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489727

Sigma-Aldrich

Hexanoic acid-6,6,6-d3

99 atom % D

Synonym(s):

Caproic acid-6,6,6-d3

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About This Item

Linear Formula:
CD3(CH2)4CO2H
CAS Number:
Molecular Weight:
119.18
MDL number:
UNSPSC Code:
12352106
PubChem Substance ID:
NACRES:
NA.12

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

SMILES string

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

InChI

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

InChI key

FUZZWVXGSFPDMH-FIBGUPNXSA-N

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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

Signal Word

Danger

Hazard Statements

Hazard Classifications

Eye Dam. 1 - Skin Corr. 1C

Storage Class Code

8A - Combustible corrosive hazardous materials

WGK

WGK 1

Flash Point(F)

215.6 °F - closed cup

Flash Point(C)

102 °C - closed cup


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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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