Sensitive Determination of Moxifloxacin HCl in Pharmaceuticals or Human Plasma Using Luminescence or Eye Vision

A new probe based on the complex of 1,2 dihydro-2-oxoquinoloine-4-carboxylic acid (DOCA) as a ligand with Europium (III) ion was developed for the quantitation of Moxifloxacin HCl (Moxi.HCl) in pharmaceuticals and human plasma using a luminescence method. The metal to ligand ratio of the complex is 1:2 as determined by a Job plot. The determination of Moxi.HCl is based on static quenching of the luminescence of the probe upon coordination of Moxi.HCl. The negative value for ΔG proves that this reaction is spontaneous. The calibration curve was constructed based on a Stern–Volmer equation and the quantitation range was 0.05–80 µg mL−1. This is low enough to determine the drug in blood plasma, even hours after administration, which is not feasible with the methods published so far. The LOD was 15 ng mL−1. The accuracy of the method was demonstrated by good recoveries of spiking experiments in tablets, ophthalmic eyedrops and human blood plasma, where the mean recovery was 99% with RSDs below 5%. The method was validated by closely matching concentrations of the drug found in all these real samples by HPLC. Additionally, Moxi.HCl can be assessed semi-quantitatively by eye vision upon excitation with a UV lamp at 365 nm by a gradual color shift from red to blue with increasing concentrations of Moxi.HCl

K-Shell Photoabsorption Studies of the Carbon Isonuclear Sequence

K-shell photoabsorption cross sections for the isonuclear C I - C IV ions have been computed using the R-matrix method. Above the K-shell threshold, the present results are in good agreement with the independent-particle results of Reilman & Manson (1979). Below threshold, we also compute the strong 1s -> np absorption resonances with the inclusion of important spectator Auger broadening effects. For the lowest 1s -> 2p, 3p resonances, comparisons to available C II, C III, and C IV experimental results show good agreement in general for the resonance strengths and positions, but unexplained discrepancies exist. Our results also provide detailed information on the C I K-shell photoabsorption cross section including the strong resonance features, since very limited laboratory experimental data exist. The resultant R-matrix cross sections are then used to model the Chandra X-ray absorption spectrum of the blazar Mkn 421

The atypical anxiolytic drug, tofisopam, selectively blocks phosphodiesterase isoenzymes and is active in the mouse model of negative symptoms of psychosis

Tofisopam is a member of the 2,3-benzodiazepine compound family which is marketed for the treatment of anxiety in some European countries. In contrast to classical 1,4-benzodiazepines, the compound does not bind to the benzodiazepine binding site of the γ-aminobutyric acid receptor and its psychopharmacological profile differs from such compounds. In addition to anxiolytic properties, antipsychotic effects are reported. We now show that tofisopam, 50 mg/kg intraperitoneally (i.p.), administered in parallel to repeated doses of dizocilpine 0.2 mg/kg i.p. can ameliorate dizocilpine-induced prolongation of immobility, which is considered to be a model of negative symptoms of psychosis. We further show that tofisopam acts as an isoenzyme-selective inhibitor of phosphodiesterases (PDEs) with highest affinity to PDE-4A1 (0.42 μM) followed by PDE-10A1 (0.92 μM), PDE-3 (1.98 μM) and PDE-2A3 (2.11 μM). The data indicate that tofisopam is an interesting candidate for the adjuvant treatment of psychosis with focus on negative symptoms. Combined partial inhibition of PDE-4 and PDE-10 as well as PDE-2 may be the underlying mechanism to this activity. Due to the good safety profile of tofisopam as evident from long-term use of this agent in patients, it may be concluded that dual or triple inhibition of PDE isoenzymes with additive or synergistic effects may be an interesting approach to pharmacological activity, resulting in active compounds with beneficial safety profile. Dose-limiting side effects such as emesis induced by selective inhibition of PDE-4 may be prevented by such strategies