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Ketoprofen (Monograph)

Drug class: Other Nonsteroidal Anti-inflammatory Agents
Chemical name: 3-Benzoyl-α-methylbenzeneacetic acid
Molecular formula: C16H14O3
CAS number: 22071-15-4

Medically reviewed by on Nov 20, 2023. Written by ASHP.


    Cardiovascular Risk
  • Increased risk of serious (sometimes fatal) cardiovascular thrombotic events (e.g., MI, stroke). Risk may occur early in treatment and may increase with duration of use. (See Cardiovascular Thrombotic Effects under Cautions.)

  • Contraindicated in the setting of CABG surgery.

    GI Risk
  • Increased risk of serious (sometimes fatal) GI events (e.g., bleeding, ulceration, perforation of the stomach or intestine). Serious GI events can occur at any time and may not be preceded by warning signs and symptoms. Geriatric individuals are at greater risk for serious GI events. (See GI Effects under Cautions.)


Prototypical NSAIA; propionic acid derivative.

Uses for Ketoprofen

Consider potential benefits and risks of ketoprofen therapy as well as alternative therapies before initiating therapy with the drug. Use lowest possible effective dosage and shortest duration of therapy consistent with patient’s treatment goals.

Inflammatory Diseases

Symptomatic treatment of osteoarthritis and rheumatoid arthritis.

Has been used in the symptomatic treatment of ankylosing spondylitis [off-label].


Relief of pain.


Symptomatic management of primary dysmenorrhea.

Ketoprofen Dosage and Administration



Oral Administration

Administer orally once daily as extended-release capsules or 3 or 4 times daily as conventional capsules.

Administration with antacids, food, or milk may minimize adverse GI effects.

Ketoprofen extended-release capsules are not recommended for the management of acute pain because of slow onset of action.


To minimize the potential risk of adverse cardiovascular and/or GI events, use lowest effective dosage and shortest duration of therapy consistent with the patient’s treatment goals. Adjust dosage based on individual requirements and response; attempt to titrate to the lowest effective dosage.


Inflammatory Diseases
Osteoarthritis or Rheumatoid Arthritis

Conventional capsules: Initially, 75 mg 3 times daily or 50 mg 4 times daily. Base subsequent dosage on clinical response and tolerance.

Extended-release capsules: Initially, 200 mg once daily. Base subsequent dosage on clinical response and tolerance.


Conventional capsules: Usual dosage is 25–50 mg every 6–8 hours as needed.


Conventional capsules: Usual dosage is 25–50 mg every 6–8 hours as needed.

Prescribing Limits


Inflammatory Diseases
Osteoarthritis or Rheumatoid Arthritis

Conventional capsules: Maximum 300 mg daily.

Extended-release capsules: Maximum 200 mg daily.

Pain or Dysmenorrhea

Conventional capsules: Maximum 300 mg daily.

Special Populations

Hepatic Impairment

Maximum recommended initial total dosage is 100 mg daily in patients with hepatic impairment and serum albumin concentrations <3.5 g/dL.

Renal Impairment

Mild renal impairment: Maximum recommended dosage is 150 mg daily.

Severe renal impairment (GFR <25 mL/minute per 1.73 m2 or end-stage renal impairment): Maximum recommended dosage is 100 mg daily. (See Renal Impairment under Cautions.)

Geriatric Patients

Consider reduced initial dosage in patients >75 years of age.

Cautions for Ketoprofen




Cardiovascular Thrombotic Effects

NSAIAs (selective COX-2 inhibitors, prototypical NSAIAs) increase the risk of serious adverse cardiovascular thrombotic events (e.g., MI, stroke) in patients with or without cardiovascular disease or risk factors for cardiovascular disease.

Findings of FDA review of observational studies, meta-analysis of randomized controlled trials, and other published information indicate that NSAIAs may increase the risk of such events by 10–50% or more, depending on the drugs and dosages studied.

Relative increase in risk appears to be similar in patients with or without known underlying cardiovascular disease or risk factors for cardiovascular disease, but the absolute incidence of serious NSAIA-associated cardiovascular thrombotic events is higher in those with cardiovascular disease or risk factors for cardiovascular disease because of their elevated baseline risk.

Increased risk may occur early (within the first weeks) following initiation of therapy and may increase with higher dosages and longer durations of use.

