Gathering the record
Relay is organizing the evidence and source boundaries.
Experimental N-acetylated and C-amidated Semax analog
A modified version of Semax, discussed for focus, cognition, and stress. It is a different molecule from parent Semax.
Evidence is explained by question. Dosing references show their own check dates.
60-second overview
Why people look into it, what studies found, and what is still unknown.
Educational information only. Evidence reviewed through July 31, 2026. Published studies, sponsor announcements, and trials without results are labeled separately. Evidence gaps apply to the specific finding beside them.
Research questions
Each label shows how much evidence supports that question.
What studies show
No direct human evidence was identified. No exact-compound peer-reviewed animal efficacy or pharmacokinetic study was identified either.
It keeps the seven-residue Semax core but caps both termini with an N-terminal acetyl group and a C-terminal amide.
Terminal acetylation and amidation can change charge, enzymatic susceptibility, metal coordination, distribution, and target interactions.
Claims about stronger potency, longer duration, cognition, focus, mood, neuroprotection, or intranasal effectiveness remain unverified for this exact analog.
They provide evidence that acetylation changes chemical and biological behavior, not proof of the doubly modified product's performance.
Terminal modification does not automatically mean a better or more potent molecule.
Keeping the same core sequence does not guarantee the same absorption, binding, brain distribution, metabolism, potency, or safety after both termini are modified.
Research-market descriptions and parent-Semax use patterns do not create a validated standard for the modified analog.
Risks & unknowns
No direct peer-reviewed efficacy, pharmacokinetic, safety, or human-exposure evidence for NA Semax was identified by Relay.
No direct evidenceA future exact-compound study could change the evidence state, but current parent and mono-acetyl evidence cannot fill this gap.
Open sourceThe available information does not reliably show how often particular side effects occur.
Evidence boundaryUnder-detected or under-reported events must not be described as rare.
Relay has not verified which side effects led people to stop treatment in studies.
Evidence boundaryThis is an evidence gap, not proof that discontinuations did not occur.
Relay has not verified a compound-specific warning summary for this profile.
Evidence boundaryNot FDA approved; no direct peer-reviewed efficacy, pharmacokinetic, safety, or human-exposure record identified Nearly every clinically relevant property: exact target engagement, absorption, nose-to-brain exposure, systemic distribution, half-life, metabolites, potency, efficacy, repeated-use safety, immunogenicity, and research-product identity.
This profile does not contain verified, product-specific emergency instructions.
Evidence boundaryRelay does not infer emergency guidance from study discontinuations, mechanism, or incomplete adverse-event reporting.
Dosing references
Each table labels its source and applies only to the named route, product, or study. An online example or community report is not an approved dose.
Semax nasal studies do not establish dosing for N-acetyl Semax or N-acetyl Semax amidate. The derivative and formulation must match the source.
What would fill this gap: A direct human protocol for the exact N-acetyl derivative.
Dosing review checked Oct 20, 2026. Additional sources are available below.No route-specific preparation instructions were verified. A different route or product does not supply them.
Starting dose: the amount used at the beginning of the named label schedule or trial.
Maintenance: the ongoing amount described by that product label.
Trial target: the amount assigned to a study group. Different groups may stop increasing at different targets.
No verified direct study was located for the exact peptide with both N-terminal acetylation and C-terminal amidation. Related-molecule studies do not establish this analog's behavior.
Population: No directly studied human population was verified for this identity.
Design: No direct efficacy, pharmacokinetic, safety, animal-outcome, or human study located
No direct primary administration source was verified for this exact identity.
Mechanisms
NA Semax is Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH2, a doubly terminal-modified analog of the ACTH(4-7)-Pro-Gly-Pro peptide Semax. N-terminal acetylation removes the free amino group and C-terminal amidation replaces the terminal carboxylate. Exact-compound searches did not identify peer-reviewed pharmacokinetic, efficacy, safety, animal-outcome, or human-exposure studies. Mono-acetylated Semax research found altered proteolysis and materially changed copper coordination and cell behavior, demonstrating that terminal chemistry can change function. Parent Semax animal studies involving BDNF, trkB, binding, and neuroprotection remain parent-only evidence. No potency multiplier, extended half-life, preferred route, dose, or product standard can be established for NA Semax.
