ACE-031 (1mg)


Size: 1mg
Contents: ACE-031 (1mg)
Form: Lyophilized powder
Purity: >99%
SKU: P-ACE031-1

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ACE-031 Peptide – the Potent Muscle Protectant

Muscle development, followed by its growth and thereby regeneration, all processes take place throughout the course of human life. These are vital functions of the body which occur right from embryogenic, followed by fetal, and then adult life.

Early discovery in 1997 (1) showed that a protein, named Myostatin, is produced endogenously by the myocyte cells which act on muscle cells and then inhibit their growth. Studies (1) showed that mice in which these proteins were absent had twice the amount of muscle growth. In order to prevent muscle growth inhibition, it was crucial to understand how Myostatin works, and then reverse, if not prevent, its mechanism.

This is where the peptide ACE-031 comes into play. This peptide aims to disrupt the working of Myostatin protein and promote muscle growth in individuals in whom muscle development is scarce.

ACE-031 Peptide Basics

ACE-031 peptide, also known as ACVR2B (activin receptor type IIB) peptide, is a fusion compound consisting of the activin receptor called type IIB and recombinant immunoglobulin IgG1 FC, which is a form of human antibody (2).

This peptide is of soluble kind, and it’s known to easily bind with myostatin protein to prevent its inhibitory effects on muscle growth. Besides this, the peptide also shows positive effects on the metabolism activities, fat storage and sperm health.

Historical Background

As previously mentioned, the endogenous myostatin protein was first discovered in 1997 where its inhibitory effects on muscle growth also became known due to the comparative studies in mice (1).

This peptide is the engineered (or synthetic) version of the naturally occurring ACV2RB receptors. Once synthesized, the peptide was developed by Acceleron Pharma, exclusively for the treatment of Duchenne Muscular Dystrophy (DMD). Clinical trials conducted so far have scientifically affirmed that the peptide can be safely administered in the human body. This will be described in detail in the article below.

Peptide Mechanism of Action

In layman terms, we can say that muscle growth is regulated in the body via proteins which function as ‘on’ and ‘off’ switches. The compound works by preventing the ‘off’ switch and inhibits the ‘off’ signal from being circulated in the body.

ACE-031 peptide binds with the myostatin protein and neutralizes its effects. Consequently, it turns off the ‘off’ signal and promotes muscle production. The peptide helps to build up the muscle mass and improve muscle strength.

Biological Uses of ACE-031

ACE-031, or the ACVR2B peptide, has shown various advantageous biological effects including:

  • Increases lean body muscle mass
  • Promotes muscle protection
  • Boosts energy
  • Increases metabolism
  • Improves body strength
  • Promotes tissue and muscle repair
  • Increases bone density
  • Potential treatment of Duchenne Muscular Dystrophy (DMD)
  • Potential Cancer treatment
  • Prevents muscle loss

Research and Clinical Studies

Studies Associated with Muscle Protection

A clinical trial (3) was conducted in healthy, postmenopausal women to determine the safety and efficacy of the peptide in muscle protection.

As part of the study, 48 female candidates were selected who were divided into two groups – one group received the placebo while the others received ACE-031 peptide at the dose of 0.02 to 3 mg/kg via subcutaneous route.

After 15 days, all female candidates were examined. The participants who were treated with the peptide showed a 3.3% increase in their body muscle mass and 5.1% increase in their thigh muscle mass. Further bioanalysis also suggested that the compound improved the fat and bone metabolism in these participants.

While ACE-031 was well tolerated in all candidates, the most common side effect seen was erythema at the injection site (i.e. swelling, redness at the site).

This study proved that a single dose treatment of the peptide is generally well tolerated in middle aged women (after menopause) and is effective in increasing, and thereby protecting, overall muscle mass.

Studies with Maximum Muscle Cell Protection

Based on scientific research (4), it was known that proteins like Myostatin are negative regulators of skeletal muscle growth. These proteins primarily send off the signal in the body via the activin receptor type IIB on skeletal muscles and cause muscle wasting conditions.

The fact that the peptide, which is a soluble form of the activin receptor type IIB, acts by binding with Myostatin and reversing its effects, suggests that the peptide may lead to maximum muscle protection and prevent muscle wasting in humans.

While this is based on scientific research and facts, clinical studies are yet to be conducted to confirm this hypothesis.

Increased Metabolism and Energy

Scientific research (5) in mice has shown that myostatin not only prevents muscle growth but also negatively affects the energy metabolism in muscles. In simpler words, excessive myostatin leads to increased fatigue and lethargy.

