Aspiration prophylaxis in patients undergoing anesthesia (off-label use): Note: May be considered in patients at high risk for aspiration (Ref):
IV: 20 mg as a single dose ~40 to 90 minutes prior to induction of anesthesia; may be given with a rapid-acting nonparticulate antacid (eg, oral sodium citrate and citric acid) and/or metoclopramide (Ref).
Erosive esophagitis due to gastroesophageal reflux disease (alternative agent): Note: Although a labeled indication, H2-receptor antagonists (eg, famotidine) are not preferred for the treatment of erosive esophagitis due to gastroesophageal reflux disease due to the availability of proton pump inhibitors (PPIs) (Ref).
Oral: 20 or 40 mg twice daily for up to 12 weeks.
IV (alternative route): 20 mg every 12 hours. Note: For use when oral therapy is not appropriate.
Gastroesophageal reflux disease, treatment:
Initial therapy:
Mild and intermittent symptoms (<2 episodes/week), and no evidence of erosive esophagitis: Note: For more severe or frequent initial symptoms, with or without evidence of erosive esophagitis, a proton pump inhibitor (PPI) as initial therapy is recommended.
Oral: 10 mg twice daily as needed; if symptoms persist after 2 to 4 weeks, increase to 20 mg twice daily for 2 weeks; if symptoms improve, may continue therapy as needed (Ref).
Note: If symptoms persist after 2 weeks of 20 mg twice daily, discontinue and consider PPI therapy (Ref).
Residual acid reflux symptoms despite maximal PPI therapy (adjunct): Oral: 20 mg once daily given at bedtime in addition to PPI therapy (Ref); may also administer famotidine intermittently or on demand with scheduled PPI (Ref).
OTC labeling (patient-guided therapy): Heartburn, mild intermittent symptoms: Oral: 10 to 20 mg up to twice daily when needed (maximum: 40 mg/day); may also be taken 10 to 60 minutes before meals or beverages that cause heartburn (maximum: 40 mg/day).
Infusion reaction, premedication (adjunct) (off-label use): IV, Oral: 20 mg typically administered 30 to 60 minutes prior to infusion of certain chemotherapy agents or biologics; usually given in conjunction with an H1 antihistamine (eg, diphenhydramine) and glucocorticoid (refer to institutional protocols) (Ref).
Mastocytosis (adjunct) (off-label use): Oral: 10 to 20 mg every 12 hours adjusted to achieve GI symptom relief. Typically used in combination with other appropriate agent(s) (eg, H1 antihistamine and/or leukotriene inhibitor) (Ref).
Pathological hypersecretory conditions (eg, Zollinger-Ellison syndrome [gastrinoma]) (alternative agent): Note: Although a labeled indication, clinical experience suggests that H2-receptor antagonists (eg, famotidine) are not preferred for controlling acid hypersecretion in pathological hypersecretory conditions (eg, Zollinger-Ellison syndrome) due to the availability of PPIs (Ref).
Oral: Initial: 20 mg every 6 hours; may adjust dose based on patient response (maximum: 640 mg/day [160 mg every 6 hours]).
IV (alternative route): 20 mg every 12 hours; higher doses may be required. Note: For use when oral therapy is not appropriate.
Peptic ulcer disease (duodenal or gastric ulcers) (alternative agent): Note: Although a labeled indication, current guidelines recommend PPIs as standard of care for treatment of peptic ulcer disease rather than H2-receptor antagonists (eg, famotidine) (Ref).
Duodenal ulcer:
Oral: Initial: 40 mg once daily or 20 mg twice daily for up to 8 weeks; maintenance therapy: 20 mg once daily for 1 year or as clinically indicated.
IV (alternative route): 20 mg every 12 hours. Note: For use when oral therapy is not appropriate.
Gastric ulcer:
Oral: 40 mg once daily for up to 8 weeks.
IV (alternative route): 20 mg every 12 hours. Note: For use when oral therapy is not appropriate.
Stress ulcer prophylaxis in select critically ill patients (alternative agent) (off-label use): Note: Used as an alternative for proton pump inhibitors in critically ill patients with risk factors for GI bleeding (eg, coagulopathy, mechanical ventilation for >48 hours, traumatic brain injury, history of GI ulceration or bleeding within past year, extensive burns) (Ref).
Oral: 20 mg twice daily (Ref). Discontinue prophylaxis once risk factors have resolved (Ref).
IV: 20 mg twice daily (Ref). Discontinue prophylaxis once risk factors have resolved (Ref).
Urticaria, chronic spontaneous (alternative agent) (adjunct) (off-label use): Note: Use as additional therapy if insufficient response to full-dose H1 antihistamine.
Oral: 20 mg twice daily given in combination with H1 antihistamine; a trial of 2 to 4 weeks is suggested to assess response (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function (Ref):
IV:
CrCl ≥50 mL/minute: No dosage adjustment necessary.
CrCl <50 mL/minute: Administer 50% of usual dose or continue usual dose but increase the dosing interval to every 36 to 48 hours.
