Pepcid

H2 Antagonists

May be administered without regard to meals.

Tablets: May administer with food, water, or milk to minimize gastric irritation.
Orally disintegrating tablets: No water is needed for administration. Instruct patients to open the tablet blister pack with dry hands, place the tablet on the tongue, allow to disintegrate, then swallow with saliva.

Oral suspension
Reconstitute by slowly adding 46 mL of purified water. Shake vigorously for 5 to 10 seconds after adding water.
After reconstitution, each 5 mL contains 40 mg of famotidine.
Shake suspension well before each use. Measure dosage with a calibrated device for accuracy.
Storage of reconstituted suspension: Store at room temperature for up to 30 days.[51477]

Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.[51456]
Updates for coronavirus disease 2019 (COVID-19): The FDA is allowing famotidine 10 mg/mL to be used beyond the labeled in-use time to help ensure access during COVID-related drug shortages. This period should be as short as possible, and for a maximum of 2 hours at room temperature or 4 hours when refrigerated. In-use time is defined as the maximum amount of time allowed to elapse between penetration of a closed-container system or after reconstitution of a lyophilized drug before patient administration.[65833]

Intermittent IV Injection
Dilute 20 mg of famotidine injection to a total of 5 or 10 mL with 0.9% Sodium Chloride Injection or other compatible solution to give concentrations of 4 or 2 mg/mL, respectively.
Inject appropriate dose over 2 minutes or more and at a rate of 10 mg/minute or less.[51456]
 
Intermittent IV Infusion (vials)
Dilute 20 mg of famotidine in 100 mL of 5% Dextrose Injection or 0.9% Sodium Chloride Injection or other compatible IV solution to give a final concentration of 0.2 mg/mL.
Infuse over 15 to 30 minutes.
Storage: If not used immediately, store diluted solutions under refrigeration and use within 48 hours of preparation. Although when diluted in common compatible solutions (e.g., 0.9% Sodium Chloride Injection, 5% Dextrose Injection, Lactated Ringer's Injection), famotidine is stable for 7 days at room temperature, there are no data available to confirm sterility under these conditions.[51456]
 
Intermittent IV Infusion (Galaxy containers)
The premixed infusion container contains famotidine 20 mg per 50 mL 0.9% Sodium Chloride Injection.
Check the container for leaks before use by squeezing the bag firmly. If leaks are found, discard solution as sterility may be impaired.
Do not add supplementary medication.
Do not use unless solution is clear, and the seal is intact.
Do not use plastic containers in series connections. Such use could result in air embolism due to residual air being drawn from the primary container before administration of the fluid from the secondary container is complete.
Suspend container from eyelet support.
Remove plastic protector from outlet port at bottom of container.
Attach administration set. Refer to complete directions accompanying set.
Infuse over 15 to 30 minutes.[51456]
 
Continuous IV Infusion
For adults, dilute 40 mg of famotidine in 250 mL of 5% Dextrose Injection or 0.9% Sodium Chloride Injection or other compatible solution. Infuse over 24 hours at a rate of 11 mL/hour or as specified by a physician.
Use a controlled-rate infusion device.
Storage: The diluted solution is stable for up to 48 hours at room temperature.
Alternatively, the dosage may be added to a compatible TPN solution for administration over 24 hours.[51493]

seizures / Delayed / Incidence not known
toxic epidermal necrolysis / Delayed / Incidence not known
Stevens-Johnson syndrome / Delayed / Incidence not known
anaphylactoid reactions / Rapid / Incidence not known
angioedema / Rapid / Incidence not known
atrophic gastritis / Delayed / Incidence not known
arrhythmia exacerbation / Early / Incidence not known
AV block / Early / Incidence not known
agranulocytosis / Delayed / Incidence not known
pancytopenia / Delayed / Incidence not known
bronchospasm / Rapid / Incidence not known
rhabdomyolysis / Delayed / Incidence not known

constipation / Delayed / 1.2-1.2
jaundice / Delayed / Incidence not known
cholestasis / Delayed / Incidence not known
hepatitis / Delayed / Incidence not known
delirium / Early / Incidence not known
depression / Delayed / Incidence not known
confusion / Early / Incidence not known
hallucinations / Early / Incidence not known
edema / Delayed / Incidence not known
conjunctivitis / Delayed / Incidence not known
palpitations / Early / Incidence not known
QT prolongation / Rapid / Incidence not known
leukopenia / Delayed / Incidence not known
thrombocytopenia / Delayed / Incidence not known
impotence (erectile dysfunction) / Delayed / Incidence not known
vitamin B12 deficiency / Delayed / Incidence not known
pernicious anemia / Delayed / Incidence not known

headache / Early / 4.7-4.7
diarrhea / Early / 1.7-1.7
dizziness / Early / 1.3-1.3
nausea / Early / Incidence not known
anorexia / Delayed / Incidence not known
dysgeusia / Early / Incidence not known
vomiting / Early / Incidence not known
xerostomia / Early / Incidence not known
agitation / Early / Incidence not known
drowsiness / Early / Incidence not known
paranoia / Early / Incidence not known
paresthesias / Delayed / Incidence not known
insomnia / Early / Incidence not known
anxiety / Delayed / Incidence not known
libido decrease / Delayed / Incidence not known
urticaria / Rapid / Incidence not known
flushing / Rapid / Incidence not known
xerosis / Delayed / Incidence not known
pruritus / Rapid / Incidence not known
acne vulgaris / Delayed / Incidence not known
rash / Early / Incidence not known
alopecia / Delayed / Incidence not known
infection / Delayed / Incidence not known
fever / Early / Incidence not known
musculoskeletal pain / Early / Incidence not known
arthralgia / Delayed / Incidence not known
gynecomastia / Delayed / Incidence not known
lethargy / Early / Incidence not known
fatigue / Early / Incidence not known
tinnitus / Delayed / Incidence not known
asthenia / Delayed / Incidence not known
muscle cramps / Delayed / Incidence not known

Heartburn Relief, Pepcid, Pepcid AC, Pepcid AC Maximum Strength, Zantac, Zantac 360

OTC, Rx

Oral/parenteral histamine type 2-receptor antagonist
Used for GI disorders such as peptic ulcer and gastroesophageal reflux disease
Fewer drug interactions than cimetidine

10 to 20 mg PO twice daily as needed. Max: 40 mg/day.

