n-acetyl-seryl-aspartyl-lysyl-proline

**N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP)** is a naturally occurring endogenous tetrapeptide generated from the N-terminal sequence of thymosin β4 by the enzyme prolyl oligopeptidase. AcSDKP acts as an alternative substrate for angiotensin-converting enzyme (ACE) and is widely distributed in plasma, urine, and tissues. Its primary physiological and pharmacological actions are anti-fibrotic and anti-inflammatory effects: it inhibits fibroblast proliferation, collagen synthesis, and tissue fibrosis, and has shown efficacy in reducing inflammation and fibrosis in preclinical models of cardiovascular, renal, hepatic, pulmonary, and intestinal diseases. AcSDKP modulates immune responses and inflammation partially through inhibition of the MEK-ERK signaling pathway and is primarily degraded by the N-domain of ACE. Some benefits of ACE inhibitors in cardiovascular and kidney disease may be partially mediated by increased AcSDKP levels. AcSDKP does not lower blood pressure but confers structural protection against fibrosis.

Other names

N-acetyl-seryl-aspartyl-lysyl-prolineAcSDKPAc-SDKPN-acetyl-L-seryl-D-α-aspartyl-L-lysyl-L-proline