I8132
scyllo-肌醇
≥98%, Myo-inositol isomer
别名:
DTLET, 青蟹肌醇
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关于此项目
经验公式（希尔记法）:
C6H12O6
化学文摘社编号:
分子量:
180.16
UNSPSC Code:
12352207
PubChem Substance ID:
NACRES:
NA.77
MDL number:
Assay:
≥98%
Quality level:
Other Notes
肌醇的天然异构体。
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)
Christophe Michon et al.
Communications biology, 3(1), 93-93 (2020-03-04)
A rare stereoisomer of inositol, scyllo-inositol, is a therapeutic agent that has shown potential efficacy in preventing Alzheimer's disease. Mycobacterium tuberculosis ino1 encoding myo-inositol-1-phosphate (MI1P) synthase (MI1PS) was introduced into Bacillus subtilis to convert glucose-6-phosphate (G6P) into MI1P. We found that
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
Yedi Sun et al.
Bioorganic & medicinal chemistry, 16(15), 7177-7184 (2008-07-19)
scyllo-Inositol has shown promise as a potential therapeutic for Alzheimer's disease, by directly interacting with the amyloid beta (Abeta) peptide to inhibit Abeta42 fiber formation. To explore the molecular details of the inositol-Abeta42 interaction, a series of scyllo-inositol derivatives have
Cheryl A Hawkes et al.
Current Alzheimer research, 9(8), 890-901 (2012-01-26)
The role of microglia in β-amyloid (Aβ) deposition or clearance in the Alzheimer's disease (AD) brain remains unclear. Previous in vivo studies have focused primarily on the association of microglia with Aβ-positive parenchymal plaques, but have given little consideration to
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