Current therapies for the treatment of seasonal allergic rhinitis include a
llergen avoidance; pharmacologic interventions such as sympathomimetics, to
pical and systemic corticosteroids, and chromones; and immunotherapy. In an
attempt to create a novel therapy, therapeutic agents have been designed t
o inhibit IgE responses that are intimately involved in the induction of th
e allergic response. Omalizumab, a humanized monoclonal antibody against Ig
E, represents a novel therapeutic intervention for seasonal allergic rhinit
is. Complex formation of omalizumab with serum-free IgE reduces the amount
of IgE available for binding to effector cells and thus has the potential t
o reduce IgE-mediated allergic symptoms. Clinical trial results confirmed t
hat omalizumab reduces free IgE to a level that is associated with suppress
ed allergic symptoms. reduces concomitant rescue medication use, and improv
es rhinitis-specific quality of lire. Patients treated with omalizumab duri
ng one pollen season can be re-treated during the subsequent season with mi
nimal risk of adverse events. Omalizumab is non-allergen-specific and does
not induce acute anaphylaxis because of the lack or IgE crosslinking with b
asophil- or mast-celt-bound IgE. Furthermore, subcutaneous or intravenous a
dministration of omalizumab does not invoke the generation of anti-omalizum
ab antibodies. Thus, omalizumab represents a novel agent that should assist
in the treatment of allergic rhinitis.