Class: Other Nonsteroidal Anti-inflammatory Agents
VA Class: MS120
Molecular Formula: C30H26CaO6•2H2O
CAS Number: 53746-45-5
- Cardiovascular Risk
Increased risk of serious (sometimes fatal) cardiovascular thrombotic events (e.g., MI, stroke).137 500 502 508 b Risk may occur early in treatment and may increase with duration of use.500 502 505 506 508 (See Cardiovascular Thrombotic Effects under Cautions.)
Contraindicated in the setting of CABG surgery.508
- GI Risk
Increased risk of serious (sometimes fatal) GI events (e.g., bleeding, ulceration, perforation of the stomach or intestine).137 b Serious GI events can occur at any time and may not be preceded by warning signs and symptoms.137 b Geriatric individuals are at greater risk for serious GI events.100 137 b (See GI Effects under Cautions.)
Prototypical NSAIA;100 b propionic acid derivative;b structurally and pharmacologically related to flurbiprofen, ibuprofen, ketoprofen, and naproxen.b d
Uses for Fenoprofen Calcium
Consider potential benefits and risks of fenoprofen therapy as well as alternative therapies before initiating therapy with the drug.100 137 b Use lowest possible effective dosage and shortest duration of therapy consistent with patient’s treatment goals.100 137 b
Relief of mild to moderate pain in adults.100 b
Symptomatic treatment of osteoarthritis and rheumatoid arthritis.100 b d
Has been used in the symptomatic treatment of juvenile rheumatoid arthritis†.b c
Fenoprofen Calcium Dosage and Administration
Consider potential benefits and risks of fenoprofen therapy as well as alternative therapies before initiating therapy with the drug.100 137 b
Administer orally.100 b
Administration with meals, milk, or antacids may minimize adverse GI effects.100 b d
Available as fenoprofen calcium; dosage expressed in terms of fenoprofen.100 b
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.100 137 b Adjust dosage based on individual requirements and response; attempt to titrate to the lowest effective dosage.100 137 b
For mild to moderate pain, 200 mg every 4–6 hours as needed.100 b
Osteoarthritis or Rheumatoid ArthritisOral
Initially, 400–600 mg 3 or 4 times daily.146 508 Adjust dose and frequency as necessary based on severity of symptoms and clinical response (maximum 3.2 g daily).100 b
Patients with rheumatoid arthritis may require higher dosages than those with osteoarthritis.100 b
Symptomatic improvement usually begins in a few days, but an additional 2–3 weeks may be needed to determine response.100 b
Osteoarthritis or Rheumatoid ArthritisOral
Maximum 3.2 g daily.100 b
No dosage adjustments recommended.100
Use not recommended in patients with advanced renal disease.100
No dosage adjustments recommended.
Cautions for Fenoprofen Calcium
Known hypersensitivity to fenoprofen or any ingredient in the formulation.100 d
History of asthma, urticaria, or other sensitivity reaction precipitated by aspirin or other NSAIAs.100 137 d
In the setting of CABG surgery.508
History of significant renal impairment.100
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.500 502 508
Findings of FDA review of observational studies, meta-analysis of randomized controlled trials, and other published information500 501 502 indicate that NSAIAs may increase the risk of such events by 10–50% or more, depending on the drugs and dosages studied.500
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.500 502 506 508
Increased risk may occur early (within the first weeks) following initiation of therapy and may increase with higher dosages and longer durations of use.500 502 505 506 508
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.508
In patients receiving NSAIAs following MI, increased risk of reinfarction and death observed beginning in the first week of treatment.505 508
Increased 1-year mortality rate observed in patients receiving NSAIAs following MI;500 508 511 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.508 511
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.141 142 143 145 500 501 502 503 506 FDA states that limitations of these studies and indirect comparisons preclude definitive conclusions regarding relative risks of NSAIAs.500
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.100 137 500 508
Some clinicians suggest that it may be prudent to avoid NSAIA use, whenever possible, in patients with cardiovascular disease.505 511 512 516 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.508 Contraindicated in the setting of CABG surgery.508
No consistent evidence that concomitant use of low-dose aspirin mitigates the increased risk of serious adverse cardiovascular events associated with NSAIAs.100 137 138 502 508 (See Specific Drugs under Interactions.)
