Follistatin / ACE-031
Myostatin Inhibition, Big Muscle Claims, Failed Clinical Programs
Evidence grade 2 of 5, Thin. Read how the Atlas grades evidence.
The written rationale for this grade is still being prepared.
- FDA
- Not FDA-approved; ACE-031 clinical program halted (2011) and discontinued (2013)
Reference only. Not medical advice.
What can go wrong
The ActRIIB approach carries documented vascular bleeding risks (epistaxis, gum bleeding, telangiectasias) from off-target BMP-9/BMP-10 inhibition, the reason ACE-031's real trials stopped. Gray-market 'follistatin' products are unregulated proteins of unknown purity, identity, and activity; injecting them has no safety data. Powerful muscle-growth signaling also has unstudied long-term consequences.
This is something to take to a clinician. The Atlas can tell you what is known about follistatin / ace-031 in general. It cannot tell you what is happening in your body, and the difference matters most for exactly the symptoms that bring people to this page.
Follistatin and ACE-031 both target the myostatin/activin pathway that limits muscle growth, the biology behind naturally 'double-muscled' animals. Follistatin is an endogenous protein that binds and neutralizes myostatin; gray-market 'follistatin-344' is sold to bodybuilders. ACE-031 (ramatercept) was a genuine drug candidate from Acceleron Pharma: a soluble ActRIIB-Fc fusion protein that trapped myostatin and related ligands. Its clinical program in Duchenne muscular dystrophy was halted in 2011 and discontinued in 2013 over vascular safety signals, a cautionary tale the muscle-growth marketing omits.
The 'double-muscle' dream, with a real clinical cautionary tale attached.
What people take it for
These are the reasons people give for taking it. They are not effects it has been shown to have.
How it is supposed to work
Myostatin (GDF-8) signals through ActRIIB to restrain muscle growth. Follistatin binds myostatin (and activins) directly, releasing that brake. ACE-031 was a decoy receptor, the ActRIIB extracellular domain fused to IgG1 Fc, that soaked up myostatin and related ligands, increasing lean mass in early study.
Why the ActRIIB program failed
ActRIIB is not a myostatin-only receptor; it also mediates BMP-9 and BMP-10 signaling important to vascular integrity. In Acceleron's Phase 2 ACE-031 trial in boys with Duchenne muscular dystrophy, subjects developed nosebleeds, gum bleeding, and telangiectasias (small dilated skin vessels), a vascular safety signal attributed to off-target BMP inhibition. The trial was halted in April 2011 despite trends toward increased lean mass, and development was discontinued in 2013. Broad ligand-trapping was too non-specific to be safe.
What people get wrong
Often said'Myostatin inhibitors safely make you superhuman.'
ActuallyThe most advanced real myostatin-trap program (ACE-031) was halted for vascular safety and abandoned; gray-market follistatin is unregulated and unproven. The 'double-muscle' framing ignores this clinical failure.
Who profits, and who pushes back
Nobody is named here yet, because we have not done that work on this entry. Read that as unfinished. Somebody almost certainly sells this, and somebody almost certainly disputes it. Assume both until we have checked.
What we do not know
- Can any myostatin-pathway agent achieve muscle benefit without the vascular/off-target problems that sank ACE-031?
- Is injected gray-market 'follistatin' even the active protein it claims to be?
The market for this
What follows describes how this is bought and sold. It is not a buying guide and it is not an endorsement of any seller.
Follistatin is sold as an unregulated research-chemical protein; ACE-031 has no legitimate supply and was never marketed. Identity and activity of gray-market 'follistatin' are especially hard to verify.
At a glance
- Target
- Myostatin / activin (ActRIIB) pathway
- ACE-031 structure
- ActRIIB extracellular domain-IgG1 Fc fusion
- Developer (ACE-031)
- Acceleron Pharma
- Program halted
- 2011; discontinued 2013
What this entry does not yet cover
What follows is unfinished work on our side, not a finding about Follistatin / ACE-031. A short entry is not a safe entry.
- Cost and market. We have not documented what it sells for or who sells it.
- Supply chain. We have not mapped where it is made.
- Who uses it. We have not documented the user groups.
- What could change. No forward-looking summary yet.
- How it compares. We have not set it against the alternatives.
- Children and teenagers. We have not checked what is known about younger people.
- Where we land. We have not taken a position on this yet.
Sources
The studies below are named and described, but not linked. You cannot open them from here and check our reading against them, which means this page is our summary of the literature rather than a document you can verify. Weigh it accordingly until the links exist.
The studies that matter
ACE-031 Phase 2 in Duchenne muscular dystrophy (Acceleron/Shire)2011
Trends toward increased lean and reduced fat mass, but halted over vascular safety signals (nosebleeds, gum bleeding, telangiectasias)
Program discontinuation2013
Acceleron discontinued ACE-031 development