Figure 2From: Elevation of the antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline: a blood pressure-independent beneficial effect of angiotensin I-converting enzyme inhibitorsAmino-acid sequence of thymosin β4 and endogenous formation of N -acetyl-seryl-aspartyl-lysyl-proline (AcSDKP). G actin binding peptide thymosin β4 is cleaved by an endopeptidase, likely prolyl oligopeptidase (POP), and subsequently its N-terminal tetrapeptide AcSDKP is synthesized. AcSDKP is hydrolyzed and degraded by angiotensin-converting enzyme (ACE). Therefore, when ACE inhibitors are used, the concentration of AcSDKP increases.Back to article page