Drugs online research references
Antimicrob Agents Chemother. 1995 Feb;39(2):567-70.
Inhibitory action of lansoprazole and its analogs against Helicobacter pylori: inhibition of growth is not related to inhibition of urease.
Nagata K, Takagi E, Tsuda M, Nakazawa T, Satoh H, Nakao M, Okamura H, Tamura T.
Department of Bacteriology, Hyogo College of Medicine, Japan.
The proton pump inhibitors omeprazole and lansoprazole and its acid-activated derivative AG-2000, which are potent and specific inhibitors of urease of Helicobacter pylori (K. Nagata, H. Satoh, T. Iwahi, T. Shimoyama, and T. Tamura, Antimicrob. Agents Chemother. 37:769-774, 1993), inhibited the growth of H. pylori. The growth was inhibited not only in urease-positive clinical isolates but also in their urease-negative derivatives which had no urease polypeptides. AG-1789, a derivative of lansoprazole with no inhibitory activity against H. pylori urease, also inhibited the growth of both strains even more strongly than the urease inhibitors lansoprazole and AG-2000. Furthermore, the antibacterial activity of omeprazole and lansoprazole was not affected by glutathione or dithiothreitol, which completely abolished the inhibitory activity of lansoprazole against H. pylori urease. These results indicated that the inhibitory action of these compounds against the growth of H. pylori was independent from the inhibitory action against urease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7726537&dopt=Abstract
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unisi.it
Lansoprazole is a gastric parietal cell proton pump inhibitor that is also active against Helicobacter pylori in vitro. We aimed to investigate further the mechanism of its antimicrobial effect. The antimicrobial activity of lansoprazole and of its sulfenamide, a rearrangement product occurring spontaneously in acid environments, was studied by determining the MICs and MBCs for 11 cytotoxic and eight non-cytotoxic H. pylori strains and by measuring the rapidity of bacterial killing. The MIC90 and MBC90 were 2.5 mg/L and 10 mg/L, respectively, both for lansoprazole and for its sulfenamide. Cytotoxic strains were as susceptible as non-cytotoxic strains. The sulfenamide exhibited faster bactericidal activity. Lansoprazole did not inhibit the toxin-induced vacuolization of HeLa cells by a cytotoxic strain, hence its anti-H. pylori activity does not depend on inhibition of a v-ATPase-mediated, toxin-induced activity. Sulfenamide formation is likely to occur in vivo in the gastric environment, thus enhancing the bactericidal activity of the drug. Lansoprazole is likely to be useful, in association with antibiotics, in the treatment of H. pylori infection regardless of the cytotoxicity of the infecting strain.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9184356&dopt=Abstract
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J Pharm Biomed Anal. 1999 Jul;20(3):599-606.
Determination of Lansoprazole in pharmaceutical dosage forms by two different spectroscopic methods.
Ozaltin N.
Department of Analytical Chemistry, Faculty of Pharmacy, Hacettepe University, Ankara, Turkey.
Two different ultraviolet (UV) spectroscopic methods were developed for determination of Lansoprazole in pharmaceutical dosage forms. The solutions of the standard and the sample were prepared in 0.1 M NaOH and phosphate buffer pH 6.6. Both UV spectrophotometric and derivative spectroscopic techniques were applied. Second-order derivative spectra were generated between 200 and 400 nm at N = 9, deltalambda = 31.5. The linear range for the UV spectrophotometric method was 3.0-25.0 microg ml(-1) and that for the derivative spectroscopic method was 0.5-25.0 microg ml(-1). The developed methods were applied to three different pharmaceutical preparations. The percentage recovery was 100.2%.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10701978&dopt=Abstract
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