Abstract: The present invention provides anti-KDR monoclonal antibodies and related compositions, which may be used in any of a variety of therapeutic methods for the treatment of a variety of cancers, rheumatoid arthritis, diabetic retinopathy and other diseases associated with aberrant VEGF or KDR expression and/or activity.

Abstract: The present invention is directed to optimized anti-CD3 variable sequences for use in a variety of bispecific formats, including those that utilize scFv components. The invention further relates to nucleic acids encoding for the polypeptide, to vectors comprising the same and to host cells comprising the vector. In another aspect, the invention provides for a pharmaceutical composition comprising the mentioned polypeptide and medical uses of the polypeptide.

Abstract: The present invention relates to the discovery that the disruption of inflammasome function leads to an altered microbiota that affects the development and progression of inflammatory diseases and disorders. Thus, the invention relates to compositions and methods for detecting and determining the relative proportions of the constituents of a subject's microbiota, methods of modifying an altered microbiota population in a subject, and compositions and methods for treating inflammatory diseases and disorders in a subject in need thereof.

Abstract: Antibody formulations are described comprising a mixture of a non-reducing sugar, an anti-?4?7 antibody and at least one amino acid. The disclosed formulations have improved stability, reduced aggregate formation, and may retard degradation of the anti-?4?7 antibody therein or exhibit any combinations thereof. The present invention further provides a safe dosing regimen of these antibody formulations that is easy to follow, and which results in a therapeutically effective amount of the anti-?4?7 anti body in vivo.

Abstract: In an aspect, a method of augmenting an immune response in a subject in need thereof, comprising identifying the subject, and treating the subject to inhibit the immune suppressive effect of CD71+ cells is provided. Further provided is a method of preventing, treating or ameliorating an infection in a subject, comprising administering to the subject an agent that reduces the level of CD71+ cells in the subject.

Abstract: The present invention provides antibodies which bind to CXC chemokine receptor 4 (CXCR4) and which do not induce significant apoptosis of CXCR4 expressing cells. Also provided are inter alia immunoconjugates and compositions comprising such antibodies and methods and uses involving such antibodies, particularly in the medical and diagnostic fields.

Abstract: The present invention provides monoclonal antibodies which specifically recognize the shorter A? peptides obtained after cleavage of the APP protein mediated by ?-secretase, i.e. the A?-peptide fragments A?1-37, A?3-37, A?3p-37, A?1-37 and A?11p-37, and other like fragments ending at the 37th amino acid of APP, hereinafter also referred to as the A?x-37 peptides. It further provides hybridoma cells producing the monoclonal antibodies as well as methods for producing the antibodies and the hybridoma cells; and an immunoassay for an A?x-37 peptide by a competitive method or a sandwich method using the antibody of the present invention; and methods for measuring the level of A?x-37 peptides in a sample, such as a biological sample.

Abstract: The present invention concerns methods for treating progressive multiple sclerosis (MS) in a patient, and an article of manufacture with instructions for such use.

Abstract: Antibodies and fragments thereof have high affinity for human ?-synuclein protofibrils and low binding of ?-synuclein monomers, wherein the antibodies or fragments have specified Complementarity Determining Region (CDR) sequences. Compositions comprise such an antibody or fragment and methods of detecting ?-synuclein protofibrils use such an antibody or fragment. In further embodiments, methods of preventing, delaying onset of or treating a neurodegenerative disorder with ?-synuclein pathology comprise administering such an antibody or fragment, and such an antibody or fragment is used in the manufacture of a pharmaceutical composition for treatment of a neurodegenerative disorder with ?-synuclein pathology. Such an antibody or fragment is used in the diagnosis or monitoring of the development of a neurodegenerative disorder with ?-synuclein pathology, and in methods for reducing or inhibiting ?-synuclein aggregation by administration of such an antibody or fragment.

Abstract: The use of anti-CD20 antibodies as in vivo purging agents for patients receiving bone marrow or peripheral blood stem cell transplant during treatment of B-cell-related diseases, e.g., B-cell lymphomas or leukemias, is disclosed. Such purging may enhance engraftment and/or prevent disease relapse in such patients.

