Date: 2015-01-09
Type of information: R&D agreement
Compound:
Company: BiogenIdec (USA - MA) Columbia University Medical Center (USA - NY)
Therapeutic area: Lung diseases - Respiratory diseases - Rare diseases - Neurodegenerative diseases
Type agreement: R&D
Action mechanism:
Disease: diseases with significant unmet clinical need such as amyotrophic lateral sclerosis and idiopathic pulmonary fibrosis
Details: * On January 9, 2015, Biogen Idec and Columbia University Medical Center have formed a $30 million strategic alliance to conduct genetics discovery research on the underlying causes of disease and to identify new treatment approaches. As part of this agreement, a sequencing and analysis facility and shared postdoctoral program will be established at Columbia to support collaborative genetics studies. The new facility will have broad genetic research capabilities and the capacity to launch and complete whole-genome sequencing projects rapidly. It will allow for rapid population-scale DNA sequencing across a broad range of disease areas, focusing on diseases with significant unmet clinical need such as amyotrophic lateral sclerosis (ALS) and idiopathic pulmonary fibrosis. The agreement will integrate genomics research conducted at Columbia with Biogen Idec’s understanding of disease mechanisms and pathways, and expertise in discovering new medicines. The collaboration will enable Biogen Idec and Columbia to investigate the genomes of patients showing unusual treatment responses or unique disease presentations and to explore the connections among genes, pathways, and disease processes. The ultimate goal will be to provide multiple qualified targets for new therapeutic approaches, increasing the potential for the development of new treatments.
Financial terms:
Latest news: * On February 19, 2015, an international consortium that includes scientists and clinicians from Columbia University Medical Center (CUMC), Biogen Idec and HudsonAlpha Institute for Biotechnology has identified a new gene that is associated with sporadic amyotrophic lateral sclerosis. The newly associated gene, called TBK1 (TANK-Binding Kinase 1), plays a key role at the intersection of two essential cellular pathways: inflammation (a reaction to injury or infection) and autophagy (a cellular process involved in the removal of damaged cellular components). The study was published in the online edition of Science.
The next-generation genetic sequencing of the exomes (protein-coding portions) of 2,874 ALS patients and 6,405 controls represents the largest number of ALS patients to have been sequenced in a single study to date. Though much is known about the genetic underpinnings of familial ALS, only a handful of genes have been definitively linked to sporadic ALS, which accounts for about 90 percent of all ALS cases. Searching through the enormous database generated in the ALS study, Goldstein and his colleagues found several genes that appear to contribute to ALS, most notably TBK1, which had not been detected in previous, smaller-scale studies. TBK1 mutations appeared in about one percent of the ALS patients – a large proportion in the context of a complex disease with multiple genetic components, according to Goldstein. The study also found that a gene, called OPTN, previously thought to play a minor role in ALS, may actually be a major player in the disease.
The researchers are currently using patient-derived, induced pluripotent embryonic stem cells (iPS cells) and mouse models with mutations in TBK1 or OPTN to study ALS disease mechanisms and to screen for drug candidates. Several compounds that affect TBK1 signaling have already been developed for use in cancer, where the gene is thought to play a role in tumor cell survival.
