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A specimen of the Cognitive drawer Drawer E · Cognitive

N-Acetyl Semax Amidate

Research Only

A chemically modified version of Semax with N-terminal acetylation and C-terminal amidation designed to enhance peptide stability. While parent Semax is approved in Russia for nootropic and neuroprotective applications, this specific modification has no independent clinical research.

NA-Semax · N-Acetyl Semax · Acetyl-Semax-Amidate · NASA-Semax

Research evidence
Very Low

Preclinical evidence only

Preclinical
100%
Human research
0%

Based on 2 cited sources

Numeric assessment unreviewed

A historical numeric score is recorded but has not passed a current, compound-specific assessment review. No numeric score is displayed.

This is a limitation of the numeric assessment, not a measured absence of benefit. It does not re-review the separately recorded catalogue classification or establish efficacy or safety.

Scoring context and limitations
!!
Evidence Level
very low
Not FDA-approved.
Research Only
Identity
SCALE · 1:1 N-TERMINUS C-TERMINUS 7 AA · ~855 Da
Also Known As
NA-Semax • N-Acetyl Semax • Acetyl-Semax-Amidate • NASA-Semax
Class
Heptapeptide (modified)
Length
7 amino acids
Mol. weight
~855 Da
Sequence
Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH2
Molecular Structure
Ac-M
E
H
F
P
G
P-NH2
Hydrophobic
Polar
Positive
Negative

The proposed mechanisms of N-Acetyl Semax Amidate are extrapolated entirely from parent compound Semax research. No direct studies exist on this modified form.

How It Works (Simplified)

N-Acetyl Semax Amidate is proposed to work through the same pathways as Semax, with enhanced stability from terminal modifications:

Neurotrophic Enhancement

Parent Semax increases BDNF, NGF, and GDNF expression. Whether modifications preserve this activity is unknown.

Neurotransmitter Modulation

Semax affects dopamine and serotonin systems. The modified form’s receptor affinity has never been tested.

TrkB Receptor Signaling

Semax activates TrkB receptors for neuroplasticity. Impact of terminal modifications on binding is uncharacterized.

Enhanced Stability

N-acetylation blocks aminopeptidases, C-amidation blocks carboxypeptidases. Actual half-life extension not measured.

Key Research: Dolotov OV et al. (Russia, 2006) demonstrated BDNF and TrkB expression effects with Semax in the rat hippocampus. PMID:16996037

Important Limitations

  • Zero published studies on N-Acetyl Semax Amidate specifically
  • All mechanisms extrapolated from parent Semax research
  • Whether modifications preserve biological activity is untested
  • No human pharmacokinetic data exists for this compound
i. Neurotrophic Pathway · Extrapolated from Semax
NA-Semax-Amidate (theoretical)Same as Semax?BDNF/NGF upregulationTrkB activationNeuroplasticity & neuroprotection
ii. Dopaminergic Modulation · Extrapolated from Semax
NA-Semax-Amidate (theoretical)Dopamine systemEnhanced cognition/motivationSerotonin systemMood modulation
Mechanism BDNF/TrkB pathway activation promoting neuroplasticity
Emerging 0 direct studies
Benefit may enhance cognitive function and memory
Evidence Level
Very Low
Mechanism Dopaminergic and serotonergic system modulation
Emerging 0 direct studies
Benefit may improve mood and motivation
Evidence Level
Very Low
Mechanism NGF/GDNF upregulation for neuroprotection
Emerging 0 direct studies
Benefit may provide neuroprotective effects
Evidence Level
Very Low
Mechanism N-acetylation and C-amidation for enhanced peptide stability
Emerging 0 direct studies
Benefit may extend duration of action compared to parent Semax
Evidence Level
Very Low
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low

Reported positives

  • Stronger and longer-lasting than standard semax reported
  • Enhanced cognitive stimulation and focus
  • Modified form provides improved bioavailability
  • Nasal administration convenient

Reported negatives

  • Overstimulation and anxiety at higher amounts
  • More expensive than standard semax
  • Hair loss concerns carried over from semax reports
  • Limited supplier options

“Considered the potent version of semax. Popular in nootropic stacks.”

Self-reported, unverified accounts — not clinical evidence and no substitute for the cited research. Anecdotes are prone to selection bias and placebo effects.

Phase 01 1
Week 1-2

No human data available. Based on parent Semax pharmacology: Acute cognitive effects may be noticed. Russian Semax studies suggest rapid onset of action. Whether modifications alter timeline is unknown.

PMID:16996037
Phase 02 2
Week 2-4

Extrapolated from Semax: Neurotrophic factor expression changes may develop. Parent compound shows BDNF modulation in animal models within this timeframe. No data specific to NA-Semax-Amidate.

PMID:17353092
Phase 03 3
Week 4-8

Based on general nootropic peptide research: Neuroplasticity effects may accumulate with continued use. No long-term studies exist for this modified compound.

PMID:15088389
Phase 04 4
Week 8+

Completely unknown. No studies have evaluated extended use of N-Acetyl Semax Amidate. Long-term safety and efficacy data do not exist.

Research-based observations

This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.

Synergistic
Compatible
Caution
Avoid

Semax

Synergistic
Synergistic

Parent compound with identical core sequence. NA-Semax-Amidate is designed to extend duration of action through terminal modifications. No studies comparing direct combination.

Both are modified Russian nootropic peptides with different mechanisms (Semax: neurotrophic focus vs Selank: anxiolytic focus). Commonly discussed together but no interaction studies exist.

Different mechanism profiles. Selank focuses on anxiolytic effects while Semax derivatives target cognitive enhancement. No known contraindications.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength labels summarize the cited material for this entry and should be read alongside its population, model, and study limitations.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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