Neuroprotective peptide that binds to amyloid beta (Aβ). Protects neurons against toxic effects of Aβ (1-42) in vitro and in vivo. Potential therapeutic in the treatment of Alzheimer's Disease.
(Modifications: Asp-5 = C-terminal amide)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble to 2 mg/ml in 10% acetonitrile / water|
Preparing Stock Solutions
The following data is based on the product molecular weight 652.75. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.53 mL||7.66 mL||15.32 mL|
|5 mM||0.31 mL||1.53 mL||3.06 mL|
|10 mM||0.15 mL||0.77 mL||1.53 mL|
|50 mM||0.03 mL||0.15 mL||0.31 mL|
References are publications that support the biological activity of the product.
Szegedi et al (2005) Pentapeptides derived from Aβ1-42 protect neurons from the modulatory effects of Aβ fibrils- an in vitro and in vivo electrophysiological study. Neurobiology of Disease 18 499 PMID: 15755677
Juhasz et al (2009) An intraperitoneally administered pentapeptide protects against Aβ (1-42) induced neuronal excitation in vivo. J.Alzheimer's Dis. 16 189
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Keywords: LPYFD-NH2, LPYFD-NH2 supplier, LPYFDNH2, neuroprotective, amyloid, sequence-derived, peptides, binds, beta, Ab, Aβ, Alzheimers, amyloidbeta, amyloidb, amyloidβ, Amyloid, Beta, Peptides, 4084, Tocris Bioscience
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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* or download 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.