Mitobridge Adds NAD+ Modulation As A Therapeutic Approach For Improving Mitochondrial Function
Published: Sep 18, 2017
Company Licenses Intellectual Property from École polytechnique fédérale de Lausanne
CAMBRIDGE, Mass.--(BUSINESS WIRE)--Mitobridge, Inc., a biopharmaceutical company pioneering the discovery and development of products that improve mitochondrial function, broadens its therapeutic approach to include Nicotinamide Adenine Dinucleotide (NAD+) pathway modulation. The company entered into a license agreement with École polytechnique fédérale de Lausanne (EPFL) for intellectual property (IP) related to the treatment of a broad range of diseases as well as conditions of aging utilizing compounds that boost NAD+ levels. The company is advancing therapeutics for muscular dystrophies and myopathies as well as kidney, liver and neurodegenerative diseases that will benefit from improved mitochondrial function.
NAD+ is an essential coenzyme that plays a key role in metabolism, mitochondrial energy production and cell signaling. Numerous studies have demonstrated that reduced NAD+ levels are associated with mitochondrial dysfunction and that maintaining or raising NAD+ levels in cells that are under stress diminishes the deleterious effects. Compounds that protect or elevate NAD+ levels could provide therapeutic benefits in many medical and age-associated conditions. Mitobridge is developing drug candidates that are directed at multiple points in the NAD+ biosynthetic and metabolic pathway. Our approach to modulating NAD+ levels includes programs targeting Poly ADP Ribose Polymerase (PARP), Aminocarboxymuconate Semialdehyde Decarboxylase (ACMSD) and N'-Nicotinamide Methyltransferase (NNMT).
The exclusive worldwide license includes IP based on research from the laboratory of Johan Auwerx, MD, PhD. Dr. Auwerx, a leader in the field of NAD+ modulation, is a Professor at EPFL in Lausanne, Switzerland. “Modulating NAD+ levels represents an innovative strategy for improving mitochondrial function and holds great promise for therapeutic development. I am delighted that Mitobridge is pursuing this approach and look forward to working with the team to progress new product candidates,” stated Dr. Auwerx.
This intellectual property expands Mitobridge’s NAD+ modulation patent portfolio, which also includes composition of matter patent applications. “Our goal is to develop novel therapeutics for restoring healthy mitochondria and impacting severe diseases with limited treatment options. This license strengthens our IP estate and expands our opportunities to address multiple medical conditions associated with mitochondrial dysfunction,” stated George Mulligan, PhD, Senior Vice President, Translational Medicine.
Mitobridge is employing several therapeutic strategies for improving mitochondrial function. The first compound to enter clinical development is MA-0211 (MTB-1), an orally bioavailable PPARd modulator being tested in healthy volunteers in preparation for a trial in Duchenne Muscular Dystrophy (DMD). As DMD is characterized by mitochondrial defects, inadequate energy supply and muscle fibrosis, intervening with MA-0211 may be therapeutically beneficial for all DMD patients, regardless of their underlying dystrophin mutation. Additional clinical studies of MA-0211 in other diseases characterized by mitochondrial defects are currently being planned.
Mitobridge is dedicated to delivering therapeutics that improve mitochondrial function. Our team of experienced drug discovery, translational and development scientists are leveraging their exceptional knowledge of mitochondria biology to deliver a pipeline of innovative programs for the treatment of muscle and kidney diseases as well as other serious medical conditions. Headquartered in Cambridge, MA, Mitobridge was launched in October 2013 with funding from Astellas Pharma Inc., MPM Capital and Longwood Ventures. For more information about the Company, please visit www.mitobridge.com.
Lisa Paborsky, PhD, 617-401-9108
Senior Vice President, Corporate Development and Strategic Relations
MacDougall Biomedical Communications
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Dr. Stephanie May
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