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Methoxy-X04
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Methoxy-X04图片
CAS NO:863918-78-9
包装与价格:
包装价格(元)
5mg电议
10mg电议

产品介绍

化学性质

Physical AppearanceA crystalline solid
StorageStore at -20°C
M.Wt344.4
Cas No.863918-78-9
FormulaC23H20O3
Solubility≥51.9 mg/mL in DMSO; insoluble in EtOH; insoluble in H2O
Chemical Name4,4'-((1E,1'E)-(2-methoxy-1,4-phenylene)bis(ethene-2,1-diyl))diphenol
Canonical SMILESCOC1=C(C=CC(/C([H])=C([H])/C2=CC=C(O)C=C2)=C1)/C([H])=C([H])/C3=CC=C(O)C=C3
运输条件蓝冰运输或根据您的需求运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。

资料参考

Methoxy-X04, a derivative of Congo red and Chrysamine-G, is a brain-permeable fluorescent probe for amyloid-β (Aβ) [1].

Aβ peptides, proposed as a cause of Alzheimer’s disease, exists in multiple conformations, including soluble monomers, aggregated soluble oligomers, and insoluble fibrils. Soluble low-n molecular weight oligomers (including dimers and trimers, up to dodecamers) may be a major driver of neurotoxicity. Furthermore, soluble Aβ oligomers concentrate around the dense core of plaques, generating a neurotoxic halo that contributes to local neuritic dystrophy, synaptic loss, and neurodegeneration [2].

Inin vitro binding studies, compared with Chrysamine-G (Ki = 25.3 nM), Methoxy-X04 exhibited similar binding affinity for Aβ fibrils (Ki = 26.8 nM) [1]. On brain slices of 12-month-old APP-PS1 (dE9) mice, 145 μM Methoxy-X04 was used for labelling fibrillary amyloid deposits [3].

In PS1/APP mice, a single i.v. injection of 5 to 10 mg/kg Methoxy-X04 distinguished individual plaques from brain fluorescent images, within 30 to 60 min after treatment. A single i.p. injection of 10 mg/kg Methoxy-X04 also produced high contrast images of plaques and cerebrovascular amyloid in PS1/APP mouse brains [1].

References:

[1]. Klunk W E, Backsai B J, Mathis C A, et al. Imaging Aβ plaques in living transgenic mice with multiphoton microscopy and methoxy-X04, a systemically administered Congo red derivative. Journal of Neuropathology & Experimental Neurology, 2002, 61(9): 797-805.

[2]. Meilandt W J, Maloney J A, Imperio J, et al. Characterization of the selective in vitro and in vivo binding properties of crenezumab to oligomeric Aβ. Alzheimer's Research & Therapy, 2019, 11(1): 97.

[3]. Jung C K, Keppler K, Steinbach S, et al. Fibrillar amyloid plaque formation precedes microglial activation. PLoS One, 2015, 10(3): e0119768.