Antibody-based therapy for cancer has become established and is considered as one of the most successful and important strategies for treating patients with hematological malignancies and solid tumors. However, their success is often limited by the tumors’ ability to evade destruction by upregulating masking molecules. For example, in lymphoma, cancer cells upregulate complement regulatory proteins (CRPs) to avoid clearance by complement dependent cytotoxicity (CDC), a mechanism that rituximab therapy utilizes for tumor cell killing in non-Hodgkins lymphoma. BRM132, a unique and novel combination of: 1) a recombinant protein based on the adenovirus serotype 35 fiber knob (AD35K); and 2) rituximab, has the potential to overcome rituximab-resistance of cancer cells in patients. Binding of AD35K recombinant protein to CRPs causes internalization and removal of CRPs from the cell surface, which subsequently restore the sensitivity of cancer cells to rituximab therapy.
BRM132 MOA Video