Pantozol® is a proton pump inhibitor with two forms oral and IV form. This drug can be used in GERD, peptic ulcer diseases and GI bleeding. 

The actions of Lorsec® are mediated by inhibition of the H+- K+ ATPase in gastric parietal cells. Lorsec® is a weak base and a prodrug which is converted at low pH to a reactive sulfenamide intermediate which binds to SH groups in the extracellular sequence of the catalytic ??subunit. Covalent binding to systemic residues inactivates the H+-K+ ATPase, leading to prolonged inhibition of acid secretion. Lorsec® is a highly specific drug whose site of action is essentially limited to the parietal cell. In vivo, Lorsec® is an extremely effective antisecretory agent which is able to completely absolish acid secretion. The drug has been demonstrated to cause prolonged inhibition of basal and stimulated acid output in a variety of animal models. 

Lansulin® causes a fall in blood glucose concentration. It facilitates glucose transport into cells and glucose metabolism within them. It inhibits ketogenesis and glycogenolysis, while increasing lipid and glycogen synthesis. It reduces amino acid release from skeletal muscle, and increases amino acid transport into cells. It causes shifts of potassium and magnesium from the extracellular fluid into cells. 

Metforex® reduces elevated blood glucose concentrations in patients with diabetes, but it does not increase insulin secretion. There is no bloodglucose- lowering effect in non-diabetic subjects. Augmentation of muscular glucose uptake and utilization. and reduction of increased hepatic glucose production through an antigluconeogenic action explain the blood-glucoselowering effect. but the contribution of each of these processes to the overall effect has not been defined. The intestinal glucose absorption may be slightly delayed. Increased glucose utilization by the intestines and erythrocytes results in increased lactate formation.The mechanism of action involves binding of the apolar biguanide hydrocarbon side-chain to membrane phospholipids, evoking a change in the electrostatic surface potential.