# tb500prescribed.com # TB-500 Prescribed — Is TB-500 a prescription drug? A wall-label reading of the evidence > TB-500 is a synthetic 7-amino-acid fragment of Thymosin Beta-4. It is not FDA-approved, not eligible for compounding, and not prescribable. A curated reading of the actual research record. TB-500 is a synthetic seven-amino-acid fragment of Thymosin Beta-4. The forty-three-amino-acid parent peptide has reached Phase III in ophthalmology and a halted Phase II in cardiology. The fragment has never been in a registered human trial — and as of September 29, 2023, it cannot be compounded in the United States. ## The wall label, briefly TB-500 is a seven-amino-acid synthetic peptide — the sequence Ac-LKKTETQ, residues 17 to 23 of the parent protein Thymosin Beta-4. Most of the encouraging science in this field used the full 43-residue protein, not this fragment. No controlled human trial has ever run on the fragment itself. As of September 2023, a U.S. compounding pharmacy cannot legally make TB-500 for a patient; the FDA placed it in Category 2 of the interim 503A Bulks List, meaning significant safety concerns. WADA classifies it as prohibited for competitive athletes. The name on this domain uses *prescribed* the way a museum uses an empty plinth — to mark a category that does not yet exist, not to claim the object is there. [Read what the research record actually says](/research) and [what people using TB-500 report anecdotally](/effects). ## What this site is, and what it isn't TB-500 Prescribed is a reading room. It is not a clinic, not a pharmacy, not a vendor, not a telehealth service. It does not sell TB-500 and it does not write prescriptions. The whole site exists to do one thing carefully: explain what the published Thymosin Beta-4 record actually says about a compound whose marketed name carries the word *prescribed* as if a prescription were available. A prescription is not available. That is the wall label. The sections that follow walk through the chemistry, the animal work, the human trials of the parent peptide, the FDA's September 2023 compounding decision, and the World Anti-Doping Agency's continuing position [1][26]. Where the published evidence is strong, it is described in detail. Where it is thin, that thinness is named. Where vendor literature has filled the gap with confident dosing tables, those tables are noted as vendor literature and not treated as clinical recommendations [22]. ## Fragment, not full peptide The molecule sold and discussed under the name *TB-500* is N-acetyl-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH, a synthetic peptide of seven amino acids carrying CAS 885340-08-9 and a molecular weight of roughly 889 Da. It corresponds to residues 17 through 23 of native human Thymosin Beta-4 (Tβ4), a 43-amino-acid intracellular peptide encoded by the *TMSB4X* gene and expressed in essentially every nucleated cell type [1][25]. Those seven residues contain the central LKKTET motif, the actin-binding region that does most of Tβ4's signature work — binding monomeric G-actin in a one-to-one complex and blocking its addition to growing filaments [1][2]. The fragment retains the binding sequence; it does not retain most of the parent peptide's downstream interaction surfaces. This distinction matters because nearly every published animal study of *Thymosin Beta-4* — the corneal-healing work, the cardiac-repair work, the stroke work, the hair-follicle work — was performed with the full 43-residue molecule [3][4][6][7][12][24]. Every registered human clinical trial likewise used full-length recombinant Tβ4, not the fragment [13][14][15][16][17]. The FDA cited that identity gap — fragment marketed, parent peptide studied — as one of its safety concerns when it restricted TB-500 from compounding [26]. ## What the research actually shows Read as a body of work, the Thymosin Beta-4 literature is consistent on a few things and unfinished on most. It is consistent on mechanism. Tβ4 binds monomeric actin one-to-one through its LKKTET core [1][2]. It induces angiogenesis, including VEGF expression in endothelial cells [25]. It activates the PINCH-Tβ4-ILK signaling complex upstream of Akt, which promotes cardiomyocyte survival and migration after ischemic injury [6][7]. It directly inhibits NF-κB transactivation, which dampens inflammation independent of its actin work [11]. It is consistent on small-animal wound healing. Topical Tβ4 accelerated re-epithelialization of full-thickness rat skin wounds by 42% at four days and 61% at seven days [3]. Topical Tβ4 accelerated corneal healing after alkali burn in mice [4]. Both observations have been replicated, including in diabetic and aged mouse models [5]. It is unfinished on humans. Phase I IV safety trials of full-length recombinant Tβ4 — one in the United States in 40 volunteers up to 1,260 mg [13], one in China in 84 volunteers up to 25 μg/kg [14] — established acceptable tolerability and no serious adverse events. The Phase III ARISE-3 trial of topical RGN-259 (a 0.1% Tβ4 ophthalmic solution) in roughly 700 dry-eye patients missed its prespecified co-primary endpoints, though it produced significant improvement in ocular grittiness and in a defined-subpopulation corneal-staining measure [15]. An earlier Phase III neurotrophic-keratopathy trial of the same product showed 60% complete corneal healing at day 29 in treated subjects versus 12.5% in placebo (p=0.066) and statistically significant healing at day 43 (p=0.036) [16]. The cardiac program, RGN-352, enrolled into Phase II with 450 mg or 1,200 mg IV regimens after acute myocardial infarction, was placed on FDA clinical hold in 2011 over contract-manufacturer cGMP issues, and has not reported efficacy [17]. ## Why nobody can write a prescription Prescriptions exist for approved drugs. They also exist, in the off-label sense, for unapproved indications of approved drugs. They do not exist for substances with no approved product anywhere in the regulatory record. No TB-500 product is FDA-approved. No full-length Tβ4 product is FDA-approved either. RGN-259 and RGN-352 remain investigational [15][16][17]. No marketing authorization has been granted by the EMA, MHRA, TGA, PMDA or any comparable agency. There is therefore no on-label prescription, and because off-label prescribing requires an approved product as the starting point, there is no off-label path either. Until September 2023, a parallel route remained open in the United States: a state-licensed compounding pharmacy operating under Section 503A could prepare TB-500 for a patient if the substance was on the FDA's 503A Bulks List. On September 29, 2023, the FDA placed *Thymosin Beta-4, Fragment (LKKTETQ)* — TB-500 by its chemical identity — in Category 2 of the Interim 503A Bulks List, the bin for substances the agency has determined raise significant safety concerns and that may not be used in compounding while under review [26]. The same placement effectively closed the Section 503B outsourcing-facility route. As of 2025, TB-500 remains in Category 2; it was not among the substances voted on at the October or December 2024 Pharmacy Compounding Advisory Committee meetings, which considered a different group of peptides [27]. This is the wall label. The site's name uses the word *prescribed* the way a museum places an empty plinth: as a position relative to the absent object, not a claim that the object is there. ## How to read the rest The /research page walks the published evidence in roughly chronological order, from the 1992 actin-sequestration biochemistry through the 2025 hydrogel-delivery work [1][20]. The /dosage page summarizes the doses and routes used in the published animal and human studies and is explicit that no clinical dosing protocol exists for the fragment [22]. The /faq page answers the questions readers actually arrive with, including the WADA and athlete-sanction question [26]. The /references page lists every