The next few slides will focus on drug metabolism. Some important preventable drug interactions are due to their effects on drug metabolizing enzymes, resulting in either inhibition of the enzyme or induction of the enzyme. There are many potential consequences of changes in drug metabolism for a given drug. It is made more complex by the fact that there are multiple pathways of metabolism for many drugs.

The majority of drugs that are metabolized are converted to inactive metabolites. This is the most common fate for most drugs. Of the remaining drugs, some are converted to metabolites that retain the same activity as the parent. An example of this is fexofenadine (Allegra), the active metabolite of terfenadine that has equal potency at the histamine receptor and now is on the market and used clinically for allergic rhinitis. However, fexofenadine is is more than 50 times less active in blocking potassium channels in the heart and therefore, unlike terfenadine, does not cause torsades de pointes.{Woosley}
In some cases the metabolites are actually more potent than the parent. For example, a pro-drug such as enalapril must be hydrolyzed to enalaprilat to become active.
In some cases, the metabolites have entirely new pharmacologic actions not seen with the parent drug. Metabolites can also be toxic, such as the metabolites of acetaminophen which can cause liver failure or the metabolite of meperidine which can cause seizures.
Inhibition of metabolism could result in potentially toxic concentrations of the parent compound. On the other hand, if the parent drug needs to be metabolized to the active compound, therapeutic failure could result (as happens, for example, if codeine is not metabolized to morphine). Induction of drug metabolizing enzymes could similarly result in a subtherapeutic effect by reducing drug levels below that required for efficacy.

Woosley RL, Chen Y, Freiman JP, Gillis RA. Mechanism of the cardiotoxic actions of terfenadine. JAMA 1993; 269(12):1532-1536.