# TB-500: The Ac-LKKTETQ Fragment of Thymosin Beta-4, Read From the Record > TB-500 is the synthetic Ac-LKKTETQ heptapeptide fragment of thymosin beta-4. A monitored digest of what the cardiac and tissue-repair literature establishes, where the human data stop, and the FDA 503A standing. Most of the efficacy record runs on the full-length 43-residue protein, not the 7-mer. Every finding here is tagged to the molecule it actually came from, the species, the dose, and the source. ## What this console reads, and the one thing it never lets you forget TB-500 is the synthetic, N-acetylated heptapeptide Ac-LKKTETQ — seven residues (17-23) lifted from the actin-binding core of thymosin beta-4, a 43-amino-acid protein present in nearly every human cell [5]. That single sentence carries this site's whole problem. The molecule sold, marketed, and detected in anti-doping work as `TB-500` weighs about 889 Da. The molecule that produced almost all of the efficacy data weighs about 4963 Da. They are not the same thing, and whether the 7-mer reproduces the parent protein's effects at the doses used in peptide research has never been tested in a controlled human trial [5]. So this page reads like an instrument panel, not a sales sheet. Findings that used the actual fragment carry a FRAGMENT tag. Findings that used full-length thymosin beta-4 carry a FULL-LENGTH tag. The established results stay bright; the gaps stay labeled. There are zero completed controlled clinical trials of the TB-500 heptapeptide for any indication [12]. Thymosin beta-4's mechanism is well characterized: it binds monomeric (globular) actin one-to-one, capping the monomer at both ends to hold a buffered pool of unpolymerized actin and regulate cytoskeletal dynamics and cell migration [1]. In injury models the parent protein is released by platelets and macrophages and is associated with accelerated cell migration, angiogenesis, reduced scarring, and anti-inflammatory signaling [5]. The corpus angle on this site is cardiac — see [TB-500 cardiac research](/cardiac-research) for the PINCH-ILK-Akt survival pathway, the epicardial-progenitor work, and the completed human acute-MI trial. ## TB-500 as a Research Peptide: The Ac-LKKTETQ Fragment of Thymosin Beta-4 TB-500 the research peptide is a defined chemical object: the sequence Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln, molecular formula C38H68N10O14, molecular weight ~889 Da. That heptapeptide is residues 17-23 of thymosin beta-4 — the conserved WH2-type actin-binding motif of the beta-thymosins [1]. It is supplied for laboratory use as a lyophilized powder and reconstituted in sterile or bacteriostatic water; as a short acetylated peptide it is more chemically robust than the full-length protein but still subject to proteolysis and freeze-thaw degradation. The identity matters because the fragment and the protein behave as different research objects. Full-length thymosin beta-4 is the body's principal G-actin sequestering molecule. Its N-terminal cleavage product Ac-SDKP has its own anti-fibrotic and angiogenic activity — and Ac-SDKP is generated from the N-terminus, not from the C-terminal-region LKKTETQ segment that TB-500 represents [5]. A reader who treats every `thymosin beta-4` result as a `TB-500` result has imported claims the fragment has not earned. `TB-500 peptide`, on this console, always means the 889 Da Ac-LKKTETQ construct, tagged FRAGMENT, distinct from its 4963 Da parent. ## Thymosin Beta-4: The Parent Protein Behind TB-500 Thymosin beta-4 (gene TMSB4X, UniProt P62328) is a ubiquitous 43-residue peptide and the body's major G-actin sequestering molecule. A 2 Angstrom X-ray structure of a gelsolin-domain-1/thymosin beta-4 hybrid bound to actin established that the protein forms a 1:1 complex with the monomer and prevents polymerization by capping both ends [1]. From that single biochemical fact a wide repair literature follows: the protein promotes migration of keratinocytes, endothelial cells, myoblasts and progenitor cells; it reduces myofibroblast number and scar formation; and it is released at injury sites by platelets and macrophages to limit apoptosis and inflammation [5]. This is where the central caveat lives. The randomized human safety study, the wound-healing figures, the stroke dose-response, the cardiac-repair results — the studies that make `thymosin beta-4` sound impressive — were almost all run with the full-length protein, not the 7-mer [5][12]. The corpus carries that distinction into every finding on this site, and so does the [thymosin beta-4 parent protein](/research) breakdown on the research page. The protein's record is real. The fragment's human efficacy is unproven. ## Four readouts that frame the record Four numbers anchor the panel above, and each is molecule-honest. The fragment's molecular weight is ~889 Da; the parent protein's is ~4963 Da — a roughly five-fold difference that is the whole reason the two cannot be read interchangeably [5]. The count of completed controlled human trials of the 7-mer is zero [12]. The highest intravenous dose tolerated in a Phase 1 study was 1260 mg — but that was full-length thymosin beta-4 in 40 healthy volunteers, not the fragment [6]. And the number of FDA-approved therapeutic indications for TB-500 is none [12]. From there the site splits into monitored channels: a mechanism and tissue-repair channel on the [how TB-500 works](/research) page, a dedicated [TB-500 cardiac research](/cardiac-research) channel for the dealt corpus lens, a research-dose channel on [TB-500 dosage in the research literature](/dosage), and a [TB-500 legal status and 503A category](/legal-status) channel for the regulatory record. The [frequently asked questions about TB-500](/faq) index ties the questions back to their answers, and every quantitative claim resolves to [TB-500 references and citations](/references). --- A pure-black analytics console querying the TB-500 and thymosin beta-4 record — the established findings held live in volt, the full-length-protein substitutions and the empty human-trial channel logged plainly, and the FDA 503A standing read before anything else; no clinic runs this console and nothing here is dispensed or sold.