NA-Semax Amidate
An N-acetylated, amidated form of Semax designed for enhanced stability, studied for nootropic and neuroprotective effects via BDNF upregulation and melanocortin receptor activity.
Also referenced as: N-Acetyl Semax Amidate, NAMSA
Also appears in: Neuroprotection
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This name primarily lives in the research market and should not be read like an approved pharmaceutical product.
Primary research area: Cognitive. Also surfaces under Neuroprotection for browsing and discovery.
N-Acetyl Semax Amidate, NAMSA
No FDA label signal · 63 trials · 21 PubMed results
Current evidence for NA-Semax Amidate is limited to laboratory or animal studies — there are no name-matched human trials with reported results. Any claims about effects in people are not yet backed by clinical data.
NA-Semax Amidate has no clinical trials that name it and 21 PubMed-indexed publications and is not FDA-approved. Current evidence is preclinical or mechanistic.
Re-checked nightly against the registries — tracked since 2026-07-09. No band changes yet.
Grades evidence strength, not efficacy or safety. Research-use context; not medical advice. Graded 2026-10-05 from PubMed, ClinicalTrials.gov, ISRCTN, openFDA, Health Canada, and OpenAlex — computed deterministically and refreshed nightly, with a retraction check. How we grade →
What is NA-Semax Amidate?
NA-Semax Amidate is a stabilized version of Semax, a synthetic heptapeptide analog of ACTH(4-10) — the fragment of adrenocorticotropic hormone responsible for its nootropic effects without the hormonal (adrenal) activity. The N-acetylation and C-terminal amidation modifications improve enzymatic resistance and extend biological half-life compared to unmodified Semax.
How it works
The core mechanism is shared with Semax:
- BDNF upregulation — Semax increases brain-derived neurotrophic factor expression in the hippocampus and cortex, supporting neuronal survival and synaptic plasticity (Dolotov et al., Neuroscience, 2006)
- Melanocortin pathway — as an ACTH(4-10) analog, Semax interacts with melanocortin receptors (MC3R, MC4R) in the CNS, which modulate attention, learning, and memory (Eremin et al., Neuroscience and Behavioral Physiology, 2004)
- NGF modulation — Semax has been shown to influence nerve growth factor expression and signaling in brain tissue (Shadrina et al., Doklady Biological Sciences, 2001)
- Enhanced stability — the N-acetyl and amide modifications reduce aminopeptidase and carboxypeptidase degradation
Research status
Semax (the parent peptide) has clinical data, primarily from Russian research:
- Semax is approved in Russia as an intranasal nootropic and neuroprotective agent (registration: P N000456)
- Eremin et al. (2004) demonstrated cognitive-enhancing effects of Semax in healthy volunteers (Neuroscience and Behavioral Physiology, 34(8):851–854)
- Dolotov et al. (2006) showed Semax-induced BDNF upregulation in rat hippocampus and cortex (Neuroscience, 137(1):93–102)
- Gusev et al. (1997) reported neuroprotective effects of Semax in acute ischemic stroke patients in a controlled trial (Zhurnal Nevrologii i Psikhiatrii, 97(6):26–34)
The NA-Amidate modification has not been separately studied in clinical trials — it is a vendor-driven formulation.
Key considerations
- Semax (parent compound) has Russian regulatory approval for both cognitive enhancement and stroke neuroprotection
- The NA-Amidate form is not the version used in clinical trials
- Typically administered intranasally; often stacked with NA-Selank Amidate
- Available from research vendors as nasal spray formulations or lyophilized powder