N-Acetyl Semax

Dosing from the Literature

Published for focus: parent Semax's Russian label doses for its 0.1% nasal drops, and nasal doses from short studies in healthy adults. Not published: any dose of the capped version.

Semax's Russian label covers two strengths of nasal drops: 0.1% (50 mcg per drop), for memory and thinking problems in vascular brain disease, mental fatigue and other uses, and 1% (500 mcg per drop), for the acute period of ischemic stroke (Russian product instructions, Semax). The table gives those label doses and the doses of published Semax studies, all for Semax, then what user reports describe for the capped analog.

What It Is

N-Acetyl Semax is a chemically modified analog of Semax — the Russian synthetic heptapeptide (a chain of 7 amino acids) nootropic developed in the 1980s at the Institute of Molecular Genetics of the Russian Academy of Sciences under Nikolai F. Myasoedov and Ivan P. Ashmarin. Semax itself (Met-Glu-His-Phe-Pro-Gly-Pro) is constructed by appending the stabilizing Pro-Gly-Pro tripeptide (a chain of 3 amino acids) to the ACTH(4-7) (a short fragment of the stress hormone ACTH) fragment. ACTH(4-10) is a natural fragment of adrenocorticotropic hormone that retains neurotrophic and behavioral activity without stimulating cortisol release; the PGP tail dramatically extends half-life by blocking C-terminal carboxypeptidase cleavage. Semax is therefore, structurally, the truncated ACTH(4-7) with a stabilizing PGP "tail" — a design choice that preserves the neurotrophic pharmacology while eliminating the HPA-axis activation of native ACTH.

The "N-Acetyl" modification adds further stabilization. The N-terminal methionine is acetylated (capping the free alpha-amine that would otherwise be the target of aminopeptidase cleavage), and the C-terminal proline is amidated (converting the terminal -COOH to -CONH₂, which blocks residual carboxypeptidase activity). That the N-terminus is where the parent gets cut was measured early: 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, and an inhibitor study put most of the hydrolysis of Semax on aminopeptidases and angiotensin-converting enzyme (Potaman 1991, PMID 1851003; Potaman 1993, PMID 8392718). This acetyl-amide double-capping strategy is a classical medicinal-chemistry approach to raising peptide serum and mucosal half-life; it was applied in parallel to Selank to produce N-Acetyl Selank. The expected pharmacokinetic effect is slower clearance and a longer duration of CNS receptor engagement at equivalent molar doses.

Parent Semax is registered and prescribed in Russia under the trade name Semax (0.1% for cognitive indications; 1% for acute stroke) for ischemic stroke, chronic cerebrovascular insufficiency, transient ischemic attacks, encephalopathy, post-anesthesia cognitive impairment, optic-nerve pathology (including glaucoma), and pediatric cognitive disorders including attention deficit. It has not been approved by the FDA, EMA, MHRA, TGA, or Health Canada. The N-Acetyl amide analog has no regulatory approval anywhere.

A note on nomenclature: the "N-Acetyl Semax Amidate" sold as a research peptide is structurally the same molecule that is also referred to as "Adamax" in some community literature. Kalios treats "Adamax" in stack and product names as N-Acetyl Semax Amidate (NASA).

Mechanism of Action

FDA's reviewers describe Semax as pleiotropic in rodents, acting through poorly understood mechanisms (FDA Semax briefing, 2026). Almost everything below was measured with the parent; whether the acetyl and amide caps leave it unchanged is untested, and in one cell study N-terminal acetylation removed Semax's protection against copper toxicity (Magrì 2016, PMID 27586814).

