# tb500legal.com # TB-500 Legal — The regulatory record on Ac-LKKTETQ-OH, read like a passport > A customs-form reading of the regulatory record on TB-500: FDA 503A Category 2, WADA S2 and S0, IFHA Article 6, USADA enforcement. Mechanism, evidence, and jurisdictional status of the seven-amino-acid fragment of Thymosin Beta-4. Ac-LKKTETQ-OH, fragment of Thymosin Beta-4. A reading of the customs forms — every clearance, every refused entry. ## The short version TB-500 is a synthetic seven-amino-acid peptide — Ac-LKKTETQ-OH — derived from the actin-binding region of a protein your body already makes in every cell. Researchers study the parent protein (Thymosin Beta-4) for tissue repair, but TB-500 itself, the short fragment, has never been tested in a registered human clinical trial. The FDA placed it on its list of substances too risky for compounding pharmacies to use. The World Anti-Doping Agency bans it for all athletes, in and out of competition. This site documents those regulatory findings jurisdiction by jurisdiction — not to endorse any use, but to read the record straight. [See what people report and the honest cautions on the effects page.](/effects) ## What this site documents TB-500 is a synthetic seven-amino-acid peptide with the sequence N-acetyl-Leu-Lys-Lys-Thr-Glu-Thr-Gln (Ac-LKKTETQ-OH). The sequence corresponds to residues 17–23 of full-length human Thymosin Beta-4 (Tβ4), a 43-amino-acid intracellular peptide encoded by the X-linked TMSB4X gene [1]. The fragment carries the conserved LKKTET central motif that mediates binding to monomeric actin in the parent peptide. The N-terminal acetyl group blocks aminopeptidase cleavage and improves solution stability. The distinction matters at every level of the regulatory record. Every registered human clinical trial of 'thymosin beta-4' has used the full 43-amino-acid recombinant protein. The synthetic seven-amino-acid fragment marketed as TB-500 has never been evaluated in a registered human clinical trial. Vendor literature treats the two molecules as interchangeable; the published structural work treats them as related but pharmacologically distinct [22]. This site reads the regulatory record on TB-500 the way a customs officer reads a passport: jurisdiction by jurisdiction, stamp by stamp. The FDA placed it on Category 2 of the interim 503A bulks list in 2023 [20]. The World Anti-Doping Agency lists it under sections S2 and S0 of the 2025 Prohibited List [21]. The International Federation of Horseracing Authorities prohibits it under Article 6 of the International Agreement on Breeding, Racing and Wagering. The U.S. Anti-Doping Agency has issued four-year ineligibility sanctions for possession alone [22]. The site documents these findings as observational record, not as prescription or proscription. ## Where TB-500 stands today TB-500 is not approved for any human indication by any major regulatory authority — not the FDA, EMA, MHRA, TGA, PMDA, or NMPA. The molecule is not currently scheduled as a controlled substance under the federal Controlled Substances Act or under the controlled-substance acts of California, Texas, New York, or Florida. The FDA's 2023 placement of TB-500 on the Category 2 interim 503A bulks list was the formal finding that the substance presents 'significant safety risks' that licensed compounding pharmacies are prohibited from using [20]. The classification followed a multi-year FDA review of bulk peptides nominated for compounding and warning-letter enforcement actions issued at intervals between 2017 and 2023. The World Anti-Doping Agency lists TB-500 and thymosin-β4 explicitly in the 2025 Prohibited List under section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics), prohibited at all times — in competition and out of competition — for athletes under the World Anti-Doping Code [21]. The S0 catch-all also applies, because the molecule has no marketing authorization in any jurisdiction. The S0 status carries a mandatory four-year ineligibility period on first offense unless the athlete establishes no significant fault. Mere possession is sufficient grounds for sanction under the Code. The USADA case against weightlifter Michael Nackoul — a four-year ineligibility for possession of prohibited growth factors including Thymosin Beta-4 — was published as a deterrent precedent [22]. ## What the science says, briefly The biology of the parent peptide is extensively characterized. Full-length Tβ4 is the principal G-actin-sequestering protein in eukaryotic cells, binding monomeric actin in a 1:1 complex through its central LKKTET motif [4]. Beyond actin sequestration, Tβ4 induces angiogenesis by stabilizing HIF-1α and inducing VEGF transcription [1], suppresses NF-κB-driven inflammatory cytokine expression [3], activates the PINCH–ILK–Akt cell-survival axis in cardiomyocytes [10], and is enzymatically cleaved to release the antifibrotic tetrapeptide AcSDKP [19]. The most-developed clinical program for full-length Tβ4 is RGN-259, a 0.1% topical ophthalmic solution. A Phase III trial in neurotrophic keratopathy (NCT02600429, n=18) reported complete corneal healing at day 29 in 60% of treated patients versus 12.5% on placebo and statistically significant healing at day 43 [14]. Subsequent Phase III trials in dry eye (ARISE-3) and European neurotrophic keratitis (SEER-3) missed their prespecified primary endpoints. Phase IIb cardiac trial NCT05984134 in 90 acute-MI patients post-PCI completed in 2023; primary results have not yet been published [13]. What the synthetic TB-500 fragment does in a human body is not documented in the peer-reviewed literature. The class of LKKTET-containing peptides shows preserved corneal-healing activity in rodent models [16], and equine doping-control work confirms systemic exposure after IV administration in horses [15]. Beyond that, the fragment's human pharmacology is the territory of vendor literature, not science. ## How the site is organized The remaining pages follow the customs-form structure. /research documents the mechanism and the published evidence, organized by tissue system and citation. /dosage catalogs the dose ranges that appear in the published research literature — these are study-attributed values, not recommendations. /faq answers the questions readers actually arrive with: is TB-500 legal in the United States, is it controlled, why did the FDA classify it, is it banned by WADA, what sanction follows. /references is the customs manifest — every citation, sortable and searchable. /about establishes who publishes the site and on what basis. /contact provides editorial correspondence channels. The site does not sell anything. It is not a clinic. It is not affiliated with any vendor, supplier, compounding pharmacy, anti-doping organization, or regulatory authority. The content is editorial commentary on publicly available science and publicly