NeuroVive signs mitochondrial medicine research agreement with US key opinion leader
Lund, Sweden, January 23, 2017 - NeuroVive Pharmaceutical AB (Nasdaq Stockholm: NVP, OTCQX: NEVPF), today announces that NeuroVive has signed a preclinical collaboration agreement with the Children’s Hospital of Philadelphia (CHOP) and Marni J. Falk, M.D., a US key opinion leader in the mitochondrial medicine field.
Dr. Falk’s research team at CHOP will evaluate compounds from NeuroVive’s research program, NVP015, in certain experimental disease models. The research team will study energy metabolism and disease development in models of mitochondrial complex I dysfunction.
Marni J. Falk. is an attending physician and director of the Mitochondrial Disease Clinical Center at CHOP, US, which is a large center for children and adults with mitochondrial disorders and a leading mitochondrial disease research center. Dr. Falk’s experience spans all the way from early experimental research through to clinical development and covers the whole drug development process. CHOP is one of the world’s largest children’s hospitals and has consistently been ranked as one of the best hospitals for children in the US.
“We feel fortunate to be able to initiate this collaboration with a well-recognized institution like CHOP and Dr. Marni Falk, a well-esteemed leader in the mitochondrial disease field. This is an important step in further advancing and strengthening our NVP015 program, as well as in the development of novel treatment opportunities for people with mitochondrial medicine disorders”, commented NeuroVive’s CMO Magnus Hansson.
About NeuroVive’s discovery program NVP015
The NVP015 discovery program is based on a concept from NeuroVive’s CSO, Dr. Eskil Elmér and collaborators to create a cell permeable prodrug of the endogenous energy substrate succinate. A prodrug is an inactive drug which is not activated until when entering the cell and the chemical structure is altered. A successful candidate from this discovery program in pediatric mitochondrial disorders would classify as an orphan drug.
About complex I dysfunction
One of the most common causes of mitochondrial diseases relates to complex I dysfunction, which occurs when energy conversion in the first of the five protein complexes in the mitochondrion that are involved in effective energy conversion does not function normally. This is apparent in disorders such as Leigh Syndrome and MELAS, both of which are very serious diseases with symptoms such as muscle weakness, epilepsy, and other severe neurological manifestations. Mitochondrial diseases usually present early in life and deteriorate progressively.
NeuroVive Pharmaceutical AB is a leader in mitochondrial medicine. The company is committed to the discovery and development of medicines that preserve mitochondrial integrity and function in areas of unmet medical need. The company’s strategy is to take drugs for rare diseases through
clinical development and into the market. The strategy for projects within larger indications outside the core focus area is out-licensing in the preclinical phase. NeuroVive enhances the value of its projects in an organization that includes strong international partnerships and a network of mitochondrial research institutions, as well as having expertise in drug development and production.
NeuroVive has a project in early clinical phase II development for the prevention of moderate to severe traumatic brain injury (NeuroSTAT®). NeuroSTAT has orphan drug designation in Europe and in the US. The R&D portfolio consists of several late stage research programs in areas ranging from genetic mitochondrial disorders to cancer and metabolic diseases such as NASH.
NeuroVive is listed on Nasdaq Stockholm, Sweden (ticker: NVP). The share is also traded on the OTCQX Best Market in the US (OTC: NEVPF).
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This information is information that NeuroVive Pharmaceutical AB (publ) is obliged to make public pursuant to the EU Market Abuse Regulation. The information was submitted for publication, through the agency of the contact person set out above, at 08:30 a.m. CET on January 23, 2017.