ACID REDUCER
  • ACID REDUCER

  • (Generic for PEPCID)
  • QTY 60 • 20 MG • Tablet • Near 77381

FAMOTIDINE (fa MOE ti deen) is a type of antihistamine that blocks the release of stomach acid. It is used to treat stomach or intestinal ulcers. It can also relieve heartburn from acid reflux.

ACID REDUCER Pediatric Monographs
  • General Administration Information
    For storage information, see the specific product information within the How Supplied section.

    Route-Specific Administration

    Oral Administration
    -May be administered without regard to meals. Administer with food, water, or milk to minimize gastric irritation.
    Oral Solid Formulations
    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 Liquid Formulations
    Oral suspension:
    -Reconstitute by slowly adding 46 ml of purified water.
    -Shake vigorously for 5-10 seconds after adding water and again immediately prior to administration.
    -After reconstitution, each 5 ml contains 40 mg of famotidine.
    -Measure dosage with calibrated device for accuracy.
    -Storage of reconstituted suspension: Store at room temperature (15-30 degrees C, 59-86 degrees F) for up to 30 days.



    Injectable Administration
    -Visually inspect parenteral products for particulate matter and discoloration prior to administration whenever solution and container permit.
    Intravenous Administration
    Intermittent intravenous injection:
    -Dilute 20 mg of famotidine to a total of 5 or 10 ml with NS or other compatible solution to give concentrations of 4 or 2 mg/ml, respectively.
    -Inject appropriate dose over >= 2 minutes and at a rate <= 10 mg/minute.

    Intermittent intravenous (IV) infusion:
    -Dilute 20 mg of famotidine in 100 ml of D5W or other compatible IV solution to give a final concentration of 0.2 mg/ml.
    -Infuse over 15-30 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., NS, D5W, Lactated Ringers), famotidine is stable for 7 days at room temperature, the manufacturer warns that there are no data available to confirm sterility under these conditions.

    Continuous 24-hour intravenous infusion:
    -Famotidine may be added to a compatible TPN solution for administration over 24 hours.

    In a clinical study of famotidine in 35 infants < 1 year of age with GERD symptoms, agitation was reported in 5 patients and resolved when famotidine was discontinued. Reversible mental status changes, including agitation, confusion, delirium, hallucinations, hostility, paranoia, depression, insomnia, and disorientation have been reported rarely after famotidine therapy. Anxiety, paresthesias, and drowsiness have also been reported. A review of central nervous system reactions to H2-antagonists revealed that the incidence varies widely depending on the specific report, and that no single H2-antagonist is more likely to induce CNS reactions than another. Central nervous system reactions are more likely to occur in patients with renal impairment. Seizures have been rarely reported in patients with renal impairment.

    Gastric acid suppression with H2-receptor antagonists has been associated with an increased risk of infection in pediatric patients. A causal relationship between the use of famotidine and infection, such as pneumonia, has not been established; however, several studies have assessed the risk of infection with another H2-receptor antagonist. however, several studies have assessed the risk of infection with another H2-receptor blocker. A study in premature neonates (gestational age 24 to 32 weeks) found a statistically significantly increased risk of overall infection (37.4% vs 9.8%, p less than 0.001), including sepsis, pneumonia, and urinary tract infection, in neonates receiving an H2-blocker; there was also a significantly higher risk of developing necrotizing enterocolitis (9.8% vs 1.6%, p = 0.003) and a significantly higher mortality rate (9.9% vs 1.6%, p = 0.003). One study in previously healthy infants and young children found an increased risk in community-acquired pneumonia (12% vs 2%, p less than .05) and acute gastroenteritis (47% vs 20%, p is less than .05) in patients receiving gastric acid inhibitors compared to controls. Another study in critically ill pediatric patients (n = 60) did not find an increased incidence of ventilator-associated pneumonia in patients receiving acid-suppression therapy compared to those not receiving treatment. Until more is known about the relationship between acid-suppression and pneumonia, clinicians are encouraged to carefully select patients before empirically initiating acid-suppressive therapy with H2-blockers or proton pump inhibitors (PPIs). Increasing evidence in adults suggests a link between acid-suppression therapy and respiratory infection, specifically pneumonia. Several mechanisms have been proposed to account for this association, including the disruption of gastric pH as a barrier against pathogenic colonization of the gastrointestinal tract and as a stimulant of the cough reflex that allows for the clearing of infectious agents from the respiratory tract. Finally, the fact that acid-suppressive therapy may impair white blood cell function, which in turn may lead to a depressed immune response to an infection, is listed among possible mechanisms.

