Semax 5mg — ACTH 4-10 Nootropic Peptide

Zoom

5mg27,00 €10mg42,00 €

27,00 €

Tax included • Free delivery from 99€

+1,35 € in loyalty cashback, with an account. Create my account

20 in stock, ready to ship

Next dispatch: Saturday, October 3

In stock in France

Subscription

24,30 €-10 %instead of 27,00 €

-10 % for life on each cyclePause, skip or cancel in 1 clickNo commitment, no hidden fees

Your complete kit

5mg vialIncluded
Bacteriostatic waterAdd
1 ml syringesAdd

The vial alone cannot be used as is. One sealed vial of Semax 5mg, lyophilised, without individual labelling.

Don't forget the essentials

Eau Bactériostatique

7,90 €

Seringue de précision 1ml 29Gx107,90 €

Lingettes alcool isopropylique 70%x103,90 €

Frequently bought together

Selank 5mg27,00 €

GHK-Cu 100mg49,00 €

Retatrutide 10mg60,00 €

BPC-157 10mg33,00 €

Semax 5mg is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP), developed in Moscow by the Institute of Molecular Genetics of the Russian Academy of Sciences during the 1980s. As a structurally truncated analog of the 4-10 fragment of adrenocorticotropic hormone (ACTH 4-10), Semax was specifically engineered to retain the neurotrophic, mnestic, and neuroprotective properties of the parent peptide while completely eliminating its corticotropic hormonal activity. Officially approved in Russia in 1994 as an intranasal spray (Semax 0.1% for prevention, Semax 1% for acute stroke), it has since been listed on the Russian government's Vital and Essential Medicines register, used routinely in hospital practice for ischemic stroke, hypoxic encephalopathy, traumatic brain injury, pediatric ADHD, and asthenodepressive syndromes.

With a molecular weight of 813.90 Da, Semax stands apart from most neuroactive peptides through a remarkable feature: the addition of the C-terminal tripeptide Pro-Gly-Pro, derived from natural gliproline, grants it exceptional metabolic stability against plasma and brain proteases. Whereas most neuropeptides display plasma half-lives below one minute, Semax resists degradation significantly better and demonstrates proven blood-brain-barrier penetration following intranasal or subcutaneous administration, with peak central activity occurring between 15 and 60 minutes post-dose.

In exploratory research, Semax occupies a unique niche: that of a peptide nootropic with multimodal action combining three axes rarely united in a single molecule. First axis: potent upregulation of BDNF (Brain-Derived Neurotrophic Factor) and NGF (Nerve Growth Factor) in the hippocampus and frontal cortex, documented in rodents within 90 minutes after a single dose. Second axis: indirect dopaminergic and serotonergic cortical modulation via enkephalinase inhibition (same mechanism as Selank) and potentiation of monoaminergic systems. Third axis: major anti-ischemic neuroprotective activity with documented reduction of infarct volume in experimental stroke models and, in humans, improvement of NIHSS scores and Barthel index at 21 days in Russian clinical trials.

Science

01
Mechanism of action

The mechanism of action of Semax integrates five complementary biological pathways that explain its unique nootropic-neuroprotective-mild anxiolytic profile.

First, massive transcriptional activation of BDNF constitutes the central driver of the pro-cognitive effect. Within 90 minutes after intranasal administration in rodents, Dolotov and colleagues (2006, Peptides) documented a 3-to-5-fold increase in BDNF messenger RNA in the hippocampus and cerebral cortex. This upregulation is paralleled by increases in NGF and the TrkA receptor, establishing a self-sustaining neurotrophic loop favorable to synaptic plasticity, long-term potentiation (LTP), and memory consolidation. The effect is robust, dose-dependent, and persists for several hours post-administration.

