EditorialIt has been well recognized that an increasing percentage of the population is using herbal products for both preventive and therapeutic purposes. Often times the use of herbals is associated with attenuating side-effects produced from therapeutic drugs such as chemotherapeutic regimen. The basis of this usage of herbal products is the concept that being a natural product, the herbal must be safe to use. However, contrary to this perception it has been well documented that significant pharmacokinetic and/or pharmacodynamic effects can occur through herb-drug interaction [1,2] which has led to an increased concern regarding the safety and even toxicity of the coadministration of these products with therapeutic drugs [3][4][5][6][7]. This effect is exacerbated more so for drugs that have a narrow therapeutic index (e.g., warfarin, digoxin, and many chemotherapeutic agents). The mechanisms of herbal-drug interaction are generally pharmacokinetic in nature and result in changes in absorption and metabolism of the therapeutic agent. In addition to the chemical/physical properties of drugs that effect absorption after oral dosing (e.g., lipid/water solubility, molecular size, degree of ionization, etc), the inhibition or induction of drug transporters can have a substantial effect on the amount of drug absorbed. Perhaps the best characterized drug transporter is P-glycoprotein (P-gp) which has been found in the apical membrane of cells in various organs including the gastrointestinal tract, liver, lungs, and kidneys. Active compounds in the herbal product have been shown to function as transporter substrates resulting in either inhibition or induction of P-gp causing either elevated or reduced drug concentrations, respectively [7,8]. These alterations in drug concentration could result in either a sub-therapeutic level of exposure or potentially produce toxic side effects.Herbal products also have components which function as cytochrome P450 (CYP450) substrates which may also result in the inhibition [9] or induction [10] of the metabolizing enzymes. For inhibition of CYP450 enzymes, herbal products do so in a mixed competitive/noncompetitive manner depending on the particular isozyme and active compounds in the product [9,11]. Competitive inhibition is reversible and is usually simple competition between the drug and the active herbal component for the reactive site on the enzyme. Noncompetitive inhibition is typically characterized by reversible binding of the inhibitor at an allosteric site on the enzyme resulting in a change in its conformation where the drug substrate can still bind but the enzyme cannot catalyze the biotransformation of the drug. Additionally, active components of the herbal may bind irreversibly through covalent interactions with the enzyme thereby reducing the concentration of the enzyme. Alternatively, metabolites of the herbal may also bind irreversibly to the enzyme (mechanism based inhibition) again reducing the pool of enzymes available to catalyze biotransformations of the drug....