Identity
a fully human monoclonal antibody (~150 kDa, modified IgG1) that binds the activin type II receptors (ActRIIA and ActRIIB) with far higher affinity than their natural ligands — thereby blocking myostatin, activin and related signals that limit muscle growth. Given roughly once monthly (originally IV, now also subcutaneous). This is the same myostatin/activin pathway as Follistatin (#40) — but reached by blocking the receptor with an antibody rather than mopping up ligands with a protein.
Mechanism (as proposed)
bimagrumab competitively occupies ActRIIA/ActRIIB, blocking myostatin, activin A and GDF-11 from signalling → skeletal-muscle hypertrophy, plus increased fat oxidation and improved insulin sensitivity. The fat loss is driven both by the metabolic lift from added muscle and by direct effects on adipose tissue — which is how it uncouples "lose fat" from "lose weight."