Thymosin Beta 4, 8mg (4 vial pack)
Thymosin Beta-4 is a thymic peptide and research chemical that is 43 amino acids long. Thymosin Beta-4 is not a thymic hormone in the true sense of the word, but is found in many tissues throughout the human body. The thymosins were isolated by Allan Goldstein in the 1960s, with recognition of clinical and therapeutic potential coming in later decades. Thymosin Beta-4 has recently been marketed extensively for performance enhancement in horses, where regulation is nonexistent relative to the human pharmaceutical industry. When TB4 is sold as a performance enhancement drug for greyhounds, horses, and other racing animals it is marketed under the name TB-500.
According to Millipore, a supplier of research-supply Thymosin Beta 4, it has been shown to regulate angiogenesis, wound healing, development, and inflammation, as well as promote corneal healing.
In rats with traumatic brain injury (TBI), TB(4) treatment "did not affect lesion volume but ... reduced hippocampal cell loss, enhanced angiogenesis and neurogenesis in the injured cortex and hippocampus...and significantly improved sensorimotor functional recovery and spatial learning." TB4 was previously known to be an effective prophylactic against TBI, which is obviously not practical for human use; Xiong et al concluded that the data "demonstrate that delayed administration...improves histological and functional outcomes in rats...indicating...therapeutic potential for patients with TBI."
Thymosin Beta-4 also shows potential for treating other injuries.
Tokura et al found that in mice, endogenous expression of Thymosin Beta-4 was upregulated in early stages of skeletal muscle injury, and that it significantly accelerated wound closure.
Tokura also found that Thymosin Beta-4 induces skeletal muscle regeneration through novel means:
…we showed that primary myoblasts and myocytes derived from muscle satellite cells of adult mice were chemoattracted to sulphoxized form of Tβ4. These data indicate that muscle injury enhances the local production of Tβ4, thereby promoting the migration of myoblasts to facilitate skeletal muscle regeneration.
Endogenous autocrine/paracrine growth factors such as IGF-1 are also known to act in a capacity to induce healing at injury sites. The fact that upregulation of certain local growth factors including TB4 results in healing effects would suggest that similar therapeutic benefits could be achieved; however, as yet the ideal delivery system to emulate endogenous expression of growth factors is unknown.
Rabinovsky et al find that transgenic expression of human IGF-1 in rats results in enhanced muscle and nerve repair:
Growth factors, such as IGF-I, that affect motor neuron survival and regeneration have potential for enhancing nerve repair. Using a mouse transgenic line expressing the human IGF-1 in skeletal muscle, we show that the local expression of IGF-1 is capable of accelerating the regeneration of peripheral nerves and muscle after a nerve injury by enhancing muscle myogenesis and peripheral nerve growth and function.
Thymosin Beta 4 does fit into the category of "growth factors...that affect motor neuron and survival," but the regulatory hurdles that transgenic therapies face are significant. A simpler solution is direct injection into the injury site.
Kurtz et al found that direct application (after transection in an experimental rat model) of growth factors to the site of an injury via injection accelerated functional recovery and reduced functional deficits through anti-inflammatory action.
TB4 may hold potential as a treatment for MD: Hara, Nakayama, and Nara found that TB4 is downregulated in animal models of muscular dystrophy, which may contribute to the degenerative symptoms of the disease.
In addition to the brain and skeletal muscle, TB4 also shows therapeutic potential in the heart:
Kumar and Gupta induced stress in a line of rat cardiac fibroblast cells using H2O2 (hydrogen peroxide); one group had been pretreated with TB4 and the other had not. They found TB4 enhanced endogenous antioxidant expression. While the research chem GHRP-6 has been shown to act as a local antioxidant in cardiac tissues, TB4 has a novel mechanism for cardioprotection unlike any other research chemical.
Kumar and Gupta concluded that “findings indicate that Tβ4 selectively targets and upregulates catalase, Cu/Zn-SOD and Bcl(2), thereby, preventing H(2)O(2)-induced profibrotic changes in the myocardium.” TB4 could eventually be administered in patients at risk of myocardial infarction or other heart disease in order to improve prognosis.
However, Zhou et al found that when applied after myocardial infarction (MI), TB4 does not “reprogram” epicardial cells into myocardiocytes, which would have been of potential use to aid recovery from MI:
Recently it was reported that in mice pretreated with thymosin beta 4 (TB4) and subsequently subjected to experimental MI, a subset of epicardial cells differentiated into cardiomyocytes. In clinical settings, epicardial priming with TB4 prior to MI is impractical. … we found post-MI TB4 treatment significantly increased the thickness of epicardium and coronary capillary density. However, epicardium-derived cells did not adopt cardiomyocyte fate, nor did they migrate into myocardium to become coronary endothelial cells. Our result thus indicates that TB4 treatment after MI does not alter epicardial cell fate to include the cardiomyocyte lineage…
Research of complex-role growth factors such as TB4 is in its infancy. Although the peptide hormone has been known since the 1960s, science is only beginning to catalog the many ways it behaves in the body and in which it may be useful: wound closure, healing of skeletal muscle, formation of new blood vessels, regulation of inflammation, nerve repair, and cardioprotective potential through the antioxidant pathway.
As delivery systems become more advanced and precise, and knowledge of such compounds improves, medical science will literally be transformed. The medical revolution of the 21st century is not one of fighting disease with compounds found outside the body, but of better treating and understanding disease states by studying and isolating the thousands of peptides found inside the human body, such as Thymosin Beta-4.
 Goldstein, AL. (October 2007). History of the Discovery of the Thymosins. Annals NY Acad Vol. 1112.
 Millipore Inc., "Anti-Thymosin beta-4, clone 1H2.1" Product Page. Accessed 12-13-2011.
 Xiong Y, Mahmood A, et al. (January 2011). Treatment of traumatic brain injury with thymosin B4 in rats. J Neurosurg. 114(1):102-15.
Tokura Y et al. (January 2011). Muscle injury-induced thymosin β4 acts as a chemoattractant for myoblasts. J Biochem. 149(1):43-8.
Rabinovsky ED, Gelir E, Gelir S, Lui H, et al. (January 2003). Targeted expression of IGF-1 transgene to skeletal muscle accelerates muscle and motor neuron regeneration. The FASEB Journal. 2003;17:53-55.
Kurtz C A, Loebig T G, Anderson D D, DeMeo P J, Campbell P G. (1999). Insulin-like growth factor I accelerates functional recovery from Achilles tendon injury in a rat model. Am J Sports Med May-Jun;27(3):363-69,
 Hara T, Nakayama Y, Nara N. (November 2005). [Regenerative medicine of skeletal muscle – Trans. from Japanese]. Rinsho Shinkeigaku. 45(11):880-2.
 Kumar S, Gupta S. (October 2011). Thymosin beta 4 prevents oxidative stress by targeting antioxidant and anti-apoptotic genes in cardiac fibroblasts. PLoS One. 2011;6(10):e26912.
 Zhou B, et al. (August 2011). Thymosin beta 4 treatment after myocardial infarction does not reprogram epicardial cells into cardiomyocytes. J Mol Cell Cardiol.