Antacids and anti-ulcer agents — histamine H2-receptor antagonist
H2-receptor antagonist indicated for active duodenal ulcer, active gastric ulcer, symptomatic nonerosive GERD and erosive esophagitis due to GERD, and reduction of duodenal ulcer recurrence risk.
Also known as: Pepcid, famotidine
DailyMed approved label (Ibuprofen and Famotidine Tablet, Doctor Reddy; setID 9f5de6af-e555-4efd-a3ed-b72c34c051b6).
DailyMed approved label (Ibuprofen and Famotidine Tablet, Doctor Reddy; setID 9f5de6af-e555-4efd-a3ed-b72c34c051b6).
No documented drug–drug interactions for this medicine.
Food does not clinically affect famotidine absorption.
May be taken with or without food, as preferred.
EMC-UK (MHRA) — approved Famotidine SmPC: https://www.medicines.org.uk/emc/product/100584/smpc
Famotidine is predominantly renally eliminated; its half-life is prolonged in severe renal impairment.
Reduce the dose in severe renal impairment.
EMC-UK (MHRA) — approved Famotidine SmPC: https://www.medicines.org.uk/emc/product/100584/smpc
Data on famotidine in pregnancy are limited; H2 antagonists are used when antacids are insufficient.
Use only if the benefit outweighs the risk, preferably in the 2nd/3rd trimester.
Excreted into breast milk in small amounts; compatible with breastfeeding.
No specific additional contraception.
EMC-UK (MHRA) — approved Famotidine SmPC: https://www.medicines.org.uk/emc/product/100584/smpc
Clinical and educational support tool. The information does not replace a medical prescription or the opinion of a qualified healthcare professional.
H2 antagonist that inhibits basal and nocturnal gastric acid secretion, as well as food- and pentagastrin-stimulated secretion. Inhibition of 86% (20 mg) and 94% (40 mg) of nocturnal acid secretion, for at least 10 hours.
Competitive inhibition of histamine H2 receptors on parietal cells, suppressing acid concentration and volume of gastric secretion; pepsin secretion varies proportionally to volume.
Incomplete absorption (oral bioavailability 40–45%); plasma peaks at 1–3 hours; plasma protein binding 15–20%. Bioavailability may slightly increase with food and decrease with antacids.
Minimal first-pass metabolism; 25–30% of an oral dose is recovered unchanged in urine. The only metabolite identified in humans is the S-oxide.
Elimination half-life of 2.5–3.5 h; eliminated by renal (65–70%) and metabolic (30–35%) routes.
Medicines from the same therapeutic group (ATC classification) or the same pharmacological class.
