Aspirin, also known as acetylsalicylic acid, is a nonsteroidal anti-inflammatory drug NSAID that is commonly used to relieve pain, reduce inflammation, and lower fever. Its mechanism of action at the molecular level involves the inhibition of cyclooxygenase COX enzymes, which play a crucial role in the synthesis of prostaglandins.Prostaglandins are hormone-like substances that are involved in various physiological processes, including the mediation of pain, inflammation, and fever. They are synthesized from arachidonic acid, a polyunsaturated fatty acid, through a series of enzymatic reactions. The first step in this process is catalyzed by the COX enzymes, which exist in two isoforms: COX-1 and COX-2.COX-1 is constitutively expressed in most tissues and is responsible for the production of prostaglandins that regulate normal physiological functions, such as gastric mucosal protection and platelet aggregation. On the other hand, COX-2 is induced during inflammation and is responsible for the production of prostaglandins that mediate pain, inflammation, and fever.Aspirin exerts its therapeutic effects by irreversibly inhibiting both COX-1 and COX-2 enzymes through the acetylation of a serine residue in their active sites. This modification prevents the access of arachidonic acid to the enzymes, thereby blocking the synthesis of prostaglandins. As a result, aspirin reduces the levels of prostaglandins that cause pain, inflammation, and fever.In addition to its anti-inflammatory and analgesic effects, aspirin also has antithrombotic properties due to its ability to inhibit platelet aggregation. This is mainly attributed to the inhibition of COX-1 in platelets, which leads to a decrease in the production of thromboxane A2, a potent platelet aggregator, and vasoconstrictor.In summary, aspirin works to reduce pain and inflammation by inhibiting the cyclooxygenase enzymes, which are responsible for the synthesis of prostaglandins that mediate these processes. Its mechanism of action at the molecular level involves the acetylation of a serine residue in the active sites of COX-1 and COX-2, thereby blocking the production of prostaglandins and reducing their levels in the body.