Semax
Semax is a synthetic ACTH-derived heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) studied primarily in Russia in ischemic-stroke and neurobiology research. The literature includes human clinical reports and a substantial preclinical mechanistic body of work.
What kind of evidence exists?
Semax has human publications, but much of the clinical literature is older, regionally concentrated, and not equivalent to large modern multicenter trials.
Semax has more human literature than many research peptides, but quality still matters.
The existence of clinical publications is meaningful. Their age, design, geography, sample size, and replication still determine how much confidence should be placed in the findings.
Selected studies.
Selected sources are grouped by study type so model limitations remain visible.
Effectiveness of semax in acute period of hemispheric ischemic stroke
A clinical report studied Semax in 30 patients during the acute period of hemispheric ischemic stroke. The small study should not be treated as definitive modern efficacy evidence.
The efficacy of semax in the treatment of patients at different stages of rehabilitation after ischemic stroke
In 110 post-stroke patients, investigators examined Semax, timing of rehabilitation, plasma BDNF, motor function, and Barthel-index recovery. The publication reported higher BDNF and faster functional recovery in Semax-treated subgroups.
Semax in prevention of disease progress and development of exacerbations in patients with cerebrovascular insufficiency
This comparative clinical publication reported tolerability and clinical outcomes in cerebrovascular insufficiency. Study design limitations should be considered before drawing causal conclusions.
Semax, an analog of ACTH(4-7), regulates expression of immune and vascular genes during cerebral ischemia
Transcriptomic analysis in rat focal cerebral ischemia found Semax-associated changes in immune-response, cytokine, stress-response, and related gene-expression pathways.
The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain after focal ischemia
This rat study examined gene-expression changes after focal ischemia and Semax exposure, adding mechanistic context to its proposed neuroprotective actions.
The effect of Semax and its C-end peptide PGP on the morphology and proliferative activity of rat brain cells during ischemia
Histologic work in normal and ischemic rat brain reported changes in glia, vascular endothelium, progenitor cells, and ischemic-damage morphology after Semax or PGP treatment.
Primary sources.
Direct PubMed links are used wherever possible.