N-Acetyl Semax Amidate
Also known as: Enhanced Semax, Stabilized Semax, NASMA
Evidence: Anecdotal
Overview
Acetylated, amidated analog of Semax, a synthetic ACTH(4-10) fragment; research on the parent peptide reports BDNF/NGF upregulation and neuroprotection in stroke models.
N-Acetyl Semax Amidate is a terminally modified analog of Semax, a synthetic fragment of ACTH(4-10) with the melanocortin activity removed. Studies of the parent peptide - mostly Russian, including human stroke and optic neuropathy trials - report increased BDNF and NGF expression, neuroprotection, and effects on attention and memory. The acetylated-amidated analog has no published human or animal data of its own; claims that it exceeds Semax in potency are extrapolation from its chemistry plus user reports.
Benefits
Cognitive enhancement, focus
Dosing reference
- Research dose
- Vendor/community range 200 to 600 mcg once or twice daily, intranasal; no published human or animal dose for this analog.
- Range
- 200 to 600 mcg, 1-2x daily
- Reconstitution
- 2 mL bacteriostatic water
- Common vial sizes
- 5 mg, 10 mg
Intranasal per vendors. No pharmacology has been published for the acetylated, amidated analog; data for the parent Semax do not transfer automatically.
Mechanism
No pharmacology of the acetylated, amidated form is published. The one study of Semax N-terminal acetylation found that it changed copper(II) and zinc(II) binding and did not protect cells against Cu(II) toxicity (Magri et al., 2016). Claims that the modifications extend half-life or improve CNS penetration have no source. For unmodified Semax, intranasal dosing raised BDNF and trkB expression in rat hippocampus (Dolotov et al., 2006).
Evidence
Anecdotal: no peer-reviewed data
- N-terminal acetylation of Semax altered its copper and zinc coordination and did not protect against Cu(II) toxicity in cells (Magri et al., 2016)
- Unmodified Semax raised BDNF and trkB expression in rat hippocampus (Dolotov et al., 2006)
- Unmodified Semax was given at 6000 mcg/day to Russian ischemic stroke patients (Gusev et al., 2018)
- Human-trial status: no study of N-acetyl Semax amidate in any species. All human data are for unmodified Semax in Russian trials; Russian peptide drug registrations are reviewed in Deigin et al., 2022
References
- 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. Magrì A, Tabbì G, Giuffrida A, et al., Journal of Inorganic Biochemistry, 2016
- Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Dolotov OV, Karpenko EA, Inozemtseva LS, et al., Brain Research, 2006
- The efficacy of semax in the tretament of patients at different stages of ischemic stroke. Gusev EI, Martynov MY, Kostenko EV, et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2018
- Development of Peptide Biopharmaceuticals in Russia. Deigin VI, Poluektova EA, Beniashvili AG, et al., Pharmaceutics, 2022
Side effects
Nasal irritation, headache, and overstimulation or irritability at higher doses are the reported effects. Safety data for this modified analog specifically is limited; the available evidence comes from unmodified Semax in Russian trials.
Storage
- Storage
- Refrigerate 2-8°C (36-46°F)
- Lyophilized
- 2+ years at room temp, 3+ years refrigerated
- Reconstituted
- 28-30 days refrigerated
Pharmacology
- Half-life
- Not measured in any species
- Bioavailability
- Not measured in any species
- Molecular weight
- 855 Da
- Sequence
- Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH2 (N-acetyl, C-amide)