Abstract: The present invention relates to VWF compounds as well as compositions suitable for treatment of blood clotting diseases.

Abstract: The present invention relates to VWF compounds as well as compositions suitable for treatment of blood clotting diseases.

Abstract: The present invention relates to Von Willebrand (VWF) compounds as well as compositions suitable for treatment of blood clotting diseases. The present invention also relates to pharmaceutical compositions, freeze-dried or liquid, comprising (i) a Factor VIII molecule and (ii) a VWF compound.

Abstract: The present invention relates to pharmaceutical compositions suitable for treatment of haemophilia.

Abstract: The present invention relates to Von Willebrand (VWF) compounds as well as compositions suitable for treatment of blood clotting diseases. The present invention also relates to pharmaceutical compositions, freeze-dried or liquid, comprising (i) a Factor VIII molecule and (ii) a VWF compound.

Abstract: The present invention relates to VWF compounds as well as compositions suitable for treatment of blood clotting diseases.

Abstract: The present invention relates to pharmaceutical compositions suitable for treatment of haemophilia.

Abstract: The present invention relates to Von Willebrand (VWF) compounds as well as compositions suitable for treatment of blood clotting diseases. The present invention also relates to pharmaceutical compositions, freeze-dried or liquid, comprising (i) a Factor VIII molecule and (ii) a VWF compound.

Abstract: A method is disclosed for inducing cell-mediated immunity against cellular antigens. More specifically, the invention provides for a method for inducing cytotoxic T-lymphocyte immunity against weak antigens, notably self-proteins. The method entails that antigen presenting cells are induced to present at least one CTL epitope of the weak antigen and at the same time presenting at least one foreign T-helper lymphocyte epitope. In a preferred embodiment, the antigen is a cancer specific antigen, e.g. PSM, Her2, or FGF8b. The method can be exercised by using traditional polypeptide vaccination, but also by using live attenuated vaccines or nucleic acid vaccination. The invention furthermore provides immunogenic analogues of PSM, Her2 and FGF8b, as well as nucleic acid molecules encoding these analogues. Also vectors and transformed cells are disclosed. The invention also provides for a method for identification of immunogenic analogues of weak or non-immunogenic antigens.

Abstract: A method is disclosed for inducing cell-mediated immunity against cellular antigens. More specifically, the invention provides for a method for inducing cytotoxic T-lymphocyte immunity against weak antigens, notably self-proteins. The method entails that antigen presenting cells are induced to present at least one CTL epitope of the weak antigen and at the same time presenting at least one foreign T-helper lymphocyte epitope. In a preferred embodiment, the antigen is a cancer specific antigen, e.g. PSM, Her2, or FGF8b. The method can be exercised by using traditional polypeptide vaccination, but also by using live attenuated vaccines or nucleic acid vaccination. The invention furthermore provides immunogenic analogues of PSM, Her2 and FGF8b, as well as nucleic acid molecules encoding these analogues. Also vectors and transformed cells are disclosed. The invention also provides for a method for identification of immunogenic analogues of weak or non-immunogenic antigens.

Abstract: Gla domain variants of human Factor VII or human Factor VIIa, comprising 1-15 amino acid modifications relative to human Factor VII or human Factor VIIa, wherein a hydrophobic amino acid residue has been introduced by substitution in position 34; or having an amino acid substitution in position 36; and use of the variants for the treatment of intracerebral haemorrhage (ICH) or trauma.

Abstract: Variants of FVII or FVIIa comprising at least one amino acid modification in position 196, 237 or 341 relative to hFVII or hFVIIa. The variants exhibit an increased clotting activity, i.e. reduced clotting time, compared to rhFVIIa.

Abstract: The present invention relates to novel polypeptide variants of factor VII (FVII) or factor VIIa (FVIIa) polypeptides, where said variants comprise an amino acid substitution in position 10 and 32 and where said variants further comprise a sugar moiety covalently attached to an introduced in vivo N-glycosylation site located outside of the Gla domain. Such polypeptide variants are useful in therapy, in particular for the treatment of a variety of coagulation-related disorders, such as trauma.

Abstract: The present invention relates to novel polypeptide variants of factor VII (FVII) or factor VIIa (FVIIa) polypeptides, where said variants comprise an amino acid substitution in position 10 and 32 and where said variants further comprise a sugar moiety covalently attached to an introduced in vivo N-glycosylation site located outside of the Gla domain. Such polypeptide variants are useful in therapy, in particular for the treatment of a variety of coagulation-related disorders, such as trauma.

Abstract: The present invention relates to novel polypeptide variants of factor VII (FVII) or factor VIIa (FVIIa) polypeptides, where said variants comprise an amino acid substitution in position 10 and 32 and where said variants further comprise a sugar moiety covalently attached to an introduced in vivo N-glycosylation site located outside of the Gla domain. Such polypeptide variants are useful in therapy, in particular for the treatment of a variety of coagulation-related disorders, such as trauma.

Abstract: The present invention relates to novel polypeptide variants of factor VII (FVII) or factor VIIa (FVIIa) polypeptides, where said variants comprise an amino acid substitution in position 10 and 32 and where said variants further comprise a sugar moiety covalently attached to an introduced in vivo N-glycosylation site located outside of the Gla domain. Such polypeptide variants are useful in therapy, in particular for the treatment of a variety of coagulation-related disorders, such as trauma.

Abstract: Gla domain variants of human Factor VII or human Factor VIIa, comprising 1-15 amino acid modifications relative to human Factor VII or human Factor VIIa, wherein a hydrophobic amino acid residue has been introduced by substitution in position 34; or having an amino acid substitution in position 36; and use of the variants for the treatment of intracerebral haemorrhage (ICH) or trauma.

Abstract: Gla domain variants of human Factor VII or human Factor VIIa, comprising 1-15 amino acid modifications relative to human Factor VII or human Factor VIIa, wherein a hydrophobic amino acid residue has been introduced by substitution in position 34; or having an amino acid substitution in position 36; and use of the variants for the treatment of intracerebral haemorrhage (ICH) or trauma.

Abstract: Gla domain variants of human Factor VII or human Factor VIIa, comprising 1-15 amino acid modifications relative to human Factor VII or human Factor VIIa, wherein a hydrophobic amino acid residue has been introduced by substitution in position 34; or having an amino acid substitution in position 36; and use of the variants for the treatment of intracerebral haemorrhage (ICH) or trauma.

Abstract: The present invention relates to novel Factor VII or VIIa variants comprising a substitution in at least one position selected from the group consisting of L39, 142, S43, K62, L65, F71, E82 and F275. Such variants exhibit increased clotting activity as compared to human wild-type Factor VIIa. The present invention also relates to use of such Factor VII or VIIa variants in therapy, in particular for the treatment of a variety of coagulation-related disorders.