In controlled studies, increased risk of MI and stroke observed in patients receiving a selective COX-2 inhibitor for analgesia in first 10–14 days following CABG surgery.

In patients receiving NSAIAs following MI, increased risk of reinfarction and death observed beginning in the first week of treatment.

Increased 1-year mortality rate observed in patients receiving NSAIAs following MI; absolute mortality rate declined somewhat after the first post-MI year, but the increased relative risk of death persisted over at least the next 4 years.

Some systematic reviews of controlled observational studies and meta-analyses of randomized studies suggest naproxen may be associated with lower risk of cardiovascular thrombotic events compared with other NSAIAs. FDA states that limitations of these studies and indirect comparisons preclude definitive conclusions regarding relative risks of NSAIAs.

Use NSAIAs with caution and careful monitoring (e.g., monitor for development of cardiovascular events throughout therapy, even in those without prior cardiovascular symptoms) and at the lowest effective dosage for the shortest duration necessary.

Some clinicians suggest that it may be prudent to avoid NSAIA use, whenever possible, in patients with cardiovascular disease. Avoid use in patients with recent MI unless benefits of therapy are expected to outweigh risk of recurrent cardiovascular thrombotic events; if used, monitor for cardiac ischemia. Contraindicated in the setting of CABG surgery.

No consistent evidence that concomitant use of low-dose aspirin mitigates the increased risk of serious adverse cardiovascular events associated with NSAIAs. (See Specific Drugs under Interactions.)

GI Effects

Serious GI toxicity (e.g., bleeding, ulceration, perforation) can occur with or without warning symptoms; increased risk in those with a history of GI bleeding or ulceration, geriatric patients, smokers, those with alcohol dependence, and those in poor general health.

For patients at high risk for complications from NSAIA-induced GI ulceration (e.g., bleeding, perforation), consider concomitant use of misoprostol; alternatively, consider concomitant use of a proton-pump inhibitor (e.g., omeprazole) or use of an NSAIA that is a selective inhibitor of COX-2 (e.g., celecoxib).


Hypertension and worsening of preexisting hypertension reported; either event may contribute to the increased incidence of cardiovascular events. Use with caution in patients with hypertension; monitor BP.

Impaired response to ACE inhibitors, angiotensin II receptor antagonists, β-blockers, and certain diuretics may occur. (See Specific Drugs under Interactions.)

Heart Failure and Edema

Fluid retention and edema reported.

NSAIAs (selective COX-2 inhibitors, prototypical NSAIAs) may increase morbidity and mortality in patients with heart failure.

NSAIAs may diminish cardiovascular effects of diuretics, ACE inhibitors, or angiotensin II receptor antagonists used to treat heart failure or edema. (See Specific Drugs under Interactions.)

Manufacturer recommends avoiding use in patients with severe heart failure unless benefits of therapy are expected to outweigh risk of worsening heart failure; if used, monitor for worsening heart failure.

Some experts recommend avoiding use, whenever possible, in patients with reduced left ventricular ejection fraction and current or prior symptoms of heart failure.

Renal Effects

Direct renal injury, including renal papillary necrosis, reported in patients receiving long-term NSAIA therapy.

Potential for overt renal decompensation. Increased risk of renal toxicity in patients with renal or hepatic impairment or heart failure, in geriatric patients, in patients with volume depletion, and in those receiving a diuretic, ACE inhibitor, or angiotensin II receptor antagonist. (See Renal Impairment under Cautions.)

Sensitivity Reactions

Hypersensitivity Reactions

Anaphylactoid reactions reported. Immediate medical intervention and discontinuance for anaphylaxis.

Avoid in patients with aspirin triad (aspirin sensitivity, asthma, nasal polyps); caution in patients with asthma.

Potentially fatal or life-threatening syndrome of multi-organ hypersensitivity (i.e., drug reaction with eosinophilia and systemic symptoms [DRESS]) reported in patients receiving NSAIAs. Clinical presentation is variable, but typically includes eosinophilia, fever, rash, lymphadenopathy, and/or facial swelling, possibly associated with other organ system involvement (e.g., hepatitis, nephritis, hematologic abnormalities, myocarditis, myositis). Symptoms may resemble those of acute viral infection. Early manifestations of hypersensitivity (e.g., fever, lymphadenopathy) may be present in the absence of rash. If signs or symptoms of DRESS develop, discontinue ketoprofen and immediately evaluate the patient.

