Health Canada has completed a safety review confirming that the use of nonsteroidal anti-inflammatory drugs (NSAIDs) starting from approximately 20 weeks of pregnancy or later may cause rare but serious kidney problems in an unborn baby. This can lead to low levels of amniotic fluid and possible complications, such as impaired lung maturation and limb contractures in the newborn baby. Health Canada is advising that pregnant women not use NSAIDs from approximately 20 to 28 weeks of pregnancy unless advised to do so by their health care provider. If a health care provider decides the use of NSAIDs between 20 and 28 weeks of pregnancy is necessary, Health Canada recommends that they use the lowest effective dose for the shortest duration possible and consider monitoring amniotic fluid levels via ultrasound if treatment extends beyond 48 hours. The use of NSAIDs remains contraindicated in the last trimester of pregnancy. The recommendations do not apply to the use of low-dose (81 mg) aspirin, pediatric-only formulations (those indicated only for children younger than 12 years), or ophthalmic formulations. Prescription and nonprescription NSAID product labels will be updated with this new information.
Further information is available at https://healthycanadians.gc.ca/recall-alert-rappel-avis/hc-sc/2021/75763a-eng.php.
Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction, and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use.
Ibuprofen is contraindicated in the setting of coronary artery bypass graft (CABG) surgery.
NSAIDs cause an increased risk of serious gastrointestinal (GI) adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients and patients with a prior history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events.
Note: Oral liquid products are available in 2 concentrations (concentrated infant drops: 50 mg/1.25 mL [40 mg/mL] and suspension: 100 mg/5 mL [20 mg/mL]); precautions should be taken to verify and avoid confusion between the different concentrations; dose should be clearly presented as "mg".
Patent ductus arteriosus (PDA), treatment: Note: Use birth weight to calculate all doses; monitor urine output; a decrease in urine output may require dose adjustment or holding of therapy.
IV:
Standard-dose therapy: Preterm neonates: IV: Initial dose: 10 mg/kg, followed by 2 doses of 5 mg/kg/dose at 24 and 48 hours after the initial dose. A second course of treatment, alternative pharmacologic therapy, or surgery may be needed if the ductus arteriosus fails to close or reopens following the initial course of therapy (Hirt 2008; Meißner 2012; manufacturer's labeling).
High-dose therapy: Limited data available: GA 24 to <40 weeks: IV: Initial dose: 20 mg/kg, followed by 2 doses of 10 mg/kg/dose administered at 24-hour intervals has been evaluated in a total of 58 neonates in 2 studies (GA: 24 to 39 weeks, PNA: ≤5 days for majority of patients). In comparison to the standard dose, these studies found a higher rate of PDA closure using high-dose therapy without an increase in adverse effects (Dani 2012; Meißner 2012). Pharmacokinetic data suggest that clearance increases with postnatal age; therefore, doses at the higher end of the dosage range may be necessary in older neonates (Hirt 2008; Van Overmeire 2001).
Oral suspension: Limited data available: GA <34 weeks weighing <1,500 g at birth: Oral: Initial dose: 10 mg/kg, followed by 2 doses of 5 mg/kg/dose at 24 and 48 hours after the initial dose; doses were administered undiluted through a feeding tube and immediately followed with a flush (~1 mL) of distilled water; this dosing regimen has been used in several trials and has been shown to be safe and as effective as IV ibuprofen and IV indomethacin (Erdeve 2012; Heyman 2003; Lee 2012); in one retrospective study, oral ibuprofen (n=52) was associated with lower rates of elevated serum creatinine compared to IV indomethacin (n=88) (Lee 2012).
Dosing adjustment in renal impairment: IV: Ibuprofen lysine (Neoprofen): If anuria or marked oliguria (urinary output <0.6 mL/kg/hour) is evident at the scheduled time of the second or third dose, hold dose until renal function returns to normal. Use is contraindicated in preterm infants with significant renal impairment.
Note: To reduce the risk of adverse cardiovascular and GI effects, use the lowest effective dose for the shortest period of time to achieve treatment goals. Oral liquid products are available in 2 concentrations (concentrated infant drops: 50 mg/1.25 mL [40 mg/mL] and suspension: 100 mg/5 mL [20 mg/mL]); precautions should be taken to verify and avoid confusion between the different concentrations; dose should be clearly presented as "mg".
Analgesic:
IV: Ibuprofen injection (Caldolor): Note: Patients should be well hydrated prior to administration.
Infants ≥6 months and Children <12 years: IV: 10 mg/kg/dose (maximum dose: 400 mg/dose) every 4 to 6 hours as needed; maximum daily dose: 40 mg/kg/day or 2,400 mg/day, whichever is less.
Children ≥12 years and Adolescents ≤17 years: IV: 400 mg every 4 to 6 hours as needed; maximum daily dose: 2,400 mg/day.
Adolescents ≥18 years: IV: 400 to 800 mg every 6 hours as needed; maximum daily dose: 3,200 mg/day.
Oral:
Weight-directed dosing: Infants, Children, and Adolescents: Limited data available in infants <6 months: Oral: 4 to 10 mg/kg/dose every 6 to 8 hours; maximum dose: 400 mg/dose; maximum daily dose: 40 mg/kg/day or 3,200 mg/day, whichever is less (APS 2016; Berde 1990; Berde 2002; Kliegman 2020; O'Donnell 2014).
Fixed dosing:
Infants ≥6 months and Children ≤11 years: Oral: See table based upon manufacturer's labeling; use of weight to select dose is preferred; if weight is not available, then use age; doses may be repeated every 6 to 8 hours; maximum: 4 doses/day; treatment of sore throat for >2 days or use in infants and children <3 years of age with sore throat is not recommended, unless directed by health care provider.
Weight (preferred)a |
Age |
Dosage (mg) | |
---|---|---|---|
kg |
lbs | ||
5.4 to 8.1 |
12 to 17 |
6 to 11 months |
50 |
8.2 to 10.8 |
18 to 23 |
12 to 23 months |
75 to 80 |
10.9 to 16.3 |
24 to 35 |
2 to 3 years |
100 |
16.4 to 21.7 |
36 to 47 |
4 to 5 years |
150 |
21.8 to 27.2 |
48 to 59 |
6 to 8 years |
200 |
27.3 to 32.6 |
60 to 71 |
9 to 10 years |
200 to 250 |
32.7 to 43.2 |
72 to 95 |
11 years |
300 |
a Manufacturer's recommendations are based on weight in pounds (OTC labeling); weight in kg listed here is derived from pounds and rounded; kg weight listed also is adjusted to allow for continuous weight ranges in kg. |
Children ≥12 years and Adolescents: Oral: 200 to 400 mg every 4 to 6 hours as needed; maximum daily dose: 3,200 mg/day (APS 2016; manufacturer's labeling); treatment of pain for >10 days is not recommended, unless directed by health care provider.
Antipyretic:
IV: Ibuprofen injection (Caldolor): Note: Patients should be well hydrated prior to administration.
Infants ≥6 months and Children <12 years: IV: 10 mg/kg/dose (maximum dose: 400 mg/dose) every 4 to 6 hours as needed; maximum daily dose: 40 mg/kg/day or 2,400 mg/day, whichever is less.
Children ≥12 years and Adolescents ≤17 years: IV: 400 mg every 4 to 6 hours as needed; maximum daily dose: 2,400 mg/day.
Adolescents ≥18 years: IV: Initial dose: 400 mg once, followed by 400 mg every 4 to 6 hours or 100 to 200 mg every 4 hours as needed; maximum daily dose: 3,200 mg/day.
Oral:
Weight-directed dosing: Infants ≥3 months weighing ≥5 kg, Children, and Adolescents: Limited data available in infants <6 months: Oral: 5 to 10 mg/kg/dose every 6 to 8 hours; maximum dose: 400 mg/dose; maximum daily dose: 40 mg/kg/day or 2,400 mg/day, whichever is less (Kliegman 2020; Litalien 2001; Sullivan 2011; Ziesenitz 2017).
Fixed dosing: Note: Treatment for >3 days is not recommended unless directed by health care provider.
Infants ≥6 months and Children ≤11 years: Oral: See table based upon manufacturer's labeling; use of weight to select dose is preferred; if weight is not available, then use age; doses may be repeated every 6 to 8 hours; maximum: 4 doses/day.
Weight (preferred)a |
Age |
Dosage (mg) | |
---|---|---|---|
kg |
lbs | ||
5.4 to 8.1 |
12 to 17 |
6 to 11 months |
50 |
8.2 to 10.8 |
18 to 23 |
12 to 23 months |
75 to 80 |
10.9 to 16.3 |
24 to 35 |
2 to 3 years |
100 |
16.4 to 21.7 |
36 to 47 |
4 to 5 years |
150 |
21.8 to 27.2 |
48 to 59 |
6 to 8 years |
200 |
27.3 to 32.6 |
60 to 71 |
9 to 10 years |
200 to 250 |
32.7 to 43.2 |
72 to 95 |
11 years |
300 |
a Manufacturer's recommendations are based on weight in pounds (OTC labeling); weight in kg listed here is derived from pounds and rounded; kg weight listed also is adjusted to allow for continuous weight ranges in kg. |
Children ≥12 years and Adolescents: Oral: 200 mg every 4 to 6 hours as needed; if fever does not respond may increase to 400 mg; maximum daily dose: 2,400 mg/day (Sullivan 2011; manufacturer's labeling).
Cystic fibrosis, mild disease (to slow lung disease progression): Limited data available: Children and Adolescents 6 to 17 years with FEV1 >60% predicted (Mogayzel 2013): Oral: Initial: 20 to 30 mg/kg/dose twice daily; titrate to achieve peak plasma concentrations of 50 to 100 mcg/mL; should not eat or take pancreatic enzymes for 2 hours after the ibuprofen dose. Dosing based on a study of 41 patients (ages: 5 to 39 years); mean required dose: ~25 mg/kg/dose twice daily; reported range: 16.2 to 31.6 mg/kg/dose every 12 hours required to achieve target concentration; results showed that chronic ibuprofen use (over 4 years) slowed the rate of decline in FEV1; patients 5 to 13 years of age with mild lung disease were observed to have greatest benefit (Konstan 1995). A follow up observational study (n=1,365; ages: 6 to 17 years) under noncontrolled conditions (real world) showed significant improvement in the rate of decline of lung disease progression with chronic ibuprofen therapy (Konstan 2007). Note: Timing of blood sampling postdose is based on dosage form: Oral suspension: Obtain blood samples at 30, 45, and 60 minutes postdose; tablets: Obtain blood samples at 1, 2, and 3 hours postdose (Litalien 2001; Scott 1999).
Juvenile idiopathic arthritis (JIA): Children and Adolescents: Oral: Usual range: 30 to 40 mg/kg/day in 3 to 4 divided doses; start at lower end of dosing range and titrate; patients with more severe disease may require up to 50 mg/kg/day; maximum dose: 800 mg/dose; maximum daily dose: 2,400 mg/day (Giannini 1990; Kim 2010; Kliegman 2020; Litalien 2001; Petty 2016).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Infants, Children, and Adolescents: Oral, IV (Caldolor): There are no dosage adjustments provided in the manufacturer's labeling; avoid use in advanced disease.
KDIGO guidelines provide the following recommendations for NSAIDs (KDIGO 2013):
eGFR 30 to <60 mL/minute/1.73 m2: Avoid use in patients with intercurrent disease that increases risk of acute kidney injury.
eGFR <30 mL/minute/1.73 m2: Avoid use.