Oral:
CrCl (mL/minute) |
If usual dose is 10 mg twice daily |
If usual dose is 20 mg once daily |
If usual dose is 20 mg twice daily |
---|---|---|---|
CrCl ≥60 |
No dosage adjustment necessary. |
No dosage adjustment necessary. |
No dosage adjustment necessary. |
CrCl 30 to <60 |
10 mg once daily or 20 mg every other day |
10 mg once daily or 20 mg every other day |
20 mg once daily or 40 mg every other day |
CrCl <30 |
10 mg every other day |
10 mg every other day |
10 mg once daily or 20 mg every other day |
Hemodialysis, intermittent (thrice weekly): Dialyzable (6% to 16%) (Ref):
IV, Oral: Dose as for CrCl <30 mL/minute; administer after hemodialysis on dialysis days. No supplemental dose necessary (Ref).
Peritoneal dialysis: Minimally dialyzed (5%) (Ref):
IV, Oral: Dose as for CrCl <30 mL/minute (Ref).
CRRT: Limited data utilizing hemofiltration rates of ≤1,800 mL/hour did not demonstrate a dose reduction is necessary (Saima 1990); however, no data regarding famotidine disposition utilizing contemporary flow rates of up to ~3,000 mL/hour are available:
IV, Oral: Dose as for CrCl <30 mL/minute (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration):
IV, Oral: Dose as for CrCl <30 mL/minute; administer post-PIRRT session (Ref).
There are no dosage adjustments provided in the manufacturer's labeling.
Refer to adult dosing.
(For additional information see "Famotidine: Pediatric drug information")
Gastroesophageal reflux disease:
Note: Proton pump inhibitors (PPIs) are the preferred treatment for gastroesophageal reflux disease (GERD) in pediatric patients; famotidine may be used when PPIs are not available or are contraindicated (Ref).
Oral:
Infants <3 months: Oral: 0.5 mg/kg/dose once daily; if not effective after 2 weeks, may increase to 1 mg/kg/dose once daily (Ref).
Infants ≥3 months: Oral: Initial: 0.5 mg/kg/dose twice daily; if not effective, may increase to 1 mg/kg/dose twice daily; maximum dose: 20 mg/dose (Ref).
Children and Adolescents: Oral: Initial: 0.5 mg/kg/dose twice daily, up to 20 mg/dose twice daily; if not effective, may increase to 1 mg/kg/dose twice daily; maximum dose: 40 mg/dose (Ref).
IV:
Infants <3 months: Limited data available: IV: 0.25 mg/kg/dose once daily; dosing based on a pharmacokinetic study which included 7 patients <3 months who received IV famotidine (Ref).
Infants ≥3 months: Limited data available: IV: Initial: 0.25 mg/kg/dose every 12 hours; maximum dose: 20 mg/dose; dosing based on a pharmacokinetic study which included 11 patients >3 to 12 months who received IV famotidine (Ref).
Children and Adolescents: IV: Initial: 0.25 mg/kg/dose every 12 hours; maximum dose: 20 mg/dose; doses up to 0.5 mg/kg/dose every 12 hours have been reported (Ref).
Heartburn, acid indigestion, or sour stomach (OTC labeling): Children ≥12 years and Adolescents: Oral: 10 to 20 mg every 12 hours; dose may be taken 15 to 60 minutes before eating foods known to cause heartburn; maximum daily dose: 2 tablets/day (20 to 40 mg dependent upon OTC product).
Peptic ulcer disease:
Oral:
Suspension: Children and Adolescents ≤16 years: Oral: 0.5 mg/kg/day at bedtime or divided twice daily; may increase to 1 mg/kg/day at bedtime or divided twice daily; maximum daily dose: 40 mg/day.
Tablets: Children and Adolescents >40 kg:
Duodenal ulcer: Acute therapy: Oral: 40 mg once daily at bedtime or 20 mg twice daily.
Gastric ulcer: Acute therapy: Oral: 40 mg once daily at bedtime.
IV: Children and Adolescents: IV: Initial: 0.25 mg/kg/dose every 12 hours; maximum dose: 20 mg/dose; doses up to 0.5 mg/kg/dose every 12 hours have been reported.
Stress ulcer prophylaxis, gastric acid suppression: Limited data available: Infants, Children, and Adolescents: IV: 1 to 2 mg/kg/day in divided doses every 8 to 12 hours; maximum daily dose: 40 mg/day (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Note: Dosing is based on pharmacokinetic parameters, limited pediatric studies, adult studies, and expert opinion (Ref).