• BDNF / TrkB (BDNF's receptor — how brain growth signals reach neurons) upregulation (hippocampus) — A single intranasal dose of Semax at 50 mcg/kg produced a 1.4-fold increase in BDNF protein, a 1.6-fold increase in TrkB tyrosine phosphorylation, and a 3-fold increase in exon-III BDNF mRNA plus a 2-fold increase in TrkB mRNA in rat hippocampus (Dolotov 2006, PMID 16996037). The treated rats also made more conditioned avoidance responses, and the authors suggest Semax acts on learning through this hippocampal BDNF/TrkB system (Dolotov 2006).
• NGF upregulation and glial-mediated trophic support — In rat glial cell cultures, Semax raised BDNF mRNA eight-fold and NGF mRNA five-fold within 30 minutes; the authors proposed this neurotrophin induction as the route to the neuron-survival effect they had seen in culture (Shadrina 2001, PMID 11457573).
• Enkephalinase inhibition — In the test tube, Semax (and Selank) inhibited enkephalin-degrading enzymes from human serum, Semax with an IC50 of 10 µM; the authors suggest this may be one of the ways the peptides act (Kost 2001, PMID 11443939).
• Dopaminergic (related to dopamine signaling) and serotonergic (related to serotonin signaling) modulation — In rodents, Semax (0.15 mg/kg by injection) raised the serotonin breakdown product 5-HIAA outside cells in the striatum, to up to 180% of baseline over 1–4 hours, without changing dopamine on its own; given before amphetamine, it amplified amphetamine's release of dopamine and its effect on movement (Eremin 2005, PMID 16362768).
• Inflammation genes after ischemia — The rat stroke models disagree: 24 hours after a transient arterial occlusion, Semax lowered inflammation-related genes such as Il1b and Il6 (Dergunova 2023, PMID 37239313), but after a permanent occlusion it mainly raised immune genes, chemokines and immunoglobulins among them (Medvedeva 2014, PMID 24661604). The authors read both as part of its neuroprotection.
• Oxidative-stress effects — What was measured directly is nitric oxide: after incomplete global ischemia in rats, nitric oxide and indices of lipid peroxidation were elevated, and Semax — unlike glycine, tested beside it — abated the rise in nitric oxide and restored neurological functioning (Bashkatova 2001, PMID 11245825).
• Enhanced pharmacokinetics via acetyl-amide capping — Specific to N-Acetyl Semax. Rat blood enzymes break Semax down from its N-terminal end, mostly through aminopeptidases (Potaman 1991, PMID 1851003; Potaman 1993, PMID 8392718); the acetyl cap targets that step, and what the C-terminal amide adds has not been measured. What has been measured is the singly capped form — N-acetyl Semax without the C-terminal amide: in vitro it 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 the parent’s (Shevchenko 2013, PMID 23652441, reported in Shevchenko 2019, DOI 10.1007/s11094-019-01960-x).
• Lack of HPA-axis activation — Semax's Russian label describes it as entirely devoid of hormonal activity (Russian product instructions, Semax), and FDA's reviewers note that the ACTH(4-10) fragment it is modeled on lacks ACTH's corticotropic and melanotropic properties (FDA Semax briefing, 2026). No published study has measured cortisol or other hormones after N-Acetyl Semax.
• Nasal-to-brain delivery — In rats given radiolabeled Semax, a larger share of the dose reached the brain by nose than by vein (about 0.07% against 0.005%), which, FDA's reviewers note, is thought to happen partly through transport along olfactory nerve cells; no human pharmacokinetic study exists (FDA Semax briefing, 2026). Semax's label reports up to 60–70% of a nasal dose absorbed (Russian product instructions, Semax). Semax is registered as nasal drops and the capped analog is sold for nasal spray; how the analog reaches the brain has not been measured.
• Translation from rat to human — The BDNF, TrkB and NGF data come from rats and rat cells (Dolotov 2006, PMID 16996037; Shadrina 2001, PMID 11457573); in people, plasma BDNF rose with Semax after stroke (Gusev 2018, PMID 29798983). The human efficacy evidence is the Russian stroke studies; FDA's 2026 review set them aside because their full texts are in Russian only, and found insufficient evidence that Semax works for cerebral ischemia. In healthy people, the published studies gave one or two days of nasal doses to 14–19 adults (FDA Semax briefing, 2026).
• Dergunova RNA-seq transcriptomics — RNA sequencing by the Dergunova group, 24 hours after a transient middle cerebral artery occlusion in rats, found several hundred genes whose expression differed with Semax compared with saline: inflammation-related genes went down and neurotransmission-related genes went up, the reverse of what the ischemia did (Dergunova 2023, PMID 37239313).
• Immune and vascular gene-expression modulation — Medvedeva 2014 genome-wide transcriptional analysis documented Semax effects on immune and vascular gene expression in rat focal cerebral ischemia. The authors propose these immune and vascular effects as the key mechanisms of its neuroprotection (Medvedeva 2014).

