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Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) used to control pain, fever, and inflammation.

Other members of drugs in the NSAID family include aspirin, naproxen (Aleve), indomethacin (Indocin), and nabumetone (Relafen).

3D Model of the molecule of Ibuprofen.
Source: Wikimedia Commons.[1]


Other Names

Ibuprofen is branded under several tradenames including Advil and Motrin.


Ibuprofen is most commonly used to manage mild to moderate pain, fever and inflammation that accompany the following conditions:

How Ibuprofen is Taken

Ibuprofen is available over-the-counter (OTC) in 200-mg and 400-mg doses. The recommended dose varies with body mass and indication. Typically, the oral dose is 200–400 mg (5–10 mg/kg in children) taken every 4–6 hours; 1200 mg is considered the maximum daily dose for OTC use. However, under medical direction, a maximum daily dose of 3200 mg may be used if it is taken in separated doses of 600–800 mg.

Ibuprofen is also available in topical form, which is absorbed through the skin. This topical form is typically indicated for sports injuries.

How Ibuprofen Works

Ibuprofen works through the inhibition of an enzyme called cyclooxygenase (COX). By inhibiting COX, ibuprofen inhibits prostaglandin synthesis. Among other things, prostaglandins regulate the inflammatory response, sensitize spinal neurons to pain, and induce fever.

COX has two known variants: COX-1 and COX-2. To varying degrees, Ibuprofen inhibits both COX-1 and COX-2. Ibuprofen's pain-relieving (analgesic), fever-reducing (antipyretic), and anti-inflammatory activities are likely achieved primarily through inhibition of the COX-2 variant. On the other hand, ibuprofen's inhibition of the COX-1 variant results in its undesirable side effects on blood platelets and the GI tract.

How The Body Affects Ibuprofen

Ibuprofen is rapidly absorbed. Peak levels generally appear within 1.5 to 2 hours. Both the rate of absorption and peak plasma concentrations are reduced when the drug is taken with food.

Ibuprofen has a half-life of approximately 2 hours. It is rapidly metabolized and excreted within 24 hours. Clinical studies indicate a duration of clinical effect for up to 8 hours for fever, and 6+ hours for pain.

Side Effects

The most common side effects of ibuprofen include the following:

Infrequent adverse effects include:

Risks and Precautions

Heart attack and stroke

Clinical trials of NSAIDs have shown an increased risk of heart attack and stroke. Patients with known heart disease or risk factors for heart disease may be at greater risk. To minimize the risk of heart attack or stroke in patients treated with an NSAID, the lowest effective dose should be used for the shortest duration possible.

High blood pressure (hypertension)

NSAIDs like ibuprofen can lead to onset of new high blood pressure or worsening of pre-existing high blood pressure. NSAIDs, including ibuprofen, should be used with caution in patients with high blood pressure. Blood pressure should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

Congestive heart failure and edema

Fluid retention and edema have been observed in some patients taking NSAIDs like ibuprofen.

Gastrointestinal effects

NSAIDs, including ibuprofen, can cause serious gastrointestinal (GI) events including inflammation, bleeding, ulceration, and perforation of the stomach, small intestine, or large intestine, which can be fatal. Most of these serious adverse events are rare, but they can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. Only one in five patients, who develop a serious upper GI adverse event on NSAID therapy, is symptomatic.

NSAIDs are prescribed with extreme caution in those with a prior history of ulcer disease or gastrointestinal bleeding. Patients with a prior history of peptic ulcer disease and/or gastrointestinal bleeding who use NSAIDs have a greater than 10-fold increased risk of developing a GI bleed compared to patients with neither of these risk factors. Other factors that increase the risk of GI bleeding in patients treated with NSAIDs include concomitant use of oral corticosteroids or anticoagulants, longer duration of NSAID therapy, smoking, use of alcohol, older age, and poor general health status. Most spontaneous reports of fatal GI events are in elderly or debilitated people and therefore, special care is taken in treating them.

To minimize the potential risk for an adverse GI event in patients treated with an NSAID, the lowest effective dose needs to be used for the shortest possible duration.

Kidney (renal) effects

Long-term administration of NSAIDs has resulted in injury to the kidneys. Patients at greatest risk are those with impaired kidney function, heart failure, liver dysfunction, those taking diuretics and ACE inhibitors, and the elderly. Discontinuation of NSAID therapy is usually followed by recovery to the pretreatment state.

Allergic reactions

As with other NSAIDs, allergic reactions may occur in patients without known prior exposure to ibuprofen.

Skin reactions

NSAIDs, including ibuprofen, can cause serious skin reactions such as exfoliative dermatitis, Stevens-Johnson Syndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal. These serious events are rare but may occur without warning.


In late pregnancy, as with other NSAIDs, ibuprofen should be avoided because it may cause premature closure of the ductus arteriosus - an important structure in the fetal heart.

Drug Interactions


Reports suggest that NSAIDs may diminish the antihypertensive effect of ACE-inhibitors. This interaction should be given consideration in patients taking NSAIDs along with ACE-inhibitors.


Concurrent administration of ibuprofen and aspirin is not generally recommended because of the potential for increased adverse effects.


