Semax Research
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Semax: Neuropeptide Research and Cognitive Signalling
Semax is a synthetic heptapeptide analogue of the N-terminal fragment of adrenocorticotropic hormone ACTH(4-10). It was developed by researchers at the Institute of Molecular Genetics in Moscow and has been studied extensively in laboratory settings for its role in neuropeptide receptor research, cognitive signalling pathway studies, and neurotrophic factor biology.
Semax: Structure and Neuropeptide Targets
Chemical and Molecular Data
| Property | Value |
|---|---|
| Molecular formula | C37H51N9O10S |
| Molecular weight | 813.93 g/mol |
| CAS number | 80714-61-0 |
| Sequence | Met-Glu-His-Phe-Pro-Gly-Pro |
| Amino acid count | 7 |
| Parent peptide | ACTH(4-10) |
| Purity | greater than or equal to 98% as verified by HPLC |
| Form | Lyophilised powder |
| Storage | -20 degrees C, protected from light and moisture |
| Reconstitution | Bacteriostatic water recommended |
Semax: Structure and Neuropeptide Targets
ACTH(4-10) and Semax Design
Native ACTH(4-10) (Met-Glu-His-Phe-Arg-Trp-Gly) is the minimal active fragment of ACTH responsible for its non-steroidal neurological effects. Semax modifies this sequence by replacing the C-terminal Arg-Trp-Gly with Pro-Gly-Pro, which significantly increases the peptide's resistance to enzymatic degradation and extends its biological activity window in research settings.
The Pro-Gly-Pro extension is notable: Pro-Gly-Pro is itself a bioactive tripeptide studied for its role in leukocyte chemotaxis and as a product of collagen degradation, potentially contributing additional biological properties.
Neurotrophic Factor Research
One of the most studied aspects of Semax in laboratory settings is its relationship with brain-derived neurotrophic factor (BDNF) and its receptor TrkB. Research in rodent models has found associations between Semax administration and changes in BDNF expression in hippocampal and cortical tissues. BDNF plays roles in synaptic plasticity, neuronal survival, and long-term potentiation — all active areas of neuroscience research.
Research has also examined Semax's effects on nerve growth factor (NGF) expression and the expression of neurotrophin receptors, making it a tool compound of interest in neurotrophin biology research.
Dopaminergic and Serotonergic Research
Laboratory studies have examined Semax's effects on dopaminergic and serotonergic neurotransmission in rodent models. Research has investigated changes in dopamine and serotonin receptor expression following Semax treatment in various brain regions, including the striatum, prefrontal cortex, and hippocampus.
Neuroprotection Research Models
Semax has been studied as a tool compound in neuroprotection research models. Laboratory studies have examined its effects in models of ischaemia, oxidative stress, and excitotoxicity at the cellular level, investigating potential interactions with the nitric oxide system and inflammatory pathways relevant to neural tissue biology.
Research Applications
Semax is used in neuropeptide receptor pharmacology studies, BDNF and neurotrophin signalling research, dopaminergic and serotonergic neurotransmitter system studies, neuroprotection model research, and hippocampal plasticity research.
Semax vs Related Neuropeptide Research Tools
| Property | Semax | Selank | N-Acetyl Semax |
|---|---|---|---|
| Sequence | Met-Glu-His-Phe-Pro-Gly-Pro | Thr-Lys-Pro-Arg-Pro-Gly-Pro | N-Acetyl + Semax |
| Parent peptide | ACTH(4-10) | Tuftsin fragment | Semax |
| Primary research | BDNF / dopamine / serotonin | Anxiolytic / GABA | Extended stability |
| Stability | Moderate | Moderate | Improved |
| CAS | 80714-61-0 | 129954-34-3 | 181186-66-3 |
BDNF Pathway in Semax Research
Brain-derived neurotrophic factor (BDNF) is a neurotrophin that signals through two receptors: TrkB (high affinity, mediates neuroplasticity and survival effects) and p75NTR (low affinity, mediates apoptotic effects). Laboratory research examining Semax has investigated changes in BDNF mRNA and protein expression in hippocampal and cortical tissues, with several rodent studies reporting increased BDNF expression following Semax administration.
The BDNF-TrkB signalling axis activates downstream pathways including MAPK/ERK (involved in synaptic plasticity), PI3K/Akt (cell survival), and PLCgamma/PKC (calcium-dependent signalling). Research examining Semax's effects on BDNF therefore connects to investigation of these downstream cascades and their roles in hippocampal long-term potentiation (LTP) — a cellular model of learning and memory.
Frequently Asked Questions
What is the Pro-Gly-Pro extension in Semax and does it have independent biological activity?
Pro-Gly-Pro is the C-terminal extension that distinguishes Semax from the native ACTH(4-10) sequence. This tripeptide is itself biologically active: it is a known chemotactic factor for leukocytes and is generated naturally as a collagen degradation product. Its inclusion in Semax increases the peptide's resistance to enzymatic degradation and may contribute additional biological properties to the research compound. Some published studies have examined Pro-Gly-Pro in isolation for comparison with full-length Semax activity.
How stable is Semax in biological media compared to native ACTH(4-10)?
Native ACTH(4-10) has a very short plasma half-life due to rapid cleavage by various proteases. The Pro-Gly-Pro C-terminal extension in Semax significantly improves resistance to carboxypeptidase degradation. The Met residue at position 1 remains a potential oxidation site — researchers working with Semax over extended incubation periods should be aware that Met oxidation can inactivate the peptide and should store lyophilised Semax protected from oxidising conditions.
Published Research References
For laboratory and analytical research purposes only. Not for human or veterinary use. No dosage or administration guidance is provided or implied.
Related research peptides: KPV | Kisspeptin-10 | BPC-157