D-Glutamic acid
Need Assistance?
  • US & Canada:
    +
  • UK: +

D-Glutamic acid

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

D-Glutamic acid is a non-essential amino acid acting at NMDA receptors. D-Glutamic is less active than the L-isomer.

Category
D-Amino Acids
Catalog number
BAT-008125
CAS number
6893-26-1
Molecular Formula
C5H9NO4
Molecular Weight
147.13
D-Glutamic acid
IUPAC Name
(2R)-2-aminopentanedioic acid
Synonyms
(R)-1-Aminopropane-1,3-dicarboxylic acid; (2R)-2-aminopentanedioic acid
Appearance
White powder
Purity
99%
Density
1.409 g/cm3
Melting Point
205°C (dec)
Boiling Point
333.8°C at 760 mmHg
Storage
Store at RT
Solubility
Soluble in Water
InChI
InChI=1S/C5H9NO4/c6-3(5(9)10)1-2-4(7)8/h3H,1-2,6H2,(H,7,8)(H,9,10)/t3-/m1/s1
InChI Key
WHUUTDBJXJRKMK-GSVOUGTGSA-N
Canonical SMILES
C(CC(=O)O)C(C(=O)O)N
1.A possible link between parathyroid hormone secretion and local regulation of GABA in human parathyroid adenomas.
Ram Hong A1, Kim YA2,3, Hyun Bae J1, Sook Min H3, Hee Kim J1, Soo Shin C1, Yeon Kim S1, Kim SW1,4. J Clin Endocrinol Metab. 2016 Apr 12:jc20154329. [Epub ahead of print]
CONTEXT: Gamma-aminobutyric acid-B receptor 1 (GABABR1) forms a heterodimeric complex with calcium-sensing receptor (CaSR) in human brain tissue. However, the expression and implication of GABABR1 in human parathyroid adenoma has not yet been examined.
2.Design, synthesis and biological evaluation of 6-substituted pyrrolo[2,3-d]pyrimidines as dual inhibitors of TS and AICARFTase and as potential antitumor agents.
Liu Y1, Li M2, Zhang H2, Yuan J2, Zhang C2, Zhang K2, Guo H1, Zhao L1, Du Y2, Wang L3, Ren L4. Eur J Med Chem. 2016 Jun 10;115:245-56. doi: 10.1016/j.ejmech.2016.03.032. Epub 2016 Mar 21.
A new series of 2-amino-4-oxo-6-substituted pyrrolo[2,3-d]pyrimidines, with an isosteric replacement of the side chain amide moiety to a sulfur atom, were designed and synthesized as multitargeted antifolates as well as potential antitumor agents. Starting from previously synthesized 2-amino-4-oxo-pyrrolo[2,3-d]pyrimidin-6-yl-acetic acid, a reduction by lithium triethylborohydride and successive mesylation afforded the key mesylate. Nucleophilic substitution by mercaptoacetic or mercaptopropionic acid methyl esters, followed by hydrolysis and condensation with pyridinyl-methylamines provided the nonclassical compounds 1-6, whereas condensation with glutamic acid diethyl ester hydrochloride and saponification afforded the classical analogs 7-8. All target compounds exhibited inhibitory activities toward KB, SW620 and A549 tumor cell lines. The most potent compounds of this series, 7 and 8, are better inhibitors against A549 cells than methotrexate (MTX) and pemetrexed (PMX).
3.Immunization with a novel Clostridium perfringens epsilon toxin mutant rETX(Y196E)-C confers strong protection in mice.
Yao W1, Kang J1, Kang L1, Gao S1, Yang H1, Ji B1, Li P1, Liu J1, Xin W1, Wang J1. Sci Rep. 2016 Apr 6;6:24162. doi: 10.1038/srep24162.
Epsilon toxin (ETX) is produced by toxinotypes B and D of Clostridium perfringens. It can induce lethal enterotoxemia in domestic animals, mainly in sheep, goats and cattle, causing serious economic losses to global animal husbandry. In this study, a novel and stable epsilon toxin mutant rETX(Y196E)-C, obtained by substituting the 196th tyrosine (Y196) with glutamic acid (E) and introducing of 23 amino acids long C-terminal peptide, was determined as a promising recombinant vaccine candidate against enterotoxemia. After the third vaccination, the antibody titers against recombinant wild type (rETX) could reach 1:10(5) in each immunized group, and the mice were completely protected from 100 × LD50 (50% lethal dose) of rETX challenge. The mice in 15 μg subcutaneously immunized group fully survived at the dose of 500 × LD50 of rETX challenge and 80% of mice survived at 180 μg (1000 × LD50) of rETX administration. In vitro, immune sera from 15 μg subcutaneously immunized group could completely protect MDCK cells from 16 × CT50 (50% lethal dose of cells) of rETX challenge and protect against 10 × LD50 dose (1.
4.Neuronal antibodies in pediatric epilepsy: Clinical features and long-term outcomes of a historical cohort not treated with immunotherapy.
Wright S1, Geerts AT2, Jol-van der Zijde CM3, Jacobson L1, Lang B1, Waters P1, van Tol MJ3, Stroink H4, Neuteboom RF2, Brouwer OF5, Vincent A1. Epilepsia. 2016 Mar 21. doi: 10.1111/epi.13356. [Epub ahead of print]
OBJECTIVE: In autoimmune encephalitis the etiologic role of neuronal cell-surface antibodies is clear; patients diagnosed and treated early have better outcomes. Neuronal antibodies have also been described in patients with pediatric epilepsy without encephalitis. The aim was to assess whether antibody presence had any effect on long-term outcomes in these patients.
Online Inquiry
Verification code
Inquiry Basket