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 July 2026 compounding review, and the WADA prohibition from the source.
Effects and cautions, separated by evidence
The rev3 corpus adds a reader-facing TB-500 effects board. It separates frequently repeated community reports from clinical evidence, then lays out the updated cautions with their source citations. No anecdote is treated as a trial result, and no safety gap is filled with a dosing claim.