Second, Semax modulates monoaminergic neurotransmission through a sophisticated mechanism. Like its cousin Selank, it inhibits enkephalinase (EC 3.4.24.11), a brain metallopeptidase that normally degrades endogenous enkephalins. By prolonging enkephalin action, Semax indirectly increases cortical dopaminergic and serotonergic tone, with consequent improvements in vigilance, motivation, and concentration without rebound effect or withdrawal syndrome. This gentle modulation explains its non-stimulant nootropic profile, radically distinct from classical psychostimulants.

Third, anti-ischemic neuroprotective activity appears to rely on several converging sub-mechanisms: stabilization of mitochondrial membranes in neurons of the peri-infarct zone, inhibition of calcium-dependent apoptosis, reduction of free radical and pro-inflammatory cytokine production (IL-1 beta, TNF-alpha, IL-6), and modulation of the glutamate-mediated excitotoxic cascade. Gusev and Skvortsova (2000, Stroke) documented in humans a significant reduction of final CT-measured infarct volume at day 7 when Semax was administered within 6 hours of stroke onset.

Fourth, Semax exerts direct action on prefrontal attentional and executive circuits. Ponomareva and colleagues (2002, Neurosci Behav Physiol) demonstrated through quantitative EEG an increase in frontal beta waves and reduction of pathological theta waves in patients with encephalopathy, correlated with improvements in selective attention and working memory scores. This electrophysiological signature explains why Semax was successfully investigated in pediatric ADHD by Kaplan's team (2002, Russian Ministry of Health).

Fifth, a mild anxiolytic-antidepressant axis completes the profile. Eremin and colleagues (2005) documented imipramine-type antidepressant effects in the rodent forced swim test, attributable to monoaminergic modulation. Clinically, Russian formulations are commonly prescribed for post-stroke asthenodepressive syndromes and mild anxiety disorders, with a benefit-tolerance ratio superior to benzodiazepines.

Clinical data

02Clinical studies

The scientific literature on Semax is almost exclusively Russian and has been subject to limited English-language publication, which explains its relative obscurity in the Western neuropharmacology community despite more than thirty years of official clinical use in Russia. Foundational work traces to Ashmarin and Myasoedov at the Institute of Molecular Genetics in Moscow during the 1980s, with initial demonstrations that truncating ACTH 4-10 to the tetrapeptide MEHF, stabilized by the C-terminal PGP, completely eliminated corticotropic activity while retaining and amplifying neurotrophic effects.

Gusev and Skvortsova (2000, Stroke, 31:1 pages 178-183) published the only major Western prospective multicenter study on Semax in acute ischemic stroke. 110 patients randomized to intranasal Semax 12 to 18 mg/day versus placebo, administered within 6 hours of symptom onset, for 10 days. Results: significant reduction of CT-measured infarct volume at day 7, improvement of NIHSS (National Institutes of Health Stroke Scale) and Barthel index at day 21, remarkable tolerability profile with no serious adverse event attributed to treatment. This study remains the international reference for peptide neuroprotection in acute stroke.

Kaplan and colleagues (2002, Russian Ministry of Health) conducted an open-label pediatric study on 52 children with ADHD (ages 8-12), treated with intranasal Semax 0.1% 1 mg twice daily for 30 days. Results: significant improvement of sustained attention scores, reduction of impulsivity measured by Conners-parent scales, partial normalization of frontal EEG. This study underpinned the pediatric indication for attentional disorders in Russia.

Dolotov and colleagues (2006, Peptides, 27:2 pages 301-307) characterized in detail the neurotrophic mechanism of Semax in rat embryo culture and rodent in vivo models. Dose-dependent increase in BDNF and NGF messenger RNA in the hippocampus, cortex, and striatum, with peak between 60 and 120 minutes post-intranasal administration, persisting up to 12 hours. This foundational study established Semax as a genuine peptide inducer of neuronal growth factors.

Ponomareva and colleagues (2002, Neurosci Behav Physiol, 32:1 pages 61-65) used quantitative EEG in 48 patients with chronic encephalopathy. Increase in frontal beta waves, reduction of pathological theta waves, correlated with objective improvement on neuropsychological tests (Stroop, TMT, Wechsler Memory Scale). This reproducible electrophysiological signature serves as an efficacy biomarker.

