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EPI-X4Health SIGNED

Therapeutic potential of optimized derivatives of an endogenous CXCR4 antagonist for the treatment of cancers and inflammatory diseases

Total Cost €

0

EC-Contrib. €

0

Partnership

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 EPI-X4Health project word cloud

Explore the words cloud of the EPI-X4Health project. It provides you a very rough idea of what is the project "EPI-X4Health" about.

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Project "EPI-X4Health" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITAET ULM 

Organization address
address: HELMHOLTZSTRASSE 16
city: ULM
postcode: 89081
website: www.uni-ulm.de

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 Germany [DE]
 Total cost 149˙156 €
 EC max contribution 149˙156 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-PoC
 Funding Scheme ERC-POC
 Starting year 2018
 Duration (year-month-day) from 2018-09-01   to  2020-02-29

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAET ULM DE (ULM) coordinator 95˙256.00
2    FRAUNHOFER GESELLSCHAFT ZUR FOERDERUNG DER ANGEWANDTEN FORSCHUNG E.V. DE (MUNCHEN) participant 26˙950.00
3    UNIVERSITE DE STRASBOURG FR (STRASBOURG) participant 26˙950.00

Map

 Project objective

Deregulation of CXCL12 signaling via the CXCR4 chemokine receptor plays a key role in many diseases, including cancer, rheumatoid arthritis, chronic inflammation and cardiovascular disorders. Thus, agents modulating CXCR4 signaling offer many prospects for therapeutic development. CXCR4 is also a major coreceptor for HIV entry. Thus, we used HIV as tool to screen peptide libraries encompassing the entire blood peptidome for novel CXCR4 ligands. This approach allowed the identification of a small fragment of human serum albumin as potent HIV inhibitor. Remarkably, this naturally occurring peptide, named EPI-X4 (Endogenous Peptide Inhibitor of CXCR4), blocks CXCL12/CXCR4 signaling and suppresses cancer cell migration and invasion. Preclinical studies in mice show that EPI-X4 mobilizes hematopoietic stem/progenitor cells and inhibits lung inflammation in an asthma model. Preliminary analyses suggest that EPI-X4 is more specific and better tolerated than Mozobiol® (AMD3100), the only CXCR4 antagonist approved for clinical application. Recently, we developed synthetic derivatives of EPI-X4 showing about three orders of magnitude improved potency against HIV as well as increased plasma stability. Key goals of this project are to determine the therapeutic potential of these improved derivatives against cancers (Aim 1) and inflammatory diseases (Aim 2) using established mouse models of colon carcinoma, osteosarcoma, glioblastoma, airway inflammation and dermatitis. These disorders were selected from the large number of CXCR4-linked diseases because no safe and effective treatment exists and since preclinical mouse models are available to determine whether EPI-X4 derived agents are more efficient and better tolerated than other compounds. In parallel to the experimental assessment of the therapeutic potential of these novel CXCR4 antagonists, we will perform market analyses and develop an IPR strategy to pave the way towards commercialization and future clinical application.

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