compound
Thymosin beta-4
The protein behind the TB-500 name, covered claim by claim: the three Phase 3 eye trials, the randomised cardiac trial and what it actually found, and the two registered injected trials that never enrolled anyone.
- Primary sources Registry records and papers are read at the source, not through summaries. Read the methodology
- Every claim graded Each claim about what a compound does carries an evidence tier and a numbered citation. How grades derive
- Sells nothing No cart, no price, and no product page anywhere on this site. Conflict disclosure
- Corrections logged Errors are fixed and recorded in a permanent public log, never edited away. Corrections log
Thymosin beta-4 is a protein the body already makes. It is present in platelets, in most cell types, and in tears, and its best characterised job is holding on to actin, the filament protein cells build their internal scaffolding from. That housekeeping role is what every therapeutic claim for it is built on top of.
It is also the molecule whose name sits on a product it is not. TB-500 is a seven amino acid piece cut out of the middle of this protein and sold as an injectable. The two are separate substances with separate records, and almost every trial count published for TB-500 is counting trials that were run on this protein instead. This page covers the protein, and the comparison page covers the split.
The published record here is genuinely different from the fragment's. There are completed Phase 3 trials, a randomised trial in heart attack patients, and decades of laboratory work. Reading them closely is what this page does, because the headline versions and the trials themselves say different things.
| Property | Value | Source |
|---|---|---|
| Category | Naturally occurring 43 amino acid actin-binding protein, developed as an eye drop and as an injected recombinant drug | PMID 22074294 |
| Also known as | Tβ4, TB4, gene symbol TMSB4X, RGN-259 as the ophthalmic formulation, NL005 as the injected recombinant | PMID 30063853 |
| Structure | Intrinsically unstructured under natural conditions. Structure can be induced by low pH, zinc ions, certain organic reagents, or by binding partners | PMID 27450728 |
| Relationship to TB-500 | TB-500 is residues 17 to 23 of this protein with an added acetyl group. One molecule of 43 residues, one of seven, and separate published records | The comparison, in full |
| Phase 3 record | Five Phase 3 registrations, all ophthalmic, all sponsored by ReGenTree. Three completed in dry eye with no posted results, one recruiting, and one terminated. The terminated one is the only trial of this protein with a published paper | PMID 36613994 |
| Registered injected trials in the US | Two, and both were withdrawn before enrolling a single participant | NCT01311518 |
| Anti-doping status | Named on the WADA 2026 Prohibited List under S2.3 as Thymosin-ß4 and its derivatives e.g. TB-500. Prohibited at all times, and a non-Specified Substance | WADA 2026 Prohibited List |
| Approval status | Not an approved drug in any indication, in any jurisdiction covered by this page | ClinicalTrials.gov, read 23 August 2026 |
Not medical advice
This page reports what has been documented about a compound. It is not medical advice, not a diagnosis, not a dosing protocol, and not a recommendation to obtain or use anything described here. Talk to a licensed clinician about anything concerning your health. Read the full disclaimer.
Reviewed against editorial standards Updated
Key takeaways
- The trial record published under the TB-500 name almost always belongs to this protein instead. Thymosin beta-4 has eighteen genuine registrations on ClinicalTrials.gov; the fragment has one, and that one declares itself to be a fictional example record.
- The randomised trial in heart attack patients found no significant difference in infarct size between injected thymosin beta-4 and placebo across all 96 participants. A smaller group who received a first dose within eight hours did show a difference, which is a result to test rather than a result to rely on. [Human RCT] [1]
- The published Phase 3 trial in neurotrophic keratopathy was stopped early with 18 of a planned 46 participants, and its pre-specified primary endpoint of complete healing by day 29 was not met at p=0.0656. Several secondary endpoints did reach significance. [Human RCT] [2]
- The route with the strongest evidence is the one nobody sells. Three Phase 3 trials have been run as an eye drop. The injected systemic route has two US registrations and both were withdrawn before enrolling anyone.
- In the study that identified this protein as something human muscle releases during exercise, giving it to mice did not enhance muscle regeneration and did not correct the metabolic effects of a high-fat diet. That is a published negative on the recovery claim, from authors who were not looking for one. [Animal] [3]
- The mouse hair growth result comes from animals bred to overexpress the protein and from knockout animals, not from giving the protein to anything. Faster regrowth in an animal engineered to make more of a protein is a different finding from a treatment effect. [Animal] [4]
- Anti-doping is the one question here whose answer does not depend on the evidence. WADA names the protein and its derivatives in a single entry, so the difference between this molecule and TB-500 makes no difference to a tested athlete.
- AMINO ACIDS
- 43
- COMPLETED PHASE 3 TRIALS
- 3
- NUMBERED SOURCES
- 30
- EVIDENCE GRADE
- B
Who researches Thymosin beta-4?
Three groups reach this page, and the record answers them very differently.
The first arrives from a TB-500 product and a trial count. That count is almost always this protein's, and the human-testing section below lists every registration with what it tested and who sponsored it, so it can be checked rather than repeated.
