D-Aspartic acid dimethyl ester hydrochloride
Need Assistance?
  • US & Canada:
    +
  • UK: +

D-Aspartic acid dimethyl ester hydrochloride

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

Category
D-Amino Acids
Catalog number
BAT-003481
CAS number
69630-50-8
Molecular Formula
C6H11NO4·HCl
Molecular Weight
197.66
D-Aspartic acid dimethyl ester hydrochloride
IUPAC Name
dimethyl (2R)-2-aminobutanedioate;hydrochloride
Synonyms
D-Asp(OMe)-OMe HCl
Appearance
White to off-white powder
Purity
≥ 99% (HPLC)
Melting Point
114-119 °C
Storage
Store at 2-8°C
InChI
InChI=1S/C6H11NO4.ClH/c1-10-5(8)3-4(7)6(9)11-2;/h4H,3,7H2,1-2H3;1H/t4-;/m1./s1
InChI Key
PNLXWGDXZOYUKB-PGMHMLKASA-N
Canonical SMILES
COC(=O)CC(C(=O)OC)N.Cl
1. Effects of dibenzylbutyrolactone lignans arctigenin and trachelogenin on the motility of isolated rat ileum
Peter Kiplang'at Koech, Imre Boldizsár, Arpád Dobolyi, Petra Varró Toxicol Rep. 2022 May 27;9:1222-1232. doi: 10.1016/j.toxrep.2022.05.019. eCollection 2022.
Dibenzylbutyrolactone-type lignans are phenolic compounds of medical importance. The purpose of the study was to determine the effects of two such lignans, arctigenin and trachelogenin on the motility of isolated rat ileum and obtain indications on their mechanism of action. They were isolated from Arctium lappa and Cirsium arvense, respectively, which have been used traditionally to treat gastrointestinal disorders. 1-1.5 cm long segments of distal ileum were obtained from adult male Wistar rats. The intestinal segments were suspended vertically in a well-aerated organ-bath according to Magnus mounting method. The intestinal motility was monitored for 30 min before treatment to obtain the baseline, followed by treatment with 1 µM, 10 µM, 20 µM and 40 µM concentrations of arctigenin and 0.5 µM, 1 µM, 10 µM and 20 µM of trachelogenin concentrations. The amplitude, tone, and period of spontaneous contractions were measured after 15 and 30 min of treatment. To investigate their mechanism of action, cholinergic, glutamatergic, adrenergic antagonists and compounds inhibiting nitric oxide synthase and L-type calcium channels were also tested. Arctigenin and trachelogenin decreased the frequency of contractions in a dose-dependent manner. At the concentration of 20 µM and 40 µM of trachelogenin and arctigenin, respectively, there was a marked alteration in spontaneous contraction pattern with an observable increase in the period time. This activity was comparable to 0.5 µM nifedipine (L-type calcium channel blocker) treatment. Our results demonstrate relaxant effect of arctigenin and trachelogenin on the ileum motility that may be mediated by L-type calcium ion channel blockade.
2. Effects of onopordia, a novel isolated compound from Onopordon acanthium, on pentylenetetrazole-induced seizures in mice: Possible involvement of nitric oxide pathway
Malihe Hassanzadeh, Niusha Sharifi, Shabnam Mahernia, Nastaran Rahimi, Ahmad Reza Dehpour, Massoud Amanlou J Tradit Complement Med. 2019 Nov 30;11(1):22-26. doi: 10.1016/j.jtcme.2019.11.005. eCollection 2021 Jan.
Epilepsy is identified as a brain disorder and characterized by unpredictable disruption of normal brain function. Due to adverse side effect associated with antiepileptic drugs and also resistance profile, improvement of antiepileptic medications with more beneficial anticonvulsant activity is essential. Natural products have demonstrated their therapeutic properties such as anxiolytic, antidepressant and anticonvulsant activities and a source for identification of novel lead compounds. Therefore, the purpose of this study was to evaluate the effects of Onopordon acanthium secondary metabolite, onopordia, on pentylenetetrazole (PTZ)-induced seizure in male mice and investigate the possible role of nitric oxide pathway. Different doses of onopordia (0.1, 1 and 10 mg/kg) and phenobarbital (20 mg/kg) were administered intraperitoneally (i.p., 30, 60 and 120 min) prior to induction of epileptic seizure and compared to control groups. Onopordia demonstrated anticonvulsant effects when administrated at dose of 10 mg/kg, i.p. and optimum time 60 min prior to induction of seizure. Anticonvulsant effect of onopordia was blocked by applying a single dose of a non-selective nitric oxide synthase (NOS) inhibitor, Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME; 10 mg/kg, i.p.), and also a single dose of a selective neuronal NOS (nNOS) inhibitor, 7-nitroindazole (7-NI; 30 mg/kg, i.p.). Administration of ketamine as a N-Methyl-d-aspartic acid (NMDA) receptor antagonist (0.5 mg/kg; i.p.) with onopordia did not change the anticonvulsant effect of onopordia. The results of the present study demonstrated the anticonvulsant effect of onopordia as a new lead compound and also contribution of NO/nNOS pathway on PTZ-induced seizure in mice.
3. Subanesthetic doses of ketamine transiently decrease serotonin transporter activity: a PET study in conscious monkeys
Shigeyuki Yamamoto, Hiroyuki Ohba, Shingo Nishiyama, Norihiro Harada, Takeharu Kakiuchi, Hideo Tsukada, Edward F Domino Neuropsychopharmacology. 2013 Dec;38(13):2666-74. doi: 10.1038/npp.2013.176. Epub 2013 Jul 24.
Subanesthetic doses of ketamine, an N-methyl-D-aspartic acid (NMDA) antagonist, have a rapid antidepressant effect which lasts for up to 2 weeks. However, the neurobiological mechanism regarding this effect remains unclear. In the present study, the effects of subanesthetic doses of ketamine on serotonergic systems in conscious monkey brain were investigated. Five young monkeys underwent four positron emission tomography measurements with [(11)C]-3-amino-4-(2-dimethylaminomethyl-phenylsulfanyl)benzonitrile ([(11)C]DASB) for the serotonin transporter (SERT), during and after intravenous infusion of vehicle or ketamine hydrochloride in a dose of 0.5 or 1.5 mg/kg for 40 min, and 24 h post infusion. Global reduction of [(11)C]DASB binding to SERT was observed during ketamine infusion in a dose-dependent manner, but not 24 h later. The effect of ketamine on the serotonin 1A receptor (5-HT1A-R) and dopamine transporter (DAT) was also investigated in the same subjects studied with [(11)C]DASB. No significant changes were observed in either 5-HT1A-R or DAT binding after ketamine infusion. Microdialysis analysis indicated that ketamine infusion transiently increased serotonin levels in the extracellular fluid of the prefrontal cortex. The present study demonstrates that subanesthetic ketamine selectively enhanced serotonergic transmission by inhibition of SERT activity. This action coexists with the rapid antidepressant effect of subanesthetic doses of ketamine. Further studies are needed to investigate whether the transient combination of SERT and NMDA reception inhibition enhances each other's antidepressant actions.
Online Inquiry
Verification code
Inquiry Basket