Immunomedics Inc fka IMMU

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9:03AM Immunomedics reports that epratuzumab mediates the reduction of select proteins on the surface of B cells via a process known as trogocytosis, and that such reduction could modulate B-cell activities (IMMU) 4.26 : Co reported that epratuzumab, the Company's humanized anti-CD22 antibody, mediates the reduction of select proteins on the surface of B cells via a process known as trogocytosis, and that such reduction could modulate B-cell activities.Results from this study were presented by Edmund A. Rossi, Ph.D., Executive Director, Recombinant Technology.

Epratuzumab is currently in two UCB-conducted Phase III pivotal trials for the treatment of patients with systemic lupus erythematosus. UCB holds the worldwide development rights for epratuzumab in autoimmune diseases, while the Company retains all rights in oncology. In earlier clinical studies in SLE and in non-Hodgkin lymphoma, epratuzumab has been shown to deplete about 30-40% of circulating B cells in patients. However, the mechanism of action of epratuzumab, especially its involvement in regulating B-cell antigen receptor signaling, has yet to be fully elucidated. In this preclinical study, treatment of peripheral blood mononuclear cells with epratuzumab significantly reduced the levels of select B-cell surface proteins, including CD22, CD19, CD21 and CD79b. Corroboratively, SLE patients on epratuzumab therapy also showed significantly lower levels of CD22, CD19 and CD21, compared to treatment-na?ve patients.

Another key finding from this study is the formation of immunological synapses between B cells and effector cells, such as monocytes, natural killer cells and granulocytes, induced by epratuzumab. By binding to B cells and effector cells simultaneously, epratuzumab serves as a conduit for the transfer of the BCR-associated receptors, lowering their presence on B cells.