# Clinic TB-500 — A research console for Thymosin Beta-4 and the LKKTETQ fragment > An independent dark-mode console summarising the published research on TB-500 (Ac-LKKTETQ-OH) and its 43-amino-acid parent peptide Thymosin Beta-4. Twenty-six peer-reviewed citations, three published human safety datasets, and the disambiguation that almost nobody else prints clearly: the 7-amino-acid fragment is not the 43-amino-acid parent peptide that ran the trials. ## The short version TB-500 is a synthetic seven-amino-acid peptide — sequence `Ac-LKKTETQ-OH` — corresponding to residues 17–23 of full-length Thymosin Beta-4 (Tβ4). That short fragment carries the actin-binding motif of the parent protein. In cell and animal studies, the parent peptide accelerates wound closure, helps cardiac tissue survive injury, and supports neurological recovery after stroke [1][3][6][8]. People in research-use communities reach for TB-500 mainly for injury recovery and joint relief; those reports are anecdotal, not clinical evidence — [read what they say on the effects page](/effects). The core disambiguation to keep in mind: almost every encouraging trial result — including five human Phase I/II/III datasets — used full-length recombinant Tβ4, not the seven-amino-acid TB-500 synthetic [25]. No completed controlled human study of TB-500 itself exists. It is not FDA-approved for any indication and is prohibited by WADA at all times [16][26]. ## What is TB-500 TB-500 is a synthetic, N-acetylated seven-amino-acid peptide with the sequence `Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH`, CAS 885340-08-9, molecular weight 889.0 Da [1]. It corresponds to residues 17 through 23 of human Thymosin Beta-4, the 43-amino-acid intracellular peptide encoded by the TMSB4X gene. Those seven residues encompass the LKKTET motif — the conserved central sequence that mediates one-to-one binding to monomeric (G-) actin in the parent protein [1] [2]. The fragment is not the parent. Almost every published animal study and every registered human clinical trial that uses the phrase "thymosin beta-4" refers to the full 43-amino-acid recombinant peptide, not the seven-residue TB-500 synthetic [16] [21] [25]. This site treats that distinction as the first piece of editorial information a reader needs. The N-terminal acetyl cap blocks aminopeptidase cleavage and improves solution stability versus unprotected LKKTETQ. The molecule has been studied in equine doping-control work [16] but has never been the subject of a registered human pharmacokinetic or efficacy trial published in the peer-reviewed literature. ## Why this site exists TB-500 sits in a region of the research peptide literature where vendor copy outweighs peer-reviewed signal. Search results for the term return a steady stream of "healing peptide" pages that cite Phase III ophthalmic data without noting that the trial molecule (RGN-259, 0.1% Thymosin Beta-4 ophthalmic solution) is the full-length parent, not the seven-amino-acid heptapeptide [10] [22]. This console reads the record the other way around. It treats the published evidence — Cassimeris 1992 on actin binding [1], Irobi 2004 on the WH2-domain structure [2], Malinda 1999 on dermal wound healing in rats [3], Sosne 2002 on corneal alkali burn in mice [4], Bock-Marquette 2004 on cardiac repair in Nature [6], Smart 2007 on epicardial progenitor mobilisation in Nature [7], Morris 2010 and 2014 on rat stroke recovery [8] [9], Ruff 2010 and Wang 2021 on human Phase I safety [13] [14], Sosne 2022 on the RGN-259 Phase III neurotrophic keratopathy trial [15], Esposito 2012 on equine TB-500 detection [16], Wei 2016 on the negative porcine cardiac result [17] — as the substance of the page. The fragment-versus-parent distinction is the frame around it. The site does not sell TB-500. It does not refer readers to a vendor. It does not claim a clinical-services role. The "clinic" in the domain name is editorial framing — a position the publisher takes relative to the literature — and is treated explicitly as such on the about page. ## How the evidence breaks down The Thymosin Beta-4 record divides cleanly into three categorical layers: **Preclinical findings (lime).** The bulk of the record. Rodent dermal wound healing [3] [5], murine corneal re-epithelialisation [4], cardiac repair in mouse coronary ligation [6], adult epicardial progenitor mobilisation [7], rat embolic stroke recovery [8] [9], hair follicle stem cell activation [11], skeletal muscle satellite cell chemotaxis [12], HUVEC angiogenesis via Notch [13], and in-vitro biochemistry on actin binding [1] [2] [10]. Doses range from 5 μg per wound topical to 150 μg every 3 days intraperitoneal to 3.75 mg/kg intravenous in stroke models. These are research-context numbers, not human dosing guidance. **Clinical evidence (cyan).** Five published human-trial datasets. Ruff 2010 — US Phase I IV safety up to 1,260 mg single dose in 40 healthy adults [13]. Wang 2021 — Chinese Phase I, IV recombinant Tβ4 at 0.05–25 μg/kg in 84 healthy adults, dose-linear PK with no SAEs [14]. RGN-259 Phase II/III ophthalmic — ARISE dry eye programme (missed prespecified co-primary endpoints, positive secondary signals) and SEER neurotrophic keratopathy programme (Phase III NCT02600429: 60% vs 12.5% complete corneal healing at day 29, p=0.066, narrowly missed; significant at day 43, p=0.036) [15]. RGN-352 Phase II — IV Tβ4 at 450 mg or 1,200 mg daily × 3 then weekly × 4 in approximately 75 post-AMI patients [25]. **Regulatory and disambiguation (orange).** TB-500 is not approved for any human indication by any major regulator. The molecule was nominated for the FDA Section 503A Bulks List and is scheduled for Pharmacy Compounding Advisory Committee review on 23 July 2026 (docket FDA-2025-N-6895). It is prohibited at all times under both S2 (peptide hormones, growth factors) and the catch-all S0 (non-approved substances) of the WADA Prohibited List in the 2024, 2025, and 2026 editions [16]. ## What you will find on this site Five reading pages: a deeper research page that walks the mechanism, the preclinical evidence, the registered human trials, and the modern hydrogel and exosome combination work [20]; a dosage page that surveys published research doses by route and by species and explicitly refuses to translate them into human-use guidance; an FAQ that takes the questions readers actually search for and answers them with attached citations; a references console that renders all 26 citations as a sortable, searchable table; and an about page that names the editorial scope and what this project is not. Every quantitative claim on every page is attached to a citation in the references console. Every page footer carries the research-only disclaimer. The publisher does not employ clinicians and does not provide medical advice. --- An independent editorial console for the peer-reviewed record — not a clinic, not a vendor, not medical advice.