DRAFTING DIGEST / Ac-LKKTETQ — THYMOSIN BETA-4 FRAGMENT
TB-500 is the Ac-LKKTETQ fragment of thymosin beta-4, drawn to spec from the literature.
Most published efficacy data describe the full-length thymosin beta-4 protein, not the seven-residue fragment sold as TB-500. This digest keeps the two apart, dimensions every figure to its study, and reads the regulatory standing straight.
TB-500, specified
TB-500 is the synthetic, N-acetylated heptapeptide Ac-LKKTETQ — residues 17 to 23 of thymosin beta-4, a 43-amino-acid protein present in nearly every human cell. Those seven residues are the actin-binding core of the parent protein. The fragment weighs about 889 Da; the full-length protein weighs about 4963 Da [1]. That gap is the most important thing on this site.
Here is the honest version of the TB-500 story. In commerce and in the anti-doping literature, "TB-500" means the heptapeptide. In the research literature, the overwhelming majority of efficacy studies used full-length thymosin beta-4, not the seven-mer. Whether the isolated fragment reproduces the parent protein's effects at the doses circulated in peptide-research communities has not been established in controlled human trials [1].
This digest is built around that distinction. Findings drawn from the full-length protein are flagged as parent-protein data. Findings about the fragment itself are kept separate. Every quantitative claim is dimensioned to a numbered study, and the regulatory standing — not FDA-approved, WADA-prohibited, placed by FDA in 503A Category 2 — is stated plainly rather than buried. The result reads like a spec sheet, because that is what an honest TB-500 page is: a verification document, not a vendor.
TB-500 Peptide: The Ac-LKKTETQ Fragment of Thymosin Beta-4
The TB-500 peptide is a short construct, not the endogenous molecule. Thymosin beta-4 (gene TMSB4X) is the body's principal G-actin-sequestering peptide, released by platelets and macrophages at sites of injury. The LKKTETQ segment that TB-500 carries is the conserved actin-binding motif of the beta-thymosins [1].
Structurally, the fragment is Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH, molecular formula C38H68N10O14. Because it is a short acetylated peptide, it is more chemically robust than the full-length protein, but it is still subject to proteolysis and freeze-thaw degradation. There is no single PubChem CID or CAS number consistently registered for the Ac-LKKTETQ fragment under the name TB-500; the parent protein maps to UniProt P62328.
One nuance the marketing rarely mentions: the parent protein also yields Ac-SDKP, an N-terminal cleavage product with its own anti-fibrotic and angiogenic activity. Ac-SDKP comes from the N-terminus and is not generated by the C-terminal-region TB-500 fragment — so claims that borrow Ac-SDKP biology for TB-500 are borrowing from the wrong end of the protein.
What the literature actually measured
Read against the parent protein, the thymosin beta-4 record is substantial. X-ray crystallography established that thymosin beta-4 forms a 1:1 complex with monomeric (G-) actin and sequesters it by capping both ends, preventing polymerization [2]. In a rat full-thickness wound model, thymosin beta-4 raised re-epithelialization by 42% at four days and up to 61% at seven days versus saline [3]. After coronary artery ligation in mice, thymosin beta-4 activated PINCH-ILK-Akt survival signaling and improved cardiac function [4].
The human record is narrower and belongs to the full-length protein. A randomized, placebo-controlled Phase 1 study gave intravenous synthetic thymosin beta-4 to 40 healthy volunteers and found it well tolerated up to 1260 mg, with no dose-limiting toxicities [5]. There are no completed controlled clinical trials of the TB-500 heptapeptide for any indication [1].
For the tissue-repair angle most readers arrive for, the TB-500 tissue repair research page collects the TB-500 wound healing studies, corneal, and connective-tissue findings in one place. For the binding chemistry, the TB-500 mechanism of action is set out study by study, alongside the thymosin beta-4 parent protein that carries most of the actual evidence.
Where TB-500 stands
TB-500 is not an approved medicine. It has no approved therapeutic indication, it is prohibited in sport by the World Anti-Doping Agency, and the FDA has placed "Thymosin beta-4, fragment (LKKTETQ), also known as TB-500" in 503A Category 2 — bulk substances identified as raising significant safety risks for compounding [6]. The TB-500 legal status and FDA 503A category page sets that record out as a title-block status stamp, and answers is TB-500 FDA approved directly.
The forward-looking note, kept honest: TB-500 is named on the published agenda of the FDA Pharmacy Compounding Advisory Committee meeting scheduled for July 23-24, 2026 as a substance being considered for inclusion on the 503A Bulks List [6][7]. That is a scheduled evaluation, not a decision and not a change in current status.
What is TB-500 used for in research?
In the literature, thymosin beta-4 and the LKKTETQ region carried by TB-500 are studied for tissue repair and wound healing, cell migration, angiogenesis, anti-inflammatory and anti-fibrotic effects, and cardiac, corneal, and neurological injury models — predominantly in animals and in vitro [10]. The fragment's human efficacy is not established [1].
What is TB-500?
TB-500 is the synthetic, N-acetylated heptapeptide Ac-LKKTETQ — residues 17 to 23 (the actin-binding motif) of the 43-amino-acid protein thymosin beta-4. It is sold for research and veterinary use; most published efficacy data are on the full-length protein, not the seven-mer [1].
What does TB-500 stand for and what does TB stand for in TB-500?
TB references thymosin beta (thymosin beta-4); TB-500 is the research and veterinary designation for the synthetic Ac-LKKTETQ fragment of that protein, not an abbreviation with an official chemical expansion beyond its thymosin-beta-4 origin [1].