# TB-500: Research Overview — Peptide Emporium > A plain-English research summary of TB-500 (Ac-LKKTETQ): the fragment-versus-full-protein distinction, actin biology, the Phase 1 human safety study, and key cautions. Citations throughout. The short Ac-LKKTETQ peptide holds the actin-binding motif of thymosin beta-4 — but most of the healing evidence in the literature comes from the full parent protein, not the fragment itself. ## The short version TB-500 is a small synthetic peptide — just seven amino acids — with the sequence Ac-LKKTETQ. That sequence is the *actin-binding* region of a larger natural protein called thymosin beta-4. Actin is part of the internal skeleton cells use to hold their shape and to crawl toward a wound, so the parent protein is closely involved in cell movement, healing, and new blood-vessel growth [10]. The single most important thing to know about TB-500 is a naming gap. In commerce and in anti-doping labs, "TB-500" means the short seven-amino-acid fragment. But most of the published *effectiveness* research was conducted with full-length thymosin beta-4 — which is about five times larger [8]. It is not established that the small fragment reproduces what the whole protein does. TB-500 is not an approved medicine, it is banned in sport, and this page reports doses only as they appear in the studies — never as a recommendation. ## What it is TB-500 is a synthetic, N-terminally acetylated heptapeptide (a seven-amino-acid peptide with a small acetyl cap on one end), sequence Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln. This `LKKTETQ` stretch corresponds to residues 17-23 of thymosin beta-4 (Tβ4), a 43-amino-acid protein encoded by the TMSB4X gene, and it is the conserved *actin-binding* region shared across the beta-thymosin family. The distinction matters throughout this page: the fragment sold and detected as "TB-500" weighs about 889 daltons, while full-length Tβ4 is about 4,963 daltons. Wherever a study used the full protein rather than the fragment, this page flags it — because that is exactly where TB-500 marketing tends to borrow a bigger molecule's data [8]. ## How it works Full-length thymosin beta-4 is the body's major intracellular G-actin sequestering protein. "G-actin" is the free, single-unit form of actin; "sequestering" means Tβ4 holds those units in reserve so they can be called up when a cell needs to change shape or crawl somewhere. A 2-angstrom X-ray crystal structure established that Tβ4 forms a 1:1 complex with G-actin and caps both ends of the monomer, preventing assembly — the structural basis for its actin-buffering role [12]. Why does that matter for repair? By governing the actin skeleton, Tβ4 (and its LKKTETQ motif) is associated with faster cell migration, new blood-vessel growth, reduced scarring, anti-inflammatory signaling, and recruitment of progenitor cells into damaged tissue — consolidated across skin-wound, corneal, cardiac and CNS models [10]. Whether the isolated seven-amino-acid fragment reproduces all of that at doses used in peptide research has not been shown in controlled human trials [10]. ## What the research shows *Structural basis.* The crystallography work established the precise 1:1 actin-capping mechanism [12], and a multi-model review consolidated Tβ4's actin-binding, pro-migratory, anti-scarring, anti-inflammatory and angiogenic functions as the rationale for clinical development [10]. *Human safety (full-length protein).* In a randomized, placebo-controlled Phase 1 study, synthetic thymosin beta-4 was given intravenously to 40 healthy volunteers — single dose then daily for 14 days at 42, 140, 420 or 1260 mg. It was well tolerated, with only infrequent mild-to-moderate adverse events, no dose-limiting toxicities, no serious adverse events, and dose-proportional pharmacokinetics [11]. Crucial note: this used full-length Tβ4, not the TB-500 fragment. *Animal dose-response.* In rats with an embolic stroke model, intraperitoneal thymosin beta-4 (2, 12 or 18 mg/kg starting 24 hours after stroke, then every three days) improved neurological function at 2 and 12 mg/kg, but not at 18 mg/kg — a *non-monotonic* result where higher was not better [9]. *Broader safety context.* A 2026 Sports Medicine review naming TB-500/thymosin beta-4 among unapproved peptides concluded that while animal-model results are often favorable, rigorous human safety data are scarce, potential for serious harm exists, and these compounds operate largely outside regulatory oversight [8]. ## Reported effects, cautions & safety The cautions for TB-500 are concrete and several are specific to this compound: - *Identity confusion.* "TB-500" is the fragment, but most efficacy data come from full-length Tβ4; efficacy claims for the fragment in humans are unproven [8]. No completed controlled clinical trials of the TB-500 fragment exist for any indication. - *Tumor and angiogenesis signal.* Thymosin beta-4 is overexpressed in several cancers and is implicated in metastasis and tumor blood-vessel growth; the same pro-migratory, pro-angiogenic properties that aid repair could, theoretically, support tumor progression [10]. - *Mixed preclinical results.* In dystrophin-deficient mice, chronic Tβ4 increased regenerating fibers but did not improve muscle strength, cardiac function or fibrosis; a porcine study found no benefit against myocardial ischemia-reperfusion injury [8][10]. - *Non-monotonic dosing.* The stroke study found 18 mg/kg helped less than 12 mg/kg — higher is not necessarily better, which undermines loading-protocol rationales [9]. - *Regulatory status.* TB-500 is WADA-prohibited and is classified as a prescription medicine in some jurisdictions; it has appeared as a doping agent in racehorses, with dedicated LC-MS detection assays developed [8]. No community-anecdote reports are included in this site's source material for TB-500 as a single compound; the points above are drawn from the cited literature. ## Where it fits in recovery research TB-500 occupies a particular position here: a compound whose *mechanism* — actin regulation driving cell migration — is well described at the protein level, but whose evidence as *the actual fragment sold* is the thinnest of the four singles [8]. Where [BPC-157](/bpc-157) leads with angiogenesis and [GHK-Cu](/ghk-cu) leads with matrix-building and human topical data, TB-500's story is really thymosin beta-4's story, borrowed. That makes it the clearest example of why this field rewards careful reading. It also appears as one half of the [Wolverine](/wolverine) blend and one component of [KLOW](/klow). See how all six compare on the [compare page](/compare). ![TB-500 actin filament and heptapeptide binding illustration in cold petrol tones](/images/tb-500.webp) --- A plain-English reading guide to the peer-reviewed recovery-peptide literature — research summaries only, never clinical advice and never a product for sale.