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.

Provided are bispecific and multi-specific antibodies that target both claudin 18.2 (CLDN18.2) and 4-1BB. These antibodies, in the absence of CLDN18.2-expressing cells, can bind to 4-1BB but are unable to activate 4-1BB signaling. In the presence of CLDN18.2-expressing cells, however, these antibodies can trigger CLDN18.2-dependent 4-1BB signaling, leading to potent immune response to the CLDN18.2-expressing tumor cells.

Provided are bispecific and multi-specific antibodies that target both claudin 18.2 (CLDN18.2) and 4-1BB. These antibodies, in the absence of CLDN18.2-expressing cells, can bind to 4-1BB but are unable to activate 4-1BB signaling. In the presence of CLDN18.2-expressing cells, however, these antibodies can trigger CLDN18.2-dependent 4-1BB signaling, leading to potent immune response to the CLDN18.2-expressing tumor cells.

The invention features methods for preventing or treating CGRP associated disorders such as vasomotor symptoms, including headaches (e.g., migraine, cluster headache, and tension headache) and hot flushes, by administering an anti-CGRP antagonist antibody. Antagonist antibody G1 and antibodies derived from G1 directed to CGRP are also described.

The present invention relates to CD3-binding molecules capable of binding to human and non-human CD3, and in particular to such molecules that are cross-reactive with CD3 of a non-human mammal (e.g., a cynomolgus monkey). The invention also pertains to uses of such antibodies and antigen-binding fragments in the treatment of cancer, autoimmune and/or inflammatory diseases and other conditions.

The present invention provides caninized human anti-human IL-4Rα antibodies that have specific sequences and a high binding affinity for canine IL-4Rα. The invention also relates to use of these antibodies in the treatment of dogs against atopic dermatitis.

The present invention relates to antigen-binding compounds that inhibit CD39. The invention also relates to cells producing such compounds; methods of making such compounds, and antibodies, fragments, variants, and derivatives thereof; pharmaceutical compositions comprising the same; methods of using the compounds to diagnose, treat or prevent diseases, e.g. cancer.

This invention relates to anti-LAG-3 antibodies and methods of using them in treating diseases and conditions that benefit from modulating LAG-3 activity, e.g., cancer.

The present application relates to optimized IgG immunoglobulin variants, engineering methods for their generation, and their application, particularly for therapeutic purposes.

Herein is reported a method for the production of a polypeptide that is biologically active as n-mer comprising a nucleic acid encoding a fusion polypeptide according to the following formula (B.sub.n-CS.sub.o-I.sub.s-CS.sub.p-FC-CS.sub.q-I.sub.t-CS.sub.r-B.sub.m).sub.u, wherein B denotes a polypeptide that is biologically active as n-mer and forms non-defined aggregates/multimers upon expression in the absence of a fused Fc-region, FC denotes a heavy chain Fc-region polypeptide, CS denotes a cleavage site, and I denotes an intervening amino acid sequence, wherein FC does not substantially bind to an Fc-receptor, recovering the fusion polypeptide from the cell or the cultivation medium, optionally cleaving the fusion polypeptide with a protease, and thereby producing a polypeptide that is biologically active as n-mer and forms non-defined aggregates/multimers upon expression in the absence of a fused Fc-region.