There are no dosage adjustments provided in the manufacturer's labeling; use caution and discontinue if hepatic function worsens.
(For additional information see "Ibuprofen: Drug information")
Note: Safety: Use the lowest effective dose for the shortest duration of time. Avoid or use with caution in patients at risk for or with existing cardiovascular disease, GI disease, kidney impairment, chronic liver disease, or a bleeding diathesis due to greater risk for adverse events. Consider administering in combination with a proton pump inhibitor in patients at risk for GI bleeding (eg, taking dual antiplatelet therapy or an anticoagulant, ≥60 years of age, high doses) (ACCF/ACG/AHA [Abraham 2010]; ACCF/ACG/AHA [Bhatt 2008]).
Anti-inflammatory (eg, for arthritis associated with rheumatic disease):
Oral: 400 to 800 mg every 6 to 8 hours; maximum dose: 3.2 g/day. Some experts generally recommend a maximum dose of 2.4 g/day for chronic use, except during a disease flare when up to 3.2 g/day may be considered for several weeks until flare resolves (Gladman 2020).
Dysmenorrhea:
Oral: Initial: 400 mg every 4 hours as needed or 600 to 800 mg every 6 to 8 hours as needed; maximum dose: 3.2 g/day. Begin at menses onset or 1 to 2 days prior to onset of menses for severe symptoms; usual duration: 1 to 5 days (Marjoribanks 2015; Smith 2020; manufacturer's labeling).
Fever (alternative agent):
IV, Oral: 200 to 400 mg every 4 to 6 hours as needed; if fever persists, may titrate up to 600 to 800 mg every 6 hours as needed; maximum dose: 3.2 g/day (Promes 2011; Rainsford 2009; manufacturer's labeling).
OTC labeling (patient-guided therapy): Oral: 200 mg every 4 to 6 hours as needed; if no relief, may increase to 400 mg every 4 to 6 hours as needed; maximum dose: 1.2 g/day. Use for >3 days is not recommended unless directed by health care provider.
Gout, treatment (acute flares) (off-label use):
Note: Some experts reserve use for patients who are not candidates for intra-articular glucocorticoids or when intra-articular glucocorticoid administration is not feasible (Gaffo 2022).
Oral: Initial: 800 mg every 8 hours within 24 to 48 hours of flare onset; reduce dose as symptoms improve; discontinue 2 to 3 days after resolution of clinical signs; usual duration: 5 to 7 days (ACR [FitzGerald 2020]; Gaffo 2022; Schweitz 1978).
Migraine, acute treatment:
Note: Limit use to ≤14 days per month to avoid medication-overuse headache (AHS [Ailani 2021]). For use as monotherapy in mild to moderate attacks not associated with vomiting or severe nausea; may be used in combination with triptans for severe migraine (AHS [Pringsheim 2016]; Schwedt 2021). Administration early in the course of a migraine attack, at the first sign of pain, may improve response to treatment (AHS [Ailani 2021]).
Oral: 400 to 600 mg once (CHS [Worthington 2013]; Rabbie 2013).
OTC labeling (patient-guided therapy): Oral: 400 mg at onset of symptoms.
Pain (monotherapy or as an adjunctive agent):
IV, Oral: 200 to 400 mg every 4 to 6 hours as needed or 600 to 800 mg every 6 to 8 hours as needed; maximum dose: 3.2 g/day (APS 2016; Derry 2009; Roelofs 2008). For postoperative pain, doses may be scheduled initially (Mariano 2020). Some experts suggest a usual maximum of 2.4 g/day for chronic use due to increased adverse effects with higher doses (Knight 2020; Pandharipande 2020).
OTC labeling (patient-guided therapy): Oral: 200 mg every 4 to 6 hours as needed; if no relief, may increase to 400 mg every 4 to 6 hours as needed; maximum dose: 1.2 g/day. Use for >10 days is not recommended unless directed by health care provider.
Pericarditis, acute or recurrent (off-label use):
Note: In patients with an indication for aspirin (eg, coronary artery disease), aspirin is generally preferred over other nonsteroidal anti-inflammatory drugs (NSAIDs). If pericarditis occurs after a myocardial infarction (MI), avoid anti-inflammatory agents (other than once-daily, low-dose aspirin for treatment of MI) for 7 to 10 days and use acetaminophen for analgesia. If this does not suffice or if treatment is necessary after 7 to 10 days, aspirin is preferred and other NSAIDs should be avoided (ACCF/AHA [O’Gara 2013]; LeWinter 2020).
Oral: Initial: 600 to 800 mg every 8 hours or 600 mg every 6 hours until resolution of symptoms for at least 24 hours and normalization of inflammatory biomarkers (eg, C-reactive protein); initial therapy typically lasts for at least 1 to 2 weeks. Gradually taper off over several weeks by decreasing each dose by 200 to 400 mg every 1 to 2 weeks; during taper, ensure patient remains asymptomatic and inflammatory biomarkers are normal. Use in combination with colchicine. In patients at risk of NSAID-related GI toxicity, prophylaxis (generally with a proton pump inhibitor) is recommended (ESC [Adler 2015]; Imazio 2021).
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.
IV, Oral:
Altered kidney function:
CrCl ≥60 mL/minute: No dosage adjustment necessary (Antal 1986; expert opinion).
CrCl >30 to <60 mL/minute: No dosage adjustment necessary (Antal 1986; expert opinion). Use of analgesics other than nonsteroidal anti-inflammatory drugs may be preferred. If necessary, use the lowest effective dose for the shortest duration possible; avoid in patients at high risk for acute kidney injury (ie, volume depleted, hypotensive, elderly, or taking concurrent nephrotoxic medications) (Baker 2020; KDIGO 2013; expert opinion).
CrCl ≤ 30 mL/minute: Avoid use due to increased risk of acute kidney injury (KDIGO 2013).
Hemodialysis, intermittent (thrice weekly): Not significantly dialyzable (Antal 1986): No dosage adjustment necessary. Avoid use in patients with residual kidney function (expert opinion).
Peritoneal dialysis: No dosage adjustment necessary. Avoid use in patients with residual kidney function (expert opinion).
CRRT: Avoid use (expert opinion).
PIRRT (eg, sustained, low-efficiency diafiltration): Avoid use (expert opinion).
There are no dosage adjustments provided in the manufacturer’s labeling; use caution and discontinue if hepatic function worsens.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Capsule, Oral:
Advil: 200 mg
Advil Liqui-Gels minis: 200 mg
Advil Migraine: 200 mg
GoodSense Ibuprofen: 200 mg [gluten free; contains brilliant blue fcf (fd&c blue #1)]
KS Ibuprofen: 200 mg [DSC] [contains fd&c blue #2 (indigotine)]
Motrin IB: 200 mg
Generic: 200 mg
Kit, Combination:
Ibuprofen Comfort Pac: 800 mg [DSC] [contains methylparaben, trolamine (triethanolamine)]
Kit, Oral:
IBU 600-EZS: 600 mg [DSC] [contains sodium benzoate]
Ibupak: 600 mg [contains sodium benzoate]
Solution, Intravenous [preservative free]:
Caldolor: 800 mg/200 mL (200 mL); 800 mg/8 mL (8 mL)
Solution, Intravenous, as lysine [preservative free]:
NeoProfen: 10 mg/mL (2 mL)
Generic: 10 mg/mL (2 mL)
Suspension, Oral:
Childrens Advil: 100 mg/5 mL (120 mL) [fruit flavor]
Childrens Advil: 100 mg/5 mL (120 mL) [contains edetate (edta) disodium, fd&c red #40, polysorbate 80, propylene glycol, sodium benzoate]
Childrens Advil: 100 mg/5 mL (120 mL) [alcohol free; grape flavor]
Childrens Advil: 100 mg/5 mL (120 mL) [alcohol free; contains brilliant blue fcf (fd&c blue #1), edetate (edta) disodium, fd&c red #40, polysorbate 80, propylene glycol, sodium benzoate; grape flavor]
Childrens Advil: 100 mg/5 mL (120 mL) [alcohol free; contains brilliant blue fcf (fd&c blue #1), propylene glycol, sodium benzoate; blue raspberry flavor]
Childrens Advil: 100 mg/5 mL (30 mL, 120 mL) [alcohol free, dye free; contains edetate (edta) disodium, polysorbate 80, propylene glycol, sodium benzoate; white grape flavor]
Childrens Advil: 100 mg/5 mL (120 mL) [alcohol free, dye free, sugar free; contains edetate (edta) disodium, polysorbate 80, propylene glycol, sodium benzoate; berry flavor]
Childrens Ibuprofen: 100 mg/5 mL (5 mL) [contains fd&c red #40, fd&c yellow #10 (quinoline yellow), polysorbate 80, sodium benzoate]
Childrens Ibuprofen: 100 mg/5 mL (5 mL) [alcohol free, dye free; contains corn starch, polysorbate 80, sodium benzoate; berry flavor]
Childrens Motrin: 100 mg/5 mL (120 mL) [alcohol free; contains fd&c blue #1 aluminum lake, fd&c red #40, polysorbate 80, sodium benzoate]
Childrens Motrin: 100 mg/5 mL (30 mL, 120 mL) [alcohol free; contains fd&c red #40, fd&c yellow #10 (quinoline yellow), polysorbate 80, sodium benzoate; berry flavor]
Childrens Motrin: 100 mg/5 mL (120 mL) [alcohol free; contains fd&c red #40, polysorbate 80, sodium benzoate]
Childrens Motrin: 100 mg/5 mL (120 mL, 240 mL) [alcohol free, dye free; contains polysorbate 80, sodium benzoate; berry flavor]
GoodSense Ibuprofen Childrens: 100 mg/5 mL (120 mL) [alcohol free, dye free, gluten free; contains polysorbate 80, sodium benzoate, sorbitol; berry flavor]
GoodSense Ibuprofen Childrens: 100 mg/5 mL (240 mL) [alcohol free, gluten free; contains fd&c red #40, polysorbate 80, sodium benzoate; bubble-gum flavor]
Ibuprofen Childrens: 100 mg/5 mL (118 mL, 237 mL) [contains brilliant blue fcf (fd&c blue #1), polysorbate 80, propylene glycol, sodium benzoate]
Ibuprofen Childrens: 100 mg/5 mL (118 mL, 237 mL) [contains fd&c red #40, polysorbate 80, propylene glycol, sodium benzoate]
Ibuprofen Childrens: 100 mg/5 mL (5 mL, 10 mL) [alcohol free; contains brilliant blue fcf (fd&c blue #1), corn starch, fd&c red #40, polysorbate 80, sodium benzoate; grape flavor]
Ibuprofen Childrens: 100 mg/5 mL (118 mL [DSC]) [alcohol free; contains corn starch, fd&c red #40, fd&c yellow #10 (quinoline yellow), polysorbate 80, sodium benzoate; berry flavor]
Ibuprofen Childrens: 100 mg/5 mL (118 mL) [alcohol free; contains corn starch, fd&c red #40, polysorbate 80, sodium benzoate; bubble-gum flavor]
Ibuprofen Childrens: 100 mg/5 mL (118 mL, 237 mL) [alcohol free; contains fd&c red #40, fd&c yellow #10 (quinoline yellow), polysorbate 80, propylene glycol, sodium benzoate; berry flavor]
Ibuprofen Childrens: 100 mg/5 mL (120 mL, 240 mL) [alcohol free; contains fd&c red #40, fd&c yellow #10 (quinoline yellow), polysorbate 80, sodium benzoate]
Ibuprofen Childrens: 100 mg/5 mL (120 mL, 240 mL) [alcohol free; contains fd&c red #40, fd&c yellow #10 (quinoline yellow), polysorbate 80, sodium benzoate; berry flavor]
Ibuprofen Childrens: 100 mg/5 mL (118 mL) [alcohol free, dye free; contains corn starch, polysorbate 80, sodium benzoate; berry flavor]
Ibuprofen Childrens: 100 mg/5 mL (118 mL, 237 mL) [dye free; contains polysorbate 80, propylene glycol, sodium benzoate; berry flavor]
Infants Advil: 50 mg/1.25 mL (30 mL) [alcohol free, dye free; contains edetate (edta) disodium, polysorbate 80, propylene glycol, sodium benzoate]
Infants Advil: 50 mg/1.25 mL (15 mL) [alcohol free, dye free; contains edetate (edta) disodium, polysorbate 80, propylene glycol, sodium benzoate; white grape flavor]
Motrin Infants Drops: 50 mg/1.25 mL (15 mL) [alcohol free; contains fd&c red #40, polysorbate 80, sodium benzoate, sorbitol]
Motrin Infants Drops: 50 mg/1.25 mL (15 mL) [alcohol free; contains fd&c red #40, polysorbate 80, sodium benzoate, sorbitol; berry flavor]
Motrin Infants Drops: 50 mg/1.25 mL (30 mL) [alcohol free, dye free; contains polysorbate 80, sodium benzoate, sorbitol]
Generic: 100 mg/5 mL (5 mL, 118 mL, 120 mL, 473 mL)
Tablet, Oral:
Addaprin: 200 mg [DSC]
Addaprin: 200 mg [DSC] [contains corn starch]
Advil: 200 mg
Advil: 200 mg [contains methylparaben, propylparaben, sodium benzoate]
Advil Junior Strength: 100 mg
Dyspel: 200 mg [DSC]
Genpril: 200 mg [DSC]
GoodSense Ibuprofen: 200 mg [gluten free; contains corn starch, fd&c red #40 aluminum lake, fd&c yellow #6 aluminum lake]
I-Prin: 200 mg [DSC]
IBU: 400 mg, 600 mg, 800 mg
IBU-200: 200 mg [dye free; contains corn starch]
Motrin IB: 200 mg [contains corn starch, fd&c red #40 aluminum lake, fd&c yellow #6 aluminum lake]
Motrin IB: 200 mg [contains fd&c yellow #6 (sunset yellow)]
Provil: 200 mg
Generic: 200 mg, 400 mg, 600 mg, 800 mg
Tablet Chewable, Oral:
Advil Junior Strength: 100 mg [scored; contains aspartame, fd&c blue #2 aluminum lake; grape flavor]
Motrin Childrens: 100 mg [contains aspartame, fd&c blue #1 aluminum lake, soybean oil]
Motrin Childrens: 100 mg [dye free; contains aspartame]
May be product dependent
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous:
Caldolor: 100 mg/mL (4 mL, 8 mL)
Tablet, Oral:
Generic: 600 mg
EnovaRX-Ibuprofen cream is compounded from a kit. Refer to manufacturer’s labeling for compounding instructions.