Abstract: The current invention is directed to particulate or vesicular immunomodulators, like e.g. cytokines, for use in combination therapy with antibodies for treatments of a range of conditions and diseases, in particular cancer, as well as methods, compositions, and kits thereof.

Abstract: This invention relates to a novel target for production of immune and non-immune based therapeutics and for disease diagnosis. More particularly, the invention provides therapeutic antibodies against VSIG1, ILDR1, LOC253012, AI216611, C1ORF32 or FXYD3 antigens, which are predicted co-stimulatory family members and which are differentially expressed in cancers including, lung cancer, ovarian cancer, and colon cancer, and diagnostic and therapeutic usages. The use of these antibodies for modulating B7 costimulation and related therapies such as the treatment of autoimmunity are also provided. This invention further relates to the discovery of extracellular domains of VSIG1 and its variants, FXYD3 and its variants, ILDR1 and its variants, LOC253012 and its variants, AI216611 and its variants, and C1ORF32 and its variants awhich are suitable targets for immunotherapy, cancer therapy, and drug development.

Abstract: This invention provides monoclonal antibodies that recognize the Toll-like Receptor 4/MD-2 receptor complex, and monoclonal antibodies that recognize the TLR4/MD2 complex as well as TLR4 when not complexed with MD-2. The invention further provides methods of using the monoclonal antibodies as therapeutics. This invention also provides soluble chimeric proteins, methods of expressing and purifying soluble chimeric proteins, and methods of using soluble chimeric proteins as therapeutics, in screening assays and in the production of antibodies.

Abstract: The present invention relates to antibodies (including anti-B7-H4 antibodies) and their antigen-binding fragments and to other molecules (including fusion proteins that bind to the cognate antigen/receptor, etc.) that are capable of immunospecifically binding to B7-H4 and the uses of such molecules in the diagnosis and the treatment of cancer and other diseases. The invention particularly concerns the use of such molecules to retard or prevent tumor growth, inhibit tumor-mediated suppression, eliminate tumors and/or deplete or block the activity of tumor associated macrophages (“TAMs”) so as to alter their activity and/or decrease TAM—mediated immune suppression.

Abstract: The present disclosure is directed to methods of treating and preventing breast cancer or recurrence of breast cancer with compositions comprising anti-progastrin antibodies.

Abstract: The present invention relates to an antibody binding to the domain 2 of human intercellular adhesion molecules-1 (ICAM-1) where the antibody is able to modulate the differentiation status of dendritic cells and induce antigen-specific T cell tolerance, thereby be effective in the prevention and/or treatment of T cell-mediated immune disorders such as transplantation rejection, graft-versus-host disease, and autoimmune disease. In addition, the present invention provides a pharmaceutical composition comprising the antibody, and method of using them for the treatment of disease.

Abstract: A method for manufacturing a drug-delivery composition includes providing at least one pharmaceutically active compound, a dry powder comprising at least a polymer, and an aqueous solution. The dry powder, the pharmaceutically active compound and the aqueous solution are mixed to form a paste-like or semi-solid drug-delivery composition, wherein the aqueous solution is added in an amount of less than or equal to twice the total dry mass of the dry powder.

Abstract: Methods for treating or preventing neointima stenosis are disclosed. The methods generally involve the use of a TGF? inhibitor, a SMAD2 inhibitor, an FGF Receptor agonist, a Let-7 agonist, or a combination thereof, to inhibit endothelial-to-mesenchymal transition (Endo-MT) of vascular endothelial cells into smooth muscle cells (SMC) at sites of endothelial damage. The disclosed methods can therefore be used to prevent or inhibit neointimal stenosis or restenosis, e.g., after angioplasty, vascular graft, or stent. Also disclosed are methods for increasing the patency of biodegradable, synthetic vascular grafts using a composition that inhibits Endo-MT. A cell-free tissue engineered vascular graft (TEVG) produced by this method is also disclosed.

Abstract: Provided are felinized antibodies and methods for treating or reducing the likelihood of developing a retroviral infection in a feline, decreasing retroviral virion entry into a feline cell, decreasing retroviral virion budding from a feline cell, or decreasing syncytium transmission in a feline. These methods require the administration of at least one felinized antibody or fragment thereof that specifically binds to CD11a and/or CD18, or ICAM-1, and/or decreases or prevents the binding of LFA-1 (CD11a/CD18 heterodimer) to ICAM-1. Also provided are veterinary compositions and methods of identifying candidate agents useful for treating or reducing retroviral infection in a feline, decreasing retroviral virion entry into a feline cell, decreasing retroviral virion budding from a feline cell, or decreasing syncytium transmission in a feline.