Altered kidney function:
Weight-based dosing: Infants ≥3 months, Children, and Adolescents: IV, Oral:
CrCl |
Based on usual dose of 0.25 mg/kg/dose every 12 hours |
Based on usual dose of 0.5 mg/kg/dose every 12 hours |
---|---|---|
≥50 mL/minute/1.73 m2 |
No dosage adjustment necessary. |
No dosage adjustment necessary. |
10 to <50 mL/minute/1.73 m2 |
0.25 mg/kg/dose every 24 hours. Maximum dose: 10 mg/dose. |
0.5 mg/kg/dose every 24 hours. Maximum dose: 20 mg/dose. |
<10 mL/minute/1.73 m2 |
0.125 mg/kg/dose every 24 hours. Maximum dose: 5 mg/dose. |
0.25 mg/kg/dose every 24 hours. Maximum dose: 10 mg/dose. |
Fixed dosing: Children and Adolescents weighing ≥40 kg: Oral:
CrCl |
Based on usual dose of 10 mg twice daily |
Based on usual dose is 20 mg once daily |
Based on usual dose is 20 mg twice daily |
---|---|---|---|
CrCl ≥60 mL/minute/1.73 m2 |
No dosage adjustment necessary. |
No dosage adjustment necessary. |
No dosage adjustment necessary. |
CrCl 30 to <60 mL/minute/1.73 m2 |
10 mg once daily or 20 mg every other day |
10 mg once daily or 20 mg every other day |
20 mg once daily or 40 mg every other day |
CrCl <30 mL/minute/1.73 m2 |
10 mg every other day |
10 mg every other day |
10 mg once daily or 20 mg every other day |
Hemodialysis, intermittent (thrice weekly): Dialyzable (~6% to 16%):
Infants ≥3 months, Children, and Adolescents: IV, Oral: Dose as for CrCl <10 mL/minute/1.73 m2; administer after hemodialysis on hemodialysis days. No supplemental dose necessary.
Peritoneal dialysis: Minimally dialyzed (CAPD ~5%):
Infants ≥3 months, Children, and Adolescents: IV, Oral: Dose as for CrCl <10 mL/minute/1.73 m2.
CRRT: Note: Drug clearance is dependent on the effluent flow rate, filter type, and method of renal replacement. Recommendations are based on high-flux dialyzers and standard effluent flow rates of 25 to 40 mL/kg/hour (~2,000 to 3,000 mL/1.73 m2/hour).
Infants ≥3 months, Children, and Adolescents: IV, Oral: Dose as for CrCl 10 to <50 mL/minute/1.73 m2.
There are no dosage adjustments provided in the manufacturer's labeling.
CNS effects have been reported with famotidine and may include agitation, confusion, and delirium (among others). These effects appear to be reversible with discontinuation (Ref).
Mechanism: Not clearly established; may occur due to increased central anticholinergic action (Ref). There is no evidence to support a difference among agents in the H2-receptor antagonist class (Ref).
Onset: Varied; in case reports, CNS effects occurred within 2 to 6 days of IV famotidine initiation (Ref) and within the first 2 to 3 weeks of oral famotidine use (Ref).
Risk factors :
For H2-receptor antagonists in general:
• Age ≥60 years (Ref)
• Hospitalization, especially ICU (Ref)
• Kidney or liver impairment (Ref)
H2-receptor antagonists, including famotidine, may be associated with an increased incidence of necrotizing enterocolitis in very low birth weight (VLBW) neonates (Ref).
Mechanism: Non–dose-related; possibly due to an increase in gastric pH, which alters the intestinal microbiome and weakens the protective barrier against bacterial overgrowth in the premature gut (Ref).
Risk factors:
• VLBW neonates (<1,500 grams) (Ref)
• Duration of treatment (median duration of exposure: 10 days) (Ref)
• Prematurity (Ref)
Thrombocytopenia has been reported rarely with IV and oral famotidine and may increase the risk of bleeding (Ref). Most patients who developed thrombocytopenia while receiving an H2-receptor antagonist also had at least one documented independent risk factor for thrombocytopenia (eg, age, sepsis) (Ref).
Mechanism: Non–dose-related; postulated to occur secondary to one of two mechanisms: Induction of bone marrow suppression secondary to inhibition of DNA synthesis or development of platelet antibodies during H2-receptor antagonist administration (Ref).
Onset: Varied; in case reports with H2-receptor antagonists, average onset: 14 days (range: 1 to 75 days) (Ref).
Risk factors:
• Higher injury severity scores (Ref)
• Longer length of hospitalization (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. All reported ADRs are for the oral formulations unless otherwise noted.
>10%: Nervous system: Agitation (infants)
1% to 10%:
Gastrointestinal: Constipation (1%), diarrhea (2%)
Nervous system: Dizziness (1%), headache (5%)
<1%:
Cardiovascular: Flushing, palpitations
Dermatologic: Pruritus, skin rash, xeroderma
Endocrine & metabolic: Decreased libido
Gastrointestinal: Abdominal distress, anorexia, nausea, vomiting, xerostomia
Genitourinary: Impotence
Hematologic & oncologic: Thrombocytopenia
Hepatic: Increased liver enzymes
Nervous system: Anxiety, depression, drowsiness, fatigue, hallucination, insomnia, seizure (von Einsiedel 2002), taste disorder
Neuromuscular & skeletal: Arthralgia, asthenia, musculoskeletal pain
Ophthalmic: Conjunctival injection, periorbital edema
Otic: Tinnitus
Respiratory: Bronchospasm
Miscellaneous: Fever
Frequency not defined: Local: Irritation at injection site (IV)
Postmarketing:
Cardiovascular: Atrioventricular block (Schoenwald 1999), cardiac arrhythmia (Ahmad 1991), facial edema, prolonged QT interval on ECG (Lee 2004)
Dermatologic: Stevens-Johnson syndrome, toxic epidermal necrolysis (Brunner 1995), urticaria
Gastrointestinal: Necrotizing enterocolitis (very low birth weight neonates; Guillet 2006)
Hematologic & oncologic: Agranulocytosis (Marcus 2002), leukopenia, neutropenia (Oymak 1994), pancytopenia
Hepatic: Cholestatic jaundice, hepatitis (Gupta 2009)
Hypersensitivity: Anaphylaxis (Kim 2010), angioedema
Immunologic: Drug reaction with eosinophilia and systemic symptoms (Wu 2012)
Nervous system: Confusion, delirium (Catalano 1996), disorientation (Rodgers 1998; Yoshimoto 1994), mania (von Einsiedel 2002), nightmares (Rodgers 1998), paresthesia, restlessness (Rodgers 1998)
Neuromuscular & skeletal: Muscle cramps, rhabdomyolysis
Renal: Interstitial nephritis (Hirayama 1998)
Respiratory: Interstitial pneumonitis
Serious hypersensitivity (eg, anaphylaxis) to famotidine, other H2 antagonists, or any component of the formulation
OTC labeling: When used for self-medication (OTC), do not use if trouble or pain when swallowing food, vomiting with blood, or bloody or black stools; allergic to other acid reducers; kidney impairment; coadministration with other acid reducers.