What the Research Shows

The interpretable human efficacy evidence comes from the parent Semax molecule. The N-acetyl amide analog has preclinical rationale but no published clinical trials.

• Ischemic stroke — Gusev 1997 (PMID 11517472) — Hemispheric ischemic stroke trial of Semax in 30 patients vs 80 matched controls receiving conventional therapy. Semax added to standard care improved the rate of recovery of general cerebral and focal motor symptoms; EEG, somatosensory evoked potentials, and clinical scales all showed favorable shifts. This study and follow-ups anchor the Russian stroke indication.
• Ischemic stroke — Gusev 2018 (PMID 29798983) — Evaluation of Semax plus early rehabilitation on plasma BDNF levels, motor performance, and Barthel Index in post-ischemic-stroke patients. Conclusion: early rehabilitation plus Semax increases plasma BDNF, speeds functional recovery, and improves motor performance.
• Chronic cerebrovascular insufficiency — Gusev (Zh Nevrol Psikhiatr Im S S Korsakova 2005) reported Semax benefit in prevention of disease progression and exacerbations in patients with chronic cerebrovascular insufficiency (PMID 15792140).
• Cerebral ischemia gene expression — Medvedeva, Dergunova and colleagues have published genome-wide transcriptional studies showing Semax-induced changes in immune- and vascular-system gene expression after permanent middle cerebral artery occlusion in rats (Medvedeva et al., BMC Genomics 2014; PMID 24661604). These studies provide the mechanistic substrate for the stroke clinical signal.
• BDNF and TrkB (Dolotov 2006, PMID 16996037) — Brain Research publication establishing the hippocampal BDNF / TrkB signaling effect at a single 50 mcg/kg intranasal dose. Defining mechanistic paper for the Semax nootropic claim.
• Enkephalinase inhibition (Kost 2001, PMID 11443939) — Semax and Selank both inhibit enkephalin-degrading enzymes from human serum.
• Focal cortical ischemia (Romanova 2006, PMID 17603664) — In rats, six days of intranasal Semax after photoinduced ischemia of the prefrontal cortex decreased the volume of the cortical infarction and improved retention and performance of a conditioned passive-avoidance response.
• Attention and learning (preclinical) — Semax produces consistent improvements in learning, attention, and memory in rodent active-avoidance, passive-avoidance, and radial-arm-maze tasks.
• Anxiolytic signature without sedation — Modest anxiolytic signal likely mediated through melanocortin and serotonergic modulation, distinct from benzodiazepine-class GABAergic (related to GABA signaling) sedation.
• N-Acetyl Semax analog data — No published study measures the acetyl-amide analog itself; the pharmacokinetic work is on the singly capped N-acetyl Semax, and the rest is extrapolation. No controlled human data exist for the stabilized form as of April 2026. The one published study of an acetylated Semax is chemistry rather than behavior: acetylating the N-terminal amine 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). In the parent’s own structure-activity work, changing that same residue was not a neutral act: attaching a gluconic-acid residue or swapping methionine for lysine kept the nootropic effect in rat learning tests, swapping it for tryptophan or serine weakened it, and swapping it for glycine, threonine or alanine abolished it (Glazova 2005, PMID 16212268).

