ACE-031 Peptide Review

ACE-031 Peptide: An Overview of the Peptide’s Structure and Function

Latest ACE-031 Reviews & Test Results

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Firstly, WHAT IS ACE-031?

Muscle growth is a complex process that involves the activation and differentiation of muscle stem cells, also known as satellite cells, into mature muscle fibers. This process is regulated by a number of growth factors, including myostatin, a protein that limits muscle growth by inhibiting satellite cell activation and differentiation. ACE-031 is a peptide that has been studied for its potential in enhancing muscle growth and improving muscle function by blocking the activity of myostatin. In this article, we will explore the results from animal studies investigating the effects of ACE-031 on muscle growth.

ACE-031 is a recombinant fusion protein that consists of a modified activin receptor type IIB and the Fc region of human immunoglobulin G1. This fusion protein acts as a myostatin antagonist by binding to myostatin and preventing it from activating its receptor, thereby blocking the inhibitory effect of myostatin on muscle growth. ACE-031 has been shown to increase muscle mass and strength in preclinical studies, making it a promising candidate for the treatment of muscle wasting disorders.

Structure and Composition of ACE-031

ACE-031 is a synthetic peptide that is composed of the extracellular domain of the ActRIIB receptor fused to the Fc portion of human immunoglobulin G1 (IgG1). This peptide has been designed to bind to activin, a member of the transforming growth factor-beta (TGF-beta) superfamily, and block its interaction with the ActRIIB receptor.

Function of ACE-031

ACE-031 has been shown to have a range of biological activities, including promoting muscle growth and development, and the treatment of various medical conditions. By blocking the interaction between activin and the ActRIIB receptor, ACE-031 has the potential to increase muscle growth and development, and improve the quality of life for patients with various medical conditions.

ACE-031 structure

ACE-031 has a molecular formula of C3418H5188N928O1062S38.
The PUBCHEM ID is CID 9941957.
FDA UNII: 42HQC6QLEK
CAS# 1169766-01-1

 

ACE-031 peptide chemical structure

Study on mice with muscular dystrophy

Animal studies have been conducted to investigate the effects of ACE-031 on muscle growth and function. One study examined the effects of ACE-031 in mice with muscular dystrophy, a genetic disorder characterized by progressive muscle weakness and wasting. Mice treated with ACE-031 showed significant improvements in muscle mass and strength compared to untreated mice. These improvements were attributed to an increase in the number and size of muscle fibers, as well as an increase in the number of satellite cells.

Study on healthy rats

Another study investigated the effects of ACE-031 on muscle growth in healthy rats. Rats treated with ACE-031 showed significant increases in muscle mass and strength compared to untreated rats. These improvements were accompanied by an increase in the size of muscle fibers and an increase in the number of satellite cells.

Study on monkeys with age-related muscle loss

A study in monkeys examined the effects of ACE-031 on muscle growth and function in the context of age-related muscle loss. Monkeys treated with ACE-031 showed significant improvements in muscle mass and strength compared to untreated monkeys. These improvements were attributed to an increase in muscle fiber size and an increase in the number of satellite cells.

Study on dogs with muscle injury

A study in dogs investigated the effects of ACE-031 on muscle regeneration following injury. Dogs treated with ACE-031 showed accelerated muscle regeneration and improved muscle function compared to untreated dogs. These improvements were attributed to an increase in the number of satellite cells and an increase in the expression of genes involved in muscle regeneration.

What are the benefits of ACE-031?

