Description

A meta-analysis (study of studies) conducted in 2015 showed broad applicability of TB500 in various disease processes, including improvement of tissue regeneration, repair of the heart after heart attack, healing of the brain following stroke, trauma and neurological diseases. Further, it showed clinical improvement in kidney and liver diseases, and repair of spinal cord, bone and ligament injuries, as well as reducing consequences of aging and viral infection.[1]

TB500 treated mice were found to have substantially improved strength in healed fractures compared to untreated mice. Treated mice showed a 41% increase in peak force to failure, and healed fractures were 25% stiffer than untreated mice. 21-day post-fracture imaging showed improvement up to 26% better than untreated subjects. They also showed 23% smaller callus, and a 31% increase in trabecular bone area/total callus area. Overall, TB500 demonstrated substantially faster healing, with better-healed injury sites when compared to placebo subjects. [2]

Spinal cord injury has been studied in rats, with potential applicability to human subjects. In a 2014 study, TB500 was administered to rats 30 minutes, 3 days, or 5 days after mild compression induced spinal cord injury in rats. Locomotor and behavioral assessments were all markedly improved with the TB500 treated group. Inflammatory cytokines were reduced, the size of scars reduced, and levels of myelin proteins were 57.8% above the control group. The study suggested that, with the known safety of TB500, that it should be considered for treatment of spinal cord injury in humans. [3]

While no animal model perfectly mimics humans for head injury research, rats are considered a close second due to our understanding of their behaviors. TB500 has been studied in traumatic brain injury (TBI), and has been demonstrated to markedly improve function after TBI. TB500 exerts both neuroprotective and neurorestorative effects on rats, including proliferation of blood flow, new brain cells, and new connections between brain cells. [4]

Multiple sclerosis has also been shown, in rat models, to benefit from administration of TB500. Zhang et al, in their 2016 study, showed that administration of TB500 significantly increased the number of newly generated oligodendrocytes and reduced axonal damage in the mice compared with control group. Importantly, the newly generated oligodendrocytes remyelinated axons, and this correlated with functional improvement. [5]

References

1 – Expert Opin Biol Ther. 2015;15 Suppl 1:S139-45.doi:10.1517/14712598.2015. 1011617. Epub 2015 Jun 22. Advances in the basic and clinical applications of thymosin β4. Goldstein AL1, Kleinman HK.

2 – J Orthop Res. 2014 Oct;32(10):1277-82. doi: 10.1002/jor.22686. Epub 2014 Jul 8. Thymosin β4 administration enhances fracture healing in mice. Brady RD1, Grills BL, Schuijers JA, Ward AR, Tonkin BA, Walsh NC, McDonald SJ.

3 – Neuropharmacology. 2014 Oct;85:408-16. doi: 10.1016/j.neuropharm.2014.06.004. Epub 2014 Jun 14. Beneficial effects of thymosin β4 on spinal cord injury in the rat. Cheng P1, Kuang F1, Zhang H1, Ju G2, Wang J3.

4 – Ann N Y Acad Sci. 2012 Oct;1270:51-8. doi: 10.1111/j.1749-6632.2012.06683.x. Neuroprotective and neurorestorative effects of thymosin β4 treatment following experimental traumatic brain injury. Xiong Y1, Mahmood A, Meng Y, Zhang Y, Zhang ZG, Morris DC, Chopp M.

5 – Neurobiol Dis. 2016 Apr;88:85-95. doi: 10.1016/j.nbd.2016.01.010. Epub 2016 Jan 12. Thymosin beta4 promotes oligodendrogenesis in the demyelinating central nervous system. Zhang J1, Zhang ZG2, Li Y2, Lu M3, Zhang Y2, Elias SB2, Chopp M4.