Inhibitor of γ-secretase that selectively inhibits βAPP cleavage without affecting other γ-secretase-mediated pathways. Prevents recovery of Aβ40 and Aβ42 from HEK293 cell overexpressing wild-type or Swedish-mutated βAPP (IC50 ~ 30 μM) but displays no effect on Notch cleavage and Notch-mediated intracellular signaling. Displays no activity on BACE1, BACE2, α-secretase, the proteosome or GSK3β.
|Storage||Store at RT|
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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 225.63. 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||4.43 mL||22.16 mL||44.32 mL|
|5 mM||0.89 mL||4.43 mL||8.86 mL|
|10 mM||0.44 mL||2.22 mL||4.43 mL|
|50 mM||0.09 mL||0.44 mL||0.89 mL|
References are publications that support the products' biological activity.
Petit et al (2001) New protease inhibitors prevent γ-secretase-mediated production of Aβ40/42 without affecting Notch cleavage. Nat.Cell.Biol. 3 507 PMID: 11331880
Petit et al (2003) JLK isocoumarin inhibitors: selective γ-secretase inhibitors that do not interfere with Notch pathway in vitro or in vivo. J.Neurosci.Res. 74 370 PMID: 14598313
Hellstrom et al (2007) DII4 signalling through Notch1 regulates formation of tip cells during angiogenesis. Nature 445 776 PMID: 17259973
If you know of a relevant reference for JLK 6, please let us know.
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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.