Aspirin, also known as acetylsalicylic acid, is a widely used non-steroidal anti-inflammatory drug NSAID that exhibits anti-inflammatory, analgesic pain-relieving , and antipyretic fever-reducing properties. The primary target of aspirin in the body is an enzyme called cyclooxygenase COX , which exists in two main isoforms: COX-1 and COX-2. These enzymes play a crucial role in the synthesis of prostaglandins, which are lipid compounds that mediate various physiological processes such as inflammation, pain, and fever.The chemical mechanism behind aspirin's action involves the irreversible inhibition of the COX enzymes. Aspirin achieves this by acetylating a serine residue Ser-530 in COX-1 and Ser-516 in COX-2 in the active site of the enzyme. The acetylation process involves the transfer of an acetyl group from aspirin to the hydroxyl group of the serine residue. This modification blocks the access of arachidonic acid, the substrate for prostaglandin synthesis, to the active site of the enzyme, thereby preventing the formation of prostaglandins.The inhibition of prostaglandin synthesis is responsible for aspirin's anti-inflammatory and analgesic properties. Prostaglandins, such as prostaglandin E2 PGE2 , are produced in response to tissue injury or inflammation and contribute to the sensitization of pain receptors, the induction of fever, and the promotion of inflammation. By inhibiting the COX enzymes and reducing the production of prostaglandins, aspirin effectively alleviates pain, reduces fever, and suppresses inflammation.It is important to note that aspirin's inhibition of COX-1 and COX-2 is non-selective, meaning it affects both isoforms of the enzyme. While this non-selectivity contributes to its therapeutic effects, it can also lead to side effects, such as gastrointestinal irritation and increased risk of bleeding, due to the inhibition of COX-1, which is involved in the maintenance of the gastrointestinal mucosa and platelet function.