TB-500
The fragment that is sold on its parent molecule's evidence
TB-500 is a seven-amino-acid fragment of thymosin β4, a 43-residue protein that has been through Phase 2 human trials for venous ulcers and Phase 3 for eye disease. Almost everything published under the name ‘TB-500’ is really about the parent. That gap between the two is the most important thing on this page.
What is it?
Thymosin β4 is one of the most abundant proteins inside mammalian cells. It is a 43-amino-acid peptide whose main job is holding a reserve pool of actin monomers — the raw material cells use to build and dismantle their internal scaffolding every time they move, divide, or close a wound. Platelets dump it at injury sites. Macrophages release it. It has been studied for four decades, it has a substantial clinical file, and it is the molecule behind essentially every claim made for TB-500.
TB-500 is not that molecule. It is LKKTETQ: seven residues lifted out of the middle of thymosin β4, the stretch that does the actin binding. The logic behind the fragment is reasonable on its face — isolate the active motif, keep the function, lose the size and the cost. Whether that logic survives contact with a living organism is a separate question, and it is one the published literature has not answered. There is no pharmacokinetic profile for LKKTETQ in humans. There is no dose-finding study. There is no trial.
This matters more than it might sound. Thymosin β4's clinical results are not hypothetical: a randomised, placebo-controlled study gave healthy volunteers intravenous doses up to 1,260 mg daily for two weeks and found adverse events infrequent and mild; a double-blind dose-escalation study in Italy and Poland tested it topically on venous ulcers; Phase 3 programmes have run in dry eye and neurotrophic keratopathy. Every one of those results belongs to the 43-residue protein. Reading them as evidence for a seven-residue fragment is the substitution this entry exists to make visible.
Where TB-500 does have a track record is veterinary — particularly in racehorses, where it has been used and, notably, banned. That history is worth knowing precisely because it is not a clinical file. It is a pattern of use that ran ahead of the evidence, in a species where the incentive to accelerate healing is measured in prize money. The human peptide community has largely reproduced that pattern, generally stacking TB-500 with BPC-157 for soft-tissue injury, on protocols that no trial has tested.
Mechanism of Action
The mechanism below is thymosin β4's. It is well characterised, it is genuinely interesting, and the honest position is that the seven-residue fragment is assumed rather than shown to reproduce it. LKKTETQ carries the actin-binding motif; a protein is more than its motif, and the parts of thymosin β4 that TB-500 leaves behind are the parts that make it a folded molecule with a measurable half-life.
This is the full protein's mechanism. TB-500 is sold as a fragment of it, and no study shows the fragment reproduces any step.
Each step is tagged with where it was shown. A dashed red arrow marks a link the evidence does not establish.
The pathway in words
- Thymosin beta-4. The protein behind TB-500: released by platelets, macrophages and other cells after injury, where it limits further damage. Shown in: review. Source: PubMed 22074294.
- Holds actin monomers. Binds single actin molecules and stops them joining filaments, acting mainly as a monomer-sequestering protein. Shown in: lab. Source: PubMed 8416954.
- Cells migrate and survive. With PINCH and integrin-linked kinase it activates Akt, driving migration of heart and endothelial cells and the survival of heart-muscle cells in culture. Shown in: cells. Source: PubMed 17600280.
- Heart repair in mice. After a coronary artery was tied off, treatment raised ILK and Akt activity, improved early heart-muscle survival and improved cardiac function. Shown in: animals. Source: PubMed 17600280.
- the TB-500 fragment never tested. In people. The whole protein was well tolerated intravenously in 40 healthy volunteers and has been tested on venous ulcers. The fragment sold as TB-500 has no human study. Shown in: people. Source: PubMed 20536472, 17495250.
G-actin sequestration
Thymosin β4 is the major G-actin-sequestering molecule in mammalian cells: it binds actin monomers and holds them out of polymerisation, creating a buffered reserve that a cell can draw on when it needs to build filaments fast. Work in J Biol Chem established this by expressing thymosin β4 and its homolog β10 in bacteria and characterising both against skeletal muscle actin directly. This is the function LKKTETQ is the motif for.