Dermatologic Reactions

Serious skin reactions (e.g., exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis) reported; can occur without warning. Discontinue at first appearance of rash or any other signs of hypersensitivity (e.g., blisters, fever, pruritus).

General Precautions

Hepatic Effects

Severe reactions including jaundice, fatal fulminant hepatitis, liver necrosis, and hepatic failure (sometimes fatal) reported rarely with NSAIAs.

Elevations of serum ALT or AST reported.

Monitor for symptoms and/or signs suggesting liver dysfunction; monitor abnormal liver function test results. Discontinue if signs or symptoms of liver disease or systemic manifestations (e.g., eosinophilia, rash) occur or if liver function test abnormalities persist or worsen.

Hematologic Effects

Anemia reported rarely. Determine hemoglobin concentration or hematocrit in patients receiving long-term therapy if signs or symptoms of anemia occur.

May inhibit platelet aggregation and prolong bleeding time.

Other Precautions

Not a substitute for corticosteroid therapy; not effective in the management of adrenal insufficiency.

May mask certain signs of infection.

Obtain CBC and chemistry profile periodically during long-term use.

Specific Populations


Use of NSAIAs during pregnancy at about ≥30 weeks’ gestation can cause premature closure of the fetal ductus arteriosus; use at about ≥20 weeks’ gestation associated with fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment.

Effects of NSAIAs on the human fetus during third trimester of pregnancy include prenatal constriction of the ductus arteriosus, tricuspid incompetence, and pulmonary hypertension; nonclosure of the ductus arteriosus during the postnatal period (which may be resistant to medical management); and myocardial degenerative changes, platelet dysfunction with resultant bleeding, intracranial bleeding, renal dysfunction or renal failure, renal injury or dysgenesis potentially resulting in prolonged or permanent renal failure, oligohydramnios, GI bleeding or perforation, and increased risk of necrotizing enterocolitis.

Avoid use of NSAIAs in pregnant women at about ≥30 weeks’ gestation; if use required between about 20 and 30 weeks’ gestation, use lowest effective dosage and shortest possible duration of treatment, and consider monitoring amniotic fluid volume via ultrasound examination if treatment duration >48 hours; if oligohydramnios occurs, discontinue drug and follow up according to clinical practice. (See Advice to Patients.)

Fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment observed, on average, following days to weeks of maternal NSAIA use; infrequently, oligohydramnios observed as early as 48 hours after initiation of NSAIAs. Oligohydramnios is often, but not always, reversible (generally within 3–6 days) following NSAIA discontinuance. Complications of prolonged oligohydramnios may include limb contracture and delayed lung maturation. In limited number of cases, neonatal renal dysfunction (sometimes irreversible) occurred without oligohydramnios. Some neonates have required invasive procedures (e.g., exchange transfusion, dialysis). Deaths associated with neonatal renal failure also reported. Limitations of available data (lack of control group; limited information regarding dosage, duration, and timing of drug exposure; concomitant use of other drugs) preclude a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal NSAIA use. Available data on neonatal outcomes generally involved preterm infants; extent to which risks can be generalized to full-term infants is uncertain.

Animal data indicate important roles for prostaglandins in kidney development and endometrial vascular permeability, blastocyst implantation, and decidualization. In animal studies, inhibitors of prostaglandin synthesis increased pre- and post-implantation losses; also impaired kidney development at clinically relevant doses. Maternally toxic ketoprofen dosages associated with embryotoxicity but not teratogenicity in rabbits.

Effects of ketoprofen on labor and delivery not known; delayed parturition observed in animal studies.


Not known whether distributed into milk in humans. Use not recommended.


NSAIAs may be associated with reversible infertility in some women. Reversible delays in ovulation observed in limited studies in women receiving NSAIAs; animal studies indicate that inhibitors of prostaglandin synthesis can disrupt prostaglandin-mediated follicular rupture required for ovulation.

Consider withdrawal of NSAIAs in women experiencing difficulty conceiving or undergoing evaluation of infertility.

Pediatric Use

Safety and efficacy not established in children <18 years of age.

Geriatric Use

Caution advised. Geriatric adults appear to tolerate NSAIA-induced adverse effects less well than younger individuals. Fatal adverse GI effects reported more frequently in geriatric patients than younger adults.

