Benign stomach ulcer. Peptic ulcer disease duodenal ulcer (treatment and relapse prevention). Hypersecretory conditions such as Zollinger-Ellison syndrome. Treatment of gastroesophageal reflux disease (reflux-esophagitis).
active substance: famotidine;
1 tablet contains famotidine 40 mg;
excipients: microcrystalline cellulose, lactose monohydrate, copovidone, croscarmellose sodium, magnesium stearate, colloidal anhydrous silica, azorubin (E 122); dry mixture “Opadry II white” containing titanium dioxide (E 171), talc, polyethylene glycol, polyvinyl alcohol.
Famatel Dosage form
Main physical and chemical properties: coated tablets, from pink to dark pink. In cross section, two layers are visible.
Famatel Pharmacotherapeutic group
Remedies for peptic ulcer and gastroesophageal reflux disease. H2-receptor antagonists. Famotidine. ATX code A02B A03.
Pharmacodynamics. Famotidine is a selective antagonist of H2 ‑ histamine receptors of the III generation.
The mechanism of action is due to the competitive inhibition of H2 ‑ histamine receptors in the stomach wall, resulting in reduced secretion of gastric juice (its volume). Inhibits basal and stimulated production of hydrochloric acid and raises the pH of gastric juice. At the same time reduces the activity of pepsin.
Strengthens the protective mechanisms of the gastric mucosa by increasing the formation of gastric mucus and its content of glycoproteins, promotes healing of its damage (including scarring of stress ulcers).
After oral administration, the action begins in 1 hour, reaches a maximum within 3 hours and lasts, depending on the dose, 10-24 hours. The effect of famotidine at a dose of 20-40 mg lasts for 10-12 hours.
Pharmacokinetics. After oral administration, famotidine is rapidly absorbed in the digestive tract; concomitant consumption does not affect absorption. Cmax in blood plasma is reached in 1-3 hours. The binding to blood proteins is 15-20%. The relative bioavailability of famotidine is 40-45%. The state of gastric filling does not affect bioavailability. It enters the cerebrospinal fluid, the placental barrier and breast milk.
The drug is metabolized in the liver to form an inactive sulfoxide metabolite. Excreted mainly by the kidneys (65-70%) by glomerular filtration and tubular secretion; in unchanged form 25-30% of the accepted dose is deduced. The plasma half-life (T½) is approximately 3 hours.
In patients with severe renal insufficiency (creatinine clearance less than 10 ml / min) T½ is prolonged and may exceed 20 hours; in patients with anuria it is approximately 24 hours.
Benign gastric ulcer.
Peptic ulcer of the duodenum (treatment and prevention of recurrence).
Hypersecretory conditions such as Zollinger-Ellison syndrome.
Treatment of gastroesophageal reflux disease (reflux esophagitis).
Hypersensitivity to the components of the drug, other antagonists of H2 ‑ histamine receptors.
Childhood, pregnancy or breastfeeding (due to lack of necessary clinical experience).
Interaction with other medicinal products and other forms of interaction
Absorption of certain drugs (eg, ketoconazole, amoxicillin, iron supplements) depends on the acidity of gastric juice. Therefore, famotidine should be used at least 2 hours after taking such drugs.
Concomitant use with other H2-receptor antagonists may significantly reduce the effectiveness of tolazoline. Although there is no confirmed interaction between famotidine and tolazoline, the likelihood of its existence is quite high, so the effects of tolazoline should be monitored at the beginning and after completion of concomitant treatment. If the effect of tolazoline decreases, its dose should be gradually increased or treatment with famotidine should be discontinued.
Food and antacids have no significant effect on famotidine treatment.
Famotidine does not affect the hepatic cytochrome P450 oxidase system, so the metabolism of oral anticoagulants, antipyrine, aminopyrine, theophylline, phenytoin, diazepam, ethanol and propranolol remains unchanged.
Probenecid may slow the release of famotidine.