Gathering the record
Relay is organizing the evidence and source boundaries.
Synthetic ACTH-fragment-derived neuroactive heptapeptide
Semax is a seven-amino-acid peptide researched mostly for brain recovery, cognition, and neuroprotection. Small and older human studies report signals, but the evidence does not establish a reliable focus, memory, stroke, migraine, or pain treatment.
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.
Semax is a seven-amino-acid peptide developed from part of an adrenocorticotropic hormone sequence but without the parent hormone's main endocrine activity. It is researched mainly in neurology.
Researchers have explored brain recovery, cognition, pain, and neurotrophin signaling. Human studies are small or old, while much of the detailed mechanism record comes from animals and cells.
A 24-person placebo-comparison imaging study found an acute brain-network change but did not measure better focus or memory. Older stroke reports described recovery or BDNF signals with unclear modern randomization and blinding. An uncontrolled migraine report produced mixed results across tiny groups.
Reproducible clinical benefit, effect size, human pharmacokinetics, product-form differences, route-specific exposure, interactions, bleeding risk, immunogenicity, and repeated-use safety remain uncertain. Mechanism and imaging changes are not patient outcomes.
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.
A small placebo-comparison study investigated acute intranasal Semax in healthy adults and measured resting brain-network activity before and shortly after exposure.
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.
Small human imaging, stroke, and pain reports exist alongside extensive animal and mechanistic research, but no modern pivotal program was located.
Research depth describes how large and mature the overall record is. It does not tell you whether the results were positive.
Human findings are small, old, incompletely controlled, and not independently replicated across modern clinical outcomes.
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: The study included twenty-four people, and allocation and masking details were not clear in the accessible abstract. A brain-network change does not establish improved focus, memory, learning, mood, productivity, recovery, or durable benefit. 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.
A 24-person placebo-comparison fMRI study found an acute default-mode-network change, while two older stroke reports involving 110 participants each described recovery or BDNF signals. None provides a modern, independently replicated, blinded efficacy record.
This is the strongest supported conclusion in the current human evidence—not a summary of every claim made about the compound.
Whether Semax produces meaningful, reproducible clinical benefit and what its human pharmacokinetics, product-form differences, route-specific exposure, repeated-use safety, immunogenicity, bleeding risk, and interaction profile look like.
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.
Its sequence is Met-Glu-His-Phe-Pro-Gly-Pro, often described as ACTH(4-7)-PGP or an ACTH(4-10) analogue.
They share the same active moiety but differ in chemical identity and may differ in solubility, stability, impurities, pharmacokinetics, and product performance.
Animal and cell studies report changes in BDNF/TrkB, NGF, immune signaling, monoamines, ischemia-related gene expression, and copper chemistry, but no single validated human therapeutic receptor explains the promoted effects.
A small placebo-comparison fMRI study found a larger rostral default-mode-network subcomponent after intranasal Semax.
Two Russian-language reports associated Semax with neurological or functional recovery and higher BDNF after ischemic stroke.
One small uncontrolled study reported headache cessation in four of 12 migraine participants, no benefit in typical trigeminal neuralgia, and limited subjective findings in dental plexalgia.
The traceable modern human record includes a small acute fMRI finding rather than validated cognitive or functional improvement.
The best-developed mechanistic record comes from rodent hippocampus and experimental cerebral ischemia.
Semax changed copper chemistry, reactive oxygen species, and cell toxicity in artificial systems and cultured cells.
FDA found rat disposition studies but no human pharmacokinetic study by any route.
Proposed subcutaneous use is not supported by a human PK, safety, or efficacy program in the FDA review.
FDA found sparse adverse-event reporting, no human PK, no subcutaneous clinical safety data, no clinical immunogenicity studies, and no adequate repeat-dose toxicology package.
FDA noted Semax-related coagulation findings in animals and an inadequately reported human abstract.
Historical studies used intranasal products and different study schedules, while supplier stability statements are not an approved U.S. product label.
A July 2026 advisory committee voted to recommend possible 503A compounding-list inclusion, but that recommendation is nonbinding and is not drug approval.