An FDA-approved patient medication guide, which is available with the product information and at http://www.fda.gov/downloads/Drugs/DrugSafety/UCM387559.pdf, must be dispensed with this medication.
Oral: Administer with food or milk to decrease GI upset.
Oral suspension: Shake suspension well before use. Administer with an accurate measuring device (calibrated oral syringe or measuring cup); do not use a household teaspoon or tablespoon to measure dose (overdosage may occur).
IV:
Ibuprofen injection (Caldolor): For IV administration only; in pediatric patients, doses are infused over ≥10 minutes; in adults, doses are infused over ≥30 minutes.
Ibuprofen lysine injection (NeoProfen): For IV administration only; administration via umbilical arterial line has not been evaluated. Infuse over 15 minutes through IV port closest to insertion site. Avoid extravasation. Do not administer simultaneously via same line with TPN. If needed, interrupt TPN for 15 minutes prior to and after ibuprofen administration, keeping line open with dextrose or saline.
Oral: Administer with food or milk.
IV: Caldolor: For IV administration only; infuse over at least 30 minutes (adults).
Ibuprofen injection (Caldolor): Store intact vials and ready-to-use bags at 20°C to 25°C (68°F to 77°F); excursions permitted to 15°C to 30°C (59°F to 86°F). Vials must be diluted prior to use. Diluted solutions are stable in D5W, LR, or NS for 24 hours at 20°C to 25°C (68°F to 77°F).
Ibuprofen lysine injection (NeoProfen): Store at 20°C to 25°C (68°F to 77°F); excursions are permitted between 15°C and 30°C (59°F and 86°F). Protect from light. Store vials in carton until use. After first withdrawal from vial, discard remaining solution (preservative free). Following dilution in D5W or NS, use within 30 minutes.
Suspension: Store at 15°C to 30°C (59°F to 86°F).
Tablet: Store at 20°C to 25°C (68°F to 77°F).
Oral:
OTC products:
Infant drops, suspension, and chewable tablets: Relief of minor aches and pains due to the common cold, flu, sore throat, headaches, and toothaches; reduction of fever (All indications: OTC products: FDA approved in ages 6 months to 11 years; consult specific product formulation for appropriate age group).
Capsule/Tablet: Relief of minor aches and pains due to the common cold, headaches, minor pain of arthritis, backache, menstrual cramps, muscle aches, and toothaches (All indications: OTC products: FDA approved in ages ≥12 years and adults).
Capsule (Advil Migraine): Treatment of migraines (OTC products: FDA approved in adults).
Prescription strength (400, 600, and 800 mg tablets): Relief of mild to moderate pain; relief of signs and symptoms of osteoarthritis and rheumatoid arthritis; treatment of primary dysmenorrhea (All indications: FDA approved in adults).
Oral ibuprofen has also been used for juvenile idiopathic arthritis (JIA), cystic fibrosis, migraine pain, gout, and for patent ductus arteriosus (PDA) closure.
Parenteral:
Ibuprofen injection (Caldolor): Management of mild to moderate pain; management of moderate to severe pain when used concurrently with an opioid analgesic; reduction of fever (All indications: FDA approved in ages ≥6 months and adults).
Ibuprofen lysine injection (NeoProfen): Treatment (ie, closure) of a clinically significant PDA when usual treatments are ineffective (FDA approved in premature neonates ≤32 weeks GA and weighing 500 to 1,500 g).
Haltran may be confused with Halfprin
Motrin may be confused with Neurontin
Beers Criteria: Ibuprofen is identified in the Beers Criteria as a potentially inappropriate medication to be avoided for chronic use in patients 65 years and older (unless alternative agents ineffective and patient can receive concomitant gastroprotective agent) due to increased risk of GI bleeding and peptic ulcer disease in older adults in high risk category (eg, older than 75 years of age or receiving concomitant oral/parenteral corticosteroids, anticoagulants, or antiplatelet agents) (Beers Criteria [AGS 2019]).
Injectable formulations: Both ibuprofen and ibuprofen lysine are available for parenteral use. Ibuprofen lysine is only indicated for closure of a clinically-significant patent ductus arteriosus.
Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with an increased risk of serious adverse cardiovascular (CV) events, including acute myocardial infarction (MI), cerebrovascular accident, and CV death. New-onset hypertension or exacerbation of hypertension may occur with NSAID use which may also contribute to an increased risk of CV events (Ref). New-onset or exacerbation of heart failure may also occur with cyclooxygenase (COX) NSAIDs (ie, coxibs) and nonselective NSAIDs, including ibuprofen, resulting in an increased risk of hospitalizations for heart failure and death in patients with heart failure (Ref).
Data collected by the Coxib and traditional NSAID Trialists’ (CNT) Collaborative have shown that high-dose ibuprofen (2,400 mg daily) and diclofenac are associated with a similar CV risk as compared to coxibs and that naproxen may have the most favorable CV risk profile among NSAIDs analyzed (Ref); however, data from the PRECISION trial showed no difference with regards to risk between naproxen, ibuprofen, or celecoxib after a treatment duration of therapy of ~3 years (Ref). The FDA states that there are insufficient data to determine if risk of MI or stroke is definitely higher or lower for any particular NSAID as compared to another (Ref).
Mechanism: Dose- and time-related; inhibition of COX-2 by NSAIDs results in a reduction in the production of prostaglandin I2 (prostacyclin) in the vascular endothelium (Ref); animal studies have shown that reduced prostacyclin activity may result in a predisposition to vascular injury (Ref). In addition, NSAIDs may inhibit sodium resorption in the thick ascending loop of Henle and collecting tubule, thereby causing sodium and fluid retention; as a result, NSAID use may result in hypertension and decreased efficacy of diuretics (Ref).
Onset: Variable; increased risk may be apparent within the first weeks following initiation of treatment (Ref); longer duration of therapy may further increase risk (Ref).
Risk factors:
• ≥65 years of age
• Higher doses (especially with regards to CV thrombotic risk (Ref))
• Longer duration of use and frequent use (eg, ≥22 days per month (Ref)
• Preexisting cardiovascular disease (CVD) or presence of risk factors for CVD, including use following coronary artery bypass graft surgery (Ref)
- Note: Relative risk appears to be similar in those with and without known CVD or risk factors for CVD; however, absolute incidence of serious CV thrombotic events appears to be higher in patients with known CVD or risk factors for CVD due to an increased baseline risk (Ref)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs), especially nonselective NSAIDs, such as ibuprofen, is associated with an increased risk of serious GI adverse events, including gastrointestinal inflammation, gastrointestinal hemorrhage, gastrointestinal ulcer, and gastrointestinal perforation; severity may range from asymptomatic to fatal (Ref).
Mechanism: Dose- and time-related; inhibition of cyclooxygenase (COX)-1 by NSAIDs results in a reduction in the production of mucosal-protective prostaglandin E2 (Ref).
Onset: Varied; GI events can occur at any time during use and without warning symptoms. A longer duration of use (eg, ≥7 days (Ref)) is associated with a greater risk.
Risk factors:
• ≥65 years of age (Ref)
• Longer duration of use (eg, ≥7 days (Ref))
• Higher doses (Ref)
• Prior history of peptic ulcer disease and/or GI bleeding (Ref)
• Concomitant use of agents known to increase the risk of GI bleeding (eg, aspirin (Ref), anticoagulants, corticosteroids (Ref), selective serotonin reuptake inhibitors (Ref))
• Comorbid Helicobacter pylori infection (Ref)
• Advanced liver disease/cirrhosis
• Coagulopathy
• Smoking
• Consumption of alcohol
• People with poor general health status
• Small intestine damage: Small intestine bacterial overgrowth (SIBO), including SIBO induced by proton pump inhibitor therapy, may be associated with an increased risk of small intestine damage (Ref)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen, is associated with prolonged bleeding time and an increased risk for hemorrhage (Ref).
In addition, drug-induced hemolytic anemia may occur (Ref). Rarely, NSAID use has been associated with potentially severe blood dyscrasias (eg, agranulocytosis, aplastic anemia, neutropenia, thrombocytopenia) (Ref).
Mechanism:
Prolonged bleeding time: Inhibition of cyclooxygenase (COX)-1 by nonselective NSAIDs causes a decrease in the production of prostaglandins, prostacyclins, and thromboxanes, including thromboxane A2 (TxA2) (Ref). As a result, patients may exhibit a decrease in platelet adhesion and aggregation and subsequent prolonged bleeding time (Ref).
Blood dyscrasias: Not clearly established; anemia may be due to occult or gross blood loss, fluid retention, or an incompletely described effect on erythropoiesis.