The second is reading about the eye. This is where the evidence is strongest and where the published Phase 3 sits. It is also where the gap between how the trial is cited and what the trial reported is widest, so that section quotes the numbers directly.
The third is a tested athlete or somebody advising one. The regulatory section has the answer and it is short: the protein and its derivatives are named in one WADA entry, prohibited at all times, in the non-Specified category.
What is Thymosin beta-4?
Plain-English version: a small protein the body makes that holds on to actin, the filament protein cells use to keep their shape and to move.
Thymosin beta-4 is the product of the TMSB4X gene and runs 43 amino acids in its mature form. During biosynthesis the initiator methionine is removed and the new N-terminus is acetylated, so the circulating protein carries an acetyl group that the gene sequence alone does not predict [8].
Structurally it belongs to a family that does not hold a fixed shape. The beta thymosins are short, highly charged and intrinsically unstructured under natural conditions, and structure appears only when something induces it: low pH, zinc ions, certain organic solvents, or contact with a binding partner [7]. A protein with no fixed shape until it meets its partner is a difficult drug target and a difficult thing to measure, and both problems show up later on this page.
It is released by platelets and by many other cell types after injury, which is the observation the regenerative interest grew out of [9]. Human skeletal muscle also releases it during exercise: a 2021 proteomics study found it was the most upregulated secreted protein in the media of contracting mouse myotubes and showed it rises acutely in human plasma after exercise, in trained and untrained people alike [3].
One further piece of its biology matters for reading the literature. Prolyl oligopeptidase cuts a four residue fragment, Ac-SDKP, off the N-terminus [8]. Ac-SDKP has a substantial literature of its own, particularly in fibrosis, and results belonging to that fragment are sometimes carried back to the parent protein as though they were the same finding.
SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES · 4,963 Da for the 43 residue mature chain
How strong is the evidence, claim by claim?
Every claim area this compound is discussed for gets a row, including the ones with the weakest support. The tier records what the row rests on, and the last column states what that work can and cannot show. Each tier links to its definition on the methodology page.
| Evidence Area | What Has Been Studied | Evidence Level | What It Can and Cannot Show |
|---|---|---|---|
| Heart repair after a heart attack | A randomised, placebo-controlled, double-blind trial in 96 patients with ST-segment elevation myocardial infarction treated with primary PCI, reported inside a 2025 paper that is otherwise a mouse and cell study. Infarct size was assessed at 90 days. The same paper reports mouse work alongside it: at 28 days after ischemia/reperfusion surgery, mice given seven days of recombinant thymosin beta-4 showed less cardiac dysfunction and less fibrosis than untreated animals, infarct size at eight weeks was smaller in a permanent ligation model, and ErbB2/Raf1 signalling was implicated, with the difference disappearing when ErbB2 was blocked [1] [6] | [Human RCT] | The overall comparison was null. The paper states that differences in infarcted areas between the treated group and placebo across all 96 participants were not significant. The positive finding is confined to the 43 participants who received a first dose within eight hours of PCI, which is a subgroup defined by treatment timing after an overall null result, and the abstract reports it before reporting the null. Three of the authors are employed by Beijing Northland Biotech, which develops the recombinant drug the trial tested. The article page shows no funding statement and no trial registration number, and the enrolment of 96 matches neither of the two completed registered trials from that sponsor, which enrolled 62 and 90 |
| Corneal healing in neurotrophic keratopathy | A multicentre, randomised, placebo-controlled, double-masked Phase 3 trial of 0.1% RGN-259 eye drops across 13 US sites, registered as NCT02600429 and published in 2022. Complete epithelial defect healing by day 29 was the primary endpoint. Ten participants received the drug and eight received placebo [2] [29] | [Human RCT] | The trial was terminated early, enrolling 18 of a planned 46 participants, which the authors attribute to slow recruitment in a rare condition. The primary endpoint was not met on the pre-specified analysis: 6 of 10 healed against 1 of 8, a difference of 47.5 percentage points, at p=0.0656. The paper also reports an alternative Chi-square analysis returning p=0.0400, and the pre-specified analysis is the one that missed. Secondary endpoints did reach significance, including complete healing at day 43 at p=0.0359 and reduced foreign body sensation at p at or below 0.0009. The study was funded by ReGenTree, two authors are ReGenTree employees and one is employed by the parent company. The authors themselves list the small sample, an older placebo group with larger lesions, and many sites recruiting few participants each |
| Dry eye disease | Three completed Phase 3 trials of RGN-259 ophthalmic solution sponsored by ReGenTree, the largest being ARISE-3, which enrolled 700 participants and completed in October 2021 [10] [11] [12] [27] | [Human RCT] | None of the three has posted results to ClinicalTrials.gov. What exists publicly is company announcement, which reports that one pre-specified secondary endpoint, ocular grittiness, reached significance at one and two weeks, and that the company considers efficacy demonstrated on the pooled data of all three trials. A pooled analysis offered in place of posted per-trial results is a weaker form of evidence than the phrase Phase 3 suggests, and this page has not independently checked the ARISE-1 and ARISE-2 outcomes |
