Abstract: Diagnosis, treatment and prophylaxis of diseases and conditions associated with smooth muscle cell (SMC) dysfunction are provided through the inhibition of IL-11-mediated signalling.

Abstract: The invention provides methods and dosing regimens for safely and effectively treating androgen-dependent prostate cancer with a gonadotrophin releasing hormone (GnRH) antagonist without causing a testosterone spike and/or other side effect of GnRH agonist therapy such as a urinary tract infection, or an arthralgia-related or cardiovascular side effect. The present disclosure also provides for methods for treating prostate cancer in a patient with a history of at least one cardiovascular event, wherein administration of degarelix to the subject decreases the likelihood of developing or experiencing an additional cardiovascular event compared to treatment with a gonadotrophin releasing hormone (GnRH) agonist.

Abstract: The present invention provides a PEGylated IFN-? variant and a composition for preventing or treating hyperproliferative diseases, inflammatory diseases, autoimmune diseases or viral infectious diseases, the composition comprising the PEGylated IFN-? variant as an effective ingredient. The PEGylated IFN-? variant of the present invention has an excellent anti-viral efficacy, immune regulatory function and anti-cell growth efficacy by virtue of better pharmacokinetic properties compared to native IFN-? and non-PEGylated IFN-? variants, and therefore can be used usefully against various diseases. The present invention provides good patient convenience in terms of administration due to exhibition of an excellent pharmacological activity effect upon administration and a significant increase of half-life in blood over existing interferon formulations.

Abstract: A mutant thyroid stimulating hormone receptor (TSHR) or fragment thereof comprises one or more mutations, wherein the mutant TSHR has increased thermostability with respect to the equivalent wild type TSHR or fragment. The one or more mutation is preferably within the extracellular leucine-rich repeat domain (LRD) of the TSHR, or within residues 22 to 260 (TSHR260) of the TSHR, or may be in the transmembrane domain (TMD), A mutant TSHR or fragment thereof of the invention preferably consists of, or consists essentially of, the subdomain TSHR260 of the TSHR receptor. A mutant TSHR or fragment thereof according to the invention has a greater thermostability than the equivalent wild type TSHR or fragment as determined by its half-life at a given temperature, and can be purified whilst retaining activity. A mutant TSHR or fragment thereof according to the invention may also be deglycosylated whilst retaining activity.

Abstract: The present invention relates to CXCR6-transduced (a) T cell(s) such as (a) CD8+ T cell(s), (a) CD4+ T cell(s), (a) CD3+ T cell(s), (a) ?? T cell(s) or (a) natural killer (NK) T cell(s) for targeted tumor therapy, nucleic acid sequences, vectors capable of transducing such (a) T cell(s), (a) transduced T cell(s) carrying the nucleic acid sequences or vectors of the present invention, methods and kits comprising the nucleic acid sequences or vectors of the present invention. The invention also provides the use of said transduced T cell(s) in a method for the treatment of diseases characterized by CXCL16 overexpression as well as a pharmaceutical composition/medicament comprising (a) transduced T cell(s) expressing the CXCR6 for use in methods of treating diseases characterized by CXCL16 overexpression.

Abstract: The present invention provides compositions and methods for treating cancer in a human. The invention relates to targeting the stromal cell population in a tumor microenvironment. For example, in one embodiment, the invention provides a composition that is targeted to fibroblast activation protein (FAP). The invention includes a chimeric antigen receptor (CAR) which comprises an anti-FAP domain, a transmembrane domain, and a CD3zeta signaling domain.

Abstract: In various embodiments methods of producing a cell population enriched for CLEC9A+ dendritic cells are provided where the methods involve culturing stem cells and/or progenitor cells in a cell culture comprising culture medium, a notch ligand, stem cell factor (SCF), FLT3 ligand (FLT3L); thrombopoietin (TPO); and IL-3 and/or GMCSF.

Abstract: The invention relates to antibodies, and in particular, to antibodies exhibiting specificity for Receptor tyrosine kinase-like Orphan Receptors (ROR), and to uses thereof for example in the treatment of cancer. The invention extends to polynucleotide and polypeptide sequences encoding the antibodies, and therapeutic uses thereof, and to diagnostic kits comprising these molecules. The invention also extends to antibody-drug conjugates and to uses thereof in therapy.

