LY-411575 has been used as a potent γ-secretase inhibitor and Notch inhibitor.[1][2][3]
Biochem./physiol. Wirkung
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.
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
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
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)
Frontiers in cell and developmental biology, 8, 586651-586651 (2020-10-27)
Pancreatic islets, discrete microorgans embedded within the exocrine pancreas, contain beta cells which are critical for glucose homeostasis. Loss or dysfunction of beta cells leads to diabetes, a disease with expanding global prevalence, and for which regenerative therapies are actively
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