<p><strong>Esomeprazole</strong>&nbsp;exerts its stomach acid-suppressing effects by preventing the final step in gastric acid production by covalently binding to sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of esomeprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, esomeprazole&#39;s duration of antisecretory effect that persists longer than 24 hours<br />
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<strong>Amoxicillin&nbsp;</strong>is similar to&nbsp;penicillin&nbsp;in its bactericidal action against susceptible bacteria during the stage of active multiplication. It acts through the inhibition of cell wall biosynthesis that leads to the death of the bacteria.<br />
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<strong>Clarithromycin&nbsp;</strong>acts by inhibiting microsomal protein synthesis in susceptible organisms mainly by binding to the donor site on the 50S subunit of the bacterial ribosome and preventing translocation to that site.</p>