3,4-Dihydroxy-L-phenylalanine methyl ester hydrochloride (BAT-006770)
* For research use only

3,4-Dihydroxy-L-phenylalanine methyl ester hydrochloride is a selective Dopamine D1 receptor agonist (1,2,3).

Category
L-Amino Acids
Catalog number
BAT-006770
CAS number
1421-65-4
Molecular Formula
C10H14ClNO4
Molecular Weight
247.68
3,4-Dihydroxy-L-phenylalanine methyl ester hydrochloride
Synonyms
H-Phe{3,4-(OH)2}-OMe HCl; H-Tyr(3-OH)-OMe HCl; 3-Hydroxy-L-tyrosine methyl ester hydrochloride
Appearance
White Solid
Purity
98%
Density
1.322g/cm3
Melting Point
163-165 °C
Boiling Point
384.4°C at 760 mmHg
Storage
Store at -20°C, (under N2)
InChI
InChI=1S/C10H13NO4.ClH/c1-15-10(14)7(11)4-6-2-3-8(12)9(13)5-6;/h2-3,5,7,12-13H,4,11H2,1H3;1H/t7-;/m0./s1
InChI Key
WFGNJLMSYIJWII-FJXQXJEOSA-N
Canonical SMILES
COC(=O)C(CC1=CC(=C(C=C1)O)O)N.Cl
1.Design and evaluation of levodopa methyl ester intranasal delivery systems.
Chun IK1, Lee YH, Lee KE, Gwak HS. J Parkinsons Dis. 2011;1(1):101-7. doi: 10.3233/JPD-2011-10011.
OBJECTIVES: This study aimed to examine the feasibility of nasal powder formulations for the delivery of levodopa (L-dopa) into the brain using highly water-soluble levodopa methyl ester hydrochloride (LDME).
2.Antiparkinsonian effects of remacemide hydrochloride, a glutamate antagonist, in rodent and primate models of Parkinson's disease.
Greenamyre JT1, Eller RV, Zhang Z, Ovadia A, Kurlan R, Gash DM. Ann Neurol. 1994 Jun;35(6):655-61.
Loss of dopaminergic innervation of the striatum results in overactivity of the glutamatergic pathways from the subthalamic nucleus to the internal segment of the globus pallidus and the substantia nigra pars reticulata, the output nuclei of the basal ganglia. Previous work has shown that local blockade of glutamate receptors in the internal segment of the globus pallidus or substantia nigra pars reticulata leads to marked suppression of parkinsonian signs. We have now examined whether systemic administration of a glutamate receptor antagonist has antiparkinsonian effects in rodent and primate models of Parkinson's disease. Remacemide hydrochloride is an anticonvulsant, neuroprotective compound with antagonist activity at the N-methyl-D-aspartate receptor ion channel. In normal rats and monoamine-depleted rats, remacemide hydrochloride did not cause locomotor hyperactivity, unlike MK-801. When monoamine-depleted rats were treated with a subthreshold dose of levodopa methylester, remacemide hydrochloride (5-40 mg/kg, orally) caused a dose-dependent increase in locomotor activity.
3.Pharmacokinetic evaluation of formulated levodopa methyl ester nasal delivery systems.
Lee YH1, Kim KH, Yoon IK, Lee KE, Chun IK, Rhie JY, Gwak HS. Eur J Drug Metab Pharmacokinet. 2014 Dec;39(4):237-42. doi: 10.1007/s13318-013-0171-8. Epub 2013 Dec 21.
The objective of this study was to investigate the pharmacokinetic characteristics of levodopa (L-dopa) from nasal powder formulations using highly water-soluble levodopa methyl ester hydrochloride (LDME). In vivo pharmacokinetic studies were carried out with formulated LDME nasal powders. After oral and intravenous administration of L-dopa and carbidopa and intranasal administration LDME to the rat, L-dopa concentrations were determined in plasma and the brain using high-performance liquid chromatography. The absolute bioavailabilities of nasal preparations with and without Carbopol were 82.4 and 66.7 %, respectively, which were much higher than that of oral delivery (16.2 %). The drug-targeting efficiencies [area under the curve (AUC) in brain/AUC in plasma] of L-dopa in the nasal formulations (0.98-1.08) were much higher than that of oral preparation (0.69). These results suggest that LDME nasal powder formulations would be useful delivery systems of L-dopa to the brain.
4.Striatal inhibition of PKA prevents levodopa-induced behavioural and molecular changes in the hemiparkinsonian rat.
Lebel M1, Chagniel L, Bureau G, Cyr M. Neurobiol Dis. 2010 Apr;38(1):59-67. doi: 10.1016/j.nbd.2009.12.027. Epub 2010 Jan 11.
l-3,4-dihydroxyphenylalanine methyl ester hydrochloride (l-DOPA) is the gold standard for symptomatic treatment of Parkinson's disease (PD), but long-term therapy is associated with the emergence of abnormal involuntary movements (AIMS) known as l-DOPA-induced dyskinesias (LID). The molecular changes underlying LID are not completely understood. Using the 6-hydroxydopamine-lesioned rat model of PD, we showed that l-DOPA elicits profound alterations in the activity of three LID molecular markers, namely DeltaFosB, dopamine, cAMP-regulated phosphoprotein of 32 kDa (DARPP-32) and extracellular signal-regulated kinases 1 and 2 (ERK1/2), as well as in phosphorylation levels of the cytoskeletal-associated protein tau. These modifications are triggered by protein kinase A (PKA) activation and intermittent stimulation of dopamine receptors as they are totally prevented by intrastriatal injections of Rp-cAMPS, a PKA inhibitor, or by continuous administration of l-DOPA via subcutaneous mini-pump.
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