citation with DOI and PubMed or PMC link. The whole site reads in one direction: from the research record outward to the regulatory record, then to the practical question of what *TB-500 prescribed* means in 2026. The answer is that it means almost nothing, because the noun phrase does not yet refer to anything the United States regulatory system has accepted. --- A curated wall-label reading of peer-reviewed science — not a clinic, not a vendor, not a prescription. --- # TB-500 reported effects and safety — what the community says and what the research cautions > TB-500 reported effects, real-world community signals, and safety cautions drawn from published research — anecdotal, not clinical evidence. Below are the effects people in research-use communities describe, labeled as anecdotal, alongside the safety concerns the published literature raises. These are two separate registers: personal reports are not clinical data. ## The short version TB-500 is a synthetic seven-amino-acid fragment of Thymosin Beta-4 (Tβ4), a protein the body makes and releases at injury sites to help coordinate repair. The fragment carries the actin-binding core of the parent protein. In animal models — mostly rodents — the full-length parent protein accelerated wound healing, supported heart muscle survival after a heart attack, aided nerve recovery after stroke, and activated hair follicle stem cells. Those findings are real, though they come from the 43-residue parent protein, not the seven-residue fragment sold as TB-500. People in athletic and research-use communities reach for TB-500 mostly for soft-tissue and joint recovery. They report feeling better from nagging tendon and ligament injuries and moving more freely. These are personal, uncontrolled accounts — not clinical data. There is no completed human trial of the fragment for any of these uses. The cautions are genuine: TB-500 is WADA-prohibited, banned from U.S. pharmacy compounding as of September 2023, and its safety in people is largely unstudied. The [research record](/research) lays out the evidence; this page covers what people anecdotally report and what the science honestly cautions. ## What people report The following signals come from peptide-use communities, athletic forums, and wellness-clinic blog write-ups. **These are anecdotal, not clinical evidence.** They are documented here because they are the reason most people arrive at this site; presenting them honestly — labeled, not amplified — is part of the editorial work. **Benefits reported:** - *Faster recovery from tendon, ligament and muscle injuries* (very commonly reported). The main reason people reach for TB-500. Users describe nagging soft-tissue injuries feeling better and returning to activity sooner. Timelines vary; no controlled human trial underpins these accounts. - *Less joint pain and stiffness, better range of motion* (frequently reported). Many users say joints feel looser and less achy after a few weeks, especially those with general wear-and-tear stiffness. No human trial underpins these reports. - *Improved overall flexibility and mobility* (frequently reported). Some people describe feeling more physically resilient during training around three to four weeks in — informal, self-tracked reports only. - *A sense of reduced inflammation or calmed soreness* (occasionally reported). A subset describe a general reduction in post-workout soreness. Vaguer than injury-recovery reports; no human trial confirms an anti-inflammatory benefit from the fragment. - *Better wound and skin healing* (occasionally reported). Some mention cuts or surgical sites healing more quickly — consistent with animal wound studies for the parent protein, though the community reports are anecdotal. - *Hair regrowth or thicker hair* (rarely reported). A minor and inconsistent signal in research-use communities. **Adverse effects reported:** - *Injection-site redness, swelling or aching* (very commonly reported). A small pink, sore or slightly swollen spot where injected, typically mild and gone within a day or two — typical of injected peptides generally. - *Temporary tiredness or lethargy* (frequently reported). Many users feel unusually sluggish for a day or two, especially after early doses, fading with continued use. - *Head rush, lightheadedness or headache* (occasionally reported). Brief and most common with larger early amounts; described as short-lived. - *Brief flu-like feeling* (occasionally reported). Mild and temporary; reported by a minority in the first day or two. - *Nausea, heightened awareness of an old injury, temporary mood changes* (rarely reported). Uncommon and vague; no clinical evidence ties any of these to the TB-500 fragment specifically. ## Safety & cautions The following cautions come from the published literature and the regulatory record. **Human safety is essentially unstudied.** There are no completed controlled human trials of the TB-500 heptapeptide for any indication. A 2026 Sports Medicine review concluded that unapproved peptides like TB-500 show promise in animal models but have scarce human safety data and carry potential for serious harm [28]. **Theoretical cancer concern.** The parent protein Tβ4 is overexpressed in several human cancers and has been linked to tumor spread and new blood-vessel formation that feeds tumors [29][30]. The same pro-migration and pro-angiogenic properties that may aid repair could in principle support tumor progression. This has not been measured for TB-500 in people. **WADA-prohibited.** TB-500 is banned under the World Anti-Doping Code. Detection methods for TB-500 and its metabolites are in routine use at accredited laboratories [31]. A positive test can end an athlete's eligibility. **Reported benefits may overstate the reality.** In dystrophin-deficient mice, long-term thymosin beta-4 increased regenerating muscle fibers but did NOT improve muscle strength, cardiac function, or fibrosis [32]. Visible regeneration did not translate into better function — a caution against assuming felt improvements mean structural repair. **TB-500 is a fragment, not the full protein.** Almost all efficacy research used the full 43-residue Tβ4. The FDA cited this gap — fragment marketed, parent studied — when restricting TB-500 from compounding [26][24]. **Research-grade quality is not guaranteed.** Identity, purity and sequence can vary between suppliers [33]. Unknown purity adds unpredictable risk. **Theoretical cautions.** Because TB-500 acts on cell migration, vascularization and platelet activity, precautionary concern extends to people with clotting disorders, those approaching surgery, and pregnant or breastfeeding individuals. None of these have been studied for the fragment in humans. --- A curated wall-label reading of peer-reviewed science — not a clinic, not a vendor, not a prescription. --- # TB-500 / Thymosin Beta-4 research record > A reading of the Thymosin Beta-4 literature from 1992 to 2025: actin sequestration, dermal and corneal healing, cardiac repair, Phase I-III human trials, and recent hydrogel work. What was studied, what replicated, what did not — and where the fragment-versus-parent distinction makes the literature mean less than it appears to. ## The short version of three decades of work The Thymosin Beta-4 literature runs from 1992 biochemistry through 2025 hydrogel-delivery papers. The clearest findings are in wound healing — rat and mouse models show real acceleration of re-epithelialization and collagen deposition. Cardiac repair work is more complicated: mouse models showed cardiomyocyte survival and epicardial progenitor mobilization, but a well-powered pig study found no reduction in infarct size. Two Phase I human safety trials of intravenous full-length Tβ4 reported no serious adverse events up to 1,260 mg. Phase III ophthalmic trials for corneal and dry-eye indications produced mixed results — one showed statistically significant healing