Abstract: 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.

Abstract: 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.

Abstract: The disclosure provides monoclonal bispecific antibodies targeting HER2 and HER3. The disclosure also provides monospecific tetravalent HER3 antigen binding antibodies. Still further provided by the disclosure are methods of treating a cancer in a subject, comprising administering to the subject a therapeutically effective amount of an antibody provided by the disclosure.

Abstract: Disclosed are methods of identifying tumor-derived exosomes as an early cancer diagnostic, as well as for staging, assessing progression and assessing therapy of cancer.

Abstract: 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.

Abstract: 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.

Abstract: The invention disclosed herein generally relates to fusion proteins for use alone or as adjuvants or antigen delivery vehicles for vaccines.

Abstract: Disclosed are methods of identifying tumor-derived exosomes as an early cancer diagnostic, as well as for staging, assessing progression and assessing therapy of cancer.

Abstract: The disclosure provides monoclonal bispecific antibodies targeting HER2 and HER3. The disclosure also provides monospecific tetravalent HER3 antigen binding antibodies. Still further provided by the disclosure are methods of treating a cancer in a subject, comprising administering to the subject a therapeutically effective amount of an antibody provided by the disclosure.

Abstract: 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.

Abstract: The present invention provides for IgG1 molecules with improved characteristics. In particular, substitution mutations are provided that, in combination, facilitate improved placental transfer, improved serum half-life and improved FcRn binding. Substitution mutations are also provided, that in combination, can be used to block FcRn function and thereby increase the clearance rates of other (endogenous or exogenous) IgGs, block placental transport of IgGs and have increased affinity/reduced pH dependence for FcRn binding.

Abstract: The present invention provides for IgG1 molecules with improved characteristics. In particular, substitution mutations are provided that, in combination, facilitate improved placental transfer, improved serum half-life and improved FcRn binding. Substitution mutations are also provided, that in combination, can be used to block FcRn function and thereby increase the clearance rates of other (endogenous or exogenous) IgGs, block placental transport of IgGs and have increased affinity/reduced pH dependence for FcRn binding.

Abstract: The present invention provides for IgG1 molecules with improved characteristics. In particular, substitution mutations are provided that, in combination, facilitate improved placental transfer, improved serum half-life and improved FcRn binding. Substitution mutations are also provided, that in combination, can be used to block FcRn function and thereby increase the clearance rates of other (endogenous or exogenous) IgGs, block placental transport of IgGs and have increased affinity/reduced pH dependence for FcRn binding.

Abstract: Disclosed are recombinant vectors encoding immunoglobulin-like domains and portions thereof, such as T-cell variable domains, antibody Fc-hinge fragments, subfragments and mutant domains with reduced biological half lives. Methods of producing large quantities of such domains, heterodimers, and fusion proteins following expression and secretion by prokaryotic host cells are also reported. Described are single chain T-cell receptors, which are folded into .beta.-pleated sheet structures similar to those of immunoglobulin variable domains; antibody Fc and Fc-hinge domains, which have the same in vivo stability as intact antibodies; and domains engineered to have reduced half lives.