118 results about "Immunotoxin" patented technology

The present invention described and shown in the specification and drawings provides novel recombinant DT-based immunotoxins, and, more specifically anti-T cell immunotoxin fusion proteins. Also provided are immunotoxins that can be expressed in bacterial, yeast, or mammalian cells. The invention also provides means for expression of the immunotoxin fusion protein.

The invention provides antibodies to a mutant form of the epidermal growth factor receptor known as EGFRvIII found only or primarily on the surface of glioblastoma cells, and on cells of breast, ovarian and non-small cell lung carcinomas. The antibodies provided by the invention have the complementarity determining regions (“CDRs”) of the scFv designated MR1, but with mutations at positions 98 and 99 in the CDR3 of the heavy chain variable region and, optionally, in other CDRs. In particular, the invention provides an antibody, designated MR1-1, which mutates MR1 in the CDR3 of the VH and VL chains. The invention provides additional antibodies in which MR1 is mutated in the CDR1 and 2 of VH or VL, or both.

An objective of the present invention is to provide a therapeutic agent for treating rheumatoid arthritis, juvenile rheumatoid arthritis, macrophage activation syndrome, septicemia, and FR-β expressing leukemia, which induces apoptosis in activated macrophages and folate receptor beta (FR-β) expressing leukemia cells to specifically destroy these cells. An FR-β monoclonal antibody of the present invention is preferably an IgG-type monoclonal antibody which specifically reacts with a human-type FR-β antigen and is produced from a clone resulting from immunization with an FR-β expressing B300-19 cell. The FR-β monoclonal antibody of the present invention specifically reacts with the FR-β antigen of activated macrophages and FR-β expressing leukemia cells and a therapeutic agent of the present invention contains an FR-β antibody immunotoxin which causes apoptosis in activated macrophages and FR-β expressing leukemia cells, as an active ingredient. Further, suitable administration form for the therapeutic agent of the present invention includes intravenous injection as well as joint injection in the case of therapeutic agents for rheumatoid arthritis and juvenile arthritis.

The present invention relates to immunotoxins, that effectively kill malignant cells having a given surface marker and nucleic acid constructs encoding them. These reagents comprise a toxic moiety that is derived from a Rana pipiens protein having ribonucleolytic activity linked to an antibody capable of specific binding with a chosen tumor cell.

The OX-40 antigen is characterized and claimed together with variants and derivatives thereof. Also described are binding agents for the antigen and the use of these in diagnosis and therapy. Examples of such use include a method for the selective depletion of activated CD4+ T-cells in vivo by using immunotoxins comprising an OX-40 antibody conjugated to a toxic molecule (such as Ricin-A chain). The administration of these specific immunotoxins is used therapeutically to deplete autoimmune reactive CD4+ T-cells which have been implicated in diseases including Multiple Sclerosis, Rheumatoid Arthritis, Sarcoidosis, and Autoimmune Uveitis as well as inflammatory bowel disease and graft-versus-host disease. This type of therapy is also beneficial for eradicating CD4+ T-cell lymphomas and alloreactive CD4+ T-cells involved with a transplantation reaction. The use of the human form of the OX-40 antibody will also help in the early diagnosis of all the diseases mentioned above.

The present invention concerns methods of reducing the antigenicity of a proteinaceous compound while maintaining the compounds biological activity, as well as proteinaceous compositions with biological activity but reduced antigenicity. These methods and compositions have significant benefits to a subject in need of such compounds and compositions. Also included are modified toxin compounds that are truncated and/or possess reduce antigenicity. Such designer toxins have therapeutic, diagnostic, and preventative benefits, particularly as immunotoxins. Methods of treating cancer using these immunotoxins are provided.

The invention relates to nucleic acid molecules encoding preproproteins having after maturation the biological activity of the mistletoe lectin dimer, to vectors comprising these nucleic acid molecules, to hosts transformed with said vectors and to polypeptides and/or polypeptide dimers which are encoded by these nucleic acid molecules. The polypeptides and/or polypeptide dimers of the invention are widely therapeutically applicable. Thus, the present invention further relates to immunotoxins as well as to pharmaceutical compositions that contain the polypeptides and/or the polypeptide dimers of the invention. Additionally, the invention relates to diagnostic compositions comprising the nucleic acid molecules of the invention, the polypeptides and/or the polypeptide dimers of the invention and/or primers which hybridize specifically to the nucleic acid molecules of the invention. Finally, the invention relates to plant protective agents comprising the polypeptides of the invention and/or the polypeptide dimers of the invention.

The invention provides uses and methods for alleviating respiratory tract symptoms of allergy, asthma, and of viral, bacterial, fungal and parasitic infections by shifting inappropriate TH2 responses to TH1 responses by administering IL-13 receptor-targeted immunotoxins to the respiratory tract.

The present invention relates to polymer conjugates of SS1P, and methods of making using the same.

Compositions and methods for treatment of focal muscle spasms. Immunotoxin conjugates comprise a toxin conjugated to an antibody reactive to a muscle specific antigen.

The present invention provides a modified toxin having an ETA moiety that has the furin site replaced with a cancer-associated protease site. The present invention also provides modified immunotoxins having a ligand that binds to a cancer cell attached to an ETA moiety that has the furin site replaced with a cancer-associated protease site. Also provided are a method of inhibiting or destroying mammalian cancer cells using the immunotoxins of the invention and pharmaceutical compositions for treating human cancer.

The present invention relates to a polynucleotide construct encoding a fusion protein consisting of a domain which binds the immunoglobulin Fc region, genetically fused to a truncated form of Pseudomonas exotoxin A (PE). In particular, the invention discloses the fusion protein, ZZ-PE38, and further provides immunotoxins, formed from complexes of the fusion protein with antibodies for targeted cell killing.

The present invention provides novel means and methods for treating unwanted side effects in transplantations, such as GVHD and allograft rejection. The invention provides immunotoxins comprising an antibody and a toxic substance, whereby cocktails of such conjugates are directed to different targets associated with one population of cells, wherein one target is chosen from CD3 or CD7. The preferred combination is a cocktail directed against both CD3 and CD7.

The invention is directed to an immunotoxin directed at fetal AchR, wherein the immunotoxin may comprises a human Fab fragment based on a human autoantibody or human combinatorial cDNA library and may be a pseudomonas exotoxin A-based single chain Fv IT (35-scFV-ETA). The invention is further directed to method of treating a patient with soft tissue tumour comprising the step of exposing the patient to the immunotoxin of the invention.

Isolated human monoclonal antibodies and antigen-binding portions thereof which specifically bind to dendritic cells are disclosed. Also disclosed are bispecifics, immunotoxins and antigen conjugates which include the antibodies or antibody portions. The human antibodies can be produced in a non-human transgenic animal, e.g., a transgenic mouse, capable of producing multiple isotypes of human monoclonal antibodies by undergoing V-D-J recombination and isotype switching. Also disclosed are pharmaceutical compositions comprising the human antibodies, non-human transgenic animals and hybridomas which produce the human antibodies, and therapeutic and diagnostic methods for using the human antibodies.

The present invention provides methods to produce immunotoxins (ITs) and cytokines with a reduced ability to promote vascular leak syndrome (VLS). The invention also provides ITs and cytokines which have been mutated to lack amino acid sequences which induce VLS. Also disclosed are methods for producing peptides that inhibit the induction of VLS by ITs and cytokines. Also disclosed are peptides comprising the (x)D(y) sequence to promote the extravasation of other molecules. Toxins mutated in the (x)D(y) motif or active site residues are disclosed for used in vaccines.