Select dosage with caution because of age-related decreases in renal function. Dosage adjustment recommended in geriatric patients >75 years of age. May be useful to monitor renal function.

Hepatic Impairment

Monitor closely. Reduced dosage may be necessary; use lowest effective dosage. (See Hepatic Impairment under Dosage and Administration.)

Renal Impairment

Use not recommended in patients with advanced renal disease; close monitoring of renal function advised if used.

Reduced maximum dosage recommended. (See Renal Impairment under Dosage and Administration.)

Common Adverse Effects

Dyspepsia, nausea, abdominal pain, diarrhea, constipation, flatulence, anorexia, vomiting, stomatitis, headache, dizziness, CNS depression, CNS excitation, tinnitus, visual disturbances, rash, renal impairment.

Drug Interactions

Protein-bound Drugs

Potential for ketoprofen to be displaced from binding sites by, or to displace from binding sites, other protein-bound drugs. Observe for adverse effects.

Specific Drugs




ACE inhibitors

Reduced BP response to the ACE inhibitor

Monitor BP

Angiotensin II receptor antagonists

Reduced BP response to the angiotensin II receptor antagonist

Monitor BP

Antacids (magnesium- or aluminum-containing)

Conventional capsules: Pharmacokinetic interaction unlikely

Anticoagulants (warfarin)

Possible bleeding complications

Increased PT reported

Caution advised


Decreased ketoprofen protein binding

Increased risk of GI ulceration or other complications

No consistent evidence that low-dose aspirin mitigates the increased risk of serious cardiovascular events associated with NSAIAs

Concomitant use not recommended

Clinical importance of pharmacokinetic changes unknown


Pharmacokinetic interaction unlikely

Diuretics (furosemide, thiazides)

Reduced natriuretic effects

Monitor for diuretic efficacy and renal failure


Increased plasma lithium concentrations

Monitor for lithium toxicity


Possible increased and prolonged blood concentrations of methotrexate

Use with caution


Possible increased risk of pemetrexed-associated myelosuppression, renal toxicity, and GI toxicity

Short half-life NSAIAs (e. g., diclofenac, indomethacin): Avoid administration beginning 2 days before and continuing through 2 days after pemetrexed administration

Longer half-life NSAIAs (e.g., meloxicam, nabumetone): In the absence of data, avoid administration beginning at least 5 days before and continuing through 2 days after pemetrexed administration

Patients with Clcr 45–79 mL/minute: Monitor for myelosuppression, renal toxicity, and GI toxicity


Decreased clearance of ketoprofen and/or its conjugates

Concomitant use not recommended


Possible altered elimination of ketoprofen; no change in the pharmacokinetics of salicylate

Clinical importance unknown

Thrombolytic agents (streptokinase)

Possible bleeding complications

Use with caution

Ketoprofen Pharmacokinetics



Well absorbed following oral administration; bioavailability is about 90%. Peak plasma concentration usually attained within 0.5–2 hours (conventional capsules) or 6–7 hours (extended-release capsules).


Food delays time to peak plasma concentration by <1 hour or about 2 hours following administration as conventional capsules or extended-release capsules, respectively.



Distributed into synovial fluid and the CNS.

Not known whether ketoprofen is distributed into human milk.

Plasma Protein Binding

>99% (mainly albumin).



Rapidly and extensively metabolized in the liver; active metabolites not identified.

Elimination Route

Excreted principally in urine.


Conventional capsules: 2–4 hours.

Extended-release capsules: 5.4 hours.

Special Populations

Renal Impairment: Half-life (when given as conventional capsules) prolonged to about 3 hours in patients with mild renal impairment and to about 5–9 hours in patients with moderate to severe renal impairment.




Conventional and Extended-release Capsules

Tight , light resistant containers at 25°C ; protect from direct light and excessive heat and humidity.


Advice to Patients


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name



Dosage Forms


Brand Names




25 mg*

Ketoprofen Capsules

50 mg*

Ketoprofen Capsules

75 mg*

Ketoprofen Capsules

Capsules, extended-release

200 mg*

Ketoprofen Extended-release Capsules

AHFS DI Essentials™. © Copyright 2024, Selected Revisions November 29, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Off-label: Use is not currently included in the labeling approved by the US Food and Drug Administration.

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