N-Acetyl Semax
Also known as: N-Acetyl Semax, NA-Semax, Acetyl Semax, Semax Acetyl
An N-terminally acetylated form of Semax, modified to resist enzymatic breakdown. The acetylation itself is documented, but nearly all of the neurotrophic and clinical research that motivates interest in this compound was performed on unmodified Semax.
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Mechanism of Action
N-Acetyl Semax shares the Semax core: a heptapeptide built from the ACTH(4-7) fragment with a C-terminal Pro-Gly-Pro extension (Met-Glu-His-Phe-Pro-Gly-Pro), derived from the ACTH(4-10) region but stripped of corticotropic activity. In the parent peptide, the documented effects are neurotrophic rather than hormonal: upregulation of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the hippocampus and cortex, modulation of dopaminergic and serotonergic signaling, interaction with melanocortin receptors, and inhibition of enkephalin-degrading enzymes. The modification in this analog is pharmacokinetic in intent: acetylating the N-terminus caps the free alpha-amino group that aminopeptidases require in order to begin cleaving the chain, and improved proteolytic stability for acetylated Semax has been measured directly across several biological media (Shevchenko et al., 2013). Two caveats belong with that. First, greater stability is not the same as greater or longer central activity, which has not been established for this analog in published human work. Second, acetylation is not pharmacologically inert: removing the free N-terminal amine measurably changes how the peptide coordinates copper(II) and zinc(II), with associated changes in biological behavior (Magri et al., 2016), so the acetylated molecule should not be assumed to be simply a longer-lasting Semax.
- Half-life
- Not characterized in humans for the acetylated form. The parent Semax is cleared from plasma within minutes while central effects persist for hours; N-terminal acetylation is intended to slow that degradation and has been shown to do so in vitro.
- Administration Routes
- intranasal, subcutaneous
- Research Status
- Research Chemical
Reported Benefits
- Acetylation measurably improves resistance to proteolysis versus unmodified Semax
- Parent compound raises BDNF and NGF and supports neuroplasticity
- Parent compound studied for focus, memory and learning
- Parent compound has Russian clinical use in stroke and cognitive indications
- Commonly used intranasally, like the parent peptide
Potential Side Effects
- Mild nasal irritation with intranasal use
- Occasional overstimulation, restlessness or difficulty sleeping
- Headache (uncommon)
- No published human safety data specific to the acetylated form
- Not approved by the FDA or EMA in any form
Common Dosing
For research use only and not personal medical advice. No approved dosing exists for the acetylated form, and no human dose-finding study has been published for it. Research-chemical references generally mirror intranasal Semax ranges of roughly 100-600 mcg per day, sometimes divided; by contrast the Russian ischemic-stroke trial of the parent peptide used a far higher 6,000 mcg per day in supervised 10-day courses, which is a clinical stroke protocol and not a nootropic range.
The dosing information above is aggregated from research literature and anecdotal community reports for educational purposes only. It is not a recommendation, prescription, or medical advice. Peptides are sold as research chemicals only and are not intended for human use.
Contraindications
- Pregnancy or breastfeeding
- Acute psychiatric agitation (theoretical, based on the parent compound's stimulating profile)
- Not approved for human use outside of certain countries
- No analog-specific human safety data to draw on
N-Acetyl Selank
An N-terminally acetylated form of Selank, the Russian anxiolytic peptide derived from tuftsin. Unlike its Semax counterpart, the acetylated form of Selank has no dedicated published literature of its own -- every finding below comes from the parent peptide.
Selank
A synthetic analog of the immunomodulatory peptide tuftsin developed in Russia for anxiety reduction and cognitive support without the sedation or dependence of benzodiazepines.
Semax
A synthetic peptide derived from ACTH(4-10) developed in Russia and used there for cognitive enhancement, stroke recovery, and neuroprotection. Often used intranasally.
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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
2016
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[The efficacy of semax in the tretament of patients at different stages of ischemic stroke]
2018
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Stability of Semax acetyl to proteolysis in various biological media
2013
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Rapid induction of neurotrophin mRNAs in rat glial cell cultures by Semax, an adrenocorticotropic hormone analog
2001