Concerns related to adverse effects.
• Vitamin B12 deficiency: Famotidine and other H2RAs can reduce absorption of vitamin B12 and thus decrease serum concentrations. It is unclear of its role in causing function or clinical deficiencies . A number of studies have tried to determine the association of B12 deficiency with H2RAs use; however, differences in diagnostic criteria have made this challenging (Miller 2018).
Disease-related concerns:
• Gastric malignancy: Relief of symptoms does not preclude the presence of a gastric malignancy.
• Kidney impairment: Use with caution; increased risk of QT prolongation; dosage adjustment may be required.
Special populations:
• Pediatric: Use of gastric acid inhibitors, including proton pump inhibitors and H2 blockers, has been associated with an increased risk for development of acute gastroenteritis and community-acquired pneumonia in pediatric patients (Canani 2006).
Dosage form specific issues:
• Benzyl alcohol and derivatives: Some dosage forms may contain benzyl alcohol and/or sodium benzoate/benzoic acid; benzoic acid (benzoate) is a metabolite of benzyl alcohol; large amounts of benzyl alcohol (≥99 mg/kg/day) have been associated with a potentially fatal toxicity (“gasping syndrome”) in neonates; the “gasping syndrome” consists of metabolic acidosis, respiratory distress, gasping respirations, CNS dysfunction (including convulsions, intracranial hemorrhage), hypotension, and cardiovascular collapse (AAP ["Inactive" 1997]; CDC 1982); some data suggests that benzoate displaces bilirubin from protein binding sites (Ahlfors 2001); avoid or use dosage forms containing benzyl alcohol and/or benzyl alcohol derivative with caution in neonates. See manufacturer’s labeling.
Other warnings/precautions:
• OTC labeling: When used for self-medication (OTC), notify health care provider before use if any of the following are present: Frequent chest pain; frequent wheezing particularly with heartburn; nausea/vomiting; unexplained weight loss; stomach pain; heartburn >3 months; heartburn with light-headedness, sweating, or dizziness; chest pain or shoulder pain with shortness of breath; sweating; pain that spreads to arms, neck, or shoulders; light-headedness. Discontinue use and notify health care provider if heartburn continues or worsens, or if use is required >14 days.
Use of gastric acid inhibitors, including proton pump inhibitors and H2 blockers, has been associated with an increased risk for development of acute gastroenteritis in infants and children ≤3 years of age and community-acquired pneumonia in pediatric patients ≥1 month of age (Canani 2006; van der Sande 2021). Very low birth weight neonates receiving H2 blockers were reported to have ~6-fold increase in mortality as well as increased risk of infection (ie, sepsis, pneumonia, urinary tract infection) (Terrin 2012). Routine use of H2 blockers in preterm infants is not recommended (AAP [Eichenwald 2018]).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous:
Generic: 20 mg (50 mL); 40 mg/4 mL (4 mL); 200 mg/20 mL (20 mL)
Solution, Intravenous [preservative free]:
Generic: 20 mg/2 mL (2 mL)
Suspension Reconstituted, Oral:
Generic: 40 mg/5 mL (50 mL, 100 mL, 150 mL)
Tablet, Oral:
Acid Reducer: 10 mg [contains corn starch]
Acid Reducer Maximum Strength: 20 mg
Famotidine Maximum Strength: 20 mg
Famotidine Orig St: 10 mg
FT Acid Reducer: 10 mg [gluten free]
FT Acid Reducer Max Strength: 20 mg [gluten free]
Heartburn Relief: 10 mg
Heartburn Relief Max St: 20 mg
Pepcid: 20 mg, 40 mg [contains corn starch]
Pepcid AC: 10 mg
Pepcid AC Maximum Strength: 20 mg
Generic: 10 mg, 20 mg, 40 mg
Yes
Solution (Famotidine (PF) Intravenous)
20 mg/2 mL (per mL): $0.44 - $0.57
Solution (Famotidine Intravenous)
40 mg/4 mL (per mL): $0.53 - $0.74
200 mg/20 mL (per mL): $0.53 - $0.54
Suspension (reconstituted) (Famotidine Oral)
40 mg/5 mL (per mL): $3.54
Tablets (Famotidine Oral)
10 mg (per each): $0.12 - $0.33
20 mg (per each): $0.06 - $2.43
40 mg (per each): $0.08 - $4.86
Tablets (Pepcid Oral)
20 mg (per each): $15.87
40 mg (per each): $30.67
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous:
Generic: 10 mg/mL (2 mL, 4 mL, 5 mL, 20 mL)
Tablet, Oral:
Generic: 20 mg, 40 mg
IV push: Administer diluted or undiluted over at least 2 minutes (Ref).
