THE EFFECT OF AN ANTI-IGE MONOCLONAL-ANTIBODY ON THE EARLY-PHASE AND LATE-PHASE RESPONSES TO ALLERGEN INHALATION IN ASTHMATIC SUBJECTS

A humanized murine monoclonal antibody directed to the FC epsilon R1-b inding domain of human IgE (rhuMAb-E25) has been shown to inhibit the binding of IgE to mast cells without provoking mast cell activation. T o examine the effects of neutralizing IgE on allergic airway responses , we assessed the effects of 9 wk of treatment with rhuMAb-E25 in a pa rallel group, randomized, double-blind, placebo-controlled study of 19 allergic asthmatic subjects. We found that treatment with rhuMAb-E25 reduced serum IgE, increased the dose of allergen needed to provoke an early asthmatic response, reduced the mean maximal fall in FEV1 durin g the early response (30 +/- 10% at baseline to 18.8 +/- 8%, versus 33 +/- 8% at baseline to 34 +/- 4% after placebo; p = 0.01), and reduced the mean maximal fall in FEV1 during the late response (24 +/- 20% at baseline to 9 +/- 10% versus 20 +/- 17% at baseline to 18 +/- 17% aft er placebo; p = 0.047). We conclude that an anti-IgE monoclonal antibo dy, which inhibits binding of IgE to its receptor, suppresses the earl y- and late-phase responses to inhaled allergen in allergic asthmatic subjects. Targeting IgE with rhuMAb-E25 might be a useful treatment fo r allergic asthma.