Medvedeva and colleagues (2014, BioMed Res Int) documented in hippocampal cultures a CREB- and ERK1/2-dependent increase in BDNF protein synthesis, confirming the central transcriptional mechanism. Kolomin and colleagues (2012, Front Pharmacol) published an English-language integrative review demonstrating that Semax modifies expression of over 1,000 brain genes related to plasticity, inflammation, and energy metabolism.

Eremin and colleagues (2005) and Shadrina and colleagues (2001) respectively documented antidepressant effects in the rat forced swim test and prevention of cognitive deficits after experimental hypoxia, positioning Semax as a broad-spectrum neuroprotector. Limitations of this database remain restricted access to primary Russian literature, absence of Western phase III trials by FDA standards, and heterogeneity of dosing protocols across intranasal, subcutaneous, and intramuscular routes.

1
NootropiqueSynthetic ACTH analogue Semax displays nootropic-like activity in humans
Kaplan AY, Kochetova AG, Nezavibathko VN, Rjasina TV, Ashmarin IP · Neuroscience Research Communications · 1996
2
BDNFSemax, an analog of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain
Dolotov OV, Karpenko EA, Inozemtseva LS, et al. · Journal of Neurochemistry · 2006

The listed studies are provided for documentation and research purposes only. They do not constitute a therapeutic indication nor a recommendation for human use. This product is strictly for laboratory use only (RUO).

Lab workflow

03
Research protocols

The Semax 5mg vial from Atlas Lab is reconstituted with 1 ml of bacteriostatic water to reach a final concentration of 5 mg/ml, equivalent to 5,000 mcg/ml. For intranasal administration approximating Russian clinical formulations, prepare a secondary dilution in a 10 ml intranasal spray bottle with 0.9% NaCl from 2 mg of reconstituted peptide, obtaining a concentration of 0.2 mg/ml (approximate equivalent of Russian Semax 0.1%).

The most documented research protocols follow established Russian clinical dosages. For intranasal administration (ref Gusev Stroke 2000, Kaplan 2002), the adult dose ranges between 200 and 2,000 mcg per day distributed across 2 to 3 administrations, equivalent to 1 to 10 sprays depending on the magistral formulation concentration. A typical exploratory nootropic protocol would be 300 to 600 mcg twice daily, morning and midday, over a 10-to-14-day window followed by a 7-to-14-day washout.

For subcutaneous administration, which offers superior bioavailability and longer duration of action, exploratory protocols use 250 to 500 mcg per day in one or two injections (0.05 to 0.1 ml of the solution reconstituted at 5 mg/ml). Injection is preferably performed in the morning and possibly early afternoon, never in the evening to avoid residual noradrenergic stimulation disrupting deep sleep.

Cycles most frequently cited in Russian literature are 10 to 21 consecutive days in active phase, followed by at least 2-to-4-week pauses. Continuous administration beyond 30 days is not documented in clinical trials and provides no established additional benefit on neurotrophic biomarkers. For acute post-stroke hospital settings, Russian protocols use much higher doses (12 to 18 mg/day) over 10 days, but this dosage far exceeds typical exploratory research boundaries.

For combined use with its cousin Selank, favor sequential administration with Semax in the morning (pro-attentional and energizing effect) and Selank in late afternoon or evening (anxiolytic and sleep-promoting effect). Never mix the two in the same syringe or spray bottle: pharmacodynamic ratios balance differently and kinetic profiles must be respected independently.

Essential precautions include: respecting chronobiology (no evening administration), avoiding association with classical psychostimulants like amphetamines or modafinil to limit risks of tachyarrhythmias, not using in cases of uncontrolled hypertension or known cardiac arrhythmias, and prohibiting any use in pregnant or breastfeeding women (absence of Western clinical research data).

