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Comparison

ACE-031 vs Follistatin-344

Both are myostatin inhibitors, so the meaningful differences are in kinetics, evidence and regulatory status.

On published evidence alone, ACE-031 is the better documented of the two (clinical trials). That is a statement about the state of the literature, not a recommendation.

ACE-031 Follistatin-344
Class Myostatin inhibitors Myostatin inhibitors
Evidence Clinical trials Animal models only
Human trials ~4 ~1
Half-life ~10-15 days ~30 minutes
Reported range 500 mcg - 3 mg 100-300 mcg
Frequency Every 2-4 weeks (trial protocols) Once daily, short cycles
Routes Subcutaneous Subcutaneous, Intramuscular
FDA approved No No
Research use only Yes Yes
Banned in sport Yes Yes
Studied for Muscular dystrophy research (discontinued), Muscle mass research Muscle hypertrophy research, Muscular dystrophy gene therapy research
Reported side effects Epistaxis, Telangiectasia, Gum bleeding, Headache, Erythema Injection-site reactions, Headache, Poorly characterised

ACE-031

ACE-031 is a fusion protein joining the extracellular domain of activin receptor type IIB to an antibody Fc region. It acts as a decoy receptor, binding myostatin and related TGF-beta family ligands before they reach the real receptor and so removing the brake myostatin places on muscle growth. Trials in Duchenne muscular dystrophy showed increases in lean mass but were halted after epistaxis and telangiectasia appeared, reflecting the vascular role of the ligands it sequesters.

Follistatin-344

Follistatin-344 is a precursor isoform of the endogenous glycoprotein follistatin, which binds and neutralises activin A and myostatin. Removing myostatin inhibition permits muscle hypertrophy and hyperplasia, an effect demonstrated dramatically in gene-therapy animal models. The injectable protein is cleared within minutes and does not reproduce those results, which is the key practical caveat: the striking animal data comes from sustained genetic expression, not from injections.

ACE-031 vs Follistatin-344: common questions

What is the difference between ACE-031 and Follistatin-344?

Both are myostatin inhibitors. ACE-031: A soluble activin receptor decoy that increased muscle mass in trials before being discontinued over vascular side effects. Follistatin-344: A natural myostatin-binding glycoprotein, of interest for muscle growth but with a very short circulating half-life.

Which has stronger evidence, ACE-031 or Follistatin-344?

ACE-031 has the stronger evidence base (clinical trials, about 4 human studies) compared with Follistatin-344 (animal models only).

Are ACE-031 and Follistatin-344 FDA approved?

Neither is FDA approved for any indication.

References

Regulatory and primary sources

  1. WADA Prohibited List ↗ · current year
  2. FDA: Unapproved drugs and "research use only" products ↗ · regulatory status of non-approved products

Published literature

  1. Campbell C, McMillan HJ, Mah JK, et al.. Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial.Muscle Nerve 2017.PubMed 27462804 · doi:10.1002/mus.25268
  2. Tsuchida K. Clinical Applications of Ligand Traps Targeting Activin Type II Receptors.Antiinflamm Antiallergy Agents Med Chem 2026.PubMed 41487000 · doi:10.2174/0118715230416604251029062751
  3. Attie KM, Borgstein NG, Yang Y, et al.. A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers.Muscle Nerve 2013.PubMed 23169607 · doi:10.1002/mus.23539
  4. Angelidi AM, Stefanakis K, Chou SH, et al.. Relative Energy Deficiency in Sport (REDs): Endocrine Manifestations, Pathophysiology and Treatments.Endocr Rev 2024.PubMed 38488566 · doi:10.1210/endrev/bnae011
  5. Seo MW, Jung SW, Kim SW, et al.. Effects of 16 Weeks of Resistance Training on Muscle Quality and Muscle Growth Factors in Older Adult Women with Sarcopenia: A Randomized Controlled Trial.Int J Environ Res Public Health 2021.PubMed 34201810 · doi:10.3390/ijerph18136762
  6. Zhang M, Song Y, Zhu J, et al.. Effectiveness of low-load resistance training with blood flow restriction vs. conventional high-intensity resistance training in older people diagnosed with sarcopenia: a randomized controlled trial.Sci Rep 2024.PubMed 39558011 · doi:10.1038/s41598-024-79506-9
  7. Ren Y, Zhao H, Yin C, et al.. Adipokines, Hepatokines and Myokines: Focus on Their Role and Molecular Mechanisms in Adipose Tissue Inflammation.Front Endocrinol (Lausanne) 2022.PubMed 35909571 · doi:10.3389/fendo.2022.873699
  8. Vannuccini S, Clemenza S, Rossi M, et al.. Hormonal treatments for endometriosis: The endocrine background.Rev Endocr Metab Disord 2022.PubMed 34405378 · doi:10.1007/s11154-021-09666-w
  9. Bolanle IO, de Liedekerke Beaufort GC, Weinberg PD. Transcytosis of LDL Across Arterial Endothelium: Mechanisms and Therapeutic Targets.Arterioscler Thromb Vasc Biol 2025.PubMed 40013359 · doi:10.1161/ATVBAHA.124.321549
  10. Stefanakis K, Kokkorakis M, Mantzoros CS. The impact of weight loss on fat-free mass, muscle, bone and hematopoiesis health: Implications for emerging pharmacotherapies aiming at fat reduction and lean mass preservation.Metabolism 2024.PubMed 39481534 · doi:10.1016/j.metabol.2024.156057
  11. Zhuang M, Gu Y, Wang Z, et al.. Effects of 12-week whole-body vibration training versus resistance training in older people with sarcopenia.Sci Rep 2025.PubMed 40011687 · doi:10.1038/s41598-025-91644-2

Literature retrieved from PubMed on October 16, 2026, favouring human studies and reviews. Numbered markers in the text show which paper supports which statement; uncited entries are background reading.

Read this first This page compares published reference data. It is not medical advice and not a recommendation to use either compound. Several compounds documented on this site are not approved for human use.