Ac-SDKP, a marker of the angiotensin-converting enzyme activity?

The tetra-peptide Acetyl-Ser-Asp-Lys-Pro (Ac-SDKP) generated by the cleavage of thymosine beta 4 inhibits the proliferation of hematopoietic stem cells and the proliferation and secretion of fibroblasts in the rnyocardium and the glomeruli. The clinical administration of Ac-SDKP has been proposed and partially investigated. The peptide could protect hematopoietic stem cells during anti-neoplastic treatments leaving cancerous cells unprotected. As it opposes the effects of TGF beta it could prevent fibrosis after myocardial infarcts and glomeruli fibrosis during the natural course of diabetic nephropathy. However, until now the expected benefits of such a treatment are based on all indirect consideration. Indeed, the degradation of Ac-SDKP is due to the action of the angiotensin-converting enzyme. Interestingly. the blocking of this enzyme both improves the above-mentioned fibrosis and increases the plasma levels of Ac-SDKP. Should the therapeutic effects prove solid, and therapeutic levels be established assaying Ac-SDKP could be an interesting marker of therapeutic efficiency.