Gathering the record
Relay is organizing the evidence and source boundaries.
Synthetic ACTH-fragment-derived neuroactive heptapeptide
An experimental peptide researched for brain conditions. People commonly look into it for focus, memory, and recovery after stroke.
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 25, 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
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.
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.
Risks & unknowns
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 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 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.
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.
Amounts reported in a human study. A studied amount is not automatically an approved dose or a recommendation for an individual.
A manufacturer-hosted report compared three treatment groups with optic-nerve disorders; 25 patients received 0.1% nasal Semax alongside other care.
| Stage / period | Amount in source | Frequency |
|---|---|---|
| 5 days to 2 weeks | 200–300 micrograms per administration | 3–4 times daily |
The report describes 2–3 drops per nostril and 600–1,200 micrograms/day. This small regional report does not establish broad cognitive benefit, injectable dosing, or a regimen for N-acetyl Semax.
Semax · optic-nerve clinical report, Materials and methods Manufacturer-hosted primary clinical report · intranasal groupThis reference checked Oct 20, 2026. The full-profile review date is shown at the top.This report used a 0.1% nasal solution. Its drop count does not transfer to a different concentration, spray device, derivative, or injectable vial.
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.
A small placebo-comparison study investigated acute intranasal Semax in healthy adults and measured resting brain-network activity before and shortly after exposure.
Population: 24 healthy adults; 11 men and 13 women, mean age 43.9 years
Design: Small placebo-comparison resting-state functional-MRI study with before-and-after imaging
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.
Research reference
A reference for the studies, populations, and routes behind this profile.
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.
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.
Community
Built by the community
Every structured report adds useful context about research setup, outcomes, and unwanted effects as the community dataset grows.
Publicly anonymous by default. Your account keeps reports editable and helps reduce duplicate submissions.Sources
2026-07-31
2026-07-24
2026-07-01
2025-06-03 · PMID 40496623 · DOI 10.1155/bca/4226220
2021-06-11 · PMID 34201112 · DOI 10.3390/ijms22126179
2018-09-01 · PMID 30225715 · DOI 10.1007/s10517-018-4234-3
2018-01-01 · PMID 29798983 · DOI 10.17116/jnevro20181183261-68
2017-06-01 · PMID 28255762 · DOI 10.1007/s00438-017-1297-1
2006-12-01 · PMID 16996037
1997-01-01 · PMID 11517472