Molecular Weight(MW): 197.19
Levodopa is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), used to treat Parkinson's symptoms.
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(A) A focused screening of Aβ generation in response to levodopa, piribedil, bromocriptine or carbidopa at indicated concentrations in SK-N-SH cells. Data are mean ± s.e.m., n = 3-4. *p < 0.05; ***p < 0.001 versus the control of each group.
PLoS ONE, 12(3), e0173240. Levodopa purchased from Selleck.
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|Description||Levodopa is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), used to treat Parkinson's symptoms.|
Levodopa produces at 25-200 μM concentrations a dose-dependent reduction of 3H-DA uptake in foetal rat midbrain cultures. Levodopa results in a decrease in the number of viable cells and tyrosine hydroxylase (TH) positive neurones, plus disruption of the overall neuritic network.  Levodopa induces dyskinesia in the absence of dopamine by excessive inhibition of neurons of the putamen-globus pallidus (GPe) projection and subsequent disinhibition of the globus pallidus (GPe). Levodopa results in a decrease in cytochrome oxidase messenger RNA expression in the globus pallidus (GPi). 
|In vivo||Levodopa elicits the development of a variety of abnormal movements in monkeys with parkinsonism induced by the neurotoxin MPTP. Levodopa administrations result in an ectopic induction of the dopamine D3receptor expression in the CdPu in 6-OHDA-lesioned rats.  Levodopa (50 mg/kg) increases anandamide concentrations throughout thebasal ganglia via activation of dopamine D1/D2 receptors in intact rats. Levodopa produces increasingly severe oro-lingual involuntary movements which are attenuated by the cannabinoid agonist R(+)-WIN55,212-2 (1 mg/kg) in lesioned rats.  Levodopa administration reverses the up-regulation of D2 dopamine receptors seen in severely lesioned rats provided evidence that Levodopa reaches a biologically active concentration at the basal ganglia. |
-  Mena MA, et al. Neuroreport, 1993, 4(4), 438-440.
-  Garcia-Effron G, et al. J Antimicrob Chemother, 2004, 53(6), 1086-1089.
-  Bordet R, et al. Proc Natl Acad Sci U S A, 1997, 94(7), 3363-3367.
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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT00089622||Completed||Parkinson Disease||National Institute of Neurological Disorders and Stroke (NINDS)|National Institutes of Health Clinical Center (CC)||August 4, 2004||Phase 2|
|NCT00086294||Completed||Parkinsons Disease|Dyskinesias||National Institute of Neurological Disorders and Stroke (NINDS)|National Institutes of Health Clinical Center (CC)||June 25, 2004||Phase 2|
|NCT02873351||Not yet recruiting||Age-related Macular Degeneration||Snyder, Robert W., M.D., Ph.D., P.C.||September 2018||Phase 2|
|NCT03023059||Not yet recruiting||Age-related Macular Degeneration||Snyder, Robert W., M.D., Ph.D., P.C.||March 2017||Phase 2|
|NCT03022318||Not yet recruiting||Age-related Macular Degeneration||Snyder, Robert W., M.D., Ph.D., P.C.||March 2017||Phase 2|
|NCT03000569||Recruiting||Parkinson Disease||Sage Therapeutics||December 2016||Phase 2|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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