Studies in mice (5) have shown that by blocking the naturally occurring ACE-031 proteins, it promotes increased lactate levels in the serum and causes severe damage to the metabolic energy of the muscles. Hence, when treated with the peptide, it not only prevents muscle growth inhibition by myostatin but also improves the oxidative capacity of the muscles. This way, the energy metabolism of the skeletal muscles increases and causes protection against excessive fatigue and against the negative effects of the radical production.

Studies with Increased Strength

Continuous research (6) by scientists has shown that the function of the peptide is beyond its ability to inhibit myostatin. By preventing oxidative stress in muscles, the peptide also improves the capacity of the muscle tissue to generate a force, and in turn preserve energy and stimulate the muscles toward oxidative respiration.

When the compound was administered in mice, it improved the maximal contractile force in mice by 40% and total contractile force in mice by 25%.

This study demonstrates that while clinical studies are yet to be conducted, the ACE-031 peptide significantly improves muscle strength.

Increased Bone Density

As part of the research (7), 32 mice were subjected to this study where the mice were divided into two groups and were either administered with placebo or the peptide once a week for 7 weeks.

After the completion of the study, it was observed that the ACE-031 peptide treated mice had increased muscle mass and excessive body weight, along with increased density in bones. Upon further study, it was observed that the increased bone density was not incidental, but was due to enhanced mineralization that boosted bone strength and overall health by almost 30% in the peptide treated mice.

This study suggested that the peptide may be a potential source to treat osteoporosis in humans. The fact that the peptide can not only boost muscle strength and bone density, but also reduce fat deposits in the body, which makes the peptide an interesting candidate.

Studies Suggesting Peptide a Potent Anti-cancer Adjunct

Chemotherapy and anti-cancer drugs are known to lead to increased muscle loss. Science has proven that both these treatments lead to increased muscle cell death and thereby necrosis (a condition characterized by limited blood supply and cellular death).

During a study (8), it was seen that when ACE-031 peptide was administered in the cell culture induced with anti-cancer medication, it prevented the activation of the signalling pathway that led to muscle loss.

Consequently, there was reduced cellular death. Furthermore, the peptide protected mitochondrial function and boosted muscle energy. Not only this, some forms of cancer forms myostatin in the body which further leads to muscle loss and wasting (9).

This is why scientists have suggested that clinical trials must be conducted on cancer patients to confirm the biological effects of the peptide. These theories suggest that the peptide can be a potent supplement to be used in conjunction with anti-cancer drugs to reduce (or preferrably eliminate) the negative effects of these medications.

Studies with DMD

Duchenne Muscular Dystrophy (DMD) is a progressive form of serious muscular dystrophy that is a genetic defect that primarily occurs in boys (10).

First Clinical Trials

A 2017 clinical trial (11) was conducted with the primary objective to study the effect of the peptide on the inhibitory mechanisms on muscle development and potentially help treat DMD.

During the clinical trial, young boys suffering from DMD were subjected to the peptide compound. The boys were divided into two groups, one was administered with placebo and the other with peptide via a subcutaneous route every 2 to 4 weeks.

While there were no serious side effects noted, the study was stopped midway due to safety concerns over epistaxis (i.e., bleeding of nostrils) and telangiectasias (i.e., dilation of blood vessels and visible veins, mainly around cheeks, chin, and nose).

Once the trial was stopped, the results were examined between both groups. A 6 minute walking test was conducted where the boys treated with the peptide had improved results as compared to the placebo treated boys. Moreover, the peptide treated group had increased body mass, improved bone density and decreased fat mass.

Additional Clinical Trials

Phase I clinical trials began in September 2008 (12) with 48 boys suffering from DMD. These patients were administered with the peptide compound via subcutaneous route at the doses of 0.02 to 3 mg/kg bodyweight.

After the trials, it was seen that the muscle volume in the boys had increased by 3.5% as compared to 0.2% in the group treated with placebo.

Phase II clinical trials were amended in April 2010 (12) with 24 subjects enrolled in this study, 6 of which were administered with placebo and 18 were treated with the peptide, for 12 weeks. Motor function tests were conducted on all patients after the completion of the study. As part of these tests, a 6 minute walk, a 10 minute walk/run, and 4 stair climb tests were conducted. All tests showed that peptide treated boys had significantly improved results compared to the placebo treated boys.

Side Effects Associated With ACE-031

Based on the research and clinical trials conducted to date, it was observed that some of the participants had noticeable side effects.

While these side effects were not prominent in all candidates, the following may be caused on the long term use of the peptide:

  • Pain, redness, and swelling at the site of peptide administration
  • Bleeding of the nose
  • Bleeding of the gums
  • Increased body temperature
  • Weakness, dizziness

Most of these side effects are known to vanish once the peptide treatment is discontinued. Hence, based on the research conducted so far, it can be stated that these effects are reversible and do not pose any serious harm to humans.

