Epratuzumab's Mechanism Of Action Featured In Blood, Official Journal Of The American Society Of Hematology

MORRIS PLAINS, N.J., Oct. 25, 2013 (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 announced that an article published yesterday in Blood described a mechanism by which epratuzumab affects B cells. Epratuzumab is a humanized anti-CD22 antibody currently in Phase III trials conducted by the Company's corporate partner, UCB (Euronext Brussels:UCB), as a therapeutic for patients with systemic lupus erythematosus (lupus).

The article was authored by several scientists of the Company, as well as a clinical collaborator, Dr. Daniel J. Wallace of Cedars-Sinai Medical Center of UCLA in Los Angeles, CA. The article was featured on the cover of this issue of Blood with a fluorescence microscopy image, showing how epratuzumab can translocate certain surface proteins on B cells to other blood cells, a process called trogocytosis.

Accompanying the article was an invited commentary by Dr. Ronald P. Taylor of the University of Virginia School of Medicine, who is a pioneer on studies of trogocytosis involving anti-B-cell antibodies, such as rituximab.

In the article by Rossi and colleagues of Immunomedics, it was demonstrated that epratuzumab can induce trogocytosis of CD22, CD21, CD19, and several other B-cell surface molecules from lymphocytes to other blood cells, such as monocytes, natural killer cells, and granulocytes. Epratuzumab is distinct from other B-cell antibodies, such as rituximab, because it does not drastically deplete B cells, but instead compromises B-cell autoimmune activity.

The Immunomedics scientists postulated that removal of CD22, CD19, CD21 and other proteins from the surface of B cells reduces the autoimmune activity of these cells. In fact, B cells obtained from lupus patients who were treated with epratuzumab showed reduced CD22, CD19 and CD21. The authors suggest that this modulation of B cells via trogocytosis could be the major mechanism of epratuzumab in patients with lupus.

If you liked this article you might like

Kite Takeover by Gilead Lifts Biotech Stocks

Biotech Movers: Immunomedics, Aerie, Exelixis

Immunomedics, Seattle Genetics Scrap License Deal

Biotech Movers: Immunomedics Shares Jump After License Pact with Seattle Genetics Is Terminated

Bullish and Bearish Reversals for This Week