published regulatory documents. --- An independent editorial survey of the published regulatory and research record — not a clinic, not a vendor, not legal counsel. --- # TB-500 reported effects and safety — what the record shows > TB-500 reported effects, community signals, and safety cautions: what research-use communities describe, what animal studies show, and what the honest risk record looks like for the synthetic Thymosin Beta-4 fragment. The effects attributed to TB-500 in research-use communities, alongside the honest safety cautions the published and regulatory record supports. ## The short version TB-500 is a seven-amino-acid fragment of a protein your body makes naturally. Animal studies show the parent protein — full-length Thymosin Beta-4 — can speed tissue repair, calm inflammation, and support cardiac and neural recovery. Whether the shorter TB-500 fragment does the same things in a human body is simply not documented in controlled clinical research. No registered human trial of TB-500 itself has ever been completed. What follows is two separate layers of information: first, what people in research-use communities say they experience (anecdotal, not clinical evidence); second, what the published and regulatory record identifies as genuine cautions. Neither layer constitutes medical advice. ## What people report **The following signals are anecdotal, not clinical evidence.** They come from peptide-user forums, wellness-clinic write-ups, and research-supplier review pages — personal accounts from people who have used TB-500 in an uncontrolled, non-research setting. They are reported here because they are part of the honest record, not because they are verified by clinical study. **Benefits most often mentioned:** - **Faster recovery from tendon, ligament, and muscle injuries** (very commonly reported). This is the main reason people in research-use communities reach for TB-500. They describe nagging soft-tissue injuries feeling better and returning to activity sooner than expected. Timelines vary widely and controlled conditions are absent. - **Less joint pain and stiffness, better range of motion** (frequently reported). People with general wear-and-tear stiffness most often mention this, typically over a few weeks. No controlled human trial underlies these joint-comfort reports. - **Improved overall flexibility and mobility** (frequently reported). Overlaps with the joint reports; people typically notice it around weeks three to four. - **Feeling of reduced inflammation or calmed-down soreness** (occasionally reported). A softer, vaguer signal than the injury-recovery reports — no human study confirms an anti-inflammatory benefit from the TB-500 fragment specifically. - **Better wound and skin healing** (occasionally reported). Some people mention cuts or surgical sites seeming to close more quickly, consistent with what animal studies show for the parent protein. - **Hair regrowth or thicker hair** (rarely reported). A minor and inconsistent signal, difficult to separate from other concurrent interventions. **Adverse effects most often mentioned:** - **Injection-site redness, swelling, or aching** (very commonly reported). The most common complaint — a small pink, sore spot that typically resolves within a day or two. Not unique to TB-500. - **Temporary tiredness or lethargy** (frequently reported). Many users describe unusual fatigue for a day or two, especially early on, that fades as use continues. - **Head rush, lightheadedness, or headache** (occasionally reported). Brief and self-resolving; less common than tiredness. - **Brief flu-like feeling** (occasionally reported). Mild and short-lived; described as the body reacting to a new peptide. - **Nausea** (rarely reported). Mild; more common at larger amounts. - **Heightened awareness of an existing injury** (rarely reported). Some users report an old injury feeling more active in the first one to two weeks. - **Temporary low mood or mood changes** (rarely reported). Vague and uncommon; no clinical evidence ties TB-500 to mood effects. ## Safety and cautions The following cautions reflect what the published and regulatory record supports. They are organized from the most firmly evidenced to the most theoretical. **Human safety is essentially unstudied.** No completed controlled human trial of the TB-500 heptapeptide exists for any indication. A 2026 Sports Medicine review of unapproved peptides concluded that compounds like TB-500 show promise in animal models but carry scarce human safety data, potential for serious harm, and operate largely outside regulatory oversight [26]. The only published human safety data are for full-length recombinant Thymosin Beta-4 — a different molecule — in a Phase I intravenous study in healthy volunteers [12]. **Theoretical cancer and tumor-growth concern (preclinical signal).** The parent protein Thymosin Beta-4 is overexpressed in several cancers — including pancreatic cancer cells, where it stimulated proinflammatory cytokine secretion [28] — and has been linked to tumor spread and to the growth of new blood vessels that feed tumors [27]. The same pro-migration, pro-angiogenic properties that may help tissue repair could, in principle, support tumor progression. This signal has not been measured for TB-500 in humans, but people with a current or past cancer, or strong family cancer risk, are the group most often identified as warranting precaution. **Banned in competitive sport.** The World Anti-Doping Agency prohibits TB-500 under its peptide and growth-factor categories. Anti-doping laboratories have validated methods to detect TB-500 and its breakdown products in both equine and human biological matrices [29]. A positive test can end an athlete's eligibility regardless of any claimed recovery benefit. **Animal evidence includes honest negative results.** A long-term animal study gave dystrophin-deficient mice thymosin beta-4 twice weekly for six months and found more regenerating muscle fibers — but no improvement in muscle strength, cardiac function, or fibrosis [30]. More apparent regeneration did not translate into better functional outcomes, which is a caution against assuming felt improvements reflect real structural repair. **TB-500 is a fragment, not the full parent protein.** Almost all encouraging efficacy research used full-length Thymosin Beta-4. TB-500 carries only the short actin-binding region (residues 17 to 23) and lacks the structural features linked to the parent protein's highest-affinity interactions [31]. Analytical work characterizing TB-500 preparations confirms it as a distinct species from the parent protein [29]. Applying the parent protein's results to the fragment is an extrapolation that has not been confirmed in controlled research. **Research-grade product quality is not guaranteed.