Rhodium(III)‐Nitroxyl Radical Complex Triggers Dual‐Pronged Disulfidptosis‐Apoptosis in Hepatocellular Carcinoma via Metabolic Sabotage and Redox Catalysis

H Hui‐Chao Lin (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China) W Wen‐Ying Shen (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China) J Jian‐Hua Wei (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China) L Liu‐Lin Chen (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China) C Chun‐Peng Jia (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China) Z Zu‐Yu. Mo (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China) L Li‐Xia Wang (Huairou Research Center of Institute of Chemistry Chinese Academy of Sciences Beijing China) C Cheng Hou (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China) Y Yang‐Han Liu (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China) J Jihu Su (CAS Key Laboratory of Microscale Magnetic Resonance and Department of Physics, School of Physical Sciences) H Hong Liang (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences) Z Zhen‐Feng Chen (Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China)

Abstract

Abstract Hepatocellular carcinoma (HCC) resists apoptosis‐targeting therapies, necessitating the development of agents targeting alternative cell death pathways. Here, we report the discovery of a nitroxyl radical‐conjugated Rh(III) complex ( OG‐Rh ) that triggers dual disulfidptosis and apoptosis via synergistic metabolic sabotage and redox catalysis. OG‐Rh inhibited glucose uptake, depleted NADPH, and induced disulfidptosis, a novel disulfide‐stress‐mediated death, by inducing actin cytoskeleton collapse via pathogenic disulfide over‐crosslinking. Simultaneously, its tumor‐selective superoxide dismutase/peroxidase (SOD)/(POD) mimetic activity converted endogenous O 2 • − and H 2 O 2 into •OH, resulting in redox attacks that suppressed AP‐1 via Mitogen‐activated protein kinases (MAPK)‐SIRT1 and amplified disulfide stress. This dual pathway mechanism overcomes apoptosis resistance and catalytic therapy limitations. In vitro, OG‐Rh showed potent cytotoxicity (IC 50  = 1.0 µM in BEL‐7402 cells) and selectivity (>10‐fold versus normal cells). In vivo, it suppressed tumor growth by 60.9% without systemic toxicity. This work pioneered a strategy via “metabolic sabotage‐redox storm” achieved by a small‐molecule metallodrug, offering a paradigm‐shifting approach against refractory HCC.

Article Details

Volume / Issue Vol. 65, Issue 3
Published January 16, 2026
ISSN 1433-7851
Publisher Wiley

Journal Info

Angewandte Chemie International Edition

Wiley

ISSN: 1433-7851 Physical Sciences

Authors (12)

H

Hui‐Chao Lin

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China

W

Wen‐Ying Shen

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China

J

Jian‐Hua Wei

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China

L

Liu‐Lin Chen

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China

C

Chun‐Peng Jia

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China

Z

Zu‐Yu. Mo

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China

L

Li‐Xia Wang

Huairou Research Center of Institute of Chemistry Chinese Academy of Sciences Beijing China

C

Cheng Hou

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China

Y

Yang‐Han Liu

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China

J

Jihu Su

CAS Key Laboratory of Microscale Magnetic Resonance and Department of Physics, School of Physical Sciences

H

Hong Liang

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences

Z

Zhen‐Feng Chen

Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), Guangxi Key Laboratory of Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmaceutical Sciences Guangxi Normal University Guilin 541004 China