Alexion Pharmaceuticals and XOMA Form Collaboration
Thursday December 18, 6:30 am ET
- Product Development Efforts to Focus on TPO Mimetic Antibody -
CHESHIRE, Conn. and BERKELEY, Calif., Dec. 18 /PRNewswire-FirstCall/ -- Alexion Pharmaceuticals, Inc. (Nasdaq: ALXN - News) and XOMA Ltd. (Nasdaq: XOMA - News) today announced a collaborative agreement for the development and commercialization of a rationally designed human c-MPL agonist antibody to treat chemotherapy-induced thrombocytopenia. The compound was discovered at Alexion Antibody Technologies (AAT), a wholly owned subsidiary of Alexion, and is in preclinical development. The c-MPL antibody was designed to mimic the activity of human thrombopoietin (TPO), a naturally occurring protein responsible for platelet production. Thrombocytopenia is an abnormal blood condition in which the number of platelets is reduced, potentially leading to bleeding complications.
"This collaboration combines XOMA's bacterial cell expression technology and its strong process development and manufacturing capabilities with Alexion's expertise in antibody engineering, providing the best development means for this compound," said Stephen P. Squinto, Ph.D., Executive Vice President and Head of Research. "This also marks a milestone for AAT and demonstrates the progression of our pipeline; we are pleased to be moving this antibody forward jointly with XOMA."
"We're enthusiastic about working with Alexion. By collaborating with them, we gain access to a promising product candidate and Alexion's antibody engineering and development expertise," John L. Castello, XOMA's Chief Executive Officer, President and Chairman said. "The c-MPL agonist antibody is particularly well suited to our process development capabilities, including our bacterial cell expression system. By combining the strengths of our two companies, we hope to accelerate getting this product into the clinic and ultimately potential marketing approval."
Under the terms of the agreement, Alexion and XOMA will jointly develop and commercialize the c-MPL agonist antibody for chemotherapy-induced thrombocytopenia. The parties will share development and commercialization expenses, including preclinical and clinical development, manufacturing and marketing costs world-wide, as well as revenues, generally on a 70-30 basis, with Alexion retaining the larger portion. In addition, Alexion will receive payments tied to initiation of the collaboration and achievement of a regulatory milestone. XOMA will be entitled to royalty payments and milestones related to its bacterial expression technology. Specific financial terms were not disclosed. The collaboration will initially focus on preclinical, process development and scale-up work, with initial clinical testing anticipated in 2005.
About the TPO Mimetic Antibodies
The rationally designed human c-MPL agonist antibody is part of a new class of therapeutic antibodies that function as receptor agonists that can stimulate their cell target, rather than blocking it, and were created using a rational design and selection process proprietary to AAT. The first rationally designed human antibody of this new class was designed to accelerate the return of blood platelet levels to normal following a toxic assault on the bone marrow, which commonly results in cancer patients undergoing chemotherapy. The TPO agonist antibody has been designed to bind to and stimulate the c-MPL receptor on the surface of platelet precursors and then to stimulate platelet-specific proliferation with a specificity and activity similar to the body's own natural platelet hormone, thrombopoietin. However, this antibody lacks any protein sequences related to native thrombopoietin, providing additional therapeutic benefit by potentially eliminating the harmful immune responses that have been associated with recombinant thrombopoietin. Alexion recently presented the status of its rationally designed human c-MPL agonist program at the American Society of Hematology Meeting held in December 2003 in San Diego. Administration of the antibody showed an increase in platelets to normal levels in an animal model following chemotherapy, without production of neutralizing antibodies against native thrombopoeitin. An abstract of the presentation, made by Dr. Yi Wang, PhD., Senior Director of Preclinical sciences at Alexion, is available at the Society's website, www.hematology.org
About Chemotherapy-induced thrombocytopenia
Chemotherapy-induced thrombocytopenia is a disease state where a patient's clot forming platelets are depleted as a byproduct of treatment with chemotherapeutic agents. Certain drugs used as chemotherapeutic agents are known to eliminate cells that are a part of the pathway that leads to formation of platelets. These cells, known as megakaryocytes, are found in the bone marrow and are the precursor cells to platelets. Platelets play a critical role in the formation of blood clots and act by sticking together at the site of a wound to help stop the blood flow out of the wound. The normal level of platelets usually is in excess of the level required to support normal clot formation. However, following chemotherapy, these levels can fall to a level that requires blood transfusions to protect the patient from excessive bleeding. |
