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-- Unique Mechanism of Action Involves Transfer of Key B-Cell Receptor Proteins From B Cells to Other White Blood Cells -- -- Study Presented at the 2012 Annual Meeting of the American Society of Hematology --
ATLANTA, Dec. 10, 2012 (GLOBE NEWSWIRE) --
Immunomedics, Inc. (Nasdaq:IMMU), a biopharmaceutical company primarily focused on the development of monoclonal antibody-based products for the targeted treatment of cancer, autoimmune and other serious diseases, today reported that its lead antibody drug candidate, epratuzumab, has a distinct way of reducing the immune response of B cells, which, in an autoimmune disease such as lupus, are responsible for producing antibodies that attack the patient's own body.
Epratuzumab is a humanized antibody targeting the CD22 receptor on B cells. Originally developed by the Company, the anti-CD22 antibody has previously demonstrated therapeutic activity in non-Hodgkin lymphoma (NHL) and systemic lupus erythematosus (SLE), and is currently in two Phase III clinical trials for the treatment of SLE (EMBODY 1 and EMBODY 2). Epratuzumab is being developed in SLE by UCB who hold the worldwide development rights for this compound in autoimmune diseases.The Company retains all rights in oncology.
While it is known that epratuzumab causes a reduction of about 45% of circulating B cells, in contrast to veltuzumab and other anti-CD20 antibodies that deplete more than 90% of B cells, the mechanism of action of epratuzumab in SLE remains to be fully understood.
Peripheral blood mononuclear cells (PBMCs) from normal donors, SLE patients, and of NHL cells spiked into normal PBMCs were used in this preclinical study. When bound to the CD22 receptor on B cells, epratuzumab promptly induced the transfer of key proteins associated with the B-cell receptor complex from B cells to other white blood cells such as monocytes, natural killer cells and granulocytes. In addition to CD22, receptors that were transferred include CD19, CD21 and CD79b. Interestingly, SLE patients currently on epratuzumab therapy showed significantly lower levels of CD22, CD19 and CD21, compared to treatment-naive patients.