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ACE-031 peptides are Synthesized and Lyophilized in the USA.
Discount per Quantity
|Quantity||5 - 9||10 +|
FREE - 30ml bottle of bacteriostatic water
(Required for reconstitution)
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What is the ACE-031 Peptide?
ACE-031 is a soluble protein comprising the type IIB activin receptor (ACVR2B) and the immunoglobulin G1-Fc (IgG1-Fc), and has been studied for its potential in 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
ACE-031 and Muscle Protection After Menopause
ACE-031 appears to enhance muscle growth and bone metabolism; it also may limit lipid accumulation. A notable improvement in lean body mass and thigh muscle volume was observed in experimental studies within a month of ACE-031 administration. The treatment outcome has the potential added benefits of improved bone and fat metabolic profile.
ACE-031 and Muscle Cell Growth
ACE-031 administration appears to reduce muscle wasting by its ability to bind myostatin in muscle cells. The most desirable outcome would be supplemented with approaches that promote muscle growth, such as the co-administration of growth hormones like IGF-1.
ACE-031 and Energy Metabolism
Research has suggested 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 potentially be overcome by ACE-031 supplementation. It may promote muscle growth by blocking myostatin-mediated wasting and may delay the onset of tiredness and oxidative damage by enhancing the oxygenation of the muscle tissues.
ACE-031 and Strength
ACE-031 has been studied for its potential influence in muscle function. Other than blocking the effects of myostatin, ACE-031 has been researched for its possible ability to 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%. Experimental studies observed that ACE-031 appears to improve muscle strength without affecting energy dynamics, or changes in ATP levels or contractile efficiency within the muscle tissues.
ACE-031 and Muscle Repair
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 suggested the ability of ACE-031 to reduce the rate of muscle damage by addressing the effects of myostatin release. The peptide appears to preserve muscle function, increase lean body mass, improve bone mineral density, and reduce fat reserves when administered once or twice a month subcutaneously, as suggested by the improved results in a 6-minute walk test.
ACE-031 and Bone Density
Researchers observed that ACE-031 appeared to improve 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 suggested the ability of ACE-031 to increase bone mass by around 30%, positing its therapeutic potential for controlling the progression of osteoporosis. Moreover, due to its suggested 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 possible myostatin inhibiting properties, studies have suggested 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.
ACE-031 and Cancer Treatment, 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 appears to avert muscle fiber atrophy due to apoptosis. In addition, the efficiency of energy consumption and the mitochondrial metabolism was also observed to improve in research studies, which is a significant outcome keeping in mind the limited nutrition in a cancer patient’s body. Moreover, the concentration of free radicals also appeared to reduce. 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 suggested 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. Experimental research reportes that ACE-031 appears to exhibit excellent bioavailability in murine models. The side effects appear minimal, and bioavailability through the oral route is low. However, its per kg dosage in rodents is not scalable to humans. ACE-031 sales 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.