Cell migration and re-epithelialisation
Actin dynamics are how cells move. By modulating the monomer pool, thymosin β4 promotes the migration of keratinocytes, endothelial cells, and stem or progenitor populations into damaged tissue — which is the step that closes a wound rather than merely stabilising it.
Angiogenesis
Released by platelets and macrophages after injury, thymosin β4 promotes blood vessel formation. In cardiac ischaemia models this is part of why it preserves function: injected or transgenic thymosin β4 increases vessel growth in both small and large animals, consistent with converting hibernating myocardium back to an actively contractile state.
Anti-inflammatory and antifibrotic activity
Thymosin β4 and its degradation products dampen inflammatory signalling and show antifibrotic effects in vitro and in vivo — relevant to why a repair peptide might improve outcome without simply accelerating scar formation. Whether a seven-residue fragment retains this is untested.
Published Research
Read the type chips on these cards carefully. Every human study here enrolled patients or volunteers on thymosin β4 — the full 43-residue protein — not on TB-500. We have not found a single published human trial of LKKTETQ, and we would list it here if it existed. The parent's file is the best evidence available and it is not the same claim.
Intravenous thymosin β4 in healthy volunteers — randomised, placebo-controlled
Four cohorts of ten healthy subjects received single ascending intravenous doses of synthetic thymosin β4 — 42, 140, 420 or 1,260 mg — then, after safety review, the same dose daily for 14 days. Adverse events were infrequent and mild. This is the safety anchor the whole field cites, and it is an anchor for the parent protein at doses roughly three orders of magnitude above what community TB-500 protocols use.
Topical thymosin β4 for venous ulcers — European dose-escalation trial
A double-blind, placebo-controlled dose-escalation study across ten sites in Italy and Poland, randomising patients 3:1 to topical thymosin β4 or placebo in sequential dose groups. Venous ulcers are a hard endpoint with a standard of care to beat, which makes this one of the more meaningful tests the molecule has faced.
Thymosin β4 and the eye: bench to bedside
Sosne's account of how thymosin β4 reached Phase 3 trials for dry eye and neurotrophic keratopathy. Worth reading for a specific reason: this is the indication where the parent molecule went furthest in humans, and it is not a musculoskeletal one. The clinical momentum behind thymosin β4 is largely ocular; the marketing behind TB-500 is almost entirely about tendons.
Thymosin β4 as a multi-functional regenerative peptide
Goldstein's synthesis of the repair biology: after injury, thymosin β4 is released by platelets, macrophages and other cell types, binds actin, and promotes the mobilisation and differentiation of stem and progenitor cells that build new vessels and regenerate tissue. The clearest statement of the case for the parent molecule.
Thymosin β4: structure, function and clinical applications
Crockford's survey of the properties supporting clinical development — cell migration, blood vessel formation, cell survival, stem cell differentiation, cytokine and chemokine modulation. Useful as a map of which claims have mechanistic support and which are extrapolation.
Thymosin β4 in heart injury: a multi-faceted repair protein
Reviews thymosin β4 as a pleiotropic actin-sequestering protein in cardiac remodelling and ulcerated tissue repair — and does not skip its involvement in tumorigenesis, which is the reason the contraindication list below leads with active malignancy rather than burying it.
Cardioprotection by thymosin β4
Treatment reduces infarct volume and preserves cardiac function in preclinical models of ischaemic injury — partly through smaller infarcts, partly through distinct antifibrotic and proangiogenic activity. Injected and transgenic thymosin β4 both increase vessel growth in small and large animals. Preclinical, and explicitly so.
Thymosin β4 as a restorative therapy for neurological injury
Given 24 hours or more after injury — i.e. on a timeline a real patient could meet — thymosin β4 enhanced angiogenesis, neurogenesis, axonal outgrowth and oligodendrogenesis, improving functional and behavioural outcomes across a range of models. The authors propose oligodendrogenesis as the common link. Animal work, but unusually well specified about timing.
Thymosin β4 and β10 are both actin monomer sequestering proteins
The foundational biochemistry. Both β-thymosins were expressed in bacteria and characterised against skeletal muscle actin; equilibrium sedimentation showed thymosin β4 behaves as a monomer in solution and binds actin monomers directly. Everything downstream on this page rests on this result.