Onset:
Prolonged bleeding time: Rapid; suppression of platelet COX-1 activity occurs within hours of administration (Ref). In patients receiving antithrombotic therapy after myocardial infarction, the use of NSAIDs has been associated with an increased risk of bleeding and excess thrombotic events, even after short-term treatment (eg, <3 days) (Ref).
Risk factors:
• Bleeding events:
- Preexisting coagulation disorders
- Concomitant use of agents known to increase the risk of bleeding (eg, anticoagulants (Ref), antithrombotics (Ref), antiplatelet agents [eg, aspirin], selective serotonin reuptake inhibitors (Ref), or serotonin norepinephrine reuptake inhibitors)
- Use during and immediately following surgical procedures (Ref)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen, may result in mild transaminase elevations, especially with higher doses (ie, ibuprofen 2,400 to 3,200 mg/day) (Ref); rarely, serious liver injury may also occur (Ref). Idiopathic liver injuries with a mixed or cholestatic pattern have been reported; these reactions may occur following severe hypersensitivity reactions (eg, toxic epidermal necrosis, Stevens-Johnson syndrome) and are characterized by immune-mediated symptoms (eg, fever rash, eosinophilia, lymphadenopathy) (Ref). Severe liver injury requiring liver transplantation has also been reported (Ref). Most cases of liver injury are likely reversible following discontinuation; full recovery may take several months (Ref). However, chronic vanishing bile duct syndrome with chronic liver failure has been described following cholestatic liver injury (Ref).
Mechanism: Not clearly established; may be a result of a toxic metabolite or an immune-mediated reaction (Ref).
Onset: Varied; liver injury that appears to be immune-mediated usually occur within a few days to 3 weeks after treatment initiation (Ref).
Risk factors:
• Prior NSAID-related liver injury (Ref)
- Note: Cross-reactivity may occur among propionic acid derivatives (eg, ibuprofen, naproxen, ketoprofen) (Ref)
Hypersensitivity reactions (immediate and delayed) involving the skin (eg, angioedema, urticaria), airways (eg, dyspnea, rhinorrhea), and/or other organs have been reported (Ref). Clinical phenotypes of nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity reactions include NSAID-exacerbated respiratory disease (NERD), NSAID-induced urticaria/angioedema (NIUA), NSAID-exacerbated cutaneous disease (NECD), and single NSAID-induced urticaria/angioedema or anaphylaxis (Ref). Delayed hypersensitivity reactions, including acute generalized exanthematous pustulosis (AGEP), drug rash with eosinophilia and systemic symptoms (DRESS), and Stevens-Johnson syndrome (SJS) have also been associated with ibuprofen (Ref).
Mechanism:
Immediate reactions: Non–dose-related; most reactions (ie, NERD, NECD, NIUA) are non-immunologic related to inhibition of cyclooxygenase-1 (COX-1) with subsequent activation of mast cells and eosinophils causing release of inflammatory mediators including cysteinyl-leukotrienes (cysLTs) (Ref). Some immediate reactions are IgE-mediated (Ref).
Delayed reactions: Delayed hypersensitivity reactions are T-cell–mediated (Ref).
Onset:
Immediate reactions: Rapid; occur within 1 hour of administration but may occur several hours after exposure (Ref).
Delayed reactions (including DRESS, AGEP, and SJS): Varied, generally occurs after 1 to 8 weeks after initiation (Ref), although some patients may develop symptoms within 24 hours (Ref).
Risk factors:
• Presence of chronic rhinosinusitis with nasal polyps, family history of NERD, and/or severe asthma may increase the risk of NERD (Ref). The prevalence of NERD in adult patients with asthma is ~10% to 20% (Ref).
• Chronic urticaria increases the risk of NECD (Ref). NSAID-induced reactions are less frequent and less intense when chronic urticaria is in remission or under control (Ref). Approximately 12% to 30% of patients with chronic idiopathic urticaria develop exacerbations of their disease with use of ibuprofen and other COX-1 inhibitors (Ref).
• Cross-reactivity between aspirin and NSAIDs, including ibuprofen (with predominant COX-1 inhibition) have been described in patients with a history of NERD, NECD, and NIUA (Ref). Cross-reactivity between aspirin/NSAID and acetaminophen, a weak COX inhibitor, and between aspirin/NSAID and nonselective COX-2 inhibitors (eg, meloxicam, nimesulide) may occur (Ref). Although selective COX-2 inhibitors (eg, celecoxib, etoricoxib) are generally tolerated in patients with NERD (Ref), cross-reactions may occur, especially in patients with histories of urticaria/angioedema (Ref).
• Cross-reactivity may occur among propionic acid derivatives (eg, ibuprofen, naproxen, ketoprofen) in patients with histories of immediate hypersensitivity reactions to ibuprofen but tolerance to aspirin (Ref)
Use of nonsteroidal anti-inflammatory drugs (NSAIDs), including ibuprofen, is associated with an increased risk of several kidney-specific effects: Acute kidney injury, interstitial nephritis (with or without nephrotic syndrome), and renal papillary necrosis.
Acute kidney injury (AKI): Hemodynamically mediated AKI may occur following use of either cyclooxygenase (COX)-2 selective NSAIDs (ie, coxibs) or nonselective NSAIDs, including ibuprofen (Ref); the risk may be greater with nonselective NSAIDs, especially indomethacin (Ref). The risk of developing AKI is decreased upon discontinuation (Ref). In patients who develop AKI, kidney function is likely to return to baseline following prompt discontinuation of the offending NSAID and supportive care (Ref); persistent kidney function abnormalities may suggest additional etiology that may or may not be related to NSAID use.
Acute interstitial nephritis (AIN) with or without nephrotic syndrome: Patients may develop NSAID-associated proteinuria combined with interstitial nephritis and varying degrees of kidney impairment; these patients generally do not present with symptoms consistent with allergic AIN (eg, fever, rash, eosinophilia, eosinophiluria) that is often seen with antibiotic-induced AIN (Ref). Kidney histology may reveal minimal change glomerulonephritis or membranous nephropathy (Ref). While use of ibuprofen has been associated with this clinical picture, the risk may be greatest with fenoprofen as compared to other NSAIDS (Ref). Proteinuria generally improves within weeks following discontinuation; full recovery may require treatment and take up to a year (Ref).
Papillary necrosis: Chronic use of NSAIDs, including ibuprofen, has resulted in the development of papillary necrosis, which may occur in conjunction with chronic interstitial nephritis and progressive decline in glomerular filtration rate as a clinical syndrome known as analgesic nephropathy (Ref). However, controversy exists on the degree to which NSAID use increases the risk for chronic kidney disease and analgesic nephropathy (Ref). Acute papillary necrosis may occur following NSAID overdose, especially in a setting of severe dehydration or intravascular volume depletion (Ref).
Mechanism:
AKI: Dose- and time-related; inhibition of cyclooxygenase (COX)-1 and COX-2 by NSAIDs results in a reduced production of nephroprotective prostaglandins and subsequent attenuation of renal vasodilation (Ref). In addition, an increase in vasoconstriction of the afferent arteriole and impaired renal blood flow causes a reduction in the glomerular capillary pressure and filtration (Ref).
AIN with or without nephrotic syndrome: Not clearly established. Following inhibition of COX-1 and COX-2 by NSAIDs, arachidonic acid is formed which may be further metabolized to leukotrienes via the lipoxygenase pathway; leukotrienes may increase vascular permeability within glomerular capillaries and peritubular capillaries and increase lymphocyte recruitment and activation (Ref).
Papillary necrosis: Time-related; exact mechanism is not clearly established; may be due to direct toxicity and/or inhibition of prostaglandin-mediated vasodilation resulting in ischemic necrosis (Ref).
Onset:
AKI: Rapid; may occur within days of treatment initiation (Ref).
AIN with or without nephrotic syndrome: Varied; mean time of onset of ~5 months (range: 2 weeks to 18 months) has been described (Ref).
Risk factors:
• AKI:
- Preexisting kidney impairment
- Chronic kidney disease
• Note: High cumulative doses (eg, ibuprofen >700 mg/day) may increase the risk for progression of chronic kidney disease (Ref)
- Nephrotic syndrome
- Volume depletion (eg, due to concomitant diuretic use, nausea, vomiting)
- ≥65 years of age (Ref)
• Note: NSAID-associated AKI may also occur in pediatric patients, even at therapeutic doses (Ref)
- Heart failure (Ref)
- Cirrhosis (Ref)
- Concomitant use of diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, or calcineurin inhibitors (Ref)
- Preexisting conditions which result in decreased renal blood flow or decreased effective arterial circulation (Ref)
- Preexisting conditions where renal blood flow/renal perfusion is dependent on prostaglandin-mediated vasodilation (Ref)
• AIN with or without nephrotic syndrome: Prior history of NSAID-induced nephrotic syndrome; recurrence has been described (Ref)
• Papillary necrosis (acute):
- Massive NSAID ingestion (Ref)
- Dehydration (Ref)
- Intravascular volume depletion (Ref)
• Papillary necrosis (chronic)/analgesic nephropathy: Chronic concomitant use of other analgesics (eg, aspirin, acetaminophen) (Ref)
Pulmonary hypertension has occurred following early (prophylactic) administration and treatment of patent ductus arteriosus (PDA) in preterm or low birth weight neonates; cases have been reported with both tromethamine ibuprofen (not available in the United States) and L-lysine ibuprofen therapy (Ref).
Mechanism: Unknown; several hypotheses have been proposed. The first relates to timing of treatment in which the administration of drug and PDA closure occurs before the normal decrease in pulmonary vascular resistance has occurred (Ref). Another hypothesis involves the effects of the acidic pH of the ibuprofen solution, namely tromethamine buffered solutions, which may lead to precipitation and microembolism of the lung (Ref).
Onset: Variable; has occurred within the first hour following the administration of the first or second dose of treatment (Ref).
