N-Acetyl Semax Amidate

N-Acetyl Semax Amidate is a stabilized, next-generation analog of the synthetic heptapeptide Semax, originally developed at the Russian Academy of Sciences in the 1980s. Semax is a synthetic analog of the ACTH(4–10) fragment—a portion of adrenocorticotropic hormone— engineered to retain the neurotrophic and cognitive-enhancing properties of ACTH while lacking its hormonal activity (no effect on cortisol levels). N-Acetyl Semax Amidate incorporates two key structural modifications: an acetyl group at the N-terminus and an amide group at the C-terminus. These modifications protect the molecule from rapid enzymatic degradation, resulting in improved metabolic stability, enhanced resistance to breakdown, and potentially greater bioavailability and longer-lasting effects compared to standard Semax. Semax has been extensively studied for over 25 years and is used as a registered pharmaceutical in Russia and CIS countries, where it is prescribed for ischemic stroke, dyscirculatory encephalopathy, optic nerve atrophy, cognitive disorders, and ADHD in children. It is listed on the Russian List of Vital and Essential Drugs. The N-Acetyl Amidate form is expected to share these properties with enhanced pharmacokinetic stability.

Key Characteristics

• Sequence (Semax): Met-Glu-His-Phe-Pro-Gly-Pro
• Molecular formula (N-Acetyl Semax Amidate): C₃₇H₅₁N₉O₁₀S
• Molecular weight: 813.92 g/mol (Semax base)
• CAS number (Semax): 80714-61-0
• Synonyms: ACTH(4–7)PGP, Pro-Gly-Pro-ACTH(4–7), MEHFPGP
• Classification: Synthetic heptapeptide, ACTH analog, nootropic neuropeptide
• Origin: Institute of Molecular Genetics, Russian Academy of Sciences
• Parent fragment: ACTH(4–10) with C-terminal Pro-Gly-Pro extension

How It Works

N-Acetyl Semax Amidate exerts its effects through multiple interconnected mechanisms that support cognitive function, neuroprotection, and brain resilience. Unlike stimulants that force neurotransmitter release, Semax improves the quality of brain signaling itself.

Neurotrophic Factor Modulation (BDNF and NGF) Semax’s most well-characterized mechanism is its ability to upregulate brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the brain. BDNF is a critical protein that supports neuroplasticity, learning, long-term memory formation, and neuronal survival. Research demonstrates that Semax rapidly increases BDNF mRNA and protein levels in the hippocampus and frontal cortex, and also upregulates the corresponding TrkB and TrkC receptors. In a clinical study of 110 stroke patients, Semax treatment at 6,000 mcg/day for 10 days significantly increased plasma BDNF levels, which remained elevated throughout the study period and correlated with improved functional outcomes (Gusev et al., 2017).

Dopaminergic and Serotonergic Modulation

Semax enhances the release and balance of key neurotransmitters including dopamine and serotonin. Dopamine modulation in the prefrontal cortex supports motivation, attention, and executive function. Serotonergic effects contribute to mood stability and emotional resilience. Importantly, these effects occur without the forced stimulation seen with amphetamines or other stimulants—there is no jitteriness, heart rate increase, or crash.

Enkephalin System Modulation

Like the related peptide Selank, Semax inhibits enzymes involved in the degradation of enkephalins, endogenous opioid peptides that play roles in pain perception, mood regulation, learning, emotional behavior, and maintaining normal brain function. By preserving endogenous enkephalin levels, Semax may contribute to its nootropic, analgesic, and mood-stabilizing effects.

Gene Expression and Transcriptomic Effects

Genome-wide transcriptional analysis has revealed that Semax produces profound changes in gene expression in the brain. In a rat model of focal cerebral ischemia, Semax affected the expression of over 1,500 genes, predominantly enhancing expression of genes related to the immune system and vascular function. Under ischemia-reperfusion conditions, Semax suppressed inflammatory gene expression while activating neurotransmission-related genes— directly opposing the damaging patterns caused by ischemia alone. This compensatory effect on disrupted mRNA expression patterns is believed to be a key mechanism underlying Semax’s neuroprotective action.

Neuroprotection via Immune and Vascular Modulation

Research has uncovered that Semax’s neuroprotective effects extend beyond direct neuronal support. The peptide increases the amount and mobility of immune cells, enhances chemokine and immunoglobulin gene expression, and affects the formation and functioning of the vascular system during ischemic conditions. These immunomodulating and vasoactive properties are now considered key mechanisms underlying Semax’s therapeutic efficacy in stroke.

