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文件

I8132

Sigma-Aldrich

scyllo-肌醇

≥98%

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别名:
DTLET, 青蟹肌醇
经验公式（希尔记法）:
C6H12O6
CAS号:
488-59-5
分子量:
180.16
MDL编号:
MFCD00065455
PubChem化学物质编号:
24896132
NACRES:
NA.77

检测方案

≥98%

SMILES string

O[C@@H]1[C@@H](O)[C@H](O)[C@@H](O)[C@H](O)[C@H]1O

InChI

1S/C6H12O6/c7-1-2(8)4(10)6(12)5(11)3(1)9/h1-12H/t1-,2-,3+,4+,5-,6-

InChI key

CDAISMWEOUEBRE-CDRYSYESSA-N

其他说明

肌醇的天然异构体。

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type N95 (US)

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H Randall Griffith et al.
NMR in biomedicine, 20(8), 709-716 (2007-02-14)
in vivo (1)H MRS reveals reduced N-acetylaspartate (NAA) and elevated myo-inositol (mI) in patients with mild Alzheimer's disease (AD) and patients with amnestic mild cognitive impairment (MCI). We are unaware of studies that have documented abnormal scyllo-inositol (sI) levels in
Aaron Y Lai et al.
Biochimica et biophysica acta, 1822(10), 1629-1637 (2012-07-18)
scyllo-Inositol (SI) is an endogenous inositol stereoisomer known to inhibit aggregation and fibril formation of the amyloid-beta peptide (Aβ). Human clinical trials using SI to treat Alzheimer disease (AD) patients have shown potential benefits. In light of the growing therapeutic
Kevin A Dasilva et al.
Experimental neurology, 223(2), 311-321 (2009-09-12)
Structural insight into the conformational changes associated with aggregation and assembly of fibrils has provided a number of targets for therapeutic intervention. Solid-state NMR, hydrogen/deuterium exchange and mutagenesis strategies have been used to probe the secondary and tertiary structure of
Daniela Fenili et al.
Journal of molecular medicine (Berlin, Germany), 85(6), 603-611 (2007-02-07)
Inositol is a simple polyol with eight naturally occurring stereoisomers. myo-Inositol, D-chiro- and epi-inositol have been examined as potential therapeutic agents for various diseases, with favorable results, but treatment with scyllo-inositol has not been previously investigated. Our laboratory has shown
Matthew Townsend et al.
Annals of neurology, 60(6), 668-676 (2006-12-29)
Despite progress in defining a pathogenic role for amyloid beta protein (Abeta) in Alzheimer's disease, orally bioavailable compounds that prevent its effects on hippocampal synaptic plasticity and cognitive function have not yet emerged. A particularly attractive therapeutic strategy is to
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