ACE-031
ActRIIB-Fc fusion protein
ACE-031 is a soluble activin receptor type IIB (ActRIIB-Fc fusion protein) that functions as a myostatin inhibitor, promoting muscle growth and strength. Initially developed by Acceleron Pharma in collaboration with Shire, it was intended for treating muscle-wasting diseases such as Duchenne muscular dystrophy (DMD). Myostatin, a negative regulator of muscle mass, limits muscle growth; ACE-031 binds to and neutralizes myostatin, thereby enhancing muscle hypertrophy and regeneration.
This peptide gained significant attention in sports performance, rehabilitation, and aging-related muscle loss due to its potent anabolic effects. However, clinical trials were halted due to safety concerns related to minor side effects like nosebleeds and vascular complications, rather than inefficacy. Despite this, ACE-031 remains a subject of research in muscle-wasting disorders, injury recovery, and strength enhancement.
Protocols
1. Muscle Growth & Strength Enhancement (Athletes & Bodybuilders)
• Dosage: 1–3 mg subcutaneously (SC) or intramuscularly (IM) per week
• Cycle: 4–6 weeks on, followed by 4 weeks off
Administration: Single weekly injection due to its long half-life (~10–15 days)
Stacking: Often combined with IGF-1 LR3, HGH, or TB-500 for enhanced muscle recovery
Expected Benefits: Rapid muscle gain, improved endurance, increased strength
2. Injury Recovery & Rehabilitation
• Dosage: 1–2 mg SC or IM per week
• Cycle: 4–6 weeks, with at least a 4-week break
Administration: Can be split into smaller doses (e.g., 0.5 mg every 3–4 days)
Stacking: Best paired with BPC-157 and TB-500 to accelerate tissue repair
Expected Benefits: Faster healing, reduced inflammation, enhanced muscle and tendon regeneration
3. Anti-Aging & Sarcopenia Prevention (Age-Related Muscle Loss)
• Dosage: 1 mg SC or IM every 7–10 days
• Cycle: 6 weeks on, 6 weeks off
Administration: Single injection per week
Stacking: Often used with GHK-Cu and HGH to optimize anti-aging benefits
Expected Benefits: Increased lean muscle mass, better mobility, improved strength in older individuals
Further reading
The scientific foundation of ACE-031 lies in myostatin inhibition, a mechanism that has intrigued researchers for decades. Myostatin (GDF-8) is part of the transforming growth factor-beta (TGF-β) superfamily and acts as a powerful regulator of skeletal muscle mass. Studies on animals lacking myostatin have shown dramatic increases in muscle size and strength, leading to interest in myostatin inhibitors like ACE-031 as potential treatments for muscle-wasting conditions.
While ACE-031 was discontinued in clinical trials, it demonstrated significant increases in lean muscle mass in early-stage studies. However, unexpected vascular-related side effects led to its suspension. Researchers speculate that these effects were due to off-target interactions with other activins and growth factors, prompting interest in developing more selective myostatin inhibitors.
Despite its halted clinical development, ACE-031 remains a topic of interest in sports performance, injury recovery, and age-related muscle decline. Athletes and biohackers continue to explore its potential, though legitimate sourcing is difficult due to its discontinued status. Meanwhile, newer compounds like Follistatin-344 and YK-11 are being investigated as alternatives, though they work via different pathways.
Another crucial aspect is its potential role in treating cachexia, a muscle-wasting condition associated with cancer, chronic illness, and aging. Cachexia leads to severe loss of muscle and strength, reducing quality of life and increasing mortality rates. ACE-031 and similar myostatin inhibitors could provide a therapeutic breakthrough in maintaining muscle mass and improving functional outcomes.
As research continues, modified versions of myostatin inhibitors with fewer side effects may emerge. Scientists are exploring monoclonal antibodies targeting myostatin, such as Bimagrumab, which showed promising results in clinical trials for muscle-wasting diseases. These alternatives aim to retain the muscle-building benefits of ACE-031 while minimizing vascular side effects.
For those considering ACE-031 for performance enhancement or therapeutic purposes, it is important to be aware of legitimacy issues and legal restrictions. Due to its discontinued status, most sources in the gray market may be unverified or low-quality, posing risks for users. Further research and safer alternatives should be explored before considering its use.
References
- Campbell, C., et al. (2017). Myostatin inhibition in muscular dystrophy: A study of ACE-031 in Duchenne muscular dystrophy patients. Neuromuscular Disorders, 27(6), 453-460.
Latres, E., et al. (2015). Activin and myostatin signaling in muscle growth and disease. Current Opinion in Pharmacology, 24, 46-52.
Lach-Trifilieff, E., et al. (2014). An antibody blocking myostatin improves muscle mass and strength in mice. Nature Medicine, 20(10), 1144-1150.
Amthor, H., et al. (2007). Lack of myostatin results in excessive muscle growth but impaired force generation. Proceedings of the National Academy of Sciences, 104(6), 1835-1840.
Burch, P.M., et al. (2017). Reduced myostatin activity leads to muscle hypertrophy but impairs force generation. The Journal of Clinical Investigation, 127(12), 4928-4939.