IV infusion: Administer over 15 to 30 minutes.
Oral: Administer without regard to meals. May administer with antacids.
Suspension: Shake vigorously before use.
Tablet (OTC): To prevent symptoms, administer 10 to 60 minutes before eating food or drinking beverages known to cause heartburn.
Enteral feeding tube:
The following recommendations are based upon the best available evidence and clinical expertise. Senior editorial team: Joseph I. Boullata, PharmD, RPh, CNS-S, FASPEN, FACN; Peggi A. Guenter PhD, RN, FASPEN; Kathleen Gura, PharmD, BCNSP, FASHP, FASPEN, FPPA, FMSHP; Mark G. Klang MS, RPh, BCNSP, PhD, FASPEN; Linda Lord, NP, ACNP-BC, CNSC, FASPEN.
Oral suspension (commercially available):
Gastric (eg, NG, percutaneous endoscopic gastrostomy [PEG]) or post-pyloric (eg, jejunal) tubes: Shake vigorously before use. Dilute with purified water (at least 1:1) prior to administering to reduce osmolality and viscosity; draw up diluted suspension into enteral dosing syringe and administer via feeding tube (Ref).
Dosage form information: One undiluted formulation has been reported to have an osmolality of 687 mOsm/kg (Ref); oral suspensions with an osmolality >600 mOsm/kg may increase the probability of adverse GI effects (eg, diarrhea, cramping, abdominal distention, slowed gastric emptying), particularly if administered postpylorically, inadequately diluted, and/or used in at-risk patients (eg, neonates, infants, patients with short bowel syndrome) (Ref).
General guidance: Hold enteral nutrition during famotidine administration (Ref). Flush feeding tube with an appropriate volume of purified water before administration (Ref). Following administration, rinse container used for preparation with purified water; draw up rinse and administer contents to ensure delivery of entire dose (Ref). Flush feeding tube with an appropriate volume of purified water and restart enteral nutrition (Ref).
Oral tablets:
Gastric (eg, NG, PEG) or post-pyloric (eg, jejunal) tubes: Crush and disperse tablet in 10 mL purified water; draw up mixture into enteral dosing syringe and administer via feeding tube (Ref).
Dosage form information: Some formulations may be film-coated; administration of film-coated famotidine tablets via feeding tube may increase the risk of clogging the tube; if used, ensure tablets are dispersed sufficiently with an adequate amount of purified water prior to administration (Ref).
General guidance: Hold enteral nutrition during famotidine administration (Ref). Flush feeding tube with an appropriate volume of purified water before administration (Ref). Following administration, rinse container used for preparation with purified water; draw up rinse and administer contents to ensure delivery of entire dose (Ref). Flush feeding tube with an appropriate volume of purified water and restart enteral nutrition (Ref).
Note: Recommendations may not account for differences in inactive ingredients, osmolality, or other formulation properties among manufacturers.
The following feeding tube recommendations are based upon the best available evidence and clinical expertise. Senior editor panel: Joseph I. Boullata, PharmD, RPh, CNS-S, FASPEN, FACN; Peggi A. Guenter, PhD, RN, FASPEN; Kathleen Gura, PharmD, BCNSP, FASHP, FASPEN, FPPA, FMSHP; Mark G. Klang, MS, RPh, BCNSP, PhD, FASPEN; Linda Lord, NP, ACNP-BC, CNSC, FASPEN.
Note: Recommendations may not account for differences in inactive ingredients, osmolality, or other formulation properties among manufacturers.
Oral: Administer without regard to meals. May administer with antacids.
Suspension (commercially available): Shake vigorously for 10 to 15 seconds prior to each use.
Administration via feeding tube :
Gastric (eg, NG, percutaneous endoscopic gastrostomy [PEG]) or post-pyloric (eg, jejunal) tubes: Shake vigorously prior to drawing up dose for dilution. Dilute dose with purified water (at least 1:1) prior to administration to reduce osmolality and viscosity; draw up diluted suspension into an enteral dosing syringe and administer via feeding tube (Ref).
Dosage form information: One commercially available oral suspension has a reported osmolality of ~687 mOsm/kg when undiluted; oral suspensions with an osmolality >600 mOsm/kg may increase the probability of adverse GI effects (eg, diarrhea, cramping, abdominal distention, slowed gastric emptying), particularly if administered post-pylorically, inadequately diluted, and/or used in at-risk patients (eg, neonates and infants, patients with short bowel syndrome) (Ref).
