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Ferroptosis is coming back to Japan! We are excited to announce the 4th  Cold Spring Harbor Asia (CSHA) meeting on “Iron, Reactive Oxygen Species & Ferroptosis in Life, Death & Disease,” organized by Quan Chen (Nankai University), Marcus Conrad (Helmholtz Zentrum München & Technical University of Munich), Xuejun Jiang (Memorial Sloan Kettering Cancer Center), Hozumi Motohashi (Tohoku University), Brent Stockwell (Columbia University), and Shinya Toyokuni (Nagoya University). The meeting will take place from November 15–20, 2026, at the beautiful Awaji Yumebutai Conference Center in Awaji, Japan. Awaji Island is conveniently located near Kobe and Osaka and is easily accessible by public transportation. Don’t miss this exciting opportunity to stay updated on the latest breakthroughs in ferroptosis reserach and connect with colleagues and friends during Japan’s beautiful autumn season! (Photo courtesy of CSHA).

Cold Spring Harbor Asia (CSHA) conference on ferroptosis

It is deeply humbling to receive this year’s CDD Jürg Tschopp Award from the European Cell Death Organization. Jürg’s pioneering work not only shaped how we understand the molecular logic of cell death and inflammation, it inspired an entire generation of scientists to think boldly, to challenge dogma, and to connect mechanism to meaning. For me, this award is a milestone along a shared journey that began more than 25 years ago in Munich — one defined by the privilege of working with extraordinary lab members, mentors, and collaborators who make science a collective adventure rather than a solitary pursuit. Thank you to everyone who has shared ideas, experiments, and late nights and very early mornings along the way. This recognition belongs as much to you as to me.

European Cell Death Organization (ECDO)

Current and former members of the DFG-funded priority programme SPP 2306 gathered from September 30 – October 2, 2025, in Feldkirchen-Westerham, Upper Bavaria, to share the latest discoveries and exciting new developments in the flourishing field of ferroptosis. Thanks to the overwhelmingly positive feedback from all participants, we are confident this was a truly unforgettable event, featuring outstanding scientific talks and poster presentations in an inspiring and highly stimulating environment. A heartfelt thank you goes to all the invited speakers from around the globe who enthusiastically joined us and contributed so much to the success of this meeting. We are already looking forward to the next opportunity to meet again. Hope to see you soon at one of our upcoming events!

DFG Priority Programme “Ferroptosis: from Molecular Basics to Clinical Applications”

We are thrilled to have been awarded a Proof of Concept (PoC) grant by the European Research Council (ERC). This support will help us identify a new lead compound—or potentially a preclinical candidate—for cancer treatment, thereby advancing ferroptosis suppressor protein-1 (FSP1) inhibitors toward preclinical and clinical development. We believe this program holds tremendous potential to deliver a substantial value proposition and open up exciting opportunities for out-licensing or co-development partnerships.

ERC PoC grant, entitled FERADICATE, awarded to Helmholtz Munich researcher

I am truly honored and humbled to receive the highly prestigious Paul-Martini-Preis 2025. This German medical award is presented annually by the Paul-Martini-Stiftung (Berlin) in recognition of outstanding achievements in clinical pharmacology and drug therapy. Named after Paul Martini, a renowned German physician and clinical pharmacologist who was instrumental in establishing the scientific foundations of modern clinical research in Germany, it is considered one of the most important awards in the country for clinical medical research, particularly in the field of pharmacology. My deepest gratitude goes to the outstanding team at the Conrad Lab, our numerous national and international collaborators, and the many funding agencies that have supported us over the past decades (Foto – courtesy from Thomas Boehm and the Paul-Martini-Stiftung).

Paul-Martini-Stiftung

Research into the mechanisms of ferroptosis is soaring due to its relevance to numerous diseases, including ischemia/reperfusion-related complications like stroke and cardiac infarction, neurodegenerative disorders, and cancer. Unlike many other forms of cell death that typically follow specific signalling cues, ferroptosis is impacted by a range of cellular and biochemical processes, including (phospho)lipid metabolism, iron handling, selenium availability, and redox metabolism. Crucially, the stark differences in redox conditions between cell culture systems and whole organisms often hinder the direct translation of in vitro findings to the in vivo context. As a result, well-controlled cellular and animal models, along with rigorously validated tools—such as small-molecule compounds, sgRNAs, and antibodies—are essential for dissecting the mechanisms underlying ferroptosis. In this Expert Recommendation, we explore best practices, highlight common pitfalls, and outline key experimental tools needed to confidently navigate this dynamic field of cell death research. We hope this guide will contribute to harmonizing methodologies across the field and inspire new exciting discoveries. (Figure adopted from Mishima, Nakamura et al., Nat Rev Mol Cell Biol 2025).

