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Raphaël Rodriguez

As seen in: Nature, MDPI, EurekAlert!, Science Magazine, Cell Press, Emerald Publishing, ChemistryViews
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Articles

Spermine is an endogenous iron chelator that inhibits ferroptosis

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By Xuexin Yu, Shuqin Ouyang, Xiaohong Chen, Huiqi Yu, Yuanji Liu, Ziwen Li, Chunhua Yu, Rui Kang, Christine Gaillet, Ludovic Colombeau, Raphaël Rodriguez, Libing Song, Guido Kroemer, Daolin Tang, Jun Li
| Nature Verified
Abstract Ferroptosis is an iron-dependent form of cell death driven by lipid peroxidation1. Here we identify spermine—a polyamine derived from spermidine2—as an endogenous iron chelator that directly suppresses ferroptosis.
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Ferroptosis inhibition enhances liver and lung graft function

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By Geraldine Veeckmans, Lene Devos, Nicholas Gilbo, Dieter Van Beersel, Camilla Scarpellini, Joris Blondeel, Magali Walravens, Greta Klejborowska, Caroline Lanthier, Michele Wölk, Sebastian Müller, Christine Gaillet, Ludovic Colombeau, Behrouz Hassannia, Matthias Längin, Jan-Michael Abicht, Bruno Reichart, Hans De Winter, Maria Fedorova, Raphaël Rodriguez, Laurens J. Ceulemans, Ina Jochmans, Koen Augustyns, Diethard Monbaliu, Arne Neyrinck, Tom Vanden Berghe, Jacques Pirenne
| Cell Press Verified
Results To complete the lead optimization of FXT-001 (Figure 1A), we conducted comprehensive absorption, distribution, metabolism, and excretion (ADME) and safety profiling. FXT-001 potently inhibited ferroptotic cell death in the nanomolar range, displayed high thermodynamic solubility across a broad pH range (pH 2–7), and showed moderate lipophilicity based on both experimental LogD7.4 and predicted calculated logP (cLogP) values (Figure 1B).
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Ether lipids influence cancer cell fate by modulating iron uptake - Nature Communications

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By Sebastian Müller, Vaishnavi Phadnis, Zhengpeng Wan, Fabien Sindikubwabo, Laurène Syx, Nicolas Servant, George Bell, Amy Deik, Clary B. Clish, Paula Hammond, Roger Kamm, Adam Cohen, Ilya Levental, Victor W. Hsu, Kandice R. Levental, Raphaël Rodriguez, Robert Weinberg
| Nature Verified
Abstract Cancer cell fate has been widely ascribed to mutational changes within protein-coding genes associated with tumor suppressors and oncogenes. In contrast, the mechanisms through which the biophysical properties of membrane lipids influence cancer cell survival, dedifferentiation and metastasis have received little scrutiny.
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