VEGF Pathway Activation

Studies on the expression of VEGF family genes (Vegf-a, Vegf-b, Vegf-c, Vegf-d, Plgf) and their receptors in the brain show that Semax and its C-terminal fragment Pro-Gly-Pro activate these pathways following ischemia. VEGF signaling supports angiogenesis and vascular repair, contributing to brain tissue recovery after injury.

Enhanced Stability of the N-Acetyl Amidate Form

The N-terminal acetylation and C-terminal amidation in N-Acetyl Semax Amidate protect the molecule from rapid enzymatic degradation. The C-terminal Pro-Gly-Pro tripeptide already provides enhanced metabolic stability compared to native ACTH fragments, extending Semax’s duration of action to 20–24 hours. The additional acetyl and amide modifications further improve this profile, potentially resulting in smoother, more consistent effects.

Benefits

The following benefits are based on extensive research with the parent compound Semax, including clinical trials in human patients. N-Acetyl Semax Amidate is expected to share these properties with potentially enhanced stability and duration.

Cognitive Enhancement

• Improved attention, concentration, and mental clarity
• Enhanced short-term and working memory
• Better information processing and learning efficiency
• Reduced mental fatigue during demanding tasks
• Sustained mental energy without stimulant-related side effects
• Improved memory and attention in healthy individuals under extreme conditions

Neuroprotection

• Upregulation of BDNF and NGF in the hippocampus and frontal cortex
• Protection of neurons under oxidative stress and hypoxia
• Reduction of neurological damage following ischemic stroke
• Compensation of disrupted gene expression patterns during ischemia
• Enhanced immune and vascular response to brain injury
• Activation of VEGF pathways supporting vascular repair

Neurological Recovery

• Accelerated functional recovery after ischemic stroke
• Improved motor performance in stroke rehabilitation
• Cognitive recovery after mental overload or brain trauma
• Support for brain resilience under chronic stress
• Enhanced neuroplasticity during rehabilitation

Mood and Motivation

• Balanced dopamine and serotonin modulation
• Improved motivation without jitteriness or crashes
• Antidepressant-like effects demonstrated in animal models
• Enhanced emotional resilience under stress
• No emotional blunting or forced mood changes

Ophthalmic Benefits

• Protection against pressure-induced nerve damage in glaucoma
• Support for optic nerve health in various neuropathies
• Used clinically in Russia for optic nerve atrophy and glaucomatous optic neuropathy

Additional Applications

• ADHD symptom management in children (approved indication in Russia)
• Gastroprotective and anti-ulcer effects (clinical evidence)
• Enhanced adaptability under extreme conditions
• Neuroprotective effects against alcohol-related neurotoxicity

What the Science Shows

Clinical Trial: Ischemic Stroke and BDNF (110 Patients) In a study of 110 patients after ischemic stroke, Semax was administered intranasally at 6,000 mcg/day in two 10-day courses with a 20-day interval. Semax increased plasma BDNF levels regardless of the timing of rehabilitation, and these elevated levels remained high throughout the study period. High BDNF levels correlated with improved Barthel index scores (functional independence) and accelerated motor performance recovery. Early rehabilitation combined with Semax administration produced the best outcomes (Gusev et al., 2017).

Clinical Trial: Nootropic Effects in Healthy Humans

In a study by Ashmarin et al. (1997), Semax was shown to stimulate operative memory and attention and increase resistance to hypoxia in both experimental animals and human subjects over a prolonged period (20–24 hours after intranasal administration at doses of 0.015–0.050 mg/kg). Semax significantly improved memory and attention in healthy men under extreme working conditions. In no case did it produce negative side effects or complications.

Pilot Study: fMRI in Healthy Subjects

In a pilot study of 24 healthy middle-aged subjects, intranasal 1% Semax solution (total dose 1.2 mg) increased resting-state fMRI signal in the default mode network rostral subcomponent relative to placebo, demonstrating measurable effects on brain activity patterns in healthy individuals (Lebedeva et al., 2018).

Human Memory Study

A study in healthy subjects using intranasal Semax at 250–1,000 mcg/kg improved attention and short-term memory and caused EEG changes similar to other established neuroprotective drugs. At higher doses (16 mcg/kg), mild stimulant-like effects were noted.

