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Merck

SML1954

Sigma-Aldrich

X-34

≥90% (HPLC), powder, amyloid-specific fluorescent dye

别名:

1,4-双(3-羧基-4-羟基苯基乙烯基)苯

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About This Item

经验公式(希尔记法):
C24H18O6
分子量:
402.40
MDL號碼:
分類程式碼代碼:
12352200
NACRES:
NA.77

product name

X-34, ≥90% (HPLC)

品質等級

化驗

≥90% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2.0 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

OC(C=C1)=C(C(O)=O)C=C1C=CC2=CC=C(C=CC3=CC=C(O)C(C(O)=O)=C3)C=C2

生化/生理作用

X-34是一种荧光淀粉样特异性染料。 它与Pittsburgh CompoundB的结合位点不同,并且是β-折叠结构的一种高度荧光标记。
X-34(1,4-双(3-羧基-4-羟基苯基乙烯基)-苯)是参与到降低Aβ42水平(淀粉样-β肽的42个残基异构体)的一种小分子γ-分泌酶调节因子(GSM)。X-34还被用于在活的转基因秀丽隐杆线虫体内对具有经典淀粉样纤维超微结构的细胞内免疫反应性沉积物进行可视化。它还可作为组织化学染色剂用于确定阿尔茨海默氏′病(AD)的病理变化。
荧光淀粉样特异性染料

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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S D Styren et al.
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 48(9), 1223-1232 (2000-08-19)
X-34, a lipophilic, highly fluorescent derivative of Congo red, was examined as a histochemical stain for pathological changes in Alzheimer's disease (AD). X-34 intensely stained neuritic and diffuse plaques, neurofibrillary tangles (NFTs), neuropil threads, and cerebrovascular amyloid. Comparison to standard
Visualization of fibrillar amyloid deposits in living, transgenic Caenorhabditis elegans animals using the sensitive amyloid dye, X-34
Link CD
Neurobiology of Aging, 22, 217-226 (2001)
Marcus Bäck et al.
Chemistry (Weinheim an der Bergstrasse, Germany), 22(51), 18335-18338 (2016-11-04)
Deposits comprised of amyloid-β (Aβ) are one of the pathological hallmarks of Alzheimer's disease (AD) and small hydrophobic ligands targeting these aggregated species are used clinically for the diagnosis of AD. Herein, we observed that anionic oligothiophenes efficiently displaced X-34
Substrate-targeting ?-secretase modulators
Kukar TL
Nature, 453, 925-929 (2008)
Heidi Olzscha et al.
Cell chemical biology, 24(1), 9-23 (2016-12-19)
Lysine acetylation is becoming increasingly recognized as a general biological principle in cellular homeostasis, and is subject to abnormal control in different human pathologies. Here, we describe a global effect on amyloid-like protein aggregation in human cells that results from

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