a vial of a given size holds once dissolved.

→ Calculator — vial-to-syringe math

Side Effects & Risks

• Nasal irritation — Mild stinging, burning, or nasal drip during or after administration. Usually dose-dependent.
• Overstimulation / insomnia — No study of the capped analog reports its side effects. Russian trials of the parent report none beyond the label’s (see Semax).
• Headache — Occasionally reported; typically mild and transient.
• Mood / anxiety — Some users describe mild agitation or elevated anxiety, particularly at higher doses. Others report the opposite — reduced anxiety and improved stress tolerance (consistent with anxiolytic signal in preclinical studies).
• Hair / skin changes (anecdotal) — Rare reports of temporary hair shedding with chronic high-dose use. Not a confirmed pharmacological effect; biological plausibility is unclear.
• Cardiac / adrenal theoretical concerns — As an ACTH-analog, any residual HPA-axis activity is theoretically possible, although the 4-10 fragment design specifically removed classical cortisol-stimulating activity.
• Pregnancy and lactation — No human safety data.
• Drug interactions — No well-characterized interactions. In theory, other dopaminergic stimulants could add restlessness, and MAO inhibitors could interact.
• Purity risk — Peptide research-chemical quality varies. Some vendors have been shown to sell mislabeled product in the Semax / Selank family.
• Long-term safety — No published chronic-dosing human safety database for the doubly-protected analog. Parent Semax has decades of Russian use without major safety signals, but Adamax is not identical to parent Semax.

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for Adamax, and no study of it has been published. The parent’s Russian instructions list no laboratory tests (Russian product instructions).

Commonly Stacked With

No published study has combined Adamax with anything. FDA’s reviewers found a US website selling a premixed 50:50 Semax and Selank spray and injection — the parent compounds, not this analog (FDA Semax briefing, 2026).

