Abstract: High affinity antibody antagonists of human interleukin-13 receptor alpha 1 are disclosed. The antibody molecules are effective in the inhibition of IL-13R?1-mediated activities and, accordingly, present desirable antagonists for the use in the treatment of conditions associated with hIL-13R?1 activity. The present invention also discloses nucleic acid encoding said antibody molecules, vectors, host cells, and compositions comprising the antibody molecules. Methods of using the antibody molecules for inhibiting or antagonizing IL-13R?1-mediated activities are also disclosed.

Abstract: The invention relates to a method for the production of acrylic acid from propane, in which a gas mixture comprising propane, water vapour and, optionally, an inert gas and/or molecular oxygen is passed over a catalyst, comprising a crystalline catalyst phase of formula (I) or (I?) TeaMolVbNbcOx (I) Sba Mol VbOy (I?), associated with a crystalline catalyst phase for activating the propane.

Abstract: The present invention provides a method for the treatment or prophylaxis of T-helper type 2 (Th2)-mediated disorders using antagonists of IL-11.

Abstract: The present invention relates generally to the treatment of an interleukin-11 (IL-11)-mediated condition. More particularly, the present invention provides the use of modified forms of IL-11 which modulate IL-11 signaling in the treatment of IL-11-mediated conditions.

Abstract: The present invention relates to the identification of a PEST motif in Suppressor of Cytokine Signalling (SOCS) proteins, the deletion/inactivation of which has been found to increase the stability of the protein whilst maintaining at least one biological activity of the protein. Such SOCS proteins with deleted/inactivated PEST motifs can be used in gene and protein therapy procedures to provide a more stable SOCS protein when compared to the native protein. The present invention also relates to the characterization of the structure of SOCS proteins, and methods of using this structural information to identify compounds which modulate the activity of SOCS.

Abstract: The present invention relates generally to the field of cancer therapy and prophylaxis. More particularly, the present invention provides growth factor antagonists which inhibit the growth of cancers including tumors and pre-cancerous tissue. Even more particularly, the present invention is directed to antagonists of vascular endothelial growth factor-B and their use to inhibit the growth of cancer including tumor tissue and pre-cancerous tissue.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: High affinity antibody antagonists of human interleukin-13 receptor alpha 1 are disclosed. The antibody molecules are effective in the inhibition of IL-13R?1-mediated activities and, accordingly, present desirable antagonists for the use in the treatment of conditions associated with hIL-13R?1 activity. The present invention also discloses nucleic acid encoding said antibody molecules, vectors, host cells, and compositions comprising the antibody molecules. Methods of using the antibody molecules for inhibiting or antagonizing IL-13R?1-mediated activities are also disclosed.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: The present invention relates generally to a method for regulating cytokine signalling and agents useful for same. The method of the present invention is predicated in part on the identification of the molecular target of suppressor of cytokine signalling (SOCS) interaction in controlling cytokine signalling. The identification of the molecular target permits the development of assays to screen for a range of agonists and antagonists useful in modulating cytokine function. The present invention further provides, therefore, screening assays and more particularly high through-put screening assays for agonists and antagonists of SOCS-receptor interaction. Such agonists and antagonists are useful in the manufacture of medicaments for controlling cytokine signalling. Control of cytokine signalling is important for the treatment of a range of conditions including cancer, inflammatory conditions, immunological disorders and any other conditions involving aberrations of signal transduction.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: The present invention relates generally to a method for regulating cytokine signaling and agents useful for same. The method of the present invention is predicated in part on the identification of the molecular target of suppressor of cytokine signaling (SOCS) interaction in controlling cytokine signaling. The identification of the molecular target permits the development of assays to screen for a range of agonists and antagonists useful in modulating cytokine function. The present invention further provides, therefore, screening assays and more particularly high through-put screening assays for agonists and antagonists of SOCS-receptor interaction. Such agonists and antagonists are useful in the manufacture of medicaments for controlling cytokine signaling. Control of cytokine signaling is important for the treatment of a range of conditions including cancer, inflammatory conditions, immunological disorders and any other conditions involving aberrations of signal transduction.

Abstract: The present invention relates to the identification of a PEST motif in Suppressor of Cytokine Signalling (SOCS) proteins, the deletion/inactivation of which has been found to increase the stability of the protein whilst maintaining at least one biological activity of the protein. Such SOCS proteins with deleted/inactivated PEST motifs can be used in gene and protein therapy procedures to provide a more stable SOCS protein when compared to the native protein. The present invention also relates to the characterization of the structure of SOCS proteins, and methods of using this structural information to identify compounds which modulate the activity of SOCS.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.

Abstract: Humanized and variant anti-VEGF antibodies and various uses therefor are disclosed. The anti-VEGF antibodies have strong binding affinities for VEGF; inhibit VEGF-induced proliferation of endothelial cells in vitro; and inhibit tumor growth in vivo.