N-Acetyl Semax
Also known as: N-Acetyl Semax Amidate, NA Semax
It is a chemically stabilized analog of the ACTH(4-7)-derived peptide Semax that, in preclinical models, binds specifically in brain tissue and raises BDNF and other neurotrophins while modulating ischemia-related inflammatory and neurotransmitter gene expression.
- Drug class
- Synthetic ACTH(4-7)-derived melanocortin neuropeptide (acetylated/amidated Semax analog)
- Primary targets
- BDNF/TrkB neurotrophin signaling, NGF/TrkA and NT-3/TrkC pathways, melanocortin (ACTH/MSH) system, dopaminergic and serotonergic neurotransmission
- Dose reference
- No established human dose for the N-acetylated/amidated analog; parent Semax was used intranasally at roughly 6,000-18,000 mcg/day in Russian stroke trials (research figures from trials, not recommendations)
- Half-life
- Not established for the analog; parent Semax plasma half-life is only minutes due to rapid aminopeptidase degradation, and vendor-claimed multi-hour half-lives lack peer-reviewed human PK data
- Developer / origin
- Institute of Molecular Genetics, Russian Academy of Sciences (parent Semax)
- Reference year
- 2000
- Evidence score
- 2/5 - Weak (analog-specific evidence essentially absent)
Weak (analog-specific evidence essentially absent)
The acetylated/amidated analog has no dedicated peer-reviewed human or animal studies; supporting science comes from parent Semax, which has solid rodent neurotrophin/gene-expression data but only small, often non-randomized, largely Russian-language human trials and no approval outside Russia and neighboring states.
Mostly animal, ex vivo, cell, or indirect evidence.
Evidence basis
- Preclinical rat studies document specific brain binding (KD ~2.4 nM) and BDNF/neurotrophin upregulation for parent Semax
- Genome-wide and protein-expression studies show modulation of ischemia-related inflammatory and neurotransmitter genes in rat MCAO models
- Human data limited to small non-randomized Russian stroke studies and resting-state fMRI studies in healthy volunteers; no Phase 3 trials outside post-Soviet states
- No published pharmacokinetics, toxicology, or human safety data for the N-acetylated/amidated analog specifically; popular half-life/bioavailability figures are not traceable to controlled studies
Key references
- Journal of Neurochemistry (2006)Semax binds specifically and increases BDNF protein in rat basal forebrain
- Cellular and Molecular Neurobiology / PMCSemax and Pro-Gly-Pro Activate Transcription of Neurotrophins and Their Receptor Genes after Cerebral Ischemia
- International Journal of Molecular Sciences (2021)Brain Protein Expression Profile Confirms the Protective Effect of ACTH(4-7)PGP (Semax) in Rat Cerebral Ischemia-Reperfusion
- Zhurnal Nevrologii i Psikhiatrii (2018)The efficacy of semax in the treatment of patients at different stages of ischemic stroke
How to read this entry
Dose references and half-life values are pulled from trial protocols, labels, reviews, or published summaries where available. They are context for research and comparison, not a personal dosing recommendation.
Status matters: approved drugs have regulated indications; investigational compounds are still being studied; research-only peptides do not have established human dosing, safety, or efficacy for consumer use.
N-Acetyl Semax guides
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TP-7
Russian-developed analog of tuftsin marketed (in Russia) as an anxiolytic. Mechanism involves modulation of GABA and stress-response pathways.
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ACTH(4-10) analog
Heptapeptide derived from ACTH(4-10). Russian neuropeptide studied for nootropic and neuroprotective effects, partly via BDNF upregulation.
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N-Acetyl Selank
NA Selank Amidate
N-Acetyl Selank is a chemically stabilized (N-acetylated, C-amidated) analog of the tuftsin-derived peptide Selank, proposed to act via GABAergic modulation, inhibition of enkephalin-degrading enzymes that raises endogenous enkephalins, and BDNF-related effects, though these mechanisms were demonstrated for the parent Selank rather than the analog.
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