Semax is a synthetic heptapeptide derived from a fragment of adrenocorticotropic hormone (ACTH 4-10) with an added Pro-Gly-Pro C-terminal tripeptide. Preclinical research investigates its role in neurotrophic factor expression and neuropeptide-mediated signaling.
Research Focus: Neurotrophic factor signaling · Neuropeptide research · BDNF pathway modulation
For research use only. Not for human consumption.
10mg
99.03%
Lyophilised Powder
£69.99
10 in stock
Semax is a synthetic heptapeptide analog based on the ACTH(4-10) fragment (Met-Glu-His-Phe-Pro-Gly-Pro), modified with a C-terminal Pro-Gly-Pro tripeptide extension designed to increase metabolic stability and resistance to enzymatic degradation. The peptide was originally developed at the Institute of Molecular Genetics of the Russian Academy of Sciences.
In preclinical laboratory research, Semax is examined as a molecular tool for studying neurotrophic factor signaling, including brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) expression pathways. Experimental models have investigated its effects on neuronal survival, synaptic plasticity markers, and transcriptional activity in in-vitro neuronal cultures and in-vivo animal systems.
Additional published preclinical work references Semax in studies of cerebrovascular signaling, oxidative stress response, and immune-associated molecular pathways in central nervous system cellular structure preparations. Its melanocortin-derived structure positions it as a research tool for investigating ACTH-related neuropeptide signaling independent of adrenal corticotropic effects.
Sequence: Met-Glu-His-Phe-Pro-Gly-Pro Molecular Formula: C₃₉H₅₁N₉O₁₀S Molecular Weight: 813.93 g/mol CAS: 80714-61-0
For non-clinical laboratory research only. Not for human consumption.
A synthetic analogue of ACTH(4-7) with a C-terminal Pro-Gly-Pro extension that enhances metabolic stability. Modulates BDNF expression, exhibits nootropic effects, and provides neuroprotection without affecting adrenal cortex function.
Neuroprotection research; cognitive enhancement models; BDNF modulation studies; stroke pathway research
1. Dolotov et al. (2006) Brain Res 1117(1):54-60
PMID: 16996037 | View Publication
Demonstrated Semax increases BDNF protein 1.4-fold and trkB phosphorylation 1.6-fold in rat hippocampus after single intranasal dose, with improved conditioned avoidance performance.
2. Dolotov et al. (2006) J Neurochem 97(Suppl 1):82-86
PMID: 16635254 | View Publication
Identified specific, high-affinity binding sites for Semax in rat basal forebrain membranes and showed intranasal Semax rapidly increases BDNF protein levels in this region.
Heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro), Lyophilised
10mg
Room temperature, dry, protect from light
only 50 vials available
≥99% lab-tested purity
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