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Highly potent γ-secretase inhibitor (Aβ40 IC50 = 0.3 nM). Exhibits >137-fold selectivity for amyloid-β precursor protein (APP) processing over Notch. Reduces plasma and brain Aβ40 and Aβ42 levels in vivo. Orally bioavailable.
|Storage||Store at +4°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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 520.89. Batch specific molecular weights may vary from batch to batch due to the degree 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||1.92 mL||9.6 mL||19.2 mL|
|5 mM||0.38 mL||1.92 mL||3.84 mL|
|10 mM||0.19 mL||0.96 mL||1.92 mL|
|50 mM||0.04 mL||0.19 mL||0.38 mL|
References are publications that support the biological activity of the product.
Gillman et al (2010) Discovery and evaluation of BMS-708163, a potent, selective and orally bioavailable γ-secretase inhibitor. ACS Med.Chem.Lett. 1 120 PMID: 24900185
Albright et al (2013) Pharmacodynamics of selective inhibition of γ-secretase by avagacestat. J.Pharmacol.Exp.Ther. 344 686 PMID: 23275065
If you know of a relevant reference for Avagacestat, please let us know.
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Keywords: Avagacestat, Avagacestat supplier, gamma, γ, secretase, inhibitors, inhibits, Abeta, AB, Aβ40, 42, amyloid-β, precursor, protein, APP, processing, highly, potent, BMS-708163, Gamma-Secretase, Amyloid, Beta, Peptides, 6363, 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* 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.