Ac-SDKP
Healing & RecoveryAlso known as: N-Acetyl-Seryl-Aspartyl-Lysyl-Proline, Goralatide, Seraspenide, AcSDKP, Thymosin Beta-4 Fragment
Mechanism
Ac-SDKP is a small four-amino-acid peptide that your body naturally produces when thymosin beta-4 (TB-500) is broken down by prolyl oligopeptidase. It is one of the most potent natural anti-fibrotic (anti-scarring) agents known. It prevents fibrosis in the heart, kidneys, liver, and lungs by blocking the transformation of normal cells into scar-producing myofibroblasts. Interestingly, ACE inhibitors (common blood pressure drugs) raise Ac-SDKP levels because ACE is the enzyme that normally breaks it down — this may partly explain why ACE inhibitors protect against organ fibrosis.
Technical detail
Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) is a tetrapeptide released from thymosin β4 by prolyl oligopeptidase (POP). It is degraded by angiotensin-converting enzyme (ACE) — hence ACE inhibitors increase circulating Ac-SDKP 5-fold. Anti-fibrotic mechanism: (1) Inhibits TGF-β/Smad2/3 signaling, the master pathway driving fibroblast-to-myofibroblast transition (FMT); (2) Blocks connective tissue growth factor (CTGF) expression; (3) Reduces collagen I and III deposition in fibrotic tissues; (4) Inhibits inflammatory macrophage infiltration and M2 macrophage-driven fibrosis; (5) Suppresses endothelial-to-mesenchymal transition (EndMT). Also regulates hematopoietic stem cell quiescence — maintains HSCs in G0 phase, protecting them from cell-cycle-specific damage (originally called goralatide for this function). Anti-fibrotic effects demonstrated in animal models of cardiac fibrosis (MI, hypertension), renal fibrosis (UUO, diabetic nephropathy), hepatic fibrosis (CCl4, BDL), and pulmonary fibrosis (bleomycin).