The development of the myostatin inhibitor known as ACE-031 has been halted by the pharmaceutical firms Acceleron Pharma and Shire. Recently, in a combined press statement [, May 2, 2013], they disclosed this information to the general public. A peculiar turn of events, considering that Muscle & Nerve had only a few weeks prior released a report indicating that ACE-031 is the kind of thing that any anyone who thinks themselves to be a chemical bodybuilder would be overjoyed to have the financial means to purchase.

An underground example of inject-able ACE-031, which may be found in the image above, is a synthesized integrin receptor class IIB. This receptor is present in muscle cells as well; it is designed to bind certain proteins such as myostatin, GDF11, and activin A and B. When myostatin binds to an activin receptor of type IIB, it impedes the creation of new muscle fibres and hence prevents hypertrophy. Myostatin can really cause the breakdown of muscle when the conditions are “just right.”

If ACE-031 is injected, this phenomenon does not take place at all. The artificial activin sensor type IIB acts as a filter, deactivating the muscle inhibitory proteins once they have been removed from the system.

In 2007, Acceleron Pharma had not yet given up hope for the ACE-031 clinical trial. At that point in time, the company’s only supporting evidence consisted of tests conducted on animals. However, in 2013, they reported the findings of a human research in which 48 young women between the ages of 45 and 75 were given a single injectable containing 0.02, 0.05, 0.1, 0.3, 1 or 3 mg of ACE-031 per kg of bodyweight. The investigation was conducted in healthy volunteers. The chemical continued to be distributed throughout the body for an extended period of time; its half-life was somewhere between ten and fifteen days.

However, the single injection did cause an increase in muscle mass. The administration of 3 milligrammes per kilogramme of body weight resulted to a rise in muscle volume of 5 percent, an increase in lean body mass of 3 percent (just over a kilogramme), and an apparent reduction in fat mass.

The injection caused a decrease in the concentration of leptin while simultaneously increasing the level of adiponectin. This would seem to show that ACE-031 is responsible for the breakdown of fat mass.

In addition to this, the myostatin inhibitor caused an increase in the concentration of bone specific alkaline phosphatase (BSAP) in the blood while simultaneously causing a decrease in the concentration of C-terminal type 1 connective telopeptide (CTX). This would seem to show that ACE-031 is beneficial to bone health. In animal tests, Acceleron was able to demonstrate similar effects using RAP-031, which is a mouse-specific version of ACE-031. [Endocrinology. September 2010; 151(9):4289-300]

If you read the article that was published in Muscle & Nerve, you might find yourself wondering why Acceleron has decided to pause the development of ACE-031. And why it does not make war on the proprietors of the web shops that are content to flout Acceleron’s patents and offer ACE-031 for prices that no regular medicines business can compete with.

You can find the response to your question in a post that’s been made just on site of the Muscular Disease Association. [ May 2, 2013] This article details a clinical study (NCT01099761) that took place in 2011 and involved the administration of ACE-031 to children suffering from muscular dystrophy. During the course of the experiment, the researchers saw undesirable consequences, which forced them to terminate the investigation.

“The adverse reactions that the trial participants experienced, which included slight bleeding from the gums and nose as well as dilatation of the blood vessels in the skin, were not, in and of themselves, regarded to be harmful. Nevertheless, the corporations and regulatory bodies involved have stated that they want further time to properly comprehend these occurrences before starting clinical research with ACE-031.

The research article that was published in Muscle & Nerve uncovered several more peculiar adverse effects as well. The administration of ACE-031 resulted in a precipitous drop in the amount of FSH that was present in the women participants. The researchers are unsure of both how this occurred and what the potential consequences of it may be.

Wyeth’s research on the myostatin blocker MYO-029 appears to be going nowhere as well. In 2008, disheartening findings from a trial including MYO-029 were revealed; the results showed that people suffering from muscular dystrophy did not see any increase in strength. [Ann Neurol. 2008 May; 63(5): 561-71.] Following that, Wyeth ceased all further development of MYO-029.

An investigation of the effects of a single ascending dosage of the muscle regulator ACE-031 in healthy volunteers.

Yang Y,  Pearsall AE, Kumar R, Willins DA, Seehra JS, Attie KM, Borgstein NG, and Sherman ML. Attie KM,  Yang Y, Condon CH, Wilson DM, Pearsall AE, and Kumar R.


Acceleron Pharmaceuticals, Inc., Department of Medical Research, 128 Sidney Street, Cambridge, Massachusetts 02139, United States of America



A soluble activin receptor type IIB, ACE-031 is a member of the activin receptor family (ActRIIB). Through its interaction with myostatin and other factors that suppress muscle mass, ACE-031 is able to stimulate the development of muscular tissue.


In this randomised, double-blind, placebo-controlled trial, the pharmacokinetics and pharmacodynamics of ACE-031 were investigated in 48 healthy postmenopausal women who were given either 1 dosage of ACE-031 (0.02-3 mg/kg s.c.) or a placebo. The study evaluated the safety of ACE-031 (3:1).

In general, ACE-031 was well tolerated by its patients. Erythema at the injection site was one of the adverse effects. The mean AUC(0-) and C(max) of ACE-031 rose linearly with dosage, and the mean T(12) was between 10 and 15 days. At day 29, the group that received 3 milligrammes per kilogramme had statistical substantial growth in median overall body fat mass (3.3 percent; P = 0.03, as measured by DXA) and leg muscle size (5.1 percent; P = 0.03, as measured by MRI). Changes in blood indicators that were statistically significant show that ACE-031 enhanced bone and fat metabolism. [Citation needed]


In healthy postmenopausal women, a single dosage of ACE-031 therapy resulted in increases in muscle mass and was usually well tolerated by the participants.

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