Licensing status

Publication and contact information

Drug platforms

Ex vivo wingless-type MMTV integration site family member 7A (WNT7A) treatment of myogenic cells prior to muscle cell transplantation to enhance both fusion with myofibrils and muscle function

Cell culture and mouse studies suggest ex vivo treatment with WNT7A could improve stem cell therapies for muscular dystrophies. In culture, WNT7A increased migration of satellite cell-derived mouse primary myoblasts compared with vehicle or WNT3A. In mice, ex vivo WNT7A increased migration of transplanted primary mouse myoblasts compared with vehicle. In a mouse model of muscular dystrophy, transplantation of human or mouse myogenic cells treated ex vivo with WNT7A improved muscle function and increased their engraftment, dispersal and fusion with myofibrils compared with transplantation of cells treated with WNT3A or vehicle. Next steps could include production of pharmaceutical-grade WNT7A.

Fate Therapeutics Inc.'s WNT7A analog FT301 is in preclinical development to treat muscular dystrophy.

SciBX 7(17); doi:10.1038/scibx.2014.504
Published online May 1, 2014

Patented; licensed to Fate Therapeutics

Bentzinger, C.F. et al. J. Cell Biol.; published online April 7, 2014;
Contact: Michael A. Rudnicki, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada