Direct myostatin inhibition looks more and more like where anabolic chemistry is headed. As I was writing this article, I almost called these drugs “the future of PEDs,” but I stopped myself—that isn’t quite right. In clinical tests, many of these drugs haven’t improved strength or performance, so I can’t really call them “performance-enhancing.” Compounds like ACE-083 and ACE-031 increased muscle size without delivering meaningful functional gains—one of the main reasons they were abandoned by big-pharma programs.
If ACE-083 was the “spot builder,” ACE-031 was pitched as the nuclear option—a circulating myostatin/activin trap meant to dial down myostatin levels across the entire body, not just where you pin it. Early human data showed lean mass moving in the right direction, and the hype machine did the rest.
Where I’m at: I haven’t run ACE-031 in my own cycles, and I’m not recommending it to my guys. My coaching isn’t about ego or forcing preferences; it’s about harm reduction and honesty. If a client is dead set on trying something experimental, I won’t play nanny—I’ll give you the straight science, the real risks, and the smartest possible way to avoid hurting yourself. Your body, your call. My job is to make sure you come out stronger, not broken.
No, I won’t personally use ACE-031 right now, nor would I advise my clients to use it; however, from here on out, I’m sticking to the best available data—the studies we have, what’s actually known, and where the limits are. So keep rocking.
| Name / Alias | ACE-031, Ramatercept, ActRIIB-IgG1, ActRIIB and Myostatin inhibitory peptide 7. |
| Category / Class | Recombinant fusion protein; activin type IIB receptor decoy (myostatin/ligand trap). |
| CAS Number | 1621169-52-5 |
| Chemical Structure / Formula | C133H227N43O33 |
| Mechanism of Action | Binds circulating myostatin and related ligands, preventing them from activating their receptor. |
| Primary Goal | Increase muscle mass by removing the “brake” on growth. |
| Status | Discontinued after early clinical trials. |
| Availability | No pharma development, but underground and “research peptide” versions are sometimes sold. |
| Benefits (What It Promises) | Muscle hypertrophy, potential lean mass gains. |
| Risks / Side Effects | Limited data; injection-site reactions, possible vascular side effects reported in trials. |
| Bodybuilder Angle | A follistatin-mimic fusion protein that circulates systemically and may boost overall muscle growth. |
| Outlook | Dropped by pharma, but knockoff versions still appear online in the research scene. |
ACE-031 is a recombinant fusion protein that works as a decoy receptor for myostatin and related growth-limiting factors. Instead of staying in one muscle like ACE-083, this one circulates systemically. That means once you inject it, ACE-031 floats through your blood and soaks up myostatin everywhere in your body.
ACE-031 was engineered by combining part of the activin type IIB receptor (the natural docking site for myostatin) with the Fc portion of an antibody. The result is a trap: when myostatin tries to bind its receptor, ACE-031 grabs it first, neutralizing it. Unlike ACE-083, which is local and muscle-specific, ACE-031 is designed for whole-body myostatin blockade.
This is a very different approach than ACE-083. Where ACE-083 is about spot growth and bringing up lagging muscles, ACE-031 targets global muscle growth. In early human trials, it pushed lean body mass up across the board—exactly the kind of signal that turns heads in the bodybuilding underground and the “for research only” online market. The catch: pharma couldn’t justify a drug that made muscles bigger without making patients stronger. It didn’t move the clinical endpoints for the diseases they were trying to treat—and that’s been a recurring theme with several myostatin inhibitors tested in humans.
ACE-031 advanced to early human trials for muscular dystrophy. It increased lean mass but did not improve muscle strength. The program was ultimately discontinued after concerns about vascular side effects—most notably nosebleeds and small blood-vessel changes—were observed in participants. Official development was shelved; however, underground “for research only” vendors now list ACE-031 for sale online.
– Systemic muscle growth across the whole body
– Potential for significant lean mass gains
– A true “bodywide myostatin inhibitor” compound, not just localized.
-Systemic Muscle Growth: In early human trials, ACE-031 increased lean body mass across the whole body. This confirmed the idea that shutting down myostatin systemically can drive hypertrophy beyond localized effects.
-Strength & Function: Even with added muscle mass, the trials didn’t show reliable improvements in strength or mobility. For pharma, that meant it wasn’t hitting the clinical endpoints they were after.
-Target Conditions: ACE-031 was aimed at Duchenne muscular dystrophy (DMD) and similar wasting diseases. While it bulked up muscle tissue, it didn’t translate into better function for patients.
-Safety: Some side effects popped up — nosebleeds, gum bleeding, and small vascular changes — thought to come from ACE-031 binding not just myostatin but also related proteins that influence blood vessels.
-Why It Was Abandoned: The combo of modest functional benefit and safety concerns pushed the brakes on development. Pharma decided it wasn’t worth the risk/reward, so the official program was shut down.
Reported issues in trials included nosebleeds, gum bleeding, and small vascular changes. These side effects likely came from ACE-031 binding not just myostatin but also other ligands in the TGF-β family that affect blood vessels. Underground versions carry the same uncertainties — purity, dosing, and safety are all up in the air.
ACE-031 is the big gun in the follistatin/myostatin world — not a calf-builder or delt-booster like ACE-083, but a full-body growth enhancer. If it ever hit the market in a clean, reliable form, it could be one of the most powerful tools for adding size we’ve ever seen. That said, it’s expensive, rare, and the knockoffs online can’t be trusted blindly.