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Merck
CN

489727

己酸-6,6,6-d3

99 atom % D

别名:

羊油酸-6,6,6-d3

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关于此项目

线性分子式:
CD3(CH2)4CO2H
化学文摘社编号:
分子量:
119.18
NACRES:
NA.12
PubChem Substance ID:
UNSPSC Code:
12352106
MDL number:
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产品名称

己酸-6,6,6-d3, 99 atom % D

InChI

1S/C6H12O2/c1-2-3-4-5-6(7)8/h2-5H2,1H3,(H,7,8)/i1D3

SMILES string

[2H]C([2H])([2H])CCCCC(O)=O

InChI key

FUZZWVXGSFPDMH-FIBGUPNXSA-N

isotopic purity

99 atom % D

assay

99% (CP)

refractive index

n20/D 1.412 (lit.)

bp

202-203 °C (lit.)

mp

-3 °C (lit.)

density

0.951 g/mL at 25 °C

mass shift

M+3

Quality Level

Packaging

This product may be available from bulk stock and can be packaged on demand. For information on pricing, availability and packaging, please contact Stable Isotopes Customer Service.

pictograms

Corrosion

signalword

Danger

hcodes

Hazard Classifications

Eye Dam. 1 - Skin Corr. 1C

存储类别

8A - Combustible corrosive hazardous materials

wgk

WGK 1

flash_point_f

215.6 °F - closed cup

flash_point_c

102 °C - closed cup

法规信息

危险化学品
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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Jingwei Cai et al.
Journal of proteome research, 15(2), 563-571 (2015-12-24)
Recent studies have identified the important role of the gut microbiota in the pathogenesis and progression of obesity and related metabolic disorders. The antioxidant tempol was shown to prevent or reduce weight gain and modulate the gut microbiota community in
Matthew V Gomez et al.
Toxicological sciences : an official journal of the Society of Toxicology, 179(1), 14-30 (2020-10-21)
The gut microbiome is a pivotal player in toxicological responses. We investigated the effects of maternal exposure to 3 human health-relevant toxicants (BDE-47, tetrabromobisphenol [TBBPA], and bisphenol S [BPS]) on the composition and metabolite levels (bile acids [BAs] and short-chain
D Nyasha Chagwedera et al.
Cell metabolism, 30(2), 364-373 (2019-05-28)
Microbial dysbiosis and inflammation are implicated in diet-induced obesity and insulin resistance. However, it is not known whether crosstalk between immunity and microbiota also regulates metabolic homeostasis in healthy animals. Here, we report that genetic deletion of tuberous sclerosis 1

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