The manufacturers in August 2009 announced success in early trials against SLE,[5] and started two Phase III clinical trials.
July 2015 : Both phase III trials (EMBODY1/2) for SLE failed to meet their primary endpoint.[6]
Mechanism of action
Epratuzumab binds to the glycoprotein CD22 of mature and malignant B-cells.
Elevated CD22 and other B-cell receptor (BCR) proteins are associated with SLE. "Epratuzumab's mechanism of action transfers these BCR proteins to helper cells called effector cells which reduces B-cell destruction and epratuzumab's impact on the body's immune system"[6] via a process called trogocytosis.[3] Other SLE therapies destroy B-cells which compromises the immune system.
References
^Carnahan J, Wang P, Kendall R, Chen C, Hu S, Boone T, et al. (September 2003). "Epratuzumab, a humanized monoclonal antibody targeting CD22: characterization of in vitro properties". Clinical Cancer Research. 9 (10 Pt 2): 3982S–90S. PMID14506197.