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Merck

H2775

DL-threo-β-Hydroxyaspartic acid

Synonym(s):

threo-2-Amino-3-hydroxysuccinic acid

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About This Item

Empirical Formula (Hill Notation):
C4H7NO5
CAS Number:
Molecular Weight:
149.10
PubChem Substance ID:
eCl@ss:
32160406
UNSPSC Code:
12352106
NACRES:
NA.32
EC Number:
224-299-4
MDL number:
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InChI key

YYLQUHNPNCGKJQ-JCYAYHJZSA-N

InChI

1S/C4H7NO5/c5-1(3(7)8)2(6)4(9)10/h1-2,6H,5H2,(H,7,8)(H,9,10)/t1-,2-/m1/s1

SMILES string

N[C@H]([C@@H](O)C(O)=O)C(O)=O

storage temp.

−20°C

Quality Level

Gene Information

human ... GLUL(2752)
mouse ... GLUL(14645)

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Application

DL-threo-β-Hydroxyaspartic acid (THA) has been used to block glutamate transport in cannulated sprague dawley rat.

General description

DL-threo-β-hydroxyaspartic acid (THA) is a glutamate uptake inhibitor.

Storage Class

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


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Nina Bionda et al.
Amino acids, 42(1), 285-293 (2010-11-18)
A simple and practical general synthetic protocol towards orthogonally protected tHyAsp derivatives fully compatible with Fmoc solid-phase peptide synthetic methodology is reported. Our approach includes enantioresolution of commercially available D: ,L: -tHyAsp racemic mixture by co-crystallization with L: -Lys, followed
Ewa Nagańska et al.
Folia neuropathologica, 48(1), 35-44 (2010-04-13)
Erythropoietin (EPO) is a chemokine hormone that is widely distributed throughout the body including nervous system. For last years its role as cytokine involved in many physiological processes out of the bone marrow has been suggested. Moreover, it plays a
Claudio Laurido et al.
TheScientificWorldJournal, 2012, 279147-279147 (2012-04-27)
N-methyl-D-aspartic acid receptor (NMDAr) activation requires the presence of D-serine, synthesized from L-serine by a pyridoxal 5'-phosphate-dependent serine racemase (SR). D-serine levels can be lowered by inhibiting the racemization of L-serine. L-serine-O-sulfate (LSOS) and L-erythro-3-hydroxyaspartate (LEHA), among others, have proven
A Hirata et al.
Brain research, 771(1), 37-44 (1998-02-12)
Excitotoxicity secondary to the loss of glutamate transporters (GluT) has been proposed as a possible pathogenetic mechanism for neuronal degeneration in amyotrophic lateral sclerosis. We therefore investigated whether prolonged in vivo pharmacologic inhibition of GluT would result in neuronal damage
A Klegeris et al.
Journal of neuroimmunology, 78(1-2), 152-161 (1997-10-23)
Glutamate, an excitatory neurotransmitter, is neurotoxic at high concentrations. Neuroglial cells, including astrocytes and microglia, play an important role in regulating its extracellular levels. Cultured human monocytic THP-1 cells increased their glutamate secretion following 18 and 68 h exposure to

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