10 to 20 mg PO twice daily as needed. Max: 40 mg/day.

20 mg PO twice daily for up to 6 weeks.

0.5 mg/kg/dose PO twice daily (Max: 40 mg PO twice daily). Treat for 6 to 12 weeks. While famotidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

0.5 mg/kg/dose PO twice daily initially, in addition to conservative measures such as thickened feedings. May increase the dose to 1 mg/kg/dose PO twice daily if needed. Treat for up to 8 weeks. While famotidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

0.5 mg/kg/dose PO once daily initially, in addition to conservative measures such as thickened feedings. May increase the dose to 1 mg/kg/dose PO once daily if needed. Treat for up to 8 weeks. While famotidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

0.5 mg/kg/dose PO once daily initially, in addition to conservative measures such as thickened feedings. May increase the dose to 1 mg/kg/dose PO once daily if needed. Treat for up to 8 weeks. While famotidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

0.25 mg/kg/dose IV every 12 hours (Max: 40 mg/day) is the FDA-approved dose; doses up to 0.5 mg/kg/dose IV every 12 hours have been used. A dose of 0.5 mg/kg/dose IV every 8 to 12 hours is supported by pharmacokinetic and pharmacodynamic data.

Safety and efficacy have not been established; however, doses of 0.25 to 0.5 mg/kg/dose IV twice daily have been used in 1 small study.

Safety and efficacy have not been established; however, doses of 0.25 to 0.5 mg/kg/dose IV once daily have been used in 1 small study.

Safety and efficacy have not been established; however, doses of 0.25 to 0.5 mg/kg/dose IV once daily have been used in 1 small study.

20 or 40 mg PO twice daily for up to 12 weeks.

0.5 mg/kg/dose PO twice daily (Max: 40 mg PO twice daily). Treat for 6 to 12 weeks. While famotidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

0.5 mg/kg/dose PO twice daily initially, in addition to conservative measures such as thickened feedings. May increase the dose to 1 mg/kg/dose PO twice daily if needed. Treat for up to 8 weeks. While famotidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

0.5 mg/kg/dose PO once daily initially, in addition to conservative measures such as thickened feedings. May increase the dose to 1 mg/kg/dose PO once daily if needed. Treat for up to 8 weeks. While famotidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

0.5 mg/kg/dose PO once daily initially, in addition to conservative measures such as thickened feedings. May increase the dose to 1 mg/kg/dose PO once daily if needed. Treat for up to 8 weeks. While famotidine may be effective in patients with less severe GERD, proton pump inhibitors (PPIs) offer more rapid symptom relief and better healing.

0.25 mg/kg/dose IV every 12 hours (Max: 40 mg/day) is the FDA-approved dose; doses up to 0.5 mg/kg/dose IV every 12 hours have been used. A dose of 0.5 mg/kg/dose IV every 8 to 12 hours is supported by pharmacokinetic and pharmacodynamic data.

Safety and efficacy have not been established; however, doses of 0.25 to 0.5 mg/kg/dose IV twice daily have been used in 1 small study.

Safety and efficacy have not been established; however, doses of 0.25 to 0.5 mg/kg/dose IV once daily have been used in 1 small study.

Safety and efficacy have not been established; however, doses of 0.25 to 0.5 mg/kg/dose IV once daily have been used in 1 small study.

40 mg PO once daily at bedtime. Most duodenal ulcer patients heal within 4 weeks and full-dose therapy is rarely needed for longer than 6 to 8 weeks.

0.5 mg/kg/day PO at bedtime or 0.25 mg/kg/dose PO twice daily initially (Max: 40 mg/day). Doses up to 1 mg/kg/day (Max: 40 mg/day) PO have been used. Individualize treatment duration and dose based on clinical response and/or pH determination (gastric or esophageal) and endoscopy. In one small study, a treatment duration of 8 weeks was effective for the treatment of gastric or duodenal ulcer.

20 mg IV every 12 hours.

0.25 mg/kg/dose IV every 12 hours (Max: 40 mg/day) is recommended by the manufacturer. An initial dose of 0.5 mg/kg/dose IV every 8 to 12 hours is supported by pharmacokinetic and pharmacodynamic data.

20 mg PO once daily at bedtime.

20 mg PO every 6 hours, initially. May titrate. Maximum: 160 mg PO every 6 hours per the manufacturer. Clinically, adjust to patient response. Doses as high as 200 mg PO every 6 hours have been reported.

20 mg IV every 6 hours when oral therapy is not feasible; higher doses may be needed and therapy should be individualized based on patient response.

40 mg PO twice daily. Data from clinical trials note that only higher doses of H2-blockers are effective at reducing risk for gastric ulceration from NSAIDs. In one trial, patients receiving a NSAID for either rheumatoid arthritis or osteoarthritis were given famotidine 20 mg PO twice daily, famotidine 40 mg PO twice daily, or placebo for 24 weeks. The cumulative incidence of gastric ulcer was significantly reduced by famotidine 40 mg but not the lower dose compared to placebo. The cumulative incidence of duodenal ulcer was significantly reduced by both famotidine doses relative to placebo.

20 mg PO every 12 hours.

20 mg IV every 12 hours.

1 to 2 mg/kg/day IV divided every 8 to 12 hours (Max: 40 mg/day).[51510] [51511] [51981]

10 mg IV bolus, followed by 1.7 mg/hour (40 mg/day) continuous IV infusion.

