The present invention is based, in part, on the discovery of anti-SIGLEC-9 composition (e.g., monoclonal antibodies and antigen-binding fragments thereof), that regulate myeloid cell inflammatory phenotypes, such as suppressive myeloid cells, monocytes, macrophages, neutrophils, and/or dendritic cells, including polarization, activation, and/or function, and methods of using such anti-SIGLEC-9 compositions for therapeutic, diagnostic, prognostic, and screening purposes.

In one aspect, the invention provides methods of inhibiting the effects of MASP-2-dependent complement activation in a living subject suffering from, or at risk for developing a thrombotic microangiopathy (TMA). The methods comprise the step of administering, to a subject in need thereof, an amount of a MASP-2 inhibitory agent effective to inhibit MASP-2-dependent complement activation. In some embodiments, the MASP-2 inhibitory agent inhibits cellular injury associated with MASP-2-mediated alternative complement pathway activation, while leaving the classical (C1q-dependent) pathway component of the immune system intact.

The present invention relates to modified antibodies. In particular, the present invention relates to recombinant monoclonal antibodies having altered ability to induce direct cell death and effector function. In addition, the present invention relates to nucleic acid molecules encoding such antibodies, and vectors and host cells comprising such nucleic acid molecules. The invention further relates to methods for producing the antibodies of the invention, and to methods of using these antibodies in treatment of disease.

The present invention relates to methods for the treatment of a bone fracture or bone defect. The invention discloses the effective use of an anti-gremlin-1 antibody to accelerate the healing and bridging of bone tissue in segmental gap defects; and demonstrates that inhibitors of gremlin-1 activity may provide improved therapies for treating or preventing fracture non-union.

The present disclosure is directed to antibodies binding to human respiratory syncytial virus F protein, including both neutralizing and non-neutralizing antibodies, and methods for use thereof.

Provided herein are isolated antibodies or antibody fragments thereof that immunospecifically bind to platelet factor 4 (PF4). In some embodiments the isolated antibodies or antigen-binding fragments thereof comprise a light chain CDR and framework region comprising SEQ ID NO: 4 and a heavy chain CDR and framework region comprising SEQ ID NO: 10. Also provided herein are methods for treating heparin-induced thrombocytopenia (HIT) and methods for reducing the likelihood that subject will become afflicted with HIT. Further disclosed are uses of the isolated antibodies or antibody fragments in the treatment of HIT or the manufacture of compositions for the treatment of HIT.

The present disclosure is directed to antibodies binding to PD-L1 and methods of using such antibodies to treat cancers, such as those that express or overexpress PD-L1.

Disclosed herein are polynucleic acid molecules, pharmaceutical compositions, and methods for treating Facioscapulohumeral muscular dystrophy.

The present application relates to antibodies which bind specifically to chelated radionuclides, including bispecific antibodies. It further relates to the use of such bispecific antibodies in applications such as radioimmunoimaging and radioimmunotherapy. It additionally relates to clearing agents and compositions useful in such methods. The chelated radionuclides may be a DOTAM-lead (Pb) chelate.

The present disclosure relates to an isolated antibody or antigen-binding fragment thereof that binds to human Sema3A. The isolated antibody or antigen-binding fragment according to the present disclosure i) binds to human Sema3A of the sequence of SEQ ID NO: 600 with a dissociation constant (KD)≤50 nM, ≤20 nM, ≤10 nM, ≤1 nM, or ≤0.1 nM; ii) cross-reacts with mouse, cynomolgus, rat, pig and/or dog Sema3A, particularly wherein said isolated antibody or antigen-binding fragment thereof binds to mouse, cynomolgus, rat, pig and/or dog Sema3A with a dissociation constant (KD)≤50 nM, ≤20 nM, ≤10 nM, ≤1 nM, or ≤0.1 nM; iii) binds to human Sema3A of the sequence of SEQ ID NO: 600 with a binding activity as measured by surface plasmon resonance (SPR) of ≥60%, ≥70%, ≥80%, or ≥90%; iv) inhibits the activity of human Sema3A of the sequence of SEQ ID NO: 600 in an in vitro mesangial cell migration assay with an EC50 of ≤10 nM, ≤5 nM, ≤2.5 nM, or ≤1 nM; v) inhibits the activity of human Sema3A of the sequence of SEQ ID NO: 600 in an in vitro growth cone collapse assay with an EC50 of ≤50 nM, ≤25 nM, ≤10 nM, or ≤5 nM; vi) inhibits the activity of human Sema3A of the sequence of SEQ ID NO: 600 in an in vitro HUVEC repulsion assay with an EC50 of ≤1 nM, or ≤0.3 nM, ≤0.1 nM, ≤0.07 nM, ≤0.06 nM and/or vii) exhibits an increased potency against cellular Sema3A, of the sequence of SEQ ID NO: 600, induced HUVEC repulsion.