● pepmg Research Desk · Peer-reviewed evidence review
What the research says about Semax
A neutral summary of the peer-reviewed literature on Semax, a synthetic analogue of ACTH(4-10) studied mainly in animal and cell models, with a small human literature concentrated in Russian-language neurology journals. Research use only.
Limited evidence — Early or small human data, or strong preclinical work. This describes the state of the published literature, not a claim that this compound works, is safe, or is for human use. Research use only.
The short version
- Semax is a synthetic heptapeptide analogue of the ACTH(4-10) fragment, studied mainly in animal and cell models as a nootropic and neuroprotective agent, with a small human literature [1][8].
- In animal work it modulates brain monoamine and neurotrophin systems, and human imaging and stroke studies examined its effects on brain connectivity and on plasma BDNF [1][2][3][5].
- The human studies are small and several are published in Russian-language neurology journals; they do not amount to large modern controlled trials [1][8].
- This page reports what the studies measured. It is not medical advice, an efficacy or safety claim, or dosing guidance. Research use only.
What Semax is
Semax is described in the literature as a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro), an analogue of the adrenocorticotropic hormone fragment ACTH(4-10) developed in Russia and reported to have nootropic and neuroprotective activity [4][8]. It is sold by third-party research-chemical vendors and is offered for laboratory and research use only.
Most of the published Semax research is preclinical, carried out in animals and cell systems; the human literature is limited to a small number of studies, several of them in Russian-language neurology journals [1][8].
What the research has measured
Limited evidenceIn animal and mechanistic studies, Semax has been reported to act on brain monoamine systems, increasing striatal serotonin turnover and enhancing amphetamine-evoked dopamine release and locomotor activity in rodents [4], and to activate the transcription of neurotrophins and their receptors in the cortex of rats subjected to experimental cerebral artery occlusion [5]. In a rat developmental-exposure model it was reported to reduce anxiety-like behaviour and normalize brain biogenic-amine levels [6], and in a cell-based Alzheimer model it was examined as a copper-binding peptide that interfered with copper-associated amyloid-beta aggregation [7].
The human data are small. A study in patients after ischemic stroke reported that adding Semax to rehabilitation was associated with higher plasma BDNF levels and with measures of motor performance and functional recovery on the Barthel index [1]. Resting-state functional-MRI studies in healthy volunteers examined how intranasal Semax alters the brain's default mode network [2] and resting-state connectivity involving the amygdala, the latter also comparing it with the related peptide Selank [3].
What the trials report on safety and adverse events
Limited evidenceThe human studies of Semax are small and their reporting of tolerability is correspondingly limited. The imaging studies were conducted in small groups of healthy volunteers and the stroke study followed a modest number of patients [1][2][3]; none was designed as a large safety trial, and much of the broader literature is not in English.
There are no large modern controlled trials establishing the safety of Semax in the general population. This is not medical advice; the human safety of Semax is not established. Consult a qualified professional and read the studies directly.
How strong is the evidence
Because the Semax evidence base is mostly preclinical with only small human studies, several published in Russian-language journals, it is characterized as limited [1][4][8]. "Limited" describes the state of the research, not a judgment of whether Semax works or is safe, and it reflects the small size and restricted reach of the human literature.
Nothing here is dosing, medical, or safety guidance. Read the studies themselves and consult a qualified professional. This page is a map to the evidence, not a recommendation.
Sources · 8
- The efficacy of semax in the treatment of patients at different stages of ischemic stroke.
- Effects of Semax on the Default Mode Network of the Brain.
- Functional connectomic approach to studying Selank and Semax effects.
- Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents.
- Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptors following cerebral ischemia.
- Semax, synthetic ACTH(4-10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in rats.
- Semax, a Synthetic Regulatory Peptide, Affects Copper-Induced Abeta Aggregation and Amyloid Formation in Artificial Model Systems.
- Therapeutic peptides in gerontology: mechanisms and applications for healthy aging.
pepmg summarizes the peer-reviewed literature and links to every source — it sells nothing, ships nothing, and gives no medical, dosing, or human-use guidance. Don't just trust this summary: follow any citation to its source and read it yourself. Research use only.