TL;DR
The double-capped Semax analog. Parent has the Russian stroke approval. This one has the duration story.
What: N-Acetyl Semax Amidate (NASA, Adamax). Parent Semax = ACTH(4-7) plus PGP, developed at Moscow's Institute of Molecular Genetics in the 1980s. Dual terminal capping slows aminopeptidase and carboxypeptidase clearance.
Does: Preserves Semax's BDNF/TrkB upregulation, NGF induction, enkephalinase inhibition, and neuroinflammation suppression. The caps don't change the mechanism. They extend duration.
Evidence: Parent Semax: Gusev 1997 (PMID 11517472) and Gusev 2018 (PMID 29798983) ischemic stroke trials. Dolotov 2006 (PMID 16996037) pinned BDNF/TrkB in hippocampus. The N-acetyl analog has no published clinical trial of its own.
Used by: Russian neurology for parent Semax (stroke, cognitive). Biohacker and nootropic communities for the N-acetyl form via research-peptide channels.
Bottom line: Parent has the data. Cap gives longer duration. Peer-reviewed analog validation absent.
What It Is
N-Acetyl Semax is a chemically modified analog of Semax — the Russian synthetic heptapeptide 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 to the ACTH(4-7) 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). 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. The stack and product-page references to "Adamax" should be understood as synonymous with N-Acetyl Semax Amidate (NASA).
Mechanism of Action
Semax's pharmacology is multimodal; the N-acetyl amide modification extends duration but does not alter the underlying mechanism. The active pharmacophore engages:
- BDNF / TrkB 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). BDNF-TrkB signaling activates PI3K/Akt and MAPK/ERK cascades that support long-term potentiation, dendritic branching, and adult hippocampal neurogenesis — the cellular substrate of learning and memory.
- NGF upregulation and glial-mediated trophic support — Shadrina 2001 documented rapid induction of NGF and BDNF mRNA in rat glial cell cultures after Semax exposure. The glial-trophic-factor limb complements the direct-hippocampal limb and contributes to the broad neuroprotective profile.
- Enkephalinase inhibition — Semax (and Selank) inhibit enkephalin-degrading enzymes from human serum (Kost 2001, PMID 11443939), raising endogenous enkephalin tone and producing mild opioidergic mood stabilization without direct opioid receptor agonism.
- Melanocortin receptor modulation — The ACTH(4-7) core engages central melanocortin pathways implicated in attention, motivation, and stress resilience. Mechanistic work suggests Semax's attention-enhancing effects are mediated in part through MC4R modulation without HPA-axis activation.
- Dopaminergic and serotonergic modulation — Semax administration alters dopamine and serotonin metabolism in frontal cortex and striatum; this pathway contributes to the reported focus-enhancing and mood-lifting profile.
- Neuroinflammation suppression — Medvedeva et al. (Gusev group) and subsequent genome-wide transcriptional studies (Dergunova, Stavchansky) documented Semax-induced changes in immune and vascular gene expression in rat cerebral ischemia, with attenuation of ischemia-driven pro-inflammatory programs. This limb is proposed to underlie Semax's stroke-recovery signal (Medvedeva 2005; Dergunova 2023).
- Antioxidant / anti-apoptotic effects — Semax reduces oxidative stress markers and caspase-3 activity in ischemic models, consistent with the cytoprotective signal in focal cerebral ischemia (Eremin 2004).
- Enhanced pharmacokinetics via acetyl-amide capping — Specific to N-Acetyl Semax: N-acetylation blocks aminopeptidase cleavage at the N-terminal methionine; C-amidation blocks residual carboxypeptidase activity at the C-terminal proline. The net effect is a longer mucosal residence time, higher CNS AUC per equivalent dose, and a prolonged duration of receptor engagement.
- Lack of HPA-axis activation — The truncation of ACTH(4-10) to ACTH(4-7) plus PGP specifically removed the adrenocortical-stimulating activity of full-length ACTH. Semax and N-Acetyl Semax do not meaningfully raise cortisol. This is the defining pharmacologic distinction from the parent hormone and the basis for their nootropic-without-glucocorticoid safety profile.