Abstract: The present invention relates to Death Receptor-6 (DR6) proteins which are members of the tumor necrosis factor (TNF) receptor family, and have now been shown to be important for regulating apoptosis in cells of the nervous system. In addition, it has been discovered that p75 is a ligand for DR6. As a result, this invention relates to methods for inhibiting the interaction of DR6 and p75 using DR6 and/or p75 antagonists. In addition, the methods described herein include methods of promoting survival of cells of the nervous system using DR6 antagonists, optionally in combination with p75 antagonists, and methods of treating neurodegenerative conditions by the administration of a DR6 antagonists, optionally in combination with a p75 antagonist.

Abstract: The invention provides methods for inhibiting the interaction of endosialin with endosialin ligands. The inhibition is effectuated on the genetic level, by inhibiting endosialin gene expression, and on the protein level, by blocking the interaction of cell-surface expressed endosialin with ligands such as fibronectin and collagen. The invention provides methods for identifying inhibitors of the interaction of endosialin with endosialin ligands. Also provided are methods for inhibiting angiogenesis and neovascularization in vivo and in vitro.

Abstract: Provided are a means for the prevention and treatment of obesity and/or insulin resistance and, particularly, pharmaceutical drugs for the treatment of obesity and/or insulin resistance under the influence of Follistatin-like 3 (FSTL3). Specifically, provided is an insulin resistance improving drug comprising an FSTL3 inhibitor as an active ingredient, particularly, the insulin resistance improving drug, wherein the FSTL3 inhibitor is one of (A) a substance specifically binding to FSTL3 to inhibit or suppress a function of FSTL3, (B) an inhibitor for expression of FSTL3, and (C) a competitor of FSTL3.

Abstract: Antibody formulations are described comprising a mixture of an anti-?4?7 antibody, an antioxidant or chelator, and at least one free amino acid. The disclosed formulations may have improved stability, reduced aggregate formation, or both. The present invention further provides a safe dosing regimen of these antibody formulations that is easy to follow, and which results in a therapeutically effective amount of the anti-?4?7 antibody in vivo.

Abstract: The invention relates to a biological system for diminishing cell growth or inducing selective killing of target cells, in particular pathogenic bacterial or fungal cells, or cancer cells. The biological system is based on toxin-antitoxin systems, as found in prokaryotic plasmids and their host chromosomes. The biological system comprises a vehicle with a first nucleic acid sequence or amino acid sequence encoding for a prokaryotic toxin of a prokaryotic toxin-antitoxin pair, and a second nucleic acid sequence or amino acid sequence encoding for the corresponding prokaryotic antitoxin of the prokaryotic toxin-antitoxin pair. The system is characterized in that the toxin and/or the antitoxin is operably linked to a protein output modifier (POM) that comprises a nucleic acid sequence or amino acid sequence that modifies the relative rate of transcription, mRNA stability, mRNA translatability or protein stability of the toxin and/or antitoxin.

Abstract: The present invention involves the reaction of a CD4 immuno-conjugate with a sample of patient whole blood. The CD4 immuno-conjugate consists of one or more antibodies with specificity for the CD4 surface receptor coupled to a signal moiety, or “label”, that is detectable by a flow cytometer. Such labels may generate a signal by such means as fluorescence properties, light scatter properties, electronic properties, or magnetic properties. The CD4 immuno-conjugate binds to both the CD4 positive lymphocytes (Helper T cells) and all monocytes. Differential detection means are employed to count immuno-conjugate labeled Helper T cells. The present invention distinguishes itself by simultaneously measuring the signal level from monocytes as a means to verify sufficient activity of the anti-CD4 antibody.

Abstract: The present invention relates to antibodies that differentially recognize multi-dimensional conformations of A?-derived diffusible ligands, also known as ADDLs. The antibodies of the invention can distinguish between Alzheimer's Disease and control human brain extracts and are useful in methods of detecting ADDLs and diagnosing Alzheimer's Disease. The present antibodies also block binding of ADDLs to neurons, assembly of ADDLS, and tau phosphorylation and are there useful in methods for the preventing and treating diseases associated with soluble oligomers of amyloid ? 1-42.

