N-Acetyl Semax
The acetylated, extended-stability form of Semax - an ACTH-derived heptapeptide with potent BDNF-upregulating, neuroprotective, and cognitive-enhancing effects.
⚠ Research & Educational Use Only. N-Acetyl Semax is a research chemical documented here for scientific education. All information references peer-reviewed literature and preclinical/clinical study data. Not for human consumption. Not medical advice. Consult a licensed researcher or healthcare professional before any laboratory use.
- Dramatically upregulates BDNF (Brain-Derived Neurotrophic Factor) - one of the most potent non-pharmacological BDNF inducers studied
- Enhanced bioavailability and stability compared to native Semax via N-acetyl modification
- Improves working memory, learning, attention, and information processing speed
- N-Acetyl Semax is not FDA-approved for human use. It is a research chemical for scientific study only.
Research At a Glance
- Dramatically upregulates BDNF (Brain-Derived Neurotrophic Factor) - one of the most potent non-pharmacological BDNF inducers studied
- Enhanced bioavailability and stability compared to native Semax via N-acetyl modification
- Improves working memory, learning, attention, and information processing speed
- Neuroprotective in stroke, traumatic brain injury, and neurodegenerative disease models
What is N-Acetyl Semax?
N-Acetyl Semax is an acetylated variant of Semax - a synthetic heptapeptide developed in Russia during the 1980s-90s, derived from the ACTH (adrenocorticotropic hormone) sequence at positions 4-10 with a Pro-Gly-Pro extension added at the C-terminus for stability. The N-acetyl group at the N-terminus further extends half-life and improves CNS bioavailability relative to the original Semax formulation.
Semax was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences with the goal of creating a neuroprotective and cognitive-enhancing compound for clinical use. It has been approved as a pharmaceutical in Russia for treatment of stroke, TIA (transient ischemic attacks), and related neurological conditions - a regulatory status that reflects a substantial body of preclinical and clinical research.
The defining pharmacological feature of Semax is its ability to rapidly and dramatically upregulate BDNF (Brain-Derived Neurotrophic Factor) in the CNS. BDNF is the primary neurotrophin responsible for neuroplasticity - the ability of the brain to form new connections, adapt to learning, and repair damage. Low BDNF is associated with depression, cognitive decline, neurodegenerative diseases, and impaired recovery from brain injury. Semax-mediated BDNF elevation has been documented in preclinical studies to be both rapid (occurring within hours) and substantial.
This BDNF elevation likely underlies multiple observed effects: improved cognitive performance (via enhanced synaptic plasticity and long-term potentiation), neuroprotection against ischemic damage (BDNF protects neurons against hypoxia and glutamate excitotoxicity), antidepressant effects (BDNF is critically reduced in depression and restored by effective antidepressant treatment), and enhanced recovery after brain injury.
Beyond BDNF, Semax modulates dopaminergic and serotonergic systems, explaining its stimulating and mood-elevating properties. It also shows effects on enkephalin metabolism and has anti-inflammatory properties in neural tissue - making it a multi-mechanism neuroprotective and cognitive-enhancing compound.
N-Acetyl Semax represents the optimised version for research use - the N-acetyl group protects the N-terminal from aminopeptidase cleavage, extending the active window of the compound. It is commonly paired with N-Acetyl Selank in research protocols combining anxiolytic and cognitive-enhancing effects.
Key Research Benefits
Documented effects observed in preclinical and clinical studies on N-Acetyl Semax. See all Cognitive Enhancement peptides for comparison.
Common Stacks
N-Acetyl Semax is frequently combined with the following peptides for synergistic effects. Click any peptide to compare profiles before deciding.
BPC-157 (angiogenic healing) and KPV (anti-cytokine) have complementary gut-protective mechanisms - the primary IBD research stack.
KPV and VIP both suppress inflammatory cytokines through different pathways (NF-kB vs. cAMP) - complementary anti-inflammatory coverage.
Side Effects & Risks
Adverse effects reported in the research literature. All data sourced from preclinical and clinical study reports.
Dosing Data from the Literature
Doses referenced below are sourced from published preclinical and clinical studies. Use the peptide dose calculator to convert these values to injection volume.
N-Acetyl Semax is typically administered intranasally or subcutaneously at 200-900 mcg per day.
Intranasal dose: 2-3 drops per nostril (at 0.1% solution), 1-2 times daily Injectable dose: 200-500 mcg subcutaneously once daily Timing: morning or mid-day to avoid sleep disruption (stimulating compound) Cycle: 1-4 weeks, with breaks to maintain sensitivity to BDNF effects
Administration in Research Settings
Standard reconstitution and administration methodology for laboratory research use.
Intranasal route is most common: use 0.1% solution nasal spray, administering 2-3 drops per nostril. For injection: reconstitute with bacteriostatic water and administer subcutaneously in the morning. Avoid evening dosing due to stimulating properties.
Explore Further
Quick Reference
Research Use Only
This information is for educational research purposes only. This is not medical advice. Consult a qualified healthcare professional.