# TB-500: The Ac-LKKTETQ Fragment of Thymosin Beta-4 — A Cited Research Dossier

> TB-500 is the synthetic Ac-LKKTETQ heptapeptide carrying the actin-binding motif of thymosin beta-4. What the literature measured — and where the data are for the full-length protein, not the fragment.

A tiled digest of the actin-binding mechanism, the muscle and ligament data, and the regulatory record — with one caveat flagged on every panel: most published efficacy data are for the full-length protein, not the 7-mer.

## What the TB-500 record actually contains

TB-500 is the synthetic, N-acetylated heptapeptide Ac-LKKTETQ — seven amino acids (Leu-Lys-Lys-Thr-Glu-Thr-Gln) that correspond to residues 17–23 of thymosin beta-4, a 43-amino-acid protein found in nearly every human cell [5]. That short stretch is the actin-binding core of the beta-thymosins. The fragment weighs roughly 889 Da; the parent protein weighs roughly 4,963 Da [1]. The gap between those two molecules is the single most important fact on this site.

Here is why. In commerce and in anti-doping science, "TB-500" denotes the heptapeptide. But the overwhelming majority of the published *efficacy* research — the wound-healing percentages, the cardiac-survival results, the stroke dose-response — was run with full-length thymosin beta-4, not the 7-mer [13]. Whether the isolated fragment reproduces the parent protein's effects at the doses circulated in peptide-research communities has not been established in any controlled human trial. Every finding tile below that drew on the full-length protein carries that flag.

The board is organized as discrete panels because the evidence is discrete: a 2-angstrom crystal structure of actin sequestration [1], a mouse cardiac-survival pathway [2], a +42% / +61% rat wound-healing result [3], a non-monotonic rat stroke dose-response [4], a myoblast-chemotaxis finding [7], a rat ligament-repair result [8], a notably null muscular-dystrophy strength result [9], and a human Phase 1 safety study of the full-length protein [6]. Read each tile on its own, check the species, and note the caveat. The athletic interest is collected under [TB-500 muscle recovery research](/muscle-recovery), and the research-context numbers under [TB-500 dosage in the literature](/dosage). For orientation across the whole record, see the [frequently asked questions about TB-500](/faq) and the [full reference list](/references).

## What Is TB-500?

TB-500 is the synthetic Ac-LKKTETQ fragment of thymosin beta-4 — a research and veterinary designation, not an acronym with an official expansion. The letters reference thymosin beta; the number is a catalog label that became the common name for the actin-binding heptapeptide. It is supplied as a lyophilized powder for laboratory use and reconstituted in sterile or bacteriostatic water.

### What is TB-500?

TB-500 is the synthetic, N-acetylated heptapeptide Ac-LKKTETQ, corresponding to residues 17–23 — the actin-binding motif — of the 43-amino-acid protein thymosin beta-4 [5]. It carries the parent protein's actin-interacting region without the rest of the molecule.

### What does TB-500 stand for?

TB references thymosin beta. TB-500 is a research and veterinary designation for the synthetic Ac-LKKTETQ fragment of thymosin beta-4, not an acronym with an official expansion. The same heptapeptide also circulates under the label TB1000.

### What is TB-500 used for in research?

It is studied as the actin-binding fragment of thymosin beta-4 across tissue-repair, wound-healing, muscle and ligament, cardiac, neurological, and angiogenesis models [5]. Critically, that body of work is overwhelmingly conducted with full-length thymosin beta-4, not the 7-mer.

## TB-500 Peptide: The Ac-LKKTETQ Fragment of Thymosin Beta-4

The TB-500 peptide is a single synthetic construct: Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH, molecular formula C38H68N10O14, molecular weight 889.02 Da. It is not endogenous. The body does make its parent — thymosin beta-4, gene TMSB4X, UniProt P62328 — which is the principal G-actin-sequestering peptide released by platelets and macrophages at sites of injury [5].

The distinction the TB-500 peptide name conceals: the 7-mer is the LKKTETQ actin-binding segment, while the full 43-residue protein also generates a separate N-terminal cleavage product, Ac-SDKP, with its own anti-fibrotic and angiogenic activity that the C-terminal-region TB-500 fragment does not produce [5]. So even mechanistically, the fragment is not a stand-in for the whole protein. A 2026 Sports Medicine review lists TB-500 and thymosin beta-4 among unapproved musculoskeletal peptides and concludes that rigorous human safety data are scarce [14].

## How TB-500 works

### How does TB-500 work?

TB-500 carries the LKKTETQ actin-binding motif of thymosin beta-4, which binds monomeric (globular) actin 1:1 and caps both ends of the monomer to hold a buffered pool of unpolymerized actin [1]. That actin-buffering controls cytoskeletal dynamics and cell migration. In injury models the parent protein is associated with angiogenesis, anti-inflammatory and anti-apoptotic signaling, reduced scarring, and progenitor-cell recruitment — see [the actin-binding mechanism of thymosin β4](/research) for the structural and signaling detail.

The identity caveat applies here too: the 1:1 sequestration mechanism was established structurally for thymosin beta-4 [1], and the downstream signaling effects were measured with the full-length protein. It is not established that the isolated heptapeptide reproduces them at research doses.

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A bento board of the TB-500 record — each finding tiled and cited, every full-length-versus-fragment caveat flagged in the corner, with no clinic behind the board and nothing here dispensed or sold.