The disclosure is directed to methods and compositions for treating cancers characterized by cells comprising chimeric antigen receptors (CARs) that bind CD70 and T-cell engaging antibody molecules (TEAMs) that bind CD33, nucleic acid molecules encoding chimeric antigen receptors (CARs) that bind CD70 and/or TEAMs that bind CD33, and compositions and methods related thereto.

The disclosure is directed to methods and compositions for treating cancers characterized by cells comprising chimeric antigen receptors (CARs) that bind CD70 and T-cell engaging antibody molecules (TEAMs) that bind CD33, nucleic acid molecules encoding chimeric antigen receptors (CARs) that bind CD70 and/or TEAMs that bind CD33, and compositions and methods related thereto.

Provided herein are compositions and methods for stimulating T-cell-based anti-tumor immunity by administration of trans-vaccenic acid (TVA), an active derivative thereof, or an inhibitor of GPR43 expression or activity. In particular embodiments, TVA, a TVA derivative, or an inhibitor of GPR43 expression or activity is administered to boost an endogenous T-cell response and/or is co-administered with a T-cell-based therapy, such as immune checkpoint blockade therapies, CAR-T therapies, monoclonal antibody therapies, bispecific T-cell engagers therapies, etc.

Provided herein are compositions and methods for stimulating T-cell-based anti-tumor immunity by administration of trans-vaccenic acid (TVA), an active derivative thereof, or an inhibitor of GPR43 expression or activity. In particular embodiments, TVA, a TVA derivative, or an inhibitor of GPR43 expression or activity is administered to boost an endogenous T-cell response and/or is co-administered with a T-cell-based therapy, such as immune checkpoint blockade therapies, CAR-T therapies, monoclonal antibody therapies, bispecific T-cell engagers therapies, etc.

The invention provides cells that have an increased immune checkpoint engagement function (Immune Checkpoint Engager ICE cells). The ICE cells comprise an engager molecule' expressed on a cell surface, wherein said engager molecule engages with an immune checkpoint molecule on an immune cell, wherein said engager molecule is expressed at least at a level that protects said ICE cell from being killed by said immune cell.

The present invention provides bispecific antibody constructs of a specific Fc modality characterized by comprising a first domain binding to a target cell surface antigen, a second domain binding to an extracellular epitope of the human and/or the Macaca CD3 chain and a third domain, which is the specific Fc modality. Moreover, the invention provides a polynucleotide, encoding the antibody construct, a vector comprising this polynucleotide, host cells, expressing the construct and a pharmaceutical composition comprising the same.

The present invention provides bispecific antibody constructs of a specific Fc modality characterized by comprising a first domain binding to a target cell surface antigen, a second domain binding to an extracellular epitope of the human and/or the Macaca CD3 chain and a third domain, which is the specific Fc modality. Moreover, the invention provides a polynucleotide, encoding the antibody construct, a vector comprising this polynucleotide, host cells, expressing the construct and a pharmaceutical composition comprising the same.

The present invention relates to FcRH5 binding domains. In particular, the invention provides single domain antibodies, antibody conjugates, chimeric antigen receptors (CARs) and immune cell engagers which comprise such binding domains.

The present invention relates to FcRH5 binding domains. In particular, the invention provides single domain antibodies, antibody conjugates, chimeric antigen receptors (CARs) and immune cell engagers which comprise such binding domains.

Disclosed herein are an anti-HER2 affibody and a switch molecule including a cotinine-conjugated anti-HER2 affibody. When applied in combination with Cot-sCART, the cotinine-conjugated anti-HER2 affibody reacts with HER2-positive cells to induce immune cell activity, thereby finding advantageous applications as switch molecules in sCART therapeutic agents.