Abstract: The disclosure relates to methods and compositions effective in the diagnosis, prognosis and treatment of human hematopoietic cancers. In particular, the disclosure provides tumor-associated genes that encode for cytokine receptors that are differentially expressed in hematopoietic tumor cells of myeloid origin compared with other cells, e.g., normal stem cells.

Abstract: The present invention relates to an anti-CD44 monoclonal antibody formulation, a process for the preparation of said formulation and uses thereof.

Abstract: The present invention relates to methods of modulating the uptake and/or clearance of cells with a disrupted cell membrane, cells infected with a pathogen, dying cells or dead cells, or a portion thereof, which can be used to treat and/or prevent diseases such as cancer, autoimmunity and infections. The present invention also relates to methods of modulating antigen recognition, processing and/or presentation, as well as immune responses to material derived from cells with a disrupted cell membrane, cells infected with a pathogen, dying cells or dead cells, or a portion thereof. The present invention further relates to methods of detecting cells with a disrupted cell membrane, cells infected with a pathogen, dying cells or dead cells, or a portion thereof.

Abstract: Methods of treating or delaying onset of a neurodegenerative disorder with ?-synuclein pathology in an individual comprise administering an antibody which is produced from a stabilized soluble ?-synuclein oligomer and capable of binding a stabilized soluble ?-synuclein oligomer, the stabilized soluble ?-synuclein oligomer having a lower formation rate to a non-soluble aggregated form than a non-stabilized soluble oligomer of the ?-synuclein. The antibody has been collected from a non-human animal to which stabilized soluble ?-synuclein oligomer had been administered or has been produced by hybridoma technology, phage display, ribosome display, mammalian cell display or bacterial display, and the disorder with ?-synuclein pathology is characterized by deposition of Lewy bodies and Lewy neurites or is selected from the group consisting of Parkinson's disease (PD), dementia with Lewy bodies (DLB), the Lewy body variant of Alzheimer's disease, and multiple system atrophy (MSA).

Abstract: Methods are disclosed for increasing the binding affinity of binding proteins using in silico affinity maturation.

Abstract: The present invention relates to antibodies targeting complement protein C5 and compositions and methods of use thereof.

Abstract: Provided are a wide concentration range, especially high concentration, substantially salt-free anti-prolactin receptor antibody formulations that are substantially isosmotic and of low viscosity.

Abstract: The present invention provides, among other aspects, methods for the treatment of Alzheimer's disease in a subject in need thereof, the method including administration of a therapeutically effective amount of a pooled human immunoglobulin G (IgG) composition to a subject with moderately severe Alzheimer's disease, a subject carrying an ApoE4 allele, or both, where the amount of pooled human IgG is from 300 mg/kg to 800 mg/kg body weight of the subject per two week period, and where the amount is administered in one or more doses during the two week period after initiation of a therapeutic regimen. Also provided, are methods for selecting a treatment regimen for a subject with Alzheimer's disease, including diagnosing the severity of the Alzheimer's disease, determining if the subject carries an APOE4 allele, or both, and assigning a treatment regimen including administration of pooled human immunoglobulin G and/or an anti-beta amyloid monoclonal antibody.

Abstract: The present invention relates to agent selected from the group consisting of an anti-S100B antibody, an anti-S100B aptamer or an inhibitor of S100B gene expression for use in a method for reducing airway hyperresponse in a subject in need thereof. The present invention also relates to a method for determining whether a subject is at risk of having or developing an airway hyperresonse comprising determining the level of S100B protein in a biological sample obtained from said subject.

Abstract: The present disclosure relates generally to compositions and methods for treating cancer with a glucopyranosyl lipid A (GLA) in the absence of antigen.

Abstract: Provided herein is are methods of reducing the number and severity of acute exacerbations of asthma in an asthma patient, comprising administering to a patient with a history of acute exacerbations of asthma an effective amount of an anti-interleukin-5 receptor (IL-5R) antibody or antigen-binding fragment thereof, for example, an anti-IL-5R? antibody or antigen-binding fragment thereof, e.g., benralizumab.

