推荐产品
方案
≥98% (HPLC)
表单
powder
旋光性
[α]/D -125 to -140°, c = 0.5 in ethanol
颜色
white to beige
溶解性
DMSO: 2 mg/mL, clear
储存温度
2-8°C
生化/生理作用
ELND006 is an allosteric γ-secretase inhibitor that selectively blocks amyloid-β (Aβ) over Notch production both in cell-free (Aβ IC50/Notch IC50 = 0.34 nM/6.6 nM) and cell-based assays (Aβ IC50/Notch IC50 = 1.3 nM/85 nM). ELND006 is orally available and blood-brain barrier-permeable (total/unbound conc in brain = 0.12 μM/1.0 nM, 0.52 μM/4.5 nM, 2.1 μM/18 nM and total/unbound conc in plasma = 0.031 μM/0.28 nM, 0.19 μM/1.7 nM, 0.90 μM/8.1 nM 3 h post 1, 3, 10 mg/kg oral dosage in rats, respectively), and shown to effectively reduce cortical Aβx-40 in mice in vivo (by 32%, 48%, and 61% 3 h post 1, 3, 10 mg/kg oral dosage).
储存分类代码
11 - Combustible Solids
WGK
WGK 3
法规信息
新产品
从最新的版本中选择一种：
Fiorenza Stagni et al.
Neurobiology of disease, 103, 11-23 (2017-04-01)
Neurogenesis impairment is considered a major determinant of the intellectual disability that characterizes Down syndrome (DS), a genetic condition caused by triplication of chromosome 21. Previous evidence obtained in the Ts65Dn mouse model of DS showed that the triplicated gene
Gary Probst et al.
Journal of medicinal chemistry, 56(13), 5261-5274 (2013-05-30)
Herein, we describe our strategy to design metabolically stable γ-secretase inhibitors which are selective for inhibition of Aβ generation over Notch. We highlight our synthetic strategy to incorporate diversity and chirality. Compounds 30 (ELND006) and 34 (ELND007) both entered human
Inger Lauritzen et al.
Acta neuropathologica, 132(2), 257-276 (2016-05-04)
Endosomal-autophagic-lysosomal (EAL) dysfunction is an early and prominent neuropathological feature of Alzheimers's disease, yet the exact molecular mechanisms contributing to this pathology remain undefined. By combined biochemical, immunohistochemical and ultrastructural approaches, we demonstrate a link between EAL pathology and the
Inger Lauritzen et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(46), 16243-1655a-16243-1655a (2012-11-16)
Triple-transgenic mice (3xTgAD) overexpressing Swedish-mutated β-amyloid precursor protein (βAPP(swe)), P310L-Tau (Tau(P301L)), and physiological levels of M146V-presenilin-1 (PS1(M146V)) display extracellular amyloid-β peptides (Aβ) deposits and Tau tangles. More disputed is the observation that these mice accumulate intraneuronal Aβ that has been
Localization and Processing of the Amyloid-β Protein Precursor in Mitochondria-Associated Membranes.
Dolores Del Prete et al.
Journal of Alzheimer's disease : JAD, 55(4), 1549-1570 (2016-12-03)
Alteration of mitochondria-associated membranes (MAMs) has been proposed to contribute to the pathogenesis of Alzheimer's disease (AD). We studied herein the subcellular distribution, the processing, and the protein interactome of the amyloid-β protein precursor (AβPP) and its proteolytic products in
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