Serious GI toxicity (e.g., bleeding, ulceration, perforation) can occur with or without warning symptoms;100 104 105 108 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.100 124 127 134
For patients at high risk for complications from NSAIA-induced GI ulceration (e.g., bleeding, perforation), consider concomitant use of misoprostol;107 124 125 126 alternatively, consider concomitant use of a proton-pump inhibitor (e.g., omeprazole)107 124 125 or use of an NSAIA that is a selective inhibitor of COX-2 (e.g., celecoxib).125
Hypertension and worsening of preexisting hypertension reported; either event may contribute to the increased incidence of cardiovascular events.100 137 Use with caution in patients with hypertension; monitor BP.100 137
Impaired response to ACE inhibitors, angiotensin II receptor antagonists, β-blockers, and certain diuretics may occur.100 137 508 (See Specific Drugs under Interactions.)
Heart Failure and Edema
Fluid retention and edema reported.100 137 508
NSAIAs (selective COX-2 inhibitors, prototypical NSAIAs) may increase morbidity and mortality in patients with heart failure.500 501 504 507 508
NSAIAs may diminish cardiovascular effects of diuretics, ACE inhibitors, or angiotensin II receptor antagonists used to treat heart failure or edema.508 (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.508
Some experts recommend avoiding use, whenever possible, in patients with reduced left ventricular ejection fraction and current or prior symptoms of heart failure.507
Direct renal injury, including renal papillary necrosis, reported in patients receiving long-term NSAIA therapy.100 137
Potential for overt renal decompensation.100 137 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.100 137 140 (See Renal Impairment under Cautions.)
Anaphylactoid reactions reported.100 137
Immediate medical intervention and discontinuance for anaphylaxis.100 137
Avoid in patients with aspirin triad (aspirin sensitivity, asthma, nasal polyps); caution in patients with asthma.100 137 d
Serious skin reactions (e.g., exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis) reported; can occur without warning.100 137 Discontinue at first appearance of rash or any other signs of hypersensitivity (e.g., blisters, fever, pruritus).100 137
Severe reactions including jaundice, fatal fulminant hepatitis, liver necrosis, and hepatic failure (sometimes fatal) reported rarely with NSAIAs.100
Elevations of serum ALT or AST reported.100
Monitor for symptoms and/or signs suggesting liver dysfunction; monitor abnormal liver function test results.100 Discontinue if signs or symptoms of liver disease or systemic manifestations (e.g., eosinophilia, rash) occur.100
Anemia reported rarely.100 137 Determine hemoglobin concentration or hematocrit in patients receiving long-term therapy if signs or symptoms of anemia occur.100 137 d
May inhibit platelet aggregation and prolong bleeding time.100 137 d
Drowsiness and dizziness reported; may impair ability to perform activities requiring mental alertness.100 b
Adverse ocular effects reported in patients receiving NSAIA therapy; ophthalmologic evaluation recommended if visual disturbances occur.100 b
Safety not established in patients with hearing impairment; auditory function tests should be performed periodically in these patients during prolonged therapy.100 b
Not a substitute for corticosteroid therapy; not effective in the management of adrenal insufficiency.100
May mask certain signs of infection.b
Obtain CBC and chemistry profile periodically during long-term use.100
Category C.100 Avoid use in third trimester because of possible premature closure of the ductus arteriosus.100
Fenoprofen is distributed into milk.b d Discontinue nursing or the drug.100 b
Safety and efficacy not established in children <18 years of age.100
Use with caution in patients ≥65 years of age.100 Geriatric patients appear to tolerate therapy less well (e.g., possible higher incidence of adverse GI effects, greater risk of developing renal decompensation) than younger individuals.100 b Fatal adverse GI effects reported more frequently in geriatric patients than younger adults.100 b
Has not been evaluated in patients with severe renal impairment.100 b Use not recommended in patients with advanced renal disease.100 b
Common Adverse Effects
Dyspepsia,100 d nausea,100 d constipation,100 d headache,100 somnolence,100 dizziness,100 nervousness,100 asthenia,100 peripheral edema.100
Interactions for Fenoprofen Calcium