20 mg PO as a single dose given 3 hours prior to the time of surgery, before induction of anesthesia. Alternatively, 40 mg PO the night prior to elective surgery. According to guidelines of the American Society of Anesthesiologists, routine preoperative use is NOT recommended in patients who have no apparent increased risk for pulmonary aspiration. However, some guidelines recommend an H2-receptor antagonist (PO or IV) for all women presenting for cesarean delivery.

20 mg IV in the morning prior to surgery, before induction of anesthesia. According to guidelines of the American Society of Anesthesiologists, routine preoperative use is NOT recommended in patients who have no apparent increased risk for pulmonary aspiration. However, some guidelines recommend an H2-receptor antagonist (PO or IV) for all women presenting for cesarean delivery.

20 mg IV as a single dose.

0.25 mg/kg/dose (Max: 20 mg/dose) IV as a single dose.

20 mg PO as a single dose.

0.25 mg/kg/dose (Max: 20 mg/dose) PO as a single dose.

†Indicates off-label use

Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.

General Recommendations
Adults
GFR more than 50 mL/minute: Administer 50% to 75% of normal dose.
GFR 10 to 50 mL/minute: Administer 10% to 50% of normal dose.
GFR less than 10 mL/minute: Administer 10% of normal dose.
Pediatrics
The following has been recommended based on a dose of 0.5 to 1 mg/kg/DAY divided every 12 hours in patients with normal renal function:
GFR 30 to 50 mL/minute/1.73 m2: 0.5 mg/kg/dose every 24 hours.
GFR 10 to 29 mL/minute/1.73 m2: 0.25 mg/kg/dose every 24 hours.
GFR less than 10 mL/minute/1.73 m2: 0.125 mg/kg/dose every 24 hours.
 
Intravenous Dosage
Adults
CrCl less than 50 mL/minute: Decrease dose 50% or extend the dosing interval to 36 to 48 hours based on clinical response.
Pediatrics
The following guidance has been recommended based on a pharmacokinetic study of pediatric patients with stable chronic renal insufficiency (n = 18):
CrCl 50 mL/minute/1.73m2 or more: 0.5 mg/kg/dose (Max: 20 mg) IV every 12 to 24 hours.
CrCl 11 to 49 mL/minute/1.73m2: 0.5 mg/kg/dose (Max: 20 mg) IV every 36 to 48 hours.
CrCl 10 mL/minute/1.73m2 or less: 0.5 mg/kg/dose (Max: 20 mg) IV every 72 to 96 hours or 0.25 mg/kg/dose (Max: 10 mg) IV every 36 to 48 hours.[51466]
 
Oral Dosage
Adults and Pediatric patients weighing 40 kg or more (maximum recommended dosage)
Active duodenal or gastric ulcer:
CrCl 30 to 60 mL/minute: 20 mg PO once daily or 40 mg PO every other day.
CrCl less than 30 mL/minute: 10 mg PO once daily or 20 mg PO every other day.
Symptomatic nonerosive GERD:
CrCl 30 to 60 mL/minute: 20 mg PO once daily.
CrCl less than 30 mL/minute: 10 mg PO once daily or 20 mg PO every other day.
Erosive esophagitis diagnosed by endoscopy:
CrCl 30 to 60 mL/minute: 20 mg PO once daily, 40 mg PO once daily, or 40 mg PO every other day.
CrCl less than 30 mL/minute: 10 mg PO once daily, 20 mg PO once daily, or 20 mg PO every other day.
Risk reduction for duodenal ulcer recurrence:
CrCl 30 to 60 mL/minute: 10 mg PO once daily or 20 mg PO every other day.
CrCl less than 30 mL/minute: 10 mg PO every other day.
Pathological hypersecretory conditions: Avoid use.
 
Intermittent hemodialysis
Adults
Dose after dialysis.
Pediatrics
0.125 mg/kg/dose every 24 hours.
 
Peritoneal dialysis
Adults
Administer 10% of normal dose.
Pediatrics
0.125 mg/kg/dose every 24 hours.
 
Continuous renal replacement therapy (CRRT)
Adults
Administer 10% to 50% of normal dose.
Pediatrics
0.5 mg/kg/dose every 24 hours.

