|BITR2101||TNFR2||Oncology / Infectious Disease||IND Enabling|
|BITD401412||CD40||Autoimmunity / Inflammation||Lead Optimization|
|Undisclosed||CD27||Autoimmunity / Inflammation||Discovery|
Tumor necrosis factor receptor 2 (TNFR2) is expressed on the most potent population of TNFR2 regulatory T cells (Tregs) in the tumor microenvironment. The TNFR2 epitope is densely expressed on the immunosuppressive Tregs that protect tumors and play a role in resistance to checkpoint inhibitors, including PD1 and CTLA4. TNFR2 is also expressed on the surface of certain cancers as an NFkB-driven growth receptor oncogene.
CD40 is a tumor necrosis factor receptor (TNFR) superfamily member that mediates T-dependent B cell responses and efficient T cell priming. CD40 has been identified as playing a role in autoimmune diseases in which activated T and B cells cause pathology, including autoimmune thyroiditis, type 1 diabetes, inflammatory bowel disease, psoriasis, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus.
Chronic infections, as well as some acute infections, can become disguised once inside the host, inducing suppression of the host response through Tregs. BITT has developed an approach to infectious disease that targets the host Tregs, not the microorganism, through TNFR2 antagonism. This approach has two major advantages. First, it avoids issues related to antibiotic resistance and, second, it provides a platform to target multiple infectious diseases (i.e., it is not specific to a particular pathogen).