MorphoSys granted U.S. patent on antibodies against GM-CSF to treat inflammatory disorders
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MorphoSys AG and the University of Melbourne announced today that the U.S. Patent & Trademark Office (USPTO) has confirmed that it will issue U.S. Patent No. 7,455,836, covering key uses of antibodies against GM-CSF.
The patent stems from a provisional patent application filed in the USPTO in 2000 by the University of Melbourne. In 2007, MorphoSys signed an agreement with the University of Melbourne, providing MorphoSys with an exclusive license to this patent family. The claims of the patent are directed to methods of ameliorating the effects of inflammation by administering to a patient an antibody directed against GM-CSF.
Human cytokine GM-CSF (Granulocyte macrophage-colony stimulating factor) is the target molecule of MorphoSys’s proprietary MOR103 antibody program for the treatment of rheumatoid arthritis (RA). MOR103 is the first fully human antibody against GM-CSF in clinical trials. The drug could offer an innovative treatment option for RA based on a mechanism of action distinct from anti-TNF and other competing approaches. In 2004, the market for biopharmaceuticals to treat RA amounted to US$ six billion worldwide and is expected to further increase to US$ 14 billion in 2009.
“This new patent provides us with broad protection for our proprietary antibody program MOR103 in the United States, which is by far the largest market for RA drugs”, commented Dr. Simon Moroney, Chief Executive Officer of MorphoSys AG. “Our patent portfolio around this promising antibody-based program now extends beyond the specific MOR103 lead antibody, itself, and we anticipate that MOR103 will find application in other inflammatory disorders as well.”
Rheumatoid arthritis (RA) is traditionally considered a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints and affects in particular a membrane, called synovium, which lines each movable joint. It is a disabling and painful inflammatory condition, which can lead to substantial loss of mobility due to pain and joint destruction. As a systemic disease, RA often affects extra-articular tissues throughout the body including the skin, blood vessels, heart, lungs, and muscles. The disease affects approximately 4-6 million people worldwide. In patients suffering from RA, white blood cells move from the bloodstream into the synovium. Here, these blood cells appear to play an important role in causing the synovial membrane to become inflamed. The HuCAL-based antibody MOR103 targets GM-CSF as a means to treat inflammatory diseases such as psoriasis, multiple sclerosis (MS), chronic obstructive pulmonary disease (COPD), asthma, and especially RA. The granulocyte macrophage colony-stimulating factor (GM-CSF) stimulates stem cells to produce granulocytes and macrophages and subsequently activates these differentiated immune cells. GM-CSF is part of the natural immune and inflammatory cascade but has also been identified as an inflammatory mediator in autoimmune disorders like RA leading to an increased production of pro-inflammatory cytokines, chemokines and proteases and thereby ultimately to articular destruction. By neutralizing GM-CSF the HuCAL-based antibody MOR103 reduces undesired proliferation and activation of inflammatory granulocytes and macrophages and intervenes in several pathophysiological pathways.
MorphoSys AG and Galapagos NV announced today the launch of a long term co-development alliance aimed at discovering and developing antibody therapies based on novel modes of action in bone and joint disease, including rheumatoid arthritis, osteoporosis and osteoarthritis. The alliance spans all activities from target discovery through to completion of proof of concept clinical
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Rheumatoid arthritis is a painful, inflammatory type of arthritis that occurs when the body’s immune system attacks itself. A new paper, published in this week’s issue of PLoS Biology, reports a breakthrough in the understanding of how autoimmune responses can be controlled, offering a promising new strategy for therapy development for rheumatoid arthritis. Normally, immune
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