Possible pharmacokinetic interaction; potential for fenoprofen to be displaced from binding sites by, or to displace from binding sites, other protein-bound drugs (e.g., oral anticoagulants, hydantoins, salicylates, sulfonamides, and sulfonylureas).100 b d Observe for adverse effects if used with other protein-bound drugs.100 b
Reduced BP response to ACE inhibitor possible 100 137 144
Possible deterioration of renal function in individuals with renal impairment144
Monitor BP100 144 b
Angiotensin II receptor antagonists
Reduced BP response to angiotensin II receptor antagonist possible144
Possible deterioration of renal function in individuals with renal impairment144
Monitor BP144 b
Antacids (aluminum- and magnesium-containing)
Did not affect fenoprofen absorption in one study; other antacids not evaluated for possible interactionsa b d
Anticoagulants (e.g., warfarin)
Possible bleeding complications100 137 144
Caution and careful monitoring advised100 144 b
Increased risk of GI ulceration or other complications 100 137
Possible decreased plasma concentrations and half-life of fenoprofen100 b d
No consistent evidence that low-dose aspirin mitigates the increased risk of serious cardiovascular events associated with NSAIAs 100 138 502 508
Concomitant use generally not recommended100 d
Diuretics (furosemide and thiazides)
Reduced natriuretic effects100 137
Monitor for diuretic efficacy and renal failure100 137
Increased plasma lithium concentrations100 137
Monitor for lithium toxicity 100 137
Possible toxicity associated with increased plasma methotrexate concentrations during concomitant NSAIA use100 b
Caution advised100 b
Possible decreased plasma concentrations and plasma half-life of fenoprofen100 b d
Dosage adjustment may be necessary when phenobarbital is initiated or discontinued100 b d
Fenoprofen Calcium Pharmacokinetics
Rapidly and almost completely absorbed following oral administration.100 b d Peak plasma concentrations usually attained within 2 hours.100 b
Onset of analgesic activity reportedly occurs within 15–30 minutes following oral administration.b
Duration of analgesic activity: 4–6 hours.b
Food delays and diminishes peak plasma fenoprofen concentrations.100 a b d
Distributed into milk;b d does not appear to cross the placenta.b d
Plasma Protein Binding
Approximately 99% (mainly to albumin).100 b d
Extensively metabolized in the liver.b d Fenoprofen’s major metabolite, 4′-hydroxyfenoprofen, probably is inactive.b
Eliminated principally in urine as unchanged drug (2–5%), 4′-hydroxyfenoprofen (2–5%), their glucuronide or other conjugates (90%), and unidentified conjugates (2–5%).100 b d
2.5–3 hours.100 b d
Not substantially removed by hemodialysis or peritoneal dialysis.100
Capsules and Tablets
Tight containers at 20–25°C.100
Inhibits cyclooxygenase-1 (COX-1) and COX-2.118 119 120 121 122 123 b
Pharmacologic actions similar to those of other prototypical NSAIAs; exhibits anti-inflammatory, analgesic, and antipyretic activity.100 118 119 120 121 122 123 b d
Advice to Patients
Importance of reading the medication guide for NSAIAs that is provided each time the drug is dispensed.100 137
Risk of serious cardiovascular events (e.g., MI, stroke).100 500 508 b Importance of seeking immediate medical attention if signs and symptoms of a cardiovascular event (chest pain, dyspnea, weakness, slurred speech) occur.100 500 508 b
Risk of GI bleeding and ulceration.100 111 115 b Importance of notifying a clinician if signs and symptoms of serious adverse GI effects occur.100 b
Risk of serious skin reactions.100 b Importance of discontinuing fenoprofen calcium and contacting clinician if rash or other signs of hypersensitivity (blisters, fever, pruritus) develop.100 b
Risk of anaphylactoid and other sensitivity reactions.100 b Importance of seeking immediate medical attention if an anaphylactic reaction occurs.100 b
Risk of hepatotoxicity.100 b Importance of discontinuing therapy and contacting a clinician immediately if signs and symptoms of hepatotoxicity (nausea, fatigue, lethargy, pruritus, jaundice, upper right quadrant tenderness, flu-like symptoms) occur.100 b
Risk of heart failure or edema; importance of reporting dyspnea, unexplained weight gain, or edema.100 508
Risk of dizziness and potential for drug to impair mental alertness; use caution when driving or operating machinery until effects on individual are known.100 b
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.100 Importance of avoiding fenoprofen in late pregnancy (third trimester).100 b
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant diseases.100
Importance of informing patients of other important precautionary information.100 (See Cautions.)