at day 43, another missed its primary endpoint. The critical caveat behind every finding: almost every study used full-length 43-residue Tβ4, not the seven-residue TB-500 fragment. The FDA specifically cited that identity gap when it placed TB-500 in Category 2 in September 2023. The pages below walk through the evidence in roughly chronological order, naming that distinction at every turn. ## The biochemistry, 1992-2004 The starting point is biochemical. In 1992, Cassimeris and colleagues demonstrated that Tβ4 forms a one-to-one complex with monomeric G-actin in resting platelets and in rabbit skeletal muscle preparations, establishing it as the principal actin-sequestering peptide in the cell types where it is most abundant [1]. The 2004 crystallographic work of Irobi and colleagues defined how the binding actually works: the C-terminal α-helix of Tβ4 sterically blocks both barbed-end and pointed-end addition of the bound monomer to a growing filament [2]. Out of this came the WH2-domain framework for understanding actin-monomer regulation that still organizes the field. The LKKTET motif sits at the structural center of this binding. That centrality is what made the fragment commercially attractive: if the binding is what matters, perhaps the seven residues that mediate it are what matters. The trouble with this inference is that the parent peptide does more than sequester actin. It signals through PINCH and integrin-linked kinase to activate Akt [6]. It directly binds NF-κB RelA/p65 to suppress inflammatory cytokine transcription [11]. It is enzymatically cleaved at its N-terminus to release N-acetyl-Ser-Asp-Lys-Pro (AcSDKP, also called Goralatide), a separately bioactive antifibrotic and proangiogenic tetrapeptide. None of those activities is shared by the seven-residue fragment in any published study. ## Dermal and corneal wound healing The dermal-wound work begins with Malinda and colleagues in 1999. Topical or intraperitoneal Tβ4 at 5 μg per wound accelerated re-epithelialization of 8-mm full-thickness punch wounds in Sprague-Dawley rats by 42% at four days and 61% at seven days, with parallel increases in angiogenesis and collagen deposition [3]. Philp and colleagues extended this to impaired-healing models in 2003, showing that both full-length Tβ4 and a synthetic peptide containing the actin-binding domain accelerated dermal wound repair in db/db diabetic mice and in aged mice at doses from 0.1 to 5 μg per wound [5]. This is the closest the dermal literature comes to direct fragment-versus-parent comparison. The corneal work begins with Sosne and colleagues in 2002. Topical Tβ4 at 5 μg twice daily accelerated corneal re-epithelialization at all time points after alkali burn in mice and significantly reduced IL-1β, KC and MIP-2 inflammatory mRNA [4]. This single study underwrites essentially the entire RGN-259 clinical program. A 2024 paper by the same group showed that an engineered tandem repeat of the LKKTET actin-binding motif — the same class of construct TB-500 belongs to — accelerated corneal epithelial wound closure in rat models, suggesting that synthetic fragment constructs can preserve and amplify the corneal-healing activity originally demonstrated for the full peptide [19]. ## Cardiac repair: rodent yes, pig no The cardiac story is the most ambitious chapter in the Tβ4 record and the one most frustrated by translation. The founding paper is Bock-Marquette and colleagues in 2004. In a mouse coronary-ligation model of myocardial infarction, Tβ4 formed a functional complex with PINCH and ILK, activated Akt, increased early cardiomyocyte survival, reduced infarct scar, and improved fractional shortening at four weeks [6]. Smart and colleagues followed in 2007 by showing that Tβ4 at 150 μg intraperitoneally every three days mobilized adult epicardial progenitor cells in mice, re-expressed the embryonic WT1 and Tbx18 epicardial program, and produced new coronary vessels in the injured adult heart [7]. This was the conceptual high-water mark: an endogenous peptide that could reawaken a developmental program in adult cardiac tissue. The large-mammal record is more equivocal. In a 2008 porcine study, Hinkel and colleagues showed that intracoronary retroperfusion of Tβ4 (alongside embryonic endothelial progenitor cells) increased cardiomyocyte survival and improved regional contractility 24 hours after reperfusion in a percutaneous LAD-occlusion model [8]. But Wei and colleagues in 2016, using a closed-chest porcine 90-minute ischemia / 24-hour reperfusion model with 24 randomized animals, found no reduction in global myocardial infarct size when Tβ4 was given at 150 μg/kg IV bolus plus maintenance, either before or after ischemia [23]. The negative pig result is the clearest sign of the rodent-to-large-mammal gap that animates the unfinished translational story. A 2022 mouse study by Stark and colleagues using AAV9-delivered Tβ4 expression (10^12 vg) showed reduced oxidative damage, less inflammation, smaller scar and improved ejection fraction at four weeks after permanent LAD ligation [18], reaffirming the rodent benefit while leaving the pig discrepancy intact. ## Brain, muscle, hair follicle Beyond skin, eye and heart, three other organ systems anchor the preclinical record. In an embolic middle-cerebral-artery occlusion model in rats, Morris and colleagues showed in 2010 that a single intravenous Tβ4 dose of 3.75 mg/kg administered 24 hours after stroke improved adhesive-removal and modified Neurological Severity Score performance from day 14 through day 56 and reduced ischemic brain damage [12]. This is the preclinical foundation for the neurorestorative interest in Tβ4, an interest that has not yet matured into a registered human trial. In skeletal muscle, Tokura and colleagues showed in 2011 that Tβ4 released from injured muscle fibers and surrounding immune cells acts as a chemoattractant for satellite-cell-derived myoblasts, accelerating regeneration in cardiotoxin and freeze-injury models in mice [10]. The implication — that Tβ4 participates in resident-progenitor mobilization in muscle as it does in heart — has been picked up by the underground market more than by the clinical pipeline. In hair-follicle work, Philp and colleagues showed in 2004 that Tβ4 at nanomolar concentrations increased clonogenic hair-follicle keratinocyte migration in rat vibrissa follicles and accelerated hair regrowth in mice [9]. This is the seed of every hair-regrowth claim made for TB-500 — though the original work used the parent peptide. ## Inflammation and the NF-κB axis The 2011 Qiu paper added a mechanistic layer not predicted by the actin work. In human HCT116 and HeLa cell lines, Tβ4 directly bound NF-κB RelA/p65 and blocked TNF-α-driven NF-κB activation and downstream IL-8 transcription, with PINCH-1 and ILK functioning as sensitizers [11]. This provides a molecular basis for the anti-inflammatory effects observed across the corneal, cardiac and dermal models — effects that the actin-sequestration mechanism alone does not explain. The inflammation work also implicates the C-terminal regions of Tβ4 that the seven-residue fragment lacks. None of the NF-κB binding studies have been replicated with the LKKTETQ fragment, and the published mechanism therefore does not transfer cleanly to TB-500. ## Human clinical trials Three human datasets matter. The Ruff 2010 Phase I study enrolled 40 healthy adult volunteers in a randomized, placebo-controlled, single-dose escalation of intravenous recombinant Tβ4 at 42 mg, 140 mg, 420 mg and 1,260 mg, followed by a multiple-dose extension [13]. No dose-limiting toxicities, no serious adverse events, mild-to-moderate adverse events only. This is the first published human safety dataset for recombinant Tβ4 and remains the upper-bound dose reference. The Wang 2021 Chinese Phase I study enrolled 84 healthy adults in a single-dose escalation from 0.05 to 25 μg/kg IV and a multiple-dose