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In pharmacology, the term mechanism of action (MOA) refers to the specific biochemical interaction through which a drug substance produces its pharmacological effect. [2] A mechanism of action usually includes mention of the specific molecular targets to which the drug binds, such as an enzyme or receptor . [ 3 ]
The action of drugs on the human body (or any other organism's body) is called pharmacodynamics, and the body's response to drugs is called pharmacokinetics. The drugs that enter an individual tend to stimulate certain receptors, ion channels, act on enzymes or transport proteins. As a result, they cause the human body to react in a specific way.
Receptor theory is the application of receptor models to explain drug behavior. [1] Pharmacological receptor models preceded accurate knowledge of receptors by many years. [2] John Newport Langley and Paul Ehrlich introduced the concept that receptors can mediate drug action at the beginning of the 20th century.
Early forms of the receptor theory of pharmacology stated that a drug's effect is directly proportional to the number of receptors that are occupied. [14] Furthermore, a drug effect ceases as a drug-receptor complex dissociates. Ariëns & Stephenson introduced the terms "affinity" & "efficacy" to describe the action of ligands bound to receptors.
In pharmaceutical sciences, drug interactions occur when a drug's mechanism of action is affected by the concomitant administration of substances such as foods, beverages, or other drugs. A popular example of drug–food interaction is the effect of grapefruit on the metabolism of drugs .
Mechanisms of action There are three different types of antagonists. ... This drug is a non-selective α-adrenergic antagonist, which means it binds to both alpha ...
Newer NSAID drugs called COX-2 selective inhibitors have been developed that inhibit only COX-2, with the hope for reduction of gastrointestinal side-effects. [8] However, several COX-2 selective inhibitors have subsequently been withdrawn after evidence emerged that COX-2 inhibitors increase the risk of heart attack. [ 9 ]
Thiazolidinedione ligand dependent transactivation is responsible for the majority of anti-diabetic effects. The activated PPAR/RXR heterodimer binds to peroxisome proliferator hormone response elements upstream of target genes in complex with a number of coactivators such as nuclear receptor coactivator 1 and CREB binding protein, this causes upregulation of genes (for a full list see PPARγ):