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γ-secretase pseudo-inhibitor. Inhibits Aβ secretion from cells in vitro and increases accumulation of γ-secretase products and long Aβ species in vitro and in vivo. Also attenuates the accumulation of activated microglia and neurological injury in a traumatic brain injury animal model.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 361.44. 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||2.77 mL||13.83 mL||27.67 mL|
|5 mM||0.55 mL||2.77 mL||5.53 mL|
|10 mM||0.28 mL||1.38 mL||2.77 mL|
|50 mM||0.06 mL||0.28 mL||0.55 mL|
References are publications that support the biological activity of the product.
Henley et al (2009) Development of semagacestat (LY450139), a functional gamma-secretase inhibitor, for the treatment of Alzheimer's disease. Expert Opin.Pharmacother. 10 1657 PMID: 19527190
Lanz et al (2006) Concentration-dependent modulation of amyloid-beta in vivo and in vitro using the gamma-secretase inhibitor, LY-450139. J.Pharmacol.Exp.Ther. 319 924 PMID: 16920992
Tagami et al (2017) Semagacestat is a pseudo-inhibitor of γ-secretase. Cell Rep. 21 259 PMID: 28978478
Lin et al (2017) Gamma-secretase inhibitors attenuate neurotrauma and neurogenic acute lung injury in rats by rescuing the accumulation of hypertrophic microglia. Cell Physiol.Biochem. 44 1726 PMID: 29227981
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Literature in this Area
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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.