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 a multispecific binding moiety comprising a PD-1 binding domain and a TGF-?RII binding domain, wherein the PD-1 binding domain blocks PD-1 mediated signaling and the TGF-?RII binding domain blocks TGF-?RII-mediated signaling. The present disclosure further relates to a pharmaceutical composition comprising such multispecific binding moiety, a method of treatment using such multispecific binding moiety, and a cell producing such multispecific binding moiety.

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 multispecific binding moieties comprising novel PD-1 binding domains that have a higher binding affinity for human PD-1 than a reference PD-1 binding domain. Such multispecific binding moieties 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 in particular relates to multispecific binding moieties comprising a novel PD-1 binding domain and a LAG-3 binding domain. Also provided is a method for treating a disease, in particular a disease associated with a suppressed immune system, such as cancer, with a multispecific binding moiety of the present disclosure. The present disclosure further relates to a vector and cell comprising nucleic acids encoding a novel PD-1 binding domain and a LAG-3 binding domain.

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.