extension of 0.5 to 5 μg/kg daily for ten days [14]. PK was dose-linear, no SAEs, no DLTs, and the immunogenicity profile was favorable. This is the second major safety dataset. The RGN-259 ophthalmic program is the most-developed efficacy program. The Phase III ARISE-3 dry-eye trial in roughly 700 patients (NCT03937882) missed its prespecified co-primary endpoints but produced statistically significant improvement in ocular grittiness versus placebo and a significant two-week corneal-staining improvement in a defined subpopulation [15]. The Phase III neurotrophic-keratopathy trial of the same product (NCT02600429, n=18) showed 60% complete corneal healing at day 29 in treated subjects versus 12.5% in placebo (p=0.066), with statistically significant healing at day 43 (p=0.036) and durable effect two weeks after stopping treatment [16]. The European SEER-3 neurotrophic-keratitis Phase III missed its primary endpoint. The RGN-352 cardiac program is the unfinished one. NCT01311518 was designed to enroll approximately 75 post-AMI patients across 20 sites in the United States, Israel and Russia at 450 mg or 1,200 mg IV daily for three days followed by weekly for four weeks. The trial was placed on FDA clinical hold in 2011 over contract-manufacturer cGMP non-compliance and never reported efficacy data [17]. No registered human trial has ever evaluated the synthetic seven-residue TB-500 fragment. Every human number above belongs to the parent peptide. ## Recent direction: 2023-2025 The current direction of Tβ4 research is delivery-mediated and combination-oriented, not free-peptide. A 2025 *Materials Today Bio* paper used Tβ4-overexpressing adipose-derived stem cell exosomes delivered in a HAMA/PLMA dual-photopolymerizable hydrogel to accelerate diabetic wound closure in streptozotocin-induced type-1 diabetic mice, with increased CD31+ neovascularization and altered macrophage polarization through the PI3K/AKT/mTOR/HIF-1α pathway [20]. This is representative of where the field is moving: the peptide as cargo for a biomaterial system, not as a stand-alone injectable. A 2024 *International Journal of Molecular Sciences* paper engineered a tandem repeat of the Tβ4 actin-binding motif and showed accelerated corneal healing in rat models — direct support for the proposition that synthetic LKKTET-containing constructs can preserve and amplify the parent peptide's corneal activity [19]. A 2023 *Cells* paper used conditional deletion of Tβ4 in hepatic stellate cells in a CCl4 mouse model and found that the knockout ameliorated liver fibrosis [21]. Tβ4 turns out to be pro-fibrotic in hepatic stellate cells, the opposite of its action in skin, cornea and heart. This is the most consequential finding in the recent record for any framing of systemic Tβ4 administration: the molecule is not biologically neutral across tissues, and indiscriminate dosing presumes a uniformity the biology does not have. ## What the record does not include Three things are notably absent. First, no peer-reviewed pharmacokinetic study of the synthetic seven-residue TB-500 fragment exists in humans. The closest published fragment-specific PK data come from equine doping-control work by Esposito and colleagues in 2012, which validated an LC-MS method for detecting TB-500 in horse plasma and urine after IV administration [22]. Rodent half-life estimates for the heptapeptide (1.5 to 3 hours plasma half-life after SC or IM injection) circulate widely but originate from vendor pages, not primary literature [22]. Second, no head-to-head efficacy comparison between the fragment and the parent peptide exists in any model system. The 2003 Philp paper showing that 'a synthetic peptide containing the actin-binding domain' produced wound-healing effects in diabetic mice [5] is the closest the literature comes, and the synthetic construct in that paper is not the same molecule sold as TB-500. Third, no clinical-trial registry currently lists a Phase I, II or III study of the seven-residue TB-500 fragment. The investigational-product line for full-length Tβ4 ends at RGN-259 and RGN-352, and even those programs have not produced a regulator-grade efficacy outcome that could support a marketing application [15][16][17]. The 2012 review by Goldstein and colleagues catalogued Tβ4's preclinical breadth across more than 30 models and explicitly noted that strict comparison studies between the parent peptide and its shorter fragments remain sparse — a literature gap the FDA cited when restricting TB-500 from compounding [24][26]. The 2021 Frontiers in Endocrinology review reached the same summary at a higher altitude [25]. The research record is real. It is also smaller, in the places that matter for prescribing, than the marketed name implies. --- A curated wall-label reading of peer-reviewed science — not a clinic, not a vendor, not a prescription. --- # TB-500 / Thymosin Beta-4 dosing in the published research > A research-context summary of the doses and routes used in published Thymosin Beta-4 studies. No clinical dosing protocol exists for the synthetic TB-500 fragment. Every number on this page describes a published research administration in an animal or a clinical trial of the parent peptide. No clinical dosing protocol exists for the seven-residue TB-500 fragment. ## What the studies administered This page lists the doses, routes and species from published research — not a prescribing protocol. No clinical protocol exists for the TB-500 fragment because the fragment has never been in a registered human trial. The numbers here come from animal studies (rats, mice, pigs, horses) and from the two published Phase I trials of full-length intravenous Tβ4 in healthy volunteers. Vendor-circulated figures — '2 to 10 mg per week subcutaneous' — appear nowhere in peer-reviewed literature and are noted as market-origin claims. The study doses are listed so readers can place those vendor numbers against the actual published record. ## A note on what this page is This page summarizes the doses and routes used in published animal and human studies of Thymosin Beta-4 and the synthetic TB-500 fragment. It is research-context only. It is not a dosing protocol. It is not a prescribing schedule. No clinical dosing protocol exists for the synthetic seven-residue TB-500 fragment, because the fragment has never been the subject of a registered human trial and is not a prescribable substance under United States regulation [22][26]. The numbers below describe what was administered in published experiments, in the units the experiments used, with the routes the experiments used. They are presented so that readers can place vendor marketing claims and underground-use anecdotes against the actual published record. ## Routes used in the published work Published studies of Tβ4 and TB-500 have used six routes of administration: - **Topical**, for dermal wound healing in rats and mice and for corneal surface application in mice [3][4][5]. - **Intraperitoneal**, for systemic rodent dosing in cardiac and epicardial models [6][7]. - **Intravenous**, for rodent cardiac and stroke models, for the porcine ischemia-reperfusion work, and for every published human Phase I trial of recombinant Tβ4 [6][12][13][14][17][23]. - **Subcutaneous**, in rodent and equine doping-control studies [22]. - **Intracoronary retroperfusion**, in the 2008 porcine LAD-occlusion model that combined Tβ4 with embryonic endothelial progenitor cells [8]. - **Intramyocardial AAV-delivered overexpression**, in mouse fibrosis models — a delivery system that is not the peptide itself but a viral vector encoding it [18]. Oral administration has not been studied in any peer-reviewed efficacy trial because both the parent peptide and the fragment are inactivated by gastric proteases [22]. All published preclinical and clinical work has used parenteral or topical routes. ## Doses used in the animal research In the dermal-wound work that