Mishima E., Nakamura T. et al. (2025) Recommendations for robust and reproducible research on ferroptosis. Nature Reviews Molecular Cell Biology

In our most recent review article, we provide a highly detailed and granular perspective on the intersection of ferroptotic cell death and cellular metabolism. Unlike many other forms of cell death, ferroptosis is intricately linked to multiple metabolic processes, including (phospho)lipid metabolism, iron homeostasis, the cholesterol pathway, and redox metabolism and signaling. Given this complexity, a comprehensive understanding of metabolic pathways and key regulatory nodes that continuously monitor the process of (phospho)lipid peroxidation is essential when designing novel therapeutic strategies. Such approaches aim either to prevent ferroptosis in the context of (neuro)degenerative diseases or to induce this form of cell death in certain malignancies (Cover adopted from Physiological Reviews, Volume 105, Issue 2, Apr 2025).

Zheng and Conrad (2025) Ferroptosis: when metabolism meets cell death. Physiological Reviews

The trace element selenium, discovered over 200 years ago, is a vital component of a select group of selenocysteine-containing enzymes, known as selenoproteins. Among these, glutathione peroxidase 4 (GPX4) serves as the primary guardian against ferroptosis. In this study, we reveal a novel role for peroxiredoxin-6 (PRDX6), a member of the thiol-specific antioxidant protein family. In addition to its established phospholipase and hydroperoxidase activities, PRDX6 exhibits a previously unrecognized “moonlighting” function: binding and delivering selenium to selenophosphate synthetase 2 (SEPHS2). SEPHS2 is a critical enzyme that facilitates the biosynthesis of selenocysteine-loaded tRNA by phosphorylating selenide, a process indispensable for the synthesis of selenoproteins, including GPX4. Notably, the loss of PRDX6 expression significantly increased the sensitivity of tumor xenografts to ferroptosis-inducing conditions and severely impaired selenoprotein expression particularly in the brain, highlighting its essential in vivo role. These findings position PRDX6’s selenium trafficking activity as more pivotal in regulating cellular ferroptosis sensitivity than its previously recognized phospholipase and peroxidase functions (Cover adopted from Mol Cell Volume 84, Issue 23, December 5, 2024)(see also “Novel Selenium Carrier Protein Regulates Ferroptosis in Cancer and Brain“).

Ito, J. et al. (2024) PRDX6 dictates ferroptosis sensitivity by directing cellular selenium utilization. Molecular Cell

Truly honored and absolutely thrilled to be named a Highly Cited Researcher (“Biology and Biochemistry” & “Molecular Biology and Genetics”) for the 5^th year in a row! This achievement wouldn’t be possible without an incredible and motivated team, as well as many successful national and international collaborations. A huge thank you to everyone who made this happen!

Highly Cited Researchers

The 3^rd Cold Spring Harbor Asia (CSHA) conference on “Iron, Reactive Oxygen Species & Ferroptosis in Life, Death & Disease” organized by Drs. Quan Chen (Nankai University, China), Marcus Conrad (Helmholtz Munich, Germany), Xuejun Jiang (Memorial Sloan-Kettering Cancer Center, USA), Hozumi Motohashi (Tohoku University, Japan), Brent Stockwell Columbias University, USA) and Shinya Toyokuni (Nagoya University, Japan) took place from November 03 to 07, 2024, this time in Suzhou, CHINA. As the two previous meetings, it was incredibly fruitful, fostering a dynamic exchange of ideas and offering novel and exciting insights into the field of ferroptosis. It was characterized by engaging discussions and interactive sessions sparking new collaborations, with participants actively sharing knowledge and challenging perspectives. The environment was not only highly stimulating but also socially enriching, as many attendees connected on a personal level, forming new friendships that promise to extend beyond the conference (Foto taken from CSHA).

