TB-500 is a synthetic variant of the naturally occurring Thymosin Beta-4 peptide, which is typically present in all mammal cells. This presumably effective biological peptide is a member of a large family of 16 similar compounds. These molecules have high sequence conservation and are found in most tissues and circulating cells. To trap and inhibit the polymerization of actin in eukaryotic cells, Thymosin Beta-4 was created.

Research suggests that during the early stages of angiogenesis, the expression of Thymosin beta-4 seems to rise by a factor of four to six. Studies suggest that it may accelerate the formation of new blood cells from the existing vessels, improve the repair of muscle damage and development, and facilitate the speedier healing of wounds.[i] Research findings suggest that “Delineating the molecular pathways impacted by T4 to promote vascular growth and remodeling may uncover novel targets for prevention and treatment of vascular disease.” It just so happens that the actin-binding domain is a rather brief core length of amino acids. It has a role in controlling blood cell division possibly mediated by Thymosin Beta-4, as well as the healing of tissue repair, migration of endothelial cells and keratinocytes, and possible increased production of enzymes that degrade extracellular matrix.

Research on Thymosin beta-4 suggests that the peptide may have the ability to act as an efficient wound-healing molecule that also has anti-inflammatory effects.[ii] A study’s findings purport that “It may act by increasing angiogenesis and cell migration, and it is currently in experimental trials for wound repair.” Findings imply that in contrast to other naturally occurring growth factors, Thymosin beta-4 may promote the migration of endothelium and keratinocyte cells. Investigations purport that due to its very low molecular weight and the fact that it does not adhere to the extracellular matrix, it may travel great distances across tissues. This is made possible by its extremely low molecular weight. Actin’s polymerization and function are controlled by this factor, as described.

Thymosin Beta-4 Peptide Research

Research has been done on the Thymosin Beta-4 peptide to investigate its potential ability to mediate several activities, including the following:

  • The healing of tissues
  • Differentiation of endothelial cells (found in blood vessels)
  • The process of angiogenesis in the dermal tissues [iii]
  • The accumulation of collagen
  • The migration of keratinocytes [iv]
  • Decrease in the inflammation of the tissue that is seen in joints [v]
  • An increase in the number of muscle fibers leads to an increase in both strength and endurance
  • The reduction of muscular spasms, as well as an increase in overall muscle tone
  • An increase in the amount of chemicals being traded inside the cells
  • The regulation of the flexibility of connective tissue
  • Protection against the development of adhesions and fibrous bands in the tissues of the muscles, tendons, and ligaments

What is the Thymosin Beta-4 Peptide?

The thymus gland is in charge of producing the hormone known as thymosin. The thymus is an organ that plays a part in the regulation of the immune system as well as the repair of damaged tissue. It has been speculated that Thymosin beta-4 may play a significant part in protecting, regenerating, and redesigning wounded or damaged tissue. Research is being done on it for potential use in managing acute injuries, as well as for wound healing and surgical repair. Researchers speculate that after a cardiac injury, the peptide may potentially support cardial tissue to recover more quickly by possibly acting as a key actin-sequestering molecule.

What Potential Does Thymosin Beta-4 Have?

Both skeletal muscles (the muscles responsible for movement) and smooth muscles (such as those in the heart) are likely to have some level of Thymosin beta-4. Upregulation of Thymosin Beta-4 appears to occur following tissue injury. Thymosin Beta-4 is thought to be secreted to aid recovery after tissue trauma. Studies suggest that during recovery following an injury, it may work to lessen the amount of scar tissue that forms and increase flexibility. Research suggests that it may have anti-inflammatory potential.

Findings imply that TB4 has been speculated to decrease inflammation of tissue in joints, relax muscular spasms, enhance muscle tone, promote the interchange of chemicals between cells, induce tissue healing, and assist in preserving flexibility. Additionally, it has been hypothesized to help retain flexibility. Moreover, investigations purport that this peptide may possibly promote the development of new blood cells in the tissue, boost physical stamina and strength, and inhibit the production of adhesions and fibrous bands in the muscles, tendons, and ligaments.

Click here to be redirected to Core Peptides’ website to find more educational and informative peptide articles.


[i] Dubé, K. N., & Smart, N. (2018). Thymosin β4 and the vasculature: multiple roles in development, repair and protection against disease. Expert opinion on biological therapy, 18(sup1), 131–139. doi:10.1080/14712598.2018.1459558

[ii] Philp, D., Goldstein, A. L., & Kleinman, H. K. (2004). Thymosin beta4 promotes angiogenesis, wound healing, and hair follicle development. Mechanisms of ageing and development, 125(2), 113–115. doi:10.1016/j.mad.2003.11.005

[iii] Maar K, Hetenyi R, Maar S, et al. Utilizing Developmentally Essential Secreted Peptides Such as Thymosin Beta-4 to Remind the Adult Organs of Their Embryonic State-New Directions in Anti-Aging Regenerative Therapies. Cells. 2021;10(6):1343. Published 2021 May 28. doi:10.3390/cells10061343

[iv] Malinda, K. M., Sidhu, G. S., Mani, H., Banaudha, K., Maheshwari, R. K., Goldstein, A. L., & Kleinman, H. K. (1999). Thymosin beta4 accelerates wound healing. The Journal of investigative dermatology, 113(3), 364–368. doi:10.1046/j.1523-1747.1999.00708.x

[v] Song, R., Choi, H. M., Yang, H. I., Yoo, M. C., Park, Y. B., & Kim, K. S. (2012). Association between serum thymosin β4 levels of rheumatoid arthritis patients and disease activity and response to therapy. Clinical rheumatology, 31(8), 1253–1258. doi:10.1007/s10067-012-2011-7

Share this article

Facebook Comments