- Nasal-to-brain delivery — Intranasal administration bypasses first-pass hepatic metabolism and delivers peptide along olfactory and trigeminal routes directly into the CNS, avoiding BBB-related pharmacokinetic losses. Standard delivery for both parent Semax and the stabilized analog.
- Translation from rat to human — The BDNF / TrkB / NGF upregulation and neuroprotection data are primarily rat-model. Human clinical confirmation comes from the ischemic-stroke trial program, which validates the translation to human CNS pathology. Community-use cognitive-enhancement data in healthy humans is experiential rather than RCT-level.
- Dergunova RNA-seq transcriptomics — Recent work from the Dergunova group applying RNA-sequencing to Semax-treated rat brain after transient middle-cerebral-artery occlusion has mapped hundreds of ischemia-related differentially expressed genes rescued by Semax treatment. This transcriptomic depth is unusual for the peptide-therapeutic literature and adds mechanistic granularity to the stroke-recovery claim.
- 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. This limb of the mechanism may underlie post-stroke recovery signals that extend beyond pure BDNF-mediated plasticity.
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.
- Cerebral ischemia gene expression — Medvedeva, Dergunova, Stavchansky, and colleagues have published a series of genome-wide transcriptional studies showing Semax-induced changes in immune, vascular, and neurosignaling gene expression after transient MCAO in rats (Medvedeva 2005, PMID 16962082; Stavchansky 2012, PMID 22585422; Dergunova 2023). 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.
- Ischemic focal cerebral ischemia (Eremin 2004) — Semax neuroprotective effects in focal cerebral ischemia rat models.
- 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 sedation.
- N-Acetyl Semax analog data — The published literature on the acetyl-amide analog specifically is primarily preclinical pharmacokinetic characterization plus extrapolation. No controlled human data exist for the stabilized form as of April 2026.
Research Limitations
Semax has a meaningful Russian clinical trial base — primarily in ischemic stroke and chronic cerebrovascular disease, primarily in Russian-language journals, and primarily authored by institutions involved in the peptide's original development. This is a real but sponsor-concentrated evidence base. The N-Acetyl amide analog is not independently trialed. Marketing claims of "2–3× greater BDNF elevation" specifically from the acetylated form are not supported by peer-reviewed human data; they appear to be extrapolations from pharmacokinetic half-life comparisons.
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 prevents disease progression and exacerbations in chronic cerebrovascular insufficiency.
- 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 2005 (PMID 16962082) — Semax regulates immune and vascular system gene expression in rat focal cerebral ischemia.
- Ashmarin 1997 (PMID 9234274) — 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.
- Dergunova 2023 (MDPI Genes) — RNA-seq analysis of Semax and ACTH(6-9)PGP in dorsolateral frontal cortex after transient MCAO; hundreds of ischemia-related differentially expressed genes partially rescued by Semax.
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.
Dosing from the Literature
Russian clinical dosing uses the 0.1% Semax nasal solution (cognitive / outpatient) and the 1% Semax nasal solution (acute stroke / inpatient). The table below summarizes those ranges and the community-use range for the stabilized N-acetyl analog.
| Application | Dose | Frequency | Notes |
|---|
| Semax clinical (Russia) — cognitive / chronic | 200–600 mcg (0.1%) | 2–3 ×/day × 10–14 days | Intranasal; typical outpatient course 2 weeks, may be repeated. |
| Semax clinical (Russia) — acute stroke | ~6–18 mg/day (1%) | Divided intranasal doses × 10 days | Hospital-supervised dosing; paired with standard stroke care. |
| N-Acetyl Semax (community-use range) — cognitive | 100–400 mcg per nostril | 1–2 ×/day morning / midday | Avoid late-day dosing (may disrupt sleep). Enhanced half-life reduces frequency. |
| N-Acetyl Semax (community-use range) — acute performance | 200–600 mcg per nostril | Single dose pre-task | Used before cognitive-demanding tasks; not a validated clinical protocol. |
Dosing Disclaimer
N-Acetyl Semax has no validated dosing. The ranges above are extrapolations from parent-Semax clinical practice adjusted for the analog's longer half-life. They are not recommendations. Consult a licensed healthcare provider. Stroke-indication dosing is a hospital-supervised medical protocol, not a research-use guideline.