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
200 mg (of fenoprofen)
400 mg (of fenoprofen)
600 mg (of fenoprofen)*
Fenoprofen Calcium Tablets
AHFS DI Essentials. © Copyright 2018, Selected Revisions March 6, 2017. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.
100. Pedinol Pharmacal Inc. Nalfon (fenoprofen calcium) capsules prescribing information. Farmingdale, NY; 2006 Jan.
101. Gurney JR, Mills RJ. Assessment of thyroid function: complications after treatment with fenoprofen. BMJ. 1986; 292:1560. [PubMed 3087516]
102. Tillman J, Leask JTS, Logue FC et al. Assessment of thyroid function: complications after treatment with fenoprofen. BMJ. 1986; 293:206. [PubMed 3089454]
103. Thornes HM, Carr D. Fenoprofen and free triiodothyronine measurement. Lancet. 1986; 2:101. [PubMed 2873356]
104. Palmer JF. Letter sent to Talbott MW of Eli Lilly and Company regarding labeling revisions about gastrointestinal adverse reactions to Nalfon (fenoprofen). Rockville, MD: Food and Drug Administration, Division of Oncology and Radiopharmaceutical Drug Products; 1988 Sep.
105. Food and Drug Administration. Labeling revisions for NSAIDs. FDA Drug Bull. 1989; 19:3-4.
106. Searle. Cytotec (misoprostol) prescribing information. 1989 Jan.
107. Anon. Drug for rheumatoid arthritis. Med Lett Drugs Ther. 2000; 42:57-64. [PubMed 10887424]
108. Soll AH, Weinstein WM, Kurata J et al. Nonsteroidal anti-inflammatory drugs and peptic ulcer disease. Ann Intern Med. 1991; 114:307-19. [PubMed 1987878]
109. Kolodzik JM, Eilers MA, Angelos MG. Nonsteroidal anti-inflammatory drugs and coma: a case report of fenoprofen overdose. Ann Emerg Med. 1990; 19:378-81. [PubMed 2321822]
110. Corticosteroid interactions: nonsteroidal anti-inflammatory drugs (NSAIDs). In: Hansten PD, Horn JR. Drug interactions and updates. Vancouver, WA: Applied Therapeutics, Inc; 1993:562.
111. Garcia Rodriguez LA, Jick H. Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs. Lancet. 1994; 343:769-72. [PubMed 7907735]
112. Hollander D. Gastrointestinal complications of nonsteroidal anti-inflammatory drugs: prophylactic and therapeutic strategies. Am J Med. 1994; 96:274-81. [PubMed 8154516]
113. Schubert TT, Bologna SD, Yawer N et al. Ulcer risk factors: interaction between Helicobacter pylori infection, nonsteroidal use, and age. Am J Med. 1993; 94:413-7. [PubMed 8475935]
114. Piper JM, Ray WA, Daugherty JR et al. Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs. Ann Intern Med. 1991; 114:735-40. [PubMed 2012355]
115. Bateman DN, Kennedy JG. Non-steroidal anti-inflammatory drugs and elderly patients: the medicine may be worse than the disease. BMJ. 1995; 310:817-8. [PubMed 7711609]
116. Ciba Geigy, Ardsley, NY: Personal communication on diclofenac 28:08.04.
117. Reviewers’ comments (personal observation) on diclofenac 28:08.04.
118. Hawkey CJ. COX-2 inhibitors. Lancet. 1999; 353:307-14. [PubMed 9929039]
119. Kurumbail RG, Stevens AM, Gierse JK et al. Structural basis for selective inhibition of cyclooxygenase-2 by anti-inflammatory agents. Nature. 1996; 384:644-8. [PubMed 8967954]
120. Riendeau D, Charleson S, Cromlish W et al. Comparison of the cyclooxygenase-1 inhibitory properties of nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors, using sensitive microsomal and platelet assays. Can J Physiol Pharmacol. 1997; 75:1088-95. [PubMed 9365818]
121. DeWitt DL, Bhattacharyya D, Lecomte M et al. The differential susceptibility of prostaglandin endoperoxide H synthases-1 and -2 to nonsteroidal anti-inflammatory drugs; aspirin derivatives as selective inhibtors. Med Chem Res. 1995; 5:325-43.
