171255
Oxalacetic acid
98%
Synonym(s):
2-Oxosuccinic acid, Oxobutanedioic acid
Sign In to View Organizational & Contract Pricing.
Select a Size
About This Item
Linear Formula:
HO2CCH2COCO2H
CAS Number:
Molecular Weight:
132.07
UNSPSC Code:
12352204
EC Number:
206-329-8
Beilstein/REAXYS Number:
1705475
MDL number:
SMILES string
OC(=O)CC(=O)C(O)=O
assay
98%
mp
161 °C (dec.) (lit.)
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2
Storage Class
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Faceshields, Gloves, type P3 (EN 143) respirator cartridges
Regulatory Information
新产品
This item has
Choose from one of the most recent versions:
Already Own This Product?
Find documentation for the products that you have recently purchased in the Document Library.
L T Wong et al.
Pediatric research, 20(3), 274-279 (1986-03-01)
An infant with the acute neonatal form of pyruvate carboxylase deficiency (cross-reacting material negative) presented with severe intractable lactic acidosis within 4 h after birth. He also had hyperammonemia, hypercitrullinemia, and hyperlysinemia. Plasma glutamine was not elevated. He had a
Lee Hua Long et al.
Biochemical and biophysical research communications, 417(1), 446-450 (2011-12-15)
Several phenolic compounds as well as ascorbate can oxidise in certain cell culture media (especially Dulbecco's modified Eagle's medium (DMEM)) to generate hydrogen peroxide. Addition of oxaloacetate decreased the levels of H(2)O(2) detected and the oxaloacetate was depleted. Oxaloacetate was
Tonya N Zeczycki et al.
Biochemistry, 50(45), 9724-9737 (2011-10-01)
The catalytic mechanism of the MgATP-dependent carboxylation of biotin in the biotin carboxylase domain of pyruvate carboxylase from R. etli (RePC) is common to the biotin-dependent carboxylases. The current site-directed mutagenesis study has clarified the catalytic functions of several residues
Alexander Zlotnik et al.
Anesthesiology, 116(1), 73-83 (2011-12-02)
Decreasing blood glutamate concentrations after traumatic brain injury accelerates brain-to-blood glutamate efflux, leading to improved neurologic outcomes. The authors hypothesize that treatment with blood glutamate scavengers should reduce neuronal cell loss, whereas administration of glutamate should worsen outcomes. The authors
Randy J Giedt et al.
Free radical biology & medicine, 52(2), 348-356 (2011-11-22)
Ischemia (I)/reperfusion (RP)-induced endothelial cell (EC) injury is thought to be due to mitochondrial reactive oxygen species (mtROS) production. MtROS have been implicated in mitochondrial fission. We determined whether cultured EC exposure to simulated I/RP causes morphological changes in the
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
Contact Technical Service