Acalabrutinib: (Moderate) Separate the administration of acalabrutinib capsules and H2-blockers if these agents are used together; administer acalabrutinib capusles 2 hours before the H2-blocker. Acalabrutinib capsule solubility decreases with increasing pH values; therefore, coadministration may result in decreased acalabrutinib exposure and effectiveness.
Albuterol; Budesonide: (Moderate) Monitor for loss of oral, enteric-coated budesonide efficacy during concomitant famotidine use. Since the dissolution of oral, enteric-coated budesonide is pH dependent, the release properties and uptake of the drug may be altered when used after H2-blockers.
Alogliptin; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Amphetamine; Dextroamphetamine Salts: (Moderate) Use amphetamine; dextroamphetamine and H2-blockers concomitantly with caution. Gastrointestinal alkalinizing agents may increase exposure to amphetamine; dextroamphetamine and exacerbate its actions.
Aripiprazole: (Minor) Coadministration of aripiprazole with famotidine decreases aripiprazole's solubility and rate of absorption. The Cmax of aripiprazole and the metabolite dehydroaripiprazole are decreased by 37% and 21%, respectively, and the AUC of aripiprazole and the dehydroaripiprazole metabolite are decreased by 13% and 15%, respectively. This interaction does not appear to cause clinically relevant effects and therefore no dosage adjustments are required.
Atazanavir: (Major) Coadministration of H2-blockers with atazanavir reduces serum atazanavir concentrations; however, H2-blockers can be used under specific administration restrictions. Although data are insufficient to recommend atazanavir dosing in children < 40 kg receiving concomitant H2-blockers, the same recommendations regarding timing and maximum doses of concomitant H2-blockers should be followed. In treatment-naive patients >= 40 kg, do not exceed an H2- blocker dose equivalent to famotidine 40 mg twice daily, and give atazanavir 300 mg with ritonavir 100 mg once daily with food. Give atazanavir simultaneously with and/or at least 10 hours after the H2- blocker. If a treatment-naive adult or adolescent (>= 40 kg) cannot tolerate ritonavir, do not exceed an H2- blocker dose equivalent to famotidine 20 mg twice daily, and the atazanavir dose should be increased to 400 mg once daily with food given at least 2 hours before or 10 hours after the H2- blocker. Data are insufficent to recommend atazanavir dosing in children or adolescents < 40 kg not receiving ritonavir boosting. In treatment-naive patients on a cobicistat-boosted regimen, cobicistat and atazanavir may be administered without dosage adjustment if given at the same time or a minimum of 10 hours after dosing of the H2-blocker. The H2-blocker dose should not exceed a dose that is comparable to 40 mg/day of famotidine in treatment-naive patients. In treatment-experienced patients >= 40 kg, do not exceed an H2- blocker dose equivalent to famotidine 20 mg twice daily, and give atazanavir 300 mg with ritonavir 100 mg once daily with food. Give atazanavir simultaneously with and/or at least 10 hours after the H2- blocker. In treatment-experienced patients >= 40 kg receiving H2-antagonists and tenofovir, atazanavir should be dosed 400 mg with ritonavir 100 mg once daily with food. In antiretroviral-experienced patients on a cobicistat-boosted regimen, the dosage of cobicistat with atazanavir needs to be increased if administered with H2-blockers; the recommended dose is cobicistat 150 mg/day with atazanavir 400 mg/day and 20 mg/day or less of famotidine or other comparably dosed H2-blocker. Significant reductions in atazanavir serum concentrations may lead to therapeutic failure and the development of HIV resistance. Closely monitor patients for antiretroviral therapeutic failure and resistance development during treatment with an H2- blocker.
Atazanavir; Cobicistat: (Major) Coadministration of H2-blockers with atazanavir reduces serum atazanavir concentrations; however, H2-blockers can be used under specific administration restrictions. Although data are insufficient to recommend atazanavir dosing in children < 40 kg receiving concomitant H2-blockers, the same recommendations regarding timing and maximum doses of concomitant H2-blockers should be followed. In treatment-naive patients >= 40 kg, do not exceed an H2- blocker dose equivalent to famotidine 40 mg twice daily, and give atazanavir 300 mg with ritonavir 100 mg once daily with food. Give atazanavir simultaneously with and/or at least 10 hours after the H2- blocker. If a treatment-naive adult or adolescent (>= 40 kg) cannot tolerate ritonavir, do not exceed an H2- blocker dose equivalent to famotidine 20 mg twice daily, and the atazanavir dose should be increased to 400 mg once daily with food given at least 2 hours before or 10 hours after the H2- blocker. Data are insufficent to recommend atazanavir dosing in children or adolescents < 40 kg not receiving ritonavir boosting. In treatment-naive patients on a cobicistat-boosted regimen, cobicistat and atazanavir may be administered without dosage adjustment if given at the same time or a minimum of 10 hours after dosing of the H2-blocker. The H2-blocker dose should not exceed a dose that is comparable to 40 mg/day of famotidine in treatment-naive patients. In treatment-experienced patients >= 40 kg, do not exceed an H2- blocker dose equivalent to famotidine 20 mg twice daily, and give atazanavir 300 mg with ritonavir 100 mg once daily with food. Give atazanavir simultaneously with and/or at least 10 hours after the H2- blocker. In treatment-experienced patients >= 40 kg receiving H2-antagonists and tenofovir, atazanavir should be dosed 400 mg with ritonavir 100 mg once daily with food. In antiretroviral-experienced patients on a cobicistat-boosted regimen, the dosage of cobicistat with atazanavir needs to be increased if administered with H2-blockers; the recommended dose is cobicistat 150 mg/day with atazanavir 400 mg/day and 20 mg/day or less of famotidine or other comparably dosed H2-blocker. Significant reductions in atazanavir serum concentrations may lead to therapeutic failure and the development of HIV resistance. Closely monitor patients for antiretroviral therapeutic failure and resistance development during treatment with an H2- blocker.
Bisacodyl: (Minor) The concomitant use of bisacodyl tablets with H2-blockers can cause the enteric coating of the bisacody tablet to dissolve prematurely, leading to possible gastric irritation or dyspepsia. Avoid H2-blockers within 1 hour before or after the bisacodyl dosage.
Bismuth Subsalicylate: (Minor) H2-blockers may increase the systemic absorption of bismuth from bismuth-containing compounds like bismuth subsalicylate.
Bismuth Subsalicylate; Metronidazole; Tetracycline: (Minor) H2-blockers may increase the systemic absorption of bismuth from bismuth-containing compounds like bismuth subsalicylate.