122. Cryer B, Dubois A. The advent of highly selective inhibitors of cyclooxygenase—a review. Prostaglandins Other Lipid Mediators. 1998; 56:341-61. [PubMed 9990677]
123. Simon LS. Role and regulation of cyclooxygenase-2 during inflammation. Am J Med. 1999; 106(Suppl 5B):37-42S.
124. Wolfe MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. 1999; 340:1888-99. [PubMed 10369853]
125. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines.. Guidelines for the management of rheumatoid arthritis: 2002 update. Arthritis Rheum. 2002; 46:328-46. [PubMed 11840435]
126. Lanza FL and the members of the Ad Hoc Committee on Practice Parameters of the American College of Gastroenterology. A guideline for the treatment and prevention of NSAID-induced ulcers. Am J Gastroenterol. 1998; 93:2037-46. [PubMed 9820370]
127. Singh G, Triadafilopoulos G. Epidemiology of NSAID induced gastrointestinal complications. J Rheumatol. 1999; 26(suppl 56):18-24.
128. in’t Veld BA, Ruitenberg A, Hofman A et al. Nonsteroidal antiinflammatory drugs and the risk of Alzheimer’s disease. N Engl J Med. 2001; 345:1515-21. [PubMed 11794217]
129. Breitner JCS, Zandi PP. Do nonsteroidal antiinflammatory drugs reduce the risk of Alzheimer’s disease? N Engl J Med. 2001; 345:1567-8. Editorial.
130. McGeer PL, Schulzer M, McGeer EG. Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer’s disease: a review of 17 epidemiologic studies. Neurology. 1996; 47:425-32. [PubMed 8757015]
131. Beard CM, Waring SC, O’sBrien PC et al. Nonsteroidal anti-inflammatory drug use and Alzheimer’s disease : a case-control study in Rochester, Minnesota, 1980 through 1984. Mayo Clin Proc. 1998; 73:951-5. [PubMed 9787743]
132. in’t Veld BA, Launer LJ, Hoes AW et al. NSAIDs and incident Alzheimer’s disease: the Rotterdam Study. Neurobiol Aging. 1998; 19:607-11. [PubMed 10192221]
133. Stewart WF, Kawas C, Corrada M et al. Risk of Alzheimer’s disease and duration of NSAID use. Neurology. 1997; 48:626-32. [PubMed 9065537]
134. Pharmacia. Daypro (oxaprozin) caplets prescribing information. Chicago, IL; 2002 May.
135. Chan FKL, Hung LCT, Suen BY et al. Celecoxib versus diclofenac and omeprazole in reducing the risk of recurrent ulcer bleeding in patients with arthritis. N Engl J Med. 2002; 347:2104-10. [PubMed 12501222]
136. Graham DY. NSAIDs, Helicobacter pylori, and Pandora’s box. N Engl J Med. 2002; 347:2162-4. [PubMed 12501230]
137. US Food and Drug Administration. Proposed NSAID Package Insert Labeling Template 1. From the FDA website (). Accessed 10 Oct 2005.
138. Food and Drug Administration. Analysis and recommendations for agency action regarding non-steroidal anti-inflammatory drugs and cardiovascular risk. 2005 Apr 6.
139. Cush JJ. The safety of COX-2 inhibitors: deliberations from the February 16-18, 2005, FDA meeting. From the American College of Rheumatology website (). Accessed 2005 Oct 12.
140. Novartis Pharmaceuticals. Diovan (valsartan) capsules prescribing information (dated 1997 Apr). In: Physicians’ desk reference. 53rd ed. Montvale, NJ: Medical Economics Company Inc; 1999:2013-5.
141. McGettigan P, Henry D. Cardiovascular risk and inhibition of cyclooxygenase: a systematic review of observational studies of selective and nonselective inhibitors of cyclooxygenase 2. JAMA. 2006; 296: 1633-44. [PubMed 16968831]
142. Kearney PM, Baigent C, Godwin J et al. Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials. BMJ. 2006; 332: 1302-5. [PubMed 16740558]
143. Graham DJ. COX-2 inhibitors, other NSAIDs, and cardiovascular risk; the seduction of common sense. JAMA. 2006; 296:1653-6. [PubMed 16968830]
144. Merck & Co. Clinoril (sulindac) tablets prescribing information. Whitehouse Station, NJ; 2006 Feb.
145. Chou R, Helfand M, Peterson K et al. Comparative effectiveness and safety of analgesics for osteoarthritis. Comparative effectiveness review no. 4. (Prepared by the Oregon evidence-based practice center under contract no. 290-02-0024.) . Rockville, MD: Agency for Healthcare Research and Quality. 2006 Sep. Available at: .
