The desired activity of a drug is mainly due to successful targeting of one of the following:
*Cellular membrane disruption
*Chemical reaction with downstream effects
*Interaction with enzyme proteins
*Interaction with structural proteins
*Interaction with carrier proteins
*Interaction with ion channels
*Ligand binding to receptors:
**Hormone receptors
**Neuromodulator receptors
**Neurotransmitter receptors
General anesthetics were once thought to work by disordering the neural membranes, thereby altering the Na influx. Antacids and chelating agents combine chemically in the body. Enzyme-substrate binding is a way to alter the production or metabolism of key endogenous chemicals, for example aspirin irreversibly inhibits the enzyme prostaglandin synthetase (cyclooxygenase) thereby preventing inflammatory response. Colchicine, a drug for gout, interferes with the function of the structural protein tubulin, while digitalis, a drug still used in heart failure, inhibits the activity of the carrier molecule, Na-K-ATPase pump. The widest class of drugs act as ligands that bind to receptors that determine cellular effects. Upon drug binding, receptors can elicit their normal action (agonist), blocked action (antagonist), or even action opposite to normal (inverse agonist).
In principle, a pharmacologist would aim for a target plasma concentration of the drug for a desired level of response. In reality, there are many factors affecting this goal. Pharmacokinetic factors determine peak concentrations, and concentrations cannot be maintained with absolute consistency because of metabolic breakdown and excretory clearance. Genetic factors may exist which would alter metabolism or drug action itself, and a patient's immediate status may also affect indicated dosage.