Epratuzumab's B-Cell Modulation Effect Elucidated in Preclinical Study

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| Source: Immunomedics, Inc.

-- 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.

The transfer of these membrane proteins is mediated through the interaction of the tail region of epratuzumab, known as the fragment crystalline (Fc) region, and the Fc receptors on the effector cells. Furthermore, epratuzumab induces the reduction of B-cell surface proteins over a broad concentration range on healthy, malignant and lupus B cells.

Importantly, PBMCs treated with epratuzumab at concentrations ranging from 1 ng/mL to 10 mg/mL produced a U-shaped curve of CD22 with substantial dampening at concentrations lower than 10 ng/mL or greater than 1 mg/mL. These observations may explain why epratuzumab was found in a number of lymphoma and SLE clinical trials to be effective at the mid-doses given and less so at the lower or higher doses.

A similar profile was observed for CD19, which was reduced to a similar level over a broad concentration range (10 ng/mL – 100 µg/mL) of epratuzumab.

"This is the first time that epratuzumab was reported to induce a quick reduction of CD22, CD19, CD21 and CD79b on the surface of B cells," remarked Cynthia L. Sullivan, President and Chief Executive Officer. "The findings of reduced levels of CD19 are particularly interesting since elevated CD19 has been correlated with susceptibility to SLE in animal models as well as in patients," Ms. Sullivan continued. "We believe this study opens up a whole new field of science, which may help us design more effective therapeutics in autoimmune disease, determine what the right dosing might be, and in the management of the B-cell lymphomas and leukemia that express these B-cell receptors," concluded Ms. Sullivan.

About Immunomedics

Immunomedics is a New Jersey-based biopharmaceutical company primarily focused on the development of monoclonal antibody-based products for the targeted treatment of cancer, autoimmune and other serious diseases. We have developed a number of advanced proprietary technologies that allow us to create humanized antibodies that can be used either alone in unlabeled or "naked" form, or conjugated with radioactive isotopes, chemotherapeutics, cytokines or toxins, in each case to create highly targeted agents. Using these technologies, we have built a pipeline of therapeutic product candidates that utilize several different mechanisms of action. We also have a majority ownership in IBC Pharmaceuticals, Inc., which is developing a novel DOCK-AND-LOCK™ (DNL™) method with us for making fusion proteins and multifunctional antibodies, and a new method of delivering imaging and therapeutic agents selectively to disease, especially different solid cancers (colorectal, lung, pancreas, etc.), by proprietary, antibody-based, pretargeting methods. We believe that our portfolio of intellectual property, which includes approximately 209 active patents in the United States and more than 400 foreign patents, protects our product candidates and technologies. For additional information on us, please visit our website at www.immunomedics.com. The information on our website does not, however, form a part of this press release.

This release, in addition to historical information, may contain forward-looking statements made pursuant to the Private Securities Litigation Reform Act of 1995. Such statements, including statements regarding clinical trials, out-licensing arrangements (including the timing and amount of contingent payments), forecasts of future operating results, potential collaborations, and capital raising activities, involve significant risks and uncertainties and actual results could differ materially from those expressed or implied herein. Factors that could cause such differences include, but are not limited to, risks associated with any cash payment that the Company might receive in connection with a sublicense involving a third party and UCB, which is not within the Company's control, new product development (including clinical trials outcome and regulatory requirements/actions), our dependence on our licensing partners for the further development of epratuzumab and veltuzumab for non-cancer indications, competitive risks to marketed products and availability of required financing and other sources of funds on acceptable terms, if at all, as well as the risks discussed in the Company's filings with the Securities and Exchange Commission. The Company is not under any obligation, and the Company expressly disclaims any obligation, to update or alter any forward-looking statements, whether as a result of new information, future events or otherwise.

Dr. Chau Cheng
Senior Director, Investor Relations & Grant Management
(973) 605-8200, extension 123