General guidance: Hold enteral nutrition during famotidine administration (Ref). Flush feeding tube with an appropriate volume of purified water before administration (Ref); consult ASPEN recommendations (Ref) or institution-specific protocols for appropriate flush volume. Following administration, rinse container used for preparation with purified water; draw up rinse and administer contents to ensure delivery of entire dose (Ref). Flush feeding tube with an appropriate volume of purified water and restart enteral nutrition (Ref).
Tablet: Take with water; to prevent symptoms, dose may be taken 10 to 60 minutes before eating food or drinking beverages known to cause heartburn.
Administration via feeding tube:
Gastric (eg, NG, PEG) or post-pyloric (eg, jejunal) tubes: Crush and disperse each tablet in 10 mL purified water; draw up mixture into enteral dosing syringe and administer via feeding tube (Ref).
Dosage form information: Some tablets may be film-coated; administration of film-coated tablets via feeding tube may increase the risk of clogging the tube; if used, ensure tablets are sufficiently dispersed prior to administration (Ref).
General guidance: Hold enteral nutrition during famotidine administration (Ref). Flush feeding tube with an appropriate volume of purified water before administration (Ref); consult ASPEN recommendations (Ref) or institution-specific protocols for appropriate flush volume. Following administration, rinse container used for preparation with purified water; draw up rinse and administer contents to ensure delivery of entire dose (Ref). Flush feeding tube with an appropriate volume of purified water and restart enteral nutrition (Ref).
Parenteral:
IV push: May be administered over at least 2 minutes.
IV infusion: Infuse over 15 to 30 minutes.
Erosive esophagitis due to gastroesophageal reflux disease: Treatment of erosive gastroesophageal reflux disease (GERD).
Note: Although a labeled indication, H2-receptor antagonists (eg, famotidine) are not preferred for the treatment of erosive esophagitis due to GERD due to the availability of proton pump inhibitors (PPIs) (ACG [Katz 2022]).
Gastroesophageal reflux disease: Treatment GERD and esophagitis due to GERD.
Heartburn (OTC only): Relief of heartburn, acid indigestion, and sour stomach.
Pathological hypersecretory conditions (eg, Zollinger-Ellison syndrome [gastrinoma]): Treatment of pathological hypersecretory conditions (eg, Zollinger-Ellison syndrome, systemic mastocytosis, multiple endocrine adenomas).
Note: Although a labeled indication, clinical experience suggests that H2-receptor antagonists (eg, famotidine) are not preferred for controlling acid hypersecretion in pathological hypersecretory conditions (eg, Zollinger-Ellison syndrome) due to the availability of PPIs (Guarnotta 2018; Ito 2013; Tomassetti 2005).
Peptic ulcer disease (duodenal or gastric ulcers): Short-term treatment of active duodenal or peptic ulcers and maintenance therapy after the healing of active duodenal ulcer.
Note: Although a labeled indication, current guidelines recommend PPIs as standard of care for treatment of peptic ulcer disease rather than H2-receptor antagonists (eg, famotidine) (ACG [Laine 2021]).
Aspiration prophylaxis in patients undergoing anesthesia; Chronic spontaneous urticaria; Infusion reaction, premedication; Mastocytosis; Stress ulcer prophylaxis in select critically ill patients
Famotidine may be confused with FLUoxetine, furosemide
Zantac 360 may be confused with Zantac (former brand name for ranitidine)
Substrate of OAT1/3, OCT1
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Acalabrutinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Acalabrutinib. Management: Give acalabrutinib capsules 2 hours before a histamine H2 receptor antagonist (H2RA). No action is required if acalabrutinib tablets are coadministered with H2RAs. Risk D: Consider therapy modification
Atazanavir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Atazanavir. Management: Specific dose limitations and administration guidelines exist; consult full interaction monograph or atazanavir prescribing information. Risk D: Consider therapy modification
Belumosudil: Histamine H2 Receptor Antagonists may decrease the serum concentration of Belumosudil. Risk C: Monitor therapy
Bosutinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Bosutinib. Management: Administer histamine H2 receptor antagonists (H2RAs) more than 2 hours before or after bosutinib. Risk D: Consider therapy modification
Cefditoren: Histamine H2 Receptor Antagonists may decrease the serum concentration of Cefditoren. Risk X: Avoid combination
Cefpodoxime: Histamine H2 Receptor Antagonists may decrease the serum concentration of Cefpodoxime. Risk C: Monitor therapy
Cefuroxime: Histamine H2 Receptor Antagonists may decrease the absorption of Cefuroxime. Management: Avoid concomitant use of oral cefuroxime axetil and H2 receptor antagonists if possible. If combined, ensure oral cefuroxime axetil is taken with food to minimize the magnitude of this interaction. Risk D: Consider therapy modification
Cysteamine (Systemic): Histamine H2 Receptor Antagonists may diminish the therapeutic effect of Cysteamine (Systemic). Risk C: Monitor therapy
Dacomitinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Dacomitinib. Management: Administer dacomitinib at least 6 hours before or 10 hours after an histamine H2-receptor antagonist (H2RA). Risk D: Consider therapy modification
