Pharmacology · Nonsteroidal anti-inflammatory drugs (NSAIDs)

Acetylsalicylic acid !

An NSAID that permanently blocks platelet cyclooxygenase: at low doses it prevents clots in the heart and brain; at higher doses it eases pain and fever.

Updated 2026-11-01

Class: Nonsteroidal anti-inflammatory drugs (NSAIDs)
Enzyme: Cyclooxygenase 1 and 2 (COX-1/COX-2)
ATC code: N02BA01
WHO Model List of Essential Medicines

Also called: aspirin

Cyclooxygenase 1 and 2 (COX-1/COX-2)Acetylsalicylic acid

The figure shows human COX-2 already acetylated by the drug: there is no free drug molecule, only the acetyl group attached to the channel serine (Ser530 in classic numbering; Ser516 in the human COX-2 sequence and Ser529 in COX-1). The salicylate leaves after the reaction.

Target in 3D: Cyclooxygenase 1 and 2 (COX-1/COX-2). PDB structure 5F19 (RCSB PDB, public domain). View the structure at RCSB PDB

Mechanism of action

Aspirin enters the cyclooxygenase channel and transfers its acetyl group to a serine, permanently blocking the path of arachidonic acid. In the platelet, which cannot make new enzyme, thromboxane A2 synthesis is suppressed for the cell's whole life and aggregation drops. At higher doses it also lowers the prostaglandins of pain, fever and inflammation.

Transfers its acetyl group to the COX channel serine (Ser530)
Platelet COX-1 is blocked for the platelet's lifetime
Thromboxane A2 falls and platelets aggregate less
Less arterial thrombosis: fewer heart attacks and ischemic strokes

Pharmacokinetics

Absorption: Absorbed quickly from the stomach and small intestine.
Distribution: Salicylate is highly bound to albumin and reaches most tissues.
Metabolism: Hydrolyzed within minutes to salicylate; salicylate is conjugated in the liver.
Elimination: Kidney, as salicylate and its conjugates.
Half-life: Intact drug about 15 to 20 minutes; salicylate about 3.5 to 4.5 hours. The antiplatelet effect lasts 7 to 10 days.

Indications

Early treatment and secondary prevention of acute myocardial infarction Myocardial Infarction (Heart Attack) →
Secondary prevention after ischemic stroke Ischaemic stroke →
Stable angina and chronic coronary disease Stable angina →
Mild to moderate pain, fever and migraine attacks in adults
Kawasaki disease and acute rheumatic fever, under specialist care (rheumatic fever still matters in Colombia)

Adverse effects

Common

Dyspepsia, nausea and epigastric pain
Minor bleeding (bruising, gums)
Tinnitus at high concentrations

Contraindications

Children and teenagers with a viral infection, except specialist indications such as Kawasaki disease
Active peptic ulcer or gastrointestinal bleeding
Bleeding disorders such as hemophilia
Asthma or urticaria triggered by NSAIDs
Third trimester of pregnancy at analgesic doses

Key interactions

Ibuprofen and other NSAIDs: If they occupy the COX-1 channel first, they stop aspirin from acetylating the serine and blunt its antiplatelet effect; they also add gastric risk.
Anticoagulants (warfarin, heparins, direct oral anticoagulants): Higher bleeding risk.
SSRIs: More risk of gastrointestinal bleeding.
Methotrexate: Reduced renal clearance of methotrexate and more toxicity.

What is monitored

Signs of gastrointestinal bleeding (melena, hematemesis)
Tinnitus or hearing loss as a sign of salicylate excess

Test yourself

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

Why does aspirin's antiplatelet effect last days even though the drug leaves the blood within minutes?

It acetylates COX-1 irreversibly and the anucleate platelet cannot make new enzyme. The effect wears off only as the bone marrow releases new platelets, over about 7 to 10 days.

Which serious complication limits aspirin use in children with influenza or chickenpox?

Reye syndrome: acute encephalopathy with fatty liver injury, linked to salicylate use during viral infections in children and teenagers.

Which acid-base disorder is typical of salicylate poisoning in adults?

A mixed disorder: early respiratory alkalosis from direct stimulation of the respiratory center plus a high anion gap metabolic acidosis.

Why can ibuprofen reduce aspirin's cardiovascular benefit?

Ibuprofen reversibly occupies the COX-1 channel and, if it gets there first, keeps aspirin from reaching the serine it needs to acetylate.

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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: Aspirin: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2025); Aspirin (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.