Thymosin beta 4 (Tβ4) may, due to its fibrinolysis and other activities, be useful in treating COVID-19 patients. Tβ4 prevents actin from binding to fibrin, a major blood clot component. Increased fibrinolysis may be achieved by increasing ACE or administering Tβ4 (1).
Fibrinolysis is fibrin breakdown in blood clots. In patients with COVID-19, blood clots have led to extensive morbidity and death. Elevated bradykinin levels in multiple tissues and systems may cause increased vascular dilation, vascular permeability, and hypotension. High bradykinin levels induce pain and cause blood vessels to expand and become leaky, leading to swelling and inflammation of the surrounding tissue. In COVID-19 patients, bradykinin storm induces fluid leakage into the lungs, elevates hyaluronic acid release, impacts oxygen uptake and carbon dioxide release, and causes many severe symptoms (1).
Women have two X chromosomes while men only have one. The Tβ4 gene resides on the X chromosome, which is interesting since men are 2.4 times more likely than women to die from COVID-19. Higher Tβ4 levels may explain why women have a lower incidence of COVID-19-induced mortality than men. If this is correct, pharmacological Tβ4 administration to COVID-19 patients may significantly reduce morbidity and improve survival (1).
Tβ4 not only down-regulates inflammatory chemokines, cytokines, and pro-inflammatory processes, such as bradykinin storm, but also increases fibrinolysis and accelerates wound repair in organs often affected by COVID-19, including the heart, lungs, and kidneys. The Tβ4 levels decrease significantly in blood, tears, and saliva by age (1). Therefore, treatment with Tβ4, which dampens bradykinin storm, may successfully treat COVID-19, particularly in elderly and vulnerable patients.
References
1. Garvin MR, Alvarez C, Miller JI, Prates ET, Walker AM, Amos BK, Mast AE, Justice A, Aronow B, Jacobson D. A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm. Elife 2020;9:e59177. doi: 10.7554/eLife.59177.
