The non-steroidal anti-inflammatory drugs (NSAIDs) is 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 analgesic and anti-inflammatory properties acts by inhibiting two recognized isoenzymes of prostaglandin G/H synthase also known as cycl-oxygenase (COX), which are COX 1 and COX 2.The pharmacodynamic action of these drugs is mostly mediated by inhibition of COX2, while the adverse reactions are largely due to COX1 inhibition.. The NSAID selectively inhibiting COX2 were developed in the 90s to reduce the risk of gastrointestinal toxicity. NSAID use has been found to be associated with an increased risk of heart failure in several randomized clinical trials and observational studies. Nevertheless, there is still limited information on the risk of heart failure associated with the use of individual NSAIDs (both COX 2 inhibitors and traditional NSAIDs) in clinical practice in resource poor communities, and especially on their doseresponse associations. The most prominent members of this group of drugs, are aspirin, ibuprofen, naproxen, that are all available over the counter in most countries. Paracetamol (acetaminophen) is generally not considered an NSAID because it has only little antiinflammatory 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 (COX-1) and COX2, and thereby the synthesis of prostalglandin 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. This review attempts to give a comprehensive view of NSAIDs pharmacological activities, the drug class, mode of action and usage in a low income economy.