Clinical pharmacology of famotidine: a summary.

Famotidine is a competitive histamine H2-receptor antagonist. Its main pharmacodynamic effect in humans is inhibition of gastric acid secretion. Dose-related suppression of basal and stimulated (meal, pentagastrin) gastric acid output has been shown with oral doses of 5-40 mg. The 40 mg dose is associated with the highest inhibitory effect, the longest duration of action, and the greatest response uniformity. After oral administration, antisecretory activity begins within 1 h, reaches a maximum in 1-3 h, and lasts 10-12 h. In addition to the earlier onset of effect, intravenous famotidine is about twice as potent as oral, a result consistent with a systemic bioavailability of oral famotidine of about 43%. Studies in patients and in healthy volunteers have shown that famotidine does not affect cardiovascular, renal, endocrine, pancreatic exocrine, or gastrointestinal motility functions. Oral famotidine is incompletely absorbed, reaching peak plasma concentrations in 1-3 h. It is eliminated primarily through the kidneys (about 70%), mostly as the parent compound. Its average elimination half-life in healthy subjects is 2.8 h. Half-life is prolonged nonlinearly in patients with decreased renal function. To date, clinically important interactions with other drugs have not been described for famotidine.