Fexofenadine is a selective, non-sedating
H1 receptor antagonist, marketed in the United States since 2000. The FDA approved an oral
suspension in 2006, for the treatment of
seasonal allergic rhinitis and
chronic idiopathic urticaria in children. The
tablet,
capsule, and oral
suspension are bioequivalent. Although
fexofenadine does not use P450 CYP 3A4 it does interact with a number of drugs at
P-glycoprotein and
organic anion transporter polypeptides. The risk of toxicity from other drugs may increase with the administration of
fexofenadine. Orange and grapefruit juices reduce the bioavailability of
fexofenadine.
Fexofenadine has been shown to have an impact on inflammatory mediators, other than
histamine, such as decreasing the production of LTC(4), LTD(4), LTE(4),
PGE(2), and
PGF(2α); inhibiting
cyclo-oxygenase 2,
thromboxane; limiting iNOS generation of NO; decreasing
cytokine levels (ICAM-1, ELAM-1, VCAM-1,
RANTES, I-TAC, MDC, TARC,
MMP-2,
MMP-9,
tryptase); and diminishing eosinophil adherence, chemotaxis, and opsonization of particles. These effects may provide benefit to some of the inflammatory responses of an acute
allergic reaction and provide a basis for future development of H1 antagonists with stronger anti-inflammatory effects. These studies also support the contention that
fexofenadine is effective for the treatment of allergic rhinits and
chronic idiopathic urticaria.