As part of the agreement, Edison will receive $35m upfront and $15m for R&D in exchange for granting development and commercialization rights to DSP. Besides, Edison will be eligible to receive $10-35m in development milestones per indication and up to $460m in commercial milestone payments as well as royalties on commercial sales.
The initial scope of the deal comprises both pediatric orphan inherited mitochondrial and adult central nervous system diseases.
DSP will take up activities required for development, approval, and commercialization of EPI-743 in Japan. The work will first focus on orphan pediatric mitochondrial disease.
On the other hand, Edison will retain complete ownership and direct all research, clinical, and commercial development of EPI-743 and EPI-589 outside the country.
The companies will collaborate on the research and development of EPI-589 with a focus on adult central nervous system disease.
Edison’s translational platform is based on redox biochemistry and it bridges important learnings derived from genetically confirmed pediatric rare mitochondrial disease to adult central nervous system disorders where redox and mitochondrial dysfunction may also play a critical role.
The Edison redox platform comprises proprietary laboratory and clinical tools that allow the discovery, optimization, and clinical validation of redox-directed drugs.
Edison will use the proceeds from the partnership to advance the late stage development and commercialization of EPI-743 for Leigh syndrome and Friedreich’s ataxia, and to advance EPI-743 in other exploratory phase 2 trials for rare pediatric diseases with shared mitochondrial mechanisms.
Edison chairman and CEO Guy Miller said that the partnership with Dainippon Sumitomo Pharma will allow Edison to accelerate the development and approval of the first drug for inherited respiratory chain diseases of the mitochondria.
"Our shared vision of the role of redox control and the mitochondria in human disease will help us extend our learnings derived from rare pediatric diseases to poorly treated acute and chronic adult CNS diseases," Miller added.