TB-500 is the Ac-LKKTETQ thymosin beta-4 fragment, routed study by study with its safety net flagged first.

What TB-500 is, drawn as one net

TB-500 is the synthetic, N-acetylated heptapeptide Ac-LKKTETQ — leucine, lysine, lysine, threonine, glutamate, threonine, glutamine — corresponding to residues 17–23 of the 43-amino-acid protein thymosin β4 (Tβ4). Those seven residues are the conserved actin-binding motif of the beta-thymosins. The molecular weight is roughly 889 Da (formula C38H68N10O14); the parent protein it is carved from weighs about 4963 Da. That weight gap is the first thing to read on this board, because it is the source of nearly every misunderstanding about the compound.

The commercial and anti-doping name "TB-500" denotes the fragment. The overwhelming majority of the efficacy literature — wound healing, cardiac repair, stroke recovery, hair-follicle activation — was run with full-length recombinant or synthetic Tβ4, not the seven-residue fragment ^[5][10]. Throughout this site, each finding carries the net tag of the molecule it was actually measured on: a FRAGMENT tag for the Ac-LKKTETQ heptapeptide, a FULL-LENGTH tag for Tβ4. Whether the isolated fragment reproduces the parent protein's effects at the doses used in peptide research has not been established in controlled human trials.

TB-500 has no FDA-approved therapeutic indication. It is supplied for laboratory research and is encountered in a veterinary context; it is also prohibited in sport by the World Anti-Doping Agency ^[15]. The dealt focus of this board is the safety net — the same pro-migratory, pro-angiogenic activity that aids repair is the activity implicated in tumor angiogenesis ^[7][8] — and that net is routed first, not buried in a footnote. Read TB-500 side effects and safety signals for the full risk picture, and TB-500 legal status and 503A category for the regulatory standing.

The TB-500 peptide: the Ac-LKKTETQ fragment of thymosin beta-4

As a research peptide, TB-500 is a single, defined molecule: the acetylated LKKTETQ heptapeptide. It is not a blend, not an extract, and not the whole protein. The endogenous parent, thymosin β4, 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][10]. The fragment isolates the parent's actin-binding core but leaves behind most of the chain, including the N-terminal segment that is cleaved to form Ac-SDKP, a separate anti-fibrotic, angiogenic peptide. Ac-SDKP comes from the opposite end of the protein and is not produced by the TB-500 fragment.

This matters for how to read any TB-500 claim. A structural study established the mechanism with precision: thymosin β4 binds monomeric G-actin 1:1 and caps both ends of the monomer to hold a buffered pool of unpolymerized actin ^[1]. That is solid biochemistry — but it is the parent protein's behavior, established in a structural complex, not a demonstration that the seven-residue fragment buffers actin identically in a living organism. The honest position is that the fragment carries the motif; what the motif does in isolation, in humans, at research doses, is not characterized in controlled trials.

The findings that hold, and the ones that don't

Three findings are worth surfacing as genuinely established in their models. In a rat full-thickness wound model, topical or intraperitoneal thymosin β4 increased re-epithelialization by 42% at 4 days and up to 61% at 7 days versus saline, with as little as 10 pg stimulating keratinocyte migration two- to three-fold ^[3]. After coronary artery ligation in mice, thymosin β4 activated PINCH–ILK–Akt survival signaling and improved early cardiomyocyte survival and cardiac function ^[2]. And a randomized, placebo-controlled Phase 1 study gave intravenous synthetic Tβ4 to 40 healthy volunteers at doses up to 1260 mg with no dose-limiting toxicities and only mild, infrequent adverse events ^[6]. All three are full-length-protein results.

The counter-evidence is on the same board, not a different one. In dystrophin-deficient mdx mice, six months of thymosin β4 increased the number of regenerating muscle fibers but produced no improvement in muscle strength, cardiac function, or fibrosis — a clean null functional result ^[9]. In the rat stroke model, 2 and 12 mg/kg improved neurological outcome but 18 mg/kg did not, a non-monotonic dose response that undercuts the idea that more is better ^[4]. And thymosin β4 is overexpressed in several cancers and implicated in metastasis and tumor angiogenesis ^[7][8]. A 2026 narrative review placed TB-500 among unapproved peptides that show favorable tissue-repair signals in animals but for which rigorous human safety data are scarce and the potential for serious harm is real ^[15].

How to read this board

Each page is a region of the same board. The research page traces how TB-500 works and the full preclinical record, with every finding tagged to the molecule it was measured on; the same page maps the thymosin beta-4 parent protein the fragment is carved from, and sets out TB-500 vs BPC-157 exactly as the 2026 review frames the two unapproved peptides. TB-500 side effects and safety signals concentrate the honest risk literature — the tumor-angiogenesis net, the null mdx result, and the absence of a human safety profile for the fragment. TB-500 dosage in the research literature frames doses as "studied at X mg/kg in [species]," never as instructions. TB-500 legal status and 503A category reads the FDA standing first. The frequently asked questions about TB-500 index the common questions, and TB-500 references and citations lists every source with its identifier.

This is an editorial reading of published work. It is not a clinic, it does not sell or supply anything, and it makes no recommendation about use. The point of routing each claim back to its node is so a reader can see, at a glance, exactly which molecule a piece of evidence is soldered to — and where the trace runs out.