Genetically modified mice are provided that express human variable (hV) sequences, including mice that express hV sequences from an endogenous mouse light chain locus, mice that express hV sequences from an endogenous mouse light chain locus, and mice that express hV sequences from a transgene or an episome wherein the hV sequence is linked to a mouse constant sequence. Mice are provided that are a source of somatically mutated human variable sequences useful for making antigen-binding proteins. Compositions and methods for making antigen-binding proteins that comprise human variable sequences, including human antibodies, are provided.

This invention pertains to monovalent agents, including Fab fragments and monovalent monoclonal antibodies analogous to MetMab, having binding specificity to human Nerve Growth Factor (NGF), and methods of treating pain in an individual wherein there is no substantial increase in the inflammatory response of the individual following administration of the monovalent agents.

A pharmaceutical composition for treating or preventing at least one disease selected from the group consisting of inflammatory bowel disease and intestinal tumor, the pharmaceutical composition comprising a dendritic cell immunoreceptor inhibitor or a binding inhibitor between a dendritic cell immunoreceptor and an asialo-biantennary N-glycan, and a pharmaceutically acceptable carrier.

Heterodimerizing domains with orthogonal mutations that drive heterodimerization, in particular heterodimerizing antibody CH3 domains, heterodimeric polypeptides comprising such heterodimerizing domains, and antibody constructs comprising such heterodimeric polypeptides, are provided.

The present invention discloses methods and platforms for generating protein binding proteins with specificity for native peptide-MHC (pMHC) complexes. The pMHC binding proteins can be used in bi-specific antibodies or for generating CAR T cells capable of binding to peptides bound to specific MHC alleles.

This disclosure relates to anti-Natriuretic Peptide Receptor 1 (NPR1) antibodies including agonist antibodies which are able to activate the NPR1 receptor, pharmaceutical compositions comprising the same, and methods of treatment comprising the same.

The disclosure pertains to antibodies that bind A-beta oligomers and methods of making and using said antibodies. Also provided are chimeric or humanized antibodies, including antibodies having CDRs in Table 2 and/or having a sequence as set forth in Table 4B or a sequence with at least 50% sequence identity thereto optionally wherein the CDR amino acid sequences are as set for forth in SEQ ID Nos: 74-79. Also provided are methods and uses thereof as well as kits comprising said antibodies.

Provided by the present invention are a bispecific T-cell engager, recombinant oncolytic virus thereof, and use thereof. The present invention provides an CD47 and CD3 bispecific T-cell engager. The present invention also provides an isolated nucleic acid molecule that encodes said bispecific T-cell engager. The present invention also provides an expression framework of said bispecific T-cell engager BiTE. The present invention also provides a recombinant oncolytic virus, and said oncolytic virus is operably inserted with or contains the expression framework of said bispecific T-cell engager BiTE. In the present invention, the bispecific T-cell engager is combined with the oncolytic virus, and in comparison with pure gene therapy or virotherapy, the oncolytic virus significantly enhances the inhibition capability on malignant tumors.

The present invention relates to methods and formulations useful for reducing the reconstitution time of lyophilized polypeptides.

The present invention provides, among other things, anti-Flt-1 antibodies and methods for treating muscular dystrophy, in particular, Duchenne muscular dystrophy (DMD). In some embodiments, a method according to the present invention includes administering to an individual who is suffering from or susceptible to DMD an effective amount of an anti-Flt-1 antibody or antigen-binding protein thereof such that at least one symptom or feature of DMD is reduced in intensity, severity, or frequency, or has delayed onset.