    Similar to other H2-antagonists, famotidine causes infrequent adverse reactions. In controlled clinical trials in adults, the incidence of adverse reactions in patients who received famotidine 40 mg at bedtime was similar to that in the placebo group. The following reactions have occurred in greater than 1% of adult patients and may be causally related to the drug: headache (4.7%), dizziness (1.3%), constipation (1.2%), and diarrhea (1.7%). Other gastrointestinal adverse events reported in clinical trials or post approval include: cholestasis with jaundice, hepatitis, hepatic enzyme abnormalities, vomiting, nausea, abdominal discomfort, anorexia, dysgeusia (reported as taste disorder), and xerostomia. The relationship between these events and famotidine therapy has been unclear in many cases.

    Few cases of toxic epidermal necrolysis and Stevens-Johnson syndrome have been reported with famotidine therapy. Anaphylactoid reactions have also been reported. Additional hypersensitivity and dermatological reactions reported for famotidine in clinical trials or post approval include: orbital or facial edema, angioedema, urticaria, rash (unspecified), conjunctivitis, alopecia, acne vulgaris, pruritus, xerosis, and flushing. The relationship between these events and famotidine therapy has been unclear in many cases.

    Atrophic gastritis, a precursor for gastric cancer, has been associated with prolonged acid suppression with high dose H2-blockers like famotidine in patients who are H. pylori positive. A 'test and treat' approach for baseline H. pylori infections is recommended for patients with reflux esophagitis on long term acid suppression therapy. Treatment of baseline infection decreases inflammation and may reverse corpus gastritis.

    Cardiovascular adverse events reported for famotidine in clinical trials or post approval include: arrhythmia exacerbation, AV block, and palpitations. The relationship between these events and famotidine therapy has been unclear in many cases. In addition, QT prolongation has been reported in patients with impaired renal function whose dose/dosing interval of famotidine may not have been adjusted appropriately.

    Hematological adverse events have been reported for famotidine in clinical trials or post approval and include cases of agranulocytosis, pancytopenia, leukopenia, and thrombocytopenia. The relationship between these events and famotidine therapy has been unclear in many cases.

    Miscellaneous adverse events reported for famotidine in clinical trials or post approval include: fever, asthenia, fatigue, lethargy, rhabdomyolysis, musculoskeletal pain including muscle cramps, arthralgia, bronchospasm, interstitial pneumonia, and tinnitus. In addition, rare cases of gynecomastia have been reported; however, in controlled clinical trials, the incidence was not greater than with placebo. The relationship between these events and famotidine therapy has been unclear in many cases.

    Long-term (e.g., generally >= 2-3 years) treatment with acid-suppressing agents, such as famotidine, can lead to malabsorption of vitamin B12 (cyanocobalamin). One large case-controlled study compared adult patients with and without an incident diagnosis of vitamin B12 deficiency (n = 25,956 and 184,199, respectively) and demonstrated a correlation between vitamin B12 deficiency and gastric acid-suppression therapy. Patients receiving >= 2 years of a proton pump inhibitor or H2-receptor antagonist were associated with having an increased risk for vitamin B12 deficiency. The precise risk in pediatric patients has not been defined. Consider the possibility of cyanocobalamin deficiency and pernicious anemia if clinical symptoms are observed. Neurological manifestations of pernicious anemia can occur in the absence of hematologic changes.

    Famotidine is contraindicated in any patient hypersensitive to the drug or its components. Cross-sensitivity in this class of compounds has been observed, so famotidine should not be administered to patients with a history of H2-blocker hypersensitivity. An incidence of cross-reactivity among this class of agents is not currently available.

