D-Aspartic acid a-methyl ester
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D-Aspartic acid a-methyl ester

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D-Aspartic acid a-methyl ester is a protected form of D-Aspartic acid. D-Aspartic acid is the unnatural isomer of L-Aspartic acid. D-Aspartic acid naturally occurs in human ovarian follicular fluid, and is thought to be linked to oocyte quality. It is also found in the white matter of human brains, more specifically in myelin proteins.

Category
β−Amino Acids
Catalog number
BAT-007644
CAS number
65414-78-0
Molecular Formula
C5H9NO4
Molecular Weight
147.13
D-Aspartic acid a-methyl ester
IUPAC Name
(3R)-3-amino-4-methoxy-4-oxobutanoic acid
Synonyms
D-Asp-OMe; h-d-asp-ome; D-Asp-OMe; D-Aspartic acid,1-methyl ester; D-Aspartic acid alpha-methyl ester; (3R)-3-amino-4-methoxy-4-oxobutanoic acid; D Asp Ome
Appearance
White to off-white powder
Purity
≥ 98% (HPLC)
Density
1.299±0.06 g/cm3 (Predicted)
Melting Point
167-172 °C
Boiling Point
272.7±30.0 °C (Predicted)
Storage
Store at 2-8 °C
InChI
InChI=1S/C5H9NO4/c1-10-5(9)3(6)2-4(7)8/h3H,2,6H2,1H3,(H,7,8)/t3-/m1/s1
InChI Key
SWWBMHIMADRNIK-GSVOUGTGSA-N
Canonical SMILES
COC(=O)C(CC(=O)O)N

D-Aspartic Acid α-Methyl Ester (DAME) is a derivative of D-aspartic acid, an amino acid that plays vital roles in the biosynthesis of proteins. As an esterified form of D-aspartic acid, DAME is known for its potential to influence the release of hormones, including luteinizing hormone and testosterone, which suggests its application in enhancing athletic performance and stimulating muscle growth. The compound is of growing interest in the fields of neurobiology, endocrinology, and sports science due to its involvement in these biochemical processes.

One of the primary applications of D-Aspartic Acid α-Methyl Ester is in the realm of sports nutrition and bodybuilding supplements. This is primarily due to its purported effect on increasing the levels of testosterone in the body, which can subsequently enhance muscle mass and strength. Athletes and bodybuilders often seek supplements that can naturally boost their hormones to improve performance, and DAME is frequently marketed as an agent that can serve in this capacity. Its potential to impact hormone levels makes it a sought-after component in pre-workout and muscle-building supplement formulations.

In the field of neurobiology, D-Aspartic Acid α-Methyl Ester is examined for its role in neurotransmission and neuroprotection. D-aspartic acid itself is a neurotransmitter in the central nervous system, and its methyl ester form could influence similar pathways. Researchers explore its potential to support cognitive function and protect against neurodegenerative diseases. The compound’s ability to modulate neurotransmitter release is a key area of interest for understanding various neurological conditions and may contribute to the development of therapeutic strategies for diseases like Alzheimer’s and Parkinson’s.

Endocrinologically, DAME is studied for its impact on reproductive hormones. Besides increasing testosterone, it may influence the production of other hormones such as luteinizing hormone, which is critical for reproductive health in both males and females. Researchers investigate its application in treating conditions associated with hormonal imbalances, such as infertility or hypogonadism. Its role in modifying hormonal pathways could potentially be harnessed to devise new treatments for these conditions, offering a non-invasive alternative to traditional hormonal therapies.

Finally, D-Aspartic Acid α-Methyl Ester is also of interest in pharmacology for its role in metabolic pathways. Its esterified form potentially offers improved bioavailability over its non-esterified counterpart, making it an attractive candidate for energy metabolism studies. Exploring its effects on metabolic functions and energy utilization could lead to innovations in metabolic health treatments and dietary supplements, aiming to enhance energy levels and improve overall metabolic efficiency. Such applications highlight the compound’s versatility and potential benefits across multiple biological systems.

