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Catabasis Pharmaceuticals Presents Preclinical Data of Edasalonexent
Catabasis Pharmaceuticals (NASDAQ:CATB) has announced preclinical data for its edasalonexent in Phase 2 development to treat Duchenne musclar dystrophy (DMD). As quoted in the press release: The data were presented at the Symposium on Muscle-Bone Interaction in Duchenne Muscular Dystrophy. Bone health is important to those affected by Duchenne as many patients experience long bone …
Catabasis Pharmaceuticals (NASDAQ:CATB) has announced preclinical data for its edasalonexent in Phase 2 development to treat Duchenne musclar dystrophy (DMD).
As quoted in the press release:
The data were presented at the Symposium on Muscle-Bone Interaction in Duchenne Muscular Dystrophy.
Bone health is important to those affected by Duchenne as many patients experience long bone and/or vertebral fractures before the age of 13. In the preclinical study sponsored by Catabasis, prednisolone treatment negatively impacted bone health in mdxmice (mouse model of DMD) compared to control, whereas edasalonexent treatment showed bone sparing effects compared to the bone loss seen with prednisolone. Mice treated with prednisolone had significantly weaker bones (both cortical density and cortical thickness) and also grew less as assessed by femur length compared to control mdx mice. These results were seen following 6 months of treatment of clinically relevant doses of prednisolone or edasalonexent. The mice receiving 6 months of edasalonexent had preserved cortical density, cortical thickness and femur length, similar to the control mice.
Corticosteroids, such as prednisolone, can negatively impact bone health by increasing osteoclast apoptosis, reducing ossification and leading to increased bone resorption and osteoporosis. Catabasis believes that the treatment of DMD by inhibiting NF-kB with edasalonexent has the potential to reduce bone loss and enhance new bone growth in those affected by DMD by increasing osteoblast maturation and decreasing osteoclast differentiation and function.
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