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Application Area

N-α-Acetyl-L-aspartic acid α-amide

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

Category

β−Amino Acids

Catalog number

BAT-005931

CAS number

60803-67-0

Molecular Formula

C6H10N2O4

Molecular Weight

174.16

IUPAC Name

(3S)-3-acetamido-4-amino-4-oxobutanoic acid

Synonyms

Ac-Asp-NH2; Ac-IsoAsn-OH; N-α-Acetyl-L-Isoasparagine

Density

1.346±0.06 g/cm3

Melting Point

162-164 °C

Boiling Point

556.8±45.0 °C

Storage

Store at -20°C

InChI

InChI=1S/C6H10N2O4/c1-3(9)8-4(6(7)12)2-5(10)11/h4H,2H2,1H3,(H2,7,12)(H,8,9)(H,10,11)/t4-/m0/s1

InChI Key

FZLYWFSBVZNFHZ-BYPYZUCNSA-N

Canonical SMILES

CC(=O)NC(CC(=O)O)C(=O)N

N-α-Acetyl-L-aspartic acid α-amide, commonly referred to as Acetylaspartylglutamic acid (NAAG), is a naturally occurring peptide neurotransmitter in the brain. It is synthesized in neurons and stored in synaptic vesicles, and is released upon neural depolarization. NAAG is comprised of N-acetylaspartic acid (NAA) linked to glutamic acid. It acts primarily as a neurotransmitter in the central nervous system with roles in modulating synaptic transmission and plasticity. NAAG is known to bind to and activate specific metabotropic glutamate receptors, playing a crucial role in balancing excitatory neurotransmission, which is vital for normal brain function and health.

One of the key applications of N-α-Acetyl-L-aspartic acid α-amide is in neurological research. Given its significant role in neurotransmission, it is extensively studied for its potential impact on neurophysiological processes and disorders. Researchers investigate its involvement in conditions such as schizophrenia and Alzheimer’s disease, where glutamatergic transmission is affected. Understanding how NAAG influences synaptic signaling provides insight into therapeutic approaches for these conditions. Additionally, exploring NAAG’s function and metabolism can lead to potential biomarkers for early detection and progression of neurological diseases.

Another important application of NAAG is in the development of neuroprotective treatments. Due to its regulatory effects on excitatory neurotransmission via inhibition of excessive glutamate activity, NAAG and its analogs are explored for their potential to protect neurons from excitotoxicity. Excitotoxicity is a pathological process that can lead to cell death and is implicated in various neurological disorders and injuries, such as stroke and traumatic brain injury. By mitigating excessive activation of glutamate receptors, NAAG offers a pathway to develop treatments that safeguard neuronal health, thereby limiting damage following acute neurological events.

NAAG also holds potential in pain management. Research indicates that it modulates synaptic plasticity at the spinal cord level, influencing the transmission of pain signals. NAAG can diminish nociceptive signaling, which might be beneficial in managing chronic pain conditions where conventional analgesics fall short. Therefore, understanding its mechanisms can assist in designing novel analgesics that target specific pathways mediated by metabotropic glutamate receptors, offering relief for patients suffering from neuropathic pain and other persistent pain syndromes.

Lastly, NAAG plays a role in cognitive enhancement. Some studies suggest that modulating NAAG levels in the brain might influence cognitive functions such as learning and memory. Because of its interaction with glutamatergic signaling pathways, manipulating NAAG concentrations has the potential to ameliorate cognitive deficits associated with aging and neurodegenerative diseases. Continuing research in this area could lead to the development of cognitive enhancers that improve mental faculties and protect against cognitive decline. This area of application holds significant promise, especially in addressing the growing prevalence of age-related cognitive impairments.

1. Alteration of substrate specificity of aspartase by directed evolution

Yasuhisa Asano, Ikuo Kira, Kenzo Yokozeki Biomol Eng. 2005 Jun;22(1-3):95-101. doi: 10.1016/j.bioeng.2004.12.002.

Aspartase (l-aspartate ammonia-lyase, EC 4.3.1.1), which catalyzes the reversible deamination of l-aspartic acid to yield fumaric acid and ammonia, is highly selective towards l-aspartic acid. We screened for enzyme variants with altered substrate specificity by a directed evolution method. Random mutagenesis was performed on an Escherichia coli aspartase gene (aspA) by error-prone PCR to construct a mutant library. The mutant library was introduced to E. coli and the transformants were screened for production of fumaric acid-mono amide from l-aspartic acid-alpha-amide. Through the screening, one mutant, MA2100, catalyzing deamination of l-aspartic acid-alpha-amide was achieved. Gene analysis of the MA2100 mutant indicated that the mutated enzyme had a K327N mutation. The characteristics of the mutated enzyme were examined. The optimum pH values for the l-aspartic acid and l-aspartic acid-alpha-amide of the mutated enzyme were pH 8.5 and 6.0, respectively. The K(m) value and V(max) value for the l-aspartic acid of the mutated enzyme were 28.3 mM and 0.26 U/mg, respectively. The K(m) value and V(max) value for the l-aspartic acid-alpha-amide of the mutated enzyme were 1450 mM and 0.47 U/mg, respectively. This is the first report describing the alteration of the substrate specificity of aspartase, an industrially important enzyme.

2. Synthesis of antimicrobial peptoids

Paul R Hansen, Jens K Munk Methods Mol Biol. 2013;1047:151-9. doi: 10.1007/978-1-62703-544-6_11.

Peptoids (N-substituted glycines) are mimics of α-peptides in which the side chains are attached to the backbone N (α) -amide nitrogen instead of the C (α) -atom. Peptoids hold promise as therapeutics since they often retain the biological activity of the parent peptide and are stable to proteases. In recent years, peptoids have attracted attention as new potential antibiotics against multiresistant bacteria. Here we describe the submonomer solid-phase synthesis of an antimicrobial peptoid, H-Nmbn-Nlys-Nlys-Nnap-Nbut-Nmbn-Nlys-NH2.

3. Methods for syntheses of N-methyl-DL-aspartic acid derivatives

M Boros, J Kökösi, J Vámos, I Kövesdi, B Noszál Amino Acids. 2007 Nov;33(4):709-17. doi: 10.1007/s00726-006-0453-4. Epub 2007 Mar 2.

A novel practical method for the synthesis of N-methyl-DL-aspartic acid 1 (NMA) and new syntheses for N-methyl-aspartic acid derivatives are described. NMA 1, the natural amino acid was synthesized by Michael addition of methylamine to dimethyl fumarate 5. Fumaric or maleic acid mono-ester and -amide were regioselectively transformed into beta-substituted aspartic acid derivatives. In the cases of maleamic 11a or fumaramic esters 11b, the alpha-amide derivative 13 was formed, but hydrolysis of the product provided N-methyl-DL-asparagine 9 via base catalyzed ring closure to DL-alpha-methylamino-succinimide 4, followed by selective ring opening. Efficient methods were developed for the preparation of NMA-alpha-amide 13 from unprotected NMA via sulphinamide anhydride 15 and aspartic anhydride 3 intermediate products. NMA diamide 16 was prepared from NMA dimethyl ester 6 and methylamino-succinimide 4 by ammonolysis. Temperature-dependent side reactions of methylamino-succinimide 4 led to diazocinone 18, resulted from self-condensation of methylamino-succinimide via nucleophyl ring opening and the subsequent ring-transformation.