78319
trans-Glutaconic acid sodium salt hydrate
≥95.0% (HPLC)
Synonym(s):
(2E)-Pentenedioic acid sodium salt hydrate, Sodium trans-glutaconate hydrate
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About This Item
Empirical Formula (Hill Notation):
C5H6O4 · xNa+ · yH2O
Molecular Weight:
130.10 (anhydrous free acid basis)
UNSPSC Code:
12352202
PubChem Substance ID:
NACRES:
NA.25
Recommended Products
assay
≥95.0% (HPLC)
form
powder
SMILES string
OC(C/C=C/C(O)=O)=O.C
InChI
1S/C5H6O4.CH4/c6-4(7)2-1-3-5(8)9;/h1-2H,3H2,(H,6,7)(H,8,9);1H4/b2-1+;
InChI key
NRJOWSDIBMLXCK-TYYBGVCCSA-N
Application
Internal reference for urine samples
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Atsuki Ikeda et al.
Biomedical chromatography : BMC, 26(5), 548-558 (2011-07-21)
Conventional tumor markers are unsuitable for detecting carcinoma at an early stage and lack clinical efficacy and utility. In this study, we attempted to investigate the differences in serum metabolite profiles of gastrointestinal cancers and healthy volunteers using a metabolomic
G F Hoffmann et al.
Journal of inherited metabolic disease, 22(4), 381-391 (1999-07-17)
The biochemical hallmark of glutaric aciduria type I (GA I) due to glutaryl-CoA dehydrogenase deficiency is the accumulation of glutaric acid, and to a lesser degree of 3-hydroxyglutaric and glutaconic acids. Abnormal metabolites vary from gross organic aciduria to only
Metabolomics of urinary organic acids in respiratory chain deficiencies in children.
Reinecke, C.J., et al.
Metabolomics, 8, 264-283 (2012)
Júlia Dénes et al.
Analytical chemistry, 84(22), 10113-10120 (2012-10-26)
A novel, single stage high resolution mass spectrometry-based method is presented for the population level screening of inborn errors of metabolism. The approach proposed here extends traditional electrospray tandem mass spectrometry screening by introducing nanospray ionization and high resolution mass
Jonathan C Schisler et al.
Journal of the American Heart Association, 4(2), doi:10-doi:10 (2015-02-26)
Long chain acyl-CoA synthetases (ACSL) catalyze long-chain fatty acids (FA) conversion to acyl-CoAs. Temporal ACSL1 inactivation in mouse hearts (Acsl1(H-/-)) impaired FA oxidation and dramatically increased glucose uptake, glucose oxidation, and mTOR activation, resulting in cardiac hypertrophy. We used unbiased
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