# TB-500 Dosage in the Research Literature — Study-attributed ranges only > The dose ranges and routes that appear in the peer-reviewed research literature on Thymosin Beta-4 and TB-500. Study-attributed values from rodent, porcine, equine, and human clinical work — not recommendations. The dose ranges that appear in the published Thymosin Beta-4 record — by species, route, and study citation. ## What these numbers are Every figure on this page comes from a specific published study. None of it is a recommendation for any person. The doses reported for full-length Thymosin Beta-4 in clinical trials — ranging from micrograms per kilogram up to 1,260 milligrams intravenously — do not translate directly to the seven-amino-acid TB-500 fragment, because the two molecules are structurally different and the fragment has never been studied in a registered human clinical trial. Vendor dose ranges circulating online are not derived from controlled research. This page records what the literature says; nothing more. ## What this page is and is not This page documents the dose ranges that appear in the published research literature on Thymosin Beta-4 and TB-500. Every figure cites a specific study. Nothing here is a dosing recommendation for any human use. TB-500 is not approved for any human indication by any regulatory authority, has been placed on FDA Category 2 of the 503A bulks list as a substance presenting significant safety risks [20], and is prohibited at all times for athletes under the WADA Prohibited List [21]. A further distinction governs every number on this page. Every published clinical and preclinical efficacy study has used full-length recombinant Tβ4 — the 43-amino-acid parent peptide. The synthetic seven-amino-acid TB-500 fragment has been characterized in published in vitro and equine PK work [15] but has never been the subject of a registered human clinical trial. Doses reported for full-length Tβ4 do not translate directly to the fragment, and the published pharmacokinetic literature does not support an equivalence assumption. Vendor literature commonly quotes 2–10 mg per week subcutaneously for TB-500. That range is not derived from any published clinical trial, has no peer-reviewed safety basis, and is not endorsed by any regulatory authority. ## Preclinical dose ranges Topical ocular and dermal dosing in rodent wound-healing models has been the most consistent setting in the Tβ4 preclinical record. Sosne and colleagues administered 5 μg of full-length Tβ4 in 5 μL PBS twice daily, topically, in a mouse alkali-burn cornea model and observed accelerated re-epithelialization at all time points [6]. The same family of corneal models has continued through engineered tandem-repeat constructs containing two LKKTET motifs, with multiple topical concentrations in rat alkali-injury studies [16]. Intraperitoneal systemic dosing in mouse cardiac-repair models has used 150 μg every three days, the regimen Smart and colleagues used for adult epicardial progenitor mobilization after coronary ligation [9]. For rat traumatic-brain-injury models, Xiong and colleagues used 6 mg/kg or 30 mg/kg intraperitoneally at six, twenty-four, and forty-eight hours post-injury [7]. For rat embolic stroke, Morris and colleagues used a single intravenous bolus of 3.75 mg/kg administered twenty-four hours post-occlusion [8]. In the porcine cardiac IR-injury work that produced the negative result, Wei and colleagues administered 150 μg/kg as an IV bolus plus maintenance — a dose roughly two orders of magnitude above the mouse epicardial-progenitor regimen on a per-kilogram basis — without reduction of infarct size at twenty-four hours [11]. The negative pig outcome remains the most-cited cautionary example in the Tβ4 translation literature. ## Human clinical dose ranges Published human dosing exists only for full-length recombinant Tβ4 in Phase I and Phase II clinical research. Ruff and colleagues' US Phase I administered single intravenous doses of 42, 140, 420, and 1,260 mg in 40 healthy adult volunteers, followed by a multiple-dose extension, with acceptable safety and tolerability across the range [12]. Wang and colleagues' Chinese first-in-human trial used single intravenous doses of 0.05–25 μg/kg and multiple-dose regimens of 0.5–5 μg/kg/day for ten days in 84 healthy volunteers, reporting dose-proportional Cmax and AUC and favorable immunogenicity [23]. For cardiac repair, the Phase IIb trial NCT05984134 evaluated recombinant Tβ4 at 0.5 μg/kg and 1.0 μg/kg administered intravenously within twelve hours of acute MI followed by daily dosing on days two through seven post-PCI [13]. For ophthalmic indications, the 0.1% RGN-259 topical solution has been administered six times per day for twenty-eight days in the Phase III neurotrophic-keratopathy program [14]. The two human Phase I dose ranges illustrate the breadth of the dosing literature for the parent peptide. Ruff 2010 went up to 1,260 mg as a single IV dose without DLTs; Wang 2021 used micrograms-per-kilogram dosing of a different formulation, both with acceptable safety. The two ranges differ by roughly four orders of magnitude in absolute milligram exposure, reflecting the formulation and pharmacokinetic differences between the two recombinant-Tβ4 products and the different clinical-development trajectories of the two sponsors. ## Half-life, routes, stability Published human pharmacokinetic data exist only for full-length recombinant Tβ4. In both Ruff 2010 and Wang 2021, intravenous recombinant Tβ4 plasma concentrations declined biphasically with rapid distribution and dose-proportional Cmax and AUC across the dose ranges studied [12, 23]. No peer-reviewed pharmacokinetic study of the synthetic seven-amino-acid TB-500 fragment has been published in humans. The figure of '2–3 hour half-life' that appears in vendor literature for TB-500 does not trace to primary research and should be treated as low-confidence. Equine pharmacokinetic detection work is the closest analogue. Esposito and colleagues validated a liquid chromatography–mass spectrometry method for TB-500 in equine urine and plasma after intravenous administration, confirming systemic exposure following injectable dosing in a large mammal [15]. The work was published to support doping-control sanctions, not as a pharmacokinetic characterization, and the half-life parameter was not fully reported. N-terminal acetylation in TB-500 blocks aminopeptidase cleavage and improves solution stability relative to the unmodified LKKTETQ heptapeptide. Full-length Tβ4 is highly water-soluble and stable in plasma because of its unstructured, hydrophilic sequence. Both molecules are inactivated by gastric proteases; oral administration is not pharmacologically meaningful, and every published preclinical and clinical study has used parenteral or topical routes [22]. Routes studied across the body of work include topical (dermal wound, corneal surface, hydrogel delivery), intraperitoneal (rodent systemic dosing across cardiac, stroke, and TBI models), intravenous (rodent, porcine, equine, human Phase I and Phase II), subcutaneous (rodent and equine doping-control studies), intracoronary (porcine IR-injury models), intramyocardial and AAV-delivered overexpression (mouse fibrosis models), and exosome-and-hydrogel-encapsulated delivery (diabetic wound, 2025) [17]. --- An independent editorial survey of the published regulatory and research record — not a clinic, not a vendor, not legal counsel.