Risk factors:
• Lower gestational age (Ref)
• Lower birthweight (less than third percentile for age) (Ref)
• Preexisting pulmonary hypertension (Ref)
• Early administration of treatment (<6 hours postnatal age in premature neonates) (Ref)
• Maternal hypertension of pregnancy (Ref)
• Maternal oligohydramnios (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
Oral:
>10%: Hematologic & oncologic: Decreased hemoglobin (17% to 23%)
1% to 10%:
Cardiovascular: Edema (1% to 3%)
Dermatologic: Maculopapular rash, pruritus (1% to 3%), skin rash (3% to 9%)
Endocrine & metabolic: Fluid retention (1% to 3%)
Gastrointestinal: Abdominal cramps (1% to 3%), abdominal distress (1% to 3%), abdominal pain (1% to 3%), bloating (1% to 3%), constipation (1% to 3%), decreased appetite (1% to 3%), diarrhea (1% to 3%), dyspepsia (1% to 3%), epigastric pain (3% to 9%), flatulence (1% to 3%), heartburn (3% to 9%), nausea (3% to 9%), nausea and vomiting (1% to 3%)
Nervous system: Dizziness (3% to 9%), headache (1% to 3%), nervousness (1% to 3%)
Otic: Tinnitus (1% to 3%)
<1%:
Cardiovascular: Cardiac arrhythmia, increased blood pressure, palpitations, sinus bradycardia, sinus tachycardia
Dermatologic: Alopecia, erythema multiforme, skin photosensitivity, urticaria, vesiculobullous dermatitis
Endocrine & metabolic: Acidosis, gynecomastia, heavy menstrual bleeding, hypoglycemia
Gastrointestinal: Duodenal ulcer, gastric ulcer, gastritis, gingival ulceration, melena, pancreatitis, xerostomia
Genitourinary: Azotemia, cystitis, hematuria
Hematologic & oncologic: Agranulocytosis, aplastic anemia, decreased hematocrit, eosinophilia, hemolytic anemia, hemorrhage, Henoch-Schonlein purpura, neutropenia, thrombocytopenia, ulcer with hemorrhage
Hepatic: Abnormal hepatic function tests, hepatitis, jaundice
Hypersensitivity: Angioedema, serum sickness
Nervous system: Abnormal dreams, chills, confusion, depression, drowsiness, emotional lability, hallucination, idiopathic intracranial hypertension, insomnia, paresthesia
Neuromuscular & skeletal: Systemic lupus erythematosus
Ophthalmic: Amblyopia, cataract, conjunctivitis, diplopia, optic neuritis, xerophthalmia
Otic: Hearing loss
Renal: Decreased creatinine clearance, polyuria, renal papillary necrosis
Respiratory: Bronchospasm, epistaxis, rhinitis
Miscellaneous: Fever
Injection: Ibuprofen (Caldolor):
>10%:
Endocrine & metabolic: Hypokalemia (4% to 19%)
Gastrointestinal: Flatulence (16%), vomiting (22%; children: ≥2%)
Hematologic & oncologic: Anemia (4% to 36%; children: ≥2%), eosinophilia (26%), hypoproteinemia (10% to 13%), neutropenia (7% to 13%) (table 1)
Drug (Ibuprofen) |
Placebo |
Population |
Dose |
Dosage Form |
Indication |
Number of Patients (Ibuprofen) |
Number of Patients (Placebo) |
---|---|---|---|---|---|---|---|
13% |
7% |
Adults |
400 mg every 4 hours for 24 hours |
IV |
Fever |
31 |
28 |
7% |
7% |
Adults |
200 mg every 4 hours for 24 hours |
IV |
Fever |
30 |
28 |
7% |
7% |
Adults |
100 mg every 4 hours for 24 hours |
IV |
Fever |
30 |
28 |
Infection: Bacteremia (13%)
Nervous system: Headache (12%; children: ≥2%)
1% to 10%:
Cardiovascular: Hypertension (≤10%) (table 2) , hypotension (7% to 10%), peripheral edema (3%)
Drug (Ibuprofen) |
Placebo |
Population |
Dose |
Dosage Form |
Indication |
Number of Patients (Ibuprofen) |
Number of Patients (Placebo) |
---|---|---|---|---|---|---|---|
10% |
0% |
Adults |
400 mg every 4 hours for 24 hours |
IV |
Fever |
31 |
28 |
0% |
0% |
Adults |
200 mg every 4 hours for 24 hours |
IV |
Fever |
30 |
28 |
0% |
0% |
Adults |
100 mg every 4 hours for 24 hours |
IV |
Fever |
30 |
28 |
Endocrine & metabolic: Hypernatremia (7% to 10%), hypoalbuminemia (10%), increased lactate dehydrogenase (7% to 10%)
Gastrointestinal: Abdominal distress (≤3%), diarrhea (10%), dyspepsia (1% to 4%), nausea (children: ≥2%)
Genitourinary: Urinary retention (5%)
Hematologic & oncologic: Hemorrhage (10%), thrombocythemia (3% to 10%), wound hemorrhage (3%)
Local: Infusion-site pain (children: ≥2%)
Nervous system: Dizziness (4% to 6%)
Renal: Increased blood urea nitrogen (10%)
Respiratory: Bacterial pneumonia (3% to 10%), cough (3%)
Injection: Ibuprofen lysine (NeoProfen) (as reported in premature infants):
>10%:
Dermatologic: Skin irritation (≤16%), skin lesion (≤16%)
Endocrine & metabolic: Hypocalcemia (12%), hypoglycemia (12%)
Gastrointestinal: Enterocolitis (22%)
Hematologic & oncologic: Anemia (32%), hemorrhage (32%; primarily intraventricular)
Infection: Sepsis (43%)
Nervous system: Intraventricular hemorrhage (29%)
Respiratory: Apnea (28%), respiratory tract infection (19%)
1% to 10%:
Cardiovascular: Edema (4%)
Endocrine & metabolic: Adrenocortical insufficiency (7%), hypernatremia (7%)
Genitourinary: Decreased urine output (3%), urinary tract infection (9%)
Renal: Increased blood urea nitrogen (7%), increased serum creatinine (3%), renal insufficiency (6%)
Respiratory: Atelectasis (4%), respiratory failure (10%)
Frequency not defined (any formulation):
Cardiovascular: Hypotension, tachycardia
Endocrine & metabolic: Hyperglycemia
Gastrointestinal: Abdominal distention, cholestasis, gastritis, gastroesophageal reflux disease, intestinal obstruction
Hematologic & oncologic: Neutropenia, prolonged bleeding time
Hepatic: Jaundice
Infection: Infection
Local: Injection site reaction
Nervous system: Seizure
Miscellaneous: Reduced intake of food/fluids
Postmarketing (any formulation):
Cardiovascular: Acute myocardial infarction (FDA 2015), cerebrovascular accident (FDA 2015), exacerbation of hypertension (Ruschitzkha 2017), heart failure (FDA 2015), thrombosis
Dermatologic: Exfoliative dermatitis, skin rash, Stevens-Johnson syndrome (Sternlieb 1978), toxic epidermal necrolysis (Balint 2014; Barry 2018)
Gastrointestinal: Gastrointestinal hemorrhage (Yeomans 2018), gastrointestinal inflammation, gastrointestinal perforation (including esophageal perforation, intestinal, stomach) (Yeomans 2018), gastrointestinal ulcer (Yeomans 2018), necrotizing enterocolitis
Genitourinary: Oliguria (Brandstetter 1978)
Hematologic & oncologic: Thrombocytopenia (Jain 1994)
Hepatic: Hepatotoxicity (idiosyncratic) (Chalasani 2021), increased serum alanine aminotransferase, increased serum aspartate aminotransferase
Hypersensitivity: Anaphylaxis (Kay 2013), hypersensitivity reaction
Immunologic: Drug reaction with eosinophilia and systemic symptoms syndrome (Koca 2016; Roales-Gómez 2014)
Nervous system: Aseptic meningitis (Pires 2019)
Ophthalmic: Blurred vision, scotoma, vision color changes, visual disturbance
Renal: Acute kidney injury (Rahman 2014), interstitial nephritis (Rahman 2014), renal failure syndrome (Marasco 1987; Poirier 1984)
Respiratory: Pulmonary hypertension (Bellini 2006)
Hypersensitivity to ibuprofen (eg, anaphylactic reactions, serious skin reactions) or any component of the formulation; history of asthma, urticaria, or allergic-type reaction to aspirin or other NSAIDs; aspirin triad (eg, bronchial asthma, aspirin intolerance, rhinitis); use in the setting of coronary artery bypass graft (CABG) surgery
Ibuprofen lysine (NeoProfen): Preterm neonates: With proven or suspected infection that is untreated; congenital heart disease in whom patency of the PDA is necessary for satisfactory pulmonary or systemic blood flow (eg, pulmonary atresia, severe coarctation of the aorta, severe tetralogy of Fallot); bleeding (especially those with active intracranial hemorrhage or GI bleeding); thrombocytopenia; coagulation defects; proven or suspected necrotizing enterocolitis; or significant renal function impairment.
Canadian labeling: Additional contraindications (not in US labeling): Cerebrovascular bleeding or other bleeding disorders; active gastric/duodenal/peptic ulcer, active GI bleeding; inflammatory bowel disease; uncontrolled heart failure; moderate [IV formulation only] to severe renal impairment (creatinine clearance [CrCl] <30 mL/minute); deteriorating renal disease; moderate [IV formulation only] to severe hepatic impairment; active hepatic disease; hyperkalemia; third trimester of pregnancy; breast-feeding; patients <18 years of age [IV formulation only]; patients <12 years of age [oral formulation only]; systemic lupus erythematosus [oral formulation only]; children suffering from dehydration as a result of acute diarrhea, vomiting, or lack of fluid intake
OTC labeling: When used for self-medication, do not use if previous allergic reaction to any other pain reliever/fever reducer; prior to or following cardiac surgery.
Concerns related to adverse effects:
• Anaphylactoid reactions: Even in patients without prior exposure anaphylactoid reactions may occur; patients with "aspirin triad" (bronchial asthma, aspirin intolerance, rhinitis) may be at increased risk. Contraindicated in patients who experience bronchospasm, asthma, rhinitis, or urticaria with nonsteroidal anti-inflammatory drug (NSAID) or aspirin therapy.
• Cardiovascular events: [US Boxed Warning]: NSAIDs cause an increased risk of serious (and potentially fatal) adverse cardiovascular thrombotic events, including fatal MI and stroke. Risk may occur early during treatment and may increase with duration of use. Relative risk appears to be similar in those with and without known cardiovascular disease or risk factors for cardiovascular disease; however, absolute incidence of cardiovascular events (which may occur early during treatment) was higher in patients with known cardiovascular disease or risk factors. New-onset hypertension or exacerbation of hypertension may occur (NSAIDs may also impair response to ACE inhibitors, thiazide diuretics, or loop diuretics); may contribute to cardiovascular events; monitor blood pressure; use with caution in patients with hypertension. May cause sodium and fluid retention; use with caution in patients with edema. Avoid use in heart failure (ACCF/AHA [Yancy 2013]). Avoid use in patients with a recent MI unless benefits outweigh risk of cardiovascular thrombotic events. Use the lowest effective dose for the shortest duration of time, consistent with individual patient goals, to reduce risk of cardiovascular events; alternate therapies should be considered for patients at high risk.
• CNS effects: May cause drowsiness, dizziness, blurred vision, and other neurologic effects which may impair physical or mental abilities; patients must be cautioned about performing tasks which require mental alertness (eg, operating machinery or driving).
• Drug reaction with eosinophilia and systemic symptoms: Potentially serious, sometimes fatal, drug reaction with eosinophilia and systemic symptoms (DRESS), also known as multiorgan hypersensitivity reactions, has been reported with NSAIDs. Monitor for signs and symptoms (eg, fever, rash, lymphadenopathy, eosinophilia) in association with other organ system involvement (eg, hepatitis, nephritis, hematological abnormalities, myocarditis, myositis). Early symptoms of hypersensitivity reaction (eg, lymphadenopathy, fever) may occur without rash; discontinue therapy and further evaluate if DRESS is suspected.
• Gastrointestinal events: [US Boxed Warning]: NSAIDs cause an increased risk of serious gastrointestinal inflammation, ulceration, bleeding, and perforation (may be fatal); elderly patients and patients with history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events. These events may occur at any time during therapy and without warning. Avoid use in patients with active GI bleeding. In patients with a history of acute lower GI bleeding, avoid use of non-aspirin NSAIDs, especially if due to angioectasia or diverticulosis (Strate 2016). Use caution with a history of GI ulcers, concurrent therapy known to increase the risk of GI bleeding (eg, aspirin, anticoagulants and/or corticosteroids, selective serotonin reuptake inhibitors), advanced hepatic disease, coagulopathy, smoking, use of alcohol, or in elderly or debilitated patients. Use the lowest effective dose for the shortest duration of time, consistent with individual patient goals, to reduce risk of GI adverse events; alternate therapies should be considered for patients at high risk. When used concomitantly with aspirin, a substantial increase in the risk of gastrointestinal complications (eg, ulcer) occurs; concomitant gastroprotective therapy (eg, proton pump inhibitors) is recommended (ACCF/ACG/AHA [Bhatt 2008]).
