The present invention relates to single-domain antibodies (sdAbs) directed against Leukocyte immunoglobulin-like receptor subfamily B member 2 (LILRB2), pharmaceutical compositions comprising

The invention provides anti-cluster of differentiation 3 (CD3) antibodies and methods of using the same.

Provided herein are methods for generating conjugated immunoglobulins, the method comprising: decapping a cysteine at amino acid position 80 (“Cys80”) in a light chain variable region of an immunoglobulin, wherein the immunoglobulin comprises a heavy chain variable region and the light chain variable region; and conjugating a thiol-reactive compound to the Cys80, wherein the thiol-reactive compound comprises a thiol-reactive group. Antigen-binding molecules and methods for generating the same, immunoglobulins as well as nucleic acid molecules encoding the immunoglobulins and host cells comprising the nucleic acid molecules, conjugated immunoglobulins, and light chain variable regions for use in a conjugated immunoglobulin are also provided.

The present disclosure relates to methods for treating Thyroid Eye Disease (e.g., Graves' Orbitopathy) using Interleukin (IL)-17 antagonists, e.g., secukinumab. Also disclosed herein are IL-17 antagonists, e.g., IL-17 antibodies, such as secukinumab, for treating patients having Thyroid Eye Disease (e.g., Graves' Orbitopathy), as well as medicaments, dosing regimens, pharmaceutical formulations, dosage forms, and kits for use in the disclosed uses and methods.

The present technology relates to the use of protein conjugates including a self-assembly and disassembly (SADA) polypeptide and a GD2-specific antigen binding domain for preventing or mitigating off-target tissue toxicity, such as brain, kidney, and/or myeloid damage, in a subject undergoing targeted alpha radioimmunotherapy. Also disclosed herein are pretargeted radioimmunotherapy (PRIT) methods that improve the durability of the anti-GD2-SADA conjugate anti-tumor response in vivo.

Provided herein are bispecific immune cell engagers with binding specificity for HLA-G and an additional antigen, including pharmaceutical compositions, diagnostic compositions, and kits.

The present disclosure provides methods for preventing, alleviating, or treating cytokine release resulting from administration of a VEGF inhibitor or side effects resulting from the cytokine release. To prevent, alleviate, or treat cytokine release or its side effects, the disclosure also provides combination therapies that use a lymphocyte-stimulating pharmaceutical agent, represented by an anti-T cell antigen-binding molecule, with a VEGF inhibitor. Among the anti-T cell antigen-binding molecules, for example, antibodies that recruit T cells as effector cells into tumor tissues are called T cell redirecting antibodies, and are known as means for treating tumors. On the other hand, when systemic cytokine production is stimulated by binding of antibodies to T cells, it is feared that this systemic action will lead to aberrations such as CRS. The present disclosure provides means for alleviating systemic cytokine production, and will enable safer use of anti-T cell antigen-binding molecules in tumor treatment.

The present application provides antibodies including antigen-binding fragment thereof that specifically recognizing Granulocyte-Macrophage Colony Stimulating Factor Receptor (GM-CSFRα). Also provided are methods of making and using these antibodies.

The invention provides antibodies that specifically bind sortilin. The antibodies inhibit or delay pathologies associated with changes in progranulin levels and associated symptomatic deterioration.

A method for generating a plurality of diverse camelid antibodies to cover functional epitopes of the target with high-resolution. Also provided is a method for generating camelid antibodies.