A plausible mechanism can explain why a study was attempted. It does not prove that the compound improves a human outcome.
Research reference
A reference for the studies, populations, and routes behind this profile.
Chemical identity is documented, but direct efficacy, pharmacokinetic, safety, animal-outcome, and human studies were not found.
Research depth describes how large and mature the overall record is. It does not tell you whether the results were positive.
Claims are largely extrapolated from parent Semax or a differently modified analogue.
Confidence describes how reliable and consistent the conclusions are. It can be high for one outcome and low for another.
The strongest evidence type shows what the best-supported conclusions are actually based on.
Human findings are more directly relevant than animal or laboratory results, but they still apply only to the populations and outcomes studied.
Route-specific record
N-Acetyl Semax Amidate direct evidence: amounts and schedules describe this route record only.
These are exposures used in cited research for a specific route and population—not an instruction for an individual.
Half-life describes how long it takes the measured amount in the body to fall by half. It is not a dosing recommendation.
Evidence can change by administration method. Findings from one route should not automatically be applied to another.
Evidence boundary: Parent Semax and N-acetyl Semax are different chemical identities. The section remains incomplete because exact-compound exposure, pharmacology, outcomes, and safety evidence are absent. Amounts shown describe cited research exposure—not a dosage recommendation.
Studies
Study arms are reported for transparency. They describe what researchers did in a defined record and do not transfer across identities, routes, formulations, or populations.
A later trial phase can ask a more mature question, but it does not guarantee a positive result, regulatory approval, or relevance outside the studied population.
Copper and zinc coordination chemistry plus neuroblastoma-cell assays
Chemical systems and SH-SY5Y neuroblastoma cells
N-terminal acetylation changed copper coordination and redox behavior. Unlike parent Semax, acetylated Semax did not protect the tested cells from copper-induced toxicity.
Study administration: Parent Semax and N-acetyl Semax; no C-terminal amidation
Limitations: The C-amidated analog was not tested. This finding demonstrates that terminal modification can change biology rather than proving that NA Semax is safer, stronger, or longer lasting.
Laboratory proteolysis testing in several biological media
Enzyme preparations and biological matrices
N-terminal acetylation altered the proteolytic stability of Semax in the tested biological media.
Study administration: N-acetyl Semax; no confirmed C-terminal amidation
Limitations: This study did not test the doubly modified N-acetylated and C-amidated NA Semax product. It cannot establish its half-life, route, potency, or human exposure.
Intranasal parent-Semax exposure with molecular and behavioral endpoints
Rats
Parent Semax altered BDNF/trkB measures and conditioned-avoidance behavior in rats.
Study administration: Parent Semax, not NA Semax
Limitations: The study does not support direct efficacy, potency, duration, or dosing claims for NA Semax.
Intranasal parent-Semax exposure and binding/BDNF analysis in rats
Rats
Parent Semax showed specific binding in rat basal-forebrain membranes and increased BDNF protein after intranasal exposure.
Study administration: Parent Semax, not NA Semax
Limitations: Parent Semax animal findings do not establish that the doubly terminal-modified analog has the same target engagement, route behavior, or effect.
PubMed and ClinicalTrials.gov searches for the doubly modified analog
Population not stated.
Relay did not identify a peer-reviewed efficacy, pharmacokinetic, safety, animal-outcome, or human trial of N-Acetyl Semax Amidate specifically.
Study administration: Not stated in the current record.
Limitations: Search results can evolve, but evidence from parent Semax or mono-acetylated Semax cannot be relabeled as direct evidence for the doubly modified analog.
Community
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2026-07-31
2026-07-31
2026-07-31
2024-12-31
2016-11-01 · PMID 27586814 · DOI 10.1016/j.jinorgbio.2016.08.013
2015-01-01 · PMID 25310602 · DOI 10.1016/j.jinorgbio.2014.09.008
2013-03-01 · PMID 23652441 · DOI 10.1134/S0012496613020166
2006-12-01 · PMID 16996037
2006-06-01 · PMID 16635254