Pepfamin

Each tablet contains Famotidine 20 mg.

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.

1. Acute duodenal ulcer and prophylaxis of recurrent duodenal ulcer.
2. Active benign gastric ulcer.
3. Gastroesophageal reflux disease (GERD), including curative treatment of esophagitis associated with gastroesophageal reflux disease.
4. Pathologic GI hypersecretory conditions e.g. Zollinger-Ellison syndrome.

Duodenal ulcer: Acute therapy: Recommended oral dose is 40 mg at bedtime or 20 mg twice daily for 4-8 weeks. In most cases healing may occur within 4 weeks. Treatment should be continued for another 4 weeks in patients whose ulcer has not healed completely within 4 weeks.
Maintenance therapy: Recommended oral dose is 20 mg at bedtime for 1 year or as clinically indicated.
Benign gastric ulcer: Recommended oral dose is 40 mg at bedtime for 6 to 8 weeks.
Gastroesophageal Reflux Disease (GERD): Recommended oral dosage is 20 mg twice daily for up to 6 weeks.
Esophagitis associated with GERD: Recommended oral dosage is 20-40 mg twice daily for up to 12 weeks.
Pathologic GI hypersecretory conditions: The usual initial adult dosage is 20 mg orally every 6 hours; may increase dose based on patient response up to maximal dosage of 160 mg every 6 hours.
Dosage in renal impairment: In adults with moderate and severe renal insufficiency, the elimination half-life will be exceeded 20 hours and up to 24 hours in anuric patients. To avoid drug accumulated, dosage should be decreased 50% of normal dose and the dosing interval should be increased to every 36 to 48 hours for preventing CNS adverse effects.
Dosage in elderly: Clinically important changes in the pharmacokinetics of Famotidine have not been observed in geriatric individuals, and dosage of the drug does not need to be modified based on age alone. However, in elderly patients with lower renal function, renal clearance will be decreased. Thus, dosage adjustment should be considered.
Dosage in hepatic impairment: Dosage adjustment is not necessary in patients with hepatic impairment.

Overdose and treatment: The adverse effects in overdose patients are similar to the adverse effects in normal clinical experience.
In acute Famotidine overdose, usual measures to remove unabsorbed drug form GI tract and clinical monitoring should be employed. Supportive and symptomatic treatment should be initiated.

1. PEPFAMIN is contraindicated in patients with a history of hypersensitivity to Famotidine or any ingredient in the formulation.
2. PEPFAMIN should not be given to the patients with a history of hypersensitivity to other drug in H₂-receptor antagonist.

For patients with renal impairment, use as directed by physician.

In patients with moderate (creatinine clearance <50 mL/min) to severe (creatinine clearance <10 mL/min) renal impairment, dosage reduction or prolong interval should be considered for preventing drug accumulated, CNS adverse effects and risk of prolonged QT interval.
PEPFAMIN should be used with caution in pregnant patients, breast-feeding mothers, and children, because there are no adequate and controlled studies to date using Famotidine in these populations. In elderly patients with impaired renal function, the dose of PEPFAMIN should be reduced.

Pregnancy: Category: B.
There are no adequate and controlled studies to date using Famotidine in pregnant women. Nevertheless, there is no evidence that histamine H₂-receptor antagonist pose a clinically significant risk to the embryo or fetus.
The physician should weigh the potential benefit of drug treatment against potential risk before prescribing this drug during pregnancy.
Lactation: Famotidine is distributed into milk in humans and in animals. In nursing infants should either stop using this drug or stop breastfeeding.

See table.

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1. Concomitant use of gastric suppressant agent, including histamine-2 receptor antagonists such as Famotidine, with ketoconazole is not recommended as systemic exposure to ketoconazole may be significantly reduced leading to ketoconazole loss of efficacy. Ketoconazole should be given two hours before Famotidine administration.
2. Concomitant use of itraconazole with Famotidine, agent that suppress gastric pH, may result in decreased gastrointestinal absorption of itraconazole and decreased itraconazole plasma concentrations.
3. Concomitant use of probenecid and Famotidine should be avoided because it has been reported to result in increased in Famotidine concentration due to a decline in renal tubular secretion.
4. Antacids appear to slightly decrease the bioavailability of Famotidine but this effect does not appear to be clinically important, Famotidine can be administered concomitantly with antacids.
5. Famotidine does not appear to inhibit the metabolism of drugs, including warfarin, theophylline, phenytoin, or diazepam, by the hepatic cytochrome P-450 (microsomal) enzyme system.
6. Concomitant use of atazanavir and Famotidine has resulted in reduced atazanavir efficacy because of alteration of gastric pH may affect absorption atazanavir.

Store below 25°C.

Antacids, Antireflux Agents & Antiulcerants

A02BA03 - famotidine ; Belongs to the class of H2-receptor antagonists. Used in the treatment of peptic ulcer and gastro-oesophageal reflux disease (GERD).

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