Cancer Drug Could Limit Lung Disease in COVID-19 Patients, Study Finds

Cancer Drug Could Limit Lung Disease in COVID-19 Patients, Study Finds

Researchers at the Hudson Institute of Medical Research have discovered that a cancer drug called idronoxil may have the potential to reduce the damaging effects of lung disease in COVID-19 patients. Inflammation plays a crucial role in controlling viral infections, including SARS-CoV-2, the virus responsible for COVID-19. However, when inflammation becomes excessive, it can be life-threatening.

Led by Associate Professor Michael Gantier, the research team found that idronoxil, initially developed as a cancer treatment, could decrease the inflammation that occurs in response to COVID-19. By targeting a specific protein activated by multiple inflammatory pathways, idronoxil can limit harmful inflammation without promoting viral replication in the lungs. The researchers demonstrated this effect by administering idronoxil three days after infection in a pre-clinical model of severe COVID-19.

The study’s findings suggest that idronoxil or similar derivatives could be used to treat lung hyperinflammation caused by emerging viruses. The COVID-19 pandemic highlighted the need for additional treatments for respiratory distress and emphasized the importance of being prepared for future outbreaks. A/Prof Gantier and his team are now working with academic and industry collaborators to develop idronoxil derivatives with enhanced anti-inflammatory properties, with funding from the Victorian Government.

The research conducted at Hudson Institute of Medical Research is a significant step toward understanding and addressing the damaging inflammatory response seen in COVID-19. By limiting excessive inflammation and restoring the body’s ability to regulate immune responses, idronoxil shows promise as a potential treatment option for severe lung disease in COVID-19 patients.

– Hudson Institute of Medical Research
– Nature Communications journal reference: Ullah, T. R., et al. (2023) Pharmacological inhibition of TBK1/IKKε blunts immunopathology in a murine model of SARS-CoV-2 infection. Nature Communications.

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