Voyager Therapeutics, Inc. and Sanofi Genzyme have restructured their gene therapy partnership under which Voyager gains worldwide rights to the VY-HTT01 Huntington’s disease program and ex-U.S. rights to the VY-FXN01 Friedreich’s ataxia program. The ex-U.S. rights to VY-FXN01 are, in turn, transferred from Voyager to Neurocrine Biosciences under the terms of their collaboration from January 2019. Additionally, Sanofi Genzyme obtains exclusive option rights to select novel AAV capsids owned or controlled by Voyager for exclusive use for up to two non-central nervous system (non-CNS) indications.  
 
“Our alliance with Sanofi Genzyme has been foundational for Voyager as we optimized the development of capsids, transgenes and gene therapy delivery,” said Andre Turenne, president and chief executive officer of Voyager. “We look forward to this new stage of the relationship and to advancing our programs and research efforts for patients with severe neurological diseases.”
 
Voyager will make a $10 million upfront payment to Sanofi Genzyme and an additional $10 million milestone upon filing of an investigational new drug (IND) application for VY-HTT01 or, if applicable, certain backup compounds for the treatment of Huntington’s disease. Preclinical studies are underway with VY-HTT01 which, if successful, are expected to support a potential filing of an IND application in late 2019.
 
In connection with the restructuring of the gene therapy relationship with Sanofi Genzyme, Voyager intends to seek a partner to advance its preclinical program for SOD1 ALS. Given this portfolio decision, Voyager no longer expects to file an IND application for VY-SOD102 in 2019. 
 
“We are committed to discovering and developing life-changing gene therapies for patients suffering from severe neurological diseases. Concentrating our efforts on HD and other promising new neurological targets will enhance our ability to achieve our maximum impact,” said Omar Khwaja, chief medical officer of Voyager. “We remain enthusiastic about the prospects for the SOD1 program and other potential program opportunities for ALS.”