Human Data

• Gusev 1997 (PMID 11517472) — Semax in acute hemispheric ischemic stroke, 30 patients vs 80 controls; improved motor and general cerebral symptom recovery.
• Gusev 2018 (PMID 29798983) — Semax + early rehabilitation increased plasma BDNF and accelerated functional and motor recovery after ischemic stroke.
• Gusev 2005 — Semax for preventing progression and exacerbations of chronic cerebrovascular insufficiency. 187 patients at different stages of the disease; the authors report clinical improvement, stabilization of the course and a reduced risk of stroke and transient ischemic attacks, with few side effects (Gusev 2005, PMID 15792140).
• Dolotov 2006 (PMID 16996037, Brain Research) — Single intranasal Semax dose at 50 mcg/kg upregulates BDNF and TrkB in rat hippocampus; defining mechanism paper.
• Kost 2001 (PMID 11443939) — Semax and Selank inhibit enkephalin-degrading enzymes from human serum.
• Medvedeva et al., BMC Genomics 2014 (PMID 24661604) — Semax altered expression of immune- and vascular-system genes in rat brain after permanent middle cerebral artery occlusion.
• Ashmarin 1997 (PMID 9173745) — Fifteen-year design and development review of the Semax nootropic program.
• Shadrina 2001 — Semax induces NGF and BDNF mRNA in rat glial cell cultures.
• Stavchansky 2011 — Effect of Semax and C-end PGP on morphology and proliferative activity of rat brain cells during experimental ischemia.
• Filippenkov 2023 (PMID 37510287) — RNA-seq of Semax and ACTH(6-9)PGP in the dorsolateral frontal cortex 4.5 hours after transient MCAO in rats: 131 differentially expressed genes for Semax and 322 for ACTH(6-9)PGP, both peptides partly preventing the change in immune- and neurosignaling-related gene expression that the ischemia caused.

No published human clinical trials specifically evaluate the N-Acetyl amide analog as of this writing. All positive clinical evidence derives from the parent Semax molecule.

Reconstitution & Storage

N-Acetyl Semax is sold as a research chemical in powder vials for nasal spray. The table is arithmetic only: what a 5 mg or 10 mg vial mixed with 2 mL or 5 mL of bacteriostatic water holds per mL and per 100 µL.

• Reconstitution — Reconstitution guides describe injecting diluent slowly down the side of the vial and swirling gently rather than shaking.
• Nasal-spray delivery — For compounded Semax nasal sprays, FDA's reviewers noted that the container, closure and pump affect how much drug each spray delivers and how evenly (FDA Semax briefing, 2026).
• Storage — No label or study gives storage conditions for N-Acetyl Semax, as powder or mixed.

→ Calculator — vial-to-syringe math

Side Effects & Risks

• Tolerability (parent Semax) — In 187 patients with chronic cerebrovascular insufficiency, the authors report few side effects and good tolerance, older patients included (Gusev 2005, PMID 15792140), and the developers' 15-year review reports no side effects or complications (Ashmarin 1997, PMID 9173745). FDA's 2026 review found too little clinical information to characterize Semax's safety; FDA's adverse-event database held one report, of eye pain and a hospital stay after Semax 0.1% nasal drops bought online; and FDA flagged a possible bleeding risk from anticlotting effects seen in rats (FDA Semax briefing, 2026).
• Nasal irritation — Semax's Russian label lists mild irritation of the nasal lining with long use (Russian product instructions, Semax); user reports compiled by an online guide also describe mild nasal irritation.
• Overstimulation / insomnia — User reports compiled by an online guide describe overstimulation and restlessness at higher doses, more often with the N-acetyl variants, and the guide notes that late-evening Semax doses may interfere with sleep.
• Headache — The same user reports describe mild headaches at higher doses, above 600–900 mcg a day.
• HPA-axis considerations — Semax's label describes it as devoid of hormonal activity (Russian product instructions, Semax); its Pro-Gly-Pro tail stabilizes it against breakdown (Dergunova 2023, PMID 37239313). No published study has measured cortisol after N-Acetyl Semax.
• Contraindications — None are set for the capped analog. Semax's Russian label lists pregnancy and breastfeeding (no clinical studies were done), acute psychiatric disorders, anxiety disorders, a history of seizures and younger children (under 7 or under 18, depending on strength and use), and calls vasoconstrictor nose drops alongside it undesirable (Russian product instructions, Semax). In rodents, Semax given before amphetamine amplified amphetamine's release of dopamine and its effect on movement (Eremin 2005, PMID 16362768).
• Purity / source — FDA's review did not cover the capped analog. For Semax itself, FDA's reviewers found no monograph in the European, Japanese or International Pharmacopoeia, and the certificates of analysis they examined reported purity but no tests for aggregates or microbial contamination (FDA Semax briefing, 2026).
• Long-term safety (analog) — Not studied: no published study has measured the acetyl-amide analog's safety, short or long term; the only papers on acetylated Semax are test-tube and cell studies (Shevchenko 2013, PMID 23652441; Magrì 2016, PMID 27586814).