Reconstitution & Storage
N-Acetyl Semax is supplied as a lyophilized powder, typically 5 mg or 10 mg per vial, for intranasal use after reconstitution with bacteriostatic water.
| Vial Size | Diluent | Resulting Concentration | Per Spray Target |
|---|
| 5 mg | 2 mL BAC water | 2.5 mg/mL (2,500 mcg/mL) | ~250 mcg per 100 µL spray |
| 5 mg | 5 mL BAC water | 1.0 mg/mL (1,000 mcg/mL) | ~100 mcg per 100 µL spray |
| 10 mg | 2 mL BAC water | 5.0 mg/mL (5,000 mcg/mL) | ~500 mcg per 100 µL spray |
| 10 mg | 5 mL BAC water | 2.0 mg/mL (2,000 mcg/mL) | ~200 mcg per 100 µL spray |
- Reconstitution — Inject diluent slowly down the side of the vial and swirl gently. Do not shake.
- Nasal-spray transfer — Transfer reconstituted solution into a calibrated nasal spray bottle; measure spray volume before first use to calculate exact per-dose mcg.
- Storage (lyophilized) — Refrigerated 2–8°C, stable 18–24 months. Protect from light.
- Storage (reconstituted) — Refrigerated 2–8°C for up to 21–28 days with BAC water. Discard at any sign of cloudiness or discoloration.
- Do not freeze reconstituted solution.
→ Use the Kalios Dosing Calculator for N-Acetyl Semax reconstitution
Side Effects & Risks
Important
Parent Semax is Russian-approved; the N-acetyl variant is not. No published clinical trial of the analog. This is a doctor conversation before intranasal self-experimentation.
- Generally well-tolerated — Parent Semax has decades of Russian clinical and pediatric use with an unusually clean safety profile for a CNS-active peptide.
- Nasal irritation — Mild stinging, transient dryness, occasional rhinorrhea with intranasal use.
- Overstimulation / insomnia — Dose late in the day and users report difficulty falling asleep. Morning / midday dosing avoids this.
- Headache — Occasionally reported at the upper end of community dose ranges.
- Hair cycling effects (rare / anecdotal) — Some community reports of increased shedding with chronic high-dose use, plausibly through melanocortin-pathway interactions with hair cycle. Not well-characterized in the literature.
- HPA-axis considerations — As an ACTH(4-7) fragment analog, Semax is specifically designed NOT to activate cortisol release — this is the entire point of the PGP truncation. Functional HPA-axis monitoring in chronic users is reasonable but unremarkable in existing data.
- Thyroid axis — Some preclinical data suggest mild melanocortin-pathway interactions with thyroid function. Chronic users may consider periodic TSH monitoring.
- Contraindications — Pregnancy and lactation (no human data). Active severe psychiatric disorder should be evaluated by a psychiatrist before use. Concurrent use with strong dopaminergic agonists or stimulants may potentiate effects.
- Purity / source — As with all research peptides, community-sourced N-Acetyl Semax varies in purity. Third-party testing recommended for research use.
- Long-term safety (analog) — Not formally characterized. Parent Semax has multi-decade pharmacovigilance data; the acetyl-amide analog does not.
Bloodwork & Monitoring
- Comprehensive metabolic panel (CMP) — Baseline renal and hepatic screening; repeat annually for chronic users. No Semax-specific abnormalities expected.
- Complete blood count (CBC) — Baseline; yearly thereafter.
- Thyroid (TSH, free T4) — Baseline plus annual for long-term users given melanocortin-thyroid axis theoretical interaction.
- Cognitive testing — Standardized assessments (n-back, digit span, trail-making, Stroop) provide the most interpretable outcome data. Repeat at course end.
- Plasma BDNF (optional) — An imperfect surrogate for central BDNF but can track neurotrophic shifts across long courses. Research context only.
- Cortisol (optional) — If subjective HPA-axis concerns. Semax is specifically designed not to activate cortisol, but baseline is reasonable for confirmation.
- Not a psychiatric substitute — Semax is not a substitute for formal evaluation of cognitive impairment, depression, or anxiety disorders. Established evidence-based care remains the primary path.