Abstract: This invention relates to methods of inducing differential stress resistance in a subject with cancer by starving the subject for a short term, administering a cell growth inhibitor to the subject, or reducing the caloric or glucose intake by the subject. The induced differential stress resistance results in improved resistance to cytotoxicity in normal cells, which, in turn, reduces cytotoxic side-effects due to chemotherapy, as well as improved effectiveness of chemotherapeutic agents.

Abstract: The present invention relates to anti-CD277 antibodies which: activates or inhibit the cytolytic function of Vy9/V?2 T cells, and/or costimulates T cells together with CD3-TCR, and/or costimulates T cells in addition to CD28-B7 costimulation, and/or increases the activity and/or survival of monocytes and dendritic cells. The invention also relates to the use of said antibodies in therapy.

Abstract: Disclosed are embryonic stem cells and motor neurons derived from mice carrying transgenic alleles of the normal or mutant human SOD1 gene. Also disclosed are in vitro systems employing such SOD1 transgenic motor neurons for the study of neural degenerative disease.

Abstract: The present invention relates to Interleukin-17 ligand and receptor family members and the discovery that IL-17 receptor A and IL-17 receptor C form a heteromeric receptor complex that is biologically active. Antagonists of the IL-17RA-IL-17RB heteromeric receptor complex are disclosed, as well as various methods of use.

Abstract: There is provided a method of treating a subject afflicted with a condition that is associated with inappropriate trafficking of cells expressing alpha4beta7 to the gastrointestinal tract, comprising administering to the subject an alpha4beta7 heterodimer specific antibody in an amount and at an interval sufficient to ameliorate the condition.

Abstract: The present invention provides an antigenically restricted subset of the highly variant PfEMP1 rosetting antigen which possess epitopes which may be exploited to raise immune responses effective against many diverse strains and isolates of the malaria parasite, Plasmodium falciparum. In this regard, the invention provides one or more P. falciparum Erythrocyte Membrane Protein-1 (PfEMP1) antigen(s) or a fragment or fragments thereof, for use in raising immune responses in humans.

Abstract: The present invention provides anti-IL-6R monoclonal antibodies and related compositions, which may be used in any of a variety of therapeutic methods for the treatment of rheumatoid arthritis and other diseases.

Abstract: A method of treating an angiogenesis related disease or disorder in a subject in need thereof is disclosed. The method comprises administering to the subject a therapeutically effective amount of an agent which regulates an amount of apolipoprotein B (ApoB), and/or an ability of ApoB to transcriptionally control vascular endothelial growth factor receptor 1 (VEGFR1).

Abstract: The present invention provides novel antibodies to human ADORA2A.

Abstract: Provided herein are methods for transporting an active agent (e.g., a therapeutic agent or an imaging agent) across the blood-brain barrier (BBB) in a patient. For example, the methods provided herein can be used to treat a brain disease in a patient, such as brain cancer. In some embodiments, the methods provided herein can be used to image the central nervous system of a patient.

Abstract: The present invention relates to pharmaceutical and medical technologies, and more particularly to novel nanobodies against pulmonary surfactant protein A (SP-A) and their preparation methods. The nanobodies of the present invention comprises an amino acid sequence having certain formula. The present invention also relates to nucleic acid sequences encoding the nanobodies, their preparation method and their applications. Immunohistochemistry and in vivo imaging show that the nanobodies of the present inventions have high lung-targeting specificity.

Abstract: Described herein are MCAM antagonists, including MCAM antagonist antibodies capable of inhibiting the interaction between MCAM and it ligand, a laminin ?4 chain, e.g., an ?4 chain of laminin 411. These MCAM antagonists, e.g., anti-MCAM antibodies, may be useful to treat neuroinflammatory conditions, for example, multiple sclerosis and Parkinson's disease, by inhibiting the infiltration of MCAM-expressing cells into the central nervous system (CNS), e.g., extravasation of TH17 cells into the CNS.

Abstract: The invention encompasses compounds having formula I-V and the compositions and methods using these compounds in the treatment of conditions in which modulation of the JAK pathway or inhibition of JAK kinases, particularly JAK3, may be therapeutically useful.