Patent classifications
G01N2333/7151
ATYPICAL HEMOLYTIC UREMIC SYNDROME (AHUS) BIOMARKER PROTEINS
The disclosure provides biomarker proteins, a change in the concentration or activity level of which are associated with atypical hemolytic uremic syndrome (aHUS) or clinically meaningful treatment of aHUS with a complement inhibitor. Also provided are compositions and methods for interrogating the concentration and/or activity of one or more of the biomarker proteins in a biological fluid. The compositions and methods are useful for, among other things, evaluating risk for developing aHUS, diagnosing aHUS, determining whether a subject is experiencing the first acute presentation of aHUS, monitoring progression or abatement of aHUS, and/or monitoring response to treatment with a complement inhibitor or optimizing such treatment.
Antibodies against glucocorticoid-induced tumor necrosis factor receptor (GITR) and uses thereof
Provided herein are antibodies, or antigen binding portions thereof, that bind to glucocorticoid-inducible TNF receptor (GITR). Also provided are uses of these proteins in therapeutic applications, such as in the treatment of cancer. Further provided are cells that produce the antibodies, polynucleotides encoding the heavy and/or light chain variable region of the antibodies, and vectors comprising the polynucleotides encoding the heavy and/or light chain variable region of the antibodies.
A COMPOSITION COMPRISING MESENCHYMAL PRECURSOR OR STEM CELLS AND THEIR USE
The present disclosure relates to improved cellular compositions and potency assays for obtaining the same. Such compositions and assays may be suitable for use in treating various inflammatory disorders.
ANTIBODY
It has been demonstrated that certain compounds bind to TNF and stabilise a conformation of trimeric TNF that binds to the TNF receptor. Antibodies which selectively bind to complexes of such compounds with TNF superfamily members are disclosed. These antibodies may be used to detect further compounds with the same activity, and as target engagement biomarker.
MECHANISM OF ACTION
The invention is in the field of TNF signalling. Compounds have been identified which are capable of modulating signalling of TNF trimers through receptors. Methods of identifying such compounds are therefore provided. The compounds themselves have utility in therapy.
Antibodies binding to trimeric TNF alpha epitopes
It has been demonstrated that certain compounds bind to TNF and stabilise a conformation of trimeric TNF that binds to the TNF receptor. Antibodies which selectively bind to complexes of such compounds with TNF superfamily members are disclosed. These antibodies may be used to detect further compounds with the same activity, and as target engagement biomarker.
Complexes between anti-TNF antibodies, trimeric TNF proteins and organic molecules binding them
It has been demonstrated that certain compounds bind to TNF and stabilise a conformation of trimeric TNF that binds to the TNF receptor. Antibodies which selectively bind to complexes of such compounds with TNF superfamily members are disclosed. These antibodies may be used to detect further compounds with the same activity, and as target engagement biomarker.
Biomarker-based methods for aiding the diagnosis of stroke
The present invention provides biomarker-based methods for diagnosing stroke in a patient suspected of having suffered a stroke, and also for discriminating between ischemic stroke and transient ischemic attack. Substrates comprising probes for specific combinations of biomarkers useful in the methods of the invention are also described.
METHOD FOR THE SELECTION OF ANTIBODIES AGAINST BCMA
An antibody specifically binding to human BCMA, characterized in that the binding of said antibody is not reduced by APRIL and not reduced by BAFF, said antibody does not alter APRIL-dependent NF-B activation, BAFF-dependent NF-B activation, and does not alter NF-B activation without BAFF and APRIL is useful as a therapeutic agent.
NOVEL TNFa STRUCTURE FOR USE IN THERAPY
A new, stable trimeric TNF structure is disclosed with distorted symmetry which can bind to the TNFR1 receptor to attenuate signalling therefrom, which can be used in the treatment and/or prevention of diseases associated with the soluble TNF/TNFR1 interaction. Membrane-bound TNF is not affected in its ability to signal through TNFR2, and thus the new structure of TNF may be used in therapies which do not significantly raise the risk of infection or malignancy.