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Legal Status

Related Compounds

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Next Steps

References

1. Dolotov OV, Karpenko EA, Inozemtseva LS, Seredenina TS, Levitskaya NG, Rozyczka J, Dubynina EV, Novosadova EV, Andreeva LA, Alfeeva LY, Kamensky AA, Grivennikov IA, Engele J, Myasoedov NF. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 2006;1117(1):54-60. PMID: 16996037.
2. Dolotov OV, Karpenko EA, Seredenina TS, Inozemtseva LS, Levitskaya NG, Kamensky AA, Andreeva LA, Alfeeva LY, Nagaev IY, Zolotarev YA, Grivennikov IA, Engele J, Myasoedov NF. Semax, an analog of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. J Neurochem. 2006;97 Suppl 1:82-86. PMID: 16635254.
3. Ashmarin IP, Nezavibatko VN, Levitskaya NG, Koshelev VB, Kamensky AA. Design and investigation of an ACTH(4-10) analog lacking D-amino acids and hydrophobic radicals. Neurosci Res Commun. 1995;16(2):105-112.
4. Kaplan AYa, Kochetova AG, Nezavibathko VN, Rjasina TV, Ashmarin IP. Synthetic ACTH analogue Semax displays nootropic-like activity in humans. Neurosci Res Commun. 1996;19(2):115-123.
5. Medvedeva EV, Dmitrieva VG, Povarova OV, Limborska SA, Skvortsova VI, Myasoedov NF, Dergunova LV. The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics. 2014;15:228. PMID: 24661604.
6. Shadrina MI, Dolotov OV, Grivennikov IA, Slominsky PA, Andreeva LA, Inozemtseva LS, Limborska SA, Myasoedov NF. Rapid induction of neurotrophin mRNAs in rat glial cell cultures by Semax, an adrenocorticotropic hormone analog. Neurosci Lett. 2001;308(2):115-118. PMID: 11457573.
7. Stavchansky VV, Yuzhakov VV, Botsina AY, Skvortsova VI, Bondurko LN, Tsyganova MG, Limborska SA, Myasoedov NF, Dergunova LV. The effect of Semax and its C-end peptide PGP on the morphology and proliferative activity of rat brain cells during experimental ischemia: a pilot study. J Mol Neurosci. 2011;45(2):177-185. PMID: 20617398.
8. Gusev EI, Skvortsova VI, Miasoedov NF, Nezavibatko VN, Zhuravleva EIu, Vanichkin AV. Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study). Zh Nevrol Psikhiatr Im S S Korsakova. 1997;97(6):26-34. PMID: 11517472.
9. Potaman VN, Antonova LV, Dubynin VA, Zaitzev DA, Kamensky AA, Myasoedov NF, Nezavibatko VN. Entry of the synthetic ACTH(4-10) analogue into the rat brain following intravenous injection. Neurosci Lett. 1991;127(1):133-136. PMID: 1652713.
10. Miasoedova NF, Skvortsova VI, Nasonov EL, Zhuravleva EY, Grivennikov IA, Arsenyeva EL, Sukhanov II. [Investigation of mechanisms of neuro-protective effect of semax in acute period of ischemic stroke]. Zh Nevrol Psikhiatr Im S S Korsakova. 1999;99(5):15-19. PMID: 10358912.
11. Romanova GA, Silachev DN, Shakova FM, Kvashennikova YuN, Viktorov IV, Shram SI, Myasoedov NF. Neuroprotective and antiamnesic effects of semax during experimental ischemic infarction of the cerebral cortex. Bull Exp Biol Med. 2006;142(6):663-666. PMID: 17603664.
12. Potaman VN, Alfeeva LY, Kamensky AA, Levitzkaya NG, Nezavibatko VN. N-terminal degradation of ACTH(4-10) and its synthetic analog semax by the rat blood enzymes. Biochem Biophys Res Commun. 1991;176(2):741-746. PMID: 1851003.
13. Shevchenko KV, Nagaev IY, Andreeva LA, Shevchenko VP, Myasoedov NF. Stability of Semax acetyl to proteolysis in various biological media. Dokl Biol Sci. 2013;449:110-112. PMID: 23652441. (The proteolysis data for N-acetyl Semax; the paper has no abstract, and its numbers are reported in the review below.)
14. Shevchenko KV, Nagaev IYu, Andreeva LA, Shevchenko VP, Myasoedov NF. Prospects for Intranasal Delivery of Neuropeptides to the Brain. Pharm Chem J. 2019;53(2):89-100. DOI: 10.1007/s11094-019-01960-x. (Russian original: Khim-Farm Zh. 2019;53(2):3-15.)
15. Kost NV, Sokolov OIu, Gabaeva MV, Grivennikov IA, Andreeva LA, Miasoedov NF, Zozulia AA. Semax and selank inhibit the enkephalin-degrading enzymes from human serum. Bioorg Khim. 2001;27(3):180-183. PMID: 11443939.
16. Magrì A, Tabbì G, Giuffrida A, Pappalardo G, Satriano C, Naletova I, Nicoletti VG, Attanasio F. Influence of the N-terminus acetylation of Semax, a synthetic analog of ACTH(4-10), on copper(II) and zinc(II) coordination and biological properties. J Inorg Biochem. 2016;164:59-69. PMID: 27586814.
17. Gusev EI, Martynov MY, Kostenko EV, Petrova LV, Bobyreva SN. The efficacy of semax in the treatment of patients at different stages of ischemic stroke. Zh Nevrol Psikhiatr Im S S Korsakova. 2018;118(3. Vyp. 2):61-68. PMID: 29798983.
18. Polunin GS, Nurieva SM, Baiandin DL, Sheremet NL, Andreeva LA. Evaluation of therapeutic effect of new Russian drug semax in optic nerve disease. Vestn Oftalmol. 2000;116(1):15-18. PMID: 10741256.
19. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
20. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.

Related Research

• N-Acetyl SemaxCanonical reference for Adamax — Stabilized ACTH(4-7) Nootropic Analog.
• SemaxNootropic & Neuroprotective (ACTH Analog)
• DS5Dihexa + Semax Nootropic Stack
• SelankAnxiolytic Nootropic (Tuftsin Analog)
• FDA TrackerPCAC voted on 7 of the 12 peptides on July 23–24, 2026; FDA plans a PCAC review of the other 5 before the end of February 2027.