Ac-SDKP (TB fragment 1-4): research, uses and evidence

Ac-SDKP is a natural tetrapeptide cut from the N-terminus of thymosin beta-4. It is studied as an anti-fibrotic and anti-inflammatory signal in the heart and kidney. ACE inhibitor drugs raise its blood levels several-fold, which may explain part of their organ-protective effect.

Structure

HydrophobicGly / ProPolarBasic (+)Acidic (−)

N-terminally acetylated. The first four residues of thymosin beta-4, released by prolyl oligopeptidase. Broken down by angiotensin-converting enzyme (ACE).

How it works

Ac-SDKP inhibits fibroblast proliferation and collagen deposition and reduces inflammatory cell infiltration. Because ACE degrades it, its levels rise with ACE inhibitors.

Research use cases

Areas where Ac-SDKP (TB fragment 1-4) has been studied. Inclusion here does not mean it works for that purpose.

Cardiac and renal fibrosis in hypertensive models
Haematopoietic stem cell protection (early work as goralatide)

What the research found

Fibrosis and blood pressure

A review of animal work describes reduced cardiac, renal and vascular fibrosis with Ac-SDKP treatment in models of hypertension and heart failure.¹

Safety and open questions

No controlled human data for the research product.

Regulatory status

Not approved. Research compound.

Status was accurate when this page was last reviewed on October 26, 2026. Regulations change; check with the relevant authority before relying on it.

Ac-SDKP (TB fragment 1-4): common questions

Why is it called a TB-500 fragment?

Because it is the first four residues (1–4) of thymosin beta-4. Its activity is different from the actin-binding region that the TB-500 name usually refers to.

Is Ac-SDKP (TB fragment 1-4) approved for human use?