Understand the source comparison
Follistatin-344 vs Other Myostatin Modulators: Research Comparison
Follistatin-344 Myostatin antagonist (direct binding) 40–60% increase in rodent models Phase I safety only. No strength endpoints published 18–32 hours (estimated); daily/EOD dosing likely required Strongest preclinical evidence but limited human validation. P
No winner is assigned.
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- Follistatin-344
- Myostatin antagonist (direct binding)
- 40–60% increase in rodent models
- Phase I safety only. No strength endpoints published
- 18–32 hours (estimated); daily/EOD dosing likely required
- Strongest preclinical evidence but limited human validation. Pharmacokinetic challenges remain unresolved
- ACE-031 (ActRIIB-IgG1)
- Activin receptor trap (blocks myostatin + activin A/B)
- 30–50% muscle mass increase in mice
- Phase II trial halted in 2013 due to epistaxis and telangiectasia
- Long-acting fusion protein; weekly dosing feasible
- More potent than follistatin but off-target vascular effects terminated development
- Bimagrumab (BYM338)
- Monoclonal antibody against ActRII
- 3.5% lean mass increase in sarcopenia patients (Phase II)
- Multiple Phase II trials completed; modest efficacy in humans
- IV infusion q4 weeks
- Only myostatin modulator with published human efficacy. Effect size smaller than animal models predicted
- Gene therapy (AAV-follistatin)
- Sustained follistatin overexpression via viral vector
- 15% muscle fiber CSA increase in primates
- Limited to muscular dystrophy trials; no strength athlete data
- Single administration; duration 6–24 months
- Most durable approach but regulatory/ethical barriers limit non-disease use
- YK-11 (myostatin inhibitor)
- Alleged selective androgen receptor modulator with myostatin inhibition
- No peer-reviewed animal data
- No clinical trials; sold as research chemical only
- Unknown pharmacokinetics
- No credible evidence of myostatin inhibition. Likely functions as weak androgen receptor agonist
- Follistatin-344 sits in a unique position: the preclinical evidence is more robust than almost any other myostatin modulator, but the human clinical translation is essentially absent. Bimagrumab, by contrast, has moved further through the clinical pipeline but shows far smaller effect sizes than animal models predicted. A pattern that raises questions about whether follistatin will face the same translational gap.