• Hematologic effects: Platelet adhesion and aggregation may be decreased; may prolong bleeding time; patients with coagulation disorders or who are receiving anticoagulants should be monitored closely. Anemia may occur; patients on long-term NSAID therapy should be monitored for anemia. Rarely, NSAID use has been associated with potentially severe blood dyscrasias (eg, agranulocytosis, thrombocytopenia, aplastic anemia).
• Hepatic effects: Transaminase elevations have been reported with use; closely monitor patients with any abnormal LFT. Rare (sometimes fatal) severe hepatic reactions (eg, fulminant hepatitis, liver necrosis, hepatic failure) have occurred with NSAID use; discontinue immediately if signs or symptoms of hepatic disease develop or if systemic manifestations occur.
• Hyperkalemia: NSAID use may increase the risk of hyperkalemia, particularly in patients ≥65 years of age, in patients with diabetes or renal disease, and with concomitant use of other agents capable of inducing hyperkalemia (eg, ACE inhibitors). Monitor potassium closely.
• Ophthalmic events: Blurred/diminished vision, scotomata, and changes in color vision have been reported. Discontinue therapy and refer for ophthalmologic evaluation if symptoms occur. Periodically evaluate vision in all patients receiving long-term therapy.
• Renal effects: NSAID use may compromise existing renal function; dose-dependent decreases in prostaglandin synthesis may result from NSAID use, reducing renal blood flow, which may cause renal decompensation (usually reversible). Patients with impaired renal function, dehydration, hypovolemia, heart failure, hepatic impairment, those taking diuretics and ACE inhibitors, and ≥65 years of age are at greater risk of renal toxicity. Rehydrate patient before starting therapy; monitor renal function closely. Long-term NSAID use may result in renal papillary necrosis and other renal injury.
• Skin reactions: NSAIDs may cause potentially fatal serious skin adverse events including exfoliative dermatitis, Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis (TEN); may occur without warning; discontinue use at first sign of skin rash (or any other hypersensitivity).
Disease-related concerns:
• Aseptic meningitis: May increase the risk of aseptic meningitis, especially in patients with systemic lupus erythematosus (SLE) and mixed connective tissue disorders.
• Asthma: Contraindicated in patients with aspirin-sensitive asthma; severe and potentially fatal bronchospasm may occur. Use caution in patients with other forms of asthma.
• Bariatric surgery: Gastric ulceration: Avoid chronic use of oral nonselective NSAIDs after bariatric surgery; development of anastomotic ulcerations/perforations may occur (Bhangu 2014; Mechanick 2020). Short-term use of celecoxib or IV ketorolac is recommended as part of a multimodal pain management strategy for postoperative pain (Chou 2016b; Horsley 2019; Thorell 2016).
• Coronary artery bypass graft surgery: [US Boxed Warning]: Use is contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Risk of MI and stroke may be increased with use following CABG surgery.
• Hepatic impairment: Use with caution in patients with hepatic impairment; patients with advanced hepatic disease are at an increased risk of GI bleeding with NSAIDs.
• Renal impairment: Avoid use in patients with advanced renal disease; discontinue use with persistent or worsening abnormal renal function tests. Use of ibuprofen lysine (NeoProfen) is contraindicated in preterm infants with significant renal impairment.
Special populations:
• Elderly: Patients ≥65 years of age are at greater risk for serious GI events; use with caution.
Dosage form specific issues:
• Benzyl alcohol and derivatives: Some dosage forms may contain 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 derivative with caution in neonates. See manufacturer's labeling.
• Ibuprofen injection (Caldolor): Must be diluted prior to administration; hemolysis can occur if not diluted.
• Ibuprofen lysine injection (NeoProfen): Hold second or third doses if urinary output is <0.6 mL/kg/hour. May alter signs of infection. May inhibit platelet aggregation; monitor for signs of bleeding. May displace bilirubin; use caution when total bilirubin is elevated. Long-term evaluations of neurodevelopment, growth, or diseases associated with prematurity following treatment have not been conducted. A second course of treatment, alternative pharmacologic therapy or surgery may be needed if the ductus arteriosus fails to close or reopens following the initial course of therapy. Avoid extravasation.
• Phenylalanine: Some products may contain phenylalanine.
• Polysorbate 80: Some dosage forms may contain polysorbate 80 (also known as Tweens). Hypersensitivity reactions, usually a delayed reaction, have been reported following exposure to pharmaceutical products containing polysorbate 80 in certain individuals (Isaksson 2002; Lucente 2000; Shelley 1995). Thrombocytopenia, ascites, pulmonary deterioration, and renal and hepatic failure have been reported in premature neonates after receiving parenteral products containing polysorbate 80 (Alade 1986; CDC 1984). See manufacturer's labeling.
• Propylene glycol: Some dosage forms may contain propylene glycol; large amounts are potentially toxic and have been associated hyperosmolality, lactic acidosis, seizures and respiratory depression; use caution (AAP ["Inactive" 1997]; Zar 2007).
Other warnings/precautions:
• Self-medication (OTC use): Prior to self-medication, patients should contact health care provider if they have had recurring stomach pain or upset, ulcers, bleeding problems, high blood pressure, heart or kidney disease, other serious medical problems, are currently taking a diuretic, aspirin, anticoagulant, or are ≥60 years of age. If patients are using for migraines, they should also contact health care provider if they have not had a migraine diagnosis by health care provider, a headache that is different from usual migraine, worst headache of life, fever and neck stiffness, headache from head injury or coughing, first headache at ≥50 years of age, daily headache, or migraine requiring bed rest. Recommended dosages should not be exceeded, due to an increased risk of GI bleeding. Stop use and consult a health care provider if symptoms do not improve within first 24 hours of use (children) get worse, or newly appear, fever lasts for >3 days or pain lasts >3 days (children) and >10 days (adults). Do not give for >10 days unless instructed by healthcare provider. Consuming ≥3 alcoholic beverages/day or taking longer than recommended may increase the risk of GI bleeding.
• Surgical/dental procedures: Withhold for at least 4 to 6 half-lives prior to surgical or dental procedures.
Oral liquid products are available in 2 concentrations (concentrated infant drops: 50 mg/1.25 mL [40 mg/mL] and suspension: 100 mg/5 mL [20 mg/mL]); precautions should be taken to verify and avoid confusion between the different concentrations; dose should be clearly presented as "mg".
A single-center, 10-year, retrospective review of pediatric patients diagnosed with acute kidney injury (AKI) (n=1,015; ages: ≤18 years) reported nonsteroidal anti-inflammatory drugs (NSAIDs) as a potential cause of AKI in 2.7% of patients (n=27); a higher incidence (6.6%) was reported when additional exclusion factors were included in the data analysis. Dosing information was available for 74% of the NSAID-associated AKI cases (n=20); dosing was within the recommended range in 75% (n=15) of these cases. The median age of children with NSAID-associated AKI was 14.7 years (range: 0.5 to 17.7 years) and 15% of patients were <5 years and more likely to require dialysis than the older patients. Some experts suggest the incidence of NSAID-associated AKI found in this study is conservative due to aggressive exclusion criteria (eg, concurrent aminoglycoside or other nephrotoxic therapy) and the actual incidence may be higher (Brophy 2013; Misurac 2013). IV ibuprofen is as effective as IV indomethacin for the treatment of patent ductus arteriosus (PDA) in preterm neonates, but is less likely to cause adverse effects on renal function (eg, oliguria, increased serum creatinine) (Aranda 2006; Lago 2002; Ohlsson 2013; Van Overmeire 2000). Ibuprofen (compared to indomethacin) also has been shown to decrease the risk of developing NEC (Ohlsson 2013).
In neonates, pulmonary hypertension has occurred following use for treatment of PDA; ten cases have been reported; three following early (prophylactic) administration of tromethamine ibuprofen (not available in United States) and 7 cases following L-lysine ibuprofen therapy (Bellini 2006; Gournay 2002; Ohlsson 2013). Avoid extravasation of ibuprofen lysine injection (NeoProfen); IV solution may be irritating to tissues. Use with caution in neonates with controlled infection or those at risk for infection; ibuprofen may alter the usual signs of infection. Use with caution in neonates when total bilirubin is elevated; ibuprofen may displace bilirubin from albumin-binding sites. Intraventricular hemorrhage has been reported; overall incidence: 29%; grade 3/4: 15%. Long-term evaluations of neurodevelopmental outcome, growth, or diseases associated with prematurity (eg, chronic lung disease, retinopathy of prematurity) following treatment have not been conducted.
Some dosage forms may contain propylene glycol; in neonates, large amounts of propylene glycol delivered orally, intravenously (eg, >3,000 mg/day), or topically have been associated with potentially fatal toxicities which can include metabolic acidosis, seizures, renal failure, and CNS depression; toxicities have also been reported in children and adults including hyperosmolality, lactic acidosis, seizures, and respiratory depression; use caution (AAP 1997; Shehab 2009).
