Studies suggest that the mechanism of ACE-031 may involve targeting multiple negative regulators of skeletal muscle growth. While myostatin is considered to be a negative regulator, other members of the transforming growth factor-β (TGF-β) superfamily, such as activin A, bone morphogenetic protein-2 (BMP-2), and BMP-7, may also play roles in inhibiting muscle development and protein synthesis.
Studies have suggested that introducing a soluble form of the activin type IIB receptor (ActRIIB), which is the receptor targeted by ACE-031, may possibly increase muscle mass more effectively than a myostatin-specific neutralizing antibody. Furthermore, in mice lacking myostatin, additional increases in muscle mass may occur when soluble ActRIIB was presented.
Based on this, it is proposed that by targeting multiple negative regulators of skeletal muscle, such as myostatin, activin A, and potentially other TGF-β family members, ACE-031 or similar agents may have a more significant impact on stimulating muscle growth in test models affected by muscle loss and degenerative conditions.(1)