    Symptomatic response to therapy with famotidine does not preclude the presence of gastric cancer. In the patient who is self-medicating with non-prescription (OTC) formulations, the continuation of heartburn, acid indigestion, or dyspepsia beyond 2 weeks signals the need to consult a health-care professional for evaluation. Patients using non-prescription famotidine products who have a suboptimal response or early symptomatic relapse after completing therapy should consider evaluation for gastric malignancy. Additionally, patients should seek immediate medical advice if any sign of GI bleeding (e.g., blood in vomit, stools) or difficult or painful swallowing (dysphagia) becomes evident.

    Symptomatic response to therapy with famotidine does not preclude the presence of H. pylori infection. Famotidine therapy does not appear to interfere with the sensitivity of gastric urease biopsy. It is controversial whether histamine type 2-receptor antagonists interfere with urea breath-tests for the detection of H. pylori; many laboratories recommend holding these drugs for 24-48 hours prior to testing. H2-blockers, as single agents, will not eradicate H. pylori infection.

    Famotidine should be used cautiously in patients with hepatic disease, renal impairment or renal failure (renal disease), because the drug can accumulate, causing toxicity. There is a close relationship between the drug's elimination half-life and creatinine clearance. Dosages of famotidine should be adjusted in patients with moderate or severe renal impairment. Confusion, delirium, hallucinations, disorientation, agitation, seizures, and lethargy have been reported in patients treated with famotidine with moderate and severe renal impairment. Rarely, QT prolongation or central nervous system (CNS) reactions have been reported in patients with impaired renal function whose dose/dosing interval of famotidine may not have been adjusted appropriately. Use famotidine with caution in patients with renal impairment and other conditions that may increase the risk of QT prolongation.

    Famotidine chewable tablets contain varying amounts of phenylalanine depending on the specific product; use cautiously in patients with phenylketonuria.

    Chronic use of gastric acid-suppressing agents should be used cautiously and with monitoring in patients who are prone to vitamin B12 deficiency. Daily treatment with a gastric acid-suppressing medication, such as famotidine, over a long period of time (e.g., generally >= 2-3 years) has been associated with malabsorption of cyanocobalamin in adults. Consider the possibility of cyanocobalamin deficiency if clinical symptoms are observed.

    Description: Famotidine is an oral and parenteral histamine type 2-receptor antagonist (H2RA) used in the treatment of gastrointestinal disorders such as peptic ulcer and gastroesophageal reflux disease (GERD). The actions and indications of famotidine differ little from the other agents in the same class, except that famotidine is less likely than cimetidine to interact with other drugs. Over-the-counter oral formulations are available for the prophylaxis and treatment of heartburn and acid indigestion in adolescent and adult patients. H2RAs are often used for stress ulcer prophylaxis in critically ill patients; however, evidence for benefit is lacking, and use may increase the risk of adverse reactions such as pneumonia and Clostridioides difficile infection. Reserve stress ulcer prophylaxis for patients with risk factors for clinically significant gastrointestinal bleeding (e.g., multiple organ dysfunction, prolonged mechanical ventilation, coagulopathy, persistent shock, concomitant corticosteroid therapy). Famotidine oral formulations are FDA-approved in pediatric patients as young as infants; the intravenous formulation is FDA-approved in children 1 year and older.

    For the self-medication of pyrosis (heartburn), acid dyspepsia (acid indigestion), or sour stomach:
    Oral dosage (OTC product, e.g., Pepcid AC and generic equivalents):
    Children < 12 years: Self-medication not recommended.
    Children >= 12 years and Adolescents: 10 mg PO given 15 minutes to 1 hour prior to eating a meal that is expected to cause symptoms for prophylaxis or 10 mg PO 1-2 times per day for treatment (Max: 20 mg/day). Patients should not take for more than 2 weeks without consulting a physician.
    Oral dosage (OTC product, e.g., Maximum Strength Pepcid AC and generic equivalents):
    Children < 12 years: Self-medication is not recommended.
    Children >= 12 years and Adolescents: 20 mg PO given 10 minutes to 1 hour prior to eating a meal that is expected to cause symptoms for prophylaxis or 20 mg PO 1-2 times per day for treatment (Max: 40 mg/day). Patients should not take for more than 2 weeks without consulting a physician.