Substrate of CYP2C19 (minor), CYP2C9 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Inhibits OAT1/3
5-Aminosalicylic Acid Derivatives: Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of 5-Aminosalicylic Acid Derivatives. Risk C: Monitor therapy
Abrocitinib: Agents with Antiplatelet Properties may enhance the antiplatelet effect of Abrocitinib. Management: Do not use antiplatelet drugs with abrocitinib during the first 3 months of abrocitinib therapy. The abrocitinib prescribing information lists this combination as contraindicated. This does not apply to low dose aspirin (81 mg/day or less). Risk X: Avoid combination
Acalabrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Acemetacin: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Risk X: Avoid combination
Agents with Antiplatelet Properties (e.g., P2Y12 inhibitors, NSAIDs, SSRIs, etc.): May enhance the antiplatelet effect of other Agents with Antiplatelet Properties. Risk C: Monitor therapy
Alcohol (Ethyl): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk of GI bleeding may be increased with this combination. Risk C: Monitor therapy
Aliskiren: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Aliskiren. Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Aliskiren. Risk C: Monitor therapy
Aminoglycosides: Nonsteroidal Anti-Inflammatory Agents may decrease the excretion of Aminoglycosides. Data only in premature infants. Risk C: Monitor therapy
Aminolevulinic Acid (Systemic): Photosensitizing Agents may enhance the photosensitizing effect of Aminolevulinic Acid (Systemic). Risk X: Avoid combination
Aminolevulinic Acid (Topical): Photosensitizing Agents may enhance the photosensitizing effect of Aminolevulinic Acid (Topical). Risk C: Monitor therapy
Angiotensin II Receptor Blockers: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the combination may result in a significant decrease in renal function. Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Angiotensin II Receptor Blockers. The combination of these two agents may also significantly decrease glomerular filtration and renal function. Risk C: Monitor therapy
Angiotensin-Converting Enzyme Inhibitors: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the combination may result in a significant decrease in renal function. Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy
Anticoagulants: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Anticoagulants. Risk C: Monitor therapy
Apixaban: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Apixaban. Specifically, the risk of bleeding may be increased. Management: A comprehensive risk to benefit assessment should be done for all patients before any concurrent use of apixaban and nonsteroidal anti-inflammatory drugs (NSAIDs). If combined, monitor patients extra closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Bemiparin: Nonsteroidal Anti-Inflammatory Agents may enhance the anticoagulant effect of Bemiparin. Management: Avoid concomitant use of bemiparin and nonsteroidal anti-inflammatory agents (NSAIDs) due to the increased risk of bleeding. If concomitant use is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Bemiparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Bemiparin. Management: Avoid concomitant use of bemiparin with antiplatelet agents. If concomitant use is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Beta-Blockers: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Beta-Blockers. Risk C: Monitor therapy
Bile Acid Sequestrants: May decrease the absorption of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Bisphosphonate Derivatives: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Bisphosphonate Derivatives. Both an increased risk of gastrointestinal ulceration and an increased risk of nephrotoxicity are of concern. Risk C: Monitor therapy
Cephalothin: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Cephalothin. Specifically, the risk for bleeding may be increased. Risk C: Monitor therapy
Collagenase (Systemic): Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Collagenase (Systemic). Specifically, the risk of injection site bruising and or bleeding may be increased. Risk C: Monitor therapy
Corticosteroids (Systemic): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor therapy
CycloSPORINE (Systemic): Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of CycloSPORINE (Systemic). Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of CycloSPORINE (Systemic). CycloSPORINE (Systemic) may increase the serum concentration of Nonsteroidal Anti-Inflammatory Agents. Management: Consider alternatives to nonsteroidal anti-inflammatory agents (NSAIDs). Monitor for evidence of nephrotoxicity, as well as increased serum cyclosporine concentrations and systemic effects (eg, hypertension) during concomitant therapy with NSAIDs. Risk D: Consider therapy modification
Dabigatran Etexilate: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Dabigatran Etexilate. Specifically, the risk of bleeding may be increased. Management: A comprehensive risk to benefit assessment should be done for all patients before any concurrent use of dabigatran and nonsteroidal anti-inflammatory drugs (NSAIDs). If combined, monitor patients extra closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Dasatinib: May enhance the anticoagulant effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Deferasirox: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk C: Monitor therapy
Deoxycholic Acid: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Deoxycholic Acid. Specifically, the risk for bleeding or bruising in the treatment area may be increased. Risk C: Monitor therapy
Desmopressin: Nonsteroidal Anti-Inflammatory Agents may enhance the hyponatremic effect of Desmopressin. Risk C: Monitor therapy
Dichlorphenamide: OAT1/3 Inhibitors may increase the serum concentration of Dichlorphenamide. Risk C: Monitor therapy
Digoxin: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Digoxin. Risk C: Monitor therapy
Drospirenone-Containing Products: May enhance the hyperkalemic effect of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Edoxaban: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Edoxaban. Specifically, the risk of bleeding may be increased. Management: A comprehensive risk to benefit assessment should be done for all patients before any concurrent use of edoxaban and nonsteroidal anti-inflammatory drugs (NSAIDs). If combined, monitor patients extra closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Enoxaparin: Nonsteroidal Anti-Inflammatory Agents may enhance the anticoagulant effect of Enoxaparin. Management: Discontinue nonsteroidal anti-inflammatory agents (NSAIDs) prior to initiating enoxaparin whenever possible. If concomitant administration is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Enoxaparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Enoxaparin. Management: Discontinue antiplatelet agents prior to initiating enoxaparin whenever possible. If concomitant administration is unavoidable, monitor closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Eplerenone: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Eplerenone. Nonsteroidal Anti-Inflammatory Agents may enhance the hyperkalemic effect of Eplerenone. Risk C: Monitor therapy
Fluconazole: May increase the serum concentration of Ibuprofen. Risk C: Monitor therapy
Heparin: Nonsteroidal Anti-Inflammatory Agents may enhance the anticoagulant effect of Heparin. Management: Decrease the dose of heparin or nonsteroidal anti-inflammatory agents (NSAIDs) if coadministration is required. Risk D: Consider therapy modification
Heparin: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Heparin. Management: Decrease the dose of heparin or agents with antiplatelet properties if coadministration is required. Risk D: Consider therapy modification
Herbal Products with Anticoagulant/Antiplatelet Effects (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Bleeding may occur. Risk C: Monitor therapy
Herbal Products with Anticoagulant/Antiplatelet Effects (eg, Alfalfa, Anise, Bilberry): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Bleeding may occur. Risk C: Monitor therapy
HydrALAZINE: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of HydrALAZINE. Risk C: Monitor therapy
Ibritumomab Tiuxetan: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Ibritumomab Tiuxetan. Both agents may contribute to impaired platelet function and an increased risk of bleeding. Risk C: Monitor therapy
Ibrutinib: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Icosapent Ethyl: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Imatinib: Ibuprofen may decrease the serum concentration of Imatinib. Specifically, ibuprofen may decrease intracellular concentrations of imatinib, leading to decreased clinical response. Management: Consider using an alternative to ibuprofen in patients who are being treated with imatinib. Available evidence suggests other NSAIDs do not interact in a similar manner. Risk D: Consider therapy modification
Inotersen: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Ketorolac (Nasal): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Risk X: Avoid combination
Ketorolac (Systemic): Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Ketorolac (Systemic). Risk X: Avoid combination
Limaprost: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Lipid Emulsion (Fish Oil Based): May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Lithium: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Lithium. Management: Consider reducing the lithium dose when initiating a NSAID. Monitor for increased lithium therapeutic/toxic effects if a NSAID is initiated/dose increased, or decreased effects if a NSAID is discontinued/dose decreased. Risk D: Consider therapy modification
Loop Diuretics: Nonsteroidal Anti-Inflammatory Agents may diminish the diuretic effect of Loop Diuretics. Loop Diuretics may enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Management: Monitor for evidence of kidney injury or decreased therapeutic effects of loop diuretics with concurrent use of an NSAID. Consider avoiding concurrent use in CHF or cirrhosis. Concomitant use of bumetanide with indomethacin is not recommended. Risk D: Consider therapy modification
Lumacaftor and Ivacaftor: May decrease the serum concentration of Ibuprofen. Risk C: Monitor therapy
Macimorelin: Nonsteroidal Anti-Inflammatory Agents may diminish the diagnostic effect of Macimorelin. Risk X: Avoid combination
MetFORMIN: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of MetFORMIN. Risk C: Monitor therapy
Methotrexate: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Methotrexate. Management: Avoid coadministration of higher dose methotrexate (such as that used for the treatment of oncologic conditions) and NSAIDs. Use caution if coadministering lower dose methotrexate and NSAIDs. Risk D: Consider therapy modification
Methoxsalen (Systemic): Photosensitizing Agents may enhance the photosensitizing effect of Methoxsalen (Systemic). Risk C: Monitor therapy
Mifamurtide: Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Mifamurtide. Risk X: Avoid combination
Multivitamins/Fluoride (with ADE): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Minerals (with ADEK, Folate, Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Multivitamins/Minerals (with AE, No Iron): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Naftazone: May enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents: May enhance the adverse/toxic effect of other Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk for gastrointestinal toxicity is increased. Risk X: Avoid combination
Nonsteroidal Anti-Inflammatory Agents (Topical): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk of gastrointestinal (GI) toxicity is increased. Management: Coadministration of systemic nonsteroidal anti-inflammatory drugs (NSAIDs) and topical NSAIDs is not recommended. If systemic NSAIDs and topical NSAIDs, ensure the benefits outweigh the risks and monitor for increased NSAID toxicities. Risk D: Consider therapy modification
Obinutuzumab: Agents with Antiplatelet Properties may enhance the adverse/toxic effect of Obinutuzumab. Specifically, the risk of serious bleeding-related events may be increased. Risk C: Monitor therapy
Omacetaxine: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Omacetaxine. Specifically, the risk for bleeding-related events may be increased. Risk C: Monitor therapy
Omega-3 Fatty Acids: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
PEMEtrexed: Ibuprofen may increase the serum concentration of PEMEtrexed. Management: In patients with an estimated creatinine clearance of 45 to 79 mL/min, avoid ibuprofen for 2 days before, the day of, and 2 days following the administration of pemetrexed. Monitor for increased pemetrexed toxicities if combined. Risk D: Consider therapy modification
Pentosan Polysulfate Sodium: May enhance the adverse/toxic effect of Agents with Antiplatelet Properties. Specifically, the risk of bleeding may be increased by concurrent use of these agents. Risk C: Monitor therapy
Pentoxifylline: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Phenylbutazone: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Risk X: Avoid combination
Porfimer: Photosensitizing Agents may enhance the photosensitizing effect of Porfimer. Risk C: Monitor therapy
Potassium Salts: Nonsteroidal Anti-Inflammatory Agents may enhance the hyperkalemic effect of Potassium Salts. Risk C: Monitor therapy
Potassium-Sparing Diuretics: Nonsteroidal Anti-Inflammatory Agents may diminish the antihypertensive effect of Potassium-Sparing Diuretics. Nonsteroidal Anti-Inflammatory Agents may enhance the hyperkalemic effect of Potassium-Sparing Diuretics. Risk C: Monitor therapy
PRALAtrexate: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of PRALAtrexate. More specifically, NSAIDS may decrease the renal excretion of pralatrexate. Management: Avoid coadministration of pralatrexate with nonsteroidal anti-inflammatory drugs (NSAIDs). If coadministration cannot be avoided, closely monitor for increased pralatrexate serum levels or toxicity. Risk D: Consider therapy modification
Probenecid: May increase the serum concentration of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Prostacyclin Analogues: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Prostaglandins (Ophthalmic): Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Prostaglandins (Ophthalmic). Nonsteroidal Anti-Inflammatory Agents may also enhance the therapeutic effects of Prostaglandins (Ophthalmic). Risk C: Monitor therapy
Quinolones: Nonsteroidal Anti-Inflammatory Agents may enhance the neuroexcitatory and/or seizure-potentiating effect of Quinolones. Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Quinolones. Risk C: Monitor therapy
Rivaroxaban: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Rivaroxaban. Specifically, the risk of bleeding may be increased. Management: A comprehensive risk to benefit assessment should be done for all patients before any concurrent use of rivaroxaban and nonsteroidal anti-inflammatory drugs (NSAIDs). If combined, monitor patients extra closely for signs and symptoms of bleeding. Risk D: Consider therapy modification
Salicylates: Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the adverse/toxic effect of Salicylates. An increased risk of bleeding may be associated with use of this combination. Nonsteroidal Anti-Inflammatory Agents (Nonselective) may diminish the cardioprotective effect of Salicylates. Salicylates may decrease the serum concentration of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Management: Nonselective NSAIDs may reduce aspirin's cardioprotective effects. Administer ibuprofen 30-120 minutes after immediate-release aspirin, 2 to 4 hours after extended-release aspirin, or 8 hours before aspirin. Risk D: Consider therapy modification
Selective Serotonin Reuptake Inhibitors: May enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Nonsteroidal Anti-Inflammatory Agents (Nonselective) may diminish the therapeutic effect of Selective Serotonin Reuptake Inhibitors. Management: Consider alternatives to NSAIDs. Monitor for evidence of bleeding and diminished antidepressant effects. It is unclear whether COX-2-selective NSAIDs reduce risk. Risk D: Consider therapy modification
Selumetinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Serotonin/Norepinephrine Reuptake Inhibitors: May enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor therapy
Sincalide: Drugs that Affect Gallbladder Function may diminish the therapeutic effect of Sincalide. Management: Consider discontinuing drugs that may affect gallbladder motility prior to the use of sincalide to stimulate gallbladder contraction. Risk D: Consider therapy modification
Sodium Phosphates: May enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Specifically, the risk of acute phosphate nephropathy may be enhanced. Management: Consider avoiding this combination by temporarily suspending treatment with NSAIDs, or seeking alternatives to oral sodium phosphate bowel preparation. If the combination cannot be avoided, maintain adequate hydration and monitor renal function closely. Risk D: Consider therapy modification
Tacrolimus (Systemic): Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Tacrolimus (Systemic). Risk C: Monitor therapy
Tenofovir Products: Nonsteroidal Anti-Inflammatory Agents may enhance the nephrotoxic effect of Tenofovir Products. Management: Seek alternatives to these combinations whenever possible. Avoid use of tenofovir with multiple NSAIDs or any NSAID given at a high dose due to a potential risk of acute renal failure. Diclofenac appears to confer the most risk. Risk D: Consider therapy modification
Tenoxicam: May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents. Risk X: Avoid combination
Thiazide and Thiazide-Like Diuretics: May enhance the nephrotoxic effect of Nonsteroidal Anti-Inflammatory Agents. Nonsteroidal Anti-Inflammatory Agents may diminish the therapeutic effect of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor therapy
Thrombolytic Agents: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Thrombolytic Agents. Risk C: Monitor therapy
Tipranavir: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Tolperisone: Nonsteroidal Anti-Inflammatory Agents may enhance the adverse/toxic effect of Tolperisone. Specifically, the risk of hypersensitivity reactions may be increased. Tolperisone may enhance the therapeutic effect of Nonsteroidal Anti-Inflammatory Agents. Risk C: Monitor therapy
Tricyclic Antidepressants (Tertiary Amine): May enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Specifically, the risk of major adverse cardiovascular events may be increased. Tricyclic Antidepressants (Tertiary Amine) may enhance the antiplatelet effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor therapy
Urokinase: Agents with Antiplatelet Properties may enhance the anticoagulant effect of Urokinase. Risk X: Avoid combination
Vancomycin: Nonsteroidal Anti-Inflammatory Agents may increase the serum concentration of Vancomycin. Risk C: Monitor therapy
Verteporfin: Photosensitizing Agents may enhance the photosensitizing effect of Verteporfin. Risk C: Monitor therapy
Vitamin E (Systemic): May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Vitamin K Antagonists (eg, warfarin): Nonsteroidal Anti-Inflammatory Agents (Nonselective) may enhance the anticoagulant effect of Vitamin K Antagonists. Management: Consider alternatives to this combination when possible. If the combination must be used, monitor coagulation status closely and advise patients to promptly report any evidence of bleeding or bruising. Risk D: Consider therapy modification
Voriconazole: May increase the serum concentration of Ibuprofen. Specifically, concentrations of the S-(+)-ibuprofen enantiomer may be increased. Risk C: Monitor therapy
Zanubrutinib: May enhance the antiplatelet effect of Agents with Antiplatelet Properties. Risk C: Monitor therapy
Some products may contain phenylalanine and/or potassium.
