Drugs online research references
Anticancer Res. 2003 Jan-Feb;23(1A):231-4.
The effect of commonly used drugs on angiogenesis.
Sartippour MR, De Leon E, Rubio R, Brooks MN.
University of California, Los Angeles, Department of Surgery, Division of Oncology, Los Angeles, CA 90095, USA.
BACKGROUND: Within the last decade, there has been much interest in the area of tumor angiogenesis, with the advent of many new anti-angiogenic drugs undergoing testing in cancer clinical Phases II and III. Many of the cancer patients also take multiple medications for a variety of chronic illnesses. Because of possible drug-drug interactions, it is important to investigate the effect that commonly prescribed medications may have on angiogenesis. MATERIALS AND METHODS: In this pilot study, we assessed the effect of the following drugs on in vitro angiogenesis: atenolol, diltiazem, enalapril, disopyramide, mexiletine, coumadin, cimetidine and omeprazole. RESULTS & CONCLUSION: We observed that, although some of these drugs at massive doses inhibited endothelial proliferation, they did not affect in vitro angiogenesis at human therapeutic ranges.
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The electrochemical oxidations of lansoprazole and omeprazole have been studied at a carbon paste electrode by cyclic and differential-pulse voltammetry in Britton-Robinson buffer solutions (0.04 M; pH 6.0-10.0). The drug produced a single oxidation step. By differential-pulse voltammetry, a linear response was obtained in B-R buffer pH 6.0 in a concentration range from 2.0 x 10(-7) to 5.0 x 10(-5) M for lansoprazole or omeprazole. The detection limits were 1.0 x 10(-8) and 2.5 x 10(-8) M for lansoprazole and omeprazole, respectively. The method was successfully applied for the analysis of omeprazole and lansoprazole in capsules. The results were comparable to those obtained by spectrophotometry. Copyright 2003 Elsevier Science B.V.
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Eur J Clin Pharmacol. 2003 Jun;59(2):103-9. Epub 2003 Apr 09.
Bioactivation of cyclophosphamide: the role of polymorphic CYP2C enzymes.
Griskevicius L, Yasar U, Sandberg M, Hidestrand M, Eliasson E, Tybring G, Hassan M, Dahl ML.
Department of Medical Laboratory Sciences and Technology, Karolinska Institutet at Huddinge University Hospital, 14186 Stockholm, Sweden.
Several-fold differences have been observed among patients in the biotransformation of cyclophosphamide. The aim of this study was to investigate the contribution of CYP2C9 and CYP2C19 and their polymorphisms to the variability of cyclophosphamide activation. The formation of 4-hydroxycyclophosphamide was studied in microsomes from a total of 32 different genotyped human livers, as well as in yeast microsomes expressing different genetic variants of CYP2C9 and CYP2C19. The kinetic data obtained in the yeast system revealed that the intrinsic clearance (V(max)/K(m)) of cyclophosphamide by CYP2C9.2 and CYP2C9.3 samples was approximately threefold lower than that by CYP2C9.1. However, in liver microsomes, there were no statistically significant differences in the intrinsic clearance of 4-hydroxycyclophosphamide formation between the group of seven CYP2C9*1/*1 livers and the remaining nine with one or two variant CYP2C9 alleles ( P>0.7). We found a statistically significant correlation ( r(s)=0.65, P=0.003) between 4-hydroxylation of cyclophosphamide and 5'-hydroxylation of R-omeprazole, a measure of CYP2C19 activity in human liver microsomes ( n=19). No correlation was found between 4-hydroxylation of cyclophosphamide and the formation rate of hydroxycelecoxib, mainly catalysed by CYP2C9 ( r(s)=0.17, P=0.55, n=32). In conclusion, based on the correlation with the formation of R-5'-hydroxyomeprazole, CYP2C19 may partly contribute to the bioactivation of cyclophosphamide in human liver microsomes, while the role of CYP2C9 appears minor.
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