    For the treatment of gastroesophageal reflux disease (GERD) or esophagitis associated with gastroesophageal reflux disease (GERD):
    Oral dosage:
    Neonates: 0.5 mg/kg/dose PO once daily initially, in addition to conservative measures such as thickened feedings. May increase 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.
    Infants 1 to 2 months: 0.5 mg/kg/dose PO once daily initially, in addition to conservative measures such as thickened feedings. May increase 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.
    Infants 3 to 11 months: 0.5 mg/kg/dose PO twice daily initially, in addition to conservative measures such as thickened feedings. May increase 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.
    Children and Adolescents: 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.
    Intravenous dosage:
    Neonates*: 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.
    Infants 1 to 3 months*: 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.
    Infants 4 to 11 months*: 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.
    Children and Adolescents: 0.25 mg/kg/dose IV every 12 hours (Max: 40 mg/day) initially is the FDA-approved dosage; 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.

    For the treatment of peptic ulcer disease (duodenal ulcer or gastric ulcer):
    Oral dosage:
    Children and Adolescents: 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 PO have been used (Max: 40 mg/day). 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.
    Intravenous dosage:
    Children and Adolescents: 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 8-12 hours is supported by pharmacokinetic and pharmacodynamic data.

    For stress gastritis prophylaxis* in critically-ill patients:
    Intravenous dosage:
    Infants, Children, and Adolescents: 1 to 2 mg/kg/day IV divided every 8 to 12 hours. Some studies did not specify a maximum dose; others did not exceed the adult maximum dose. One study administered famotidine 0.4 mg/kg/dose IV every 8 hours to 10 critically ill pediatric patients and found the mean total time gastric pH increased to 4 or more was 62.2% over 24 hours. A second study (n = 22) administered famotidine 1 mg/kg/day divided every 8 hours in patients weighing less than 10 kg and divided every 12 hours in patients weighing 10 kg or more.

    Maximum Dosage Limits:
    -Neonates
    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.
    -Infants
    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.
    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.
    -Children
    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.
    -Adolescents
    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.

    Patients with Hepatic Impairment Dosing
    Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed unless decreased renal function is also present.

    Patients with Renal Impairment Dosing
    Famotidine injection
    The FDA-approved product labeling states that dose adjustments should be considered in pediatric patients with moderate or severe renal impairment; however, data are not available to establish a safe and effective IV famotidine dose in pediatric patients with renal impairment. One pharmacokinetic study (n = 18) of pediatric patients with stable chronic renal insufficiency recommended the following adjustments for IV famotidine:
    CrCl 50 mL/minute/1.73m2 or more: 0.5 mg/kg/dose IV every 12 to 24 hours (Max: 20 mg).
    CrCl 11 to 49 mL/minute/1.73m2: 0.5 mg/kg/dose IV every 36 to 48 hours (Max: 20 mg).
    CrCl 10 mL/minute/1.73m2 or less: 0.5 mg/kg/dose IV every 72 to 96 hours (Max: 20 mg) or 0.25 mg/kg/dose IV every 36 to 48 hours (Max: 10 mg).

    Famotidine oral suspension
    No dosage adjustment is needed in patients with mild renal impairment (CrCl more than 60 mL/minute). Data are not available to establish a safe and effective dosage in pediatric patients with renal impairment. The FDA-approved product labeling recommends the following dosage adjustments in adults:
    Active DU or Active GU:
    CrCl 30 to 60 mL/minute: 20 mg once daily or 40 mg every other day.
    CrCl less than 30 mL/minute: 10 mg once daily or 20 mg every other day.
    Symptomatic nonerosive GERD:
    CrCl 30 to 60 mL/minute: 20 mg once daily.
    CrCl less than 30 mL/minute: 10 mg once daily or 20 mg every other day.
    Erosive esophagitis due to GERD, diagnosed by endoscopy:
    CrCl 30 to 60 mL/minute: 20 mg once daily or 40 mg once daily or 40 mg every other day.
    CrCl less than 30 mL/minute: 10 mg once daily or 20 mg once daily or 20 mg every other day.
    Pathological hypersecretory conditions:
    Avoid use: The dosage required to treat pathological hypersecretory conditions may exceed the maximum dosage evaluated in patients with impaired renal function. The risk for increased adverse reactions in renally impaired patients treated with famotidine for pathological hypersecretory conditions is unknown.
    Reduction of the risk of DU recurrence:
    CrCl 30 to 60 mL/minute: 10 mg once daily or 20 mg every other day.
    CrCl less than 30 mL/minute: 10 mg every other day.