** Material sold as TB-500 for research is not manufactured to medicine-grade standards; identity, purity, and exact sequence vary between suppliers. A 2023 analytical study characterizing TB500/TB1000 preparations for doping control underscores how much composition matters for any interpretation of results [32]. **Theoretical cautions in specific populations.** Because the parent protein influences blood-vessel formation and platelet activity at injury sites, people with clotting disorders or those near surgery face uncertain effects — a mechanism-based inference, not a measured finding. Pregnant or breastfeeding individuals and anyone still developing are a precautionary group for the same reason. There are no human safety data in any of these populations. --- An independent editorial survey of the published regulatory and research record — not a clinic, not a vendor, not legal counsel. --- # TB-500 Research Record — Mechanism, evidence, and clinical-program status > The peer-reviewed research record on Thymosin Beta-4 and its synthetic fragment TB-500: G-actin sequestration, HIF-1α/VEGF angiogenesis, PINCH-ILK-Akt cardiac signaling, corneal repair, neurorestoration, and the active clinical-development landscape. Mechanism, preclinical findings, and the clinical-program status. What is known and what remains, by jurisdiction of evidence. ## What the record contains The research on this page is almost entirely about the full 43-amino-acid Thymosin Beta-4 protein, not the seven-amino-acid TB-500 fragment. The distinction matters: every registered human trial has used the parent protein. The TB-500 fragment appears in equine doping-control detection work and a handful of cell and animal studies, but its human pharmacology is uncharted. What follows is the published record on how Thymosin Beta-4 works — actin sequestration, angiogenesis, cardiac signaling, corneal repair, brain injury — organized by tissue system and citation, with the fragment-versus-parent distinction preserved throughout. ## The molecule Thymosin Beta-4 is a 43-amino-acid intracellular peptide encoded by the X-linked TMSB4X gene and conserved across nearly every eukaryotic lineage examined. It is expressed in essentially every nucleated cell type, with particularly high levels in platelets, macrophages, and polymorphonuclear cells. The central biological role is G-actin sequestration: each Tβ4 molecule binds one monomeric actin unit through a flexible structure organized around the central LKKTET motif, regulating the cellular pool of polymerization-ready actin [4]. TB-500 — the synthetic peptide marketed under that name — is the heptapeptide Ac-LKKTETQ-OH, corresponding to residues 17–23 of the parent protein. Molecular formula C37H67N9O14; CAS 885340-08-9; monoisotopic mass approximately 889.5 Da. N-terminal acetylation blocks aminopeptidase cleavage and improves solution stability. The fragment carries the LKKTET motif but lacks the C-terminal α-helix that crystallographic work has identified as the principal structural determinant of high-affinity actin sequestration in the parent peptide [22]. The pharmacological consequence of that structural difference is the unresolved question at the center of the entire TB-500 literature. Vendor materials treat the fragment and the parent as functionally equivalent. The published comparison studies that would settle the matter have not been done. ## Angiogenesis: HIF-1α, VEGF, and Notch Among the best-characterized downstream effects of full-length Tβ4 is its induction of vascular endothelial growth factor. In human umbilical vein endothelial cells exposed to recombinant Tβ4 at 10–100 ng/mL, Jo and colleagues found that the peptide stabilized HIF-1α protein under both normoxic and hypoxic conditions, leading to increased VEGF transcription and secretion. HIF-1α siRNA abolished the effect [1]. The loop runs in both directions. Ryu and colleagues found that nitric oxide regulates Tβ4 expression through HIF-1α binding to the Tβ4 promoter, identifying the peptide itself as a hypoxia-responsive gene [2]. The result is a positive feedback circuit in which hypoxic stress raises Tβ4 expression, and Tβ4 in turn stabilizes HIF-1α to drive angiogenesis. A further step is Notch signaling. Kim and Kwon showed that inhibition of either Notch1 or Notch4 receptors blocked Tβ4-induced VEGF and HIF-1α expression in HUVEC cells and abolished tube formation in subcutaneous Matrigel plugs containing 1 μg Tβ4 [3]. Notch is obligate downstream of Tβ4 for angiogenic activity, not merely correlated with it. ## Anti-inflammation and the AcSDKP axis Beyond actin sequestration and angiogenesis, Tβ4 directly modulates inflammatory transcription. Qiu and colleagues found that recombinant Tβ4 bound NF-κB RelA/p65 in human HCT116 and HeLa cells, blocking TNF-α-driven NF-κB transactivation and downstream IL-8 transcription. The integrin-linked-kinase partner PINCH-1 sensitized the effect [4]. A distinct anti-inflammatory and antifibrotic effect operates through proteolytic cleavage. The N-terminal tetrapeptide AcSDKP — N-acetyl-Ser-Asp-Lys-Pro, also called Goralatide — is released from Tβ4 by meprin and prolyl oligopeptidase and carries its own antifibrotic and pro-angiogenic activity. A 2019 review in the Canadian Journal of Physiology and Pharmacology catalogued the Tβ4–AcSDKP pathway across arteries, heart, lungs, and kidneys as the dominant mechanistic frame for Tβ4's cardiovascular and renal effects [19]. Purinergic signaling adds another layer in epithelial repair contexts. Yang and colleagues found that Tβ4 promoted human corneal epithelial cell migration through increased extracellular ATP release, P2X7 receptor-mediated calcium influx, and ERK1/2 activation. P2X7 antagonists blocked the migration effect [5]. ## Tissue repair: cornea, dermis, brain, heart The seminal preclinical work on Tβ4 in corneal repair is Sosne and colleagues' 2002 alkali-burn mouse study, in which topical Tβ4 at 5 μg in 5 μL PBS, twice daily, accelerated corneal re-epithelialization at all observed time points and reduced IL-1β, KC, and MIP-2 inflammatory chemokine mRNA [6]. The study underwrites the entire RGN-259 ophthalmic clinical program. A 2024 paper from the same laboratory extended the work to engineered tandem-repeat constructs containing two LKKTET actin-binding motifs, which accelerated corneal closure and restored a thicker continuous epithelial architecture in rat alkali-injury models — evidence that short LKKTET-containing constructs preserve the parent peptide's corneal activity [16]. In the central nervous system, Xiong and colleagues administered Tβ4 intraperitoneally at 6 mg/kg or 30 mg/kg starting six hours after controlled cortical-impact traumatic brain injury in adult male Wistar rats. The intervention increased dentate gyrus neurogenesis 4.5-fold and 5.6-fold respectively over baseline and improved sensorimotor and spatial-learning outcomes [7]. Morris and