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Updated: Sep 10, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics

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Dovitinib Ameliorates Inflammation-Related Diseases by Inhibiting Necroptosis and Ferroptosis

Yingying Lin1, Jianting Feng1, Mingyuan Zhao1

  • 1The School of Basic Medical Sciences, Fujian Medical University, Fuzhou 350004, China.

ACS Chemical Biology
|August 21, 2025
PubMed

Insights

Dovitinib (Dov) effectively inhibits both necroptosis and ferroptosis, two cell death types linked to organ injury and inflammation. This dual-action compound shows potential as a therapeutic for related diseases.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Dysregulated cell death, including necroptosis and ferroptosis, significantly contributes to organ injury and inflammation.
  • Targeting these cell death pathways is a promising therapeutic strategy for various pathological conditions.

Purpose of the Study:

  • To identify novel inhibitors of necroptosis and ferroptosis.
  • To evaluate the therapeutic potential of identified compounds in disease models.

Main Methods:

  • Screening of a small-molecule compound library to identify dual inhibitors.
  • Investigating the molecular mechanisms of inhibition for necroptosis (via RIPK1) and ferroptosis (via NRF2/HMOX1 axis).
  • Assessing compound efficacy in models of TNF-induced inflammation and concanavalin A-induced acute liver injury.

Main Results:

  • Dovitinib (Dov) was identified as a potent dual inhibitor of necroptosis and ferroptosis.
  • Dov inhibited TNF-induced necroptosis by regulating RIPK1, alleviating systemic inflammation.
  • Dov inhibited ferroptosis by modulating the NRF2/HMOX1 axis and lipid peroxidation, protecting against liver injury.

Conclusions:

  • Dovitinib acts as a dual inhibitor of necroptosis and ferroptosis.
  • Dovitinib presents a potential therapeutic agent or combination therapy for diseases involving these cell death pathways.

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