Cold Spring Harbor Asia (CSHA) conference on ferroptosis

Thrilled to announce that our work has been awarded the Galenus-von-Pergamon-Preis 2024 in the category Basic Research. The Galenus-von-Pergamon-Preis is a highly prestigious award established in 1985 to recognize and promote outstanding innovations in pharmaceutical research in Germany. Named after the ancient Greek physician „Galen (Galenos) of Pergamon“, this prize is awarded annually and highlights breakthroughs in drug development and clinical pharmacology that have been introduced to the German market (Foto taken from die Aerztezeitung – copyright Marc-Steffen Unger).

It’s an incredible honor to receive this year’s European Cell Death Organisation (ECDO) Honorary Award 🏆 and to join such a distinguished group of cell death pioneers! This achievement was only made possible by the continued dedication and hard work of the talented members of the ConradLab, both current and past, as well as the many amazing collaborators over the last 25 years. I’m deeply grateful to everyone who has been a part of this journey!

In our current work, we identify and validate the first multi-species inhibitor of ferroptosis suppressor protein-1 (FSP1), called viFSP1 (versatile inhibitor of FSP1). FSP1, along with extra-mitochondrial ubiquinone (CoQ10) or vitamin K, represents one of the key ferroptosis surveillance system in mammals. Since standard therapy-resistant and metastasizing cancers show high vulnerability to ferroptosis, targeting FSP1 might attenuate tumor growth in certain tumor contexts. Moreover, a better understanding of the molecular mechanisms of FSP1 in ferroptosis prevention is of utmost importance for the rationale design of FSP1-based therapies. Using a combination of computational predictions and random mutagenesis approaches, we now unravel not only the mechanism-of-action of viFSP1 and iFSP1, another inhibitor specific for the human enzyme published earlier by us (Doll et al., Nature 2019), but also the enzymatic mechanism of how FSP1 reduces its main substrates CoQ10 and vitamin K, thereby protecting against lipid peroxidation and ferroptosis (Figure taken and modified from Nakamura et al., Nat Struct Mol Biol 2023)(see also “A Rising Star: Inducing Ferroptosis with Innovative Compounds for Cancer Therapy“).

Delighted to be listed as one of the Highly Cited Researchers again this year. This success is thanks to the tremendous efforts of an outstanding team and fantastic collaborators that I have had the pleasure of working with over the past few years! Clarivate unveiled the 2023 Highly Cited Researchers™ list with 6,849 Highly Cited Researchers in 2023, coming from more than 1,300 institutions in 67 nations and regions. Germany with 336 researchers is ranked fourth after United States, China and United Kingdom.

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In this comprehensive review article, we provide an up-to-date overview of the multiple roles that iron plays in a variety of cellular and metabolic processes. We highlight how cells handle and transport iron within cells and between organs, and how they use it in the biosynthetic pathways of haem and iron-sulphur cluster-containing proteins. We also discuss the regulatory mechanisms of how cells store and mobilise iron from professional iron storage or release proteins, and the so-called labile iron pool. We emphasise the importance of balanced cellular and tissue iron levels, as disturbances of these are ultimately associated with the development of disease and susceptibility to ferroptosis, a non-apoptotic form of cell death characterised by iron-dependent lipid peroxidation. We believe that a better understanding of the underlying regulatory nodes of iron metabolism is essential for the rational development of new therapeutic options to combat iron-related diseases (Figure adopted from Galy et al., Nat Rev Mol Cell Biol 2023).

Galy, B. et al. (2023) Mechanisms controlling cellular and systemic iron homeostasis. Nature Reviews Molecular Cell Biology

In our recent work, we demonstrate that brequinar (BQR), an established and potent inhibitor of dihydroorotate dehydrogenase (DHODH), sensitizes to ferroptosis via ferroptosis suppressor protein-1 (FSP1) and not via DHODH as previously suggested by Mao et al. (2021). The reason Mao et al. concluded that mitochondrially localised DHODH could be a therapeutic vulnerability in cancer was because of the extremely high concentrations of BQR used throughout, but which also inhibit FSP1, as shown in our recent study. Furthermore, we provide conclusive evidence that it is the short form (alias “cytosolic” or “somatic” form”) of glutathione peroxidase 4 (GPX4) that effectively protects cells from ferroptosis. Our results therefore suggest that DHODH plays only a minor role, if any, in ferroptosis surveillance, while GPX4 and FSP1 remain the major systems for suppressing ferroptosis in mammalian cells. Our study should, however, not discourage ongoing efforts to study DHODH as a valid anticancer target due to its role well-established role in pyrimidine synthesis and hence cell proliferation (Figure taken from Mishima et al., Nature 2023).

