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Biological Activity for Semax
Semax is a synthetic heptapeptide analog of adrenocorticotropic hormone (ACTH) (4-10). It increases hippocampal BDNF and TrkB expression and levels in vivo. Semax regulates cortical nitric oxide (NO) and lipid peroxidation and is neuroprotective in a rat model of global ischemia. Semax sequesters copper ions and interacts directly with Aβ:Cu2+ oligomers leading to reduced amyloid β protein (Aβ) aggregation and fibrillogenesis. Semax increases viability of d-SH-SY5Y cells pre-incubated with Aβ1-42 oligomers.
Technical Data for Semax
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for Semax
|Solubility||Soluble to 2 mg/ml in water|
References for Semax
References are publications that support the biological activity of the product.
Bashkatova (2001) Novel synthetic analogue of ACTH 4-10 (Semax) but not glycine prevents the enhanced nitric oxide generation in cerebral cortex of rats with incomplete global ischemia. Brain Res. 894 145 PMID: 11245825
Dolotov et al (2006) Semax, an analog of ACTH(4–10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. Brain Res. 1117 54 PMID: 16996037
Sciacca et al (2022) Semax, a synthetic regulatory peptide, affects copper-induced Abeta aggregation and amyloid formation in artificial membrane models. ACS Chem.Neurosci. 13 486 PMID: 35080861
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Keywords: Semax, Semax supplier, peptides, analogs, adrenocorticotropic, hormone, hippocampal, BDNF, trkB, neuroprotective, global, ischemia, amyloid, beta, Aβ, ABeta, aggregation, inhibits, fibrillogenesis, Alzheimers, Amyloid, Beta, Peptides, Other, RTKs, 7712, Tocris Bioscience
Citations for Semax
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.