colleagues administered Tβ4 intravenously at 3.75 mg/kg 24 hours after embolic middle-cerebral-artery occlusion in rats, improving adhesive-removal and modified Neurological Severity Score from day 14 to day 56 [8]. In the heart, Smart and colleagues found that Tβ4 mobilized adult epicardial progenitor cells in mice, restored their multipotent capacity, and drove neovascularization after coronary ligation [9]. Bock-Marquette and colleagues identified the PINCH–ILK–Akt complex as the cardiomyocyte survival mechanism: in coronary-ligation MI mice, Tβ4 reduced scar tissue and improved fractional shortening at four weeks [10]. ## The negative result and the context-dependence Not every preclinical model has replicated. Wei and colleagues administered Tβ4 systemically (150 μg/kg IV bolus plus maintenance) in a closed-chest porcine 90-minute ischemia / 24-hour reperfusion model, before and after ischemia, and found no reduction in infarct size by TTC or MRI at 24 hours [11]. The pig result is the clearest published counterpoint to the rodent cardiac data and the most-cited example of the rodent-to-large-mammal translation gap that shapes the present clinical-development landscape. The context-dependence runs in another direction in the liver. Lee and colleagues, working with a hepatic-stellate-cell conditional knockout in a CCl4 mouse fibrosis model, found that loss of Tβ4 reduced αSMA-positive activated stellate cells and ameliorated fibrotic scarring — Tβ4 is pro-fibrotic in that cell type, mediated through Hedgehog signaling, in apparent contrast to its broadly antifibrotic action via AcSDKP elsewhere [18]. Indiscriminate systemic dosing is not biologically neutral. ## Human clinical evidence Two published Phase I trials have established human safety for intravenous recombinant Tβ4. Ruff and colleagues administered single doses of 42, 140, 420, and 1,260 mg intravenously, then a multiple-dose extension, to 40 healthy adult volunteers in a randomized, double-blind, placebo-controlled US trial. No dose-limiting toxicities and no serious adverse events were reported; adverse events were mild to moderate only [12]. Wang and colleagues' Chinese first-in-human trial of recombinant Tβ4 (NL005) in 84 healthy volunteers — single doses 0.05–25 μg/kg IV, multiple-dose 0.5–5 μg/kg/day × 10 — reported dose-proportional pharmacokinetics, no SAEs, and favorable immunogenicity [23]. The most-developed efficacy program is ophthalmic. The Phase III neurotrophic-keratopathy trial NCT02600429 in 18 patients found complete corneal healing at day 29 in 60% of 0.1% RGN-259-treated subjects vs 12.5% of placebo (p=0.066), with statistically significant healing at day 43 (p=0.036) and a sustained effect after washout [14]. Subsequent Phase III ophthalmic trials missed their primary endpoints: ARISE-3 in dry eye and SEER-3 in European neurotrophic keratitis. The Phase IIb cardiac trial NCT05984134 enrolled 90 acute-MI patients post-PCI to receive recombinant Tβ4 0.5 μg/kg or 1.0 μg/kg or placebo IV within 12 hours, then on days 2–7; cardiac MRI infarct size and microvascular obstruction at day 5 and day 90 were the primary endpoints. Primary completion was May 2023; results have not yet been published [13]. The synthetic seven-amino-acid TB-500 fragment has never been evaluated in a registered human clinical trial. The detection record exists — Esposito and colleagues validated a liquid chromatography–mass spectrometry method for TB-500 in equine urine and plasma after intravenous administration, the method now in routine use by horse-racing authorities [15] — but a detection method is not a pharmacokinetic or efficacy study. ## The 2024–2025 direction of travel Recent work has moved away from free-peptide systemic dosing and toward combination biomaterial delivery. Yu and colleagues, in 2025, formulated an adipose-stem-cell exosome-loaded hemostatic and antibacterial HAMA/PLMA dual-photopolymerizable hydrogel overexpressing Tβ4. In streptozotocin-induced type-1 diabetic mice, the hydrogel accelerated full-thickness wound closure, increased CD31-positive neovascularization, and shifted macrophage polarization through PI3K/AKT/mTOR/HIF-1α activation [17]. The engineered-tandem-peptide and Tβ4-selenium combination work in 2024–2025 reinforces the direction: the peptide is increasingly studied as an active component of a delivery construct rather than as a standalone therapeutic [16]. A Frontiers in Endocrinology comprehensive review in 2021 catalogued Tβ4's roles across cardiovascular, neural, ocular, and hepatic systems and remains the standard reference for the clinical-translation status of the full-length molecule [24]. --- An independent editorial survey of the published regulatory and research record — not a clinic, not a vendor, not legal counsel. --- # 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. --- # TB-500 Legal FAQ — Customs, controls, and the questions readers arrive with > Plain answers to the questions readers actually ask about TB-500's legal status: FDA Category 2, WADA, USADA, NCAA, customs, controlled substance status, research-only labeling, and the difference between TB-500 and Thymosin Beta-4. What the regulatory record says, in plainer language than the regulators use. ## Is TB-500 legal in the United States? TB-500 is not approved by the FDA for any human indication, and the FDA has not authorized any human medical use of the molecule. It is also not currently scheduled as a controlled substance under the federal Controlled Substances Act or under the controlled-substance acts of California, Texas, New York, or Florida. Those two facts together produce the narrow legal posture under which TB-500 is sold in the United States: as a research chemical for in vitro use only, outside the FDA's drug-marketing jurisdiction. The FDA placed TB-500 on Category 2 of the interim 503A bulks list in 2023, formally finding that the substance presents 'significant safety risks' and prohibiting licensed compounding pharmacies from using it [20]. The agency has issued warning letters to US suppliers marketing TB-500 for human use at intervals between 2017 and 2023. ## Is TB-500 a controlled substance under state or federal law? No. As of the current writing, TB-500 is not listed as a controlled substance under the federal Controlled Substances Act and is not scheduled under the controlled-substance acts of the four largest US states by population. Controlled-substance scheduling and FDA approval status are separate regulatory tracks: a substance can be unapproved by the FDA without being scheduled by the Drug Enforcement Administration. The absence of scheduling does not constitute regulatory endorsement. The FDA's Category 2 placement on the 503A bulks list [20] and the WADA Prohibited List status [21] both apply independent of any DEA scheduling decision. ## Why did the FDA place TB-500 on the