Genome-Wide Transcriptomic Analysis (Focal Ischemia) Dergunova et al. (2014) conducted genome-wide transcriptomic analysis of Semax’s effects in rat brain cortex following permanent middle cerebral artery occlusion. The peptide affected expression of over 1,500 genes, predominantly enhancing immune system genes. At 24 hours post-ischemia, Semax significantly increased transcripts encoding transmembrane receptors, cytokines, and immunoglobulins. The immunomodulating effect and vascular system impact were identified as key mechanisms of neuroprotection.

Ischemia–Reperfusion Transcriptomic Study

Using RNA-Seq analysis under transient MCAO conditions, researchers identified 394 differentially expressed genes in Semax-treated rat brains at 24 hours. Semax suppressed inflammation-related gene expression and activated neurotransmission-related genes—directly opposing the harmful patterns caused by ischemia-reperfusion alone. This compensatory effect on disrupted mRNA expression is believed to underlie Semax’s neuroprotective action (Dergunova et al., 2020).

Neurotrophin and Receptor Activation After Ischemia

Studies demonstrated that Semax activates transcription of neurotrophins (BDNF, NGF, NT-3) and their receptors (TrkB, TrkC, TrkA) in the ischemic cortex at critical time points (3 and 24 hours post-ischemia) when penumbra cells still retain functional activity and survival potential. This activation of the neurotrophin system promotes neuroprotection and cell survival in neural tissue after cerebral ischemia.

Glaucomatous Optic Neuropathy

Clinical trials in glaucoma patients demonstrated that 0.1% intranasal Semax, used for up to 30 days, protected against pressure-induced nerve damage. When combined with anti-inflammatory treatments, Semax reduced the progression and severity of optic neuropathy.

Peptic Ulcer Study

Ivanikov et al. (2002) demonstrated that intranasal 1% Semax (2–4 drops per nostril, three times daily for 10 days) was nearly three times more effective than placebo in promoting healing of peptic ulcers, with a healing rate of approximately 90% versus just over 30% in controls.

Important Context

Semax has been studied extensively in Russia for over 25 years and is approved for clinical use. However, most published studies are in Russian, and large-scale Western clinical trials are limited. Direct research on the N-Acetyl Semax Amidate modification specifically is sparse, though the structural modifications are standard peptide chemistry techniques aimed at improving stability rather than altering mechanism.

Dosing Protocol

Dosing information is derived from clinical use of the parent compound Semax in Russia, combined with practitioner protocols for the N-Acetyl Amidate form. No official dosing guidelines exist specifically for N-Acetyl Semax Amidate.

Intranasal Administration

Intranasal delivery is the most extensively studied route and allows rapid CNS penetration via olfactory epithelium and trigeminal nerve transport, bypassing the blood–brain barrier. Absorption is approximately 60–70% of the active substance.

Protocol Dose Frequency Duration Cognitive 400–900 mcg/day 2–3x daily 10–14 days enhancement Cognitive fatigue 400–600 mcg/day 1–2x daily 3–14 days prevention Stroke (moderate) 6,000–12,000 3–4x daily 10 days mcg/day Stroke (severe) 12,000–20,000 4–6x daily 10 days mcg/day Optic nerve disorders 600–1,200 mcg/day 2–3x daily Up to 30 days ADHD (children ≥7 200–400 mcg/day 2x daily Up to 30 days yrs)

Subcutaneous Administration

Injectable Semax offers convenient once-daily dosing with consistent bioavailability.

Protocol Dose Frequency Duration Conservative start 300 mcg Once daily 14 days Standard nootropic 500–800 mcg Once daily 14–30 days Advanced protocol 800–1,000 mcg Once daily Up to 30 days

Cycling Guidelines

• Standard nootropic cycles: 10–14 days on, 1–3 months off.
• Clinical stroke protocols: Two 10-day courses with a 20-day interval between them.
• Continuous use is not recommended due to potential BDNF pathway adaptation.
• Effects persist for 20–24 hours after a single dose, supporting once-daily administration.

Important Dosing Notes

• N-Acetyl Semax Amidate may be more potent than standard Semax due to improved

stability; start conservatively.

• Morning or early-afternoon dosing is preferred to avoid potential interference with sleep.
• Higher doses (above 16 mcg/kg intranasal) may produce stimulant-like effects and

slightly elevated anxiety.

