A novel soluble recombinant ACVR1-Fc was generated.
ACVR1-Fc could suppress dysregulated ACVR1 signaling and chondro-osseous differentiation.
In vitro model for FOP based on HUVECs was established.
A novel receptor-mediated approach to block ligand-mediated ACVR1 signaling holds promise in the treatment of FOP.