Research board / thymosin beta-4 fragment
TB-500 is the Ac-LKKTETQ thymosin beta-4 fragment, studied for tissue repair in animal models.
A flat status board of the published record — most efficacy data sit on full-length thymosin beta-4, not the seven-residue fragment, and that line is drawn on every card. Each finding is tagged by evidence tier and cited.
What the TB-500 record actually shows
TB-500 is a synthetic, N-acetylated heptapeptide with the sequence Ac-LKKTETQ — residues 17–23 of thymosin beta-4, the body's principal actin-sequestering peptide [1]. That short stretch is the actin-binding motif of the parent protein, and it is the entire molecule sold and detected as TB-500 (molecular weight ~889 Da). One identity fact organizes this whole site: most of the efficacy research credited to TB-500 was run on full-length thymosin beta-4 (~4963 Da), not the seven-residue fragment. Where a finding used the full protein, this board says so on the card.
The published evidence is strong in animals and thin in humans. In a rat full-thickness wound model, thymosin beta-4 increased re-epithelialization by 42% at four days and up to 61% at seven days versus saline [2]. X-ray crystallography established that thymosin beta-4 binds monomeric actin 1:1, capping both ends to buffer the unpolymerized pool [3]. In mice, it activated PINCH–ILK–Akt survival signaling and improved cardiac function after coronary ligation [4]. Those are the kind of reproducible, mechanistically grounded results that built the interest.
The human column is nearly empty. No completed controlled clinical trial of the TB-500 fragment exists for any indication [5]. The human data that do exist are on full-length thymosin beta-4: a randomized, placebo-controlled Phase 1 study dosed it intravenously and found it well tolerated to 1260 mg [6], plus topical ophthalmic trials. Whether the isolated seven-mer reproduces the parent protein's effects at research doses has not been tested in people [5]. This page leads with that gap rather than hiding it.
TB-500 peptide: what the research describes
The TB-500 peptide is the Ac-LKKTETQ heptapeptide — leucine, lysine, lysine, threonine, glutamate, threonine, glutamine, N-terminally acetylated, formula C38H68N10O14 [1]. In commerce and in the anti-doping literature, "TB-500" means this fragment. It is supplied as a lyophilized powder for research use and reconstituted in bacteriostatic or sterile water. As a short acetylated peptide it is more chemically robust than the full-length protein, though still subject to proteolysis and freeze–thaw degradation.
The seven residues matter because they carry the actin-binding function. The LKKTETQ motif is a WH2-type actin-interacting segment, the same region thymosin beta-4 uses to sequester monomeric (G-) actin and regulate cytoskeletal dynamics, cell migration, and motility [3]. That is the mechanistic bridge between the fragment and the parent protein — but a bridge is not proof the fragment reproduces every downstream effect of the whole molecule at the doses used in peptide research [5]. The honest framing throughout this board: the actin-sequestration mechanism is shared; the human efficacy of the fragment is unestablished.
Thymosin beta-4: the parent protein behind TB-500
Thymosin beta-4 (Tβ4; gene TMSB4X, UniProt P62328) is a ubiquitous 43-amino-acid peptide present in nearly all human cells and released by platelets and macrophages at sites of injury [7]. It is the body's main G-actin-sequestering molecule. The thymosin beta-4 parent protein is where almost all of the regenerative research sits — wound healing, corneal repair, cardiac and central-nervous-system models — and a 2012 review consolidated that record: actin binding, cell mobilization, reduced myofibroblast number (less scarring), anti-inflammatory and anti-apoptotic signaling, and angiogenesis [7].
TB-500 is a fragment of this protein, not the protein itself. The distinction is not pedantry. One full-length-only example: thymosin beta-4 generates Ac-SDKP, an N-terminal cleavage product with its own anti-fibrotic and angiogenic activity — and Ac-SDKP comes from the N-terminus, not the C-terminal-region LKKTETQ fragment that is TB-500 [1]. Marketing that cites "TB-500" benefits while leaning on full-length Tβ4 data blurs exactly the line this site keeps drawn.
How to read this board
Every finding on this site carries a status chip and a citation, the way a project board tags a task. A cyan HUMAN-DATA chip marks the one human-evidence tier (the intravenous Phase 1 safety study and topical ophthalmic trials, all on full-length thymosin beta-4) [6]. A lime PRECLINICAL chip marks rodent and in-vitro findings [2]. A cyan STRUCTURAL chip marks the biochemical results [3]. A coral NO-HUMAN-DATA chip marks every place the fragment has not been tested in people [5]. Color always rides a label word, so the status reads even without the color.
From here, four routes. The TB-500 hair follicle research page covers the bulge-stem-cell findings — the allocated focus of this board. The research page covers mechanism, the cardiac and stroke models, the TB-500 and BPC-157 comparison, and the wound data. The dosage page sorts the animal milligram-per-kilogram ranges and the human Phase 1 doses, with the half-life caveat. The TB-500 legal status page reads the FDA 503A standing, the scheduled compounding review, and the WADA prohibition from the source.