EVIDENCE HEATMAP / THYMOSIN β4 (17-23) FRAGMENT

TB-500 is the actin-binding thymosin β4 fragment, graded here by how hot its evidence really runs.

The seven-residue fragment carries the actin-binding core of a forty-three-residue protein. We grade each finding by the heat of its data — the cardiac signal read first, the human record read straight.

A data-visualization heatmap matrix of small cells stepping from cold indigo to hot coral-red on a faint grid, with a vertical colorbar legend, on a deep plasma-black ground

The record, graded by heat

TB-500 is the synthetic N-acetylated heptapeptide Ac-LKKTETQ, corresponding to residues 17–23 of thymosin beta-4 (Tβ4) — the conserved actin-binding motif of the parent protein. On this site, every claim about TB-500 is graded by how hot its evidence actually runs: animal-confirmed and structurally established findings run hot, the human story for the fragment runs cold, and the borrowed-from-the-parent-protein findings are flagged so the heat is never read as more than it is.

The preclinical band is genuinely hot. The 1:1 binding of thymosin beta-4 to monomeric actin is established at 2 Å crystallographic resolution [1]. In rat wounds, thymosin beta-4 raised re-epithelialization by 42% at 4 days and up to 61% at 7 days versus saline [3]. In mice, the protein activated integrin-linked kinase and the survival kinase Akt and improved cardiac function after coronary ligation [2].

The human band is cold. No completed controlled trial of the TB-500 heptapeptide exists for any indication. The only human safety data come from full-length thymosin beta-4: a randomized Phase 1 study dosed it intravenously to 1260 mg with no dose-limiting toxicities [6]. Whether the isolated 7-mer reproduces the parent protein's effects in people is unproven.

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

The TB-500 peptide is a single synthetic molecule, not a blend. It is the acetylated heptapeptide Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln, molecular weight approximately 889 Da, formula C38H68N10O14. That sequence is the LKKTETQ actin-binding region of thymosin beta-4 — the WH2-type motif through which the parent protein binds and sequesters globular actin.

The distinction matters because the names are used loosely. In commerce and in anti-doping science, "TB-500" denotes this ~889 Da fragment. But the overwhelming majority of published efficacy work uses full-length recombinant or synthetic Tβ4 (~4963 Da), not the 7-mer [5]. It is not established that the fragment reproduces the whole protein's activity at the doses circulated in peptide research [11]. Across this site, any finding generated with full-length Tβ4 carries a parent-protein mark so that borrowed heat is visible at a glance.

Thymosin Beta-4 (Tβ4): The Parent Protein Behind TB-500

Thymosin beta-4 is a ubiquitous 43-amino-acid peptide present in nearly all human cells and released by platelets and macrophages at sites of injury. It is the body's principal G-actin-sequestering molecule: it binds monomeric actin 1:1 and holds a buffered pool of unpolymerized actin, regulating cytoskeletal dynamics, cell migration, and motility [1]. A 2012 review consolidated its reported activities — actin binding, cell mobilization, reduced myofibroblast number and scarring, anti-apoptotic and anti-inflammatory signaling, and angiogenesis — as the rationale for clinical development in dermal wounds, corneal injury, and heart and CNS repair [5].

This is why most of the literature is read through the thymosin beta-4 parent protein: the deepest efficacy data belong to the whole protein, and TB-500 carries only its actin-binding core. One mechanistic caveat is built into the chemistry — Ac-SDKP, an N-terminal Tβ4 cleavage product with its own anti-fibrotic and angiogenic activity, is generated from the protein's N-terminus and is not produced by the C-terminal-region TB-500 fragment.

Where the heat concentrates

The hottest cluster on this site is cardiac. In mouse hearts, thymosin beta-4 mobilized adult epicardial progenitor cells and drove neovascularization of ischemic myocardium [7], and it acts as a paracrine factor for the endothelial progenitors that build the coronary vasculature [8]. The full cardiac case — the PINCH-ILK-Akt survival pathway, post-infarct repair, and the mixed and negative results that cool it back down — is laid out in the TB-500 cardiac research page.

The TB-500 mechanism of action, the wound and neuro data, the tumor and angiogenesis safety signal, and how TB-500 compares with BPC-157 are graded on the research page. Research-context dosing, routes, and the TB-500 half-life question — there is no validated human pharmacokinetic value for the fragment — sit on the dosage page. Regulatory standing, the FDA 503A category, and WADA prohibition, with how compounded access actually stands, are set out on the TB-500 legal status page.