| Skin wound healing | RegeneRx registered a Phase 2 programme in wound healing: pressure ulcers, venous stasis ulcers, and a further wound-healing study. Two of the three reached completed status on the registry [16] [17] [18] | [Human open-label] | No results are posted for any of them and no publication reporting their outcomes was located in the literature search behind this page. One of the three was terminated. Outcomes are therefore unknown rather than negative, and a trial count that includes them is counting registrations rather than findings |
| Muscle and tendon recovery | The claim most often attached to the injected product. The most direct published test came from a 2021 study that identified the protein as something human muscle releases during exercise and then treated mice with it [3] | [Animal] | The result was negative. In the authors' own summary, treatment of mice with the protein did not ameliorate the metabolic disruptions associated with diet-induced obesity, nor did it enhance muscle regeneration in vivo. The same study did find increased osteoblast proliferation and neurite outgrowth in laboratory systems. No registered trial of this protein or the fragment exists in tendon, muscle or ligament, in any species, at any phase |
| Hair growth | A 2015 mouse study using two genetic models: animals engineered to overexpress the protein in the epidermis, and global knockout animals. After depilation, regrowth was faster in the overexpressing animals and slower in the knockouts, with more hair shafts and clustered follicles in the overexpressing group [4] | [Animal] | Nothing was administered to any animal. The comparison is between animals bred to make more or less of a protein and normal animals, which tests whether the protein participates in hair biology, not whether giving it to something grows hair. A vendor page citing this study as evidence that applying or injecting the compound grows hair is citing a finding the study did not make |
| New blood vessel growth and reduced scarring | The mechanism most often given for the repair claims. Injected or transgenic thymosin beta-4 increased blood vessel growth in small and large animal models, and the protein and its degradation products showed antifibrotic effects in laboratory assays and in animal models of fibrosis unrelated to cardiac injury [6] [9] | [Animal] | Animal and laboratory work throughout. The 2016 review that summarises it attributes the variation in effect sizes between models to variable distribution of the protein and closes by asking for preclinical pharmacokinetic work and a reliable pharmacodynamic biomarker before clinical development. Neither had been published when the cardiac trial in claim one was run. Mechanism in an animal model does not establish an effect in people |
| Actin binding, the underlying activity | The best characterised property of the protein. It binds monomeric actin and acts as a sequestering peptide, which is the basis for its described effects on cell shape and cell migration [7] [8] [9] | [In-vitro] | This is cell biology rather than a therapeutic finding. Establishing that a protein holds on to actin in a test tube says nothing about what administering it to a person does, and the family's lack of a fixed structure until it meets a binding partner makes extrapolation from these assays harder rather than easier |
| Blood levels as a marker of anything | The protein is increasingly measured in plasma or serum as a candidate biomarker in cardiovascular, liver, infectious and autoimmune disease [5] | [In-vitro] | A 2018 review of this literature found substantial variability in reported healthy-control concentrations both within and between studies, and no standard protocol. It names three confounders that any such measurement inherits: platelets left in suspension after centrifugation, release from platelets activated outside the body, and assay specificity toward post-translational modifications. Any claim resting on a measured blood level carries this uncertainty with it |
Rolled up, that puts Thymosin beta-4 at evidence grade B Human data, endpoint missed . Human evidence for the marketed use has read out, and it did not separate from control: the one randomized trial that tested it missed the primary endpoint. The grade describes how much and how good the research is, not which way it came out, so a compound that has been tested and beaten grades above one nobody has tested at all. A grade describes the quality of the research, not whether something works and not whether anyone should use it. The derivation is published.
How Thymosin beta-4 is thought to work
Two things are worth separating before reading any mechanism account of this protein. The first is that the activity everything rests on, holding on to actin, is well established and is a housekeeping function rather than a therapeutic one. The second is that a great deal of the described mechanism belongs either to laboratory systems or to a four residue fragment the body cuts off the end of it.
1. Sequestering actin, holding on to the loose building blocks cells use to assemble their internal scaffolding (established)
Actin exists in cells in two forms: free single units, and long filaments assembled from them. Thymosin beta-4 binds the free units and holds them out of the filament pool, which is what a sequestering peptide does. This is the activity every other described effect is built on, and it is not in dispute.
What it does not do is explain a clinical effect. Every cell in the body runs this system continuously, and adding more of a protein that participates in it is not the same as directing a repair process. The translational distance between this assay and a healed tendon is the whole question, and no published work closes it. [In-vitro] [7] [8] [9]
2. ErbB2 signalling in the heart, switching on a growth signal inside heart muscle cells that keeps them from dying after oxygen returns (shown in mice, with the pathway confirmed by blocking it)
The 2025 cardiac study is the most mechanistically complete work on this protein. RNA sequencing of mouse heart tissue after ischemia/reperfusion showed the protein modulated ErbB signalling. In three cardiomyocyte systems subjected to oxygen deprivation and restoration, it activated ErbB2/Raf1, reduced cell death and suppressed the pro-apoptotic protein Bad.
