Neuro & Cognitive · Research Compound
Semax
A synthetic peptide studied in neuroprotection, cognition, and BDNF-related research.
Semax is a synthetic peptide originally developed in Russia, based on a fragment of adrenocorticotropic hormone (ACTH) with a stabilizing modification. It is studied primarily in neuroprotection and cognitive research, where interest centers on its reported effects on brain-derived neurotrophic factor (BDNF) and related neurotrophic signaling.
Much of the published research originates from Russian institutions, where related peptides have clinical use; the broader international evidence base remains largely preclinical. Material here is for research-use-only, educational purposes.
Research areas
BDNF & Neurotrophic Signaling
Research examines effects on brain-derived neurotrophic factor expression and downstream neuroplasticity pathways.
Neuroprotection
Studied in models of ischemia and oxidative stress for neuroprotective signaling.
Cognition & Attention
Investigated for effects on learning, attention, and memory in preclinical and limited clinical research.
Neuropeptide Stability
The modified structure is studied for enhanced resistance to enzymatic breakdown.
Recent research findings
- 2024Continued neuropharmacology research on Semax and related ACTH-fragment peptides.
- 2023Reviews summarized BDNF-related signaling and neuroprotective model data.
- 2022Studies explored mechanisms in ischemia and cognitive-performance models.
Published Research & Citations
The research summarized above is drawn from published, peer-reviewed studies. Explore the 5 sources below — links open the abstract or, where marked, the full free article on the U.S. National Library of Medicine (PubMed / PMC).
- Dolotov OV, et al. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Research, 2006. Reports Semax increased hippocampal BDNF and trkB expression alongside improved conditioned responses.
- Dolotov OV, et al. Semax, an analogue of ACTH(4-10), binds specifically and increases BDNF protein in rat basal forebrain. Journal of Neurochemistry, 2006. Found specific Semax binding sites and elevated BDNF protein in the basal forebrain.
- Dergunova LV, et al. The peptide Semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia. BMC Genomics, 2014. Free full text Open-access genome-wide analysis of Semax effects on immune and vascular gene expression after ischemia.
- Filippenkov IB, et al. Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia-Reperfusion in Rats. Genes, 2020. Free full text Open-access transcriptome study of Semax neuroprotection in an ischemia-reperfusion model.
- Medvedeva EV, et al. Semax, an analog of ACTH(4-7), regulates expression of immune-response genes during ischemic brain injury in rats. Molecular Genetics and Genomics, 2017. Examines Semax modulation of immune-response gene expression after ischemic injury.