1. Chiral separation of N-methyl-DL-aspartic acid in rat brain tissue as N-ethoxycarbonylated (S)-(+)-2-octyl ester derivatives by GC-MS
Duc-Toan Nguyen, Kyoung-Rae Kim, Gwang Lee, Man-Jeong Paik Biomed Chromatogr. 2012 Nov;26(11):1353-6. doi: 10.1002/bmc.2703. Epub 2012 Jan 30.
A selective and sensitive analytical method was developed for enantiomeric separation and determination of N-methyl-DL-aspartic acid (NMA). The method involved the conversion of each enantiomer into N-ethoxycarbonylated (S)-(+)-2-octyl ester derivative for the direct separation by gas chromatography-mass spectrometry (GC-MS). The diastereomeric derivatives showed characteristic mass spectral properties for analysis by selected ion monitoring mode (SIM) and enabling enantioseparation on an achiral capillary column. Two enantiomers were baseline separated, and the detection limits for N-methyl-L-aspartic acid (NMLA) and N-methyl-D-aspartic acid (NMDA) were 0.07 and 0.03 ng/g, respectively. When applied to rat brain tissues for absolute configuration of NMA, only NMDA was determined, while NMLA was monitored as lower than the limit of detection.
2. N-methyl-D-aspartic acid receptor activation downregulates expression of δ subunit-containing GABAA receptors in cultured hippocampal neurons
Suchitra Joshi, Jaideep Kapur Mol Pharmacol. 2013 Jul;84(1):1-11. doi: 10.1124/mol.112.084715. Epub 2013 Apr 12.
Neurosteroids are endogenous allosteric modulators of GABAA receptors (GABARs), and they enhance GABAR-mediated inhibition. However, GABARs expressed on hippocampal dentate granule neurons of epileptic animals are modified such that their neurosteroid sensitivity is reduced and δ subunit expression is diminished. We explored the molecular mechanisms triggering this GABAR plasticity. In the cultured hippocampal neurons, treatment with N-methyl-D-aspartic acid (NMDA) (10 μM) for 48 hours reduced the surface expression of δ and α4 subunits but did not increase the expression of γ2 subunits. The tonic current recorded from neurons in NMDA-treated cultures was reduced, and its neurosteroid modulation was also diminished. In contrast, synaptic inhibition and its modulation by neurosteroids were preserved in these neurons. The time course of NMDA's effects on surface and total δ subunit expression was distinct; shorter (6 hours) treatment decreased surface expression, whereas longer treatment reduced both surface and total expression. Dl-2-amino-5-phosphonopentanoic acid (APV) blocked NMDA's effects on δ subunit expression. Chelation of calcium ions by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetic acid tetrakis (acetoxymethyl ester) (BAPTA-AM) or blockade of extracellular signal-regulated kinase (ERK) 1/2 activation by UO126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio] butadiene) also prevented the effects of NMDA. Thus, prolonged activation of NMDA receptors in hippocampal neurons reduced GABAR δ subunit expression through Ca(2+) entry and at least in part by ERK1/2 activation.
3. N-methyl-D-aspartic acid-induced penile erection and yawning: role of hypothalamic paraventricular nitric oxide
M R Melis, S Succu, U Iannucci, A Argiolas Eur J Pharmacol. 1997 Jun 11;328(2-3):115-23. doi: 10.1016/s0014-2999(97)83037-3.
A dose of N-methyl-D-aspartic acid (NMDA, 50 ng) that induces penile erection and yawning when injected into the paraventricular nucleus of the hypothalamus, increased the concentration of NO2- from 1.10 +/- 0.28 microM to 7.32 +/- 1.12 microM and of NO3 from 4.96 +/- 0.69 microM to 10.5 +/- 1.61 microM in the paraventricular dialysate obtained from male rats by in vivo microdialysis. NO2- concentration was not increased by (+/-)-alpha-(amino)-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA, 100 ng) or by trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (ACPD) (100 ng), which were unable to induce these behavioral responses. N-Methyl-D-aspartic acid effect on NO2- concentration, penile erection and yawning was prevented by dizolcipine (MK-801) (10-100 ng) or by the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (20 microg), but not by the oxytocin receptor antagonist [d(CH2)5,Tyr(Me)2,Orn8]vasotocin (100 ng), or by the guanylate cyclase inhibitor methylene blue (20 microg) given in the paraventricular nucleus 15 min before N-methyl-D-aspartic acid or by the dopamine receptor antagonist haloperidol (0.5 mg/kg) given intraperitoneally 30 min before N-methyl-D-aspartic acid. In contrast, the nitric oxide scavenger hemoglobin (20 microg) given in the paraventricular nucleus prevented N-methyl-D-aspartic acid-induced NO2- concentration increase, but was unable to prevent penile erection and yawning. The results suggest that N-methyl-D-aspartic acid induces penile erection and yawning by increasing nitric oxide synthase activity in the paraventricular nucleus of the hypothalamus, possibly in the cell bodies of oxytocinergic neurons projecting to extra-hypothalamic brain areas and mediating these behavioral responses.
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