Pepfamin Mechanism of Action

Pharmacology: Pharmacodynamics: PEPFAMIN is a histamine H₂-receptor antagonist, primarily inhibits both the concentration and volume of gastric secretion and pepsin of the gastric juices. It is approximately 20 to 150 times more potent at inhibiting gastric acid secretion than cimetidine and 3-20 times more potent than ranitidine.
PEPFAMIN does not appear to affect the exocrine pancreatic secretions e.g. amylase or bicarbonate. PEPFAMIN has demonstrated no effects on testosterone, estradiol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), cortisol, thyroxine (T₄), triiodothyronine (T₃) or prolactin levels. PEPFAMIN has no effect on hepatic blood flow or hepatic mixed-function oxidase systems; as a result, PEPFAMIN appears to be free of clinically significant effects on the metabolism of drugs such as warfarin, phenytoin, theophylline, or diazepam.
Pharmacokinetics: PEPFAMIN is incompletely absorbed from the GI tract following oral administration. Bioavailability of Famotidine from the tablet formulation is approximately 40-45% and is unaffected by food. The inhibition of gastric acid secretion is apparently within 1 hour following oral administration of Famotidine. The peak plasma concentration of PEPFAMIN occurs within 1 to 3 hours. The duration of antisecretory effect is 10 to 12 hours. The apparent volume of distribution of Famotidine in normal adults and in patients with renal or hepatic failure is approximately 1.2 L/Kg. Protein binding is relatively low at 15-20%.
PEPFAMIN undergoes minimal first pass metabolism and is excreted in the urine, with 25 to 30% of an orally administered dose recovered in urine as unchanged drug. The elimination half-life of PEPFAMIN in normal subject is approximately 2.5-4 hours. The elimination half-life was exceeded 20 hours in severe renal insufficiency patients with creatinine clearance below 10 mL/min and up to 24 hours in anuric patients. Thus, dosage adjustment and dosing interval should be considered.
In elderly patients with lower renal function, renal clearance will be decreased. Thus, dosage adjustment should be considered.
In patients with compensated or decompensated liver disease but normal renal function, PEPFAMIN pharmacokinetics do not appear to differ significantly from those of normal subject.