Bosutinib: (Moderate) Bosutinib displays pH-dependent aqueous solubility; therefore, concomitant use of bosutinib and H2-blockers may result in decreased plasma exposure of bosutinib. Separate the administration of bosutinib and H2-blockers by more than 2 hours.
Budesonide: (Moderate) Monitor for loss of oral, enteric-coated budesonide efficacy during concomitant famotidine use. Since the dissolution of oral, enteric-coated budesonide is pH dependent, the release properties and uptake of the drug may be altered when used after H2-blockers.
Budesonide; Formoterol: (Moderate) Monitor for loss of oral, enteric-coated budesonide efficacy during concomitant famotidine use. Since the dissolution of oral, enteric-coated budesonide is pH dependent, the release properties and uptake of the drug may be altered when used after H2-blockers.
Budesonide; Glycopyrrolate; Formoterol: (Moderate) Monitor for loss of oral, enteric-coated budesonide efficacy during concomitant famotidine use. Since the dissolution of oral, enteric-coated budesonide is pH dependent, the release properties and uptake of the drug may be altered when used after H2-blockers.
Bupivacaine; Lidocaine: (Moderate) Concomitant use of systemic lidocaine and famotidine may increase lidocaine plasma concentrations by decreasing lidocaine clearance and therefore prolonging the elimination half-life. Monitor for lidocaine toxicity if used together. Lidocaine is a CYP3A4 and CYP1A2 substrate; famotidine inhibits CYP1A2.
Cabotegravir; Rilpivirine: (Moderate) Coadministration with famotidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of famotidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Canagliflozin; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Cefpodoxime: (Moderate) H2-blockers should be avoided during treatment with cefpodoxime. Coadministration could result in antibiotic failure. H2-blockers increase gastric pH. Cefpodoxime proxetil requires low gastric pH for dissolution. While the rate of absorption is not affected, coadministration reduces cefpodoxime AUC, peak plasma concentration (by 42%), and extent of absorption (by 32%).
Cefuroxime: (Major) Avoid the concomitant use of H2-blockers and cefuroxime. Drugs that reduce gastric acidity, such as H2-blockers, can interfere with the oral absorption of cefuroxime axetil and may result in reduced antibiotic efficacy.
Cysteamine: (Major) Monitor white blood cell (WBC) cystine concentration closely when administering delayed-release cysteamine (Procysbi) with H2-blockers. Drugs that increase the gastric pH may cause the premature release of cysteamine from delayed-release capsules, leading to an increase in WBC cystine concentration.
Dacomitinib: (Moderate) Administer dacomitinib at least 6 hours before or 10 hours after taking famotidine due to the risk of decreased plasma concentrations of dacomitinib which may impact efficacy. Although the effect of H2-blockers on dacomitinib pharmacokinetics has not been studied, coadministration with a proton pump inhibitor decreased the dacomitinib Cmax and AUC by 51% and 39%, respectively.
Dapagliflozin; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Dasatinib: (Major) Do not administer H2-blockers with dasatinib due to the potential for decreased dasatinib exposure and reduced efficacy. Consider using an antacid if acid suppression therapy is needed. Administer the antacid at least 2 hours prior to or 2 hours after the dose of dasatinib. Concurrent use of an H2-blocker reduced the mean Cmax and AUC of dasatinib by 63% and 61%, respectively.
Delavirdine: (Major) Coadministration of delavirdine with H2-blockers results in decreased absorption of delavirdine. Administration of delavirdine and H2-blockers should be separated by at least 1 hour. Chronic use of H2-blockers with delavirdine is not recommended.
Dichlorphenamide: (Major) Concomitant use of dichlorphenamide and famotidine is not recommended because of an increased risk of famotidine-related adverse effects. Monitor closely for signs of famotidine-related drug toxicity if coadministration cannot be avoided. Increased famotidine exposure is possible. Dichlorphenamide inhibits OAT1. Famotidine is a sensitive OAT1 substrate. Consider if an alternative to famotidine would be appropriate for the patient.
Diphenhydramine; Naproxen: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Dolutegravir; Rilpivirine: (Moderate) Coadministration with famotidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of famotidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Empagliflozin; Linagliptin; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Empagliflozin; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Emtricitabine; Rilpivirine; Tenofovir alafenamide: (Moderate) Coadministration with famotidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of famotidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Emtricitabine; Rilpivirine; Tenofovir Disoproxil Fumarate: (Moderate) Coadministration with famotidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of famotidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Erlotinib: (Major) If concomitant use of erlotinib with famotidine is necessary, erlotinib must be taken 10 hours after the last dose of famotidine and at least 2 hours before the next dose. Erlotinib displays pH-dependent solubility with decreased solubility at a higher pH; the increased gastric pH resulting from famotidine therapy may reduce the bioavailability of erlotinib. Increasing the dose of erlotinib without modifying the administration schedule is unlikely to compensate for loss of exposure. Erlotinib exposure was decreased by 33% and the Cmax by 54% when erlotinib was administered 2 hours after a single dose of an H2-antagonist. When administered at least 10 hours after an evening dose of an H2-antagonist and 2 hours before the morning dose, erlotinib exposure was decreased by 15% and Cmax by 17%.
Ertugliflozin; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Fosamprenavir: (Moderate) Monitor for decreased fosamprenavir efficacy if coadministered with H2-blockers. Concurrent use may decrease the plasma concentrations of fosamprenavir leading to a reduction of antiretroviral efficacy and the potential development of viral resistance.
Gefitinib: (Major) Avoid coadministration of famotidine with gefitinib if possible due to decreased exposure to gefitinib, which may lead to reduced efficacy. If concomitant use is unavoidable, take gefitinib 6 hours after the last dose or 6 hours before the next dose of famotidine. Gefitinib exposure is affected by gastric pH. Coadministration with high doses of another H2-blocker to maintain gastric pH above 5 decreased gefitinib exposure by 47%.