founded the field, Malinda and colleagues used 5 μg of Tβ4 in 50 μL of PBS per wound, applied topically or by intraperitoneal injection, in Sprague-Dawley rats [3]. The 2003 Philp paper used 0.1 to 5 μg per wound topically in db/db diabetic and aged mice [5]. In the corneal work, Sosne and colleagues used 5 μg in 5 μL PBS topically twice daily in 129 Sv mice after alkali burn [4]. In the cardiac mouse work, the original Bock-Marquette paper used a single intraperitoneal bolus plus continued dosing over four weeks after coronary artery ligation [6]. Smart and colleagues used 150 μg intraperitoneally every three days to mobilize adult epicardial progenitor cells [7]. In the AAV-delivered mouse cardiac fibrosis work, a single 10^12 vg dose of AAV9-Tβ4 was administered intramyocardially or intravenously [18]. In the porcine cardiac work, the 2008 Hinkel paper used Tβ4 retroperfused to the site of injury during reperfusion [8]. The 2016 Wei paper used 150 μg/kg IV bolus plus maintenance dosing, given either before or after ischemia, and found no reduction in global infarct size at 24 hours [23]. In the stroke work, Morris and colleagues used a single 3.75 mg/kg IV dose administered 24 hours after embolic middle-cerebral-artery occlusion in rats [12]. ## Doses used in the human trials The Ruff 2010 Phase I study escalated single IV doses of recombinant Tβ4 from 42 mg through 140 mg and 420 mg to 1,260 mg in 40 healthy adult volunteers, with a multiple-dose extension [13]. No dose-limiting toxicities and no serious adverse events were observed. The Wang 2021 Chinese Phase I study escalated single IV doses from 0.05 to 0.25 to 0.5 to 2.0 to 5.0 to 12.5 to 25.0 μg/kg in 84 healthy Chinese adults, with a multiple-dose extension of 0.5 to 5.0 μg/kg per day intravenously for ten days [14]. PK was dose-proportional and no SAEs were reported. The planned RGN-352 Phase II cardiac regimen was 450 mg or 1,200 mg IV daily for three days followed by weekly for four weeks in approximately 75 post-AMI patients [17]. The trial did not complete enrollment and did not report efficacy. The RGN-259 ophthalmic clinical program used a 0.1% Tβ4 ophthalmic solution administered topically twice daily in Phase II/III dry-eye work and six times daily for 28 days in the Phase III neurotrophic-keratopathy trial [15][16]. These are the doses on the human record. Every one of them was administered with full-length recombinant Tβ4. None of them was administered with the synthetic seven-residue TB-500 fragment. ## Pharmacokinetics, such as they are Published PK data for full-length recombinant Tβ4 in humans (Ruff 2010 IV; Wang 2021 IV) show biphasic plasma concentration-time curves with rapid distribution and terminal exposure measured over hours, with no dose-dependent accumulation across the studied range [13][14]. No peer-reviewed pharmacokinetic study of the synthetic seven-residue TB-500 heptapeptide exists in humans. The closest published fragment-specific PK is the Esposito 2012 equine doping-control work, which validated an LC-MS detection method for TB-500 in horse plasma and urine after intravenous administration [22]. Rodent estimates for the heptapeptide — typically quoted as a 1.5- to 3-hour plasma half-life after SC or IM injection — come from vendor and aggregated commercial sources rather than primary literature and should be read as low-confidence [22]. The N-terminal acetylation of TB-500 blocks aminopeptidase cleavage and improves solution stability versus the unmodified LKKTETQ sequence [22]. This is a chemistry observation, not a clinical PK measurement. ## What vendor literature reports — and why it isn't here Vendor pages and underground-use writing routinely quote TB-500 dosing as 2 to 10 mg per week subcutaneously, sometimes as a loading-and-maintenance schedule [22]. These figures are not derived from any published clinical trial. They have no peer-reviewed safety basis. They cannot be a prescribing protocol because the substance cannot be prescribed in the United States [26]. This page documents their existence as a feature of the marketplace and declines to reproduce them as if they were research-grounded. The published research used the doses listed above, in the species listed above, with the routes listed above. That is the record. --- A curated wall-label reading of peer-reviewed science — not a clinic, not a vendor, not a prescription. --- # TB-500 frequently asked questions > Direct answers to the questions readers arrive with: prescription status, FDA approval, compounding, the fragment-versus-parent distinction, WADA status, and legality. Short answers, drawn from the published record and the current FDA and WADA positions. Each answer carries its citations. ## Can TB-500 be prescribed by a doctor in the United States? No. A prescription presupposes an FDA-approved product, either as an on-label prescription for the indication the agency cleared or as an off-label prescription for an unapproved use of an approved product. No TB-500 product is FDA-approved. No full-length Thymosin Beta-4 product is FDA-approved either; the investigational programs RGN-259 (ophthalmic) and RGN-352 (intravenous, halted) remain investigational [15][16][17]. With no approved product anywhere in the regulatory record, there is no on-label prescription and no off-label path. A licensed prescriber who writes for TB-500 is not writing a prescription for an approved drug; they are ordering an investigational substance [26]. ## Is TB-500 available by prescription anywhere? Not in any major regulated market. No TB-500 product holds marketing authorization from the FDA in the United States, the EMA in Europe, the MHRA in the United Kingdom, the TGA in Australia, the PMDA in Japan, or any other comparable agency [26]. The full-length parent peptide has been studied in registered human trials — including in China — but has not received marketing authorization in any indication in any country. ## Has any TB-500 or Thymosin Beta-4 product been FDA-approved? No. The most-developed clinical program for the parent peptide is RGN-259, a 0.1% Thymosin Beta-4 ophthalmic solution developed by RegeneRx and its partners (most recently HLB Therapeutics and the ReGenTree joint venture). Phase III ARISE-3 in dry eye missed its prespecified co-primary endpoints [15]. The Phase III neurotrophic-keratopathy trial (NCT02600429, n=18) showed statistically significant healing at day 43 (p=0.036) [16], but neither trial has produced a regulator-grade efficacy result that could anchor an approval pathway. The cardiac program RGN-352 was halted in 2011 over manufacturing issues and never read out [17]. The synthetic seven-residue TB-500 fragment has never been the subject of a registered human IND. ## Why can't a compounding pharmacy make TB-500 for me? Compounding pharmacies operate under specific federal authority. A traditional, patient-specific compounding pharmacy works under Section 503A of the Food, Drug, and Cosmetic Act. A larger outsourcing facility works under Section 503B. Either route, when compounding from a bulk drug substance, requires that the substance appear on the relevant FDA Bulks List or otherwise meet specific statutory criteria. On September 29, 2023, the FDA placed *Thymosin Beta-4, Fragment (LKKTETQ)* — TB-500 by its chemical identity — in Category 2 of the Interim 503A Bulks List. Category 2 is the agency's designation for substances it has determined raise significant safety concerns and that may not be used in pharmacy compounding while the agency completes its review [26]. The same placement effectively closed the Section 503B route. State boards of pharmacy and major outsourcing facilities have since stopped accepting orders for the substance. ## What is the FDA Category 2 / 503A bulks list, and how does it affect TB-500? The Interim 503A Bulks List is the FDA's working categorization of bulk drug substances that have been nominated for use in