# TB-500 Doctor — Independent research summaries on the Thymosin Beta-4 7-AA fragment (Ac-LKKTETQ-OH) > Plain-English summaries of the TB-500 and Thymosin Beta-4 research literature: actin-binding mechanism, wound-healing animal studies, RGN-259 clinical trials, and the synthetic fragment versus parent peptide distinction. An editorial framing of the Thymosin Beta-4 literature, structured so the fragment-versus-parent distinction is visible on every page. ## The short version TB-500 is a seven-amino-acid research peptide — the actin-binding core of a much larger protein called Thymosin Beta-4. The important thing most vendor pages skip: almost every encouraging study you will find was run on the full 43-amino-acid parent protein, not on this short fragment. The animal research for wound healing, cardiac protection and tissue repair is real. Whether the fragment reproduces those effects in people is a genuinely open question — there are no completed controlled human trials of TB-500 itself. TB-500 is also prohibited in competitive sport under WADA and is not FDA-approved for any use. This site is a structured reading of the literature, built to keep the fragment-versus-parent distinction visible on every page. Start with [the effects page](/effects) for what research-use communities report, then work through the research record and citation table. ## What TB-500 actually is TB-500 is a synthetic peptide with the sequence `Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH`. It is seven amino acids long, weighs roughly 889 daltons, and carries CAS number 885340-08-9. The sequence corresponds to residues 17 through 23 of human Thymosin Beta-4 (Tβ4), a 43-amino-acid intracellular peptide encoded by the TMSB4X gene and expressed in nearly every nucleated cell type [1]. The central `LKKTET` motif inside TB-500 is the actin-binding core of the parent Tβ4 protein. The N-terminal acetyl group is a stability modification — it blocks aminopeptidase cleavage and slows degradation in solution. Beyond that, TB-500 carries none of the parent peptide's C-terminal sequence, none of its other interaction surfaces, and is missing the AcSDKP tetrapeptide that endogenous Tβ4 proteolysis liberates as a separately bioactive fragment [22]. In other words: TB-500 is a research analog of Thymosin Beta-4, sharing only the actin-binding domain. ## The disambiguation this site is built around Vendor pages and forum threads routinely refer to TB-500 and Thymosin Beta-4 interchangeably. The research record does not. Every published animal study cited on this site used full-length recombinant or synthetic 43-amino-acid Tβ4. Every registered human clinical trial — RGN-259 ophthalmic solution in dry eye and neurotrophic keratopathy [15][16], RGN-352 intravenous Tβ4 in post-myocardial infarction [22], the US Phase I dose-escalation by Ruff and colleagues [13], and the Chinese Phase I by Wang and colleagues [14] — used full-length Tβ4. The 7-amino-acid fragment marketed as TB-500 has never been the subject of a registered human trial or a published human pharmacokinetic study [12][22]. The scientific transfer from parent to fragment is plausible. Two papers have shown that constructs containing the actin-binding domain retain dermal and corneal healing activity in mice [5][20]. But the published large-mammal and human data sit with the parent peptide, and the gap is the editorial point of this publication. ## What the literature actually shows The strongest preclinical signal for Tβ4 is in tissue repair, in three lanes: **Dermal and corneal wound healing.** Topical Tβ4 at 5 micrograms accelerated reepithelialization of 8 mm full-thickness rat wounds by 42% at day 4 and 61% at day 7 [3]. The same molecule at 5 micrograms twice daily accelerated corneal healing and lowered IL-1β and chemokine mRNA after alkali burn in mice [4]. This preclinical foundation underwrites the entire RGN-259 ophthalmic program. **Cardiac repair.** Tβ4 binds PINCH and integrin-linked kinase (ILK) to activate Akt, improving cardiomyocyte survival after coronary ligation in mice [6]. It also mobilizes adult epicardial progenitor cells, restoring multipotency and driving new coronary vessels in the injured adult heart [7]. A porcine ischemia-reperfusion study did, however, fail to show global infarct-size reduction with systemic dosing [21] — a negative result that has shaped how the cardiac program reads in 2025. **Stem-cell mobilization and angiogenesis.** Tβ4 induces VEGF in endothelial cells, recruits skeletal-muscle satellite cells [10], increases hair-follicle keratinocyte migration [9], and, most recently, has been packaged into adipose-stem-cell exosomes inside dual-photopolymerizable hydrogels for diabetic wound closure (2025) [18]. ## What the literature does not show There is no published human pharmacokinetic study of the synthetic 7-amino-acid TB-500 heptapeptide. Half-life figures of two to three hours that circulate online originate from vendor pages, not primary literature [12]. The Phase III ARISE-3 trial of 0.1% RGN-259 ophthalmic solution in approximately 700 dry-eye patients missed its prespecified co-primary endpoints, with positive secondary signals in ocular grittiness and two-week corneal staining [15]. A separate Phase III neurotrophic keratopathy trial showed 60% versus 12.5% complete corneal healing at day 29 (p=0.066, a narrow miss) and statistically significant healing at day 43 [16] — meaningful but not yet a regulator-grade efficacy result. Tβ4 biology is also context-dependent. Conditional deletion of Tβ4 in hepatic stellate cells reduced liver fibrosis in a mouse CCl4 model [19], indicating that systemic Tβ4 is not biologically neutral across organs. Finally: TB-500 is prohibited at all times under the World Anti-Doping Code, listed under section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) and the catch-all S0 (Non-Approved Substances). Equine doping-control labs have validated LC-MS detection in plasma and urine [20]. ## How to read the rest of this site Each page below is structured as a sequence of framed blocks. Color-coded fills carry editorial categories: pink for mechanism, sky blue for clinical trials, lime for safety and preclinical animal data, gold for regulatory and WADA notes. The framing is the disclosure — every claim sits in a labeled box, every citation is a tile. Start with [the research record](/research) for the mechanism and the trial detail. Move to [dosage](/dosage) for the research-context dose information and a frank note on the gap between published rodent dosing and the multi-milligram per-week schedules vendor literature promotes for the fragment. Use [the FAQ](/faq) for the questions readers most commonly bring to this molecule, and [the references](/references) for the sortable citation table. --- An editorial record of the peer-reviewed Thymosin Beta-4 literature — not a clinic, not a vendor, not medical guidance.