secretion by selectively interacting with the gastric proton pump (H+/K+-ATPase) in the parietal cell secretory membrane [183, 186]. The molecular formula is C16H14F2N3NaO4S×1. 5 H2O and molecular weight is 432.4 g/Mol[185]. Because of gradual degradation of pantoprazole sodium during heating, the melting point cannot be accurately determined. It is a white to off-white crystalline powder. The structural formula is: [185] Pantoprazole has numerous advantages compared to its analogues (e.g., Omeprazole and lansoprazole) such as greater stability in a neutral PH environment, specific site of binding, and longer duration of action [187]. In addition, it shows no potential to either induce or inhibit the CYP 450 [183,184, 188]. It is a more selective inhibitor of acid secretion than other proton pump inhibitors [189]. Pantoprazole is used for treatment of erosive esophagitis, or “heartburn” caused by gatroesophageal reflux disease (GERD), a condition where the acid in the stomach washes back up into the esophagus. Pantoprazole can also be used to treat Zollinger-Ellison syndrome, a condition where the stomach produces too much acid. The most common side effects of pantoprazole include blurred vision, dry mouth, abdominal pain, fatigue, flushed, dry skin, increased hunger, increased thirst, and increased urination. The other side effects are excess air or gas in either stomach or intestine and trouble in sleeping. Mechanism of action: In low PH values, pantoprazole is transformed into cationic sulfenamide, which is its active form [184, 190] , this drug accumulates in the highly acidic environment of the parietal-cell canalicular lumen and it is activated. The active form, tetracyclic cationic sulfonamide, reacts with thiol groups of cysteines 813 and 822 of transmembranal H+ / K+ ATPase[183, 186]. This conversion must take place b>