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for N-Acetyl Semax, and Semax's Russian label lists none (Russian product instructions, Semax). Semax's own trials measured neurological rating scales, EEG and evoked potentials in acute stroke (Gusev 1997, PMID 11517472), and plasma BDNF, motor performance and the Barthel index of daily living after stroke (Gusev 2018, PMID 29798983).

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References

1. Gusev EI, Skvortsova VI, Miasoedov NF, Nezavibat'ko 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.
2. 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.
3. Dolotov OV, Karpenko EA, Inozemtseva LS, Seredenina TS, Levitskaya NG, Rozyczka J, Dubynina EV, Novosadova EV, Andreeva LA, Alfeeva LY, Kamensky AA, Grivennikov IA, Myasoedov NF, Engele J. 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.
4. Kost NV, Sokolov OYu, 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.
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. Ashmarin IP, Nezavibat'ko VN, Myasoedov NF, Kamenskii AA, Grivennikov IA, Ponomareva-Stepnaia MA, Andreeva LA, Kaplan AIa, Koshelev VB, Riasina TV. A nootropic adrenocorticotropin analog 4-10-semax (15 years experience in its design and study). Zh Vyssh Nerv Deiat Im I P Pavlova. 1997;47(2):420-430. PMID: 9173745.
7. 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.
8. 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.
9. Eremin KO, Kudrin VS, Saransaari P, Oja SS, Grivennikov IA, Myasoedov NF, Rayevsky KS. Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents. Neurochem Res. 2005;30(12):1493-1500. PMID: 16362768.
10. Dergunova LV, Filippenkov IB, Limborska SA, Myasoedov NF. Neuroprotective Peptides and New Strategies for Ischemic Stroke Drug Discoveries. Genes (Basel). 2023;14(5):953. PMID: 37239313.
11. 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.
12. Potaman VN, Alfeeva LY, Kamensky AA, Nezavibatko VN. Degradation of ACTH/MSH(4-10) and its synthetic analog semax by rat serum enzymes: an inhibitor study. Peptides. 1993;14(3):491-495. PMID: 8392718.
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. 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.
16. Glazova NIu, Sebentsova EA, Levitskaia NG, Andreeva LA, Alfeeva LIu, Kamenskii AA, Miasoedov NF. Effect of modification of the N-terminal region of molecule on the expression of neotropic effect of semax analogues. Izv Akad Nauk Ser Biol. 2005;(4):460-466. PMID: 16212268.
17. Gusev EI, Skvortsova VI, Chukanova EI. Semax in prevention of disease progress and development of exacerbations in patients with cerebrovascular insufficiency. Zh Nevrol Psikhiatr Im S S Korsakova. 2005;105(2):35-40. PMID: 15792140.
18. 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.)
19. Peptogen. Семакс (Semax) 0.1% and 1% nasal drops: instructions for medical use, registrations ЛС-002553 (0.1%) of December 30, 2011, reissued November 10, 2015, and Р N000812/01 (1%) of December 29, 2011, reissued November 16, 2015. peptogen.ru/products/semaks-0-1/ and peptogen.ru/products/semaks-1/ (instructions and registration certificates). Read October 4, 2026. (In Russian. Indications, doses (50 µg per drop of the 0.1% solution, 500 µg per drop of the 1%), contraindications, side effects, nasal absorption, storage; prescription only.)
20. FDA. Evaluation of Semax-Related Bulk Drug Substances (Semax (Free Base) and Semax Acetate) for Inclusion on the 503A Bulk Drug Substances List. FDA Briefing Document, Pharmacy Compounding Advisory Committee meeting of July 23–24, 2026; memorandum dated May 11, 2026. fda.gov/media/193348/download. Read October 4, 2026.
21. 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.

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