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  • 1
    Electronic Resource
    Electronic Resource
    The continuing development of proton pump inhibitors with particular reference to pantoprazole (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 9 (1995), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Inhibition of the gastric proton pump is gaining acceptance as the treatment of choice for severe gastrooesophageal reflux disease, and for treatment of duodenal and gastric ulceration. Three of these drugs are now available (omeprazole, lansoprazole and pantoprazole) and more are being developed. Proton pump inhibitors share the same core structure, but differ in terms of substituents on this core. The substitutions are able to modify some important chemical properties of the compounds. For example, pantoprazole is significantly more acid-stable than omeprazole or lansoprazole. E3810 is significantly less stable than the other compounds. We present an explanation for this finding that depends on the relative pK values for the pyridine and benzimidazole nitrogens, especially the former.Pantoprazole formulated in an enteric-coated tablet displays high bioavailability and linear pharmacokinetics whether on single or multiple dose regimens. Although all three proton pump inhibitors provide a similar chemical conversion to sulphenamides, which are highly reactive cysteine reagents, these reagents derivatize different cysteines in the extracytoplasmic or membrane domain of the pump and inhibit the pump at different rates.Whereas the differences in chemical reactivity can be explained by the solution chemistry of the compounds, selective derivatization of different cysteines on the protein argues for an involvement of pump structure in response to the presence of the proton pump inhibitor on its luminal surface. This suggests that the proton pump inhibitors, which were originally designed to take advantage of only the highly acidic space generated in the parietal cell by the production of the sulphenamide, are made even more selective by the protein they target.Pantoprazole is metabolized by a combination of phase I and phase II metabolism, and has also been shown to have a very low potential for drug interaction. Studies of acid secretion in man have shown this compound to be an effective and long lasting inhibitor of acid secretion. The pharmacodynamics explain the cumulative effect of repeated doses and maximal acid secretory capacity with a once daily dosage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.1995.tb00394.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Stimulation by McN-A-343 and blockade by telenzepine of acid secretion in the mouse isolated stomach at histamine-liberating cells (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 68-75 
    Details
    ISSN: 1432-1912
    Keywords: Antimuscarinics ; Gastric acid secretion ; Mouse isolated stomach ; Telenzepine ; McN-A-343 ; Histamine release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary (1) In the lumen-perfused mouse stomach in vitro, potential sites of gastric antisecretory action of the muscarine M1-receptor antagonist telenzepine were investigated. Acid secretion was stimulated by the muscarinic agonist McN-A-343 (1–1000 μmol/l). Neither basal nor McN-A343-stimulated acid secretion was affected by 1 μmol/l TTX indicating that neuronal structures were probably not involved. (2) Acid secretion stimulated by 10 μmol/l McNA-343 was inhibited by telenzepine (0.1-1.4 μmol/l) and cimetidine (10–140 μmol/l). Neither of the antagonists affected basal acid secretion. TTX had no inhibitory influence on the antagonist effect of telenzepine and cimetidine. (3) Compound 48/80 (100 pmol/l), which depletes histamine stores, initially mimicked but subsequently prevented the effect of McN-A-343. Prenylamine (50 μmol/l), which prevents histamine release, also abolished the secretagogue effect of subsequently administered McN-A-343. (4) Up to concentrations greater than 100 μmol/l, McN-A-343 did not stimulate acid production in rabbit isolated fundic glands and guinea-pig isolated parietal cells. Thus, parietal cells are not directly stimulated by McN-A-343. (5) Based on the site of action of the agonist McN-A-343 in the mouse isolated stomach and its failure to stimulate parietal cells from different species directly, it is concluded that telenzepine blocks, in the mouse isolated stomach, muscarine receptors located on paracrine cells to reduce endogenous histamine release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169209
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    Paper (German National Licenses)
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