Argenx Bv

Argen-x N.v.

Argenx Bvba

The University of Texas System

Universitè Catholique De Louvain

Université Catholique De Louvian

Torsten Dreier

Johannes Joseph Wilhelmus De Haard

Peter Ulrichts

Natalie De Jonge

Christophe Blanchetot

Karen Silence

Sebastian Paul Van Der Woning

Christophe Frederic Jerome Blanchetot

Johannes De Haard

Michael John Scott Saunders

Anna Hultberg

Mahan Moshir

Sofie Maria Elvire Gabriels

Harald Wajant

Michael Saunders

Paolo Michieli

Cristina Basilico

Els Festjens

Pierre G Coulie

Sophie Lucas

Gitte De Boeck

Lore Mariën

Filip Borgions

E Sally Ward Ober

Stéphanie Liénart

Nicolas G H Ongenae

Nicolas Leupin

Nicolas Ongenae

Antonio Guglietta

Hans De Haard

Stéphanie Lienart

Tonke Van Bragt

Thierry Cousin

Johannes Joseph De Haard

Stëphanie Liénart

Paulo Michieli

Stephanie Lienart

Lore Marien

Michael John Saunders

Sofie Maria Gabriels

Christophe Frederic Blanchetot

Johannes Joesph De Haard

Nicolas Gh Ongenae

Lore MARIËN

Johannes Joesph Wilhelmus De Haard

Provided are novel methods of treating generalized myasthenia gravis in a subject. These methods generally comprise administering to the subject an effective amount of an isolated FcRn antagonist. In certain embodiments the FcRn antagonist binds to FcRn with increased affinity and reduced pH dependence relative to native Fc region.

Use of FCRN antagonists for treatment of generalized myasthenia gravis

A method is disclosed for the treatment of human subjects diagnosed with immune thrombocytopenia (ITP). The method comprises administering to a human subject a human neonatal Fc receptor (hFcRn) antagonist, optionally in combination with standard-of-care ITP treatment. In certain embodiments, the hFcRn antagonist is efgartigimod (ARGX-113). Standard-of-care ITP treatment may comprise administration of corticosteroids, immunosuppressants, and/or thrombopoietin receptor (TPO-R) agonists.

Compositions and methods for treating immune thrombocytopenia

The present invention provides binding molecules (e.g., antibodies or antigen binding fragments thereof) that specifically bind to and inhibit the biological activity of IL-6 (e.g., human, mouse and non-human primate IL-6). In a preferred embodiment, the antibodies or antigen binding fragments of the invention bind to IL-6 and inhibit its binding to an IL-6 receptor. Such antibodies or antigen binding fragments are particularly useful for treating IL-6-associated diseases or disorders (e.g., inflammatory disease and cancer).

IL-6 binding molecules

Provided are novel FcRn antagonist compositions comprising a variant Fc region that binds specifically to FcRn with increased affinity and reduced pH dependence relative to the native Fc region. Also provided are FcRn antagonists with enhanced CD16 binding affinity. Also provided are methods of treating antibody-mediated disorders (e.g. autoimmune diseases) using the these FcRn antagonist compositions, nucleic acids encoding the FcRn antagonist compositions, recombinant expression vectors and host cells for making the FcRn antagonist compositions, and pharmaceutical compositions comprising the FcRn antagonist compositions.

FcRn antagonists and methods of use

The present invention relates to antibodies and antigen binding fragments thereof which bind to the human CD70 protein with high affinity and display potent inhibition of tumour cell growth.

Antibodies to CD70

The present invention relates to antibodies and antigen binding fragments thereof which bind to the human CD70 protein with high affinity and display potent inhibition of tumor cell growth.

The present invention relates to antibodies and antigen binding fragments thereof, which bind to a complex of GARP and TGF-&#x3b2;1, particularly a complex of human GARP and human TGF-&#x3b2;1. These antibodies and antigen binding fragments exhibit a combination of advantageous properties including high affinity antigen binding and the ability to inhibit the release of active TGF-&#x3b2; from regulatory T cells. The antibodies and antigen binding fragments of the present invention are relatively resistant to deamidation, isomerization and oxidation, such that they display improved stability.

Nucleic acids encoding GARP-TGF-beta 1 antibodies

GARP-TGF-&#x3b2; 1 IGG antibodies

The present invention relates to antibodies that specifically bind to the human c-Met receptor protein and that act as strict antagonists of hepatocyte growth factor (HGF)-mediated activation of the c-Met receptor and also inhibit HGF-independent activation of the human c-Met protein.

Anti c-Met antibodies

GARP-TGF-beta 1 antibodies

FCRN antagonists and methods of use

Provided are chimeric, camelid-human (e.g., llama-human) polypeptides comprising a first antigenic polypeptide portion and a second antigenic polypeptide portion wherein the first antigenic portion is a derived from a first portion of a camelid (e.g., llama) and the second antigenic portion is a human polypeptide homolog of a second portion of the camedid antigen. The chimeric polypeptides are useful inter alia for epitope mapping and generation of antibodies that bind to a desired region of human antigen.

Chimeric human-llama antigens and methods of use

Growing community of inventors

Sint-Martens-Latem, Belgium

Torsten Dreier