Argenx Bv

Ablynx N.v.

Argenx Bvba

University of Texas System

Universiteit Gent

Vib Vzw

Argen-x N.v.

Argenx Iip Bv

New York University

Christophe Blanchetot

Johannes Joseph Wilhelmus De Haard

Torsten Dreier

Michael John Scott Saunders

Sebastian Paul Van Der Woning

Peter Vanlandschoot

Hans De Haard

Johannes De Haard

Natalie De Jonge

Regorius Leurs

Martine Smit

Sven Jähnichen

Karen Silence

Peter Ulrichts

Bart Lambrecht

Dominique Schols

Peter Verheesen

Michael Saunders

E Sally Ward Ober

Kenneth Verstraete

Savvas Savvides

Hamida Hammad

Emma Persson

Nicolas G H Ongenae

Jean-Michel Percier

Nicolas Ongenae

Catelijne Stortelers

Shohei Koide

Akiko Koide

Francis Descamps

Maria Gonzalez Pajuelo

Philippe Van Rompaey

Anna Hultberg

Maarten Van Roy

Pascal Gerard Merchiers

Steven J Burden

David Andre Baptiste Maussang-Detaille

Vladimir Bobkov

Jolien Van Santbergen

Julien Oury

René Bigirimana

Judith Baumeister

Jacobus Cornelis Rasser

Erik Hofman

Marie Godar

Roeland Vanhauwaert

Nadia Leloup

Hendrik Adams

Inge Van De Walle

Kevin Budding

Erik Hack

Ludo Van Der Pol

Sebastian Van Der Woning

Nicolas Gh Ongenae

Provided herein are binding molecules comprising a human neonatal Fc receptor (FcRn) binding molecule and at least one antigen-binding domain linked to the FcRn binding molecule. Polynucleotides, vectors, host cells, and methods of production are also provided herein. Methods of treating an antibody-mediated disorder with an FcRn/antigen-binding molecule are further provided.

FcRn/HSA binding molecules and methods of use

The present invention relates to bispecific and other multispecific antigen binding constructs. In certain aspects, the invention relates to bispecific antigen binding constructs comprising a single domain antibody (VHH) antigen binding region fused to an IgG Fc domain; a heavy chain-Fc domain portion of a conventional IgG antibody, and a light chain portion of a conventional IgG antibody. The bispecific antigen binding constructs of the invention are capable of targeting two different antigens separately or in a protein complex.

Bispecific antigen binding construct

Methods for preparing engineered antibodies exhibiting improved pH-dependent antigen binding are disclosed. The methods are based on introduction of histidine residues at a subset of defined amino acid positions within the antibody CDRs. The set of amino acid positions selected for histidine substitution is derived from a heat-map of histidine occurrence within the CDRs of functional antibodies from a natural antibody repertoire. The methods provide a simpler and less time-consuming approach to the identification of pH-dependent antibody variants.

Method of preparing pH-dependent antibodies

The present invention relates to combination therapies and to their use in the treatment of chronic airway disease, particularly use in the treatment of asthma. The combination therapies comprise (i) an antagonist of IL-5:IL-5R and (ii) an antagonist of IL-4:IL-4R and/or an antagonist of IL-13:IL-13R. The present invention also provides bispecific antibodies comprising an antigen binding domain that binds to IL-4Rα and an antigen binding domain that binds to IL-5. The bispecific antibodies may be used for the treatment of chronic airway disease, particularly asthma.

Multispecific antibodies against IL-5 and IL-4R

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

The present invention relates to antagonists, particularly antibodies and antigen binding fragments thereof, that bind to the protein galectin-10, particularly human galectin-10. The galectin-10 antagonists disrupt the crystallization of galectin-10 and are therefore useful in methods of preventing and treating diseases and conditions wherein the pathology is linked to the formation/presence of Charcot-Leyden crystals (CLCs).

Galectin-10 antibodies

Provided are antibodies and antigen-binding fragments thereof that bind specifically to human complement factor C2 and are capable of inhibiting activation of the classical and lectin pathways of the complement system. The antibodies and antigen-binding fragment exhibit improved manufacturability, pharmacokinetics, and antigen sweeping. Also provided are pharmaceutical compositions comprising the antibodies and antigen-binding fragments, nucleic acids and vectors encoding the antibodies and antigen-binding fragments, host cells comprising the nucleic acids or vectors, and methods of making and using the antibodies and antigen-binding fragments. The antibodies and antigen-binding fragments can be used to inhibit the classical pathway of complement activation in a subject, e.g., a human. The antibodies and antigen-binding fragments can also be used to inhibit the lectin pathway of complement activation in a subject, e.g., a human.

Antibodies to human complement factor C2B and methods of use

Antibodies to human complement C2B

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 antibody-based molecules, including full-length antibodies, antigen-binding domains thereof, and antibody derivatives that are capable of binding to and activating human muscle-specific tyrosine protein kinase (MuSK). The present invention further discloses methods of treating neuromuscular conditions using the aforementioned MuSK antibodies.

Therapeutic musk antibodies

Antibodies that specifically bind to human complement factor C2b

FCRN antagonists and methods of use

Growing community of inventors

Destelbergen, Belgium

Christophe Blanchetot