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Pharmacology · Nonsteroidal anti-inflammatory drugs (NSAIDs)

Ibuprofen !

A widely used NSAID for pain, fever and inflammation. It reversibly blocks both cyclooxygenases.

Updated 2026-11-01

The figure shows ibuprofen in the channel of mouse COX-2, which keeps the same site as the human enzyme.

Target in 3D: Cyclooxygenase 1 and 2 (COX-1/COX-2). PDB structure 4PH9 (RCSB PDB, public domain). View the structure at RCSB PDB

Mechanism of action

Ibuprofen, a propionic acid derivative, reversibly occupies the channel of COX-1 and COX-2 and keeps arachidonic acid from reaching the catalytic site. Prostaglandins that sensitize nociceptors, raise the thermal set point and sustain inflammation fall. Because it lets go of the enzyme, its antiplatelet effect is mild and short-lived.

  1. Reversibly occupies the COX-1 and COX-2 channel
  2. Arachidonic acid is not converted to prostaglandin H2
  3. Less PGE2: calmer nociceptors and a lower thermal set point
  4. Relief of pain, fever and inflammation

Pharmacokinetics

Absorption
Well absorbed by mouth.
Distribution
Almost completely bound to albumin.
Metabolism
Liver, mainly CYP2C9, to inactive metabolites.
Elimination
Kidney, as metabolites.
Half-life
About 2 hours; longer in liver disease.

Indications

Adverse effects

Common

  • Dyspepsia, nausea and abdominal pain
  • Fluid retention and edema
  • Raised blood pressure

Contraindications

  • The period right before or after coronary artery bypass surgery
  • Active peptic ulcer or gastrointestinal bleeding
  • Severe kidney failure or severe heart failure
  • Pregnancy from week 20 onward, unless specialist-directed
  • Asthma or urticaria triggered by NSAIDs

Key interactions

Aspirin
Can block its antiplatelet effect if it occupies COX-1 first.
ACE inhibitors or ARBs with diuretics
Higher risk of acute kidney injury and a weaker antihypertensive effect.
Anticoagulants and SSRIs
More risk of gastrointestinal bleeding.
Lithium and methotrexate
Reduced renal clearance and risk of toxicity.

What is monitored

  • Blood pressure and kidney function with prolonged use
  • Signs of gastrointestinal bleeding

Test yourself

Think of the answer, then tap the question to see it.

How does COX inhibition by ibuprofen differ from that by aspirin?

Ibuprofen binds reversibly and competitively, so its effect lasts only while the drug stays in the site; aspirin acetylates the enzyme irreversibly.

Why do NSAIDs such as ibuprofen relieve primary dysmenorrhea?

The pain comes mainly from excess endometrial prostaglandins, which drive strong uterine contractions and ischemia; lowering them reduces contractions and pain.

Which drug combination with ibuprofen raises the risk of acute kidney injury?

An ACE inhibitor or ARB plus a diuretic. The NSAID constricts the afferent arteriole, the ACE inhibitor or ARB dilates the efferent one and the diuretic lowers volume: filtration falls.

Why is ibuprofen contraindicated from week 20 of pregnancy?

Fetal prostaglandins support fetal kidney function and keep the ductus arteriosus open; inhibiting them can cause oligohydramnios and premature ductal closure.

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Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: Ibuprofen: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2023); Ibuprofen, (+-)- (PubChem (NCBI), 2026); eEML - Electronic Essential Medicines List (World Health Organization, 2025); ATCDDD - ATC/DDD Index (WHO Collaborating Centre for Drug Statistics Methodology, 2026).

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Representative model, for educational purposes only.