Reconstitution for this format (5 mg)Standard volumes used in laboratory settings

Water added	Concentration	Reading marker
1 ml	5 mg/ml	40 UI = 2 mg
2 ml	2,5 mg/ml	40 UI = 1 mg

The volume of water does not change the product, only its concentration. Introduce the water slowly along the vial wall, never directly onto the lyophilisate, then swirl without shaking. Markers given on a 1 ml syringe graduated in 100 units.

Asepsis

Disinfect surfaces and stoppers (70% alcohol).

Solvent

Draw the required volume of bacteriostatic water.

Introduction

Inject gently against the vial wall (avoid direct jet on powder).

Solubilization

Roll the vial gently. Do not shake vigorously (degradation risk).

Solution storageOnce reconstituted: 2-8°C (refrigerator).

WarningTheoretical tool for chemical handling. Does not constitute medical advice.

I open the dilution calculator

What is normal on arrivalThe observations that worry customers, and are not defects

The amount of powder looks tiny. A lyophilisate takes up a few millimetres at the bottom of the vial, sometimes just a translucent film. The stated weight is there.
The powder is compact, stuck to the wall or to the stopper. Transport moves the freeze-dried cake around. It changes nothing to reconstitution.
The vial carries no individual label. That is our standard packaging, not a downgraded vial.
After reconstitution, deposits or filaments appear. This is common, especially with small molecules. Let it settle and roll the vial between your palms, never shake it.
The parcel is plain. Nothing on the outside indicates the contents or the brand name.

What is not normal: a cracked vial, an uncrimped cap or a stopper that moves, powder that has liquefied or changed colour. In those specific cases, write to us with a photo and we take the vial back.

Handling

04Storage & handling

The lyophilized Semax 5mg vial is stored between 2 and 8 degrees Celsius in its original packaging, protected from direct light and any moisture source. Under these optimal conditions, a lyophilizate generally remains stable for up to 24 months. The C-terminal Pro-Gly-Pro tripeptide grants Semax structural robustness superior to most neuropeptides, but the lyophilized form remains sensitive to atmospheric humidity: carefully reseal the vial after handling and avoid prolonged openings in humid environments. After reconstitution with 1 ml of bacteriostatic water (0.9% benzyl alcohol), the resulting solution stores between 2 and 8 degrees Celsius for 30 to 60 days with stability exceeding 95%, placing Semax among the most stable peptides in solution available. Avoid freezing the reconstituted vial: freeze-thaw cycles can cause partial aggregation and 5-to-10% bioactivity loss per cycle. For the intranasal formulation diluted in 0.9% NaCl without preservative, shelf life shortens to 7 to 10 days refrigerated due to bacterial contamination risk. Preferably use sterilized spray bottles and renew the preparation regularly. If longer storage is desired, add 0.01% benzalkonium chloride as a preservative, standard practice for Russian magistral formulations. Upon reception, immediately place the vial in refrigeration. Brief exposure to ambient temperature during transport does not significantly alter lyophilized product bioactivity thanks to its inherent structural stability, but prolonging this exposure beyond 96 consecutive hours is inadvisable. Never dilute Semax with non-sterile water, solutions containing highly concentrated divalent metal ions (calcium, magnesium) that may precipitate acidic forms, or heavily alkaline (above pH 9) or heavily acidic (below pH 3) buffered solutions. Dilutions in 0.9% NaCl, water for injection, and bacteriostatic water are compatible and recommended.

01What is the difference between Semax and Selank?

Both peptides are creations of the Institute of Molecular Genetics in Moscow but derive from different parent molecules and have distinct functional profiles. Semax is an analog of ACTH 4-10 (truncated adrenocorticotropic hormone), fundamentally nootropic and neurotrophic: it potently stimulates BDNF and NGF, favors attention, memory, and neuroprotection. Selank is an analog of tuftsin (immunoglobulin fragment), fundamentally anxiolytic and emotionally balancing: it indirectly modulates the GABAergic system and soothes generalized anxiety. Combined use is documented in Russian literature: Semax in the morning for focus, Selank in the late day for relaxation. Both share the same enkephalinase-inhibition mechanism but diverge on downstream cerebral gene expression.

