Semax
A synthetic ACTH-derived peptide studied for cognitive signalling, neurotrophic factor interaction, and attention research.
⏱ Half-Life
Short duration profile
Semax demonstrates a short half-life characteristic in research literature, shaping how observation windows and study timelines are typically structured.
⚡ Onset Characteristics
Fast measurable response
Onset is observed as fast — a property that influences how researchers structure comparative studies versus other compounds in the cognitive research category.
🧠 Key Notes
What makes it distinct
- 01Often studied alongside Selank
- 02Short systemic half-life with rapid measurable effect
- 03Investigated via intranasal research delivery
🧬 Mechanism of Action
How it works
Semax is a synthetic heptapeptide modelled on the ACTH(4–10) fragment, with a stabilising C-terminal Pro-Gly-Pro tail that resists enzymatic degradation. It acts centrally to upregulate brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), enhancing neuronal plasticity, dendritic growth, and synaptic resilience. It also modulates dopaminergic and serotonergic signalling and supports the body's endogenous opioid balance. Despite a short plasma half-life, downstream central effects persist for hours, indicating durable transcriptional changes rather than direct receptor occupancy.
✨ Documented Benefits
What the research shows it supports
🔍 Research Insights
What the literature shows
Increases BDNF and NGF expression in central tissue research — neurotrophic factors tied to plasticity and learning.
Despite a short plasma half-life, central effects persist for hours, suggesting durable downstream signalling.
Originally developed in Russian neuroscience research as a stable analog of ACTH(4–10).
🧪 Typical Research Use Cases
Where it appears in study design
Attention, memory, and learning research models.
Stress-response and neuroprotection studies.
Intranasal pharmacokinetic and bioavailability work.
📚 References
Peer-reviewed literature
Primary research sources cited on this profile. All links resolve to PubMed or the publishing journal.
- [01]
Dolotov, O. V. et al. (2006). Semax, an analog of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. Journal of Neurochemistry, 97(Suppl 1), 82–86.
Journal of Neurochemistry ↗ - [02]
Gusev, E. I., Skvortsova, V. I., Miasoedov, N. F., Nezavibat'ko, V. N., Zhuravleva, E. I., & Vanichkin, A. V. (1997). Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study). Zhurnal Nevrologii i Psikhiatrii, 97(6), 26–34.
Zh Nevrol Psikhiatr ↗ - [03]
Shadrina, M. I. et al. (2010). Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action. Journal of Molecular Neuroscience, 41(1), 30–35.
Journal of Molecular Neuroscience ↗ - [04]
Medvedeva, E. V. et al. (2014). The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics, 15, 228.
BMC Genomics ↗
Continue Exploring
Also explore: Selank, PT-141, MOTS-c
