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Trio unites in lupus agreement
04-03-2014
by Kelsey Kaustinen  |  Email the author
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ROCKLAND, Mass.—EMD Serono, a subsidiary of Merck KGaA, has announced the signing of a research agreement with Pfizer Inc. and the Broad Institute of MIT and Harvard. The three organizations will be collaborating on the genomic profiling of patients with systemic lupus erythematosus (SLE) and lupus nephritis (LN).
 
“We are thrilled to align with EMD Serono and Pfizer on an innovative project to stratify SLE patients and identify candidate immune pathways underlying lupus nephritis,” Prof. Nir Hacohen, associate professor at Massachusetts General Hospital and Harvard Medical School, and senior associate member at the Broad Institute, said in a press release. “Technical advances now make it possible for us to sequence RNA in very small numbers of cells, enabling us to be more comprehensive in our analysis of cell types and states in lupus patients. We will collect millions of unbiased measurements from lupus patients over many time points along with key clinical variables. We will use this dataset to infer active biological pathways in these patients and develop novel dynamic models of Lupus pathogenesis.”
 
Per the terms of the agreement, EMD Serono and Pfizer will jointly fund the project, and will receive real-time access to all data and analysis. Both companies will also have the option of sending a research scientist to the Broad Institute to add their expertise in computational and experimental genomic profiling.
 
For its part, the Broad Institute will be investigating clinical samples obtained from SLE and LN patients through biochemical and next-generation sequencing technologies as well as the analysis of immune cell subpopulations. The aim of this research agreement is the identification of biomarkers that can help to better define target patient populations for future therapies. The project will also seek to use computational modeling approaches to identify key molecular drivers of SLE and LN kidney flares and in conjunction, potential novel drug targets that could serve as the basis of new therapies.
 
“The research group of Prof. Nir Hacohen from the Broad Institute is a pioneer in the field of systems immunology and has developed a unique strategy to dissect Lupus and Lupus Nephritis,” Harsukh Parmar, head of the Translational Innovation Platform Immunology & Neurodegenerative Diseases at EMD Serono, commented in a statement. “Combined with the Broad Institute’s technical know-how, we see this collaboration aiming for a significant contribution to potential future innovative treatments of Lupus and Lupus Nephritis. This is in line with our concept to integrate genomic profiling and system biology approaches throughout our preclinical and clinical programs.”
 
SLE is a systemic autoimmune disease that can cause LN, inflammation of the kidney. According to the American College of Rheumatology, SLE “can affect the skin, joints, kidneys, lungs, nervous system and other organs of the body,” with most patients suffering from symptoms such as fatigue, rashes, arthritis and fever. Lupus is the result of the immune system misfiring, producing something known as “autoantibodies,” which attack a person’s healthy tissues rather than biological intruders such as viruses. The American College of Rheumatology notes that SLE affects 10 times as many women as it does men, and there is currently no cure.
 
“We are pleased to collaborate with EMD Serono and the Broad Institute on research designed to enhance our understanding of the molecular and cellular underpinnings of Lupus, a debilitating disease that has long been a mystery to the scientific community,” said Johan Lund, senior vice president and chief scientific officer of Immunoscience at Pfizer. “This collaboration builds on Pfizer's patient-centric and precision medicine-based approach to autoimmune disease research, applying cutting edge technologies and a wealth of patient level data with a goal of advancing our understanding of disease in order to develop innovative therapies.”
 
Code: E04021401

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