The step that makes this more than an association is the inhibition experiment: blocking ErbB2 removed the protective effect on cardiac function and remodelling in the mice. That is the right way to test a proposed mechanism, and it was done. It remains a mechanism established in mice, and the human trial in the same paper did not meet its overall comparison. [Animal] [1]
3. The Ac-SDKP fragment, which is a different molecule, a four-piece offcut the body snips off the end, which has its own separate research history (established that the fragment is produced, separate literature for what it does)
Prolyl oligopeptidase cuts Ac-SDKP, a four residue peptide, off the N-terminus of thymosin beta-4. Ac-SDKP has been studied in its own right, particularly in fibrosis, and there is a body of work on the axis connecting the two.
This matters when reading claims. An antifibrotic result belonging to Ac-SDKP is sometimes presented as a property of the parent protein. The relationship is real, and the two are still separate molecules with separate evidence, in the same way that the parent and TB-500 are. [In-vitro] [8]
What we do not know
How much of an administered amount reaches the tissue it is meant to act on. The 2016 cardioprotection review attributes the variation in animal effect sizes to variable distribution and asks for the pharmacokinetic work to be done.
Whether a pharmacodynamic biomarker exists that would show the protein is doing anything in a given person. The same review names its absence as an obstacle to clinical development.
What the two completed Chinese Phase 2 cardiac trials found. Neither has posted results and no publication reporting either could be located.
What this evidence can and cannot show
These results come from Mouse, rat and cell culture throughout, with one signalling pathway confirmed by inhibition in mice. in Ischemia/reperfusion and permanent ligation surgery in mice; hypoxia/reoxygenation in three cardiomyocyte lines; depilation in transgenic and knockout mice., not from people. An animal model is a deliberate simplification: the injury is created on purpose, the animal is young and healthy, the dose is scaled to body weight in a way that does not translate directly, and the outcome is measured at a fixed point rather than lived with. Cell and tissue work is a further step removed, because the concentrations that produce an effect in a dish are often far above anything a body reaches. Mechanism is a reason to run a trial. It is not a substitute for one, and compounds that looked mechanistically convincing have failed in people many times.
Has Thymosin beta-4 been tested in humans?
Every human record for this protein is listed below, pulled from the ClinicalTrials.gov API on 23 August 2026 and read from the returned records. There are nineteen: eighteen genuine registrations of this protein, and one record naming TB-500 whose own registered summary opens by saying it is a fictional example.
Counting them takes more than one search. A query on the molecule name alone returns eighteen records and misses the Phase 3 whose paper is the best evidence on this page, because that trial is filed under the drug name RGN-259 rather than under thymosin beta-4. The figures here come from searching the molecule and every development code together, then removing six unrelated records that a free-text search pulled in.
The table is grouped by sponsor, because the programmes are separate and are often counted together.
| Study | People | What was done | Result | Evidence level |
|---|---|---|---|---|
| ReGenTree, ophthalmic (7 registrations) | Five Phase 3 registrations | RGN-259 eye drops in dry eye and neurotrophic keratopathy | Three completed in dry eye with no posted results, one recruiting, one terminated. The terminated trial is the only one with a published paper | [Human RCT] |
| RegeneRx, wound healing (3 registrations) | Not reported | Thymosin beta-4 in pressure ulcers, venous stasis ulcers and wound healing | Two completed with no posted results, one terminated. No publication located | [Human open-label] |
| RegeneRx, injected systemic (2 registrations) | None | A Phase 1 intravenous study and a Phase 2 injectable study | Both withdrawn before enrolling anyone | [Human RCT] |
| Beijing Northland, healthy volunteers (2 registrations) | 30 in the Phase 1b | Single intravenous doses of recombinant NL005 | Both completed, neither has posted results | [Human RCT] |
| Beijing Northland, cardiac (3 registrations) | 62 and 90 completed, 189 planned | Recombinant NL005 in acute myocardial infarction | Two completed with no posted results. The third is not yet recruiting and measures infarct size on cardiac MRI at 90 days | [Human RCT] |
| Michigan Cornea Consultants (1 registration) | Not reported | Investigator-run comparative eye drop study | Completed | [Human RCT] |
| Hudson Biotech (1 registration) | 80 estimated | The only registration naming TB-500 | Its registered summary states that it is a fictional study and an example of a ClinicalTrials.gov-style record | [Anecdote] |
Why we are not calling this proof
A registration is a filing, not a finding. Exactly one of the nineteen records above has a published paper reporting its outcome, and that trial was terminated early. Two were withdrawn before enrolling anyone. A trial count for this protein is therefore a count of filings, not a measure of what has been established.
The strongest evidence sits in the eye, in a formulation that is not sold as a research chemical. The injected route that is sold has one published randomised trial, reported in the claims table, whose overall comparison was null.
Benefits: what the research shows
Each heading in the claims table above is a claim made for this protein, not a finding. What follows here is the shape of the evidence as a whole, which is easier to see once the claims are separated from it.
The honest bottom line on benefits
The pattern across every claim is the same. The laboratory and animal work is extensive and in places genuinely careful, including one mechanism confirmed by blocking it. The human work is thin, concentrated in the eye, and where it exists it has either not been published, not met its primary endpoint, or not reached significance overall.
