# TB-500 | The Thymosin Beta-4 Fragment, Read Against the Research > TB-500 is the synthetic Ac-LKKTETQ fragment of thymosin beta-4, studied for tissue repair. A precise reading of the record — what is shown, what is only preclinical, and what is an outright gap. Ac-LKKTETQ is seven amino acids of a 43-residue protein. Most of the efficacy data is the protein, not the fragment, and zero controlled human trials of the fragment have been completed — so we print the headline and its health together. ## TB-500, stated precisely TB-500 is the synthetic, N-acetylated heptapeptide Ac-LKKTETQ — seven amino acids (Leu-Lys-Lys-Thr-Glu-Thr-Gln) corresponding to residues 17–23 of thymosin beta-4, the actin-binding core of that 43-residue protein [1]. That single sentence carries the most important caveat on this site: the molecule sold and tracked in the anti-doping literature as TB-500 is the ~889 Da fragment, while nearly every efficacy study cited below used full-length thymosin beta-4 (~4963 Da) [6]. It is not established that the isolated 7-mer reproduces the parent protein's effects at the doses used in peptide research. Thymosin beta-4 itself is the body's principal G-actin–sequestering peptide, present in nearly all human cells and released by platelets and macrophages at sites of injury [5]. The LKKTETQ motif in TB-500 is its actin-binding region. We read the literature on that basis throughout: where a finding used the full protein, we say so; where it used the fragment, we say that too. This is the [actin-binding mechanism of TB-500](/research), and it is the spine of everything else. The honest summary is short. The mechanism is well-characterized. The tissue-repair signals in animal models are real and, in places, large. The human record is thin and confined to the parent protein, the fragment has no completed controlled trial, and a genuine tumor/angiogenesis safety question sits underneath the repair story. Each of those is set out in its own panel below, cited to source. ## TB-500 as a Research Peptide: Sequence and Identity The TB-500 peptide is a defined chemical object: Ac-LKKTETQ, molecular formula C38H68N10O14, molecular weight ~889.02 Da. It is a synthetic construct, not an endogenous species — the body makes the full 43-residue thymosin beta-4, not the isolated heptapeptide. In commerce and in veterinary contexts the same fragment also appears under the designation TB1000; the number is a product label, not a chemical descriptor. Why the identity matters for reading the evidence: a short acetylated 7-mer and a 4963 Da protein are different molecules with different stability, distribution, and downstream biology. The full protein generates Ac-SDKP, an N-terminal cleavage product with its own anti-fibrotic and angiogenic activity — and that fragment is not produced by the C-terminal-region TB-500 sequence [5]. So when a marketing claim leans on a thymosin beta-4 study, it is borrowing data from a larger molecule. We keep the two labelled apart on every page. The parent protein's biology is genuinely well-mapped. X-ray crystallography of a gelsolin-domain-1–thymosin beta-4 hybrid bound to actin, resolved to 2 Å, established that thymosin beta-4 forms a 1:1 complex with monomeric (G-) actin and sequesters it by capping both ends, preventing polymerization [1]. That is the structural anchor for the whole beta-thymosin family — and it is the part of the TB-500 story that is fully confirmed. ## What the record establishes — and what it does not Confirmed: the actin-sequestration structure (1:1 G-actin capping) [1]; accelerated re-epithelialization in animal wounds, where full-length thymosin beta-4 raised re-epithelialization by 42% at four days and up to 61% at seven days versus saline [3]; and a randomized, placebo-controlled Phase 1 IV safety study in which synthetic thymosin beta-4 was well tolerated up to 1260 mg with no dose-limiting toxicities [6]. Those are the genuinely-on-the-record findings. Preclinical only: cardiac survival signaling via PINCH–ILK–Akt in mice [2]; dose-dependent neurological improvement after rat embolic stroke [4]; and the 2021–2026 thymosin beta-4 work — scaffold-released cardiac repair, inhaled-protein pulmonary fibrosis, zebrafish axon regeneration, an NAFLD inflammation study, and a 2025 engineered tandem corneal peptide. These are the [latest thymosin beta-4 research](/tissue-repair) signals, and they are animal or in-vitro. Outright gaps: there are zero completed controlled clinical trials of the TB-500 heptapeptide for any indication [6]. There is no validated human pharmacokinetic half-life for the fragment. And a 2026 Sports Medicine review lists TB-500 among unapproved musculoskeletal peptides with scarce rigorous human safety data and potential for serious harm. The honest record is the findings and the gaps, read together. ## Three common questions, answered up front The full question set lives on the [TB-500 side effects and safety signals](/faq) page. Three definitional ones belong here. --- A fiduciary-grade reading of the TB-500 and thymosin beta-4 record — each finding weighed against its own study and graded for evidence, the fragment-versus-protein line drawn in plain sight, with no clinic, pharmacy, or prescription behind the desk and nothing here dispensed or for sale.