Brand Names of Famotidine in Kenya
FAMOTIDINE MODE OF ACTION
Famotidine is a competitive inhibitor of histamine H2-receptors. The primary clinically important pharmacologic activity of famotidine is inhibition of gastric secretion. Both the acid concentration and volume of gastric secretion are suppressed by famotidine, while changes in pepsin secretion are proportional to volume output.
Famotidine is indicated in adult and pediatric patients 40 kg and greater for the treatment of:
– Active duodenal ulcer (DU).
– Active gastric ulcer (GU).
– Symptomatic nonerosive gastroesophageal reflux disease (GERD).
– Erosive esophagitis due to GERD, diagnosed by biopsy.
Famotidine is indicated in adults for the:
– Treatment of pathological hypersecretory conditions (e.g., Zollinger-Ellison syndrome, multiple endocrine neoplasias).
– Reduction of the risk of duodenal ulcer recurrence.
DOSAGE AND ADMINISTRATION
Initiation of treatment: The recommended dose is 40 mg of famotidine per day at bedtime. The treatment should be continued for 4-8 weeks, but it may be discontinued even earlier if it is found by endoscopic examination that the ulcer has healed. In most cases the ulcer will heal with this treatment within four weeks. Treatment should be continued for another four weeks in patients whose ulcer has not healed completely within four weeks.
Maintenance treatment: In prophylactic treatment of recurrent ulcer it is recommended that famotidine therapy be continued with a dose of 20 mg per day at bedtime.
Non-malignant gastric ulcer.
The recommended dose is 40 mg per day at bedtime. The treatment is continued for 4-8 weeks, but a shorter course of treatment is adequate if an endoscopic examination shows that the ulcer is healed.
If the patient has not previously received drugs to reduce the secretion of acid, the treatment is introduced by giving 20 mg of famotidine every 6 hours. The dosage should be adjusted according to the patient’s needs and it should be continued as long as it is clinically indicated. Daily doses up to 800 mg have been administered without any significant undesirable effects or tachyphylaxis. If the patient has received another H2 blocking agent, famotidine therapy can be introduced in a larger dose than otherwise recommended. The size of the initial dose is dependent on the severity of the condition and on the size of doses of H2 blocking agents received until that time.
The recommended dose for the relief of symptoms of reflux oesophagitis is 20 mg of famotidine twice daily. Doses should be continued for as long as indicated.
The recommended dose for the treatment of erosion or ulcer associated with reflux oesophagitis is 40 mg of famotidine twice daily. The recommended treatment length is 6-8 weeks.
If long-term management of reflux oesophagitis by famotidine is considered relevant, the recommended dose is 20 mg twice daily.
At present, this prophylactic treatment is not recommended to be extended beyond six months.
Famotidine is primarily eliminated via the kidneys. For patients with impaired renal function in whom creatinine clearance is less than 10 ml/min, the daily dose of famotidine should be reduced by 50%. Caution is advised in patients with renal impairment. Dialysis patients should also take doses that are reduced by 50%. Famotidine tablets should be administered at the end of dialysis or later since some of the active ingredient is removed by dialysis.
In patients with cirrhosis of the liver, the plasma concentration and elimination of famotidine in the urine were the same as that of healthy volunteers. Reduction of the dose is therefore not necessary in these patients.
When famotidine was administered to elderly patients in clinical studies the undesirable effects associated with the drug were not found to increase nor were they found to be different from those exhibited in younger patients. Adjustment of dose based on age is therefore not necessary.
Paediatric population: Not recommended.
During concomitant use of drugs where the absorption of the drug is affected by the amount of gastric juice, a possible effect on the absorption should be taken into consideration. The absorption of ketoconazole and itraconazole could be reduced. Ketoconazole should be given two hours before famotidine administration.
Probenecid inhibits renal tubular secretion of famotidine, and has been shown to cause a 50% increase in plasma levels of famotidine. Therefore, concomitant use of probenecid and famotidine should be avoided.
Concomitant use of famotidine and antacids could reduce the famotidine uptake and cause lower plasma levels of famotidine. Therefore, famotidine should be administered 1-2 hours before antacids.
Concomitant use of sucralfate inhibits absorption of famotidine. Therefore, sucralfate should not be administered within 2 hours after famotidine.
