Thymosin-β4 acetate (Tβ4) is a 43 amino acid peptide which is regarded as the main intracellular G-actin sequestering peptide. Extracellular thymosin β4 may contribute to physiological processes such as angiogenesis, wound healing and regulation of inflammation [1]. Thymosin-β4 has been tested in multicenter trials in patients with bed sores, ulcers caused by venostasis, epidermolysis bullosa simplex and chronic neurotrophic corneal epithelial defects, and it was found to promote repair. So it is widely used in cosmetic peptides & dermatology, inflammation research, regenerative medicine.

Over the last decade an epidemic of chronic kidney disease (CKD) has occurred, linked to increased obesity, hypertension and diabetes. Current treatment strategies control known risk factors through pharmacological inhibitors and lifestyle changes, but new therapies are urgently required. Regardless of the origin, the progression of CKD is accompanied by inflammation, fibrosis, extracellular matrix accumulation and tubular atrophy. Therefore, treatments that modulate these pathophysiological processes have the potential to reduce the morbidity and mortality associated with CKD. Thymosin-β4 is a low–molecular-weight naturally occurring peptide and the major G-actin–sequestering protein in mammalian cells. Thymosin-β4 regulates the actin filament assembly and disassembly in a dynamic balance with the actin-binding competitor profilin and the depolymerisation factor cofilin. In addition, thymosin-β4 is able to form a complex with PINCH-1 and integrin-linked kinase, both of which are necessary for cell migration and survival. Thymosin-β4 can also bind to stabilin-2, a membrane receptor involved in the engulfment of apoptotic cells. The ability of thymosin-β4 to regulate cell movement, and turnover has led to studies showing that it can stimulate coronary vasculogenesis and angiogenesis and regulate inflammation and fibrosis in mouse models of lung, heart and cornea injury. Thymosin-β4 derivatives have similar properties. Thymosin-β4 sulfoxide is anti-inflammatory, whilst the tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline is able to reduce fibrosis in animal disease models [2].

Despite recent advances in the treatment of coronary heart disease, a significant number of patients progressively develop heart failure. Reduction of infarct size after acute myocardial infarction and normalization of microvasculature in chronic myocardial ischemia could enhance cardiac survival. Thymosin-β4 might be a promising candidate for the treatment of ischemic heart disease. It has been characterized as a major G-actin-sequestering factor regulating cell motility, migration, and differentiation. During cardiac development, Thymosin-β4 seems essential for vascularization of the myocardium. In the adult organism, Thymosin-β4 has anti-inflammatory properties, increases myocyte and endothelial cell survival, accompanied by differentiation of epicardial progenitor cells. In chronic myocardial ischemia, Tβ4 overexpression enhances micro- and macrovasculature in the ischemic area and thereby improves myocardial function. A comparable effect is seen in diabetic and dyslipidemic pig ischemic hearts, suggesting an attractive therapeutic potential of adeno-associated virus encoding for Tβ4 for patients with ischemic heart disease [3].

Reference

[1]https://www.creative-peptides.com/product/thymosin-4-acetate-item-10-101-35-110.html 
[2]Elisavet Vasilopoulou, et. al., The role of thymosin-β4 in kidney disease, Expert Opinion on Biological Therapy, Volume 15, 2015, 187-190.
[3]Rabea Hinkel, et. al., Thymosin β4-mediated protective effects in the heart, Expert Opinion on Biological Therapy, Volume 18, 2018, 121-129
[4]https://pubchem.ncbi.nlm.nih.gov/compound/45382195