PubMed · 10434482
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J E Dunne. 1999. Buspirone in ODD.. https://doi.org/10.1097/00004583-199908000-00006
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Quantitative and molecular analysis have been performed on two main polymorphs of buspirone hydrochloride (BUS-HCl). Quantitative analysis of solid-state composition of pharmaceutical powders is necessary to ensure safety and efficacy of drug substance and to validate the production processes. In this study, X-ray powder diffraction and differential scanning calorimetry have been used for the quantitative analysis of two polymorphic forms of BUS-HCl. In addition, single crystal X-ray study of Form 1 revealed its crystal structure, however, a similar study on Form 2 was not possible due to the difficulties encountered in producing it. Molecular analysis including partial charge analysis has been performed by using Gaussian simulation package to find the electro-negativity pattern in molecule. 1H and 13C solid-state NMR spectra of polymorphs were recorded and also regression equations and QM theory were developed to predict the 1H and 13C NMR spectra through the use of atomic environmental descriptors. The NMR differences between the two polymorphs were discussed by using prediction and experimental results and description of each NMR shift for carbon and hydrogen atoms.
A sensitive HPLC-tandem mass spectrometry method was developed for determination of buspirone levels in human plasma. After solid phase extraction and reversed phase HPLC separation, detection of buspirone and the internal standard (prazosin) was performed using eletrospray ionization and selected reaction monitoring in the positive ion mode. Linear calibration curves were established over a concentration range of 0.025-2.5 ng/ml when 0.5 ml aliquots of plasma were used. Satisfactory results of within-day precision (RSD of 1.9-7.7%) and accuracy (% difference of 0.5-6.6%) and between-day precision (RSD of 3.7-11.1%) and accuracy (% difference of 2.2-6.8%) were obtained. The assay has been successfully applied to the analysis of buspirone levels in more than 500 human plasma samples collected from a drug interaction study.
Effective, pharmacologic approaches to the treatment of cerebellar ataxia are lacking or inadequate. We recently reported preliminary evidence that tandospirone citrate (tandospirone), a 5-HT1A agonist, improved cerebellar ataxia in patients with Machado-Joseph disease (MJD). In the course of that study, we found that such treatment also alleviated the pain associated with cold sensations in the legs, insomnia, anorexia, and depression, all of which are thought to be mediated through activation of the 5-HT1A receptor. In this paper, we reviewed the few published clinical trials that involved the use of 5-HT1A receptor agonists for the treatment of cerebellar ataxia, and discussed the current theories regarding their mechanism of action. Cortical cerebellar atrophy (CCA) was reported, in a double-blind study, to be amenable to treatment with tandospirone. Other types of spinocerebellar degeneration (SCD) i.e., olivopontocerebellar atrophy (OPCA) and Machado-Joseph disease (MJD) have also been reported to respond to the drug, but these have been small studies. Responsive patients exhibited only mild ataxia. The doses of 5-HT1A agonists that have been used successfully ranged from 12.5 mg/day to 60 mg/day (or 1 mg/kg), and were well tolerated by most patients.