TB-500 is the synthetic Ac-LKKTETQ fragment of thymosin beta-4, tracked across the cardiac and tissue-repair literature.

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 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 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 page, a dedicated TB-500 cardiac research channel for the dealt corpus lens, a research-dose channel on TB-500 dosage in the research literature, and a TB-500 legal status and 503A category channel for the regulatory record. The frequently asked questions about TB-500 index ties the questions back to their answers, and every quantitative claim resolves to TB-500 references and citations.