The NGLY1 Foundation ( is pleased to announce the appointment of Matthew Fox to its Board of Directors.

“Matt Fox brings years of experience in finance, biotech, drug development and personalized therapeutics to the board. Matt is currently CEO of Pairnomix, which identifies personalized therapies for patients with genetic epilepsy. The NGLY1 Foundation believes his expertise in achieving results for patients quickly and affordably will accelerate our search for therapies.”
… Matt Might, PhD, Chief Scientific Officer of

Matthew Fox is the Chief Executive Officer for Pairnomix, a genetic research company focused on rare neurological disease. Prior to joining Pairnomix, Matthew led corporate strategy on the executive team at Upsher-Smith Laboratories, a branded and generic pharmaceutical company. Before joining Upsher-Smith, Matthew spent a decade as a professional healthcare investor, last working as a Portfolio Manager at Bank am Bellevue in Zurich, Switzerland. Additionally, Matthew is a Board Member for Proximagen, a clinical stage biotech company, and Treasurer of the Edina School Board in his home town in Minnesota. He holds a B.A. in Neuroscience and Behavior from Wesleyan University (CT).

“We are extremely fortunate to have Matthew Fox join our organization,” said Carrie Ostrea, executive director of “He brings extensive experience in the finance and drug development fields, and his leadership is something that will be an invaluable asset as strives to finding therapies for our community.”

About the NGLY1 Foundation: The mission of the NGLY1 Foundation is to eliminate the challenges of N-glycanase Deficiency through research, awareness and support including 1] conducting and promoting science that may lead to understanding, treatments and cures for N-Glycanase Deficiency, 2] educating the scientific, medical, and general populations to improve diagnosis, understanding, and treatment of N-Glycanase Deficiency, and 3] providing guidance and community support for families of individuals (mostly children) affected by NGLY1 Deficiency.