Antibodies are provided that specifically bind seven human ELR.sup.+ CXC chemokines. The antibodies of the invention are useful for treating various inflammatory/autoimmune diseases, such as inflammatory bowel disease (IBD), plaque psoriasis, and palmoplantar pustulosis; and cancer, such as renal cancer or ovarian cancer.

The present invention is directed to antibodies and fragments thereof (especially chimeric and humanized) having binding specificity for HGF and their use in therapy and diagnosis. These antibodies inhibit or block HGF-associated activities including HGF's effects on cell proliferation, invasion, angiogenesis, metastasis and fibrosis. Particularly the antibodies may be used as a monotherapy or in combination therapies in treating cancer, other proliferative disorders and other conditions wherein inhibition of HGF and/or the HGF/HGF-R (c-met) interaction is desired.

The invention provides improved non-human vertebrates and non-vertebrate cells capable of expressing antibodies comprising human variable region sequences. The present invention is directed to the provision of long HCDR3s from non-human vertebrates and cells. The present invention is also directed to the provision of novel V, D and J pairings in immunoglobulin heavy and light chain loci. Novel, biased antibody diversities and potentially expanded diversities are provided. The invention also provides for novel and potentially expanded diversity or diversity that is biased towards variable gene usage common to antibodies useful for treating and/or preventing certain diseases or conditions, such as infectious diseases. The invention also provides methods of generating antibodies using such vertebrates, as well as the antibodies per se, therapeutic compositions thereof and uses.

Disclosed herein are low immunogenic human anti-TNF-α antibodies which can inhibit the apopotosis of cells induced by TNF-α. The invented low immunogenic human anti-TNF-α antibodies are capable of binding to TNF-α specifically. The invention presents the human anti-TNF-α antibodies which bind to TNF-α with similar affinities as Adalimumab. Most importantly, the invented human anti-TNF-α antibodies showed reduced immunogenicities in vivo, which made them safer candidate for antibody drug and other biotherapy. The invention also features method of de-immunogenicity of antibody drugs by identification, replacement of high immunogenic FR sequence(s) of the human antibody with low immunogenic FR sequences from other human IgGs, and significantly reduce the risk of human anti-human immunogenicity and improve the efficacy of antibody drugs.

Provided is a biomarker for diagnosing at-risk mental state (ARMS) that may include one or more selected from the group consisting of biopyrrin, cortisol, a KFLC or a fragment thereof, and a AFLC or a fragment thereof. Further provided is an ARMS diagnosis of a subject that may be performed quickly, easily, and accurately by measuring the amount of the biomarker for diagnosing ARMS in a biological sample.

A bispecific epitope binding protein having a multimer of four single-chain chimeric polypeptides of two single-chain chimeric heavy chains and two single-chain chimeric light chains. The bispecific epitope binding protein has a first antigen binding domain that binds specifically to HER2 and a second antigen binding domain that binds specifically to 4-1BB.

There is disclosed a chimeric infliximab-like monoclonal antibody having at least 80% NANA glycosylation terminal sialic acid and a glycosylation pattern of Gal-α(2,3/6)-Gal that binds to tumor necrosis factor alpha (TNF). The disclosed infliximab-like monoclonal antibody is a chimeric antibody having the same amino acid sequence (light chain/heavy chain of SEQ ID NO. 1/SEQ ID NO. 2) as infliximab (Remicade®) which has at least 80% NGNA terminal sialic acid and a glycosylation pattern of Gal-α(1,3)-Gal.

There is disclosed a chimeric cetuximab-like monoclonal antibody (CMAB009 mAb) having at least 80% NANA glycosylation terminal sialic acid at an N-glycosylation site Asn297 and a glycosylation pattern of Gal-α(2,3/6)-Gal. The disclosed CMAB009 monoclonal antibody is a chimeric antibody having the same amino acid sequence (light chain/heavy chain of SEQ ID NO. 1/SEQ ID NO. 3) as cetuximab (Erbitux®) which has at least 80% NGNA terminal sialic acid and a glycosylation pattern of Gal-α(1,3)-Gal.

The present invention relates to new humanized antagonistic anti-CD40 antibodies and therapeutic and diagnostic methods and compositions for using the same.

The invention provides non-human cells and mammals having a genome encoding chimeric antibodies and methods of producing transgenic cells and mammals. Certain aspects of the invention include chimeric antibodies, humanized antibodies, pharmaceutical compositions and kits. Certain aspects of the invention also relate to diagnostic and treatment methods using the antibodies of the invention.