推荐产品
质量水平
方案
≥98%
SMILES字符串
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)
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
其他客户在看
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
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
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
Sara Alam et al.
Current biology : CB, 33(11), 2175-2186 (2023-05-11)
Most eukaryotes respire oxygen, using it to generate biomass and energy. However, a few organisms have lost the capacity to respire. Understanding how they manage biomass and energy production may illuminate the critical points at which respiration feeds into central
Cheryl A Hawkes et al.
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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