Bispecific antibodies which comprise one antigen-binding region binding to an epitope of human epidermal growth factor receptor 2 (HER2) and one antigen-binding region binding to human CD3, and related antibody-based compositions and molecules, are disclosed. Pharmaceutical compositions comprising the antibodies and methods for preparing and using the antibodies are also disclosed.

Provided herein are antibodies that specifically bind Tau and methods of using the same.

The present invention relates to antigen-binding compounds that inhibit the enzymatic activity of soluble human 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.

The present invention provides novel full-length human antibodies that bind to human Fc epsilon-R1 alpha (monospecific antibodies). The present invention also provides novel bispecific antibodies (bsAbs) that bind to both Fc epsilon-R1 alpha and CD3 and activate T cells via the CD3 complex in the presence of Fc epsilon-R1 alpha-expressing cells. The bispecific antigen-binding molecules of the invention are useful for the treatment of diseases and disorders in which an upregulated or induced Fc epsilon-R1 alpha-targeted immune response is desired and/or therapeutically beneficial. For example, the bispecific antibodies of the invention are useful for the treatment of allergies, including anaphylaxis.

Described herein are methods for producing and utilizing an alternative signal 1 domain to construct an optimally signaling CAR. Alternative signal 1 domains of the present technology are based on alternatives to CD3ζ, including mutated ITAMs from CD3ζ (which contains 3 IT AM motifs), truncations of CD3ζ, and alternative splice variants known as CD3s, CD3 theta, and artificial constructs engineered to express fusions between CD3s or CD30 and CD3ζ. CAR polypeptides comprising alternative signal 1 domains are utilized to engineer CAR T cells. Further, this technology related to methods of treating cancer by administering to a subject in need thereof CAR T cells comprising alternative signal 1 domains.

This invention relates to inhibition of the complement signaling using an anti-C5 antibody. Specifically, the invention relates to methods of treating a complement-mediated disease or complement-mediated disorder in an individual by contacting the individual with an anti-C5 antibody.

The present invention relates to the fields of antibodies, antigen binding fragments and immunodiagnostics. Specifically, the invention relates to a recombinant anti-body or antigen binding fragment for binding thyroid hormone T4 (thyroxine) and halogenated bisphenol A. Also, the present invention relates to an isolated nucleic acid molecule comprising a nucleotide sequence that encodes the recombinant antibody or antigen binding fragment of the present invention, as well as an ex-pression vector and host cell comprising the nucleic acid molecule of the present invention. Still, the present invention relates to a method of producing a recombi-nant antibody or antigen binding fragment for binding T4 thyroid hormone and hal-ogenated bisphenol A, a test kit and an immunoassay comprising the recombinant antibody or antigen binding fragment of the present invention, and a method for determining T4 thyroid hormone and/or halogenated bisphenol A levels in a sam-ple of a subject. Still further, the present invention relates to a method of treating a sample, e.g. an immunoaffinity-based sample preparation method for enrich-ment of the halogenated bisphenol A from a sample.

Disclosed herein are humanized antibodies in which human germline residues are introduces to the complementarity determining regions (CDRs) of a non-human donor antibody. Also described herein are libraries of antibody variable domains (e.g., phage-display libraries) and methods for screening for humanized antibodies.

Expression of lambda antibody light chain with non-native leader sequence, wherein light chain is sequence-engineered to restore native N terminus. Immunoglobulin lambda variable domain sequence comprising N terminal deletion for expression with non-native N terminal signal peptide.

Provided are CD3 binding molecules that specifically bind to CD3, for example monospecific binding molecules that specifically bind to CD3 and multispecific binding molecules (MBMs) that specifically bind to CD3 and a tumor-associated antigen, conjugates comprising the CD3 binding molecules, and pharmaceutical compositions comprising the CD3 binding molecules and conjugates. Provided are methods of using the CD3 binding molecules, conjugates, and pharmaceutical compositions to activate T cells in a subject, for example a subject having a cancer or autoimmune disease. Provided are recombinant host cells engineered to express the CD3 binding molecules and methods of producing the CD3 binding molecules by culturing the host cells under conditions in which the CD3 binding molecules are expressed.