Category 2 bulks list? Section 503A of the Federal Food, Drug, and Cosmetic Act governs traditional patient-specific pharmacy compounding. The provision permits compounders to use bulk drug substances only when the substances meet specific criteria. The FDA maintains a tiered interim list of nominated substances: Category 1 substances are under evaluation and may be used while review proceeds; Category 2 substances have been reviewed and found to present significant safety risks. In 2023 the FDA placed TB-500, alongside BPC-157 and several other research peptides, in Category 2 [20]. The classification followed a multi-year FDA review of bulk peptides nominated for compounding and reflected concerns about purity, identity, characterization, and the absence of approved human use. Licensed compounding pharmacies that prepare TB-500 are operating outside the 503A framework. ## Is TB-500 banned by WADA, USADA, the IOC, or the NCAA? Yes — by every WADA-aligned anti-doping authority, in every context the World Anti-Doping Code reaches. The WADA 2025 Prohibited List explicitly names 'TB-500' and 'thymosin-β4' under section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics), prohibited at all times — in competition and out of competition [21]. The S0 catch-all (Non-Approved Substances) also applies, because the molecule has no marketing authorization in any jurisdiction. USADA, the IOC, the IPC, the World Athletics Anti-Doping Rules, FIFA, and the national anti-doping organizations that have adopted the Code all enforce the same list. The NCAA and most US professional sports leagues maintain banned-substance lists that incorporate WADA-listed peptide hormones and growth factors, although the exact scope and sanctions vary by league. Military and first-responder drug-testing programs that adopt WADA-aligned panels — including programs run by US Special Operations Command — likewise screen for the substance. ## What sanction does an athlete face for using TB-500? Under the World Anti-Doping Code, a first offense involving a non-specified substance such as TB-500 carries a mandatory four-year period of ineligibility unless the athlete establishes no significant fault or negligence. Possession is sufficient grounds for sanction — an in-competition positive test is not required. The USADA case against weightlifter Michael Nackoul resulted in a four-year ineligibility for possession of prohibited growth factors including Thymosin Beta-4, and the case was published as deterrent precedent [22]. Sanctions vary by sport and by tribunal: prompt admission, substantial assistance, or contaminated-supplement defenses can reduce the period in specific cases, but the published TB-500 sanction record reflects multi-year ineligibility periods as the typical outcome. ## Why can compounding pharmacies no longer make TB-500? Compounding pharmacies in the United States operate under two statutory frameworks. Section 503A of the FD&C Act covers traditional patient-specific compounding; Section 503B covers outsourcing facilities that produce larger batches. Both pathways require that any bulk drug substance used in compounding meet specific eligibility criteria. The FDA's interim 503A bulks list is the mechanism by which the agency communicates which nominated substances may be used while review is in progress. Substances placed on Category 2 of that list have been formally reviewed and found to present significant safety risks; they are not eligible for compounding under either 503A or 503B [20]. TB-500 was placed on Category 2 in 2023. Licensed compounding pharmacies that continue to prepare TB-500 after that date are operating outside the FDA's compounding framework and have been the subject of agency enforcement letters. ## What does mean on a TB-500 label? The phrase is a legal-marketing convention, not a quality assurance. By labeling a substance for non-human, in vitro research use only, a supplier remains outside the FDA's jurisdiction over drug marketing — the agency regulates substances marketed for use in or on the human body. The label does not assert that the substance is intended for human use; it explicitly disclaims that intention. The phrase also does not certify that the substance was manufactured under Good Manufacturing Practice, that lot-release testing was performed, that endotoxin or sterility specifications were met, or that the substance is what the label says it is. The Category 2 placement on the 503A bulks list [20] and the published controversies about purity, identity, and adulteration in research-chemical channels are independent of how the label reads. ## How is TB-500 detected in doping-control samples? The validated detection method most-cited in racing and human anti-doping work is liquid chromatography–mass spectrometry. Esposito and colleagues published a validated LC-MS method for TB-500 in equine urine and plasma after intravenous administration in 2012, and the method is in routine use by horse-racing laboratories [15]. Human anti-doping laboratories accredited under the WADA International Standard for Laboratories operate equivalent peptide-detection panels under the agency's technical document for biomarker and peptide hormone analysis. The detection window after a single dose depends on dose magnitude, route of administration, individual pharmacokinetics, and the analytical sensitivity of the laboratory, and the published window has not been comprehensively characterized in humans. ## Is TB-500 the same molecule as Thymosin Beta-4? No. TB-500 is a synthetic seven-amino-acid peptide with the sequence Ac-LKKTETQ-OH, corresponding to residues 17–23 of human Thymosin Beta-4 (Tβ4), the 43-amino-acid intracellular peptide encoded by the X-linked TMSB4X gene. The fragment carries the conserved LKKTET central motif that mediates G-actin binding in the parent peptide. The fragment lacks the C-terminal α-helix that crystallographic work has identified as the principal structural determinant of high-affinity actin sequestration in the parent [22]. Vendor literature treats the two molecules as interchangeable, but every registered human clinical trial of 'thymosin beta-4' has used the full 43-amino-acid recombinant protein. The synthetic seven-amino-acid TB-500 fragment has never been evaluated in a registered human clinical trial. The science transfer from full-length Tβ4 to the fragment is plausible for some endpoints — preserved corneal-healing activity has been demonstrated for short LKKTET-containing constructs [16] — but is not established. ## What does the published research actually say about TB-500? Published research on TB-500 itself — the synthetic seven-amino-acid fragment — is narrow. Esposito and colleagues established a validated LC-MS detection method in equine urine and plasma [15]. The class of LKKTET-containing constructs has been characterized in rodent