Methyldopa or Methyldopahydrazine as Levodopa Synergists

Fermaglich, Joseph; Chase, T N

doi:10.1016/s0140-6736(73)90586-2

Cited by 10 publications

(6 citation statements)

References 9 publications

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“…It should be mentioned that catechol groups are the chelating moieties of various siderophores and make up the main structure of catecholamines, which besides their physiological action as neurotransmitters [15] are of pharmacological use in such fields as the treatment of Parkinson's disease [16], hypertension [17] and breast cancer [18]. The stability of ferric complexes with catechol-type ligands has been widely studied [12,14,[16][17][18][19][20][21][22][23][24]. Nitro-catechol derivatives, which are inhibitors of catechol-O-methyltransferase, have been introduced in the treatment of Parkinson's disease.…”

Section: Introductionmentioning

confidence: 99%

Effect of substituents on complex stability aimed at designing new iron(III) and aluminum(III) chelators

Nurchi

Pivetta

Lachowicz

et al. 2009

Journal of Inorganic Biochemistry

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Section: Introductionmentioning

confidence: 99%

Effect of substituents on complex stability aimed at designing new iron(III) and aluminum(III) chelators

Nurchi

Pivetta

Lachowicz

et al. 2009

Journal of Inorganic Biochemistry

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“…The combination of benserazide and L ‐dopa is marketed under the brand name of Madopar. A number of studies showed the advantage of L ‐dopa combined with a peripheral decarboxylase inhibitor compared to L ‐dopa alone 65–72…”

Section: Steps Taken To Enhance the Effectiveness And Reduce The Advementioning

confidence: 99%

The history of dopamine and levodopa in the treatment of Parkinson's disease

2008

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The discoveries of dopamine as a neurotransmitter in the brain, its depletion in patients with Parkinson disease, and its replacement with levodopa therapy were major revolutionary events in the rise to effective therapy for patients with this disorder. This review describes these events and the persons who carried out these accomplishments. Their impact went beyond a single clinical entity of parkinsonism, for it opened up the beginning of a much better understanding of the role of dopamine in other neurologic movement disorders and also in many psychiatric diseases.

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“…Parkinson's disease (PD), a disease associated with dopamine deficiency in the brain, 1,2 has been treated by administration of levodopa (LD) since the late 1960s [3][4][5] and is currently co-administered with a peripheral decarboxylase inhibitor, such as carbidopa (CD), where advantage over LD alone has been demonstrated by numerous studies. [6][7][8][9][10][11][12][13] Compared to oral administration of LD/CD, stable exposure of LD/CD by infusion has demonstrated improved efficacy in managing PD symptoms. 14 This owes, at least in part, to the ability of an infusion to stay within the shrinking therapeutic window associated with advanced PD and avoid the LD troughs associated with "off" time motor symptoms as well as the LD peaks associated with "on" time with troublesome dyskinesia associated with orally administered LD.…”

Section: Introductionmentioning

confidence: 99%

Metabolite profiling of foslevodopa/foscarbidopa in plasma of healthy human participants by LC‐HRMS indicates no major differences compared to administration of levodopa/carbidopa intestinal gel

Savaryn,

Smith,

Rosebraugh

et al. 2024

Pharmacology Res & Perspec

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Analysis was conducted to compare levodopa/carbidopa pharmacokinetics and drug‐related material in plasma of healthy participants after receiving a continuous infusion of Levodopa/Carbidopa Intestinal Gel (LCIG) to a continuous subcutaneous infusion of foslevodopa/foscarbidopa. Study samples were from a randomized, open‐label, 2‐period crossover study in 20 healthy participants. Participants received either 24‐h foslevodopa/foscarbidopa SC infusion to the abdomen or LCIG delivered for 24 h to the jejunum through a nasogastric tube with jejunal extension. Serial blood samples were collected for PK. Comparability of the LD PK parameters between the two treatment regimens was determined. Selected plasma samples were pooled per treatment group and per time point for metabolite profiling. LC–MSn was performed using high‐resolution mass spectrometry to identify drug‐related material across the dosing regimens and time points. The LD PK parameter central values and 90% confidence intervals following the foslevodopa/foscarbidopa subcutaneous infusion were between 0.8 and 1.25 relative to the LCIG infusion. With LCIG administration, LD, CD, 3‐OMD, DHPA, DOPAC, and vanillacetic acid were identified in plasma at early and late time points (0.75 and 24 h); the metabolic profile after administration of foslevodopa/foscarbidopa demonstrated the same drug‐related compounds with the exception of the administered foslevodopa. 3‐OMD and vanillacetic acid levels increased over time in both treatment regimens. Relative quantification of LC–MS peak areas showed no major differences in the metabolite profiles. These results indicate that neither the addition of monophosphate prodrug moieties nor SC administration affects the circulating metabolite profile of foslevodopa/foscarbidopa compared to LCIG.

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Methyldopa or Methyldopahydrazine as Levodopa Synergists

Cited by 10 publications

References 9 publications

Effect of substituents on complex stability aimed at designing new iron(III) and aluminum(III) chelators

Effect of substituents on complex stability aimed at designing new iron(III) and aluminum(III) chelators

The history of dopamine and levodopa in the treatment of Parkinson's disease

Metabolite profiling of foslevodopa/foscarbidopa in plasma of healthy human participants by LC‐HRMS indicates no major differences compared to administration of levodopa/carbidopa intestinal gel

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