Glipizide; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Glyburide; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Infigratinib: (Moderate) Separate the administration of infigratinib and H2-receptor antagonists if concomitant use is necessary. Coadministration may decrease infigratinib exposure resulting in decreased efficacy. Administer infigratinib two hours before or ten hours after an H2-receptor antagonist.
Iron: (Minor) The bioavailability of oral iron salts is influenced by gastric pH, and the concomitant administration of H2-blockers can decrease iron absorption. The non-heme ferric form of iron needs an acidic intragastric pH to be reduced to ferrous and to be absorbed. Iron salts and polysaccharide-iron complex provide non-heme iron. H2-blockers have long-lasting effects on the secretion of gastric acid and thus, increase the pH of the stomach. The increase in intragastric pH can interfere with the absorption of iron salts.
Itraconazole: (Moderate) When administering H2-blockers with the 100 mg itraconazole capsule and 200 mg itraconazole tablet formulations, systemic exposure to itraconazole is decreased. Conversely, exposure to itraconazole is increased when H2-blockers are administered with the 65 mg itraconazole capsule. Administer H2-blockers at least 2 hours before or 2 hours after the 100 mg capsule or 200 mg tablet. Monitor for increased itraconazole-related adverse effects if H2-blockers are administered with itraconazole 65 mg capsules.
Ketoconazole: (Major) Avoid use of H2-blockers with ketoconazole. Medications that increase gastric pH may impair ketoconazole absorption.
Ledipasvir; Sofosbuvir: (Major) Solubility of ledipasvir decreases as gastric pH increases; thus, coadministration of ledipasvir; sofosbuvir with H2-blockers may result in lower ledipasvir plasma concentrations. Ledipasvir; sofosbuvir can be administered with H2-blockers if given simultaneously or separated by 12 hours. The H2-blocker dose should not exceed a dose that is comparable to famotidine 40 mg twice daily.
Levoketoconazole: (Major) Avoid use of H2-blockers with ketoconazole. Medications that increase gastric pH may impair ketoconazole absorption.
Lidocaine: (Moderate) Concomitant use of systemic lidocaine and famotidine may increase lidocaine plasma concentrations by decreasing lidocaine clearance and therefore prolonging the elimination half-life. Monitor for lidocaine toxicity if used together. Lidocaine is a CYP3A4 and CYP1A2 substrate; famotidine inhibits CYP1A2.
Lidocaine; Epinephrine: (Moderate) Concomitant use of systemic lidocaine and famotidine may increase lidocaine plasma concentrations by decreasing lidocaine clearance and therefore prolonging the elimination half-life. Monitor for lidocaine toxicity if used together. Lidocaine is a CYP3A4 and CYP1A2 substrate; famotidine inhibits CYP1A2.
Lidocaine; Prilocaine: (Moderate) Concomitant use of systemic lidocaine and famotidine may increase lidocaine plasma concentrations by decreasing lidocaine clearance and therefore prolonging the elimination half-life. Monitor for lidocaine toxicity if used together. Lidocaine is a CYP3A4 and CYP1A2 substrate; famotidine inhibits CYP1A2.
Linagliptin; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Mefloquine: (Moderate) H2-blockers may increase plasma concentrations of mefloquine. Patients on chronic mefloquine therapy might be at increased risk of adverse reactions, especially patients with a neurological or psychiatric history. In a small study involving 6 healthy subjects and 6 peptic ulcer patients, cimetidine increased the Cmax and AUC of mefloquine. In the study, the pharmacokinetics of mefloquine were determined after receiving a single oral mefloquine 500 mg dose alone and after 3-days of cimetidine 400 mg PO twice daily. In both healthy subjects and peptic ulcer patients, Cmax was increased 42.4% and 20.5%, respectively. The AUC was increased by 37.5% in both groups. Elimination half-life, total clearance, and volume of distribution were not significantly affected. An increase in adverse reactions was not noted.
Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Metformin; Repaglinide: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Metformin; Rosiglitazone: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Metformin; Saxagliptin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Metformin; Sitagliptin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Naproxen: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Naproxen; Esomeprazole: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Naproxen; Pseudoephedrine: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Neratinib: (Major) Take neratinib at least 2 hours before the next dose of an H2-blocker or 10 hours after the last dose of an H2-blocker due to decreased absorption and systemic exposure of neratinib; the solubility of neratinib decreases with increasing pH of the GI tract. The Cmax and AUC of neratinib were reduced by 57% and 48%, respectively, when administered 2 hours after a daily dose of ranitidine 300 mg. The Cmax and AUC of neratinib were reduced by 44% and 32%, respectively, when administered 2 hours before ranitidine 150 mg twice daily (given approximately 12 hours apart).
Nilotinib: (Moderate) If concomitant use of these agents is necessary, administer the H2-blocker approximately 10 hours before and approximately 2 hours after the nilotinib dose. Nilotinib displays pH-dependent solubility with decreased solubility at a higher pH. The concomitant use of nilotinib and H2-blockers that elevate the gastric pH may reduce the bioavailability of nilotinib. In a study in healthy subjects, there was no significant change in nilotinib pharmacokinetics when a single 400-mg nilotinib dose was given 10 hours after and 2 hours prior to famotidine.
Octreotide: (Moderate) Coadministration of oral octreotide with H2-blockers may require increased doses of octreotide. Coadministration of oral octreotide with drugs that alter the pH of the upper GI tract, including H2-blockers, may alter the absorption of octreotide and lead to a reduction in bioavailability.
Pazopanib: (Major) Avoid coadministration of pazopanib with H2-blockers due to decreased absorption of pazopanib, which may decrease efficacy. If concomitant administration with a gastric acid-reducing agent is unavoidable, consider the use of a short-acting antacid in place of an H2-blocker; separate administration of the short-acting antacid and pazopanib by several hours to avoid a reduction in pazopanib exposure. Concomitant use of pazopanib with a proton pump inhibitor decreased pazopanib exposure (AUC and Cmax) by approximately 40%.
Pexidartinib: (Moderate) Administer pexidartinib 2 hours before or 10 hours after H2-blockers as concurrent administration may reduce pexidartinib exposure. Although the effects of H2-blockers on pexidartinib pharmacokinetics have not been studied, other acid-reducing agents have been shown to decrease pexidartinib exposure by 50%.