Clinical studies have shown that ibuprofen can reduce the effect of furosemide and thiazides in some people. This response has been attributed to inhibition of renal prostaglandin synthesis. During concurrent therapy with NSAIDs, a person needs to be observed closely for signs of kidney failure, as well as to make sure that the diuretic is working properly.


Ibuprofen produced an elevation of plasma lithium levels and a reduction in renal lithium clearance in a study of eleven volunteers. This effect has been attributed to inhibition of prostaglandin synthesis in the kidneys caused by ibuprofen. Thus, when ibuprofen and lithium are administered concurrently, people need to be observed carefully for signs of increased lithium levels and toxicity.[2]


NSAIDs like ibuprofen have been reported to competitively inhibit methotrexate accumulation in studies done on rabbit kidneys. This may indicate that NSAIDs could enhance the toxicity of methotrexate. Caution should be used when NSAIDs are taken at the same time as methotrexate.

Coumarin-type anticoagulants

Because bleeding has been reported when ibuprofen and other NSAIDs have been given to patients on coumarin-type anticoagulants (like Coumadin), physicians are usually cautious when administering ibuprofen to patients on anticoagulants. The effects of coumarin and NSAIDs on GI bleeding are additive, such that the users of both drugs together have a risk of serious GI bleeding higher than users of either drug alone.

History and Development

Ibuprofen was discovered by Stewart Adams, John Nicholson, and Colin Burrows. The drug was patented in 1961 and was further developed by the research arm of Boots Group. The drug was approved as a treatment for rheumatoid arthritis in the U.K. in 1969, and in the U.S. in 1974.


Ibuprofen is well-established as a treatment for many specific types of pain. Published studies have demonstrated the utility of this drug in headaches[3], migraine headaches [4], backaches [5], and toothaches [6]. It is also established in treating muscular pain and soft tissue injury [7] and menstrual cramps.[8][9][10][11]

Ibuprofen is useful in the treatment of sore throat[12][13], the common cold [14], and fever.[15][16]

Epidemiological evidence suggests that ibuprofen may also act to reduce the risk or delay the onset of Alzheimer disease, suggesting a link between inflammation and neurodegenerative diseases.[17]


  1. http://commons.wikimedia.org/wiki/Image:Ibuprofen_3D_Model.png
  2. Ragheb M. The clinical significance of lithium-nonsteroidal anti-inflammatory drug interactions. J Clin Psychopharmacol. 1990 Oct;10(5):350-4. Abstract
  3. Noyelle RM et al. Ibuprofen, aspirin, and paracetamol compared in a community study. Pharm J 1987;238:561-4
  4. Pearce I et al. Ibuprofen, a prostaglandin synthetase inhibitor compared to paracetamol, a peripheral analgesic, on classical migraine. Practitioner 1983;227:465-7
  5. Hosie GAC. The topical NSAID, felbinac, versus oral ibuprofen; a comparison of efficacy in the treatment of acute lower back injury. Br J Clin Res 1993;4:5-17
  6. Jain AK, Ryan JR, McMahon FG, et al. Analgesic efficacy of low-dose ibuprofen in dental extraction pain. Pharmacotherapy 1986;6:318-22 Abstract
  7. Valtonen EJ, Busson M. A comparative study on ibuprofen (Brufen) and indomethacin in non-articular rheumatism. Scand J Rheumatol 1978;7:183-7
  8. Shapiro SS, Diem K. The effect of ibuprofen in the treatment of dysmenorrhoea. Curr Ther Res 1981;30:327-34 Abstract
  9. Morrison JC et al. Analgesic efficacy of ibuprofen for treatment of primary dysmenorrhoea. South Med J 1980;73:999-1002 Abstract
  10. Milsom I, Andersch B. Effect of ibuprofen, naproxen sodium and paracetamol on intrauterine pressure and menstrual pain in dysmenorrhoea. Br J Obstet Gynaecol 1984;91:1129-35 Abstract
  11. Gookin KS et al. Comparative efficacy of ibuprofen, indomethacin, and placebo in the treatment of primary dysmenorrhea. South Med J 1983;76:1361-2, 1367 [Abstract
  12. Boureau F et al. Evaluation of ibuprofen vs. paracetamol analgesic activity using a sore throat pain model. Clin Drug Invest 1999;17:1-8
  13. Schactel BP, Thoden WR. A placebo-controlled model for assaying systemic analgesics in children. Clin Pharmacol Ther 1993;53:593-601 Abstract
  14. Winther B. The therapeutic effectiveness of ibuprofen on the symptoms of naturally acquired common colds. Am J Rhinology 2001;15:239-42Abstract
  15. Czaykowski D et al. Evaluation of the antipyretic efficacy of single dose ibuprofen suspension compared to acetaminophen elixir in febrile children. Paediatric Research, April 1994;Vol 35 (4) Part2, Abstr.829
  16. Autret E, Breart G, Jonville AP,et al. Comparative efficacy and tolerance of ibuprofen syrup and acetaminophen syrup in children with pyrexia associated with infectious diseases and treated with antibiotics. Eur J Clin Pharmacol 1994;46(3):197-201. Abstract
  17. Dokmeci D. Ibuprofen and Alzheimer's disease. Folia Med (Plovdiv). 2004;46(2):5-10. [1]

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