Reaction SMILES: CO[C:3]1[CH:38]=[CH:37][C:6]2[N:7]([S:23]([C:26]3[CH:36]=[CH:35][C:29]([O:30][CH2:31][C:32]([NH2:34])=[O:33])=[CH:28][CH:27]=3)(=[O:25])=[O:24])[C:8]([S:10]([CH2:12]C3C(C)=C(OC)C(C)=CN=3)=[O:11])=[N:9][C:5]=2[CH:4]=1.COC1C=CC2N=C(S(CC3C(C)=C(OC)C(C)=CN=3)=O)N(S(C3C=CC([O:69][CH2:70][C:71]([NH2:73])=[O:72])=CC=3)(=O)=O)C=2C=1.C[C:78]1[CH:79]=[N:80][C:81](C[S+]([O-])C2NC3C=CC(OC)=CC=3N=2)=[C:82]([CH3:86])[C:83]=1[O:84][CH3:85]>>[C:71]([CH2:70][O:69][C:28]1[CH:27]=[C:26]([S:23]([N:7]2[C:6]3[CH:37]=[CH:38][CH:3]=[CH:4][C:5]=3[N:9]=[C:8]2[SH:10]([C:81]2[C:82]([CH3:86])=[C:83]([O:84][CH2:85][CH2:28][CH2:29][O:30][CH3:31])[CH:78]=[CH:79][N:80]=2)([CH3:12])=[O:11])(=[O:24])=[O:25])[CH:36]=[CH:35][C:29]=1[O:30][CH2:31][C:32]([NH2:34])=[O:33])(=[O:72])[NH2:73]
Reactant: COc1ccc2c(c1)nc(S(=O)Cc1ncc(C)c(OC)c1C)n2S(=O)(=O)c1ccc(OCC(N)=O)cc1
Reactant: COc1ccc2nc(S(=O)Cc3ncc(C)c(OC)c3C)n(S(=O)(=O)c3ccc(OCC(N)=O)cc3)c2c1
Reactant: COc1ccc2[nH]c([S+]([O-])Cc3ncc(C)c(OC)c3C)nc2c1
Product: COCCCOc1ccnc([SH](C)(=O)c2nc3ccccc3n2S(=O)(=O)c2ccc(OCC(N)=O)c(OCC(N)=O)c2)c1C

Procedure:
Additional experiments, described below, with further compounds of the invention showed good inhibition of gastric acid secretion. For example, when a mixture of 2-{2-carbamoylmethoxy-4-[5-methoxy-2-((4-methoxy-3,5-dimethyl pyridin-2-yl)methanesulfinyl)benzimidazole-1-sulfonyl]phenoxy}acetamide and 2-{2-carbamoylmethoxy-4-[6-methoxy-2-((4-methoxy-3,5-dimethyl pyridin-2-yl)methanesulfinyl)benzimidazole-1-sulfonyl]phenoxy}acetamide (1:1 mixture of isomers) was administrated to male rat, gastric acid secretion was observed to be significantly and continuously inhibited. Using pylorus-ligated male rats, when acid-output stimulated by histamine was measured, intraduodenal administration of 10 μmole of 2-{2-carbamoylmethoxy-4-[5-methoxy-2-((4-methoxy-3,5-dimethyl pyridin-2-yl)methanesulfinyl)benzimidazole-1-sulfonyl]phenoxy}acetamide and 2-{2-carbamoylmethoxy-4-[6-methoxy-2-((4-methoxy-3,5-dimethyl pyridin-2-yl)methanesulfinyl)benzimidazole-1-sulfonyl]phenoxy}acetamide (1:1 mixture of isomers) provided 64.2% inhibition, while OMEPRAZOLE provided only 54.6% under identical condition. Also, when acid-output stimulated by histamine and carbachol was measured after 5.5 hr of oral administration, the latter mixture of isomers provided 49.7% inhibition, while OMEPRAZOLE provided only 19.6% inhibition. Under similar condition, (pyridine-3-sulfonyl)OMEPRAZOLE (the compound of Example 25) inhibited 61% and a mixture of 2-{4-[(5-methoxy-2-{[(3,5-dimethyl-4-methoxy-2-pyridyl)methyl]sulfinyl } benzimidazol-1-yl)sulfonyl]phenoxy} acetamide and 2-{4-[(6-methoxy-2-{[(3,5-dimethyl-4-methoxy-2-pyridyl)methyl]sulfinyl} benzimidazol-1-yl)sulfonyl]phenoxy}acetamide inhibited 65%, while OMEPRAZOLE showed relatively rapid decline of inhibition (about 20%) with fast elimination of drug in the plasma level. Similarly, 2-(2-carbamoylmethoxy-4-{2-[4-(3-methoxypropoxy)-3-methyl pyridin-2-yl methylsulfinyl]benzimidazole-1-sulfonyl}phenoxy)acetamide provided 56% inhibition after 5 hr of oral administration, while the parent RABEPRAZOLE showed 32% of inhibition under the same condition. 2-(4-{[2-({[3-Methyl-4-(2,2,2-trifluoroethoxy)-2-pyridyl]methyl}sulfinyl) benzimidazol-1-yl]sulfonyl}phenoxy)acetamide provided 46.9% inhibition and 2-(2-carbamoylmethoxy-4-{2-[3-methyl-4-(2,2,2-trifluoro-ethoxy)-pyridin-2-yl methanesulfinyl]-benzimidazole-1-sulfonyl}-phenoxy)-acetamide gave 36.8% inhibition, while the parent LANSOPRAZOLE showed only 29% inhibition after 4 hour of oral administration.