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Marki, F.1
Breitenstein, W.2
Beriger, E.3
Bernasconi, R.4
Caravatti, G.5
Francis, J.E.6
Paioni, R.7
Wehrli, H.U.8
Wiederkehr, R.9
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0028172301
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(a)
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(a) Tramposch, K. M.; Chilton, F. H.; Stanley, P. L.; Franson, R. C.; Havens, M. B.; Nettleton, D. O.; Davern, L. D.; Darling, I. M.; Bonney, R. J. J. Pharmacol. Expt. Therapeut. 1994, 271, 852.
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(1994)
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Tramposch, K.M.1
Chilton, F.H.2
Stanley, P.L.3
Franson, R.C.4
Havens, M.B.5
Nettleton, D.O.6
Davern, L.D.7
Darling, I.M.8
Bonney, R.J.9
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66
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0025790158
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(b)
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(b) Stanley, P. L.; Steiner, S.; Havens, M.; Tramposch, K. M. Skin Pharmacol. 1991, 4, 262.
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(1991)
Skin Pharmacol.
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Stanley, P.L.1
Steiner, S.2
Havens, M.3
Tramposch, K.M.4
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68
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0343468322
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note
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The compounds tested in the chronic inflammation in vivo assay (2, 4, 28, 36b, 36i) were not evaluated as potential inhibitors of MPO in a control experiment. Thus, the possibility exists that some (or all) of the in vivo activity reported for these compounds in the tables is a consequence of direct inhibition of the enzyme marker MPO rather than a reflection of reduced influx of neutrophils (PMNs). However, animals treated with compound 28 had significant, dose-dependent ear weight reductions that paralleled the measured reduction of myeloperoxidase activity. This implies that the drug is reducing general hyperplasia (and inflammation), and that it is not acting simply as a MPO inhibitor. Many other structurally similar (but non-biaryl) compounds were evaluated in the chronic assay for both ear weight reduction and inhibition of MPO activity. The compounds tested almost always displayed ear weight reductions that paralleled the measured reduction of myeloperoxidase activity.
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69
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0343032599
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note
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2), although other explanations are possible.
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