摘要:
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.
摘要:
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.
摘要:
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.
摘要:
The present invention relates generally to a method for modulating cell survival. Modulation of cell survival includes inducing, enhancing or otherwise promoting cell survival such as the survival of neural cells as well as facilitating cell death such as the death of targeted cancer cells. The modulation of cell survival is mediated by a region identified on the p75 neurotrophin receptor (p75NTR) required for death signalling. The present invention further provides genetic molecules which encode the death signalling region of p75NTR which are useful in antagonising death signal function as well as promoting cell death when expressed in targeted cells. The present invention also contemplates recombinant peptides, polypeptides and proteins s well as chemical equivalents, derivatives and homologues thereof which comprise the death signalling portion of p75NTR. Particularly useful molecules of the present invention comprise peptides corresponding to soluble forms of the death signalling portion of p75NTR. These molecules antagonise p75NTR-mediated cell death.
摘要:
High affinity antibody antagonists of human interleukin-13 receptor alpha 1 are disclosed. The antibody molecules are effective in the inhibition of IL-13Rα1-mediated activities and, accordingly, present desirable antagonists for the use in the treatment of conditions associated with hIL-13Rα1 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-13Rα1-mediated activities are also disclosed.
摘要:
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.
摘要:
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.
摘要:
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.
摘要:
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.