What people say, and what was measured
TB-500 is sold as a healing peptide and named after thymosin beta-4, the natural protein it is derived from. The distinction matters for every claim below: the human trials were run on thymosin beta-4 itself, by a company developing it as a drug, not on the product sold as TB-500.
It speeds recovery from injury, and is stacked with BPC-157 as the Wolverine protocol.
Heard in: Forbes Health, The FDA Eased Restrictions On Six Peptides: What Consumers Should Know, which describes the "Wolverine Stack" of TB-500 and BPC-157 (read October 1, 2026). Source
No trial has tested recovery from injury in people. The human work on thymosin beta-4 is a safety study in 40 healthy volunteers and a trial in venous leg ulcers; neither measured athletic or soft-tissue recovery. The repair claims rest on reviews of laboratory and animal work. PMID: 20536472, 17495250, 22074294
Never tested in peopleIt is well tolerated even at high doses.
Heard in: Grey Peptides listing review, October 1, 2026: listings present TB-500 as having no significant side effects. Sellers are not named.
This one has real support, for the parent molecule. Forty healthy volunteers received intravenous thymosin beta-4 at 42 to 1,260 mg, as a single dose and then daily for 14 days. Adverse events were infrequent and mild or moderate, with no dose-limiting toxicity. That is a pharmaceutical-grade product given intravenously under supervision, not a vial of research-chemical TB-500. PMID: 20536472
Tested in people; supportedIt repairs the heart after damage.
Heard in: Vitamins and Hormones, Cardioprotection by Thymosin Beta 4, a review of the cardiac repair literature that the claim draws on (read October 1, 2026). Source
Thymosin beta-4 protected the heart after induced heart attack in mice, and reviews have built a case for developing it in cardiac ischaemia. The safety study in healthy volunteers was run with that development in mind. No trial has given it to people with heart damage. PMID: 17600280, 27450736, 20536472
Shown in animals or cells onlyIt is a legal alternative to banned substances because it is a natural peptide.
Heard in: WADA 2026 Prohibited List, section S2.3, which names "Thymosin-ß4 and its derivatives e.g. TB-500" (read October 1, 2026). Source
WADA names TB-500 by name under S2.3, so it is prohibited at all times in tested sport. Thymosin beta-4 is a natural protein, first described as an actin-binding protein, but being natural has never been a defence: testing looks for the molecule. PMID: 8416954
Contradicted by the ruleEach claim is quoted from where it is said, never from a seller, and checked as of October 1, 2026 against the studies listed below.
Dosing Data
There is no established dose for TB-500, because establishing a dose requires a trial and no trial has been run. The figures below are what circulates in community protocols and what is reported in the grey literature. They are documented here because people use them and deserve to see them written down accurately, next to the fact that nothing validates them.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
→ Full TB-500 dosage guide — why the community numbers look the way they do, and what the parent molecule's trials actually dosed
→ Blend & Stack Calculator — TB-500 is also sold in multi-peptide vials; the calculator shows what each draw delivers of every component; our blends and stacks hub sets out what each mix contains and what has been studied.
Side Effects & Contraindications
Reported Side Effects
There is no adverse-event table for TB-500, because that is what a trial produces. What follows is drawn from the parent molecule's human safety data plus consistently reported community experience. Treat the second category as what it is: uncontrolled self-report with no denominator.
Contraindications & Cautions
The angiogenesis question is the one that deserves weight rather than a footnote. A molecule whose proposed benefit is building new blood vessels and mobilising progenitor cells is a molecule with an obvious theoretical problem in the presence of a tumour, and thymosin β4's own literature discusses its involvement in tumorigenesis.
Legal Status
TB-500 is not approved as a medicine anywhere. It is sold as a research chemical, which is a category defined by what it is not licensed for rather than by any assessment of what it does. The sporting position is more clear-cut than the pharmaceutical one.
Frequently Asked Questions
?Is TB-500 the same thing as thymosin β4?
No, and this is the single most important distinction on the page. Thymosin β4 is a 43-amino-acid protein with human trial data. TB-500 is LKKTETQ — seven residues from its actin-binding region. Vendors and forum posts routinely cite thymosin β4's trials as TB-500 evidence. They are two different molecules and only one of them has been in a clinical trial.
