The present invention pertains to humanized anti-Lewis Y antibodies which specifically bind to Lewis Y and do not show any cross-reactivity. Especially, the humanized anti-Lewis Y antibodies do not bind to Lewis b or any other blood group carbohydrate antigen. In particular, the present invention is directed to humanized anti-Lewis Y antibodies which are useful in the treatment of cancer.

This invention relates generally to antibodies that bind to human B and T lymphocyte attenuator (BTLA) and uses thereof. More specifically, the invention relates to agonistic antibodies that bind human BTLA and modulate its activity, and their use in treating inflammatory, autoimmune and proliferative diseases and disorders. Suitably, the antibodies also possess an Fc modification that enhances signalling through FcγR2B.

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

The claimed invention relates to treating cancer by targeting CD36, a fatty acid receptor. The claimed invention also relates to treating cancer metastases by targeting CD36. The invention involves using anti-CD36 antibodies as blockers or inhibitors of CD36 activity.

The present disclosure relates to antibodies binding to tumor discoidin domain receptor 1 (DDR1) and the uses of the antibodies in detecting and treating cancer.

Methods of treating cancer are provided that include administering glycan-interacting antibodies. Included are anti-sialyl Tn antigen antibodies and related compositions and formulations suitable to achieve desirable bioactivity, bioavailability, and toxicity levels.

The present application provides anti-CD93 constructs that bind to CD93 (e.g., anti-CD93 antibodies), nucleic acid molecules encoding an amino acid sequence of the anti-CD93, vectors comprising the nucleic acid molecules, host cells containing the vectors, methods of preparing the anti-CD93 construct, pharmaceutical compositions containing the anti-CD93 construct, and methods of using the anti-CD93 construct or compositions.

The present disclosure provides a method of treating cancer in a subject in need thereof comprising administering a checkpoint inhibitor to the subject, and administering a MALT-1 inhibitor according to an intermittent dosage regimen.

Disclosed are compositions and methods for targeted treatment of SSTR-expressing cancers. In particular, chimeric antigen receptor (CAR) polypeptides are disclosed that can be used with adoptive cell transfer to target and kill SSTR-expressing cancers. Also disclosed are immune effector cells, such as T cells or Natural Killer (NK) cells, that are engineered to express these CARs. Therefore, also disclosed are methods of providing an anti-tumor immunity in a subject with a SSTR-expressing cancer, such as a neuroendocrine tumor, that involves adoptive transfer of the disclosed immune effector cells engineered to express the disclosed CARs.

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