Gathering the record
Relay is organizing the evidence and source boundaries.
Experimental N-acetylated and C-amidated Semax analog
NA Semax is N-Acetyl Semax Amidate: the Semax core sequence with both ends chemically capped. Relay found no direct study of this exact analog in humans or animals. Published work on parent Semax and N-acetyl Semax tests different molecules and cannot establish that NA Semax is stronger, longer lasting, cognitively effective, neuroprotective, or safe.
60-Second Overview
Start with what it is, why it matters, what research has shown, and what remains unknown. The science follows after the orientation.
Start here. These four answers explain why the compound matters before the page introduces the deeper science.
NA Semax is a name for N-Acetyl Semax Amidate, a chemically modified version of the Semax sequence with both ends capped. It is a different molecule from parent Semax.
Terminal modifications may change how a peptide breaks down or interacts with other molecules. That possibility has led to claims of greater strength or duration, but those claims require direct testing of the exact analog.
Relay found no direct efficacy, pharmacokinetic, safety, animal-outcome, or human study of the doubly modified analog. Laboratory work on N-acetyl Semax and animal work on parent Semax tested different molecules and sometimes showed that modification changed biological behavior.
Absorption, nose-to-brain exposure, half-life, metabolites, potency, target engagement, clinical effects, repeated-use safety, immunogenicity, and product identity remain unknown. Evidence from parent or singly modified Semax cannot be transferred.
The research depth, routes, studies, and primary sources below explain how Relay knows—and where the evidence stops.
Research context
Published research has investigated this compound using the following study designs.
These records explain what researchers did. They are not instructions, recommendations, or a transferable protocol.
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.
Reported study administration—not a recommendation.
Research at a glance
Evidence depth, confidence, and route context explain how Relay knows—not what anyone should do.
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
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.
Detailed evidence
Start with the strongest supported conclusion and its main uncertainty. Claim-level records below show how the evidence changes by question, population, route, formulation, and study design.
No direct human evidence was identified. No exact-compound peer-reviewed animal efficacy or pharmacokinetic study was identified either.
This is the strongest supported conclusion in the current human evidence—not a summary of every claim made about the compound.
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.
Keeping the main uncertainty visible prevents an early or promising finding from looking more settled than it is.
Questions people bring to the evidence
Research questions—not promises of benefit.
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.
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.
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.
Safety snapshot
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 current record does not support a reliable common-versus-uncommon frequency split.
Evidence boundaryUnder-detected or under-reported events must not be described as rare.
No source-qualified compound-specific warning or contraindication is encoded in the current record.
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.
The current record does not identify a reliable compound-specific pattern of events that caused study discontinuation.
Evidence boundaryThis is an evidence gap, not proof that discontinuations did not occur.
No compound-specific patient-facing urgent-action threshold is established in the current Relay record.
Evidence boundaryRelay does not infer emergency guidance from study discontinuations, mechanism, or incomplete adverse-event reporting.
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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
No direct primary administration source was verified for this exact identity. The limitation is the finding.