TB-500 / Thymosin beta 4 is made up of 43 amino acids, making it a oligopeptide, and has a molecular weight of 4.9 kDa. It is considered to be present in most tissues, with the exception of erythrocytes (red blood cells). The peptide was initially discovered as a protein isolate in the mammalian thymus gland. It belongs to a family of thymosins, acidic molecules that are light in weight and that function to produce cells. With that said, the motion and distinction of cells may potentially be manipulated by counteracting the power of singular monomers (or actin proteins) to polymerize into thin strands. In contrast, thymosins assemble the actin monomers, which may permit or deny the production of coming filaments. This may, to a degree, facilitate or inhibit the differentiation of a cell – such as a pluripotent stem cell into another (e.g. neurons or bone cells).
It follows that thymosin-like molecules (thymosin beta-4 being most prevalent in mammals) may potentially play a major function in tissue, cell regeneration or even postnatal development. TB-500’s potential influence over actin may extend to manipulating the migration of cells and the formation of new blood vessels. It is available as a lab-grade, synthetic peptide called TB-500 (Thymosin Beta 4).
Thymosin Beta 4 (TB-500) Peptide Research
The function of TB-500 to repair and regenerate tissue has been suggested through various experimental research studies. Thymosin Beta 4 has appeared to exhibit the ability to slow or prevent scar formation, microbial growth, cell death, and inflammation. TB-500, derived externally, may potentially act to hasten the repair of injured corneal, dermal, and cardiac tissues.
Studies in the peptide have suggested that it may play a role in repairing and regenerating various tissues, such as those of the peripheral nervous system, brain, heart, and spinal cord. TB-500 has been suggested to induce anti-inflammatory impacts as well as potentially presenting the power to weaken the discharge of prostaglandin EP4 and nitric oxide in cell models exposed to reactive oxygen species. Nevertheless, it may increase the stimulus response of pro-inflammatory chemokines and several interleukins in cells of the periodontium. Yet another research hypothesis for the action of TB-500 is that it may exhibit in the management of bone production, as these are osteoclastogenic molecules as well.In one study, NF-κB activation in murine macrophages appeared hindered by the peptide.
TB-500 is considered to be involved with the release of an anti-inflammatory peptide fragment called acSDKP – the metabolism of which is regulated by a number of interesting factors. The preparation of TB 500 together with integrated kidney tissue of rats reportedly produced a significant increase in the release of acSDKP7. Before the acSDKP split, this process is governed by an intricate governing mechanism which necessitates peptidases that split only the molecules of particular fragments, potentially involving TB-500 hydrolysis by meprin-alpha.
Researchers may find Thymosin beta-4 a possible research candidate within the context of fibrotic scarring of organs. Recently, results from a team of researchers have been published that present notable inflammation reductions in a rodent replica of pulmonary fibrosis. Also, acSDKP has presented a renal fibrosis reduction in rodents. The exposure to the fragment reportedly produced a decreased discharge of the major components of scar tissue (collagen and fibronectin), as well as a decrease in myofibroblast and macrophage migration to the damaged sites.
Hepatic stellate cell activation also appears to be associated with the up-regulation of TB-500. Generally, TB-500 considered to be connected with the intricate developmental and governing processes that take place in organisms in vivo. TB-500 appears to be a possible factor of tissue regeneration management, inflammation, and cell differentiation and may potentially prove interesting within the context of research on replicas of issues like rheumatoid arthritis, abnormal fibrosis, various states of postnatal development, and other forms of osteolytic inflammation.
Injury Repair
In one study using a murine model, TB 500 presented possible wound healing potential after being exposed to damaged tissue. Tissues were re-epithelialized by 42% over saline controls on the fourth day of the study; 61% on the seventh day after the injury occurred. An elevation in the discharge of collagen and formation of new blood vessels were reported in the exposed wound.
Eyes and Vision
In animal studies of various models, TB 500 was suggested to potentially restore eye-related impairments effectively – including injuries related to UV exposure, alkali, exposure to smoke, heptanol debridement, and ethanol exposure. In every situation, cell migration apparently induced by TB 500 appeared responsible for the repairs made to the injured/wounded region. The damaged eyes recovered quickly, and the migration increase with this peptide was reported.
Heart Muscles
In one study, TB-500 was exposed to soft tissue wounds in rodents. The wounds were in the center of the palate, and were three millimeters in diameter. Pictures of the wounded regions were taken and examined microscopically seven days after the procedure. The wound closure was reported to be significantly enhanced in rats that were exposed to Thymosin Beta 4, as compared to controls. In most cases, healing of oral cavity wounds is considered to happen more rapidly and may not scar as much as dermal tissue, which may result from the distinct phenotype of oral fibroblasts, and from particular salivary components. Nonetheless, damaged tissues resulting from implant and periodontal procedures are constantly confronted with a bacterial infection in the oral cavity, requiring detailed, cautious oral hygiene maintenance and increased management of plaque, regardless of the fairly quick wound healing. That is why, TB-500, which is suggested to improve the reconstruction of various tissue types, is anticipated to speed up the healing of mucosal wounds as well.
References:
- Kim J, Wang S, Hyun J, et al. Hepatic Stellate Cells Express Thymosin Beta 4 in Chronically Damaged Liver. PloS one journal, 2015.
- Philip D, Goldstein AL, Kleinman HK. Thymosin beta4 promotes angiogenesis, wound healing, and hair follicle development. Mechanisms of ageing and development, 2004.
- Lee S-I, Yi J-K, Bae W-J, et al. Thymosin Beta-4 Suppresses Osteoclastic Differentiation and Inflammatory Responses in Human Periodontal Ligament Cells. PloS one journal, 2016.
- Conte E, Genovese T, Gili E, et al. Protective effects of thymosin beta4 in a mouse model of lung fibrosis. Annals of the New York Academy of Sciences, 2012.
- Sosne G, Kleinman HK; Primary Mechanisms of Thymosin β4 Repair Activity in Dry Eye Disorders and Other Tissue Injuries. Invest. Ophthalmol. Vis. Sci, 2015.
- Goldstein AL, Hannappel E, Sosne G & Kleinman HK. Thymosin β4: a multi-functional regenerative peptide. Basic properties and clinical applications, Expert Opinion on Biological Therapy, 2012.
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