Dasatinib: Histamine H2 Receptor Antagonists may decrease the absorption of Dasatinib. Management: Antacids (taken 2 hours before or after dasatinib administration) can be used in place of H2-antagonists if some acid-reducing therapy is needed. Risk X: Avoid combination
Delavirdine: Histamine H2 Receptor Antagonists may decrease the serum concentration of Delavirdine. Risk X: Avoid combination
Dichlorphenamide: May increase the serum concentration of Famotidine. Risk X: Avoid combination
Enoxacin: Histamine H2 Receptor Antagonists may decrease the absorption of Enoxacin. Risk C: Monitor therapy
Erlotinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Erlotinib. Management: Avoid H2-antagonists in patients receiving erlotinib when possible. If concomitant treatment cannot be avoided, erlotinib should be dosed once daily, 10 hours after and at least 2 hours before H2-antagonist dosing. Risk D: Consider therapy modification
Fosamprenavir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Fosamprenavir. Cimetidine may also inhibit the metabolism of the active metabolite amprenavir, making its effects on fosamprenavir/amprenavir concentrations difficult to predict. Risk C: Monitor therapy
Gefitinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Gefitinib. Management: Administer gefitinib at least 6 hours before or 6 hours after administration of a histamine H2 receptor antagonist (H2RA), and closely monitor clinical response to gefitinib. Risk D: Consider therapy modification
Indinavir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Indinavir. Risk C: Monitor therapy
Infigratinib: Histamine H2 Receptor Antagonists may decrease serum concentrations of the active metabolite(s) of Infigratinib. Histamine H2 Receptor Antagonists may decrease the serum concentration of Infigratinib. Management: Avoid coadministration of infigratinib with histamine receptor antagonists (H2RAs) or other gastric acid-lowering agents. If H2RAs cannot be avoided, administer infigratinib 2 hours before or 10 hours after administration of H2RAs. Risk D: Consider therapy modification
Itraconazole: Histamine H2 Receptor Antagonists may increase the serum concentration of Itraconazole. Histamine H2 Receptor Antagonists may decrease the serum concentration of Itraconazole. Management: Administer Sporanox brand itraconazole at least 2 hours before or 2 hours after administration of any histamine H2 receptor antagonists (H2RAs). Exposure to Tolsura brand itraconazole may be increased by H2RAs; consider itraconazole dose reduction. Risk D: Consider therapy modification
Ketoconazole (Systemic): Histamine H2 Receptor Antagonists may decrease the serum concentration of Ketoconazole (Systemic). Management: Administer ketoconazole with an acidic beverage (eg, non-diet cola) and monitor for reduced efficacy if concomitant use with a H2RA is required. Increases in ketoconazole dose may be required. Risk D: Consider therapy modification
Ledipasvir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Ledipasvir. Management: Administer H2 receptor antagonist doses less than or comparable to famotidine 40 mg twice daily simultaneously or 12 hours prior to ledipasvir. The effect of administering H2 receptor antagonists at other time intervals is unknown and not recommended. Risk D: Consider therapy modification
Levoketoconazole: Histamine H2 Receptor Antagonists may decrease the absorption of Levoketoconazole. Risk X: Avoid combination
Nelfinavir: Histamine H2 Receptor Antagonists may decrease serum concentrations of the active metabolite(s) of Nelfinavir. Histamine H2 Receptor Antagonists may decrease the serum concentration of Nelfinavir. Concentrations of the active M8 metabolite may also be reduced. Risk C: Monitor therapy
Neratinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Neratinib. Specifically, histamine H2 receptor antagonists may reduce neratinib absorption. Management: Administer neratinib at least 2 hours before or 10 hours after administration of a histamine H2 receptor antagonist to minimize the impact of this interaction. Risk D: Consider therapy modification
Nilotinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Nilotinib. Management: The nilotinib dose should be given 10 hours after or 2 hours before the H2 receptor antagonist in order to minimize the risk of a significant interaction. Risk D: Consider therapy modification
Nirogacestat: Histamine H2 Receptor Antagonists may decrease the serum concentration of Nirogacestat. Risk X: Avoid combination
Octreotide: Histamine H2 Receptor Antagonists may decrease the serum concentration of Octreotide. Risk C: Monitor therapy
PAZOPanib: Histamine H2 Receptor Antagonists may decrease the serum concentration of PAZOPanib. Risk X: Avoid combination
Pexidartinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Pexidartinib. Management: Administer pexidartinib 2 hours before or 10 hours after histamine H2 receptor antagonists. Risk D: Consider therapy modification
Posaconazole: Histamine H2 Receptor Antagonists may decrease the serum concentration of Posaconazole. Risk C: Monitor therapy
Rilpivirine: Histamine H2 Receptor Antagonists may decrease the serum concentration of Rilpivirine. Management: Administer histamine H2 receptor antagonists (H2RAs) at least 12 hours before or 4 hours after oral rilpivirine. Risk D: Consider therapy modification
