LY-411575 has been used as a potent γ-secretase inhibitor and Notch inhibitor.[1][2][3]
Biochem/physiol Actions
LY-411575 is potent, cell permeable and selective γ-secretase inhibitor that reduces Aβ/42 after acute or chronic treatment, and blocks Notch activation. Studies (Cancer Cell) have shown that treatment with LSN-411575 arrests KrasG12V-driven NSCLCs in association with inhibition of HES1 expression and ERK phosphorylation.
LY-411575 is potent, cell permeable and selective γ-secretase inhibitor that reduces Aβ40/42 after acute or chronic treatment, and blocks Notch activation.
Enzymatic assays for studying intramembrane proteolysis.
Bolduc D M, et al.
Methods in Enzymology, 584, 295-308 (2017)
Prion-protein-interacting amyloid-β oligomers of high molecular weight are tightly correlated with memory impairment in multiple Alzheimer mouse models.
Kostylev M A, et al.
The Journal of Biological Chemistry, 290(28), 17415-17438 (2015)
British journal of cancer, 105(6), 796-806 (2011-08-19)
We reported that Notch-1, a potent breast oncogene, is activated in response to trastuzumab and contributes to trastuzumab resistance in vitro. We sought to determine the preclinical benefit of combining a Notch inhibitor (γ-secretase inhibitor (GSI)) and trastuzumab in both
Different developmental histories of beta-cells generate functional and proliferative heterogeneity during islet growth.
Molecular therapy : the journal of the American Society of Gene Therapy, 29(7), 2294-2307 (2021-03-02)
Numerous aggregation inhibitors have been developed with the goal of blocking or reversing toxic amyloid formation in vivo. Previous studies have used short peptide inhibitors targeting different amyloid β (Aβ) amyloidogenic regions to prevent aggregation. Despite the specificity that can be
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