    Famotidine oral tablet
    No dosage adjustment is needed in patients with mild renal impairment (CrCl more than 60 mL/minute). The FDA-approved product labeling recommends the following dosage adjustments in pediatric patients 40 kg or more:
    Active DU or Active GU:
    CrCl 30 to 60 mL/minute: 20 mg once daily or 40 mg every other day.
    CrCl less than 30 mL/minute: 20 mg every other day.
    Symptomatic nonerosive GERD:
    CrCl 30 to 60 mL/minute: 20 mg once daily.
    CrCl less than 30 mL/minute: 20 mg every other day.
    Erosive esophagitis due to GERD, diagnosed by endoscopy:
    CrCl 30 to 60 mL/minute: 20 mg once daily or 40 mg once daily or 40 mg every other day.
    CrCl less than 30 mL/minute: 20 mg once daily or 20 mg every other day.
    Pathological hypersecretory conditions:
    Avoid use: The dosage required to treat pathological hypersecretory conditions may exceed the maximum dosage evaluated in patients with impaired renal function. The risk for increased adverse reactions in renally impaired patients treated with famotidine for pathological hypersecretory conditions is unknown.
    Reduction of the risk of DU recurrence:
    CrCl 30 to 60 mL/minute: 20 mg every other day.
    CrCl less than 30 mL/minute: 10 mg every other day.

    *non-FDA-approved indication

    Monograph content under development

    Mechanism of Action: 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 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.

    Pharmacokinetics: 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-1

    Famotidine 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).


    -Route-Specific Pharmacokinetics
    Oral Route
    Bioavailability of famotidine is approximately 42% in infants and 50% in children and adolescents, which are similar to adult values. 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.

    Intravenous Route
    Sixty-five to 70% of an intravenous dose of famotidine is excreted in urine as unchanged drug.


    -Special Populations
    Pediatrics
    Neonates and Infants
    After a single administration of 0.5 mg/kg orally in patients from birth to 12 months of age, the bioavailability was approximately 42%. The AUC increased 1.4-fold after a single oral dose of 1 mg/kg compared to 0.5 mg/kg and 2.7-fold after multiple oral doses of 1 mg/kg compared to 0.5 mg/kg. The half-life was 5.82 in infants birth to 12 months of age. Plasma clearance was reduced, and elimination half-life was prolonged in pediatric patients from birth to 3 months of age compared to older pediatric patients. After intravenous administration of 0.5 mg/kg, total clearance was 0.13 +/- 0.06 L/hour/kg, 0.21 +/- 0.06 L/hour/kg, and 0.49 +/- 0.17 L/hour/kg in pediatric patients younger than 1 month of age, younger than 3 months of age, and 4 to 12 months of age, respectively. Elimination half-life was 10.5 hours, 8.1 hours, and 4.5 hours in pediatric patients younger than 1 month of age, younger than 3 months of age, and 4 to 12 months of age, respectively. The duration of acid suppression was longer in pediatric patients from birth to 3 months of age compared to older pediatric patients.

    Children and Adolescents
    The mean oral bioavailability in 8 pediatric patients 11 to 15 years of age was 50%. The mean half-life was 2 to 3.4 hours in pediatric patients 1 to 15 years of age.

    Renal Impairment
    There is a close relationship between famotidine elimination half-life and creatinine clearance (CrCl). In a small pharmacokinetic study (n = 18) of pediatric patients with stable chronic renal insufficiency, mean famotidine elimination half-life was 3.72 hours, 6.75 hours, and 14.66 hours in patients with mild (CrCl 50 to 89 mL/minute/1.73m2), moderate (CrCl 25 to 49 mL/minute/1.73m2), and severe (0 to 10 mL/minute/1.73m2) renal impairment, respectively.

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