Mechanism of Action

RSO-021 is a novel first-in-class small molecule that irreversibly binds and inhibits mitochondrial peroxiredoxin 3 (PRX3).

Inhibition of the PRX3 antioxidant signaling network in mitochondria results in selective killing of malignant cells by upregulation of oxidative stress; in contrast, healthy tissue is spared. In pre-clinical models RSO-021 reduces tumor growth in mice, sensitizes tumor cells to apoptosis and reduces the expression of pro-metastatic epithelial to mesenchymal (EMT) genes.  See our publications for additional information.

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In pre-clinical models RSO-021 reduces tumor growth in mice, sensitizes tumor cells to apoptosis and reduces the expression of pro-metastatic epithelial to mesenchymal (EMT) genes.

Scientific Research

Altered metabolism and oxidative stress are now considered a hallmark of cancer. Cancer cells upregulate their antioxidant capacity and redox-responsive signaling pathways to survive and grow under otherwise inhospitable conditions. A promising therapeutic approach is to increase the reactive oxygen species (ROS) to levels incompatible with tumor cell survival. Mitochondrial peroxiredoxin 3 (PRX3) plays a significant role in detoxifying ROS. Targeting PRX3 with RSO-021 elicits significant tumor cell death in preclinical and clinical studies.

 

Mitochondria (yellow) are constantly changing shape, size and location to support cell (purple) processes including invasion and metastasis. Optimal mitochondrial bioenergetics are critical to support tumor growth.

 

 

 

We utilize advanced in vitro and in vivo models to evaluate tumor cell metabolism and response to therapeutic intervention. Advanced 3-dimensional patient derived tumor organoid and explant models (Video) are foundational to understanding pre-clinical drug responses. By using biochemical, genetic, and phenotypic assays we are identifying the next generation of targeted therapies for aggressive cancers.