Ucbbiopharma Srl

Brian John Sutton

Ralph Adams

Alistair James Henry

Thomas Allen Ceska

Xiaofeng Liu

James Michael McDonnell

Anna Marie Davies

Marta Katarzyna Westwood

The present invention relates to the area of improved anti-IgE antibodies and antigen binding agents, and compositions thereof, which target IgE, for instance: for use in treating disorders caused by IgE (such as allergic responses, or certain autoimmune responses); and, in particular, disorders caused by the interaction of IgE with the FcεRI receptor. In particular, this invention relates to improved anti-IgE antibodies and antigen binding agents related to novel mutants of omalizumab (Xolair®). The improved anti-IgE antibodies and antigen binding agents of the invention may have improved affinity for IgE and/or an improved interaction with the Cε2 domain of IgE and/or an improved modified epitope on IgE (for instance further involving the Cε2 domain of IgE) and/or the ability to disassociate IgE from the FcεRI receptor for instance at pharmaceutically-relevant concentrations. In one aspect, improved or novel treatments for IgE mediated disorders are disclosed in which IgE is targeted (for instance free IgE and/or IgE complexed with the FcεRI receptor).

Anti-IgE antibodies

The present invention relates to the area of improved anti-IgE antibodies and antigen binding agents, and compositions thereof, which target IgE, for instance: for use in treating disorders caused by IgE (such as allergic responses, or certain autoimmune responses); and, in particular, disorders caused by the interaction of IgE with the Fc&#x3b5;RI receptor. In particular, this invention relates to improved anti-IgE antibodies and antigen binding agents related to novel mutants of omalizumab (Xolair&#xae;). The improved anti-IgE antibodies and antigen binding agents of the invention may have improved affinity for IgE and/or an improved interaction with the C&#x3b5;2 domain of IgE and/or an improved modified epitope on IgE (for instance further involving the C&#x3b5;2 domain of IgE) and/or the ability to disassociate IgE from the Fc&#x3b5;RI receptor for instance at pharmaceutically-relevant concentrations. In one aspect, improved or novel treatments for IgE mediated disorders are disclosed in which IgE is targeted (for instance free IgE and/or IgE complexed with the Fc&#x3b5;RI receptor).

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London, United Kingdom

Brian John Sutton