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ACE-031, also known as ramatercept, is not a synthetic peptide but a recombinant fusion protein: the extracellular ligand-binding domain of the human activin receptor type IIB joined to the Fc region of human immunoglobulin G1. It works as a decoy. Myostatin, also called GDF-8, is a transforming growth factor beta family member secreted by muscle that limits its own growth by signalling through ActRIIB and downstream SMAD2/3. By presenting a soluble copy of that receptor domain into circulation, ACE-031 binds myostatin before it can reach receptors on the muscle cell surface, and the Fc portion gives the construct a long half-life through neonatal Fc receptor recycling. The mechanism is not selective for myostatin alone — ActRIIB also binds activin A, GDF-11 and several bone morphogenetic proteins, so the trap captures all of them. That breadth is what ended its clinical development: trials in Duchenne muscular dystrophy were halted after nosebleeds, gum bleeding and telangiectasia, adverse effects attributed to cross-inhibition of BMP9 and BMP10, which regulate vascular endothelium.