Abstract: Disclosed are combination therapies comprising administration of a CD73 inhibitor and an adenosine A2A or A2B receptor inhibitor. The disclosed combination therapies are useful in the treatment of diseases related to the activity of adenosine receptors and/or CD73 including, for example, cancer, inflammatory diseases, cardiovascular diseases, and neurodegenerative diseases. Anti-CD73 antibodies and A2A/A2B inhibitors are also disclosed.

Abstract: The present disclosure relates to novel PD-1 binding domains that have a higher binding affinity for human PD-1 than a reference PD-1 binding domain. The PD-1 binding domains of the present disclosure further provide a comparable, or equal or higher, potency in blocking ligand binding to human PD-1 than a reference PD-1 antibody. The present disclosure further relates to binding moieties comprising such PD-1 binding domains. Also provided is a method for treating a disease, in particular a disease associated with a suppressed immune system, such as cancer, with a PD-1 binding domain or binding moiety of the present disclosure. The present disclosure further relates to nucleic acids encoding the heavy chain variable region of the PD-1 binding domains, and a vector and cell comprising such nucleic acid.

Abstract: The present disclosure relates to novel PD-1 binding domains that have a higher binding affinity for human PD-1 than a reference PD-1 binding domain. The PD-1 binding domains of the present disclosure further provide a comparable, or equal or higher, potency in blocking ligand binding to human PD-1 than a reference PD-1 antibody. The present disclosure further relates to binding moieties comprising such PD-1 binding domains. Also provided is a method for treating a disease, in particular a disease associated with a suppressed immune system, such as cancer, with a PD-1 binding domain or binding moiety of the present disclosure. The present disclosure further relates to nucleic acids encoding the heavy chain variable region of the PD-1 binding domains, and a vector and cell comprising such nucleic acid.

Abstract: Anti-CD73 antibodies are disclosed. Also disclosed are related nucleic acids, vectors, cells, and pharmaceutical compositions. Methods of treating cancer with the anti-CD73 antibodies are also disclosed.

Abstract: Disclosed are combination therapies comprising administration of a CD73 inhibitor and an adenosine A2A or A2B receptor inhibitor. The disclosed combination therapies are useful in the treatment of diseases related to the activity of adenosine receptors and/or CD73 including, for example, cancer, inflammatory diseases, cardiovascular diseases, and neurodegenerative diseases. Anti-CD73 antibodies and A2A/A2B inhibitors are also disclosed.

Abstract: Anti-CD73 antibodies are disclosed. Also disclosed are related nucleic acids, vectors, cells, and pharmaceutical compositions. Methods of treating cancer with the anti-CD73 antibodies are also disclosed.

Abstract: The present disclosure relates to novel PD-1 binding domains that have a higher binding affinity for human PD-1 than a reference PD-1 binding domain. The PD-1 binding domains of the present disclosure further provide a comparable, or equal or higher, potency in blocking ligand binding to human PD-1 than a reference PD-1 antibody. The present disclosure further relates to binding moieties comprising such PD-1 binding domains. Also provided is a method for treating a disease, in particular a disease associated with a suppressed immune system, such as cancer, with a PD-1 binding domain or binding moiety of the present disclosure. The present disclosure further relates to nucleic acids encoding the heavy chain variable region of the PD-1 binding domains, and a vector and cell comprising such nucleic acid.

Abstract: Anti-mutant calreticulin (mutCALR) antibodies are disclosed. Also disclosed are related nucleic acids, vectors, cells, kits, and pharmaceutical compositions. Methods of treating or diagnosing myeloproliferative neoplasms with the anti-mutCALR antibodies are also disclosed.

Abstract: The present disclosure relates to novel PD-1 binding domains that have a higher binding affinity for human PD-1 than a reference PD-1 binding domain. The PD-1 binding domains of the present disclosure further provide a comparable, or equal or higher, potency in blocking ligand binding to human PD-1 than a reference PD-1 antibody. The present disclosure further relates to binding moieties comprising such PD-1 binding domains. Also provided is a method for treating a disease, in particular a disease associated with a suppressed immune system, such as cancer, with a PD-1 binding domain or binding moiety of the present disclosure. The present disclosure further relates to nucleic acids encoding the heavy chain variable region of the PD-1 binding domains, and a vector and cell comprising such nucleic acid.

Abstract: Antibodies and antigen binding fragments thereof directed against Staphylococcus aureus (S. aureus) surface determinant antigens and secreted toxins are disclosed. Methods of detecting, diagnosing and treating S. aureus using the antibodies and antigen binding fragments thereof are also provided.

Abstract: Disclosed are combination therapies comprising administration of a CD73 inhibitor, an adenosine A2A or A2B receptor inhibitor, and a PD-1/PD-L1 inhibitor. The disclosed combination therapies are useful in the treatment of diseases related to the activity of adenosine receptors and/or CD73 and/or PD-1/PD-L1 including, for example, cancer, inflammatory diseases, cardiovascular diseases, and neurodegenerative diseases. Anti-CD73 antibodies, PD-1/PD-L1 inhibitors, and A2A/A2B inhibitors are also disclosed.

Abstract: Disclosed are combination therapies comprising administration of a CD73 inhibitor and an adenosine A2A or A2B receptor inhibitor. The disclosed combination therapies are useful in the treatment of diseases related to the activity of adenosine receptors and/or CD73 including, for example, cancer, inflammatory diseases, cardiovascular diseases, and neurodegenerative diseases. Anti-CD73 antibodies and A2A/A2B inhibitors are also disclosed.

Abstract: Anti-CD73 antibodies are disclosed. Also disclosed are related nucleic acids, vectors, cells, and pharmaceutical compositions. Methods of treating cancer with the anti-CD73 antibodies are also disclosed.

Abstract: The present application provides methods of treating cancer using a combination of an inhibitor of A2A and/or A2B and an inhibitor of PD-1 and/or PD-L1.

Abstract: Antibodies and antigen binding fragments thereof directed against Staphylococcus aureus (S. aureus) surface determinant antigens and secreted toxins are disclosed. Methods of detecting, diagnosing and treating S. aureus using the antibodies and antigen binding fragments thereof are also provided.

Abstract: Antibodies and antigen binding fragments thereof directed against Staphylococcus aureus (S. aureus) surface determinant antigens and secreted toxins are disclosed. Methods of detecting, diagnosing and treating S. aureus using the antibodies and antigen binding fragments thereof are also provided.

Abstract: Antibodies and antigen binding fragments thereof directed against Staphylococcus aureus (S. aureus) surface determinant antigens and secreted toxins are disclosed. Methods of detecting, diagnosing and treating S. aureus using the antibodies and antigen binding fragments thereof are also provided.

Abstract: Antibodies and antigen binding fragments thereof directed against Staphylococcus aureus (S. aureus) surface determinant antigens and secreted toxins are disclosed. Methods of detecting, diagnosing and treating S. aureus using the antibodies and antigen binding fragments thereof are also provided.

Abstract: Antibodies and antigen binding fragments thereof directed against Staphylococcus aureus (S. aureus) surface determinant antigens and secreted toxins are disclosed. Methods of detecting, diagnosing and treating S. aureus using the antibodies and antigen binding fragments thereof are also provided.

Abstract: Stabilized variable regions of the T cell receptor and methods of making the same using directed evolution through yeast display are provided. In one embodiment, the variable region is variable beta. In one embodiment, the stabilized T cell receptor variable regions have high affinity for a superantigen, such as TSST-1 or SEB. These T cell receptor variable regions are useful as therapeutics.