corneal-injury models [16]. The published clinical and preclinical efficacy literature commonly cited in connection with 'TB-500' is in fact the literature on full-length recombinant Tβ4: G-actin sequestration through the LKKTET motif [22]; HIF-1α stabilization and VEGF induction [1]; Notch-dependent angiogenesis [3]; NF-κB inhibition [4]; PINCH–ILK–Akt cardiomyocyte survival [10]; topical corneal repair [6]; rat TBI [7]; rat stroke [8]; adult epicardial progenitor mobilization [9]; the AcSDKP antifibrotic axis [19]; and the negative porcine cardiac IR-injury result [11]. The clinical-development program for the parent peptide remains active in ophthalmic and cardiac indications [13, 14] but has not produced a regulatory-grade efficacy result. ## Does Customs and Border Protection intercept TB-500 shipments? US Customs and Border Protection intercepts shipments of unapproved drug substances that arrive in the United States from international suppliers. The agency's enforcement priorities include unapproved peptide research chemicals shipped to consumer addresses. Published enforcement data do not break out interception rates by peptide identity, and the interception pattern is therefore best documented through agency enforcement-action notices and importer warning letters rather than aggregate statistics. Shipments marked as 'research chemical for in vitro use only' from overseas suppliers may be detained, refused, or destroyed at the discretion of CBP and the FDA, and personal-use exemptions that apply to certain prescription drugs do not extend to substances on the FDA's 503A Category 2 list [20]. ## Is TB-500 banned for racehorses? Yes. Horse-racing authorities worldwide treat TB-500 as a prohibited substance under the International Federation of Horseracing Authorities International Agreement on Breeding, Racing and Wagering, Article 6 (Clause 10). The validated LC-MS detection methods for TB-500 in equine urine and plasma published by Esposito and colleagues [15] are in routine use by racing laboratories. Equine sanctions have been issued. The IFHA prohibition pre-dates and operates independently of the WADA Prohibited List, although the underlying rationale — that the substance is unapproved for any therapeutic use and is sold through research-chemical channels — is similar. ## Is TB-500 unsafe? The two published Phase I trials of full-length recombinant Tβ4 — Ruff 2010 in 40 US healthy volunteers up to 1,260 mg IV [12] and Wang 2021 in 84 Chinese healthy volunteers up to 25 μg/kg IV [23] — both reported acceptable safety with no dose-limiting toxicities and no serious adverse events. That body of data established the regulatory safety baseline for the parent peptide in carefully controlled clinical settings. It does not extend to the synthetic seven-amino-acid TB-500 fragment, which has not been studied in a registered human clinical trial, and it does not characterize the safety of substances obtained through unregulated research-chemical channels where Good Manufacturing Practice, lot-release testing, endotoxin control, and sterility assurance are not provided. The FDA's Category 2 placement on the 503A bulks list reflects the agency's finding that the substance presents 'significant safety risks' in compounding contexts [20]. Theoretical concerns about effects on occult or pre-existing tumors have been raised in the literature, although no clinical safety signal of tumor promotion has been reported in the published human Phase I/II data to date. ## What is the difference between TB-500 and BPC-157 legally? The two research peptides occupy a similar regulatory posture. Both were placed on FDA Category 2 of the interim 503A bulks list in the 2023 review [20]. Both are listed on the WADA Prohibited List 2025 under section S2 and the S0 catch-all [21]. Neither is approved for any human indication by any major regulatory authority. Neither is currently scheduled as a controlled substance under federal or major-state law. The most-cited difference lies upstream of the regulatory record: BPC-157 has a substantial body of rodent musculoskeletal-repair literature behind the synthetic peptide itself, while the published efficacy literature for 'TB-500' is in fact literature on the full-length 43-amino-acid parent protein, with the synthetic seven-amino-acid fragment never having entered a registered human clinical trial. --- An independent editorial survey of the published regulatory and research record — not a clinic, not a vendor, not legal counsel. --- # TB-500 References — Customs manifest of the cited research and regulatory record > Full citation list for the TB-500 Legal research record: 24 entries spanning Thymosin Beta-4 mechanism, preclinical studies, clinical trials, and regulatory actions, with DOIs and primary-source URLs. The full reference list — twenty-four entries from in vitro biochemistry to regulatory enforcement. ## About this manifest Every claim made on this site is sourced to one or more of the entries below. The manifest spans the foundational biochemistry of Thymosin Beta-4 — actin sequestration, HIF-1α and VEGF, NF-κB inhibition, PINCH–ILK–Akt cardiac signaling, AcSDKP antifibrotic activity — through the preclinical record in mouse, rat, pig, and equine models, into the Phase I and Phase II/III clinical-development programs for the full-length recombinant peptide. It includes the regulatory enforcement record (FDA 503A Category 2 placement; WADA 2025 Prohibited List entries; USADA athlete sanction) and the validated equine doping-control detection method. Where multiple citations bear on a single topic, the most-cited or most-recent primary source is given preference. Where a regulatory finding is the citation, the original agency document is linked directly. DOIs are provided where available; PubMed, PMC, and ClinicalTrials.gov URLs are provided for primary research; agency URLs are provided for regulatory entries. The table is sortable, searchable, and filterable by year, species, journal, and authority. The customs-manifest treatment is intentional: a single document of record. ## The citation list The full reference list appears below, organized as a single sortable manifest. Each entry includes the citation, DOI or identifier, and a direct URL to the primary source. ## References [1] Jo JO, Kim SR, Bae MK, Kang YJ, Ock MS, Kleinman HK, Cha HJ. Thymosin β4 induces the expression of vascular endothelial growth factor (VEGF) in a hypoxia-inducible factor (HIF)-1α-dependent manner. Biochim Biophys Acta Mol Cell Res. 2010. https://pubmed.ncbi.nlm.nih.gov/20691219/ [2] Ryu YK, Kang JH, Moon EY. The Actin-Sequestering Protein Thymosin Beta-4 Is a Novel Target of Hypoxia-Inducible Nitric Oxide and HIF-1α Regulation. PLoS One. 2014. https://pmc.ncbi.nlm.nih.gov/articles/PMC4182666/ [3] Kim S, Kwon J. Thymosin beta4 induces angiogenesis through Notch signalling in endothelial cells. Cell Signal. 