I8132
scyllo-Inositol
≥98%
Synonym(s):
1,3,5/2,4,6-Hexahydroxycyclohexane, DTLET
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About This Item
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Assay
≥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
Other Notes
Naturally occurring isomer of myo-inositol.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
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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
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
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
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
The European journal of neuroscience, 31(2), 203-213 (2010-01-16)
Beta-amyloid (Abeta) peptides are thought to play a major role in the pathogenesis of Alzheimer's disease. Compounds that disrupt the kinetic pathways of Abeta aggregation may be useful in elucidating the role of oligomeric, protofibrillar and fibrillar Abeta in the
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