ibuprofen

Brand: Advil, Motrin

⚠ BBW Beers Criteria Prototype Drug

Drug Class: nonsteroidal anti-inflammatory drug (NSAID)

Drug Family: NSAID

Subclass: non-selective COX inhibitor (propionic acid derivative)

Organ Systems: cnsmusculoskeletal

Mechanism of Action

Non-selective inhibitor of COX-1 and COX-2; blocks conversion of arachidonic acid to prostaglandins and thromboxane. Reduced prostaglandin synthesis accounts for analgesia, antipyresis, and anti-inflammatory effects. COX-1 inhibition contributes to GI toxicity and antiplatelet effect.

COX-1 (cyclooxygenase-1)COX-2 (cyclooxygenase-2)

Indications

pain (mild to moderate)
fever
inflammation
dysmenorrhea
osteoarthritis
rheumatoid arthritis

Contraindications

active peptic ulcer disease
severe renal impairment
aspirin sensitivity/asthma triad
perioperative pain after CABG
third trimester of pregnancy (premature closure of ductus arteriosus)

Adverse Effects

Common

GI upset
dyspepsia
nausea
heartburn
fluid retention

Serious

GI bleeding/ulceration
acute kidney injury
cardiovascular events (MI, stroke) with prolonged use
hypertension
acute liver injury (rare)
anaphylaxis in aspirin-sensitive patients

Pharmacokinetics (ADME)

Absorption	well absorbed orally; bioavailability ~80%; food delays but does not reduce absorption
Distribution	protein binding >99%; Vd ~0.14-0.2 L/kg
Metabolism	primarily CYP2C9; inactive hydroxylated metabolites
Excretion	renal (90%)
Half-life	2 hours
Onset	30-60 minutes
Peak	1-2 hours
Duration	4-6 hours
Protein Binding	>99%
Vd	0.14-0.2 L/kg

Drug Interactions

Drug / Agent	Mechanism	Severity
aspirin	ibuprofen may competitively block aspirin from binding COX-1 platelet site; take aspirin before ibuprofen if both needed	moderate
anticoagulants (warfarin, DOACs)	additive bleeding risk and GI ulceration	major
ACE inhibitors/ARBs	antagonize antihypertensive effect; AKI risk via reduced renal prostaglandin synthesis	major
lithium	reduce renal lithium clearance; increase lithium levels	major

Nursing Considerations

Administer with food or milk to reduce GI irritation; consider proton pump inhibitor in patients with GI risk factors.
Monitor renal function in patients with CKD, heart failure, cirrhosis, dehydration, or concurrent nephrotoxic agents; NSAIDs reduce renal prostaglandin-mediated afferent arteriolar dilation and can precipitate AKI.
Avoid in patients with aspirin-exacerbated respiratory disease (AERD/Samter triad: aspirin sensitivity + asthma + nasal polyps) due to cross-reactivity via COX-1 inhibition.
Third trimester pregnancy: NSAIDs cause premature closure of the ductus arteriosus and neonatal renal dysfunction; absolutely contraindicated.

Clinical Pearls

Ibuprofen is the NSAID prototype for pharmacology education; understanding its mechanism, GI toxicity (COX-1), and cardiovascular risk (COX-2) provides the framework for understanding the entire NSAID class and the rationale for COX-2 selective inhibitors.
The ibuprofen-aspirin interaction is clinically important: ibuprofen taken before aspirin can interfere with the irreversible COX-1 binding needed for aspirin antiplatelet effect; patients on cardioprotective aspirin should take aspirin first and wait 30-60 minutes before taking ibuprofen.

Safety Profile

Pregnancy avoid

Lactation use-with-caution

Renal Adjustment Required

Hepatic Adjustment Required

TDM Not required

Concordance Terms

Cross-referenced clinical concepts — click any term to see all content where it appears.

Dysmenorrhea Fever Inflammation Nonsteroidal Anti-inflammatory Drug (NSAID) Osteoarthritis Pain (mild To Moderate) Rheumatoid Arthritis

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