2013. https://pubmed.ncbi.nlm.nih.gov/23749167/ [4] Qiu P, Wheater MK, Qiu Y, Sosne G. Thymosin β4 inhibits TNF-α-induced NF-κB activation, IL-8 expression, and the sensitizing effects of its partners PINCH-1 and ILK. FASEB J. 2011. https://pmc.ncbi.nlm.nih.gov/articles/PMC3101037/ [5] Yang HM, Kang SW, Sung J, Kim K, Kleinman HK. Purinergic Signaling Involvement in Thymosin β4-mediated Corneal Epithelial Cell Migration. Curr Eye Res. 2020. https://pubmed.ncbi.nlm.nih.gov/32223337/ [6] Sosne G, Szliter EA, Barrett R, Kernacki KA, Kleinman H, Hazlett LD. Thymosin beta 4 promotes corneal wound healing and decreases inflammation in vivo following alkali injury. Exp Eye Res. 2002. https://pubmed.ncbi.nlm.nih.gov/11950239/ [7] Xiong Y, Zhang Y, Mahmood A, Meng Y, Zhang ZG, Morris DC, Chopp M. Neuroprotective and neurorestorative effects of thymosin beta4 treatment initiated 6 hours post injury following traumatic brain injury in rats. J Neurosurg. 2012. https://pmc.ncbi.nlm.nih.gov/articles/PMC3392183/ [8] Morris DC, Chopp M, Zhang L, Lu M, Zhang ZG. Thymosin β4 improves functional neurological outcome in a rat model of embolic stroke. Neuroscience. 2010. https://pmc.ncbi.nlm.nih.gov/articles/PMC2907184/ [9] Smart N, Risebro CA, Melville AAD, Moses K, Schwartz RJ, Chien KR, Riley PR. Thymosin β4 induces adult epicardial progenitor mobilization and neovascularization. Nature. 2007. https://pubmed.ncbi.nlm.nih.gov/17108969/ [10] Bock-Marquette I, Saxena A, White MD, DiMaio JM, Srivastava D. Thymosin β4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature. 2004. https://pubmed.ncbi.nlm.nih.gov/15565145/ [11] Wei C, Kumar S, Kim IK, Gupta S. Systemic dosing of thymosin beta 4 before and after ischemia does not attenuate global myocardial ischemia-reperfusion injury in pigs. Front Pharmacol. 2016. https://pmc.ncbi.nlm.nih.gov/articles/PMC4853610/ [12] Ruff D, Crockford D, Girardi G, Zhang Y. A randomized, placebo-controlled, single and multiple dose study of intravenous thymosin beta4 in healthy volunteers. Ann N Y Acad Sci. 2010. https://pubmed.ncbi.nlm.nih.gov/20536472/ [13] Beijing Northland Biotech. Efficacy and Safety Study of Thymosin Beta 4 in Patients With Acute Myocardial Infarction. ClinicalTrials.gov NCT05984134. 2023. https://clinicaltrials.gov/study/NCT05984134 [14] Sosne G, Kleinman HK, Springs C, Gross RH, Sung J, Kang S. 0.1% RGN-259 (Thymosin β4) Ophthalmic Solution Promotes Healing and Improves Comfort in Neurotrophic Keratopathy Patients in a Randomized, Placebo-Controlled, Double-Masked Phase III Clinical Trial. Int J Mol Sci. 2022. https://pmc.ncbi.nlm.nih.gov/articles/PMC9820614/ [15] Esposito S, Deventer K, Goeyens L, Van Eenoo P. Doping control analysis of TB-500, a synthetic version of an active region of thymosin β4, in equine urine and plasma by liquid chromatography–mass spectrometry. Anal Chim Acta. 2012. https://www.sciencedirect.com/science/article/abs/pii/S0021967312014550 [16] Sosne G, Kleinman HK, et al. Engineered Tandem Thymosin Peptide Promotes Corneal Wound Healing. Int J Mol Sci. 2024. https://pmc.ncbi.nlm.nih.gov/articles/PMC12636994/ [17] Yu H, Wang B, Li Z, et al. Tβ4-exosome-loaded hemostatic and antibacterial hydrogel to improve vascular regeneration and modulate macrophage polarization for diabetic wound treatment. Mater Today Bio. 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC11893380/ [18] Lee S, Lee H, Bae S, Kim E, Oh GT, Park H, Yeon JE, Byun KS, Kim K. Targeted deletion of thymosin beta 4 in hepatic stellate cells ameliorates liver fibrosis in a transgenic mouse model. Cells. 2023. https://pmc.ncbi.nlm.nih.gov/articles/PMC10297343/ [19] Conte E, Genovese T, Gili E, Esposito E, Iemmolo M, Fruciano M, Fagone E, Pistorio MP, Crimi N, Cuzzocrea S, Vancheri C. Tβ4–Ac-SDKP pathway: Any relevance for the cardiovascular system? Can J Physiol Pharmacol. 2019. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6824425/ [20] U.S. Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. 21 CFR Part 216. 2023. https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks [21] World Anti-Doping Agency. The World Anti-Doping Code International Standard — Prohibited List 2025. WADA, 2024. https://www.wada-ama.org/sites/default/files/2024-09/2025list_en_final_clean_12_september_2024.pdf [22] Irobi E, Aguda AH, Larsson M, Guerin C, Yin HL, Burtnick LD, Blanchoin L, Robinson RC. Structural basis of actin sequestration by thymosin-β4: implications for WH2 proteins. EMBO J. 2004. https://pmc.ncbi.nlm.nih.gov/articles/PMC517612/ [23] Wang X, Liu L, Qi L, Lei C, Li P, Wang Y, Liu C, Bai H, Han C, Sun Y, Liu J. A first-in-human, randomized, double-blind, single- and multiple-dose, phase I study of recombinant human thymosin β4 in healthy Chinese volunteers. J Cell Mol Med. 2021. https://pmc.ncbi.nlm.nih.gov/articles/PMC8419156/ [24] Xing Y, Ye Y, Zuo H, Li Y. Progress on the function and application of thymosin β4. Front Endocrinol. 2021. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2021.767785/full [25] U.S. Anti-Doping Agency. Michael Nackoul Accepts Doping Sanction. USADA Sanction Notice, 2018. https://www.usada.org/sanction/michael-nackoul-accepts-doping-sanction/ [26] Mendias CL, Awan TM. Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance. Sports Med. 2026. https://pubmed.ncbi.nlm.nih.gov/41966639/ [27] Cha HJ, Jeong MJ, Kleinman HK. Role of thymosin beta4 in tumor metastasis and angiogenesis. J Natl Cancer Inst. 2003. https://pubmed.ncbi.nlm.nih.gov/14625258/ [28] Wang WS, et al. Thymosin beta 4 is overexpressed in human pancreatic cancer cells and stimulates proinflammatory cytokine secretion and JNK activation. Cancer Biol Ther. 2008. https://pubmed.ncbi.nlm.nih.gov/18094619/ [29] Cooper TM, et al. Doping control analysis of TB-500, a synthetic version of an active region of thymosin β4, in equine urine and plasma by liquid chromatography-mass spectrometry. J Chromatogr A. 2012. https://pubmed.ncbi.nlm.nih.gov/23084823/ [30] Spurney CF, et al. Evaluation of skeletal and cardiac muscle function after chronic administration of thymosin beta-4 in the dystrophin deficient mouse. PLoS One. 2010. https://pubmed.ncbi.nlm.nih.gov/20126456/ [31] Goldstein AL, Hannappel E, Sosne G, Kleinman HK. Thymosin β4: a multi-functional regenerative peptide. Basic properties and clinical applications. Expert Opin Biol Ther. 2012. https://pubmed.ncbi.nlm.nih.gov/22074294/ [32] Thomas A, et al. TB500/TB1000 and SGF1000: A scientific approach for a better understanding of doping-relevant peptide preparations. Drug Test Anal. 2023. https://pubmed.ncbi.nlm.nih.gov/36482504/ --- An independent editorial survey of the published regulatory and research record — not a clinic, not a vendor, not legal counsel. --- # About TB-500 Legal — Independent editorial publisher of regulatory and research summaries > TB-500 Legal is an