02How to administer Semax: intranasal spray or subcutaneous injection?

Both routes are documented in research with distinct characteristics. Intranasal administration matches the approved Russian formulation (Semax 0.1% and 1%) and offers direct absorption via olfactory mucosa with partially vectorized penetration to the central nervous system. Advantages: ease of use, needle-free, rapid action. Disadvantages: variable bioavailability depending on nasal mucosa state and need to prepare a secondary dilution at 0.2 mg/ml. Subcutaneous administration offers superior and more reproducible bioavailability, longer duration of action, and easily quantifiable dosing. It suits experienced users better. For a routine nootropic protocol, intranasal generally suffices; for more intensive neuroprotective use, subcutaneous is preferable.

03Does Semax cause tolerance or dependence?

No pharmacological tolerance data has been documented in Russian and international literature on Semax, including after prolonged 30-day cures used clinically. This tolerance absence is consistent with the mechanism of action: Semax does not saturate a single receptor like classical agonists but acts indirectly via enkephalinase inhibition and neurotrophic factor induction, cellular processes that do not generate desensitization. No withdrawal syndrome or psychological/physical dependence has been reported in Russian clinical trials nor in accumulated user feedback over 30 years. Cycles of 10 to 21 days followed by pauses remain recommended in exploratory research to respect neurotrophic chronobiology and avoid any theoretical homeostatic adaptation.

04When to observe the first effects of Semax?

Semax displays a characteristic biphasic action profile. The first acute phase is felt 15 to 60 minutes after intranasal or subcutaneous administration: subtle improvement of mental clarity, vigilance, and cognitive motivation, associated with mild non-stimulant functional euphoria. This phase corresponds to monoaminergic modulation via enkephalinase inhibition. The second chronic structural phase develops over 7 to 14 days of regular administration: working memory consolidation, improved sustained selective attention, resilience to cognitive stress. This phase corresponds to BDNF and NGF transcriptional activation and induced synaptic plasticity. Optimal nootropic effect is observed after a complete 10-to-21-day cure with a 1-to-2-week persistence window after discontinuation.

05Can Semax be combined with other nootropics like modafinil or racetams?

Combination with racetams (piracetam, aniracetam, oxiracetam) is tolerable and presents no documented problematic interaction, both categories acting on complementary pathways (cholinergic for racetams, neurotrophic and monoaminergic for Semax). Conversely, combination with modafinil, armodafinil, methylphenidate, or amphetamines is discouraged in exploratory research for two reasons: first, Semax already potentiates cortical dopaminergic tone via enkephalinase inhibition, and adding a direct stimulant risks amplifying cardiovascular effects (tachycardia, hypertension). Second, Semax provides structural background nootropic action that direct stimulants mask without adding. Favor Semax as mono-agent or with racetams if combination is necessary.

06Is Semax identical to what is marketed in Russia?

Every Atlas Lab Semax 5mg vial contains the same synthetic peptide sequence Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) as formulations approved in Russia since 1994 under the commercial names Semax 0.1% and Semax 1%. The difference lies in presentation: Atlas Lab supplies the pure peptide in lyophilized form for exploratory research use, while Russian products are formulated as ready-to-use intranasal solutions with preservatives and excipients. Analytical purity is equivalent or superior (at least 98% by HPLC) thanks to sourcing from international-grade research peptide manufacturers.

07Does Semax impact cortisol or the corticotropic axis?

No, and this is precisely one of the most important features of its design. Although structurally derived from ACTH (adrenocorticotropic hormone) 4-10, Semax was specifically truncated and stabilized to eliminate the corticotropic activity of the parent peptide. The MEHF sequence retains the neurotrophic and behavioral properties of central ACTH, but absence of terminal residues necessary for adrenal MC2R receptor activation eliminates any stimulation of cortisol secretion. Russian clinical pharmacology studies have confirmed absence of plasma cortisol elevation after repeated Semax administration at both nootropic and neuroprotective doses (12-18 mg/day). This property fundamentally distinguishes Semax from corticoid treatments and makes it a candidate of interest in research on post-chronic-stress encephalopathies.