Original publication:

In this study, we introduce the small molecule compound class of 3-phenylquinazolinones, termed icFSP1, as the first in vivo active ferroptosis suppressor protein-1 (FSP1)-specific inhibitors. Unlike the first described FSP1 inhibitor iFSP1 (Doll et al., Nature 2019), icFSP1 induces subcellular relocalisation of FSP1 from membranes and phase separation prior to lipid peroxidation and ferroptosis. (Liquid-liquid) phase separation is a physicochemical process similar to the separation of water and oil and is involved in many cellular processes, including cell signalling and transcriptional regulation. In addition, phase separation has also been linked to various pathologies such as neurodegeneration and cancer. We further show that icFSP1-induced phase separation of FSP1 requires different structural elements in FSP1 and that pharmacological treatment of tumour-bearing mice impairs tumour growth. Our results therefore establish a link between the process of phase separation and ferroptosis and should spur future efforts to develop in vivo applicable drugs for the treatment of certain cancers considered to be vulnerable to ferroptosis (Figure taken and modified from Nakamura et al., Nature 2023).

Original publication:

In this perspective article, we provide an overview of the diverse functions of vitamin K (K comes from Koagulation, the German word for coagulation) in physiology and metabolism including blood clotting and bone metabolism. As an essential cofactor of γ-carboxyglutamyl carboxylase in the canonical vitamin K cycle, vitamin K has also vitamin K-independent functions, such as regulation of gene expression. In addition, vitamin K has recently been shown to also act as a potent “anti-ferroptotic” molecule by preventing lipid peroxidation of cell membranes in cultured cells and mice (see Mishima et al., Nature 2022). This non-canonical anti-ferroptotic function, which requires regeneration of oxidized vitamin K by ferroptosis suppressor protein-1 (FSP1) and NAD(P)H, has been termed the “Mishima cycle” to clearly distinguish this function from the canonical function in blood coagulation. Future studies will shed light on whether vitamin K together with FSP1 has similar or even additional functions in organisms that are also highly dependent on vitamin K, such as plants and bacteria (Figure taken from Mishima et al., Nat Metab 2023).

Mishima, E. et al. (2023) Diverse biological functions of vitamin K: from coagulation to ferroptosis. Nature Metabolism

The first EMBO Workshop entitled “FERROPTOSIS: When metabolism meets cell death” organized by Drs. Marcus Conrad (Helmholtz Munich, DE), José Pedro Friedmann Angeli (University of Würzburg, DE), Maria Fedorova (Technical University of Dresden, DE) and Xuejun Jiang (Memorial Sloan-Kettering Cancer Center, US) took place from April 23 – 27, 2023 in Kloster Seeon, Germany, close to Lake Chiemsee and the Bavarian Alps. We had an excellent lineup of speakers, a huge number of outstanding posters and intense and fruitful discussions. There was clear consensus among the participants that this was a truly exciting and stimulating workshop, sparking new ideas and collaborations.

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FERROPTOSIS: When metabolism meets cell death

The Deutsche Forschungsgemeinschaft (DFG) has appointed Marcus Conrad as a new member of the DFG’s Hinterzarten Circle on Cancer Research. The Hinterzarten Circle is a roundtable which serves as a regular discussion forum. Membership consists of medical and biological scientists working in the field of cancer research. The annual meeting discusses novel findings in the field of cancer-related basic research and the diagnosis and therapy of malignant tumours. This annual roundtable, held in relative seclusion, aims to encourage intensive discussion between scientists from various disciplines engaged in basic research and those conducting clinical research. The five members of the Hinterzarten Circle are appointed by the DFG for five years.