independent editorial project that publishes summaries of the peer-reviewed research and regulatory record on Thymosin Beta-4 and its synthetic fragment Ac-LKKTETQ-OH. Not a clinic, not a vendor. Who publishes this site, what it does, and what it deliberately does not do. ## What this site is TB-500 Legal is an independent editorial project that publishes summaries of the peer-reviewed research literature and the regulatory record on Thymosin Beta-4 and its synthetic seven-amino-acid fragment Ac-LKKTETQ-OH. We are not a clinic. We do not employ clinicians, and we do not provide medical advice. We do not manufacture, sell, or distribute any product. Our work is editorial commentary on publicly available science and publicly published regulatory documents. The site exists because the regulatory record on TB-500 is dispersed across multiple jurisdictions and authorities — the FDA interim 503A bulks list, the World Anti-Doping Agency annual Prohibited List, the International Federation of Horseracing Authorities International Agreement, the US Anti-Doping Agency sanction archive, agency warning-letter notices — and is rarely read together. The editorial conceit of the site is to read those documents the way a customs officer reads a passport: jurisdiction by jurisdiction, stamp by stamp, with the regulatory geography in clear view. The domain name carries the word 'legal' as editorial framing — the publisher's stance toward the literature, focused on jurisdictional questions about a research peptide. It is not a claim that the site provides legal counsel, regulatory consulting, or any form of professional service. The site offers no consultation, no prescription, no representation, and no advisory relationship of any kind. ## Editorial standards Every quantitative claim on the site is cited to a specific peer-reviewed study, a registered clinical trial, or a regulatory document of record. Where the underlying record is ambiguous — for example, where vendor literature treats the synthetic TB-500 fragment as interchangeable with full-length Tβ4 while the structural biology distinguishes them — the ambiguity is preserved in the editorial copy rather than resolved by inference. Where studies have produced negative results, including the porcine cardiac IR-injury work that did not replicate the rodent cardiac findings, those negative results are reported. The site does not promote any vendor, supplier, compounding pharmacy, telehealth platform, or product. It does not link to commercial sources of TB-500 or any related research chemical. It does not solicit consultations, prescriptions, or purchases. The outbound links on the site are limited to PubMed, PubMed Central, the National Institutes of Health, ClinicalTrials.gov, peer-reviewed journal websites, the FDA, WADA, USADA, and equivalent regulatory and scientific institutions. The editorial contract of this site is a familiar one in scientific journalism: document the published record, report the regulatory findings, preserve the negative results and the contested claims alongside the favorable ones, and take no position on human use that the underlying scientific and regulatory record does not already take. An independent editorial survey of the published record — not a clinic, not a vendor, not legal counsel. ## What we deliberately do not do We do not name a 'medical team,' a 'clinical advisor,' a 'reviewing physician,' or any individual person — fictional or real — as the author or editor of this site. The site is published anonymously as an editorial project, in line with the publisher's stated role as a commentator on the regulatory and research record rather than a participant in clinical care. We do not provide medical advice, treatment recommendations, dosing guidance for human use, prescriptions, consultations, or any service that requires a licensed health-care professional. We do not refer readers to specific clinics, vendors, suppliers, or compounding pharmacies. We do not assess the legality of any specific transaction, possession, importation, or use of TB-500 in any specific jurisdiction or circumstance — those determinations require a licensed attorney with knowledge of the reader's situation. The regulatory findings documented on the site are the published findings of the relevant agencies, current as of the publication date noted on each page. Regulatory status can and does change. Readers seeking the current authoritative status of any substance in any jurisdiction should consult the relevant agency directly. --- An independent editorial survey of the published regulatory and research record — not a clinic, not a vendor, not legal counsel. --- # Contact TB-500 Legal — Editorial correspondence channels > Editorial correspondence for TB-500 Legal: corrections, source suggestions, regulatory updates, and citation queries. The site does not provide medical, legal, or commercial services. What we accept correspondence on, and what we deliberately do not. ## Editorial correspondence We accept editorial correspondence on the following topics: factual corrections to the published material; suggestions of additional peer-reviewed sources or registered clinical trials we should reference; updates to the regulatory record we may have missed (new FDA actions, revisions to the WADA Prohibited List, USADA or IFHA sanction notices); and citation queries — for example, requests for the full bibliographic record behind a numbered reference. Correspondence on any of these topics is welcome and will be reviewed. We do not provide medical advice, treatment recommendations, dosing guidance for human use, or any service that requires a licensed health-care professional. We do not provide legal counsel on the importation, possession, or use of TB-500 in any jurisdiction. We do not provide product reviews, vendor recommendations, supplier introductions, or commercial referrals. Inquiries on those topics will not be answered. The site is a one-way publication: we publish the editorial record, and we respond to corrections and additions to that record. We do not offer consultations of any kind. ## How to reach us A standard contact form is provided below for written correspondence. Inquiries should be brief and should identify the page and specific passage being addressed where applicable. We aim to respond to substantive editorial correspondence within ten business days; volume permitting, all messages are read. This form does not constitute a request for medical, legal, or commercial services. Submission of the form does not establish any advisory, professional, or commercial relationship with the publisher. The publisher reserves the right not to respond to messages outside the editorial scope described above. --- An independent editorial survey of the published regulatory and research record — not a clinic, not a vendor, not legal counsel.