Maple Semax (Met-Glu-His-Phe-Pro-Gly-Pro, or MEHFPGP) is a synthetic heptapeptide derived from the adrenocorticotropic hormone (ACTH) fragment 4-10. Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, Semax represents one of the most extensively studied synthetic neuropeptides in preclinical research, with documented effects on neurotrophic factor expression, cognitive function in animal models, and neuroprotection following experimental cerebral ischemia.
Maple Research Labs supplies research-grade Semax to Canadian laboratories, universities, and documented research buyers. Every batch ships with an independent third-party Certificate of Analysis confirming identity and purity.
For research purposes only. Not for human consumption. Not for diagnostic or therapeutic use.
Molecular Profile
| Parameter | Value |
|---|---|
| Sequence | Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) |
| CAS Number | 80714-61-0 |
| Molecular Formula | C37H51N7O10S |
| Molecular Weight | 813.4 Da (free acid) |
| Parent Structure | ACTH(4-10) with C-terminal Pro-Gly-Pro extension |
| Purity | ≥99% (HPLC) |
| Storage | -20°C, lyophilized, desiccated, protected from light |
The C-terminal Pro-Gly-Pro tripeptide extension distinguishes Semax from the native ACTH(4-10) fragment. This modification was engineered to increase resistance to aminopeptidase degradation, extending the peptide’s biological half-life in preclinical models while retaining the neurotropic activity associated with the ACTH(4-10) core sequence.
Primary Research Mechanisms
BDNF/TrkB Pathway Modulation
The most extensively documented mechanism of Semax involves modulation of brain-derived neurotrophic factor (BDNF) expression and its downstream signaling through the TrkB receptor. According to PubMed, Dolotov et al. (2006) demonstrated that a single intranasal application of Semax at 50 mcg/kg body weight produced a maximal 1.4-fold increase in BDNF protein levels accompanied by a 1.6-fold increase in TrkB tyrosine phosphorylation in the rat hippocampus (DOI: 10.1016/j.brainres.2006.07.108). The same study observed a 3-fold increase in exon III BDNF mRNA and a 2-fold increase in TrkB mRNA levels.
In a complementary study, Dolotov et al. demonstrated that Semax binds specifically to cell membranes in the rat basal forebrain with a dissociation constant (KD) of 2.4 nM and a BMAX of 33.5 fmol/mg protein. Intranasal Semax at 50 and 250 mcg/kg produced rapid increases in BDNF protein levels in the basal forebrain within 3 hours, with no corresponding increase in the cerebellum, suggesting region-specific neurotrophic modulation (DOI: 10.1111/j.1471-4159.2006.03658.x).
Neurotrophin Gene Expression
Based on articles retrieved from PubMed, Shadrina et al. (2010) characterized the temporal dynamics of NGF and BDNF gene expression across multiple brain regions following Semax administration. In the rat hippocampus and retina, expression of both neurotrophin genes decreased 20 minutes post-administration but increased in the frontal cortex. BDNF expression in the retina showed significant upregulation at 90 minutes, indicating tissue-specific and time-dependent effects on neurotrophin gene transcription (DOI: 10.1007/s12031-009-9270-z). Earlier work by Dolotov et al. (2003) confirmed BDNF expression stimulation across different brain areas in vivo (DOI: 10.1023/a:1025177812262).
Neuroprotection in Ischemia Models
Semax has been investigated for neuroprotective properties in experimental cerebral ischemia models. According to PubMed, Bashkatova et al. (2001) demonstrated that Semax prevented the enhanced nitric oxide generation in the cerebral cortex of rats subjected to incomplete global ischemia. Unlike glycine (which proved ineffective), Semax significantly reduced NO levels and restored neurological functioning in ischemic animals (DOI: 10.1016/s0006-8993(00)03324-2). The proposed mechanism involves regulation of nitric oxide synthesis pathways that contribute to ischemic neuronal damage.
Clinical investigation by Gusev et al. (2018) examined Semax administration in a study of 110 post-ischemic stroke patients. Administration of Semax increased plasma BDNF levels that remained elevated throughout the study period. The study reported a positive correlation between BDNF plasma levels and Barthel index scores, with Semax administration accelerating functional recovery outcomes (DOI: 10.17116/jnevro20181183261-68).
