NSAID

Nonsteroidal anti-inflammatory drug
Drug class
Coated 200 mg tablets of generic ibuprofen, a common NSAID
Class identifiers
Pronunciation	/ˈɛnsɛd/ EN-sed
Synonyms	nonsteroidal anti-inflammatory agents/analgesics (NSAIAs), nonsteroidal anti-inflammatory medicines (NSAIMs)
Use	Pain and fever
ATC code	M01A
Mechanism of action	Enzyme inhibitor
Biological target	COX-1 and COX-2

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a drug class that groups together drugs that provide analgesic (pain-killing) and antipyretic (fever-reducing) effects, and, in higher doses, anti-inflammatory effects.

The term nonsteroidal distinguishes these drugs from steroids, which, among a broad range of other effects, have a similar eicosanoid-depressing, anti-inflammatory action. First used in 1960, the term served to distance new drugs from steroid-related iatrogenic tragedies.

The most prominent members of this group of drugs are aspirin, ibuprofen and naproxen, all available over the counter in most countries.Paracetamol (acetaminophen) is generally not considered an NSAID because it has only little anti-inflammatory activity. It treats pain mainly by blocking COX-2 mostly in the central nervous system, but not much in the rest of the body.

Most NSAIDs inhibit the activity of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and thereby the synthesis of prostaglandins and thromboxanes. It is thought that inhibiting COX-2 leads to the anti-inflammatory, analgesic and antipyretic effects and that those NSAIDs also inhibiting COX-1, particularly aspirin, may cause gastrointestinal bleeding and ulcers.

NSAIDs are usually used for the treatment of acute or chronic conditions where pain and inflammation are present.

NSAIDs are generally used for the symptomatic relief of the following conditions:

Aspirin, the only NSAID able to irreversibly inhibit COX-1, is also indicated for inhibition of platelet aggregation. This is useful for the management of arterial thrombosis and prevention of adverse cardiovascular events. Aspirin inhibits platelet aggregation by inhibiting the action of thromboxane A₂.