Pioglitazone; Metformin: (Minor) Famotidine may decrease the renal clearance of metformin secondary to competition for renal tubular transport systems. Such an interaction has been observed when cimetidine was administered with metformin. The decrease in renal excretion led to a 40% increase in metformin AUC. Although interactions with cationic drugs remain theoretical (except for cimetidine), caution is warranted when famotidine and metformin are prescribed concurrently. Famotidine may be less likely to interact with metformin versus cimetidine or ranitidine because of less tubular excretion.
Polyethylene Glycol; Electrolytes; Bisacodyl: (Minor) The concomitant use of bisacodyl tablets with H2-blockers can cause the enteric coating of the bisacody tablet to dissolve prematurely, leading to possible gastric irritation or dyspepsia. Avoid H2-blockers within 1 hour before or after the bisacodyl dosage.
Rasagiline: (Moderate) Monitor for dopaminergic adverse effects during concurrent use of rasagiline and famotidine. Coadministration may result in increased rasagiline concentrations. A dose reduction of rasagiline may be necessary. Rasagiline is primarily metabolized by CYP1A2; famotidine is a weak CYP1A2 inhibitor. When administered with a strong CYP1A2 inhibitor, the AUC of rasagiline was increased by 83%.
Rilpivirine: (Moderate) Coadministration with famotidine may significantly decrease rilpivirine plasma concentrations, potentially resulting in treatment failure. To decrease the risk of virologic failure, avoid use of famotidine for at least 12 hours before and at least 4 hours after administering rilpivirine.
Risedronate: (Major) Use of H2-blockers with delayed-release risedronate tablets (Atelvia) is not recommended. Co-administration of drugs that raise stomach pH increases risedronate bioavailability due to faster release of the drug from the enteric coated tablet. This interaction does not apply to risedronate immediate-release tablets.
Secretin: (Major) Discontinue use of H2-blockers at least 2 days before administering secretin. Patients who are receiving H2-blockers at the time of stimulation testing may be hyperresponsive to secretin stimulation, falsely suggesting gastrinoma.
Selpercatinib: (Major) Avoid coadministration of selpercatinib with famotidine due to the risk of decreased selpercatinib exposure which may reduce its efficacy. If concomitant use is unavoidable, take selpercatinib 2 hours before or 10 hours after administration of famotidine. Coadministration with acid-reducing agents decreases selpercatinib plasma concentrations; however, no clinically significant differences in the pharmacokinetics of selpercatinib were observed when given under fasting conditions with multiple daily doses of another H2-receptor antagonist given 10 hours prior to and 2 hours after the selpercatinib dose.
Sofosbuvir; Velpatasvir: (Major) H2-blockers may be administered simultaneously with or 12 hours apart from velpatasvir. H2-blocker doses should not exceed doses comparable to famotidine 40 mg twice daily. Velpatasvir solubility decreases as pH increases; therefore, drugs that increase gastric pH are expected to decrease the concentrations of velpatasvir, potentially resulting in loss of antiviral efficacy.
Sofosbuvir; Velpatasvir; Voxilaprevir: (Major) H2-blockers may be administered simultaneously with or 12 hours apart from velpatasvir. H2-blocker doses should not exceed doses comparable to famotidine 40 mg twice daily. Velpatasvir solubility decreases as pH increases; therefore, drugs that increase gastric pH are expected to decrease the concentrations of velpatasvir, potentially resulting in loss of antiviral efficacy.
Sonidegib: (Moderate) Based on population PK analysis, the concomitant administration of a histamine-2-receptor antagonist such as famotidine decreases the geometric mean sonidegib steady-state AUC (0-24 hours) value by 34%.
Sotorasib: (Major) Avoid coadministration of sotorasib and gastric acid-reducing agents, such as H2-receptor antagonists. Coadministration may decrease sotorasib exposure resulting in decreased efficacy. If necessary, sotorasib may be administered 4 hours before or 10 hours after a locally acting antacid. Coadministration with an H2-receptor antagonist decreased sotorasib exposure by 38% under fed conditions.
Sparsentan: (Major) Avoid concurrent use of sparsentan and H2 receptor antagonists due to the risk for decreased sparsentan exposure which may reduce its efficacy. Medications that affect gastric pH may reduce sparsentan absorption.
Sumatriptan; Naproxen: (Moderate) Avoid concomitant use of enteric-coated, delayed-release naproxen and H2-blockers due to the gastric pH elevating effects of H2-blockers. Enteric-coated, delayed-release naproxen tablets are designed to dissolve at a pH of 6 or more.
Thalidomide: (Moderate) Thalidomide and other agents that slow cardiac conduction such as H2-blockers should be used cautiously due to the potential for additive bradycardia.
Theophylline, Aminophylline: (Minor) Aminophylline is a prodrug of theophylline, and is primarily metabolized in the liver by the CYP1A2 isoenzyme. In general, famotidine does not interact with aminophylline and does not affect theophylline levels in most patients. One small study documented a significant decrease in theophylline clearance after therapy with famotidine. Be alert for any evidence of interaction, and monitor the patients aminophylline therapy as per standard of care or if side effects are reported. (Minor) Theophylline is primarily metabolized in the liver by the CYP1A2 isoenzyme. In general, famotidine does not interact with theophylline and does not affect theophylline levels in most patients. One small study documented a significant decrease in theophylline clearance after therapy with famotidine. Be alert for any evidence of interaction, and monitor the patients theophylline therapy as per standard of care or if side effects are reported.
Tizanidine: (Major) Avoid concomitant use of tizanidine and famotidine as increased tizanidine exposure may occur. If use together is necessary, initiate tizanidine at 2 mg and increase by 2 to 4 mg/day based on clinical response. Discontinue tizanidine if hypotension, bradycardia, or excessive drowsiness occurs. Tizanidine is a CYP1A2 substrate and famotidine is a weak CYP1A2 inhibitor.
Warfarin: (Moderate) Closely monitor the INR if coadministration of warfarin with famotidine is necessary as concurrent use may increase the exposure of warfarin leading to increased bleeding risk. Famotidine is a CYP1A2 inhibitor and the R-enantiomer of warfarin is a CYP1A2 substrate. The S-enantiomer of warfarin exhibits 2 to 5 times more anticoagulant activity than the R-enantiomer, but the R-enantiomer generally has a slower clearance.

