Ac-SDKP
N-acetyl-seryl-aspartyl-lysyl-proline (thymosin beta-4 fragment 1-4)
Also known as: Thymosin beta-4 fragment 1-4, TB4 1-4
The N-terminal four amino acids of thymosin beta-4, a natural anti-fibrotic peptide broken down by ACE (which is why ACE inhibitors raise it); animal and human observational data, sold as capsules unlikely to survive digestion.
Overview
Ac-SDKP circulates naturally and limits fibrosis in heart, kidney and lung models. Its blood level rises in people taking ACE inhibitors, a well-documented human observation. Animal studies support anti-fibrotic and anti-inflammatory effects. As a product it is sold as an oral 'TB-4 fragment' capsule, but the peptide is cleared within minutes by ACE and there is no evidence of oral absorption.
Mechanism of action
Inhibits fibroblast proliferation and collagen deposition via TGF-beta/Smad signaling; degraded by angiotensin-converting enzyme.
Key studies & citations
- Review2021
Ac-SDKP as an anti-fibrotic peptide (review)
Consistent anti-fibrotic effects in animal models.
Clinical and Experimental Pharmacology and Physiology - Review2015
Effect of ACE inhibitors on Ac-SDKP levels: systematic review and meta-analysis
ACE inhibition raises circulating Ac-SDKP in humans.
PLoS One - Animal2017
Ac-SDKP in traumatic brain injury model
Reduced inflammation after injury in rats.
Journal of Neurosurgery
Frequently asked questions
Does an Ac-SDKP capsule work?
There is no evidence the peptide survives digestion, and it is cleared by ACE within minutes once in the blood.