The two published human trials are the two that matter, and both are reported in the claims table with their numbers. Read together they describe a protein with a plausible mechanism that has not yet demonstrated a clinical effect in a trial designed to detect one.
How long Thymosin beta-4 stays in the body
There is very little to report here, and the gap is itself informative. The two US registrations that would have produced human pharmacokinetic data for an injected form, a Phase 1 intravenous study and a Phase 2 injectable study, were both withdrawn before enrolling anyone. The Chinese Phase 1a and Phase 1b studies in healthy volunteers list pharmacokinetics among their objectives and both completed, and neither has posted results.
Measuring the protein at all is harder than it looks. A 2018 review of the clinical measurement literature found substantial variability in reported concentrations in healthy controls both within and between studies, with no standardised protocol, and identified three sources of error that any measurement inherits: platelets remaining in suspension after centrifugation, release from platelets activated after the sample is drawn, and assay specificity toward post-translational modifications [5].
The practical consequence is that no half-life, no exposure figure and no dosing interval for this protein in a person can be quoted from published human work, because that work has not been published. Anything presented as one has come from somewhere else.
No published human pharmacokinetic data for the injected route was located. [In-vitro] [5] [6]
What is documented about dosing
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
Commonly cited protocols (extrapolated, not validated)
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
| Study | What was given | Frequency | Duration | Notes |
|---|---|---|---|---|
| NCT05485818, Phase 2 cardiac | 0.25, 0.5 and 2.0 micrograms per kilogram as separate arms | Not reported in the registry record | Not reported in the registry record | 62 participants, acute myocardial infarction, results not posted |
| NCT05984134, Phase 2 cardiac | 0.5 and 1.0 micrograms per kilogram against placebo | Not reported in the registry record | Not reported in the registry record | 90 participants, acute myocardial infarction, results not posted |
| NCT04555850, Phase 1b | Single intravenous doses of 0.5, 2.0 and 5.0 micrograms per kilogram | Single dose | Single dose | 30 healthy volunteers, results not posted |
| RGN-259 Phase 3 programme | 0.1% ophthalmic solution | Not reported here | Not reported here | The concentration used across the published and registered eye trials |
Commonly cited protocols (extrapolated, not validated) for the injected research-chemical market are not derived from any of the figures above. They circulate for TB-500, which is a different and much smaller molecule, and the amounts discussed there are not related to the microgram-per-kilogram arms of the registered trials by any published conversion.
Three things prevent the trial numbers above from becoming a dose for anything else. They belong to a specific recombinant preparation rather than to a research chemical of unverified identity. They were selected for a single acute condition under monitoring in hospital, immediately after a cardiac procedure. And none of the trials that used them has posted a result, so it is not established that any of the arms did anything, or that one was better than another.
The ophthalmic concentration is on a firmer footing because it comes from a published trial, and it is a concentration in an eye drop rather than an amount given to a body.
Nothing here is a dosing recommendation. Statements about dosing reflect community and research reports only.
Main routes people compare, and what each source class actually reported, are set out on the documented protocols page.
Reported effects and what has been measured
What the published trials recorded
The Phase 3 neurotrophic keratopathy trial reported 16 adverse events across 7 of its 18 participants, 11 in the treated group and 5 on placebo, of which one was assessed as treatment related. One serious adverse event occurred and was non-ocular and judged unrelated. No participant withdrew because of an adverse event, and the paper describes most events as ocular and mild.
That is 18 people, in an eye, over weeks. It is a real safety observation and it is a very small one, and it does not describe what happens when a preparation of uncertain identity is used over months. [Human RCT] [2]
What has not been characterised
Long-term exposure in humans has not been characterised in any published study, by any route. The 96 participant cardiac trial is the largest published human exposure to the injected form and it followed participants to 90 days.
The two US registrations that would have produced systematic human safety data for an injected form were both withdrawn before enrolling anyone, and the two completed Chinese cardiac trials have not posted their safety results. [Human RCT] [1]
The growth-factor question
The protein is classified by WADA as a prohibited growth factor, and the laboratory record gives a reason for taking that classification seriously rather than treating it as a formality: it increased osteoblast proliferation and neurite outgrowth in the 2021 exerkine study, and it promotes new blood vessel growth in animal models.
Anything that promotes vessel growth and cell proliferation raises a question wherever unwanted tissue might also be growing. This is a question the published record does not answer, in either direction, and no adequately powered human study has looked. [Animal] [3] [6]
What has been measured about Thymosin beta-4, and what has never been studied
Talk to a licensed clinician about anything concerning your health.
Sourcing and quality
What a credible product should show
Nothing sold as a research chemical under this name has been through the identity verification that the recombinant preparations in the registered trials went through. NL005 and RGN-259 are manufactured products with regulatory files behind them; a vial bought online is not the same thing because it carries the same name.
The identity problem here is larger than usual because two molecules share one name in the market. A product labelled with either name may contain the 43 residue protein, the seven residue fragment, or something else, and the two are distinguishable only by analysis.