- Medication reconciliation — Document all current stimulant, SSRI / SNRI, dopaminergic, and other psychotropic medications. Semax-family interactions with validated neurology / psychiatry drugs have not been formally mapped for the N-acetyl analog.
- Post-stroke / post-TBI context — Semax's most rigorous Russian clinical data is in post-stroke and cerebrovascular-disease populations. Anyone pursuing this use case requires formal neurology supervision; self-directed use in acute neurologic disease is not appropriate.
The evidence basis for Semax-family cognitive monitoring is limited. Objective cognitive testing paired with symptom diaries is the most interpretable feedback; avoid over-interpreting subjective reports that are subject to expectancy effects.
Commonly Stacked With
The classic stabilized-Russian nootropic pairing — Semax (cognitive drive, BDNF, attention) + Selank (GABAA-allosteric calm, anxiolysis). Pharmacodynamically complementary, used in Russian outpatient practice as a paired course.
Parent (non-acetylated) Selank; same complementary logic with slightly different pharmacokinetics. Russian clinical literature has evaluated parent Semax + parent Selank extensively.
P21 (CNTF-mimetic neurogenesis peptide)
P21 engages ciliary neurotrophic factor pathways; Semax drives BDNF. Multi-trophic stack used in community literature; no clinical trial data.
Cholinergic support (alpha-GPC / citicoline)
Semax does not directly modulate acetylcholine; pairing with a choline precursor provides a complementary neurotransmitter substrate. Purely community practice.
Omega-3 (EPA/DHA 2–3 g)
Membrane phospholipid and neuroinflammation support. Synergistic with BDNF pathway work; fish-oil omega-3 is a foundational cognitive-support input with RCT-grade evidence in mood and cognitive domains.
Creatine monohydrate (3–5 g)
ATP buffering and modest cognitive-performance evidence particularly under sleep deprivation. Mechanistically independent of Semax; layered use supports ATP availability in neurons during BDNF-driven plasticity.
→ Check compound compatibility in the Stack Builder
Supportive Nutrition & Lifestyle
BDNF / nootropic peptides work best on a foundation of validated cognitive-supportive lifestyle inputs. Users considering N-Acetyl Semax should not view it as a substitute for the following:
- Aerobic exercise (150+ minutes/week) — Exercise is the highest-leverage BDNF-raising intervention known. A Semax course layered on a sedentary lifestyle produces smaller effect than optimizing exercise alone.
- Sleep (7–9 hours consolidated) — Memory consolidation and synaptic plasticity require sleep; any BDNF-elevating intervention works against a headwind in chronically sleep-deprived users.
- Cognitive load / learning — BDNF upregulation requires substrate — active learning, novel cognitive challenge, and effortful practice. Semax's neurotrophic signal supports learning; it does not substitute for it.
- Dietary omega-3 (2–3 g EPA/DHA) — Membrane fluidity and neuroinflammation support; complements BDNF pathway.
- Choline precursors (alpha-GPC 300–600 mg or CDP-choline 250–500 mg) — Semax does not directly modulate acetylcholine; choline precursors provide a complementary neurotransmitter substrate for broader cognitive support.
- Caffeine / L-theanine (balanced) — Classical acute-focus combination; complementary pharmacology to Semax's attention-enhancing signal.
- Creatine monohydrate (3–5 g) — ATP buffering with modest cognitive-performance RCT evidence under sleep deprivation; complementary mitochondrial substrate.
- Magnesium L-threonate (1,000–2,000 mg) — Hippocampal magnesium bioavailability signal; complements synaptic-plasticity mechanism.
- B-complex (methylated forms) — Supporting monoamine synthesis; mood and cognition respond to B-vitamin status.
- Alcohol reduction — Alcohol impairs hippocampal neurogenesis; reduction supports any BDNF-targeted pharmacologic intervention.
What to Expect — Timeline
Experience varies substantially by baseline cognitive load and dose.
- First dose (30–60 minutes) — Subtle lift in focus and mental clarity. Some users describe "sharper" verbal fluency and decision speed; others describe no acute change.
- Days 1–3 — Acute cognitive-clarity effects more consistent with continued dosing. BDNF upregulation builds; mild energy / alertness increase common.