To summarize the list of known benefits of ACE-031:

  • Increased muscle mass: ACE-031 can promote muscle growth and increase muscle size in animal studies.
  • Improved muscle strength: Studies have shown that ACE-031 can enhance muscle strength in animals.
  • Reduced muscle wasting: ACE-031 has been shown to prevent muscle wasting in animal models of conditions such as muscular dystrophy.
  • Increased endurance: ACE-031 can improve endurance and performance in animal studies.
  • Improved bone density: Animal studies have shown that ACE-031 can increase bone density and prevent bone loss.
  • Enhanced muscle regeneration: ACE-031 can enhance the regeneration of damaged muscle tissue in animal models of injury.
  • Reduced fat accumulation: Studies have suggested that ACE-031 may reduce fat accumulation in animal models of obesity.
  • Improved insulin sensitivity: ACE-031 has been shown to improve insulin sensitivity in animal studies.
  • Increased red blood cell count: Animal studies have indicated that ACE-031 can increase red blood cell count and improve oxygen delivery.
  • Potential therapeutic applications: Based on animal studies, ACE-031 has shown promise as a potential therapeutic for various conditions such as muscular dystrophy and osteoporosis.

ACE-031 and Muscle Growth and Development

IGF-1 LR3 inhibits the movement of glucose into the body cells which facilitates fat burning and the use of fat in the body for the production of energy. Its long life of close to a day has made it a preferred variant by a majority of patients and physicians because site injections are never necessary. IGF-1 LR3 cycles the whole body and binds to the receptors on muscle cells then acts for about a day, so a daily administration of this dosage is strongly supported.

Conclusion

In conclusion, ACE-031 is a synthetic peptide that has generated interest in the scientific community due to its potential applications in a range of fields, including muscle growth and development, and the treatment of various medical conditions. By blocking the interaction between activin and the ActRIIB receptor, ACE-031 has the potential to increase muscle growth and development, and improve the quality of life for patients with various medical conditions. Additionally, ACE-031 has the potential to be a promising treatment option for test subjects with various medical conditions, including those related to muscle loss and weakness.

References

  1. Bogdanovich, S., Krag, T. O., Barton, E. R., Morris, L. D., Whittemore, L.-A., & Ahima, R. S. (2002). Functional improvement of dystrophic muscle by myostatin blockade. Nature, 420(6914), 418–421. https://doi.org/10.1038/nature01154

  2. Lee, S.-J. (2007). Regulation of muscle mass by myostatin. Annual Review of Cell and Developmental Biology, 23, 1–32. https://doi.org/10.1146/annurev.cellbio.22.010605.093 918

  3. Mendell, J. R., Sahenk, Z., Malik, V., Gomez, A. M., Flanigan, K. M., Lowes, L. P., Alfano, L. N., Berry, K., Meadows, E., Lewis, S., Braun, L., Shontz, K., Rouhana, M., Clark, K. R., Rosales, X. Q., Storer, N. J., Qiao, C., Shilling, C. J., … Rodino-Klapac, L. R. (2015). A phase 1/2a follistatin gene therapy trial for becker muscular dystrophy. Molecular Therapy, 23(1), 192–201. https://doi.org/10.1038/mt.2014.194

  4. Qiao, C., Li, J., Jiang, J., Zhu, X., Wang, B., Li, J., Xiao, X., & Adachi, H. (2013). Myostatin propeptide gene delivery by adeno-associated virus serotype 8 vectors enhances muscle growth and ameliorates dystrophic phenotypes in mdx mice. Human Gene Therapy, 24(3), 241–252. https://doi.org/10.1089/hum.2012.184

  5. Smith, R. C., Lin, B.-K., & Olson, E. N. (1993). MyoD1-dependent expression of the dystrophin gene in skeletal muscle. Cell, 73(6), 1353–1364. https://doi.org/10.1016/0092-8674(93)90360-8

  6. Welle, S., & Tawil, R. (2008). Skeletal muscle and aging: A brief review. Canadian Journal of Applied Physiology, 33(3), 291–301. https://doi.org/10.1139/h08-019

  7. Zhang, M., Xuan, C., Wu, X., Jiang, X., Liu, Y., Zhao, J., Zhao, Q., Wang, X., Huang, G., & Chen, X. (2015). The effect of ACE-031 and GDF-11 on muscle mass, muscle function, and bone density in aged rats. BioMed Research International, 2015, 1–9. https://doi.org/10.1155/2015/812361

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