Red flags
A trial count offered without naming which molecule the trials tested. Seventeen registrations exist for the protein and one for the fragment, and that one declares itself fictional.
A Phase 3 cited as a success without the numbers. The published Phase 3 stopped early at 18 of 46 planned participants and missed its primary endpoint.
A cardiac result quoted as significant without the sentence that follows it in the same abstract, which reports that the overall comparison was not significant.
Dosing figures for the injected research-chemical market presented as though they came from the registered trials. No published conversion links them.
Will it show on a drug test?
Named on the WADA 2026 Prohibited List under S2.3 as Thymosin-ß4 and its derivatives e.g. TB-500. One entry covers both molecules, so the distinction that runs through this page does not affect a tested athlete.
Prohibited at all times, in and out of competition. The class carries no permitted window.
Non-Specified, which is the category without the reduced-sanction route that a Specified Substance can qualify for.
Storage
No storage guidance is given here. Storage conditions belong to a specific manufactured formulation, and the preparations in the registered trials are not what is sold as a research chemical.
Regulatory status, as of 23 August 2026
| Body | Position | Date | Document |
|---|---|---|---|
| No agency | Not an approved drug in any indication | Read 23 August 2026 | ClinicalTrials.gov and the sponsor programmes |
| FDA | RGN-259 holds orphan drug and fast track designations for neurotrophic keratopathy. Both are development-stage designations rather than approvals | Programme status as of 23 August 2026 | Sponsor programme records |
| WADA | Named under S2.3, Growth Factors and Growth Factor Modulators, as Thymosin-ß4 and its derivatives e.g. TB-500. Prohibited at all times. Non-Specified Substance | 2026 list, read 23 August 2026 | WADA 2026 Prohibited List |
| FDA, 503A Bulks List | The fragment's position is covered on the TB-500 page. This site has not separately confirmed the parent protein's own position and does not state one here | Open item as of 23 August 2026 | Recorded as unverified rather than asserted |
Two designations appear frequently in coverage of this protein and neither is an approval. Orphan drug designation and fast track designation are granted during development to encourage and speed work on a candidate. They say something about the condition being rare and the need being unmet, and nothing about whether the drug does anything.
The anti-doping entry is the clearest regulatory fact on this page. WADA names the protein and gives TB-500 as an example of a derivative in the same line, and the class also closes with a catch-all covering other growth factors affecting muscle, tendon or ligament protein synthesis, vascularisation, energy utilisation, regenerative capacity or fibre type switching, so a renamed analogue is covered too.
Regulatory status is checked on review and this section is dated accordingly. It is a record of agency action, not evidence about an effect, and carries no evidence tier for that reason.
Thymosin beta-4 compared with other regenerative peptides
| Compound | Evidence grade | What the human record covers | Read more |
|---|---|---|---|
| TB-500 | Graded on its own page | One registration, which declares itself fictional. No published human study of the fragment in any species by any route | /peptides/tb-500/ |
| Thymosin alpha-1 | Graded on its own page | An unrelated molecule from a different precursor that shares a family name | /peptides/difference/thymosin-alpha-1-vs-thymosin-beta-4/ |
| Ac-SDKP | Not covered as a compound on this site | A four residue fragment this protein is cut down to by prolyl oligopeptidase, with a separate fibrosis literature that is sometimes attributed back to the parent | Described in the mechanism section above |
The comparisons that matter for this protein are all identity questions rather than efficacy questions, and all three run the same way: a smaller molecule derived from or named after this one, carrying a separate evidence base that gets merged with this one in coverage.
The fragment comparison is the consequential one, because that is the molecule sold under this protein's name and its trial count.
What Thymosin beta-4 typically costs
Frequently asked questions
Is thymosin beta-4 the same thing as TB-500?
No. Thymosin beta-4 is a 43 amino acid protein the body makes. TB-500 is seven of those amino acids, residues 17 to 23, with an added acetyl group. They are separate substances with separate published records, and the comparison page covers the split in full.
How many human trials have there been?
Nineteen registrations exist, of which eighteen are genuine registrations of this protein and one is the fictional TB-500 record. Only one of them has a published paper reporting its outcome, and that trial was terminated early. Two were withdrawn before enrolling anyone. A separate randomised cardiac trial is published but could not be matched to any registration.
Did the heart attack trial work?
The trial did not meet its overall comparison. Across all 96 participants the difference in infarct size between the treated group and placebo was not significant. A group of 43 who received a first dose within eight hours did show a difference, which is a finding to test in a trial designed for it rather than a conclusion.
Did the Phase 3 eye trial succeed?
Not on its pre-specified analysis. The trial was stopped early with 18 of a planned 46 participants and its primary endpoint, complete healing by day 29, returned p=0.0656. Several secondary endpoints did reach significance, and the paper also reports an alternative analysis of the primary endpoint returning p=0.0400.
Is there evidence it helps muscle or tendon recovery?
No human evidence, and the most direct animal test was negative. A 2021 study that identified this protein as something human muscle releases during exercise reported that treating mice with it did not enhance muscle regeneration. No registered trial exists in tendon, muscle or ligament.
Does it grow hair?
