# TB-500: Live Transmission from the Bathyal Zone of the Literature > TB-500 is the N-acetylated LKKTETQ heptapeptide fragment of the 43-residue protein thymosin beta-4. Preclinical tissue-repair findings, pharmacokinetics, and regulatory status, cited from the published record. A live transmission from the deep of the literature: the seven-residue Ac-LKKTETQ peptide, its parent Tβ4, and every cited finding surfaced as a specimen against the dark. ## TB-500 Peptide Overview TB-500 is a synthetic, N-acetylated heptapeptide with the sequence Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln — `Ac-LKKTETQ`, molecular weight 889.0 Da. It corresponds to amino acids 17 through 23 of thymosin beta-4, a 43-residue protein found in most mammalian cells [1]. The fragment retains the actin-binding motif of the parent molecule, which is why most preclinical activity ascribed to TB-500 traces back, mechanistically, to Tβ4 research conducted across the past three decades [3][18]. The distinction matters. Most completed clinical-trial work uses full-length Tβ4 — RGN-259 ophthalmic drops for dry eye and neurotrophic keratopathy [12][13], RGN-352 intravenous for cardiac repair [14] — not the seven-residue fragment. The LKKTETQ heptapeptide sold under the TB-500 name has its own preclinical demonstrations of wound-healing activity in diabetic and aged mice [3], but its human pharmacokinetics have not been published in the peer-reviewed literature. When the literature talks about "TB-500," it is often shorthand for the parent peptide; when it talks about TB-500 specifically, the dataset is narrower and earlier-stage. ## What is TB-500? TB-500 is a synthetic heptapeptide (Ac-LKKTETQ) corresponding to amino acids 17-23 of the endogenous protein thymosin beta-4. It is investigated in preclinical models for tissue repair, angiogenesis, and cell migration. It is not approved by the FDA for any human therapeutic indication. The compound is prohibited at all times under WADA Section S2 (peptide hormones, growth factors, related substances and mimetics) and is treated as a Class 1 substance by the Association of Racing Commissioners International [16]. ## What is TB-500 used for in research? TB-500 and its parent Tβ4 are investigated in preclinical models of tendon, ligament, muscle, cardiac, and corneal repair. Foundational work demonstrated that Tβ4 stimulates directional migration of human umbilical vein endothelial cells four- to six-fold over media-alone controls in Boyden chamber assays — the first piece of the angiogenesis story [1]. Subsequent rodent dermal-wound studies showed accelerated re-epithelialization, increased collagen deposition, and enhanced angiogenesis [2]. None of this represents a human-approved indication; it is the preclinical literature. ## Relationship to Thymosin Beta-4 (Tβ4) TB-500 (Ac-LKKTETQ) is a synthetic peptide corresponding to amino acids 17-23 of the 43-residue endogenous protein thymosin beta-4 — it is the active region of the parent peptide, not the full protein. Tβ4 is the major intracellular G-actin-sequestering peptide in mammalian cells. The LKKTETQ motif mediates that actin binding [18]. A 2003 study demonstrated that a synthetic peptide containing only the actin-binding domain — the LKKTETQ sequence — promoted dermal wound repair in db/db diabetic mice and in aged mice [3], providing direct evidence that the fragment retains a meaningful portion of the parent peptide's wound-healing activity. The fragment, in other words, is not a placeholder for the parent; it is a smaller molecule that carries forward part of the parent's functional repertoire. This is where reading the literature gets careful. The Phase 1, 2, and 3 human trials of [Thymosin Beta-4](/#thymosin-beta-4) (RGN-259 ophthalmic, RGN-352 IV) used full-length Tβ4 [12][13][14]. The TB-500 fragment has no completed Phase 3 human trial of its own. Efficacy extrapolation from full-length-peptide trials to fragment activity in humans is not validated. ## What the preclinical record actually contains Across roughly two dozen primary preclinical papers, Tβ4 and its LKKTETQ fragment have produced a consistent vocabulary of effects: endothelial chemotaxis [1], dermal re-epithelialization [2][3], reduced scarring with organized collagen birefringence [5], improved cardiomyocyte survival and ejection fraction after coronary ligation in mice [6], adult epicardial progenitor mobilization [7], hair-follicle bulge stem-cell migration [8], NF-κB suppression in corneal epithelium [9][20], and improved fibril organization in transected medial collateral ligament [4]. The list is broad. The species list is narrow — mostly rat, mouse, and in vitro human cell lines. The clinical translation, where it exists at all, is ophthalmic [12][13]. For [tendon repair research](/research#tendon) and other musculoskeletal indications, the evidence is preclinical only. For the full dose-by-species-by-route inventory, see the [TB-500 dosage](/dosage) page. For the regulatory and adverse-event picture — including the WADA prohibition and the theoretical angiogenesis-and-tumor signal from Cha 2003 [11] — see the [TB-500 side effects](/side-effects) page. The [TB-500 half-life](/dosage#half-life) data come exclusively from full-length-Tβ4 IV dosing in healthy volunteers [14]; no validated human PK for the heptapeptide fragment exists. --- A bathyal reading log on the TB-500 and thymosin beta-4 literature — transmitted from the deep, cited at depth, sold by no one.