TB4-FRAG (Ac-SDKP)

✓Key benefits

📈What to expect

Based on community reports and published research. Individual results vary significantly.

💊Dosing protocols

Dosing information is sourced from published research and community protocols. This is not a recommendation. Consult a healthcare professional.

Overview

Ac-SDKP (N-Acetyl-Seryl-Aspartyl-Lysyl-Proline) is a four-amino-acid peptide derived from the N-terminal region of Thymosin Beta-4 (the parent molecule of TB-500). It is released endogenously by the enzyme prolyl oligopeptidase (POP) and is normally degraded by angiotensin-converting enzyme (ACE). Circulating Ac-SDKP levels increase 4-5 fold in patients taking ACE inhibitors, which led researchers to discover that many of ACE inhibitors' cardioprotective benefits are actually mediated by Ac-SDKP accumulation. Research has focused on its anti-fibrotic, anti-inflammatory, and stem cell regulatory properties.

⚙️How it works

Ac-SDKP inhibits the differentiation of bone marrow stem cells, keeping them in a quiescent state that protects them during chemotherapy or radiation. In fibrotic tissue, it blocks TGF-beta/Smad signalling - the primary pathway driving fibroblast activation and collagen overproduction. It also inhibits macrophage infiltration and inflammatory cytokine release, reduces endothelial-to-mesenchymal transition (EndMT), and promotes angiogenesis. These combined effects make it a potent anti-fibrotic agent across multiple organ systems including heart, kidney, liver, and lung.

⚡Side effects

📅Research history

The ACE inhibitor connection

ACE inhibitors (lisinopril, enalapril, ramipril) are among the most prescribed cardiovascular drugs. It was long assumed their benefits came entirely from blocking angiotensin II. However, research revealed that ACE also degrades Ac-SDKP. When ACE is inhibited, Ac-SDKP levels rise 4-5 fold. Studies now suggest that a significant portion of ACE inhibitors' anti-fibrotic and cardioprotective effects are mediated by this Ac-SDKP accumulation rather than by angiotensin II suppression alone. This finding has repositioned Ac-SDKP as a key endogenous cardioprotective molecule.

Ac-SDKP vs full TB-500

TB-500 is a 43-amino-acid synthetic version of Thymosin Beta-4. Ac-SDKP is just 4 amino acids from the N-terminal region. While TB-500 has broader effects (actin regulation, cell migration, wound healing), Ac-SDKP concentrates the anti-fibrotic and stem cell protective activity. For users primarily interested in reducing fibrosis or scar tissue, Ac-SDKP offers a more targeted approach. However, for general tissue repair and injury recovery, full TB-500 provides a wider range of benefits.

References

1. [1]Rasoul S, et al. 'Antifibrotic effect of Ac-SDKP and angiotensin-converting enzyme inhibition.' Journal of Hypertension, 2004.
2. [2]Peng H, et al. 'Ac-SDKP inhibits transforming growth factor-beta1-induced differentiation of human cardiac fibroblasts.' American Journal of Physiology - Heart and Circulatory Physiology, 2010.

Frequently asked questions

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