• Safely administered in clinical studies at doses from 600 mcg/day to 12,000 mcg/day for

up to 10 consecutive days.

• 0.1% intranasal Semax used safely for up to 30 days in glaucoma patients.

Draw Volumes – 30 mg Vial (3 mL Reconstitution = 10 mg/mL) Dose Volume Units on Insulin Syringe 300 mcg 0.03 mL 3 units 500 mcg 0.05 mL 5 units 600 mcg 0.06 mL 6 units 800 mcg 0.08 mL 8 units 1,000 mcg 0.10 mL 10 units

At 500 mcg daily, one 30 mg vial provides 60 doses. At 1,000 mcg daily, one vial provides 30 doses.

Reconstitution Instructions

Step 1: Gather supplies: N-Acetyl Semax Amidate vial, bacteriostatic water, alcohol swabs, and syringes. Step 2: Clean the stoppers on both vials with alcohol swabs. Step 3: Draw 3 mL of bacteriostatic water into a syringe. Step 4: Inject the water slowly down the inside wall of the peptide vial. Do not spray directly onto the powder. Step 5: Let the powder dissolve naturally. Gently swirl if needed. Do not shake. Step 6: Once fully dissolved, the solution is ready for use. Step 7: Label the vial with the date, concentration (10 mg/mL), and contents.

Concentration Math

• 30 mg ÷ 3 mL = 10 mg/mL = 10,000 mcg/mL
• Each 0.01 mL (1 unit) = 100 mcg

Side Effects and Cautions

Semax has been studied extensively and demonstrates an excellent safety and tolerability profile. Direct safety data on N-Acetyl Semax Amidate specifically are limited.

Reported Side Effects

• Nasal irritation or mild discomfort (intranasal route)
• Mild headache
• Slightly elevated anxiety at high doses (above 16 mcg/kg intranasal)
• Injection site reactions: redness, minor swelling (subcutaneous route)
• Potential nasal congestion with prolonged intranasal use

Safety Profile

• No addiction potential
• No tolerance buildup
• No withdrawal effects
• No emotional blunting
• No effect on cortisol levels (unlike parent ACTH molecule)
• Non-sedating; does not impair cognitive function
• Safely administered at doses from 600 mcg/day to 12,000 mcg/day in clinical studies
• No serious adverse events or complications documented across 25+ years of clinical use

Theoretical Concerns

• Continuous use may blunt BDNF pathway responsiveness; cycling is recommended.
• A potential link between elevated BDNF and increased hair loss in men predisposed to

baldness has been proposed, but no research confirms this connection with Semax use specifically.

• High doses may produce stimulant-like effects; dose titration is advisable.
• Avoid concurrent use of vasoconstrictive nasal sprays, which may reduce intranasal

absorption.

Contraindications and Precautions

Avoid

• Known hypersensitivity to Semax, ACTH fragments, or any component of the

formulation

• Pregnancy (safety not established)
• Breastfeeding (safety not established)
• Active acute psychosis or severe anxiety disorders (high-dose Semax may have

stimulant-like effects)

Use with Caution

• Concurrent use with stimulants or ADHD medications (may enhance stimulant effects)
• Concurrent use with MAO inhibitors
• History of seizure disorders
• Under age 7 (limited data outside Russian clinical protocols)

Special Considerations

Because N-Acetyl Semax Amidate modulates dopaminergic, serotonergic, and neurotrophic signaling, it may interact with medications affecting similar pathways. Discuss with a physician if you take antidepressants, stimulants, or other neuroactive medications. Cycling is recommended to prevent potential adaptation of BDNF pathways.

Comparison with Similar Compounds

N-Acetyl Semax Amidate vs. Standard Semax

N-Acetyl Semax Amidate features N-terminal acetylation and C-terminal amidation for enhanced metabolic stability and longer-lasting effects. The core mechanism of action is expected to remain the same. Standard Semax already has a 20–24-hour duration of action; the modified form may extend this further.

N-Acetyl Semax Amidate vs. N-Acetyl Selank Amidate

Both are modified Russian neuropeptides, but they target different primary systems. Semax primarily enhances BDNF, cognitive performance, and neuroprotection through neurotrophic factor modulation. Selank primarily modulates GABAergic signaling and enkephalin systems for anxiolysis. Many practitioners combine or alternate both for comprehensive cognitive and mood support.