Abstract: It is an object of the present invention to provide an antibody that binds to a human PGE2 receptor subtype EP4 and inhibits the function of EP4, or a functional fragment thereof. It is another object of the present invention to provide a medicament comprising the aforementioned antibody or a functional fragment thereof. Mice were immunized with the human PGE2 receptor subtype EP4, and a monoclonal antibody that suppresses the intracellular cAMP level increase induced by EP4 was screened. In addition, the CDR sequences of the obtained monoclonal antibody were determined.

Abstract: The present invention relates to a method for quantifying an anti-TNF antibody in a sample of a human individual comprising a step of adding to a test sample which may contain therapeutic anti-TNF antibodies a known amount of two or more labeled forms of said anti-TNF antibodies.

Abstract: The present invention relates, in general, to pattern-recognition receptors (PRRs), including toll-like receptors (TLRs), and, in particular, to a method of inhibiting nucleic acid-induced activation of, for example, endosomal TLRs using an agent that binds to the nucleic acid (“nucleic acid binding agent”), preferably, in a manner that is independent of the nucleotide sequence, the chemistry (e.g., DNA or RNA, with or without base or sugar modifications) and/or the structure (e.g., double-stranded or single-stranded, complexed or uncomplexed with, for example protein) of the nucleic acid(s) responsible for inducing TLR activation. The invention also relates to methods of identifying nucleic acid binding agents suitable for use in such methods.

Abstract: Provided herein are immunomodulatory proteins comprising ICOSL variants and nucleic acids encoding such proteins. The immunomodulatory proteins provide therapeutic utility for a variety of immunological and oncological conditions. Compositions and methods for making and using such proteins are provided.

Abstract: The present invention relates to antibodies with specificity for FGFR1. More particularly, the invention relates to monoclonal antibodies that bind specifically to and neutralize human, macaque and mouse forms of FGFR1 with high affinity. The invention also relates to nucleic acids encoding said antibodies, vectors for expression of these nucleic acids, and host cells for producing said antibodies. Further, the invention relates to the use of said antibodies in the diagnosis and/or treatment of cancers.

Abstract: The present disclosure relates to a novel polypeptide having an activity of exporting 5?-inosine monophosphate, a microorganism comprising the same, a method for preparing 5?-inosine monophosphate using the same, and a method for increasing export of 5?-inosine monophosphate.

Abstract: Provided are a method of efficiently producing an sIL-2R antigen in an amount necessary for antibody generation, and a method of producing an anti-sIL-2R antibody using the antigen. Specifically, provided are a method of producing soluble interleukin-2 receptor, including culturing SCC-3 cells and recovering soluble interleukin-2 receptor from a culture of the cells, and a method of producing an anti-soluble interleukin-2 receptor antibody, including immunizing an animal with sIL-2R produced by the method.

Abstract: The present invention relates to the use of receptor tyrosine kinase (RTK) oligomers as markers of RTK activation and signalling. Methods are described based upon determining the presence of RTK oligomers and/or determining the nanometre spatial separation between RTK molecules assembled as RTK oligomers at the cell surface. Such methods are directed to the monitoring of RTK activation in cells and the detection of mutations in RTKs. Methods are also described for determining prognosis for subjects having diseases characterised by aberrant RTK activation and for selecting subjects for treatment with RTK inhibitors.

Abstract: The present invention relates to isolated or purified or partially purified peptide derived molecules having the following general formula (S1): X-[(Pro)n-His-Pro-His-Ala-Arg-Ile-Lys]m-Y. The peptides are for medical use, in particular as anti-tumoral agents.

Abstract: The invention, in some aspects relates to light-activated ion channel molecules and methods for their use to alter cell activity and function. Light-activated ion channel molecules of the invention can be administered to subjects, expressed in cells, and activated with light, to alter membrane potential in the cells, and can be used in methods for assaying compounds, treating diseases and conditions, compound screening and more.

Abstract: The ?-glucan-binding protein contains an amino acid sequence represented by SEQ ID NO: 1.

Abstract: The present invention relates to a method for quantifying a therapeutic antibody in a sample of a human individual comprising a step of adding to a test sample which may contain therapeutic antibodies to be quantified a known amount of two or more labeled forms of said therapeutic antibodies.