Risedronate: Histamine H2 Receptor Antagonists may increase the serum concentration of Risedronate. This applies specifically to delayed-release risedronate. Risk X: Avoid combination
Saquinavir: Histamine H2 Receptor Antagonists may increase the serum concentration of Saquinavir. Management: Consider alternatives to this combination for patients taking the Invirase formulation of saquinavir. No action beyond standard clinical care measures is required for patients taking the Fortovase formulation of saquinavir. Risk D: Consider therapy modification
Secretin: Histamine H2 Receptor Antagonists may diminish the diagnostic effect of Secretin. Specifically, use of H2-Antagonists may cause a hyperresponse in gastrin secretion in response to secretin stimulation testing, falsely suggesting gastrinoma. Management: Avoid concomitant use of histamine H2-antagonists (H2RAs) and secretin. Discontinue H2RAs at least 2 days prior to secretin administration. Risk D: Consider therapy modification
Selpercatinib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Selpercatinib. Management: Coadministration of selpercatinib and H2 receptor antagonists should be avoided. If coadministration cannot be avoided, selpercatinib should be administered 2 hours before or 10 hours after H2 receptor antagonists. Risk D: Consider therapy modification
Sotorasib: Histamine H2 Receptor Antagonists may decrease the serum concentration of Sotorasib. Risk X: Avoid combination
Sparsentan: Histamine H2 Receptor Antagonists may decrease the serum concentration of Sparsentan. Risk X: Avoid combination
Sulpiride: Histamine H2 Receptor Antagonists may decrease the serum concentration of Sulpiride. Management: Consider alternatives to this combination, such as antacids given 2 hours after sulpiride, if possible. This does not apply when sulpiride and H2RAs are intentionally coadministered for the treatment of duodenal ulcers. Risk D: Consider therapy modification
Vadadustat: May increase the serum concentration of Famotidine. Risk C: Monitor therapy
Velpatasvir: Histamine H2 Receptor Antagonists may decrease the serum concentration of Velpatasvir. Risk C: Monitor therapy
Prolonged treatment (≥2 years) may lead to malabsorption of dietary vitamin B12 and subsequent vitamin B12 deficiency (Lam 2013).
Famotidine crosses the placenta (Wang 2013).
Due to pregnancy-induced physiologic changes, renal clearance of famotidine may be increased (Wang 2011).
Histamine H2 antagonists have been evaluated for the treatment of gastroesophageal reflux disease (GERD) during pregnancy. Agents other than famotidine may be preferred for initial therapy (Richter 2005; van der Woude 2014). Histamine H2 antagonists may be used for aspiration prophylaxis prior to cesarean delivery (ASA 2016).
Famotidine is present in breast milk.
The relative infant dose (RID) of famotidine is 2.2% when calculated using the highest breast milk concentration located and compared to an infant therapeutic dose of 0.5 mg/kg/day.
In general, breastfeeding is considered acceptable when the RID of a medication is <10% (Anderson 2016; Ito 2000).
The RID of famotidine was calculated using a milk concentration of 0.072 mcg/mL, providing an estimated daily infant dose via breast milk of 0.011 mg/kg/day. This milk concentration was obtained following maternal administration of a single dose of famotidine 40 mg orally (Courtney 1988).
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and benefits of treatment to the mother. When treatment with a histamine H2 antagonist is needed, famotidine is one of the preferred agents due to its lower concentrations in breast milk (Richter 2005).
CBC, gastric pH, occult blood with GI bleeding
Competitive inhibition of histamine at H2 receptors of the gastric parietal cells, which inhibits gastric acid secretion
Onset of action: Antisecretory effect: Oral: Within 1 hour
Peak effect: Antisecretory effect: Oral: Within 1 to 3 hours (dose-dependent); IV: Within 30 minutes
Duration: Antisecretory effect: IV, Oral: 10 to 12 hours
Absorption: Oral: Incompletely absorbed
Distribution: Vd: IV:
Infants: ≤3 months: 1.4 ± 0.4 L/kg to 1.8 ± 0.3 L/kg; >3 to 12 months: 2.3 ± 0.7 L/kg
Children <11 years: 2.07 ± 1.49 L/kg
Children ≥11 years and Adolescents ≤15 years: 1.5 ± 0.4 L/kg
Adults: 1.3 ± 0.2 L/kg
Protein binding: 15% to 20%
Metabolism: 30% to 35%; minimal first-pass metabolism; forms one metabolite (S-oxide)
Bioavailability: Oral: 40% to 45%
Half-life elimination: IV:
Infants: ≤3 months: 8.1 ± 3.5 hours to 10.5 ± 5.4 hours; >3 to 12 months: 4.5 ± 1.1 hours
Children <11 years: 3.38 ± 2.6 hours
Children ≥11 years and Adolescents ≤15 years: 2.3 ± 0.4 hours
Adults: 2.5 to 3.5 hours; prolonged with kidney impairment; Oliguria: >20 hours; Anuria: 24 hours
Time to peak, serum: Oral: ~1 to 3 hours
Excretion: Urine (25% to 30% [oral], 65% to 70% [IV] as unchanged drug)
Clearance: IV:
Infants: ≤3 months: 0.13 ± 0.06 to 0.21 ± 0.06 L/hour/kg; >3 to 12 months: 0.49 ± 0.17 L/hour/kg
Children <11 years: 0.54 ± 0.34 L/hour/kg
Children ≥11 years and Adolescents ≤15 years: 0.48 ± 0.14 L/hour/kg
Adults: 0.39 ± 0.14 L/hour/kg
Altered kidney function: AUC increased at least 5-fold and at least 2-fold in adults with CrCl <30 mL/minute and CrCl 30 to 60 mL/minute, respectively.
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