N-Acetyl Semax Amidate vs. Caffeine and Stimulants

Unlike caffeine and stimulant medications, Semax does not increase heart rate, cause nervousness, or produce crashes. It works by enhancing the quality of brain signaling through neurotrophic factors rather than forcing neurotransmitter release. There is no tolerance buildup or dependence risk.

N-Acetyl Semax Amidate vs. Racetams

Racetams primarily modulate acetylcholine and glutamate signaling. Semax operates through a broader set of mechanisms including BDNF upregulation, gene expression modulation, and immune/vascular effects. Semax has a more robust clinical evidence base, particularly for stroke recovery and neuroprotection.

Feature N-Acetyl Standard N-Acetyl Caffeine Racetams Semax Semax Selank Amidate Amidate Primary Nootropic + Nootropic + Anxiolytic + Stimulant Nootropic effect neuroprotective neuroprotective nootropic Key BDNF / gene BDNF / gene GABA / Adenosine ACh / mechanism expression expression enkephalin block glutamate Duration 20–24+ hrs 20–24 hrs Several hrs 4–6 hrs 4–8 hrs Crash risk None None None High Low Dependence None None None Moderate Low risk Clinical Limited Extensive Moderate Extensive Moderate evidence (analog)

Success Tips

Set Appropriate Expectations

N-Acetyl Semax Amidate is not a stimulant. It supports cognitive performance at the biological level through neurotrophic factor modulation. Effects are typically noticed as clearer thinking, improved focus, and better memory rather than a “buzz” or rush. Users often describe feeling “locked in” rather than overstimulated. Effects last 20–24 hours per dose.

Optimize Administration

• For intranasal use, clear nasal passages before application; avoid vasoconstrictive sprays.
• Tilt head slightly back during intranasal administration to prevent drainage into the

throat.

• For subcutaneous injection, rotate sites (abdomen, outer thighs, upper arms).
• Morning or early-afternoon dosing is preferred to avoid potential sleep interference.

Support Brain Health Foundations

• Quality sleep (7 to 9 hours)
• Regular aerobic exercise and cognitive training
• Balanced diet rich in omega-3 fatty acids and antioxidants
• Stress management through mindfulness or meditation
• Mental stimulation and learning new skills

Respect the Cycle

Standard protocols recommend 10- to 14-day cycles for nootropic use, followed by 1 to 3 months off. Continuous daily use is not recommended, as BDNF and neurotrophic signaling pathways can adapt with overstimulation.

Track Subjective Markers

• Focus and concentration quality
• Memory and recall accuracy
• Mental energy and stamina
• Motivation and drive
• Mood stability
• Learning speed and information retention

Consider Combining with Selank

Semax and Selank are commonly paired or alternated due to their complementary effects. Semax provides cognitive enhancement and neuroprotection, while Selank provides anxiolysis and emotional balance. A common protocol: Semax in the morning, Selank later in the day.

Storage and Handling

Before Reconstitution

• Store lyophilized powder at −20°C (−4°F) for long-term storage.
• Room temperature storage (below 25°C / 77°F) is acceptable for short periods.
• Keep in a dry location away from light.

After Reconstitution

• Refrigerate at 2–8°C (35–46°F).
• Protect from light.
• Use within 28 to 30 days.
• Do not freeze the reconstituted solution.
• Avoid repeated freeze–thaw cycles.
• Check for cloudiness or particles before each use; discard if present.

Nasal Spray Storage

• Store nasal spray formulations refrigerated at 2–8°C.
• Use within the timeframe specified by the manufacturer.

Travel

• Keep refrigerated when possible.
• A cooler with ice packs works for short trips.
• Do not expose to excessive heat.

Legal Status

Russia and CIS Countries

• Semax is a registered pharmaceutical approved for multiple neurological indications.
• Listed on the Russian List of Vital and Essential Drugs (approved December 7, 2011).
• Approved indications include ischemic stroke, dyscirculatory encephalopathy, optic

nerve atrophy, cognitive disorders, and ADHD in children.

• Available as 0.1% and 1% intranasal drops.

United States

• Not FDA-approved for any medical indication.
• Not a controlled substance.
• Available as a research peptide.
• Use is considered experimental.

International

• Regulatory status varies by country.
• Not widely approved outside of Russia and CIS countries.
• Widely sold by online vendors as a purported nootropic.

