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Research at the University of Pecs demonstrates that Proxison reverses aberrant mitochondrial function and morphology in cells from LAM patients

Released: Monday 21st January 2019

Lymphangioleiomyomatosis (LAM) is a rare disease primarily affecting younger women with the average age of diagnosis around 35. The condition is characterised by cystic lung destruction, lymphatic involvement and the growth of benign renal tumours. Proliferation of abnormal smooth-muscle-like LAM cells results in a progressive deterioration of lung function over many years. 

 

Current therapeutic options to delay progression of the condition are limited and recourse to lung transplantation is often required to manage the inevitable decline. New therapeutic strategies are desperately needed to manage this crippling orphan indication. 

 

Researchers at the University of Pecs have provided new insight into the pathogenesis of LAM highlighting the key role that mitochondrial dysfunction plays in the condition. Proxison, a novel mito-active redox molecule within the Antoxis Kromex platform, was found to be highly-effective in restoring normal mitochondrial function and morphology in patient-derived LAM cell lines. 

 

Link to full journal article    

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