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Merck

SML0506

Sigma-Aldrich

LY-411575

≥97% (HPLC)

Sinónimos:

LSN-411575, LY 411575, N2-[(2S)-2-(3,5-Difluorophenyl)-2-hydroxyethanoyl]-N1-[(7S)-5-methyl-6-oxo-6,7-dihydro-5H-dibenzo[b,d]azepin-7-yl]-L-alaninamide

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About This Item

Fórmula empírica (notación de Hill):
C26H23F2N3O4
Número de CAS:
Peso molecular:
479.48
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥97% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 5 mg/mL, clear

shipped in

wet ice

storage temp.

−20°C

SMILES string

C[C@H](NC(=O)[C@@H](O)c1cc(F)cc(F)c1)C(=O)N[C@@H]2C(=O)N(C)c3ccccc3-c4ccccc24

InChI

1S/C26H23F2N3O4/c1-14(29-25(34)23(32)15-11-16(27)13-17(28)12-15)24(33)30-22-20-9-4-3-7-18(20)19-8-5-6-10-21(19)31(2)26(22)35/h3-14,22-23,32H,1-2H3,(H,29,34)(H,30,33)/t14-,22-,23-/m0/s1

InChI key

ULSSJYNJIZWPSB-CVRXJBIPSA-N

Application

LY-411575 has been used as a potent γ-secretase inhibitor and Notch inhibitor.

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.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

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Enzymatic assays for studying intramembrane proteolysis.
Bolduc D M, et al.
Methods in Enzymology, 584, 295-308 (2017)
K Pandya et al.
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.
Singh S P, et al.
Nature Communications, 8(1), 664-664 (2017)
Kyung-Won Park et al.
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)

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