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• W1993722110 endingPage "23" @default.
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• W1993722110 abstract "The purpose of the study was to evaluate the inhibitory effect of the mucoadhesive polymers polycarbophil, chitosan and chitosan glutamate on trypsin and carboxypeptidase B (CPB) activity as well as their potential to improve the intestinal transport of the peptide drug 9-desglycinamide, 8-l-arginine vasopressin (DGAVP) in vitro. The degradation of the model substrates N-α-benzoyl-l-arginine ethylester by trypsin and hippuryl-l-arginine by CPB in the presence of the polymers was studied. Furthermore, the effect of the polymers on intestinal DGAVP transport was investigated using Caco-2 cell monolayers and the rat vertically perfused intestinal loop model. Uniquely, polycarbophil in a concentration of 1% (w/v) was able to inhibit both trypsin and CPB activities. Chitosan glutamate in concentrations of 0.4 and 1% (w/v) strongly increased the transport of DGAVP across Caco-2 cell monolayers, whereas 1% (w/v) polycarbophil showed only low transport enhancement. All polymers in concentrations of 1% (w/v), however, showed a pronounced and comparable improvement of DGAVP transport across intestinal mucosae in the vertically perfused loop model. It is concluded that the chitosans enhance the transport of DGAVP solely by increasing the paracellular permeability due to opening of intercellular junctions. The observed comparable transport effect of polycarbophil in the intestinal loop model is mainly ascribed to protection of DGAVP against proteolytic degradation in the intestinal lumen, which allows for sufficient concentration and thus transport of the peptide drug when polycarbophil induced paracellular transport is less enhanced." @default.
• W1993722110 created "2016-06-24" @default.
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• W1993722110 date "1997-03-01" @default.
• W1993722110 modified "2023-10-12" @default.
• W1993722110 title "Mucoadhesive polymers in peroral peptide drug delivery. IV. Polycarbophil and chitosan are potent enhancers of peptide transport across intestinal mucosae in vitro" @default.
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• W1993722110 doi "https://doi.org/10.1016/s0168-3659(96)01536-2" @default.
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