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63302-01-2

63302-01-2 Structure

63302-01-2 Structure
IdentificationBack Directory
[Name]

L-Tyrosine, 3-hydroxy-, monosodium salt (9CI)
[CAS]

63302-01-2
[Synonyms]

Levodopa sodium
L-Tyrosine, 3-hydroxy-, monosodium salt (9CI)
[Molecular Formula]

C9H12NNaO4
[MOL File]

63302-01-2.mol
[Molecular Weight]

221.19
Hazard InformationBack Directory
[Description]

Levodopa is the naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE.
[Uses]

L-DOPA (Levodopa) sodium is an orally active metabolic precursor of neurotransmitters dopamine. L-DOPA sodium can cross the blood-brain barrier and is converted into dopamine in the brain. L-DOPA sodium has anti-allodynic effects, and can be used for Parkinson's disease research[1][2][3].
[in vitro]

SH-SY5Y cells were treated with CA (carnosic acid) for 18 h, and then co-treated with 400 μM L-dopa for the indicated time points. The results showed that pretreatment of CA attenuated the cell death and nuclear condensation induced by L-dopa. In conclusion, CA ameliorates the development of LID via regulating the D1R signaling and prevents L-dopa-induced apoptotic cell death through modulating the ERK1/2-c-Jun and inducing the parkin._x000D_ _x000D_ Reference: Front Pharmacol. 2021 Aug 9;12:703894. https://pubmed.ncbi.nlm.nih.gov/34434108/
[in vivo]

These results confirm previous findings that rotenone-induced motor and non-motor problems were alleviated by the Active diet (AD). Levodopa showed an additive beneficial effect on rotarod performance in rotenone-treated mice fed with the AD._x000D_ _x000D_ Reference: Front Aging Neurosci. 2018 Aug 3;10:237. https://pubmed.ncbi.nlm.nih.gov/30127735/
[target]

L-DOPA (Levodopa) sodium is an orally active metabolic precursor of neurotransmitters dopamine.
[IC 50]

Human Endogenous Metabolite
[References]

[1] Hyland K, et al. Aromatic L-amino acid decarboxylase deficiency: diagnostic methodology. Clin Chem. 1992 Dec;38(12):2405-10. PMID:1281049
[2] Merims D, et al. Dopamine dysregulation syndrome, addiction and behavioral changes in Parkinson's disease. Parkinsonism Relat Disord. 2008;14(4):273-80. Epub 2007 Nov 7. DOI:10.1016/j.parkreldis.2007.09.007
[3] Perez-Pardo P, et al. Additive Effects of Levodopa and a Neurorestorative Diet in a Mouse Model of Parkinson's Disease. Front Aging Neurosci. 2018 Aug 3;10:237. DOI:10.3389/fnagi.2018.00237
[4] Park HJ, et al. Anti-allodynic effects of levodopa in neuropathic rats. Yonsei Med J. 2013 Mar 1;54(2):330-5. DOI:10.3349/ymj.2013.54.2.330
[5] M Lundblad, et al. Pharmacological validation of a mouse model of l-DOPA-induced dyskinesia. Exp Neurol. 2005 Jul;194(1):66-75. DOI:10.1016/j.expneurol.2005.02.002
[6] Jie Zhang, et al. Pharmacokinetics of L-dopa in plasma and extracellular fluid of striatum in common marmosets. Brain Res. 2003 Dec 12;993(1-2):54-8. DOI:10.1016/j.brainres.2003.08.065
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