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Effects of Antithrombotic and Results of Drug Screening
Published in Josef Hladovec, Antithrombotic Drugs in Thrombosis Models, 2020
Many drugs have been shown (2.b in the listing above) to exert some effects on prostacyclin production, release and preservation but the relative importance of such findings is often questionable. Thus nafazatrom was reported to protect prostacyclin from oxidation, and prostacyclin effects were enhanced by suloctidil, anagrelide, and clofibrate. The first attempt to look for specific stimulators of prostacyclin release and synthesis was probably that of Boeynaems et al.378 (SKF 525-A, proadifen).
Pharmacokinetic-Pharmacodynamic Modeling in Drug Development: Comments and Applications
Published in Hartmut Derendorf, Günther Hochhaus, Handbook of Pharmacokinetic/Pharmacodynamic Correlation, 2019
Joseph C. Fleishaker, James J. Ferry
During phases I and II of drug development, the metabolic profile of the compound in man should be elucidated and related to the toxicology species tested. This is accomplished in part by administration of radiolabeled compound to normal volunteers, followed by metabolic profiling of various biological fluids. This allows the detection and isolation of major metabolites which may or may not contribute to the activity and toxicity of the compound. For adinazolam, these studies indicated that the major circulating species presented following the adinazolam were the parent compound and mono-N-demethyladinazolam (NDMAD).21,22 The question then became which compound(s) should be monitored in subsequent pharmacokinetic studies. This question was answered to some extent using receptor binding studies and in vivo pharmacology. Both adinazolam and N-demethyladinazolam bind to benzodiazepine receptors, with NDMAD having higher affinity (208 vs. 6.96 nM, respectively).23 In addition, the sedative effects seen after the administration of adinazolam were found to be decreased in rats when the metabolism of adinazolam was blocked by proadifen (SKF 525A).24 This suggested that it would be important to assess the kinetics of both compounds in man. However, the contribution of these compounds to the activity and side effects of adinazolam in man could not be predicted from these data.
Evaluation of an immunoassay procedure to measure 6-monoacetylmorphine
Published in Toxicology Mechanisms and Methods, 2020
Bernardino González-de-la-Presa, Rosa Fernández-Bonifacio, Esther Fernández-Galán, Lourdes Mares, Rebeca Muñoz, Marina Parra-Robert, Jordi To-Figueras
Drugs were extracted from urine by solid phase extraction (SPE) using Bond Elut Certify columns (Agilent Technologies). Elution of drugs was performed with a dichloromethane:isopropanol (80:20) solution with 2% ammonia. The extract was evaporated dry with nitrogen and derivatized with MBTFA (N-Methyl-bis-trifluoroacetamide) and N,O-bis(trimethylsilyl)trifluoroacetamide (BSTFA) with 1% trimethylchlorosilane (TMCS) (Supelco). The final extract was injected into GC-MS. Proadifen hydrochloride (Sigma, Fluka Analytical P1061) was used as internal standard.
Role of glucocorticoid- and monoamine-metabolizing enzymes in stress-related psychopathological processes
Published in Stress, 2020
Vadim Tseilikman, Eliyahu Dremencov, Olga Tseilikman, Michaela Pavlovicova, Lubica Lacinova, Daniela Jezova
Interaction between brain monoamine transmission and liver CYP activity is reciprocal. Complementary to central monoamine regulation of hepatic CYP, the hepatic CYP activity can influence brain monoamine neuron excitability. We have recently found that CYP inhibition by proadifen hydrochloride (SKF525) resulted in inhibition of spontaneous firing of 5-HT neurons in the rat dorsal raphe nucleus (Grinchii, Paliokha, Tseilikman, & Dremencov, 2018).