Important Context

N-Acetyl Semax Amidate is sold as a research chemical in most countries outside Russia. Human use is at your own risk. No medical claims can be made about its efficacy or safety outside jurisdictions where Semax is approved.

Frequently Asked Questions

What is the difference between Semax and N-Acetyl Semax Amidate? N-Acetyl Semax Amidate is a modified version of Semax with an acetyl group at the N-terminus and an amide group at the C-terminus. These modifications improve metabolic stability and resistance to enzymatic degradation, potentially resulting in longer-lasting and more consistent effects. The core mechanism of action is expected to remain the same. How quickly will I notice effects? Semax effects are typically noticed within 15–30 minutes of intranasal administration, with peak effects lasting throughout the day (20–24-hour duration). Many users describe improved clarity, focus, and mental energy within the first dose.

Is N-Acetyl Semax Amidate a stimulant?

No. Unlike caffeine or amphetamines, Semax does not force neurotransmitter release. It supports cognitive performance by enhancing neurotrophic factors, particularly BDNF. There is no heart rate increase, jitteriness, or crash. At very high doses, mild stimulant-like effects have been noted.

Can I combine N-Acetyl Semax Amidate with Selank?

Yes. Semax and Selank are commonly paired or alternated due to complementary mechanisms. Semax provides cognitive enhancement and neuroprotection, while Selank provides anxiolysis and emotional balance. A typical approach is Semax in the morning and Selank later in the day. Does Semax affect cortisol levels? No. Although Semax is derived from the ACTH(4–10) fragment, it was specifically engineered to retain neurotrophic effects while eliminating hormonal activity. It does not stimulate cortisol release.

Is N-Acetyl Semax Amidate safe?

The parent compound Semax has been used as a registered pharmaceutical in Russia for over 25 years with an excellent safety record. No serious adverse events or complications have been documented. It is non-toxic, non-sedating, and non-addictive. Direct safety data on the N-Acetyl Amidate modification specifically are limited, but the structural modifications are standard peptide chemistry techniques.

Can I take N-Acetyl Semax Amidate long-term?

Standard protocols recommend cycled use: 10–14 days on, 1–3 months off for nootropic purposes. Continuous use is not recommended due to potential BDNF pathway adaptation. Clinical stroke protocols use two 10-day courses with a 20-day interval. Is intranasal or subcutaneous administration better? Intranasal is the most extensively studied route, with approximately 60–70% absorption and rapid CNS penetration. Subcutaneous injection offers consistent bioavailability and convenient once-daily dosing. Both routes are effective.

References

1. Gusev EI, et al. The efficacy of Semax in the treatment of patients at different stages of ischemic stroke. Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. 2017. 2. Ashmarin IP, Nezavibat’ko VN, Miasoedov NF, et al. A nootropic adrenocorticotropin analog 4–10-Semax (15 years’ experience in its design and study). Zhurnal Vysshei Nervnoi Deiatelnosti. 1997;47(2):420–430. 3. Dergunova LV, et al. 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. 4. Dergunova LV, 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;11(6):681. 5. Dolotov OV, et al. Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia. Cellular and Molecular Neurobiology. 2006. 6. Lebedeva IS, et al. Effects of Semax on the default mode network of the brain. Bulletin of Experimental Biology and Medicine. 2018. 7. Kaplan AY, et al. Synthetic ACTH analogue Semax displays nootropic-like activity in humans. Neuroscience Research Communications. 1996;19(2):115–123. 8. Ivanikov IO, et al. Gastroprotective effects of Semax in peptic ulcer disease. 2002. 9. Kolomin TA, et al. A new generation of drugs: synthetic peptides based on natural regulatory peptides. Neuroscience and Medicine. 2013;4(4):223–252. 10. Koroleva SV, Myasoedov NF. Semax as a universal drug for therapy and research. Biology Bulletin. 2018;45(6):589–600. 11. Shadrina MI, et al. Expression of BDNF and NGF genes in brain tissues following Semax administration. Doklady Biological Sciences. 2010. 12. Glazova MV, et al. Antidepressant and anxiolytic properties of the peptide Semax. Neuroscience and Behavioral Physiology. 2003;33(4):377–381. 13. Wikipedia. Semax. February 2026. 14. Peptide Sciences. N-Acetyl Semax Amidate 30mg: Enhanced metabolic stability research analog. 2024. 15. Alzheimer’s Drug Discovery Foundation. Semax: Cognitive Vitality for Researchers. 2024.