pharmacy compounding. The agency sorts nominated substances into three categories. Category 1 substances may be used in compounding while the FDA continues to consider them. Category 2 substances may not be used in compounding because the agency has identified significant safety concerns. Category 3 substances are those nominated without sufficient supporting information. TB-500 — under the chemical identity *Thymosin Beta-4, Fragment (LKKTETQ)* — was placed in Category 2 on September 29, 2023 [26]. That placement is the operative regulatory fact for any United States question about whether a pharmacy can prepare TB-500. ## When did TB-500 lose its compounding-pharmacy access, and is that decision under review? The September 29, 2023 Category 2 placement was the operative restriction [26]. The Pharmacy Compounding Advisory Committee (PCAC) — the FDA federal advisory committee that reviews bulk drug substances for the 503A Bulks Regulation — held meetings on October 29 and December 4, 2024 to begin formal review of several Category 2 peptides. TB-500 was not among the substances voted on at those December 2024 sessions, which focused on AOD-9604, CJC-1295, and Thymosin Alpha-1 [27]. As of 2025, TB-500 remains in Category 2 — still ineligible for 503A or 503B compounding — with no PCAC vote on the fragment yet scheduled. ## How is TB-500 different from full-length Thymosin Beta-4, and does that matter for prescribing? TB-500 is a synthetic seven-amino-acid peptide, N-acetyl-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH, with the central LKKTET actin-binding motif of the parent peptide. Full-length Thymosin Beta-4 is a 43-amino-acid endogenous peptide encoded by the *TMSB4X* gene [1][25]. The fragment retains the actin-binding sequence. It does not retain most of the parent peptide's downstream interaction surfaces, including the C-terminal helix that mediates inflammation-related signaling [11], the regions involved in PINCH-ILK-Akt complex formation [6], and the N-terminal sequence that is enzymatically cleaved to release AcSDKP, a separately bioactive antifibrotic and proangiogenic tetrapeptide. This matters for prescribing in two ways. First, vendor literature for TB-500 routinely cites animal and clinical studies of the parent peptide as if the data applied to the fragment, which it does not without separate study [24]. Second, the FDA explicitly cited identity ambiguity — fragment marketed, parent peptide studied — among the safety concerns supporting the September 2023 Category 2 placement [26]. ## What are the human clinical trials of Thymosin Beta-4 (RGN-259, RGN-352) and did any succeed? Three Phase III ophthalmic trials and one Phase II cardiac trial define the human record for the parent peptide. ARISE-3 (NCT03937882) tested 0.1% RGN-259 ophthalmic solution BID in roughly 700 dry-eye patients. It missed its prespecified co-primary endpoints but produced statistically significant improvement in ocular grittiness and significant central corneal fluorescein staining improvement at two weeks in a defined subpopulation [15]. The European SEER-3 neurotrophic-keratitis Phase III missed its primary endpoint. NCT02600429 tested the same 0.1% RGN-259 solution at six applications per day for 28 days in 18 neurotrophic-keratopathy patients. Complete corneal healing was observed at day 29 in 60% of treated subjects versus 12.5% in placebo (p=0.066, narrow miss) and statistically significant healing was reached at day 43 (p=0.036), with sustained healing two weeks after stopping treatment [16]. RGN-352 (NCT01311518) was the Phase II cardiac trial designed to enroll approximately 75 post-AMI patients at 450 mg or 1,200 mg IV daily for three days followed by weekly for four weeks. The trial was placed on FDA clinical hold in 2011 over contract-manufacturer cGMP non-compliance and never reported efficacy data [17]. In short: positive signals in ophthalmology, no clean primary-endpoint success, and an unfinished cardiac story. ## Is TB-500 banned by WADA for athletes? Yes. 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) of the WADA Prohibited List in the 2024, 2025 and 2026 editions [22][26]. Multiple athlete sanctions and four-year ineligibility periods have been issued under both S0 and S2. Validated LC-MS detection methods for TB-500 in equine plasma and urine have been published [22], and analogous human-sport detection methods are in routine use at WADA-accredited laboratories. The compound is not difficult to detect after recent administration. ## Is TB-500 legal to possess if it's not prescribable? TB-500 is not a federally scheduled controlled substance in the United States. Its regulatory restriction is medical-product law, not drug-scheduling law: it cannot be lawfully prescribed because no approved product exists [26], and it cannot be lawfully compounded under 503A or 503B because of its Category 2 placement on the Interim 503A Bulks List [26]. State laws and professional-licensure rules add further constraints on practitioners. Research use of TB-500 as a research chemical is a separate question that depends on the institutional setting, the source's licensing, and applicable state and federal research-chemical regulation. This site does not advise on possession or use; it documents the regulatory record. ## Are 'underground' TB-500 doses safe to use? Underground- and research-chemical-market TB-500 is sold without GMP manufacturing, lot release testing, endotoxin control, or sterility assurance. The contamination and purity risks of unregulated peptide injectables are not theoretical — they were among the stated FDA bases for the 503A Category 2 placement [26]. The commonly quoted '2 to 10 mg per week subcutaneous' regimens have no peer-reviewed safety basis [22] and are not derived from any published clinical trial. The pharmacology adds context. Tβ4 biology is not uniformly tissue-supportive: in hepatic stellate cells, conditional knockout of Tβ4 ameliorates liver fibrosis in mouse CCl4 models, suggesting that the molecule is pro-fibrotic in that compartment [21]. The largest registered cardiac efficacy study in pigs was negative for global infarct-size reduction [23]. These are the parts of the published record that vendor pages tend to leave out. ## Does TB-500 cause cancer? No clinical signal of tumor promotion has been reported in the published human safety data to date [13][14]. Theoretical concerns have been raised in the literature because Tβ4 promotes angiogenesis and cell migration — two activities that could in principle accelerate the progression of occult or pre-existing tumors. The Phase I human trials of recombinant Tβ4 enrolled small numbers of healthy adult volunteers under short observation periods and were not powered or designed to detect such a signal. The published record neither confirms nor refutes the theoretical concern. ## Does TB-500 work for hair regrowth? The hair-regrowth interest traces to a 2004 paper by Philp and colleagues showing that full-length Tβ4 at nanomolar concentrations increased clonogenic hair-follicle keratinocyte migration in rat vibrissa follicles and accelerated hair regrowth in mice [9]. The work used the parent peptide, not the seven-residue fragment, and was conducted in rodent models. No registered human clinical trial of either Tβ4 or TB-500 for hair regrowth has been published. The vendor-marketing claim is grounded in a real preclinical observation; it is not grounded in human evidence. ## Why does this site use the word 'prescribed' in its name if TB-500 isn't prescribable? Because the word *prescribed* is the search term readers actually use, and the editorial position of this site is that the term names a category absence — a thing the United States regulatory system has not yet created — rather than a product that exists. The domain modifier sits on the front of the site the way an empty plinth sits in a gallery: as a position relative to the