# TB-500: The Ac-LKKTETQ Fragment of Thymosin Beta-4, Read From the Research > TB-500 is the synthetic Ac-LKKTETQ heptapeptide carrying the actin-binding motif of thymosin beta-4. A research digest of the tissue-repair literature and where the human data stop. One synthetic seven-residue peptide, the actin-binding motif of a 43-residue parent protein. This is the mechanism, the evidence class on each finding, and the line between the two — every quantitative claim cited. ## What TB-500 is, in one read TB-500 is the synthetic N-acetylated heptapeptide `Ac-LKKTETQ` — molecular weight `~889 Da`, formula `C38H68N10O14` — corresponding to residues 17-23 of the 43-amino-acid protein thymosin beta-4 (Tβ4). That seven-residue stretch is the conserved actin-binding motif of the beta-thymosins, which is why the fragment carries the name and the repair narrative [1]. One distinction governs everything else on this site. "TB-500" in commerce and in the anti-doping literature denotes the `~889 Da` heptapeptide, but the overwhelming majority of *efficacy* research is conducted with full-length thymosin beta-4 (`~4963 Da`), not the seven-mer [5]. The full protein is the body's principal G-actin-sequestering molecule, present in nearly all cells and released by platelets and macrophages at sites of injury [5]. The fragment is a synthetic construct, not an endogenous species. Where a finding below was measured on the parent protein, it carries an identity-caveat mark — so you can see at a glance whether a result is on the molecule sold as TB-500 or on the protein it is derived from. This is a reading desk, not a clinic and not a counter. It summarizes the published record on TB-500 and Tβ4, sorts each finding by evidence class, and states the regulatory picture present-tense. It does not sell anything, dispense anything, or recommend a dose for any person. ## What is TB-500? TB-500 is the synthetic Ac-LKKTETQ heptapeptide — residues 17-23, the actin-binding motif, of the 43-amino-acid protein thymosin beta-4. Most published efficacy research uses the full-length protein, not the fragment. The structural basis of the parent protein's activity is established: X-ray crystallography of a gelsolin-domain-1–Tβ4 hybrid bound to actin resolved a `1:1` complex in which thymosin beta-4 sequesters a monomer of actin by capping both ends, preventing polymerization [1]. ## TB-500 peptide: the Ac-LKKTETQ fragment of thymosin beta-4 The TB-500 peptide is a single, defined sequence: `Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH`, abbreviated `Ac-LKKTETQ`. It is not a blend, not an analog family, and not the whole protein — it is the C-terminal-region actin-binding segment isolated and N-terminally acetylated for synthesis [5]. Naming this precisely matters because the fragment and the parent protein behave as one story in marketing and as two molecules in the laboratory. The LKKTETQ motif is a WH2-type actin-binding element, the same class of motif used by monomer-sequestering and filament-assembly proteins across the cytoskeleton [1]. Whether the isolated seven-mer reproduces the full protein's downstream effects — migration, angiogenesis, anti-scarring — at the doses used in peptide research is not established in controlled human trials [5]. One product of full-length Tβ4 makes the distinction concrete: `Ac-SDKP`, an N-terminal cleavage fragment with its own anti-fibrotic and angiogenic activity, is generated from the protein's other end and is *not* produced by the C-terminal-region TB-500 fragment [5]. The sequence you reconstitute and the protein the data describe are related, not identical. For the full mechanism, see [the actin-binding mechanism of TB-500](/research). For the parent protein, see the [thymosin beta-4 parent protein](/research) section. ## The repair pipeline, mechanism to outcome The research story for this compound is a single thread, which is why it reads as one pipeline. Full-length thymosin beta-4 binds monomeric (globular) actin `1:1`, capping both ends of the monomer to hold a buffered pool of unpolymerized actin and regulate cytoskeletal dynamics, cell migration and motility [1]. In injury models the protein is associated with accelerated cell migration, angiogenesis, anti-inflammatory and anti-apoptotic signaling, reduced myofibroblast number, and recruitment of progenitor cells — the basis for clinical development in dermal wounds, corneal injury, and heart and CNS repair [5]. The headline tissue-repair numbers come from a rat full-thickness wound model: topical or intraperitoneal thymosin beta-4 raised re-epithelialization by `42%` at four days and up to `61%` at seven days versus saline, increased wound contraction, and raised collagen deposition and angiogenesis; as little as `~10 pg` stimulated keratinocyte migration [3]. Those figures are on the full-length protein. What the fragment does at research doses in humans has not been measured in any completed controlled trial [5]. The full evidence base — cardiac, neurological, wound, and the safety signals — is organized study by study on the research page, alongside [TB-500 dosage in the research literature](/dosage) and the [TB-500 tissue repair research](/tissue-repair). ## Where the record stands, and where it stops Three facts anchor the honest version of TB-500. First, there are no completed controlled clinical trials of the TB-500 heptapeptide for any indication — human data exist only for full-length thymosin beta-4, including a randomized placebo-controlled Phase 1 intravenous safety study in which the protein was well tolerated to `1260 mg` [6]. Second, the same pro-migratory, pro-angiogenic properties that aid repair are a theoretical safety concern: thymosin beta-4 is overexpressed in several cancers and implicated in metastasis and tumor angiogenesis [9]. Third, the regulatory picture is specific and current — TB-500 is not an FDA-approved drug, the FDA has placed the LKKTETQ fragment in 503A "Category 2" (bulk substances that may present significant safety risks), and TB-500 is prohibited by the World Anti-Doping Agency in and out of competition. Those boundaries are not footnotes here. They lead the [TB-500 legal status](/legal-status) page — where the [FDA 503A and compounding access](/legal-status) picture is laid out present-tense — they recur on every finding that used the parent protein, and they are why the human-evidence count for the fragment reads zero. The 2026 Sports Medicine review of approved and unapproved peptide therapies places TB-500/thymosin beta-4 among compounds with favorable animal tissue-repair data but scarce rigorous human safety evidence and potential for serious harm [11]. --- TB-500 Store runs the thymosin beta-4 literature as a single luminous pipeline — the Ac-LKKTETQ fragment traced from actin binding to tissue repair, every full-length-protein substitution flagged in line, the empty human-trial node left lit, and FDA's 503A standing read before anything else; a research repository, not a clinic, a vendor, or a prescription.