Famotidine/Heartburn Relief/Pepcid/Pepcid AC/Pepcid AC Maximum Strength/Zantac/Zantac 360 Oral Tab: 10mg, 20mg, 40mg
Famotidine/Pepcid Intravenous Inj Sol: 1mL, 10mg, 20mg, 50mL
Famotidine/Pepcid Oral Pwd F/Recon: 5mL, 40mg

40 mg/day PO or IV for active duodenal or benign gastric ulcer; 20 mg/day PO for ulcer maintenance; 40 mg/day PO for GERD; 80 mg/day PO for esophagitis; doses may go as high as 640 mg/day or 800 mg/day (rare) PO or 80 mg/day IV for hypersecretory conditions such as Zollinger-Ellison; 40 mg/day PO for self-medication (OTC).

40 mg/day PO or IV for active duodenal or benign gastric ulcer healing; 20 mg/day PO for ulcer maintenance; 40 mg/day PO for GERD; 80 mg/day PO for esophagitis; doses may go as high as 640 mg/day or 800 mg/day (rare) PO or 80 mg/day IV for hypersecretory conditions such as Zollinger-Ellison; 40 mg/day PO for self-medication (OTC).

1 mg/kg/day PO (Max: 80 mg/day); 1 mg/kg/day IV (Max: 40 mg/day) is FDA-approved maximum; however, doses up to 2 mg/kg/day IV have been used off-label.

1 mg/kg/day PO (Max: 80 mg/day); 1 mg/kg/day IV (Max: 40 mg/day) is FDA-approved maximum; however, doses up to 2 mg/kg/day IV have been used off-label.

3 to 11 months: 2 mg/kg/day PO. Safety and efficacy of IV have not been established; however, doses up to 2 mg/kg/day IV have been used off-label.
1 to 2 months: 1 mg/kg/day PO. Safety and efficacy of IV have not been established; however, doses up to 2 mg/kg/day IV have been used off-label.

1 mg/kg/day PO. Safety and efficacy of IV have not been established; however, 0.5 mg/kg/day IV has been used off-label.

Famotidine competitively inhibits the binding of histamine to H2-receptors on the gastric basolateral membrane of parietal cells, reducing basal and nocturnal gastric acid secretions. The drug also decreases the gastric acid response to stimuli such as food, caffeine, insulin, betazole, or pentagastrin. Famotidine reduces the total volume of gastric juice, thus indirectly decreasing pepsin secretion. The drug does not appear to alter gastric motility, gastric emptying, esophageal pressures, biliary secretions, or pancreatic secretions. Famotidine may aid in gastromucosal healing, and it may protect the mucosa from the irritant effects caused by aspirin and nonsteroidal antiinflammatory agents.

Famotidine is administered orally and parenterally. Plasma protein binding is approximately 15% to 20%. There is no cumulative effect with repeat doses; plasma concentrations after multiple doses are similar to those after single doses. Famotidine undergoes minimal first-pass metabolism. The majority (65 to 70%) of a famotidine dose is excreted in the urine; 30 to 35% of the dose is metabolized by the liver. The S-oxide metabolite is the only 1 identified in humans. Famotidine elimination half-life is 2.5 to 3.5 hours in adults with normal renal function.
 
Affected cytochrome P450 isoenzymes: CYP1A2, OAT1, OAT3, MATE-1Famotidine is a weak inhibitor of CYP1A2. In vitro studies also indicate that famotidine is a substrate for human organic anion transporter (OAT) 1 and 3 and an inhibitor of multidrug and toxin extrusion protein 1 (MATE-1).

Bioavailability of famotidine is approximately 40% to 45% in adults. Famotidine tablets, oral suspension, and orally disintegrating tablets are bioequivalent. Food may slightly increase and antacids may slightly decrease the bioavailability of famotidine; however, the effects are considered clinically insignificant. The onset of action is usually within 1 hour after oral administration with maximum effects occurring within 1 to 3 hours depending on the dose. The duration of action is roughly 10 to 12 hours. Twenty-five to 30% of an oral dose is excreted in urine as unchanged drug.

Sixty-five to 70% of an intravenous dose of famotidine is excreted in urine as unchanged drug.[51456]

Animal studies and epidemiologic data during pregnancy suggest famotidine use when necessary is not harmful, even though there are no adequate and well-controlled studies evaluating famotidine use in pregnant patients.   In one such study of human data, exposure to H2-blockers, including famotidine, was not associated with an increased risk for congenital malformations (adjusted OR 1.03, 95% CI: 0.80, 1.32); also, no such association was found when therapeutic pregnancy terminations were included in the analysis (adjusted OR 1.17, 95% CI: 0.93, 1.46). Exposure to H2-blockers was not associated with perinatal mortality, premature delivery, low birth weight, or low Apgar scores. In animal reproduction studies, no adverse development effects were observed with oral famotidine at doses up to approximately 243 and 122 times, respectively, the recommended human dose of 80 mg/day for the treatment of erosive esophagitis. Guidelines recommend a trial of lifestyle modifications as first-line therapy for heartburn and gastroesophageal reflux disease (GERD) during pregnancy, followed by antacids if lifestyle adjustments are ineffective. For ongoing symptoms, H2-blockers such as famotidine can be used. Other medications should be reserved for pregnant patients who fail H2-blocker therapy. Self-medication with H2-blockers (OTC formulations) during pregnancy is not recommended. Pregnant patients should see their health care professional for a proper diagnosis and for treatment recommendations. Famotidine has been used in limited circumstances at term to prevent acid aspiration during labor; some guidelines recommend an H2-blocker (PO or IV) for all women presenting for cesarean delivery.

There are limited data suggesting the presence of famotidine in human breast milk; however, there were no effects on the breastfed infant; experts and guidelines consider use of famotidine compatible with breast-feeding. There are no data on famotidine effects on milk production. Famotidine is present in the milk of lactating rats. Famotidine is indicated for use in infants and is used in newborns at doses that are higher than those excreted in breast milk. According to guidelines, if heartburn/gastroesophageal reflux (GERD) symptoms persist after delivery, antacids and sucralfate are safe to use during lactation because they are not concentrated in breast milk. H2-blockers are excreted in breast milk, but cimetidine and famotidine are considered safe for use during lactation and may be used if symptoms persist despite antacid use. Famotidine is preferred in lactation due to the low concentration in breast milk.