Copper(II) Ion Binding and Metal-Induced Cytoprotection
Based on articles retrieved from PubMed, Tabbi et al. (2014) characterized the copper(II) binding properties of Semax, demonstrating high-affinity coordination with a 4N planar arrangement becoming predominant above pH 5. The study found that Semax reduced copper-induced cytotoxicity in SH-SY5Y neuroblastoma and RBE4 endothelial cell lines as measured by MTT assay. This metal-chelating capacity may be relevant to research on metal ion dyshomeostasis in neurodegenerative models (DOI: 10.1016/j.jinorgbio.2014.09.008).
Cognitive and Behavioral Research
Semax has been studied in multiple behavioral paradigms relevant to learning and memory. In conditioned avoidance testing, Semax-treated animals showed a distinct increase in the number of conditioned avoidance reactions, an effect the authors associated with hippocampal BDNF/TrkB system modulation (Dolotov et al., 2006). Manchenko et al. (2010) demonstrated nootropic effects in passive avoidance acquisition following both intranasal and intraperitoneal routes, with intranasal administration showing greater potency for learning improvement (PMID: 21268834).
Glazova et al. (2021) investigated whether Semax could attenuate behavioral deficits induced by neonatal fluvoxamine (SSRI) exposure in rats. Semax administration on postnatal days 15-28 reduced anxiety-like behavior, improved learning abilities in food-motivated maze tasks, and normalized brain biogenic amine levels that had been disrupted by early SSRI exposure (DOI: 10.1016/j.npep.2020.102114).
Semax vs. Selank: Research Comparison
Semax and Selank are both synthetic heptapeptides developed at the Institute of Molecular Genetics, but they derive from different parent molecules and engage distinct primary mechanisms. Semax is based on the ACTH(4-10) fragment and primarily modulates the BDNF/TrkB neurotrophic pathway. Selank is based on the endogenous immunomodulatory peptide tuftsin (Thr-Lys-Pro-Arg) with a Pro-Gly-Pro C-terminal extension and primarily influences the GABAergic and enkephalinergic systems. In research settings, the two peptides serve as complementary tools for investigating different aspects of CNS plasticity and neuroprotection.
Product Specifications
| Specification | Detail |
|---|---|
| Peptide | Semax (MEHFPGP) |
| CAS Number | 80714-61-0 |
| Purity | ≥99% (HPLC verified) |
| Form | Lyophilized powder |
| COA | Third-party Certificate of Analysis included with every order |
| Storage | -20°C, desiccated, protected from light |
| Shipping | Same-day processing from Canada |
| Use | For research purposes only |
View Semax product page and COA | How to read a Certificate of Analysis
Frequently Asked Questions
What is Semax and how does it differ from ACTH(4-10)?
Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) that retains the core ACTH(4-7) sequence (Met-Glu-His-Phe) and adds a C-terminal Pro-Gly-Pro tripeptide extension. This modification increases resistance to enzymatic degradation compared to the native ACTH(4-10) fragment, extending biological half-life while preserving the neurotropic activity associated with the parent sequence. Unlike full-length ACTH, Semax does not stimulate adrenal steroidogenesis in preclinical models.
What neurotrophic pathways does Semax modulate in research?
The primary documented mechanism involves upregulation of brain-derived neurotrophic factor (BDNF) and activation of its TrkB receptor. Published research demonstrates region-specific BDNF increases in the basal forebrain and hippocampus following Semax administration, with corresponding increases in TrkB phosphorylation. Semax also influences NGF expression with tissue-specific temporal dynamics across the hippocampus, frontal cortex, and retina.
Can I purchase Semax for research in Canada?
Yes. Maple Research Labs is a Canadian supplier of research-grade Semax verified at 99%+ purity via HPLC analysis. All orders ship from within Canada with same-day processing and include a batch-specific Certificate of Analysis. Semax is sold exclusively for in-vitro and preclinical research use and is not approved for human therapeutic applications.
How should Semax be stored for research use?
Lyophilized Semax should be stored at -20°C in a desiccated environment protected from light. Reconstituted solutions should be stored at 2-8°C and used within the timeframe appropriate for the research protocol. Avoid repeated freeze-thaw cycles to maintain peptide integrity and experimental reproducibility.
Related Research Resources
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- Understanding Certificates of Analysis — COA interpretation guide
- All Research Peptides — Complete compound catalog
For research purposes only. Not for human consumption. Not for diagnostic or therapeutic use.