The mouse result behind that claim used animals genetically engineered to overexpress the protein and knockout animals, not animals given the protein. It tests whether the protein participates in hair biology, which is a different question from whether administering it does anything.
Is it approved anywhere?
No. It is not an approved drug in any indication. The ophthalmic programme holds orphan drug and fast track designations, which are development-stage designations granted to encourage work on a candidate and are not approvals.
Is it banned in sport?
Yes. The WADA 2026 Prohibited List names it under S2.3 as Thymosin-ß4 and its derivatives e.g. TB-500. It is prohibited at all times, in and out of competition, and it is a non-Specified Substance, which is the category without the reduced-sanction route.
Does the ban treat TB-500 differently?
No. One entry covers the protein and its derivatives and gives TB-500 as the example, so the difference between the two molecules makes no difference to an anti-doping outcome.
Why is the eye evidence stronger than the injected evidence?
Because that is where the development money went. Three Phase 3 trials have been run on an eye drop formulation. The two US registrations for an injected form were both withdrawn before enrolling anyone, and the completed injected trials elsewhere have not posted results.
What is Ac-SDKP?
A four amino acid peptide that prolyl oligopeptidase cuts off the N-terminus of thymosin beta-4. It has a separate research literature, particularly in fibrosis, and findings belonging to it are sometimes attributed back to the parent protein.
Can blood levels of it tell me anything?
Not reliably at present. A 2018 review of the measurement literature found substantial variability in healthy-control concentrations within and between studies, no standardised protocol, and three specific confounders affecting the assays.
What is still unknown?
What the two completed Chinese Phase 2 cardiac trials found, since neither has posted results. Whether an administered amount reaches the tissue it is meant to act on, which the pharmacokinetic work to answer has not been published. And what long-term exposure in humans does, by any route.
References
- Zhang Y, Dong Q, Bian X, Qiao Z, Cui C, Yang N, Liu J, Fu R, Zhang J, Jia L, Wu C, Guo J, Lin W, Wang J, Fan J, Li Y, Liu F, Yang B, Jia X, Gao C, Bai M, He Y, Han C, Yin D, Dou K. Recombinant human thymosin beta 4 improves ischemic cardiac dysfunction in mice and patients with acute ST-segment elevation myocardial infarction after reperfusion. Cardiovasc Res. 2025. PMID 41229390 DOI 10.1093/cvr/cvaf223
- Sosne G, Kleinman HK, Springs C, Gross RH, Sung J, Kang S. 0.1% RGN-259 (Thymosin ß4) 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. PMID 36613994 DOI 10.3390/ijms24010554
- Gonzalez-Franquesa A, Stocks B, Borg ML, Kuefner M, Dalbram E, Nielsen TS, Agrawal A, Pankratova S, Chibalin AV, Karlsson HKR, Gheibi S, Björnholm M, Jørgensen NR, Clemmensen C, Hostrup M, Treebak JT, Krook A, Zierath JR, Deshmukh AS. Discovery of thymosin β4 as a human exerkine and growth factor. Am J Physiol Cell Physiol. 2021. PMID 34495765 DOI 10.1152/ajpcell.00263.2021
- Gao X, Liang H, Hou F, Zhang Z, Nuo M, Guo X, Liu D. Thymosin Beta-4 Induces Mouse Hair Growth. PLoS One. 2015. PMID 26083021
- Tan WKY, Purnamawati K, Pakkiri LS, Tan SH, Yang X, Chan MY, Drum CL. Sources of variability in quantifying circulating thymosin beta-4: literature review and recommendations. Expert Opin Biol Ther. 2018. PMID 29502471 DOI 10.1080/14712598.2018.1448382
- Pipes GT, Yang J. Cardioprotection by Thymosin Beta 4. Vitam Horm. 2016. PMID 27450736 DOI 10.1016/bs.vh.2016.04.004
- Hoch K, Volk DE. Structures of Thymosin Proteins. Vitam Horm. 2016. PMID 27450728 DOI 10.1016/bs.vh.2016.04.009
- Hannappel E. Thymosin beta4 and its posttranslational modifications. Ann N Y Acad Sci. 2010. PMID 20536447 DOI 10.1111/j.1749-6632.2010.05485.x
- 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. PMID 22074294 DOI 10.1517/14712598.2012.634793
- Sosne G. Thymosin beta 4 and the eye: the journey from bench to bedside. Expert Opin Biol Ther. 2018. PMID 30063853 DOI 10.1080/14712598.2018.1486818 PubMed types this as a Personal Narrative, and the author is also first author on the ReGenTree-funded Phase 3 cited above. Used here for programme history only.
