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Merck
CN

C9012

双环己酮草酰二腙

≥95% purity (TLC), powder

别名:

Cuprizon, 新铜试剂, 草酰双(环己基亚肼)

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关于此项目

经验公式(希尔记法):
C14H22N4O2
化学文摘社编号:
分子量:
278.35
NACRES:
NA.47
PubChem Substance ID:
UNSPSC Code:
12171500
EC Number:
206-729-2
MDL number:
Beilstein/REAXYS Number:
2388004
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产品名称

双环己酮草酰二腙, ≥95% (TLC)

InChI key

DSRJIHMZAQEUJV-UHFFFAOYSA-N

InChI

1S/C14H22N4O2/c19-13(17-15-11-7-3-1-4-8-11)14(20)18-16-12-9-5-2-6-10-12/h1-10H2,(H,17,19)(H,18,20)

SMILES string

O=C(N\N=C1\CCCCC1)C(=O)N\N=C2/CCCCC2

assay

≥95% (TLC)

form

powder

technique(s)

titration: suitable

color

white/clear to off-white

mp

210-214 °C (lit.)

solubility

acetic acid: 50 mg/mL, colorless to very faintly brown

application(s)

diagnostic assay manufacturing
hematology
histology

storage temp.

2-8°C

Quality Level

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Application

  • 双(环己酮)草二腙(草酸双)已被用于小鼠研究 NG2(神经/胶质抗原 2)蛋白聚糖对毒性引起的脱髓鞘的影响。
  • 已用于诱导小鼠脱髓鞘。
  • 已被用于研究草酸双诱导的小鼠胼胝体脱髓鞘和髓鞘再生。

Biochem/physiol Actions

双(环己酮)草二腙(草酸双)是铜螯合剂。它导致少突胶质细胞死亡,从而导致脱髓鞘、星形胶质细胞增生和小胶质细胞活化。草酸双被广泛用于研究胼胝体线粒体功能障碍相关的原发性脱髓鞘和髓鞘再生。

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Galanin transgenic mice with elevated circulating galanin levels alleviate demyelination in a cuprizone-induced MS mouse model.
Zhang L, et al.
PLoS ONE, 7, e33901-e33901 (2012)
Demyelination and remyelination in anatomically distinct regions of the corpus callosum following cuprizone intoxication.
Steelman AJ, et al.
Neuroscience Research, 72, 32-42 (2012)
Cortical demyelination is prominent in the murine cuprizone model and is strain-dependent.
Skripuletz T, et al.
The American Journal of Pathology, 172, 1053-1061 (2008)
Recovery from Toxic-Induced Demyelination Does Not Require the NG2 Proteoglycan.
Stefanie Albrecht et al.
PloS one, 11(10), e0163841-e0163841 (2016-10-19)
Thomas Skripuletz et al.
Brain : a journal of neurology, 136(Pt 1), 147-167 (2012-12-26)
Recent evidence suggests that astrocytes play an important role in regulating de- and remyelination in multiple sclerosis. The role of astrocytes is controversial, and both beneficial as well as detrimental effects are being discussed. We performed loss-of-function studies based on

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