13.
Bruni A. T., Ferreira M. M. C.,  “Omeprazole and analogue compounds: a case study”. Bournemouth, United Kingdom, 08-13/09/2002: 14th European Symposium on QSAR: Designing Drugs and Crop Protectants - processes, problems and solutions, Proceedings, Session 3 Posters, Eds. M. Ford, D. Livingstone, J. Dearden, H. Van de Waterbeemd, Blackwell Publishing Ltd., Oxford, UK, pp. 164-166 (2003).
[Extended Abstract. More information about the meeting see at Notes.]

Abstract (from the Book of Abstracts).
Omeprazole is a substituted benzimidazole and it presents an optically active center with the sulfur of the sulfoxide group being the chiral center. It is a pro-drug which can be easily converted into its respective sulfenamide at low pH. Figure 1 shows the decomposition reaction of omeprazole (1) to sulfenamide (4). Omeprazole has also some rotational freedom. Figure 1. Omeprazole decomposition reaction in acid medium. In this work, omeprazole and analogue compounds have been studied against Heliobacter pylori action. Heliobacter pylori usually lives in the stomach and requires urease enzyme to colonize mucus layer.1 It plays and important role in peptic ulcer disease, and the bacterium eradication decreases the ulcer recurrence.2,3 These facts motivate a search to find new treatments. Besides, some complementary studies about omeprazole behavior were performed. Conformational aspects, racemization barriers and decomposition reaction (Fig. 1) were taken in account. Initially, conformational analysis was performed for all compounds. Quantum chemistry coupled to chemometric methods PCA4 were used to find all minimum energy structures for each drug. The PM3 semi-empirical method implemented in Gaussian 98 package was used to perform conformational analysis and to find the racemization barriers values. The descriptors and the total energy involved in the decomposition reaction were calculated by using the ab initio method at Hartree-Fock level (6-31G**), implemented in Spartan Pro package. The PLS regression method was used to build the QSAR models.
1. B. J. Marshall, Am. J. Gastroenterol., 89 S116 (1994).
2. Y. Glupczynski, A. Burette, Am. J. Gastroenterol., 87 1716 (1992).
3. N. Chiba, B. V. Rao, J. W. Rademaker, R. H. Hunt, Am. J. Gastroenterol., 87 1716 (1992).
4. A. T. Bruni, B. P. Leite, M. M. C. Ferreira, J. Comp. Chem., 23 222 (2002).

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