absent object, not a claim that the object is there. The /about page explains the editorial framing in more detail. --- A curated wall-label reading of peer-reviewed science — not a clinic, not a vendor, not a prescription. --- # References — TB-500 / Thymosin Beta-4 > Full citation list for the TB-500 / Thymosin Beta-4 record, with DOIs and PubMed or PMC links. Twenty-seven peer-reviewed and regulatory primary sources. Every citation used elsewhere on the site, with DOI or registry identifier and a link to the source. ## About the bibliography The references on this page are the primary sources cited by the /index, /research, /dosage and /faq pages. They are listed below in citation-number order and rendered as a sortable, searchable table. The sources fall into four groups. Biochemistry and mechanism papers from 1992 through 2011 establish the actin-binding, NF-κB and PINCH-ILK-Akt frameworks [1][2][6][11]. Preclinical efficacy papers from 1999 through 2025 cover dermal and corneal wound healing, cardiac repair, stroke, skeletal muscle and hair follicle, plus the recent hydrogel-delivery and hepatic-stellate-cell work [3][4][5][7][8][9][10][12][18][20][21]. Human clinical trial reports and registry entries cover the Phase I safety studies, the Phase III ophthalmic program, and the halted Phase II cardiac program [13][14][15][16][17]. The Esposito 2012 equine doping-control paper provides the only published PK data specific to the seven-residue fragment [22]. Two review papers organize the field [24][25]. The FDA Interim 503A Bulks List guidance and the 2024 PCAC briefing material define the current regulatory record [26][27]. All twenty-seven sources have a DOI or a registry identifier and link to the publisher, PubMed, PMC, or ClinicalTrials.gov. ## The full list The table is sortable by citation number, year, first author and journal, and searchable across the citation text. The default sort is by citation number. ## References [1] Cassimeris L, Safer D, Nachmias VT, Zigmond SH. Interaction of thymosin beta 4 with muscle and platelet actin: implications for actin sequestration in resting platelets. Biochemistry. 1992;31(20):4628-4632. https://pubmed.ncbi.nlm.nih.gov/1627561/ [2] 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 Journal. 2004;23(18):3599-3608. https://pmc.ncbi.nlm.nih.gov/articles/PMC517612/ [3] Malinda KM, Sidhu GS, Mani H, Banaudha K, Maheshwari RK, Goldstein AL, Kleinman HK. Thymosin β4 accelerates wound healing. Journal of Investigative Dermatology. 1999;113(3):364-368. https://www.jidonline.org/article/S0022-202X(15)40595-0/fulltext [4] 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. Experimental Eye Research. 2002;74(2):293-299. https://pubmed.ncbi.nlm.nih.gov/11950239/ [5] Philp D, Badamchian M, Scheremeta B, Nguyen M, Goldstein AL, Kleinman HK. Thymosin β4 and a synthetic peptide containing its actin-binding domain promote dermal wound repair in db/db diabetic mice and in aged mice. Wound Repair and Regeneration. 2003;11(1):19-24. https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1524-475X.2003.11105.x [6] 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;432(7016):466-472. https://pubmed.ncbi.nlm.nih.gov/15565145/ [7] 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;445(7124):177-182. https://pubmed.ncbi.nlm.nih.gov/17108969/ [8] Hinkel R, El-Aouni C, Olson T, Horstkotte J, Mayer S, Müller S, Willhauck M, Spitzweg C, Gildehaus FJ, Münzing W, Hannappel E, Bock-Marquette I, DiMaio JM, Hatzopoulos AK, Boekstegers P, Kupatt C. Thymosin β4 is an essential paracrine factor of embryonic endothelial progenitor cell-mediated cardioprotection. Circulation. 2008;117(17):2232-2240. https://pmc.ncbi.nlm.nih.gov/articles/PMC2672916/ [9] Philp D, Nguyen M, Scheremeta B, St-Surin S, Villa AM, Orgel A, Kleinman HK, Elkin M. Thymosin β4 increases hair growth by activation of hair follicle stem cells. FASEB Journal. 2004;18(2):385-387. https://faseb.onlinelibrary.wiley.com/doi/10.1096/fj.03-0244fje [10] Tokura Y, Nakayama Y, Fukada S, Nara N, Yamamoto H, Matsuda R, Hara T. Muscle injury-induced thymosin β4 acts as a chemoattractant for myoblasts. Journal of Biochemistry. 2011;149(1):43-48. https://pubmed.ncbi.nlm.nih.gov/20880960/ [11] 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 Journal. 2011;25(6):1815-1826. https://pmc.ncbi.nlm.nih.gov/articles/PMC3101037/ [12] 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;169(2):674-682. https://pmc.ncbi.nlm.nih.gov/articles/PMC2907184/ [13] Ruff D, Crockford D, Girardi G, Zhang Y. A randomized, placebo-controlled, single and multiple dose study of intravenous thymosin beta4 in healthy volunteers. Annals of the New York Academy of Sciences. 2010;1194:223-229. https://pubmed.ncbi.nlm.nih.gov/20536472/ [14] 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. Journal of Cellular and Molecular Medicine. 2021;25(17):8222-8233. https://pmc.ncbi.nlm.nih.gov/articles/PMC8419156/ [15] ReGenTree LLC / RegeneRx Biopharmaceuticals (HLB Therapeutics). Assessment of the Safety and Efficacy of RGN-259 Ophthalmic Solutions for Dry Eye Syndrome (ARISE-3). ClinicalTrials.gov NCT03937882, 2020. https://clinicaltrials.gov/study/NCT03937882 [16] 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. International Journal of Molecular Sciences. 2022;24(1):554. https://pmc.ncbi.nlm.nih.gov/articles/PMC9820614/ [17] RegeneRx Biopharmaceuticals, Inc. A Study of the Safety and Efficacy of Injectable Thymosin Beta 4 for Treating Acute Myocardial Infarction. ClinicalTrials.gov NCT01311518, 2011. https://clinicaltrials.gov/study/NCT01311518 [18] Stark C, Taimen P, Tarkia M, Pärkkä J, Saraste A, Bizzarro V, Saraste M, Savunen T, Koskenvuo JW. Thymosin β4 protects against cardiac damage and subsequent cardiac fibrosis in mice with myocardial infarction. Cardiovascular Therapeutics. 2022;2022:1308651. https://pmc.ncbi.nlm.nih.gov/articles/PMC9187458/ [19] Sosne G, et al. Engineered tandem thymosin peptide promotes corneal wound healing. International Journal of Molecular Sciences. 2024;25(19):10347. https://www.mdpi.com/1422-0067/25/19/10347 [20] 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. Materials Today Bio. 2025;31:101585. https://pmc.ncbi.nlm.nih.gov/articles/PMC11893380/ [21] 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;12(12):1658. https://pmc.ncbi.nlm.nih.gov/articles/PMC10297343/ [22] 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. Analytica Chimica Acta. 2012;752:97-104. https://www.sciencedirect.com/science/article/abs/pii/S0021967312014550 [23] 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. Frontiers in Pharmacology. 2016;7:115. https://pmc.ncbi.nlm.nih.gov/articles/PMC4853610/ [24] Goldstein AL, Hannappel E, Sosne G, Kleinman HK. Thymosin β4: a multi-functional regenerative peptide. Basic properties and clinical applications. Expert Opinion on Biological Therapy. 2012;12(1):37-51. https://pubmed.ncbi.nlm.nih.gov/22074294/ [25] Xing Y, Ye Y, Zuo H, Li Y. Progress on the function and application of thymosin β4. Frontiers in Endocrinology. 2021;12:767785. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2021.767785/full [26] U.S. Food and Drug Administration. Interim Policy on Compounding Using Bulk Drug Substances Under Section 503A of the FD&C Act — Updated Categorization. September 29, 2023. Docket FDA-2017-D-1067. https://www.fda.gov/drugs/human-drug-compounding/bulk-drug-substances-used-compounding-under-section-503a-fdc-act [27] U.S. Food and Drug Administration. Pharmacy Compounding Advisory Committee Meeting Briefing Materials, October 29 and December 4, 2024. Docket FDA-2017-D-1067. https://www.fda.gov/advisory-committees/pharmacy-compounding-advisory-committee [28] Mendias CL, Awan TM. Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance. Sports Medicine. 2026. https://pubmed.ncbi.nlm.nih.gov/41966639/ [29] Cha HJ, Jeong MJ, Kleinman HK. Role of thymosin beta4 in tumor metastasis and angiogenesis. Journal of the National Cancer Institute. 