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Very honored to see that our work has been recognized again by the broader scientific community. Each year, Clarivate™ identifies the world’s most influential researchers ─ the select few who have been most frequently cited by their peers over the last decade. In 2022, fewer than 7,000, or about 0.1%, of the world’s researchers, in 21 research fields and across multiple fields, have earned this exclusive distinction. Marcus Conrad is among this elite group recognized for your exceptional research influence, demonstrated by the production of multiple highly-cited papers that rank in the top 1% by citations for field and year in the Web of Science™.

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The Cold Spring Harbor Asia (CSHA) conference on “Iron, Reactive Oxygen Species & Ferroptosis in Life, Death & Disease” organized by Drs. Quan Chen (Nankai University, China), Marcus Conrad (Helmholtz Munich, Germany), Xuejun Jiang (Memorial Sloan-Kettering Cancer Center, USA), Hozumi Motohashi (Tohoku University, Japan), Brent Stockwell Columbias University, USA) and Shinya Toyokuni (Nagoya University, Japan) took place from October 10 – October 14, 2022, at Awaji Yumebutai Conference Center, JAPAN. Despite all the hurdles with the COVID pandemics, this second openly accessible conference on ferroptosis was a true success as new findings and developments in the field were intensely discussed among basic scientists, physicians and representatives from pharma/biotech industry.

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In this study, we show that vitamin K is a potent suppressor of ferroptosis by preventing oxidative damage to cellular membranes. So far, vitamin K has been well-known for its role in blood clotting and bone calcification. Its discovery dating almost 100 year ago was awarded with the Nobel Prize in Physiology or Medicine to Henrik Carl Peter Dam and Edward Adelbert Doisy in 1943. We further report that ferroptosis suppressor protein-1 (FSP1) reduces oxidized vitamin K to its hydroquinone form, thus driving a novel non-canonical vitamin K cycle that we tentatively name the “Mishima cycle”. Finally, we demonstrate that FSP1 is the long sought-after warfarin-resistant vitamin K reductase, thus solving one of the last riddles in vitamin K biology. Findings presented in our present work will therefore have immediate implications for both vitamin K and ferroptosis research (Figure adopted from Mishima et al., Nature 2022).

Mishima, E. et al. (2022). A non-canonical vitamin K cycle is a potent ferroptosis suppressor. Nature

The newly launched consortium “FERROPath” involves six partners in Germany, located in Munich, Dresden, Regensburg and Essen, who aim to identify and validate common ferroptotic signatures and molecular mechanisms in organs mostly affected by ischemia/reperfusion injury (IRI), such as brain, liver, lung and kidney. IRI occurs when the blood flow to a certain organ is transiently interrupted causing additional damage to the affected tissue due to the generation of high levels of oxygen radicals including lipid peroxidation. IRI is therefore a serious complication, responsible for a variety of clinically important conditions including stroke, acute kidney injury and organ transplantation. As such, understanding the molecular mechanisms and elucidating common molecular signatures of ferroptosis will be of utmost importance for the development of novel therapies based on next generation ferroptosis inhibitors.

Delighted to announce that our research of the last years has again been widely appreciated by the broader scientific community, demonstrated by multiple highly-cited papers that rank in the top 1% by citations for field and year in the Web of Science™. Each year, Clarivate™ identifies the world’s most influential researchers ─ the select few who have been most frequently cited by their peers over the last decade. In 2021, 6,602 researchers from more than 70 countries and regions have earned this exclusive distinction (Germany ranks five with 331 scientists).

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On October 01, we have officially started our DFG (Deutsche Forschungsgemeinschaft) funded Priority Programme “Ferroptosis: from Molecular Basics to Clinical Applications” (SPP 2306) which will fund 25 projects scattered all over Germany for up to six years. The overall goal of the program is to better understand the molecular mechanisms of ferroptosis as the basis for the development of novel therapies based on ferroptosis modulation.

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Here, we highlight the role of lipid metabolizing enzymes, distinct (phospho)lipid species and their oxidative modification as well as relevant metabolic pathways in the context of sensitization of cells toward ferroptosis. We further discuss outstanding questions how lipid peroxidation and related secondary products may contribute to the rupturing of cellular membranes, the final step in ferroptosis execution (Cover art from Trends in Endocrinology & Metabolism. July 2021).