# TB-500: The Ac-LKKTETQ Fragment of Thymosin Beta-4, Read Panel by Panel

> TB-500 is the synthetic N-acetylated heptapeptide Ac-LKKTETQ, the actin-binding fragment of thymosin beta-4. A cited digest of the tissue-repair and neurological-recovery research, with the human data clearly flagged.

A panel-by-panel reading of what the published research measured, where the evidence is genuinely strong, and the one caveat the whole field turns on: most of the data are for the full-length protein, not the heptapeptide.

## TB-500 in one panel

TB-500 is the synthetic N-acetylated heptapeptide `Ac-LKKTETQ` — residues 17 to 23 of the 43-amino-acid protein thymosin beta-4, and the conserved actin-binding motif of that protein [1]. At roughly `889 Da` it is a fraction of the full-length protein's `~4963 Da`. It is supplied for laboratory and veterinary contexts and has no approved human therapeutic indication.

That single sentence carries the tension this whole site documents. The name **TB-500** is what commerce and the anti-doping literature put on the seven-residue fragment, but the overwhelming majority of the *efficacy* research — the wound-healing numbers, the stroke models, the cardiac data — was run on full-length thymosin beta-4, not the 7-mer [5]. Whether the isolated fragment reproduces the parent protein's effects at the doses used in peptide research has not been established in controlled human trials [10]. Where a finding below comes from the full-length protein, this digest says so.

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

The **TB-500 peptide** is one short stretch of a much larger story. Thymosin beta-4 is the body's principal G-actin-sequestering peptide — present in nearly every human cell and released by platelets and macrophages at sites of injury [5]. Its job is to bind monomeric (globular) actin one-to-one and cap both ends of the monomer, holding a buffered reserve of unpolymerized actin that the cell can draw on to remodel its cytoskeleton, migrate, and repair [1].

The `LKKTETQ` segment that TB-500 reproduces is the actin-binding core of that protein — a WH2-type motif. So the fragment carries the parent protein's docking site for actin without the rest of the molecule. That structural fact is the reason TB-500 is studied for repair at all, and the reason its evidence base has to be read carefully: a docking motif is not the whole protein. The corpus flags this fragment-versus-full-length distinction on every page where it matters.

## What the research has actually shown

In a rat full-thickness wound model, thymosin beta-4 increased re-epithelialization by `42%` at four days and up to `61%` at seven days versus saline, raised wound contraction, and increased collagen deposition and new-vessel formation; as little as `~10 pg` stimulated keratinocyte migration two- to three-fold [3]. In male Wistar rats with embolic stroke, intraperitoneal thymosin beta-4 at `2` and `12 mg/kg` improved neurological function while `18 mg/kg` did not — a non-monotonic result that quietly undercuts the "more is better" loading logic [4]. In mice, thymosin beta-4 activated the PINCH-ILK-Akt survival pathway and improved cardiac function after coronary artery ligation [2].

Those are the kinds of discrete, quotable findings this site is built around — each one a panel you can check against its source. The deep dives live on [TB-500 benefits observed in research models](/research#benefits) and the dedicated [TB-500 neuroprotection and neurological recovery research](/neuro-research) page. The recurring editor's note, in plain print: items [2], [3] and [4] all used full-length thymosin beta-4, not the TB-500 heptapeptide.

## Where the human data stop

No completed controlled clinical trial of the TB-500 heptapeptide exists for any indication [10]. The only controlled human exposure to thymosin beta-4 in this digest is a randomized, placebo-controlled Phase 1 study in which the *full-length* synthetic protein was given intravenously to 40 healthy volunteers at `42`, `140`, `420` or `1260 mg`, well tolerated to the top dose with no serious adverse events [6]. Topical ophthalmic thymosin beta-4 (RGN-259) has been studied for corneal healing and dry eye [9].

That is the honest shape of the evidence: large, reproducible effects in animal models; a clean Phase 1 safety read on the full-length protein in humans; and essentially no human efficacy data on the fragment itself. For how that lands on access, see [TB-500 legal status and FDA 503A category](/legal-status). A pro-angiogenic, pro-migratory signal that aids repair also underlies a flagged tumor-biology concern, covered in [TB-500 side effects and safety signals](/faq#side-effects).

## What is TB-500?

TB-500 is the synthetic N-acetylated heptapeptide `Ac-LKKTETQ`, corresponding to residues 17 to 23 — the actin-binding motif — of the 43-amino-acid protein thymosin beta-4 [1]. It is supplied for research and veterinary contexts and has no approved human therapeutic indication. The parent protein is abbreviated Tβ4; "TB" in TB-500 refers to thymosin beta.

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The TB-500 record drawn as a comic page — each repair figure, stroke dose and safety signal inked into its own panel and logged to its study, the fragment-versus-full-length caveat stamped on every page, with no clinic behind the gutters and nothing here dispensed or sold.