2003;95(22):1674-1680. https://pubmed.ncbi.nlm.nih.gov/14625258/ [30] Wang WS, Chen PM, Hsiao HL, Wang HS, Liang WY, Su Y. Thymosin beta 4 is overexpressed in human pancreatic cancer cells and stimulates proinflammatory cytokine secretion and JNK activation. Cancer Biology & Therapy. 2008;7(3):450-457. https://pubmed.ncbi.nlm.nih.gov/18094619/ [31] Cooper TM, Stevenson DA, Bassindale T, Jarvis AM, Robinson JL. 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. Journal of Chromatography A. 2012;1262:215-222. https://pubmed.ncbi.nlm.nih.gov/23084823/ [32] Spurney CF, Cha HJ, Sali A, Pandey GS, Pistilli E, Guerron AD, Gordish-Dressman H, Hoffman EP, Bhatt DL. Evaluation of skeletal and cardiac muscle function after chronic administration of thymosin beta-4 in the dystrophin deficient mouse. PLoS One. 2010;5(1):e8976. https://pubmed.ncbi.nlm.nih.gov/20126456/ [33] Thomas A, Thevis M, Polet M, Delahaut P, Schänzer W. TB500/TB1000 and SGF1000: A scientific approach for a better understanding of doping-relevant peptide preparations. Drug Testing and Analysis. 2023;15(3):303-313. https://pubmed.ncbi.nlm.nih.gov/36482504/ --- A curated wall-label reading of peer-reviewed science — not a clinic, not a vendor, not a prescription. --- # About — TB-500 Prescribed > TB-500 Prescribed is an independent editorial reading room that summarizes the peer-reviewed Thymosin Beta-4 research literature. Not a clinic, not a pharmacy. TB-500 Prescribed is an independent editorial project. ## What this publication is TB-500 Prescribed is an independent editorial project that publishes summaries of the peer-reviewed research literature on Thymosin Beta-4 and the synthetic seven-amino-acid fragment marketed as TB-500. 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. The modifier *prescribed* in the domain name is editorial framing — a position the publisher occupies relative to the literature, not a claim about the site's services. The site does not write prescriptions, does not connect readers to prescribers, and does not facilitate compounding or telehealth. It writes about the regulatory and research record that surrounds the prescription question. As of this publication, the answer to that question in the United States is that no prescription is available, because no FDA-approved TB-500 product exists and the substance is not eligible for pharmacy compounding [26]. ## Editorial standards The site is built around three editorial commitments. *Sources are primary.* Every quantitative claim — every dose, every percentage, every endpoint result, every regulatory date — is traced to a peer-reviewed paper, a registered clinical trial record, or a published FDA guidance document. The /references page lists twenty-seven such sources with DOIs and registry identifiers. *Distinctions are preserved.* The fragment-versus-parent-peptide distinction is treated as a structural fact about the field, not a footnote. The Phase I safety record for full-length Tβ4 [13][14] is not extrapolated to the seven-residue fragment. The animal data for the parent peptide is not represented as fragment data. Where vendor literature collapses the distinction, the site names the collapse. *The regulatory record is current.* The September 29, 2023 FDA Category 2 placement of *Thymosin Beta-4, Fragment (LKKTETQ)* on the Interim 503A Bulks List [26] is the operative United States fact for the prescription and compounding questions, and the site treats it as such. The 2024 PCAC review of related peptides is also tracked [27]. If the FDA position changes, the site will update. ## What this publication isn't It is not a clinic. There are no clinicians on staff. There is no clinical team. There are no physicians, pharmacists, or other licensed healthcare professionals associated with this publication who provide care to readers. It is not a pharmacy. The site does not manufacture, distribute, sell, compound, repackage, or ship any product. It does not collect orders. It does not maintain a formulary. It does not partner with compounding pharmacies or outsourcing facilities. It is not a vendor. The site has no commercial relationship with any peptide manufacturer, research-chemical supplier, telehealth platform, or licensed pharmaceutical company. It does not run affiliate links to product pages. It is not medical advice. Nothing on this site constitutes medical advice, prescribing recommendations, clinical guidance, or a substitute for evaluation by a qualified healthcare professional. Readers seeking care should consult a licensed clinician. ## How the wall labels read Each page is structured as a wall-label reading of one part of the record. The hero on each page carries an eyebrow section number and a one-line wall label. The body proceeds in inverted-pyramid order: the most important fact first, the supporting evidence underneath, the unresolved questions named at the end. Inline citation markers in square brackets point to the references index, which is reachable from the navigation on every page. The quiet visual register — black-on-cream typography, a single burgundy hairline accent, generous whitespace as the framing device — is the editorial argument enacted in design. TB-500 is a research peptide whose prescription status is fundamentally a category absence. The site exhibits the absence rather than performing it. --- A curated wall-label reading of peer-reviewed science — not a clinic, not a vendor, not a prescription. --- # Contact — TB-500 Prescribed > Contact the editors of TB-500 Prescribed. Editorial corrections, source suggestions, and reference updates welcome. Not a clinical service. Drop the editors a note. We read every message and update the record when a source warrants it. This is not a clinical service. ## What this form is for The form below reaches the editors. It is appropriate for: - Editorial corrections — typos, broken links, misattributions, citation errors. - Source suggestions — a peer-reviewed paper, registered trial, or FDA guidance document the site has missed. - Regulatory updates — a PCAC vote, an FDA Category change, a WADA Prohibited List update. - Questions about the editorial approach or the publisher. We read every message. We respond when a message warrants a response. We update the published record when a source warrants an update. ## What this form is not for It is not for clinical questions. The editors are not clinicians and cannot answer questions about whether a particular individual should or should not use TB-500, what dose to use, what route to use, or how to obtain the substance. Readers seeking that kind of guidance should consult a licensed healthcare professional in their jurisdiction. It is not for product inquiries. The site does not sell, manufacture, distribute, compound, or ship any product. We cannot connect readers to suppliers or compounding pharmacies. We cannot facilitate purchase. It is not for legal advice. The regulatory summaries on this site describe the published FDA, WADA and clinical-trial record. They are editorial readings of public documents, not legal opinions on individual situations. ## Editorial contact form Use the form below. Mark the subject line accurately so the right editor reads it first. We reply, when we reply, by email — typically within several business days for citation corrections and source suggestions, and not at all for clinical or product questions, which fall outside the scope of the publication. ## Disclosure TB-500 Prescribed has no commercial relationship with any manufacturer, vendor, telehealth service, compounding pharmacy, or licensed pharmaceutical company. The site does not run affiliate links to product pages and does not accept advertising. Editorial decisions are made by the editorial team without external influence. --- A curated wall-label reading of peer-reviewed science — not a clinic, not a vendor, not a prescription.