N-Acetyl Semax Amidate
| Category | Compounds |
|---|---|
| Also known as | NA-Semax, N-Acetyl Semax, N-Acetyl Semax Amidate |
| Last updated | 2026-04-14 |
| Reading time | 3 min read |
| Tags | nootropicneuropeptideacth-analogrussian-research |
Overview
N-Acetyl Semax Amidate (often abbreviated NA-Semax or NAS) is a modified form of Semax, a synthetic heptapeptide analog of the ACTH(4-10) fragment originally developed in Russia for nootropic and neuroprotective applications. The parent compound has been studied for stroke recovery, cognitive performance, and attention. The N-acetyl amidate form adds protective modifications at both termini.
The rationale for the modifications is peptide stability: an N-terminal acetyl group blocks aminopeptidase cleavage, and a C-terminal amide blocks carboxypeptidase cleavage. The result is a longer-acting analog with reported increases in potency in some preclinical assays. Much of the primary literature remains Russian-language; English-language discussions typically draw on the same originating research groups.
NA-Semax is commonly discussed alongside the related stabilized analog NA-Selank, as well as P21 peptide, Cerebrolysin, and Noopept in nootropic research communities.
Structure / Chemistry
The parent Semax sequence is Met-Glu-His-Phe-Pro-Gly-Pro. The N-acetyl amidate form adds an acetyl group on the N-terminal methionine and an amide on the C-terminal proline. These modifications do not change the core sequence but substantially alter susceptibility to exopeptidases.
Mechanism of Action
Semax and its analogs are thought to modulate BDNF, NGF, and other neurotrophin expression, influence dopaminergic and serotonergic tone, and interact indirectly with melanocortin and opioid-related systems. The compound does not activate ACTH's glucocorticoid axis. NA-Semax is expected to engage the same pathways, with enhanced duration of action from its termini modifications.
Research Summary
| Area | Finding | Reference |
|---|---|---|
| Neurotrophin | Semax upregulates BDNF in rodent hippocampus | Dolotov et al., Neurosci Lett 2006 |
| Stroke | Semax improved outcomes in ischemic stroke trials | Gusev et al., Stroke 2005 |
| Stability | Acetyl-amide modifications resist peptidases | Shevchenko et al., Bioorg Khim reports |
| Attention | Cognitive/attention effects in rodent models | Vorvul et al., Bull Exp Biol Med 2020 |
| Neuroprotection | Protective effects after cerebral ischemia | Ashmarin et al., Pathophysiology 2005 |
Pharmacokinetics
Native Semax has a very short plasma half-life after intranasal administration. NA-Semax is reported to have substantially longer biological activity in animal models. Administration in research contexts is typically intranasal. Human pharmacokinetic data on the modified analog are limited.
Common Discussion Topics
- Effective intranasal dosing and absorption questions.
- Comparisons between Semax and NA-Semax duration.
- Mechanistic overlap with Selank and NA-Selank.
- Role of BDNF upregulation in cognitive effects.
- Research context within Russian peptide neuropharmacology.
Related Compounds
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Related entries
- Cerebrolysin— A porcine brain-derived peptide preparation containing low-molecular-weight neuropeptides and free amino acids, approved in over 40 countries for stroke, traumatic brain injury, and dementia, though not FDA-approved in the United States.
- N-Acetyl Selank— N-Acetyl Selank is a stabilized analog of Selank, a tuftsin-derived neuropeptide studied for anxiolytic and nootropic activity.
- P21 Peptide— P21 is a CNTF-derived tetrapeptide designed to mimic the active region of ciliary neurotrophic factor, studied for neurogenesis and Alzheimer's disease models.
- Selank— A synthetic heptapeptide analog of the immunomodulatory peptide tuftsin, developed in Russia as an anxiolytic and nootropic with additional immunomodulatory properties.
- Semax— A synthetic heptapeptide analog of ACTH(4-10) developed in Russia as a nootropic and neuroprotective agent, studied for cognitive enhancement, stroke recovery, and BDNF modulation.