Mechanisms
Semax is the synthetic peptide Met-Glu-His-Phe-Pro-Gly-Pro, commonly described as ACTH(4-7)-PGP or an ACTH(4-10) analogue. Human evidence includes a 24-person acute resting-state fMRI study and older, methodologically limited stroke and pain reports. Rodent and cell studies show BDNF/TrkB, immune, inflammatory, monoamine, ischemia-response, and copper-related effects, but no single validated human therapeutic target or exposure-response relationship is established.
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.
Chemical binding, reactive-oxygen-species, amyloid-beta, and neuronal-cell experiments
Cell-free systems and SH-SY5Y neuroblastoma cells
Semax bound copper, reduced copper-linked reactive oxygen species, and reduced toxicity in the cell model.
Study administration: Semax added to copper/amyloid-beta chemical systems and cultured cells
Limitations: This does not demonstrate prevention or treatment of Alzheimer's disease, cognitive decline, or neurodegeneration in humans.
Small placebo-comparison resting-state functional-MRI study with before-and-after imaging
24 healthy adults; 11 men and 13 women, mean age 43.9 years
The Semax group showed a larger rostral default-mode-network subcomponent than the placebo group after administration.
Study administration: Intranasal 1% Semax in 14 participants or placebo in 10 participants; allocation and masking details were not stated in the abstract
Limitations: This tiny acute imaging study did not measure or demonstrate better focus, memory, learning, mood, productivity, or durable cognitive performance. Randomization and masking are unclear from the abstract.
Five-month clinical comparison stratified by early or late rehabilitation and Semax exposure
110 adults after ischemic stroke
The report associated Semax exposure with higher plasma BDNF and faster Barthel-index improvement, while early rehabilitation was also strongly associated with recovery.
Study administration: Rehabilitation with or without two reported intranasal Semax courses; study exposure is described for transparency and is not dosing guidance
Limitations: The accessible report does not establish a modern randomized, blinded treatment effect. Subgroup sizes, allocation, concurrent care, confounding by rehabilitation timing, and complete safety reporting are unclear.
Rat focal-ischemia transcriptome and protein-expression experiments
Rats with experimental cerebral ischemia or ischemia-reperfusion
Semax changed inflammatory, immune, neurotransmission, cell-death, and recovery-related molecular signals in ischemic rat brain tissue.
Study administration: Semax or control after experimental cerebral ischemia in rats
Limitations: These are molecular findings in artificial stroke models. They do not demonstrate improved survival, disability, cognition, or safety in people.
Controlled rat experiment measuring neurotrophin expression, TrkB phosphorylation, and conditioned avoidance
Rats
Semax increased several BDNF/TrkB measures and conditioned-avoidance responses in rats.
Study administration: Intranasal Semax or control in rats; animal exposure is not human dosing guidance
Limitations: Rodent molecular and learning-task findings do not establish human focus, memory, mood, neuroprotection, or clinical recovery.
Older clinical and electrophysiological comparison with a conventionally treated control group
30 adults with acute hemispheric ischemic stroke receiving Semax plus intensive therapy and 80 severity- and lesion-matched controls
The authors reported faster regression of cerebral and focal neurological deficits, especially motor impairment, when Semax was added.
Study administration: Semax added to conventional intensive therapy versus conventional therapy; historical study schedules are not current treatment recommendations
Limitations: Randomization and masking were not reported in the abstract, the paper is Russian-language, modern stroke-care comparability is uncertain, and detailed safety and statistical reporting are limited.
Uncontrolled, unblinded single-dose pain study summarized in the 2026 FDA briefing
12 adults with migraine plus 16 with typical trigeminal neuralgia and nine with dental plexalgia
Four of 12 migraine participants reported headache cessation at 90 to 120 minutes. The typical trigeminal-neuralgia group did not improve; some subjective improvement was described in dental plexalgia without a broad objective effect.
Study administration: One intranasal Semax exposure; FDA could not determine whether free base or acetate was used
Limitations: There was no placebo group or masking, measurement methods were poorly described, the subgroups were tiny, and FDA concluded that the evidence was insufficient for migraine or trigeminal neuralgia.
Safety snapshot
The available safety record is insufficient to characterize short- or long-term Semax risk.
No direct evidenceAbsence of a well-characterized event rate is not evidence that a product is safe.
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.
The available safety record is insufficient to characterize short- or long-term Semax risk.
No direct evidenceAbsence of a well-characterized event rate is not evidence that a product is safe.
Open sourceThe 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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