?Does TB-500 actually heal injuries faster?
No human trial has tested that question for TB-500. The parent molecule improved outcomes in animal models of cardiac, neurological and dermal injury, and was tested in humans for venous ulcers and eye disease — not for tendon or muscle injury. Anyone telling you the tendon question is settled is describing animal data about a different molecule.
?Why is it so often stacked with BPC-157?
Because the two are marketed to the same people for the same goal, and the stack has been repeated long enough to look like a protocol. There is no trial of the combination, no interaction data, and no pharmacokinetic reason to predict how they would behave together. The stack is a convention, not a finding.
?How is it dosed in the studies?
It isn't. The 2–2.5 mg twice-weekly figure that circulates has no trial behind it. For contrast, the parent molecule's human safety study ran to 1,260 mg daily intravenously — a different molecule by a different route at several hundred times the dose, which tells you how little the community number is anchored to anything published.
?Will TB-500 show up on a drug test?
It is prohibited at all times under WADA's S2 category, and detection methods for peptide growth factors have improved considerably. Assume any athlete in a testing pool is at risk. It has also been the subject of enforcement in horse racing.
?Is the cancer concern real or is it theoretical?
It is theoretical, and the theory is a reasonable one. Thymosin β4's proposed benefits are angiogenesis and progenitor cell mobilisation — mechanisms a tumour would also benefit from — and its own review literature discusses involvement in tumorigenesis. No study shows TB-500 causes or accelerates cancer. No study has looked. That is the honest state of it.
References
- [pubmed] Ruff D, et al. "A randomized, placebo-controlled, single and multiple dose study of intravenous thymosin beta4 in healthy volunteers." Ann N Y Acad Sci, 2010;1194:223-9. PMID: 20536472.
- [pubmed] Guarnera G, et al. "Thymosin beta-4 and venous ulcers: clinical remarks on a European prospective, randomized study on safety, tolerability, and enhancement on healing." Ann N Y Acad Sci, 2007;1112:407-12. PMID: 17495250.
- [review] Sosne G. "Thymosin beta 4 and the eye: the journey from bench to bedside." Expert Opin Biol Ther, 2018;18(sup1):99-104. PMID: 30063853.
- [review] Goldstein AL, et al. "Thymosin β4: a multi-functional regenerative peptide. Basic properties and clinical applications." Expert Opin Biol Ther, 2012;12(1):37-51. PMID: 22074294.
- [review] Crockford D, et al. "Thymosin beta4: structure, function, and biological properties supporting current and future clinical applications." Ann N Y Acad Sci, 2010;1194:179-89. PMID: 20536467.
- [review] Bjørklund G, et al. "Thymosin β4: A Multi-Faceted Tissue Repair Stimulating Protein in Heart Injury." Curr Med Chem, 2020;27(37):6294-6305. PMID: 31333080.
- [review] Pipes GT, et al. "Cardioprotection by Thymosin Beta 4." Vitam Horm, 2016;102:209-26. PMID: 27450736.
- [review] Chopp M, et al. "Thymosin β4 as a restorative/regenerative therapy for neurological injury and neurodegenerative diseases." Expert Opin Biol Ther, 2015;15 Suppl 1:S9-12. PMID: 25613458.
- [pubmed] Yu FX, et al. "Thymosin beta 10 and thymosin beta 4 are both actin monomer sequestering proteins." J Biol Chem, 1993;268(1):502-9. PMID: 8416954.
- [pubmed] Srivastava D, et al. "Thymosin beta4 is cardioprotective after myocardial infarction." Ann N Y Acad Sci, 2007;1112:161-70. PMID: 17600280.
- [clinical-trial] ReGenTree. "Assessment of the Safety and Efficacy of RGN-259 Ophthalmic Solutions for Dry Eye Syndrome" (phase 3, thymosin β4 eye drops). ClinicalTrials.gov NCT03937882; completed October 7, 2021.
Sources & Citations
Every citation on this page is PubMed-indexed and has been checked against its record — not just that the identifier resolves, but that the paper is about what the sentence beside it claims. Where a study is about thymosin β4 rather than TB-500, the card says so. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.