TB-500 Fragment (AC-SDKP)

AcSDKP · N-acetyl-Ser-Asp-Lys-Pro · Goralatide

Last reviewed: 2026-05-16

CAS: 98474-59-0
MW: 487.5 Da
Sequence: Ac-SDKP
Research focus: regeneration anti inflammatory

A naturally occurring N-terminal tetrapeptide cleaved from thymosin beta-4. Distinct anti-fibrotic and angiogenic profile in research models, particularly in cardiac and renal fibrosis.

Mechanism of action

AC-SDKP is constitutively released from Tβ4 by prolyl oligopeptidase and is normally degraded by angiotensin-converting enzyme (ACE). Reported effects include inhibition of cardiac and renal fibroblast proliferation, suppression of TGF-β/Smad signalling, and pro-angiogenic action on endothelial cells.

Research history

Originally identified as a haematopoietic stem-cell quiescence factor and later studied as an endogenous anti-fibrotic peptide. Plasma levels rise during ACE-inhibitor therapy, providing one explanation for ACE-inhibitor-associated anti-fibrotic benefits in cardiac and renal disease.

Summarised studies

AC-SDKP attenuates cardiac fibrosis post-MI

Yang F. et al., Hypertension · 2010

Chronic subcutaneous AC-SDKP reduced interstitial fibrosis and collagen volume fraction in murine post-infarction hearts, with parallel reductions in TGF-β1 expression.

Renal anti-fibrotic effect of AC-SDKP

Cavasin M.A., Curr Med Chem · 2011

AC-SDKP infusion reduced renal interstitial fibrosis in unilateral ureteral obstruction models, suggesting broad anti-fibrotic activity beyond cardiac tissue.

Safety profile

As an endogenous peptide circulating at low nanomolar concentrations, AC-SDKP has a clean baseline safety reputation in pre-clinical work. Exogenous administration data in humans are limited; immunogenicity is considered unlikely given its small size.

UK regulatory status

Not a licensed medicine in the UK. Research-only laboratory use is unrestricted.

Frequently asked questions

Is AC-SDKP related to TB-500?

AC-SDKP is a four-amino-acid peptide cleaved from the N-terminus of full-length thymosin beta-4. It is distinct from the central actin-binding region sold commercially as TB-500 and has its own pharmacology.

Why are ACE inhibitors relevant to AC-SDKP?

Angiotensin-converting enzyme is the principal endogenous degrader of AC-SDKP. ACE inhibition therefore raises endogenous AC-SDKP concentrations, which some authors propose contributes to the anti-fibrotic benefit of ACE inhibitors.

Where to source TB-500 Fragment (AC-SDKP) for laboratory research

The following UK-based suppliers stock research-grade, lyophilised peptides for in-vitro and pre-clinical work. Purity and provenance vary; always request a Certificate of Analysis (CoA) and confirm cold-chain storage on arrival. None of the products linked below are approved for human use.

PeptideAuthority.co.uk
UK-based research peptide supplier with batch certificates of analysis and >99% purity testing.
PeptideBarn.co.uk
Wide catalogue of research-grade lyophilised peptides shipped from the UK, including bulk vials.