Famotidine does not interact with the cytochrome P450-linked drug metabolizing enzyme system. Compounds metabolized by this system which have been tested in man have included warfarin, theophylline, phenytoin, diazepam, propranolol, aminopyrine and antipyrine. Indocyanine green as an index of hepatic blood flow and/or hepatic drug extraction has been tested and no significant effects have been found.
Studies in patients stabilized on phenprocoumon therapy have shown no pharmacokinetic interaction with famotidine and no effect on the pharmacokinetic or anticoagulant activity of phenprocoumon.
In addition, studies with famotidine have shown no augmentation of expected blood alcohol levels resulting from alcohol ingestion.
Alterations of gastric pH may affect the bioavailability of certain drugs resulting in a decrease in the absorption of atazanavir.
Risk of loss of efficacy of calcium carbonate when co-administered as phosphate binder with famotidine in hemodialysis patients.
Blood and the lymphatic system disorders
Reversible psychic disturbances including Hallucinations
Nervous system disorders
Uncommon: taste disorder
Epileptic seizures, convulsions; grand mal seizures (particularly in patients with impaired renal function);
Abdominal discomfort or distension
Intrahepatic cholestasis (visible sign: jaundice),
Hepatitis; cholestatic jaundice, Increase in liver enzyme abnormalities (transaminases, gamma GT, alkaline phosphatase, bilirubin)
Metabolism and nutrition disorders
Loss of appetite (anorexia)
Skin and subcutaneous tissue disorders
Alopecia, Stevens Johnson syndrome/toxic epidermal necrolysis sometimes fatal
Immune system disorders
Hypersensitivity reactions (angioneurotic oedema, anaphylaxis, bronchospasm)
Respiratory, thoracic and mediastinal disorders
Interstitial pneumonia sometimes fatal
Muscoskeletal, connective tissue and bone disorders
Muscle cramps, Arthralgia
AV block with H2 receptor antagonists administered intravenously
General disorders and administration site conditions:
Very rare: chest tightness
Reproductive system and breast disorders:
Very rare: impotence
Adverse Effects – Causal Relationship Unknown
Rare cases of gynecomastia, have been reported, however, in controlled clinical trials the incidences were not greater than those seen with placebo.
Reporting of suspected adverse reactions:
The PPB Department of Pharmacovigilance was set up with a vision to develop, implement and continuously upgrade an appropriate system for detecting, reporting, and monitoring adverse drug reactions (ADRs) and other relevant problems with medicines in Kenya. The department strives to ensure the safety and efficacy of pharmaceutical products in Kenya.
Reporting suspected adverse reactions after authorization of the medicinal product are important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals/ Patients are encouraged to report any suspected adverse reactions via Pharmacovigilance Yellow Form, email@example.com or clicking below button:
Famotidine in Kenya
Famotidine in Kenya
Famotidine in Kenya
Famotidine in Kenya
Famotidine in Kenya
Clinical | Pharmacokinetic data
Pregnancy Category: B (No risk in non-human studies)
Routes of Administration: By mouth (tablets), Intravenous
Bioavailability: 40–45% (by mouth)
Protein Binding: 15–20%
Onset of Action: N/A
Elimination Half life: 2.5–3.5 hours
Excretion: Kidney (25–30% unchanged [Oral]
Legal Status | Dosage forms & Strengths
Prescription only Medicine (POM) , ℞-only
Narcotic Drugs and Psychotropic Substances (Control ) Act Schedule:
This drug is not a controlled substance under Narcotic Drugs and Psychotropic Substances (Control ) Act
Dosage Forms | Strengths:
|CompTox Dashboard (EPA)|
- PPB Drugs Retention Register
- Campoli-Richards, Deborah M., and S. P. Clissold. “Famotidine.” Drugs 32.3 (1986): 197-221.
- Walt, R. P., et al. “Continuous intravenous famotidine for haemorrhage from peptic ulcer.” The Lancet 340.8827 (1992): 1058-1062.
- Echizen, Hirotoshi, and Takashi Ishizaki. “Clinical pharmacokinetics of famotidine.” Clinical pharmacokinetics 21.3 (1991): 178-194.
- Berardi, R. R., R. M. Tankanow, and T. T. Nostrant. “Comparison of famotidine with cimetidine and ranitidine.” Clinical pharmacy 7.4 (1988): 271.
- Kroemer, H., and U. Klotz. “Pharmacokinetics of famotidine in man.” International Journal of Clinical Pharmacology, Therapy, and Toxicology 25.8 (1987): 458-463.