ACE-031 peptide, also known as ACVR2B (activin receptor type IIB) peptide, is a fusion compound consisting of the activin receptor type IIB and recombinant immunoglobulin IgG1 FC, which is a form of antibody (2). Research indicates peptide is soluble, and studies suggest it may bind with myostatin protein to prevent inhibiting muscle growth. Besides this, the peptide also shows positive potential for metabolism activities, fat storage, and sperm health.
The endogenous myostatin protein was first discovered in 1997, when some inhibitory action on muscle growth was observed in comparative studies in mice (1). This ACE-031 peptide is the engineered (or synthetic) version of the naturally occurring ACV2RB receptors.
ACE-031 has been suggested by researchers to bind with the myostatin protein, possibly neutralizing its action. ACE-031, or the ACVR2B peptide, has shown various potential actions including some listed below, and is currently under scientific investigation:
- Possibly increasing lean body muscle mass
- May promote muscle protection
- May boost energy
- May increase metabolism
- Possibly promote tissue and muscle repair
- May increase bone density
Research and Clinical Studies
ACE-031 Peptide and Muscle Protection
A clinical trial (3) was conducted in postmenopausal women to determine the potential of the peptide in muscle protection. As part of the study, 48 female subjects were selected who were divided into two groups – one group received the placebo while the others received ACE-031 peptide. After 15 days, all female subjects were examined. The participants who were given the peptide exhibited an apparent 3.3% increase in their body muscle mass and 5.1% increase in their thigh muscle mass.
ACE-031 Peptide and Metabolism, Energy
Scientific research (5) in mice has suggested that myostatin not only might prevent muscle growth but also may negatively affect the energy metabolism in muscles. Studies in mice (5) have suggested that by blocking the naturally occurring ACE-031 proteins, lactate levels increase and may cause severe damage to the metabolic energy of the muscles.
ACE-031 Peptide and Strength
Continuous research (6) by scientists has suggested that the potential of the peptide may extend beyond myostatin inhibition. By potentially preventing oxidative stress in muscles, the peptide may improve 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 given to mice, it was reported by the researchers to imporve the maximal contractile force in mice by 40% and total contractile force in mice by 25%.
ACE-031 Peptide and 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 given a placebo or the peptide once a week for 7 weeks. After the completion of the study, it was observed that the ACE-031 peptide mice appeared to exhibit increased muscle mass and excessive body weight, along with increased density in bones. Upon further study, it was suggested by the researchers that the increased bone density might not be incidental, but was perhaps due to enhanced mineralization that boosted bone strength by almost 30% in the peptide mice.
ACT-031 peptide is available for research and laboratory purposes only. Please review and adhere to our Terms and Conditions before ordering.
(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. https://pubmed.ncbi.nlm.nih.gov/9139826/
(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. https://pubmed.ncbi.nlm.nih.gov/27462804/
(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. https://pubmed.ncbi.nlm.nih.gov/23169607/
(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. https://pubmed.ncbi.nlm.nih.gov/29109273/
(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. https://pubmed.ncbi.nlm.nih.gov/24861054/
(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. https://pubmed.ncbi.nlm.nih.gov/27416839/
(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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5244551/
(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. https://pubmed.ncbi.nlm.nih.gov/27259276/
(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. https://pubmed.ncbi.nlm.nih.gov/22621320/
(10) About Duchenne Muscular Dystrophy. https://www.genome.gov/Genetic-Disorders/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. https://pubmed.ncbi.nlm.nih.gov/27462804/
(12) Study of ACE-031 in Subjects With Duchenne Muscular Dystrophy. https://clinicaltrials.gov/ct2/show/NCT01099761
(13) ACE-031 for the Treatment of Duchenne Muscular Dystrophy. https://www.clinicaltrialsarena.com/projects/ace031forthetreatment/
NOTE: These products are intended for laboratory research use only. ACE-031 for sale (1mg) is not intended for personal use. Please review and adhere to our Terms and Conditions before ordering.
Dr. Marinov (MD, Ph.D.) is a researcher and chief assistant professor in Preventative Medicine & Public Health. Prior to his professorship, Dr. Marinov practiced preventative, evidence-based medicine with an emphasis on Nutrition and Dietetics. He is widely published in international peer-reviewed scientific journals and specializes in peptide therapy research.