The effect of drug depeond on the interaction between a drug and its specific molecular target which called drug–receptor interactions.
Most drugs achieve their desired therapeutic effects by interacting selectively with target molecules that play important physiologic or pathophysiologic roles.
In many cases, selectivity of drug binding to receptors also determines the undesired ( adverse ) effects on a drug. In general, drugs are molecules that interact with speciffic molecular components of an organism to cause biochemical and physiologic changes within that organism.
Given the great diversity of drug molecules, it might seem likely that the interactions between drugs and their molecular targets would be equally diverse. This is only partly true. In fact, most of the currently understood drug–receptor interactions can be classif ed into six major groups .

1. transmembrane ion channels
2. transmembrane receptors coupled to intracellular G proteins
3. transmembrane receptors with linked enzymatic domains
4. intracellular receptors, including enzymes, signal transduction molecules, transcription actors, structural proteins, and nucleic acids
5. extracellular targets
6. cell surfface adhesion receptors

A. Drugs can bind to ion channels spanning the plasma membrane, causing an alteration in the channel’s conductance.

B. Heptahelical receptors spanning the plasma membrane are functionally coupled to intracellular G proteins. Drugs can influence the actions of these receptors by binding to the extracellular surfface or transmembrane region of the receptor.

C. Drugs can bind to the extracellular domain of a transmembrane receptor and cause a change in signaling within the cell by activating or inhibiting an enzymatic intracellular domain ( rectangular box ) o the same receptor molecule.

D. Drugs can diffuse through the plasma membrane and bind to cytoplasmic or nuclear receptors. This is often the pathway used by lipophilic drugs (e.g., drugs that bind to steroid hormone receptors).

Additionally, drugs can bind to enzymes and other targets in the extracellular space and to cell sur ace adhesion receptors without the need to cross the plasma membrane

Drug metabolism is the metabolic breakdown of drugs usually through specialized enzymatic systems.

The rate of metabolism determines the duration and intensity of a drug's pharmacologic action.

Drug metabolism is goes into three phases. The first phase, enzymes such as cytochrome P450 oxidases introduce reactive or polar groups into xenobiotics.

The effect of this cytochrome (P450) can be affectd by present of other drugs

This effect of the other drugs can inhance cytochrome P450 action which lead to rapid metabolism and clear the drug very quickly, and the therapeutic concentration of the drug in the blood and tissues may not be reached. or inhibiting cytochrome P450 action leading to the drug to be metabolized so slowly that it accumulates in the blood stream. The higher concentration of the drug in the body creates a greater potential for adverse effects.

Cytochromes P450 (CYPs) are a superfamily of enzymes containing heme as a cofactor that functions as monooxygenases.In mammals, these proteins oxidize steroids, fatty acids, and xenobiotics, and are important for the clearance of various compounds, as well as for hormone synthesis and breakdown

Influence of fm(fraction metabolized by inhibited P450) on drug-drug interactions. The control represents a model drug for which cytochrome P450 (dark bar) is responsible for 20% of the clearance, with the remaining 80% being non-P450 mediated (white bar). CYP inhibited and CYP induced illustrate the effect on total clearance of a fivefold reduction or increase in the P450 activity, respectively.