ACE-031 Peptide FDA Approval

The peptide is currently under investigation for its potential treatment of Duchenne Muscular Dystrophy.

In August 2010, the peptide received an ‘orphan’ drug designation from the US FDA for treating DMD(13) to help expedite the ongoing research of the peptide. ‘Orphan’ drugs are the medications that are used to cure serious disorders that currently do not have any treatment discovered.


ACE-031 peptide, also known as ACVR2B, is a soluble fused compound consisting of the activin receptor called type IIB and recombinant immunoglobulin IgG1 FC. A potent analogue of the activin receptor, this peptide has proven to show fruitful biological effects in humans.

The peptide exerts its properties by binding with the myostatin protein, preventing the inhibitory effects of the protein on the muscle development, and thereby increasing muscle mass, muscle strength and overall well being.

Research so far has demonstrated significant results indicating that the peptide may potentially be used to treat serious ailments including osteoporosis and DMD, and can act as a potent adjunct in anti-cancer treatments. Successful clinical Phase I and II trials of the peptide in battling DMD have led the peptide to be designated as an ‘orphan drug’ to treat such genetic muscular disorders.

Research and further clinical trials continue to date to fully study the effects of ACE-031 and help establish that the compound is a potent therapeutic agent to combat various human ailments.


(1) McPherron AC, Lawler AM, Lee SJ. Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member. Nature. 1997 May 1;387(6628):83-90.

(2) Campbell C, McMillan HJ, Mah JK, Tarnopolsky M, Selby K, McClure T, Wilson DM, Sherman ML, Escolar D, Attie KM. Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial. Muscle Nerve. 2017 Apr;55(4):458-464.

(3) Attie KM, Borgstein NG, Yang Y, Condon CH, Wilson DM, Pearsall AE, Kumar R, Willins DA, Seehra JS, Sherman ML. A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers. Muscle Nerve. 2013 Mar;47(3):416-23.

(4) Morvan F, Rondeau JM, Zou C, Minetti G, Scheufler C, Scharenberg M, Jacobi C, Brebbia P, Ritter V, Toussaint G, Koelbing C, Leber X, Schilb A, Witte F, Lehmann S, Koch E, Geisse S, Glass DJ, Lach-Trifilieff E. Blockade of activin type II receptors with a dual anti-ActRIIA/IIB antibody is critical to promote maximal skeletal muscle hypertrophy. Proc Natl Acad Sci U S A. 2017 Nov 21;114(47):12448-12453.

(5) Relizani K, Mouisel E, Giannesini B, Hourdé C, Patel K, Morales Gonzalez S, Jülich K, Vignaud A, Piétri-Rouxel F, Fortin D, Garcia L, Blot S, Ritvos O, Bendahan D, Ferry A, Ventura-Clapier R, Schuelke M, Amthor H. Blockade of ActRIIB signaling triggers muscle fatigability and metabolic myopathy. Mol Ther. 2014 Aug;22(8):1423-1433.

(6) Béchir N, Pecchi E, Vilmen C, Le Fur Y, Amthor H, Bernard M, Bendahan D, Giannesini B. ActRIIB blockade increases force-generating capacity and preserves energy supply in exercising mdx mouse muscle in vivo. FASEB J. 2016 Oct;30(10):3551-3562.

(7) Puolakkainen, Tero et al. “Treatment with soluble activin type IIB-receptor improves bone mass and strength in a mouse model of Duchenne muscular dystrophy.” BMC musculoskeletal disorders vol. 18,1 20. 19 Jan. 2017.

(8) Barreto R, Waning DL, Gao H, Liu Y, Zimmers TA, Bonetto A. Chemotherapy-related cachexia is associated with mitochondrial depletion and the activation of ERK1/2 and p38 MAPKs. Oncotarget. 2016 Jul 12;7(28):43442-43460.

(9) Lokireddy S, Wijesoma IW, Bonala S, Wei M, Sze SK, McFarlane C, Kambadur R, Sharma M. Myostatin is a novel tumoral factor that induces cancer cachexia. Biochem J. 2012 Aug 15;446(1):23-36.

(10) About Duchenne Muscular Dystrophy.

(11) Campbell C, McMillan HJ, Mah JK, Tarnopolsky M, Selby K, McClure T, Wilson DM, Sherman ML, Escolar D, Attie KM. Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial. Muscle Nerve. 2017 Apr;55(4):458-464.

(12) Study of ACE-031 in Subjects With Duchenne Muscular Dystrophy.

(13) ACE-031 for the Treatment of Duchenne Muscular Dystrophy.

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