Minovia Therapeutics, Ltd. and Astellas Pharma Inc. announced a worldwide strategic collaboration and license agreement for the research, development, and commercialization of novel cell therapy programs for diseases caused by mitochondrial dysfunction.

Through this strategic collaboration, Astellas and Minovia aim to accelerate the creation of allogeneic mitochondrial cell therapy programs. The two companies will jointly research cell therapy program candidates comprised of cells derived from Astellas’ proprietary genetically-engineered, induced pluripotent stem cells and augmented with Minovia’s proprietary MAT platform technology. The goal of these programs will be to treat diseases caused by mitochondrial dysfunction, through the transfer of healthy mitochondria to restore the patients’ tissues.

“We are excited and honored to collaborate with Astellas,” stated Minovia’s Co-founder and Chief Executive Officer, Natalie Yivgi-Ohana, Ph.D. “We share with Astellas both their passion for mitochondrial science and their commitment to patients in need of new therapies. As Minovia continues the development of Mitochondrial Augmentation Therapy, we believe this partnership is critical to accelerate the development of off-the-shelf, allogeneic cell therapy programs for the many patients living with mitochondrial diseases caused by mitochondrial dysfunction.”

Naoki Okamura, Representative Director, Corporate Executive Vice President, Chief Strategy Officer and Chief Financial Officer, at Astellas said, "We, at Astellas, have positioned mitochondrial biology as one of the Primary Focuses of our research and development strategy to develop therapies for patients with unmet medical needs. One of the aspirations of this Primary Focus is to establish a mitochondrial cell therapy platform. Minovia is pioneering mitochondrial cell therapy and has unique technologies for enhancing delivery of healthy mitochondria to the patients’ cells. This strategic collaboration with Minovia will accelerate and expand our pipeline of treatment options for patients with diseases with underlying mitochodrial dysfunction.”