- Week 1 — Peak of acute-phase subjective benefit; attention, verbal fluency, and task persistence often track highest in this window.
- Weeks 2–3 — Consolidation. BDNF / TrkB-pathway effects manifest more durably; learning and memory retention improvements (if they occur for a given user) tend to emerge here.
- Course cessation — Effects wane over 1–2 weeks as CNS tone returns to baseline. No withdrawal syndrome reported in Russian clinical use; no rebound cognitive impairment.
- Non-responders — Real. A notable minority of users report no subjective effect. Dose escalation in this population is not reliably productive.
- Typical cycling pattern — 10–14 day courses separated by 2–4 week washout periods in traditional Khavinson-era Russian practice. Stabilized-analog users may titrate course length down given extended half-life.
- If you feel worse — Persistent headache, insomnia, or unusual symptom — stop and re-evaluate; consider switching dosing time from evening to morning, reducing dose, or verifying product purity.
Regulatory Status
Current Status — April 2026
Parent Semax is approved and prescribed in Russia (Semax 0.1% for chronic/cognitive use; Semax 1% for acute stroke) with indications including ischemic stroke, chronic cerebrovascular insufficiency, transient ischemic attacks, encephalopathy, optic-nerve pathology, and pediatric cognitive disorders. It is not approved by the FDA, EMA, MHRA, TGA, or Health Canada.
N-Acetyl Semax (the stabilized analog on this page) is not approved by any regulatory agency anywhere in the world. It is distributed through research-peptide suppliers labeled for laboratory research only and has no independent clinical-trial pedigree.
Semax is not specifically named on the WADA Prohibited List. Athletes should consult their sport-specific federation and the current Prohibited List; a CNS-active ACTH fragment analog could draw scrutiny under broader categories.
Neither Semax nor N-Acetyl Semax is on the FDA Category 2 Bulk Drug Substances list and neither is part of HHS Secretary Robert F. Kennedy Jr.'s February 2026 Category 2 reclassification announcement. Absent a U.S. NDA or BLA sponsor, Semax-family compounds are unlikely to enter FDA-compoundable status in the foreseeable regulatory horizon.
Cost & Access
N-Acetyl Semax is available through research-peptide suppliers labeled for laboratory research purposes only. It is not dispensed by U.S. or EU regulated pharmacies. Parent Semax is sold as a finished nasal-spray pharmaceutical in Russia and several CIS markets; personal-use import into the U.S. is restricted and legally gray.
Unregulated-channel quality varies substantially. Third-party HPLC and mass-spectrometry identity / purity testing is the practical floor for research use. Kalios does not sell compounds or endorse their use.
N-Acetyl Semax is not on the FDA Category 2 list and is not part of the February 2026 HHS reclassification. It will remain a research-only compound under U.S. regulation in the foreseeable term.
Access information as of April 2026. Actual availability and pricing vary by source and jurisdiction. Kalios does not sell compounds.
Related Compounds
People researching N-Acetyl Semax often also look at these:
ACTH(4-10) heptapeptide analogue. Russian nootropic with BDNF-upregulating and neuroprotective activity.
Adamantane-class actoprotector. Russian dopaminergic / adaptogenic nootropic.
Porcine brain-derived peptide mixture. Neurotrophic formulation used clinically in stroke and dementia.
Cerebrolysin-derived synthetic peptide engineered to retain the neurotrophic core activity.
Key References
- 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.
- 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.
- 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.
- 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.
- 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;15:1052. PMID: 25476978.
- 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: 9234274.
- 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: 11457574.
- 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: 21409522.
- 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: 16362767.
- 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: 37239312.
- Levitskaya NG, Sebentsova EA, Andreeva LA, Alfeeva LY, Kamenskii AA, Myasoedov NF. Investigation of the spectrum of physiological activities of a heptapeptide analog of ACTH(4-10) — Semax. Neurosci Behav Physiol. 2004;34(4):399-405. PMID: 15341214.
- Koroleva SV, Ashmarin IP. Neuropeptide tuftsin and semax — comparative study of regulatory functions. Biochemistry (Mosc). 2006;71(6):657-663.
Last updated: April 2026 | Profile authored by Kalios Peptides research team