BDNF & Neuroplasticity
Semax has been studied for its ability to upregulate BDNF and TrkB expression in rat hippocampus. Research has examined downstream effects on learning, memory consolidation, and synaptic plasticity markers.
Overview
What is Semax?
Semax is a synthetic heptapeptide analogue of the ACTH(4-10) fragment, extended with a C-terminal Pro-Gly-Pro sequence that confers resistance to enzymatic degradation. Unlike its parent fragment, Semax carries no documented corticotropic activity. Research has examined its influence on BDNF and TrkB expression, neuroprotection in cerebral ischemia models, and monoaminergic signaling in rodent brain tissue.
Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is supplied strictly as a reference material for in vitro and preclinical investigation. All characterization data described here is drawn from peer-reviewed literature and laboratory analysis; nothing herein constitutes a claim of clinical effect in humans.
Investigational Scope
Documented Research Areas
The following domains summarize directions explored across published studies and laboratory models. Each reflects observations reported in rodent models, in vitro systems, or the peer-reviewed record.
Ischemia & Oxidative Stress
Studies in rodent models of focal cerebral ischemia have documented effects on neuronal survival markers, calcium homeostasis under glutamate toxicity, and inflammatory gene expression in brain tissue.
Monoaminergic Modulation
Research has examined Semax's effects on dopamine and serotonin turnover in prefrontal cortex and hippocampus, connecting the peptide to attention and motivation-related circuitry in animal models.
Immune & Vascular Transcripts
Transcriptomic studies of ischemic rat brain have reported changes in genes tied to immune signaling and vascular remodeling following administration, suggesting a broad regulatory footprint.
Proposed Mechanism
Mechanistic Pathway
Mechanistic steps below are hypothesized from in vitro assays and animal-model data reported in the literature. They describe biochemical interactions observed under controlled experimental conditions.
-
1
BDNF & TrkB Pathway
Semax stimulates BDNF expression and TrkB receptor signaling in hippocampal and cortical neurons, supporting the synaptic plasticity and neuronal survival mechanisms documented in rodent research.
-
2
Pro-Gly-Pro Stabilization
The C-terminal Pro-Gly-Pro extension slows peptidase cleavage relative to the native ACTH(4-10) fragment, extending exposure while removing the steroidogenic activity of the parent hormone fragment.
-
3
Monoamine Turnover
Studies have documented altered dopamine and serotonin metabolism in rodent brain regions following administration, examined as a contributor to observed changes in attention and adaptive behavior.
-
4
Neuronal Calcium Homeostasis
Research on Semax and its Pro-Gly-Pro fragment has examined preservation of calcium homeostasis and improved neuronal survival under glutamate excitotoxicity in cell-culture systems.
Technical Data
Molecular Specifications
| Amino Acid Sequence | Met-Glu-His-Phe-Pro-Gly-Pro |
|---|---|
| Molecular Weight | 813.9 g/mol |
| Molecular Formula | C₃₇H₅₁N₉O₁₀S |
| CAS Number | 80714-61-0 |
| Storage | −20°C long-term, 4°C short-term up to 4 weeks |
References
Selected Literature
The following peer-reviewed references informed the research summaries on this page. Citations are provided for scientific context only.
- Dolotov OV, et al. (2006). Semax, an analogue of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Research, 1117(1), 54–60.
- Sebentsova EA, et al. (2008). Semax affects multiple neuropeptide systems in the brain. Neuroscience Letters, 443(1), 1–5.
- Shadrina MI, et al. (2010). Neuroprotective effect of Semax in rat model of focal cerebral ischemia. Bulletin of Experimental Biology and Medicine, 148(4), 572–574.
- Storozhevykh TP, et al. (2007). Effects of Semax and its Pro-Gly-Pro fragment on calcium homeostasis of neurons and their survival under conditions of glutamate toxicity. Bulletin of Experimental Biology and Medicine, 143(5), 601–604.
- Medvedeva EV, et al. (2014). The peptide Semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia. Molecular Biology, 48(3), 415–422.
Research Disclaimer
This product is intended strictly for laboratory research purposes only. It is not a drug, food, cosmetic, or dietary supplement and is not intended to diagnose, treat, cure, or prevent any disease. It is not for human or animal consumption. All information presented is derived from published scientific literature and is provided for educational reference only. By purchasing, the buyer affirms they are a qualified researcher or institution and assume full responsibility for the safe and lawful handling of this material.