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N-Acetyl Semax Amidate

Also known as NA Semax Amidate, Ac-MEHFPGP-NH2, Acetylated Semax Amide

N-Acetyl Semax Amidate is a modified analog of Semax, itself derived from the ACTH(4-7) fragment. It is considered the most potent and bioavailable form of Semax, incorporating both N-terminal acetylation and C-terminal amidation to resist enzymatic degradation. Used intranasally, it is studied for cognitive enhancement, neuroprotection, BDNF upregulation, and focus and mood improvement.

Last updated April 10, 2026

TL;DR

Quick summary

N-Acetyl Semax Amidate is the most potent and bioavailable form of Semax, with acetyl and amide modifications that extend the half-life from minutes to an estimated 6-12 hours. It is the preferred Semax variant for BDNF upregulation and cognitive enhancement in biohacking protocols.

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Overview

N-Acetyl Semax Amidate is a modified analog of Semax, itself derived from the ACTH(4-7) fragment. It is considered the most potent and bioavailable form of Semax, incorporating both N-terminal acetylation and C-terminal amidation to resist enzymatic degradation. Used intranasally, it is studied for cognitive enhancement, neuroprotection, BDNF upregulation, and focus and mood improvement.

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Mechanism of action

N-Acetyl Semax Amidate modulates neurotrophic and neurogenic signaling primarily through upregulation of brain-derived neurotrophic factor (BDNF) and its receptor TrkB, as well as nerve growth factor (NGF) and GAP-43. These effects promote neuroplasticity, synaptic density, and long-term potentiation. It also influences the melanocortin system via partial ACTH-receptor agonism, which affects mood, attention, and stress response. The acetyl and amide modifications substantially extend half-life compared to unmodified Semax (estimated 6–12 hours vs. 2–4 hours) by blocking aminopeptidase and carboxypeptidase cleavage sites. Dopaminergic and serotonergic modulation has been reported in preclinical models.

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Dosing protocols

PurposeRouteDosageFrequency
cognitive enhancement and neuroprotection (research)nasal300900 mcgonce to twice daily

Dosing information is for educational purposes only. Consult a qualified healthcare professional before using any peptide.

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Research summary

Semax and its analogs have been approved in Russia for stroke recovery, cognitive impairment, and optic nerve disease. Human studies (primarily Russian) demonstrate improvements in attention, processing speed, and memory consolidation. Animal models show neuroprotective effects following ischemic injury, increased BDNF expression in the hippocampus, and reduced neuroinflammation. N-Acetyl Semax Amidate's enhanced pharmacokinetics make it the preferred form in community biohacking protocols, though Western double-blind RCT data specific to this analog remain limited as of 2026.[1][2][3][4][5]

📄This section cites 5 peer-reviewed sources. View all references →
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Evidence grading

Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.

preliminary
BDNF and TrkB upregulationDolotov Brain Res 2006 (Semax parent): rat hippocampal BDNF/TrkB upregulation; mechanism extends to acetyl-amidate analog by structural inference
preliminary
Cognitive enhancement and attentionRussian clinical studies on parent Semax show attention, processing speed, memory improvements; acetyl-amidate analog has no dedicated RCTs
moderate
Neuroprotection after ischemic strokeGusev et al. 2001: Semax parent clinical study in acute hemispheric ischemic stroke; Kolomin Bull Exp Biol Med 2007 animal data; approved in Russia for stroke
preliminary
Extended half-life via acetyl/amide modificationsZayats Neuropeptides 2016: N-acetylation receptor selectivity study; PK extension is theoretical/extrapolated, no published human PK for this analog
preliminary
Dopaminergic neuroprotection (Parkinson's)Glazova Neurosci Lett 2004: MPTP-induced dopaminergic lesion model; single preclinical study of parent Semax

Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data

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Side effects

Nasal irritation or congestion
Headache
Fatigue after high doses
Vivid dreams
Mild anxiety at high doses (anecdotal)

Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.

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Common stacks

Peptides commonly paired with N-Acetyl Semax Amidate for synergistic effects.

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Sourcing & access

Research compound

N-Acetyl Semax Amidate is classified as a research compound. Regulatory status varies by jurisdiction. Always verify current legal status and source from vendors providing third-party certificates of analysis (COA).

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Frequently asked questions

N-Acetyl Semax Amidate is a modified analog of Semax with both N-terminal acetylation and C-terminal amidation. These modifications resist enzymatic degradation, substantially extending the half-life compared to unmodified Semax and making it the most potent form available.

The acetyl and amide modifications block aminopeptidase and carboxypeptidase cleavage sites, extending the estimated half-life from 2-4 hours to 6-12 hours. This enhanced pharmacokinetics results in stronger and longer-lasting BDNF upregulation and cognitive effects.

It is administered intranasally using a spray, typically starting at 300 mcg per dose once to twice daily. Common formulations come in 0.1 percent and 0.3 percent solutions. Cycles of 4 to 8 weeks with breaks are standard.

It upregulates BDNF and its receptor TrkB, as well as NGF and GAP-43, promoting neuroplasticity and synaptic density. It also modulates the dopaminergic and serotonergic systems, affecting mood, attention, and stress response.

Reported side effects include nasal irritation or congestion, headache, fatigue after high doses, vivid dreams, and mild anxiety at high doses. The side effect profile is generally mild compared to stimulant-based cognitive enhancers.

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Research references

  1. Influence of the N-terminus Acetylation of Semax, a Synthetic Analogue of ACTH(4-10), on Melanocortin Receptor Selectivity and ActivityZayats M, Efimova TA, Dolotov OV, et al.Neuropeptides, 2016PubMed
  2. Semax, an Analog of ACTH(4-10) with Cognitive Effects, Regulates BDNF and trkB Expression in the Rat HippocampusDolotov OV, Karpenko EA, Inozemtseva LS, et al.Brain Research, 2006PubMed
  3. Neuroprotective and Antiamnesic Effects of Semax during Experimental Ischemic Infarction of the Cerebral CortexKolomin T, Shadrina M, Slominsky P, et al.Bulletin of Experimental Biology and Medicine, 2007PubMed
  4. Effectiveness of Semax in Acute Period of Hemispheric Ischemic Stroke (a Clinical and Electrophysiological Study)Gusev EI, Skvortsova VI, Miasoedov NF, et al.Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2001PubMed
  5. The Neuroprotective Effects of Semax in Conditions of MPTP-Induced Lesions of the Brain Dopaminergic SystemGlazova MV, Meza E, Hernandez N, et al.Neuroscience Letters, 2004PubMed
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