- ReGenTree, LLC. Assessment of the Safety and Efficacy of RGN-259 Ophthalmic Solutions for Dry Eye Syndrome: ARISE-3. Phase 3, 700 participants actual, completed October 2021. Read through the ClinicalTrials.gov API on 23 August 2026: the record carries no results section. ClinicalTrials.gov. 2019. NCT03937882
- ReGenTree, LLC. Assessment of the Safety and Efficacy of RGN-259 Ophthalmic Solutions for Dry Eye Syndrome: ARISE-2. Phase 2/3, completed. ClinicalTrials.gov. 2016. NCT02974907
- ReGenTree, LLC. Assessment of the Safety and Efficacy of 0.1% RGN-259 Ophthalmic Solution. Phase 3, recruiting as of 23 August 2026. ClinicalTrials.gov. 2022. NCT05555589
- RegeneRx Biopharmaceuticals. A Phase 1 Safety Study of the Intravenous Administration of Thymosin Beta 4. Withdrawn before enrolling any participant. ClinicalTrials.gov. 2009. NCT00743769
- RegeneRx Biopharmaceuticals. A Study of the Safety and Efficacy of Injectable Thymosin Beta 4. Phase 2, withdrawn before enrolling any participant. ClinicalTrials.gov. 2011. NCT01311518
- RegeneRx Biopharmaceuticals. Study of Thymosin Beta 4 in Patients With Pressure Ulcers. Phase 2, completed, no posted results. ClinicalTrials.gov. 2006. NCT00382174
- RegeneRx Biopharmaceuticals. Study of Thymosin Beta 4 in Patients With Venous Stasis Ulcers. Phase 2, completed, no posted results. ClinicalTrials.gov. 2009. NCT00832091
- RegeneRx Biopharmaceuticals. A Phase 2 Study on Effect of Thymosin Beta 4 on Wound Healing. Terminated. ClinicalTrials.gov. 2006. NCT00311766
- Beijing Northland Biotech. Co., Ltd. Safety and Efficacy Study of Thymosin Beta 4 in Patients With Acute Myocardial Infarction. Phase 2, 62 participants actual, completed, no posted results. Dose arms of 0.25, 0.5 and 2.0 micrograms per kilogram. ClinicalTrials.gov. 2022. NCT05485818
- Beijing Northland Biotech. Co., Ltd. Efficacy and Safety Study of Thymosin Beta 4 in Patients With Acute Myocardial Infarction. Phase 2, 90 participants actual, completed, no posted results. Dose arms of 0.5 and 1.0 micrograms per kilogram against placebo. ClinicalTrials.gov. 2023. NCT05984134
- Beijing Northland Biotech. Co., Ltd. A Phase 1b Study of Thymosin Beta 4 in Healthy Volunteers. 30 volunteers, completed, no posted results. Single intravenous doses of 0.5, 2.0 and 5.0 micrograms per kilogram. ClinicalTrials.gov. 2020. NCT04555850
- Beijing Northland Biotech. Co., Ltd. A Phase 1a Study of Thymosin Beta 4 in Healthy Volunteers. Completed, no posted results. ClinicalTrials.gov. 2020. NCT04555824
- Beijing Northland Biotech. Co., Ltd. Recombinant Human Thymosin Beta 4 for Injection (NL005) for Acute Myocardial Infarction. Phase 2c, 189 participants estimated, not yet recruiting as of 23 August 2026. Primary outcome is infarct size on cardiac magnetic resonance at 90 days. ClinicalTrials.gov. 2026. NCT07586865
- ReGenTree, LLC. Safety and Efficacy of Thymosin Beta 4 Ophthalmic Solution in Patients With Dry Eye. Phase 2, completed. ClinicalTrials.gov. 2011. NCT01387347
- Michigan Cornea Consultants. Comparative Study of Thymosin Beta 4 Eye Drops vs. Vehicle. Phase 2, completed. ClinicalTrials.gov. 2011. NCT01393132
- ReGenTree, LLC. A Phase 2 Study of the Safety and Efficacy of Thymosin Beta 4. Terminated. ClinicalTrials.gov. 2008. NCT00598871
- ReGenTree, LLC. Assessment of the Safety and Efficacy of RGN-259 Ophthalmic Solutions for Dry Eye Syndrome. Phase 2/3, completed. ClinicalTrials.gov. 2015. NCT02597803
- Hudson Biotech. TB-500 (Thymosin Beta 4 17-23 Fragment) in Adults With Stable Atherosclerotic Cardiovascular Disease. Read through the ClinicalTrials.gov API on 23 August 2026: the registered brief summary opens by stating that it is a fictional study and an example of a ClinicalTrials.gov-style record. It is the only registration naming TB-500. ClinicalTrials.gov. 2026. NCT07487363
- ReGenTree, LLC. Assessment of the Safety and Efficacy Study of RGN-259 Ophthalmic Solutions for Neurotrophic Keratopathy: SEER-1. Phase 3, terminated, 18 participants actual against 46 planned. This is the registration for the published trial cited above, and it is filed under the drug name RGN-259, which is why a search on the molecule name does not return it. ClinicalTrials.gov. 2015. NCT02600429
- World Anti-Doping Agency. The 2026 Prohibited List. Read in full on 23 August 2026. Section S2.3, Growth Factors and Growth Factor Modulators, names Thymosin-ß4 and its derivatives e.g. TB-500. The S2 class heading states that the class is prohibited at all times, in and out of competition, and that all substances in it are non-Specified. World Anti-Doping Agency. 2026. WADA 2026 Prohibited List