Nonsteroidal anti-inflammatory drugs (NSAIDs) may delay or prevent rupture of ovarian follicles. This may be associated with infertility that is reversible upon discontinuation of the medication. Consider discontinuing use in patients having difficulty conceiving or those undergoing investigation of fertility.
Based on available information, NSAIDs can be continued in males with rheumatic and musculoskeletal diseases who are planning to father a child (ACR [Sammaritano 2020]).
The use of nonsteroidal anti-inflammatory drugs (NSAIDs) close to conception may be associated with an increased risk of miscarriage due to cyclooxygenase-2 inhibition interfering with implantation (Bermas 2014; Bloor 2013).
Birth defects have been observed following in utero NSAID exposure in some studies; however, data are conflicting (Bloor 2013). Nonteratogenic effects, including prenatal constriction of the ductus arteriosus, persistent pulmonary hypertension of the newborn, oligohydramnios, necrotizing enterocolitis, renal dysfunction or failure, and intracranial hemorrhage, have been observed in the fetus/neonate following in utero NSAID exposure (Bermas 2014; Bloor 2013). Maternal NSAID use may cause fetal renal dysfunction leading to oligohydramnios. Although rare, this may occur as early as 20 weeks' gestation and is more likely to occur with prolonged maternal use. Oligohydramnios may be reversible following discontinuation of the NSAID (Dathe 2019; FDA 2020). In addition, nonclosure of the ductus arteriosus postnatally may occur and be resistant to medical management (Bermas 2014; Bloor 2013).
Maternal use of NSAIDs should be avoided beginning at 20 weeks' gestation. If NSAID use is necessary between 20 and 30 weeks' gestation, limit use to the lowest effective dose and shortest duration possible; consider ultrasound monitoring of amniotic fluid if treatment extends beyond 48 hours, and discontinue the NSAID if oligohydramnios is found (FDA 2020). Because NSAIDs may cause premature closure of the ductus arteriosus, prescribing information for ibuprofen specifically states use should be avoided starting at 30 weeks' gestation.
Based on available information, NSAIDs can be continued during the first 2 trimesters of pregnancy in patients with rheumatic and musculoskeletal diseases; use in the third trimester is not recommended (ACR [Sammaritano 2020]).
NSAIDs may be used as part of a multimodal approach to pain relief following cesarean delivery (ACOG 2019).
NSAIDs are not preferred for the acute management of migraine during pregnancy (Burch 2020; van Casteren 2020). However, use of ibuprofen during the second trimester may be considered when an NSAID is required (Burch 2020).
CBC, serum electrolytes, occult blood loss, liver enzymes; urine output, serum BUN, and creatinine in patients receiving IV ibuprofen, concurrent diuretics, those with decreased renal function, or in patients on chronic therapy. Monitor preterm neonates for signs of bleeding and infection; serum electrolytes, glucose, calcium and bilirubin; vital signs; monitor IV site for signs of extravasation. Patients receiving long-term therapy for JIA should receive periodic ophthalmological exams.
Plasma concentrations >200 mcg/mL may be associated with severe toxicity; cystic fibrosis: therapeutic peak plasma concentration: 50 to 100 mcg/mL.
Reversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which results in decreased formation of prostaglandin precursors; has antipyretic, analgesic, and anti-inflammatory properties
Other proposed mechanisms not fully elucidated (and possibly contributing to the anti-inflammatory effect to varying degrees), include inhibiting chemotaxis, altering lymphocyte activity, inhibiting neutrophil aggregation/activation, and decreasing proinflammatory cytokine levels.
Onset of action: Oral: Analgesic: Within 30 to 60 minutes (Davies 1998; Mehlisch 2013); Antipyretic: Single oral dose 8 mg/kg (Kauffman 1992): Infants ≤1 year: 69 ± 22 minutes; Children ≥6 years: Single oral dose 8 mg/kg (Kauffman 1992): 109 ± 64 minutes; Adults: <1 hour (Sullivan 2011)
Maximum effect: Antipyretic: 2 to 4 hours
Duration: Oral: Antipyretic: 6 to 8 hours (Sullivan 2011)
Absorption: Oral: Rapid (85%)
Distribution: Vd:
Oral: Febrile children <11 years: 0.2 L/kg; Adults: 0.12 L/kg
IV: Ibuprofen (Caldolor):
Pediatric patients 6 months to <2 years: 0.31 L/kg
Pediatric patients 2 to 16 years: 0.23 L/kg
IV: Ibuprofen lysine: Premature neonates, GA <32 weeks: Variable results observed: 0.32 L/kg, others have reported: a central compartment Vd that decreases with increasing PNA and ductal closure (Van Overmeire, 2001) and a Vd, apparent: 0.062 L/kg in 21 premature neonates (GA <32 weeks, PNA: <1 day) (Aranda 1997); a 2-compartment open model was observed
Protein binding: >99%; Premature infants: ~95% (Aranda 1997)
Bioavailability: 80%
Metabolism: Hepatic via oxidation; Note: Ibuprofen is a racemic mixture of R and S isomers; the R isomer (thought to be inactive) is slowly and incompletely (~60%) converted to the S isomer (active) in adults; the amount of conversion in children is not known, but it is thought to be similar to adults; a study in preterm neonates estimated the conversion to be 61% after prophylactic ibuprofen use and 86% after curative treatment (Gregoire 2004).
Half-life elimination: IV:
Ibuprofen (Caldor):
Pediatric patients: 6 months to <2 years: 1.8 hours; 2 to 16 years: ~1.5 hours
Adults: 2.22 to 2.44 hours
Ibuprofen lysine (Neoprofen):
Premature neonates, GA <32 weeks: Reported data highly variable
R-enantiomer: 10 hours; S-enantiomer: 25.5 hours (Gregoire 2004)
Age-based observations:
PNA <1 day: 30.5 ± 4.2 hours (Aranda 1997)
PNA 3 days: 43.1 ± 26.1 hours (Van Overmeire 2001)
PNA 5 days: 26.8 ± 23.6 hours (Van Overmeire 2001)
Half-life elimination: Oral:
Children 3 months to 10 years: Oral suspension: 1.6 ± 0.7 hours (Kauffman 1992)
Adults: ~2 hours; End-stage renal disease: Unchanged (Aronoff 2007)
Time to peak: Tablets: 1 to 2 hours; Suspension: 1 hour
Children with cystic fibrosis (Scott 1999):
Suspension (n=22): 0.74 ± 0.43 hours (median: 30 minutes)
Chewable tablet (n=4): 1.5 ± 0.58 hours (median: 1.5 hours)
Tablet (n=12): 1.33 ± 0.95 hours (median: 1 hour)
Excretion: Urine (primarily as metabolites (45% to 80%); ~1% as unchanged drug and 14% as conjugated); some feces
Motrin suspension contains sucrose 0.3 g/mL and 1.6 calories/mL. Due to its effects on platelet function, ibuprofen should be withheld for at least 4 to 6 half-lives prior to surgical or dental procedures.
Capsules (Advil Liqui-Gels minis Oral)
200 mg (per each): $0.24
Capsules (Advil Migraine Oral)
200 mg (per each): $0.17
Capsules (Advil Oral)
200 mg (per each): $0.13
Capsules (Ibuprofen Oral)
200 mg (per each): $0.07 - $0.10
Capsules (Motrin IB Oral)
200 mg (per each): $0.15
Chewable (Advil Junior Strength Oral)
100 mg (per each): $0.18
Chewable (Motrin Childrens Oral)
100 mg (per each): $0.26
Kit (Ibupak Oral)
600 mg (per each): $1,523.00
Solution (Caldolor Intravenous)
800 mg/200 mL (per mL): $0.14
800 mg/8 mL (per mL): $3.26
Solution (Ibuprofen Lysine Intravenous)
10 mg/mL (per mL): $206.25 - $273.74
Solution (NeoProfen Intravenous)
10 mg/mL (per mL): $590.15
Suspension (Childrens Advil Oral)
100 mg/5 mL (per mL): $0.04
Suspension (Childrens Motrin Oral)
100 mg/5 mL (per mL): $0.05
Suspension (Ibuprofen Oral)
100 mg/5 mL (per mL): $0.25 - $0.38
Suspension (Infants Advil Oral)
50 mg/1.25 mL (per mL): $0.27
Suspension (Motrin Infants Drops Oral)
50 mg/1.25 mL (per mL): $0.36
Tablets (Advil Junior Strength Oral)
100 mg (per each): $0.18
Tablets (Advil Oral)
200 mg (per each): $0.08
Tablets (IBU Oral)
400 mg (per each): $0.21
600 mg (per each): $0.29
800 mg (per each): $0.38
Tablets (Ibuprofen Oral)
200 mg (per each): $0.02 - $0.08
400 mg (per each): $0.05 - $0.39
600 mg (per each): $0.06 - $1.02
800 mg (per each): $0.07 - $1.18
Tablets (Motrin IB Oral)
200 mg (per each): $0.11
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.