PeptideDB

TB-500 (Ac-LKKTETQ)

Moderate research

Thymosin Beta-4 Active Fragment | Healing Peptide

TB-500 (Ac-LKKTETQ) is a synthetic derivative of thymosin beta-4 consisting of the N-terminal acetylated 17-23 amino acid fragment.

Molecular & research data

Sequence
Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln
Molecular weight
844 Da
Half-life
Not precisely established; effects persist longer than 24 hours
Primary targets
vegf
Routes (research)
Injectable
Storage
Reconstituted: 2-8°C refrigerated

Overview

TB-500 (Ac-LKKTETQ) is a synthetic derivative of thymosin beta-4 consisting of the N-terminal acetylated 17-23 amino acid fragment. This sequence represents the active site within thymosin beta-4 responsible for actin binding, cell migration, and wound healing. Research shows it promotes endothelial cell differentiation, angiogenesis, keratinocyte migration, collagen deposition, and decreases inflammation. The acetylation protects against N-terminal degradation while maintaining biological activity.

Mechanism of action

TB-500 contains the LKKTETQ sequence which is the actin-binding motif of full-length thymosin beta-4. This fragment shares many properties of the parent protein regarding cell proliferation, differentiation, and migration. It promotes angiogenesis by upregulating VEGF expression and enhancing endothelial cell sprouting. The peptide undergoes serial cleavage at the C-terminus during metabolism, while the N-terminal acetylation provides protection from degradation.

Key research findings

  • Promotes wound healing
  • Enhances cell migration
  • Supports angiogenesis (new blood vessel formation)
  • Reduces inflammation
  • Promotes keratinocyte migration
  • Supports collagen deposition
  • Enhances tissue repair
  • Active region of thymosin beta-4

Research applications

Tissue Repair

  • Wound Healing — Promotes dermal wound healing through the active LKKTETQ sequence.
  • Tissue Regeneration — Supports tissue repair comparable to full thymosin beta-4 in research.
  • Skin Repair — Promotes keratinocyte migration and collagen deposition.

Vascular Support

  • Angiogenesis — Promotes endothelial cell differentiation and new blood vessel formation.

Anti-Inflammatory

  • Inflammation Reduction — Decreases inflammatory responses in damaged tissues.

TB-500 (Ac-LKKTETQ) FAQ

Is TB-500 fragment (Ac-LKKTETQ) the same as full TB-500?+

TB-500 fragment is the active 7-amino-acid sequence (LKKTETQ) of the larger 43-amino-acid thymosin beta-4. Both promote wound healing and cell migration, but the fragment is more stable due to N-terminal acetylation and may be more cost-effective while retaining core regenerative properties.

How quickly does TB-500 fragment accelerate wound healing?+

Initial wound healing acceleration appears within 1-7 days, with enhanced cell migration and angiogenesis noticeable by week 1-2. Visible tissue repair improvements typically develop over 2-4 weeks during the loading phase of 2x weekly injections.

Should TB-500 fragment be used with BPC-157 for better healing?+

Yes, TB-500 fragment and BPC-157 are commonly combined for synergistic healing. TB-500 promotes cell migration and angiogenesis while BPC-157 upregulates growth factors - together they address multiple healing pathways better than either peptide alone.

Is the N-terminal acetylation in TB-500 fragment necessary for effectiveness?+

Yes, the acetylation protects the peptide from degradation at the N-terminus during metabolism while maintaining the active LKKTETQ sequence responsible for wound healing. This modification extends the functional lifespan and improves stability versus non-acetylated versions.

References

  1. [1]Synthesis and Characterization of N-terminal Acetylated 17-23 Fragment of Thymosin Beta-4Drug Testing and Analysis
  2. [2]Doping Control Analysis of TB-500Journal of Chromatography B
  3. [3]TB-500 Metabolism and Wound HealingJournal of Chromatography B
  4. [4]Investigation of TB-500 MetabolismWADA

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Last reviewed: 2026-06-26. Information is provided for research and educational reference only — see our disclaimer.