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SIENA, Italy

Trademark
Siena Biotech S.P.A. | Date: 2008-12-09

Pharmaceutical preparations for the treatment of neurodegenerative diseases, cancer and other human chronic diseases in the nature of genetic and autoimmune diseases. Scientific research in the field of pharmacology.


Grant
Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH.2010.2.4.4-1 | Award Amount: 8.59M | Year: 2010

The Consortium will undertake clinical research activities aimed at ascertaining feasibility of a range of pharmacodynamic readouts for use in the clinical development of SEN0014196 to demonstrate the disease-modifying properties of the compound in Huntingtons Disease. SEN0014196 is a novel and selective SirT1 inhibitor, currently in Phase I clinical development, and enjoys Orphan Status in the EU as of September 2, 2009. A multi-factorial approach will be used, including assessment of both novel and compound-specific measures of molecular action as well as previously identified predictors of disease progression. The translational approaches addressed by this project are instrumental in the progression of SEN0014196 to clinical proof-of-concept and, if successful, will play a pivotal role in patient stratification and outcomes research. The Consortium will comprise four partners, all with a proven track-record in Research and Development in the Huntingtons Disease area. All Partners are based within the EU.


Grant
Agency: Cordis | Branch: FP7 | Program: MC-ITN | Phase: PEOPLE-2007-1-1-ITN | Award Amount: 2.54M | Year: 2008

Neurodegenerative diseases such as Parkinsons disease (PD) and Huntingtons disease (HD) still lack treatments that are disease modifying. The proposed network is going to address the three most important bottlenecks for finding more effective medicine in brain disorders. Those are: (i) identification and validation of pre-symptomatic and surrogate marker for disease progression, (ii) Development of model systems that translate to human pathology and are predictive of clinical efficacy, and (iii) better understanding of disease mechanisms leading to better target selection. We believe that a joint effort putting together industry and academia offers a great opportunity to cope with those bottlenecks. Therefore, we have assembled a unique consortium to which industry (5 partners) and academia (5 partners) contribute equally. Through putting together these partners into one network Neuromodel is going to achieve both organization of an excellent training program and performance of excellent research projects with a pronounced focus on intersectional transfer of knowledge. The gain for individual early stage researchers as well as for the participating research teams is obvious. On the one hand, the career chances of young researchers will improve enormously by receiving high quality training (for and by research) in areas of high demand on the employment market. On the other hand, the intersectional, interconnected and integrated research effort pursued by Neuromodel will definitively contribute towards finding more effective treatments in PD and HD. Expertise available within the consortium has lead to the definition of four structural elements (i) understanding disease mechanisms leading to target identification, (ii) approaches towards treatment, (iii) development of models predictive for efficacy and translating to human pathology, (iv) behavioural markers of animal models - that determines the training as well as the research program.


Grant
Agency: Cordis | Branch: FP7 | Program: MC-ITN | Phase: FP7-PEOPLE-2010-ITN | Award Amount: 3.76M | Year: 2011

Protein aggregation is a hallmark of many late onset neurodegenerative disorders including Parkinsons Disease (PD), Alzheimers Disease (AD), amyotrophic lateral sclerosis (ALS), prion diseases as well as the group of polyglutamine diseases (polyQ). The aim of this proposal is to create a network of European partners bridging important basic mechanisms involved in proteinopathies, research of model diseases and treatment approaches. The TreatPolyQ network will focus on two main representatives of the polyQ diseases: Huntingtons disease as the most common polyQ disease as well as spinocerebellar ataxia type 3 (SCA3) as the most frequent autosomal-dominantly inherited ataxia. Patients suffer from a multitude of neurological symptoms including movement abnormalities with late onset and in a progressive manner. Up to now, no treatment or cure is available. The network will be consisting of a rare combination of experts from basic and translational research, including a Nobel prize laureate, four industrial partners (two medium, and two small companies, all incorporated as full participants) and academic leaders of the field. The network not only focuses on one special aspect of a disease but spans several important disease-associated mechanism as well as promising treatment strategies for HD and SCA3 (protein transport, protein folding, protein degradation via both the ubiquitin-proteasome system and autophagy), likely to be important across a range of neurodegenerative diseases. In order to implement these research projects, extensive collaborations and temporarily personnel secondments of the involved researchers will take place, enhancing interdisciplinary transfer of knowledge. Beyond the personalized local training plan for each employed researcher within the Network, there will be 4 structured courses covering aspects ranging from structural biology to protein degradation to model organisms and drug development, including soft skill training.


Grant
Agency: Cordis | Branch: FP7 | Program: CP-IP | Phase: HEALTH.2011.2.1.1-1 | Award Amount: 39.64M | Year: 2011

In response to the call for a high impact initiative on the human epigenome, the BLUEPRINT Consortium has been formed with the aim of generating at least 100 reference epigenomes and studying them to advance and exploit knowledge of the underlying biological processes and mechanisms in health and disease. BLUEPRINT will focus on distinct types of haematopoietic cells from healthy individuals and on their malignant leukaemic counterparts. Reference epigenomes will be generated by state-of-the-art technologies from highly purified cells for a comprehensive set of epigenetic marks in accordance with quality standards set by IHEC. This resource-generating activity will be conducted at dedicated centres to be complemented by confederated hypothesis-driven research into blood-based diseases, including common leukaemias and autoimmune disease (T1D), by epigenetic targets and compound identification, and by discovery and validation of epigenetic markers for diagnostic use. By focussing on 100 samples of known genetic variation BLUEPRINT will complete an epigenome-wide association study, maximizing the biomedical relevance of the reference epigenomes. Key to the success of BLUEPRINT will be the integration with other data sources (i.e. ICGC, 1000 genomes and ENCODE), comprehensive bioinformatic analysis, and user-friendly dissemination to the wider scientific community. The involvement of innovative companies will energize epigenomic research in the private sector by creating new targets for compounds and the development of smart technologies for better diagnostic tests. BLUEPRINT will outreach through a network of associated members and form critical alliances with leading networks in genomics and epigenomics within Europe and worldwide. Through its interdisciplinarity and scientific excellence combined with its strong commitment to networking, training and communication BLUEPRINT strives to become the cornerstone of the EU contribution to IHEC.

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