Publications by authors named "O V Ardashov"
Monoamine oxidase B (MAO-B) inhibitors are widely used as part of combination drug therapy for Parkinson's disease. As demonstrated in both in vitro and in vivo experiments, the monoterpenoid Prottremine and some of its derivatives exhibit high antiparkinsonian activity. In this study, the inhibitory activity of Prottremine and its derivatives (including 14 new 9-- and -derivatives) against MAO-A and MAO-B enzymes has been investigated for the first time.
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- The novel antiparkinsonian agent PA-96 shows promise in supporting dopamine neuron survival and alleviating motor deficits in Parkinson's disease models.
- A validated HPLC-MS/MS method was used to investigate the pharmacokinetics of PA-96 in mice, analyzing both oral and intravenous administration at various doses.
- Bioavailability of PA-96 was approximately 7% for a 5 mg/kg dose and 35% for a 10 mg/kg dose, with pharmacokinetic variations potentially linked to saturation of enzyme or receptor binding sites.
Article Synopsis
- - Two methods for creating -menthene epoxide ((1,5,6)) are explored: one uses chlorohydrin with NaH in THF, and the other combines diacetate with sodium-butoxide.
- - A proposed mechanism addresses unexpected results in how the epoxide is formed concerning regio- and stereospecificity.
- - The epoxide ring can be opened by different nucleophiles to produce various derivatives of Prottremine, which has been noted for its potential benefits in treating Parkinson's disease.
Parkinson's disease is the second most common neurodegenerative disease. Unfortunately, there is still no definitive disease-modifying therapy. In our work, the antiparkinsonian potential of trans-epoxide (1S,2S,3R,4S,6R)-1-methyl-4-(prop-1-en-2-yl)-7-oxabicyclo [4.
View Article and Find Full Text PDFParkinson's disease (PD) is the most common age-related movement disorder characterized by the progressive loss of nigrostriatal dopaminergic neurons. To date, PD treatment strategies are mostly based on dopamine replacement medicines, which can alleviate motor symptoms but do not slow down the progression of neurodegeneration. Thus, there is a need for disease-modifying PD therapies.
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