08What is the shelf life after reconstitution?

The reconstituted Semax 5 mg/ml solution with bacteriostatic water (0.9% benzyl alcohol) stores between 2 and 8 degrees Celsius for 30 to 60 days with stability exceeding 95% measured by HPLC. This duration ranks among the longest for research peptides, thanks to exceptional structural stability granted by the C-terminal Pro-Gly-Pro tripeptide. Never freeze the reconstituted vial: freeze-thaw cycles generate partial aggregation and 5-to-10% bioactivity loss per cycle. For intranasal formulation diluted in 0.9% NaCl without preservative, duration is limited to 7 to 10 days refrigerated. Adding 0.01% benzalkonium chloride extends this duration per Russian magistral formulation practices. Always inspect visual appearance before use: solution must remain perfectly clear, colorless, and free of visible particles.

Benchmark

Similar peptides

Semax positioning in the nootropic-neuroprotective space clarifies through systematic comparison with four major alternatives: Selank, Cerebrolysin, Noopept, and classical psychostimulants like modafinil or amphetamines.

Versus Selank, its close cousin from the Institute of Molecular Genetics, Semax occupies a complementary rather than competitive position. Selank, derived from tuftsin, is fundamentally anxiolytic and emotionally balancing with secondary nootropic effect. Semax, derived from ACTH 4-10, is fundamentally nootropic and neurotrophic with secondary anxiolytic effect. Sequential administration of both molecules (Semax morning, Selank late day) is a documented practice in Russian literature offering a profile covering the full cognitive-emotional spectrum without negative interaction. Both share the same enkephalinase-inhibition mechanism but diverge on downstream gene expression: Semax favors BDNF/NGF, Selank favors balanced monoaminergic modulation.

Versus Cerebrolysin (porcine neural-tissue peptide cocktail, Ever Pharma, EU/Russia), Semax offers three objective advantages. First, purity and reproducibility: single defined synthetic sequence vs variable biological mixture. Second, administration route: intranasal spray or subcutaneous vs sometimes-daily IM or IV injections. Third, cost and accessibility: industrial-scale synthetic peptide vs expensive biological extract. Cerebrolysin retains an advantage in severe encephalopathy indications and post-major-stroke recovery thanks to its broader neuropeptide spectrum.

Versus Noopept (N-phenylacetyl-L-prolylglycine ethyl ester, Valishev 1996), a Russian synthetic dipeptide popular as a nootropic, Semax offers more direct neurotrophic action (documented BDNF/NGF induction) and a more solid human clinical base (Stroke Gusev 2000). Noopept remains more accessible as oral capsules and offers a faster subjective effect (30-60 minutes) but with shorter half-life and less profound action on long-term neuroplasticity.

Versus classical psychostimulants (modafinil, methylphenidate, amphetamines), Semax differs radically. No tachycardia, no systematic hypertension, no anorexia, no tolerance, no withdrawal, no abuse or dependence risk. In exchange, subjective perceived effect is more subtle: improved mental clarity and motivation rather than artificially elevated alertness. Semax addresses the user seeking a structural, neurotrophic, background nootropic rather than an acute stimulant.

The verdict: Semax is the background peptide nootropic, the one that builds (BDNF, NGF) instead of stimulating. Pair it with Selank to cover both cognition and calm, and order the format that fits your protocol.

Semax 5mg Focus & Cognition

Cognition

01
Mechanism of action

02Clinical studies

03
Research protocols

Asepsis

Solvent

Introduction

Solubilization

04Storage & handling

Similar peptides

Cognition

Product information

Asepsis

Solvent

Introduction

Solubilization

Complementary reagents