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ACE-031 peptides are Synthesized and Lyophilized in the USA.
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FREE - 30ml bottle of bacteriostatic water
(Required for reconstitution)
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What Is ACE-031?
The activin receptor promotes sperm development and boosts muscle mass. ACE-031, a soluble protein comprising the type IIB activin receptor (ACVR2B) and the immunoglobulin G1-Fc (IgG1-Fc), is capable of a similar role by binding and inactivating myostatin, a protein that hampers muscle growth. This has therapeutic potential towards the treatment of muscle-wasting disorders and neuromuscular conditions such as Duchenne Muscular Dystrophy (DMD) and certain cancers such as those of the prostate or colorectal regions and lipid storage and bone metabolism.
AKA: Ramatercept, ActRIIB-IgG1, ACVR2B/Fc
Sequence: Not Available
PubChem: CID 16130571
CAS Number: 1169766-01-1
Muscle Protection After Menopause
ACE-031 enhances muscle growth and bone metabolism; it also limits lipid accumulation. A notable improvement in lean body mass and thigh muscle volume is seen within a month of ACE-031 administration. The treatment outcome has the added benefits of improved bone and fat metabolic profile.
Muscle Cell Growth
ACE-031 administration reduces muscle wasting by its ability to bind myostatin in muscle cells. The most desirable outcome is supplemented with approaches that promote muscle growth, such as the co-administration of growth hormones like IGF-1.
Research has shown that inhibiting the natural ACE-031 proteins can cause failure to reduce serum lactate levels, prevent metabolic damage to muscles, and improve vascularization of the muscle tissue. These can be overcome by ACE-031 supplementation. It promotes muscle growth by blocking myostatin-mediated wasting and delays the onset of tiredness and oxidative damage by enhancing the oxygenation of the muscle tissues.
ACE-031 improves muscle function in more ways than one. Other than blocking the effects of myostatin, ACE-031 can improve muscle thermodynamics by promoting oxidative respiration, thereby improving the force-generating capacity of muscles, specifically the maximum force by 50% and total contractile force by 25%. It also showed that ACE-031 improves muscle strength without affecting energy dynamics, or changes in ATP levels or contractile efficiency within the muscle tissues.
Muscle wasting disorders such as Duchenne Muscular Dystrophy (DMD) often result in difficulty walking by the time the patient is 12 years of age. Patients display severe muscle loss due to low protein levels despite the extremely high-fat reserves—the primary reason being that the dystrophin (a group of proteins) in these patients is non-functional. Moreover, the release of myostatin from damaged muscle cells can affect surrounding cells causing their growth to slow down. However, research has shown the ability of ACE-031 to reduce the rate of muscle damage by addressing the effects of myostatin release.
The peptide preserves muscle function, increases lean body mass, improves bone mineral density, and reduces fat reserves when administered once or twice a month subcutaneously, as shown by the improved results in the 6-minute walk test.
ACE-031 improved total body weight, muscle mass, and bone mineral density when administered once a week for seven consecutive weeks. A reduction in the population of osteoclasts seems to be responsible for the improved mineral content in bones, which also improved the biomechanics, stiffness, and maximum force that the bones could tolerate.
Research has shown the ability of ACE-031 to increase bone mass by around 30%, highlighting its therapeutic potential for controlling the progression of osteoporosis. Moreover, due to its ability to promote muscle strength and bone density and reduce lipid reserves, the peptide promises to improve the physiologic effects caused due to aging.
In addition to its myostatin inhibiting property, studies have shown the ability of ACE-031 to increase bone density by almost 132% in the femur (the thigh bone, which is often damaged with age) and 27% in vertebrae.
Cancer Treatment and Muscle Loss
Molecular cascades resulting in muscle loss due to either death or necrosis are commonly seen in cancer patients or those undergoing chemotherapy. The primary reason is the metabolic stress on muscles due to changes in aerobic respiration status. In addition, there is an increase in the free radical population within cells that indirectly causes muscle damage.
Activating the ERK1/2 pathway by administering ACE-031 averts muscle fiber atrophy due to apoptosis. In addition, the efficiency of energy consumption and the mitochondrial metabolism is also seen to improve, which is a significant outcome keeping in mind the limited nutrition in a cancer patient’s body. Moreover, the concentration of free radicals also reduces. Thus, ACE-031, along with anticancer drugs, may have a better potential of preventing chemotherapy-induced muscle atrophy.
Myostatin is produced in certain cancers, which leads to muscle wasting and loss. In addition, these transformed cells are often associated with inactivated activin receptors, loss of mitochondria, and hence ATP levels. Research has shown a reversal of these effects with ACE-031 administration.
The resulting preservation of muscle composition, strength, and lean body mass increases life expectancy in such patients. Some additional benefits of myostatin inhibition include improved insulin sensitivity, reduced fat storage, reduced inflammation, and better bone metabolism and strength.
ACE-031 demonstrates excellent bioavailability upon subcutaneous administration in murine models. The side effects are minimal, and bioavailability through the oral route is low. However, its per kg dosage in rodents is not scalable to humans. ACE-031 usage and sale are limited to educational and scientific research and are not suitable for human consumption.
- Attie, K. M., Borgstein, N. G., Yang, Y., Condon, C. H., Wilson, D. M., Pearsall, A. E., Kumar, R., Willins, D. A., Seehra, J. S., & Sherman, M. L. (2013). A single ascending-dose study of muscle regulator ACE-031 in healthy volunteers. Muscle & nerve, 47(3), 416–423. https://doi.org/10.1002/mus.23539
- Cadena, S. M., Tomkinson, K. N., Monnell, T. E., Spaits, M. S., Kumar, R., Underwood, K. W., Pearsall, R. S., & Lachey, J. L. (2010). Administration of a soluble activin type IIB receptor promotes skeletal muscle growth independent of fiber type. Journal of applied physiology (Bethesda, Md. : 1985), 109(3), 635–642. https://doi.org/10.1152/japplphysiol.00866.2009
- Muramatsu, H., Kuramochi, T., Katada, H., Ueyama, A., Ruike, Y., Ohmine, K., Shida-Kawazoe, M., Miyano-Nishizawa, R., Shimizu, Y., Okuda, M., Hori, Y., Hayashi, M., Haraya, K., Ban, N., Nonaka, T., Honda, M., Kitamura, H., Hattori, K., Kitazawa, T., Igawa, T., … Nezu, J. (2021). Novel myostatin-specific antibody enhances muscle strength in muscle disease models. Scientific reports, 11(1), 2160. https://doi.org/10.1038/s41598-021-81669-8
- Campbell, C., McMillan, H. J., Mah, J. K., Tarnopolsky, M., Selby, K., McClure, T., Wilson, D. M., Sherman, M. L., Escolar, D., & Attie, K. M. (2017). Myostatin inhibitor ACE-031 treatment of ambulatory boys with Duchenne muscular dystrophy: Results of a randomized, placebo-controlled clinical trial. Muscle & nerve, 55(4), 458–464. https://doi.org/10.1002/mus.25268
- Maïmoun, L., Mariano-Goulart, D., Huguet, H., Renard, E., Lefebvre, P., Picot, M. C., Dupuy, A. M., Cristol, J. P., Courtet, P., Boudousq, V., Avignon, A., Guillaume, S., & Sultan, A. (2022). In patients with anorexia nervosa, myokine levels are altered but are not associated with bone mineral density loss and bone turnover alteration. Endocrine connections, 11(5), e210488. https://doi.org/10.1530/EC-21-0488
Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.