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Follistatin-344 Mechanism of Action Detailed: Comparison to Related Compounds
The table below compares follistatin-344's mechanism to other myostatin antagonists and anabolic agents used in muscle research protocols. | Compound | Primary Mechanism | Myostatin Binding Affinity | SMAD Pathway Impact | Satellite Cell Effect | Clinical Tria
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This page preserves a source comparison for education. It does not add a rating, recommendation or clinical judgment.
- The table below compares follistatin-344's mechanism to other myostatin antagonists and anabolic agents used in muscle research protocols.
- | Compound | Primary Mechanism | Myostatin Binding Affinity | SMAD Pathway Impact | Satellite Cell Effect | Clinical Trial Status | Professional Assessment ||—|—|—|—|—|—|| Follistatin-344 | Competitive myostatin sequestration via FS domain binding | Kd ~600 pM | Prevents SMAD2/3 phosphorylation by blocking receptor activation | Derepresses quiescence. Allows activation under training stimulus | Phase I completed (muscular dystrophy). No current active trials | Most physiologically native myostatin antagonist; selectivity over activin A reduces off-target risks but also limits potency ceiling || ACE-031 | Soluble activin receptor IIB decoy. Binds myostatin, activin A, GDF-11 | Kd ~50 pM (higher affinity than follistatin) | Broader SMAD inhibition due to activin A binding | Strong satellite cell activation but also impacts reproductive signalling | Discontinued Phase II (safety concerns. Nosebleeds, telangiectasia) | Higher potency than follistatin but non-selectivity caused vascular adv