146. Mylan Pharmaceuticals Inc. Fenoprofen calcium tablets prescribing information. Morgantown, WV; 2015 Jul.
500. Food and Drug Administration. Drug safety communication: FDA strengthens warning that non-aspirin nonsteroidal anti-inflammatory drugs (NSAIDs) can cause heart attacks or strokes. Silver Spring, MD; 2015 Jul 9. From the FDA web site. Accessed 2016 Mar 22.
501. Coxib and traditional NSAID Trialists' (CNT) Collaboration, Bhala N, Emberson J et al. Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials. Lancet. 2013; 382:769-79. [PubMed 23726390]
502. Food and Drug Administration. FDA briefing document: Joint meeting of the arthritis advisory committee and the drug safety and risk management advisory committee, February 10-11, 2014. From FDA web site
503. Trelle S, Reichenbach S, Wandel S et al. Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis. BMJ. 2011; 342:c7086. [PubMed 21224324]
504. Gislason GH, Rasmussen JN, Abildstrom SZ et al. Increased mortality and cardiovascular morbidity associated with use of nonsteroidal anti-inflammatory drugs in chronic heart failure. Arch Intern Med. 2009; 169:141-9. [PubMed 19171810]
505. Schjerning Olsen AM, Fosbøl EL, Lindhardsen J et al. Duration of treatment with nonsteroidal anti-inflammatory drugs and impact on risk of death and recurrent myocardial infarction in patients with prior myocardial infarction: a nationwide cohort study. Circulation. 2011; 123:2226-35. [PubMed 21555710]
506. McGettigan P, Henry D. Cardiovascular risk with non-steroidal anti-inflammatory drugs: systematic review of population-based controlled observational studies. PLoS Med. 2011; 8:e1001098. [PubMed 21980265]
507. Yancy CW, Jessup M, Bozkurt B et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013; 62:e147-239. [PubMed 23747642]
508. Xspire Pharma, LLC. Nalfon (fenoprofen calcium) capsules prescribing information. Ridgeland, MS; 2016 Apr.
511. Olsen AM, Fosbøl EL, Lindhardsen J et al. Long-term cardiovascular risk of nonsteroidal anti-inflammatory drug use according to time passed after first-time myocardial infarction: a nationwide cohort study. Circulation. 2012; 126:1955-63. [PubMed 22965337]
512. Olsen AM, Fosbøl EL, Lindhardsen J et al. Cause-specific cardiovascular risk associated with nonsteroidal anti-inflammatory drugs among myocardial infarction patients--a nationwide study. PLoS One. 2013; 8:e54309.
516. Bavry AA, Khaliq A, Gong Y et al. Harmful effects of NSAIDs among patients with hypertension and coronary artery disease. Am J Med. 2011; 124:614-20. [PubMed 21596367]
a. Chernish SM, Rubin A, Rodda BE et al. The physiological disposition of fenoprofen in man. IV. The effects of position of subject, food ingestion and antacid ingestion on the plasma levels of orally administered fenoprofen. J Med. 1972; 3: 249-57. [PubMed 4508566]
b. AHFS drug information 2007. McEvoy GK, ed. Fenoprofen. Bethesda, MD: American Society of Health-System Pharmacists; 2007:2054-2058.
c. Brewer EJ, Giannini EH, Baum J et al. Aspirin and fenoprofen (Nalfon) in the treatment of juvenile rheumatoid arthritis results of the double blind-trial: a segment II study. J Rheumatol. 1982; 9: 123-8.
d. Brogden RN, Pinder RM, Speight TM et al. Fenoprofen: a review of its pharmacological properties and therapeutic efficacy in rheumatic diseases. Drugs. 1977; 13: 241-65.
More about fenoprofen
- Side Effects
- During Pregnancy or Breastfeeding
- Dosage Information
- Drug Images
- Drug Interactions
- Support Group
- Pricing & Coupons
- En Español
- 2 Reviews – Add your own review/rating
- Drug class: Nonsteroidal anti-inflammatory drugs