Abstract: The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF?/?) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response. PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monocloncal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.

Abstract: The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF?/?) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monoclonal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.

Abstract: The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF?/?) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response. PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monoclonal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.

Abstract: The invention relates to the field of muscle pathologies, more particularly to the field of diseases where skeletal muscle degeneration occurs. The invention describes transgenic mice that do not produce prolyl-hydroxylase-1, -2 or -3. It is revealed that the phenotype of the prolyl-hydroxylase 1 knock-out mouse is characterized by a protection of skeletal muscle atrophy due to a variety of muscle damages, especially ischemic insults. The invention thus relates to the use of molecules that can bind to prolyl-hydroxylase-1 for the prevention and/or treatment of skeletal muscle degeneration.

Abstract: The present invention relates to the field of pathological angiogenesis and arteriogenesis and, in particular, to a stress-induced phenotype in a transgenic mouse (PIGF?/?) that does not produce Placental Growth Factor (PIGF) and that demonstrates an impaired vascular endothelial growth factor (VEGF)-dependent response. PIGF deficiency has a negative influence on diverse pathological processes of angiogenesis, arteriogenesis and vascular leakage comprising ischemic retinopathy, tumor formation, pulmonary hypertension, vascular leakage (edema formation) and inflammatory disorders. The invention thus relates to molecules that can inhibit the binding of PIGF to its receptor (VEGFR-1), such as monoclonal antibodies and tetrameric peptides, and to the use of these molecules to treat the above-mentioned pathological processes.

Abstract: The present invention relates to new antibodies and fragments and derivatives thereof, which are particularly suited for the characterization of the structure and function of Factor VIII (FVIII) of the coagulation pathway, for the design of therapeutic strategies for eradication of FVIII inhibitors and for the use as a medicament The invention also relates to cell lines producing the specific antibodies. The present invention furthermore relates to pharmaceutical compositions comprising the antibodies, fragments and/or derivatives of the Invention and to methods of preventing and treating cardiovascular disorders by using the antibodies or fragments and derivatives thereof or pharmaceutical compositions thereof.