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TRACER SIGNED

TRAF-STOP therapy to reduCe inflammation in athERosclerosis.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 TRACER project word cloud

Explore the words cloud of the TRACER project. It provides you a very rough idea of what is the project "TRACER" about.

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Project "TRACER" data sheet

The following table provides information about the project.

Coordinator
ACADEMISCH MEDISCH CENTRUM BIJ DE UNIVERSITEIT VAN AMSTERDAM 

Organization address
address: MEIBERGDREEF 15
city: AMSTERDAM
postcode: 1105AZ
website: www.amc.nl

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Netherlands [NL]
 Total cost 0 €
 EC max contribution 150˙000 € (0%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-PoC
 Funding Scheme ERC-POC-LS
 Starting year 2020
 Duration (year-month-day) from 2020-01-01   to  2021-06-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    ACADEMISCH MEDISCH CENTRUM BIJ DE UNIVERSITEIT VAN AMSTERDAM NL (AMSTERDAM) coordinator 150˙000.00

Map

 Project objective

Atherosclerosis, the underlying cause of the majority of cardiovascular diseases, is a lipid driven, inflammatory disease of the large arteries. Despite a 25% relative risk reduction achieved by lipid-lowering treatment, the vast majority of atherosclerosis induced cardiovascular disease risk remains unaddressed. Therefore, characterizing mediators of the inflammatory aspect of atherosclerosis is a widely recognized scientific goal with great therapeutic implications. Blocking the co-stimulatory CD40L-CD40 dyad reduces atherosclerosis. However, long-term inhibition of CD40L or its receptor CD40 results in suppression of the immune system and poses a risk for thromboembolic events. Therefore, we focused on the downstream signaling pathways of CD40, and found that the interaction between CD40 and TNF-receptor-associated factor 6 (TRAF6) is the driving force for atherosclerosis. Using virtual ligand screening, we identified several small molecule inhibitors termed TRAF-STOPs that were modeled to bind to the CD40-binding domain of TRAF6. TRAF-STOPs significantly reduce (existing) atherosclerosis and treatment was well tolerated. The first toxicology results in mice show that there are no side effects. Here we pursue the hypothesis that TRAF-STOPs are excellent candidates to pass the translational pipeline towards a clinical application to treat atherosclerotic cardiovascular disease. Prof. Lutgens is one of the founders of the recently established start-up company Cartesio Therapeutics to be able to valorise our novel TRAF-STOPs. By the end of the PoC grant, we expect to have an oral drug available and to have completed toxicology and bio-distribution analysis in a large animal model (mini-pig) and have tested TRAF-STOPs in a pig model of atherosclerosis. This way, we hold a solid business case in our hands. The resulting business- and (pre-)clinical development plan and patent portfolio will then be ready for seed investment and venture capital funding.

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The information about "TRACER" are provided by the European Opendata Portal: CORDIS opendata.

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