Peptide Health Lab

Repair & recovery

TB-500

FOR RESEARCH PURPOSES ONLY

Also known as: Thymosin Beta-4 fragment, TB4, N-acetylated LKKTETQ

Regulatory status
Research only
Evidence grade
Animal studies only

Last reviewed August 2, 2026 · 16 sources

What TB-500 is and how it works

The first thing to understand about TB-500 is that it is not thymosin β4, and almost every claim made for it borrows evidence generated with thymosin β4.

Thymosin β4 is a naturally occurring protein of 43 amino acids. It is the major actin-sequestering molecule in eukaryotic cells, found in essentially all cells and body fluids, and its various biological activities have been mapped to distinct regions of the molecule.[9] TB-500 is a synthetic copy of one of those regions: residues 17 through 23, the sequence LKKTETQ, which is the central actin-binding domain plus one additional amino acid, with the N-terminus artificially acetylated.[14] Seven amino acids out of forty-three.

That mapping work is the reason the fragment exists at all. Reviewing the parent protein's active sites, investigators attributed distinct functions to distinct sequences. The amino-terminal Ac-SDKP tetrapeptide is associated with blocking inflammation and reducing fibrosis, a longer amino-terminal stretch with cell survival and blocking apoptosis, and LKKTETQ specifically with angiogenesis, wound healing, and cell migration.[9] If a single short sequence carries the repair-relevant activity, a short synthetic peptide is a cheaper and more tractable molecule than the whole protein. That is a reasonable hypothesis. It is not the same thing as a tested one.

The name "TB-500" itself entered the peer-reviewed literature through doping control. A racing laboratory describing a veterinary preparation known as TB-500 characterized its main ingredient as N-acetylated LKKTETQ. It catalogued the claims made for the preparation: promoting endothelial cell differentiation, angiogenesis in dermal tissue, keratinocyte migration, collagen deposition, and decreased inflammation. Then it developed the analytical method needed to detect prior use in horses.[14] Read that sequence again: the field's engagement with TB-500 as a distinct compound began with detecting it, not with testing it.

The proposed mechanism, inherited from the parent protein, centres on actin binding and cell motility. Thymosin β4 binds G-actin and promotes migration of several cell types; in cardiac work it formed a functional complex with PINCH and integrin-linked kinase, activating the survival kinase Akt.[4] Reviews frame the whole molecule as an actin-sequestering housekeeping protein that moonlights as a repair signal.[5]

What the research actually shows

Endothelial and keratinocyte migration. Thymosin β4 stimulated directional migration of human umbilical vein endothelial cells in culture.[1] In a rat full-thickness wound model, topical or intraperitoneal thymosin β4 increased reepithelialization by roughly 42% at four days and as much as 61% at seven days over saline controls, with greater wound contraction, increased collagen deposition, and increased angiogenesis; the same paper reported two- to threefold stimulation of keratinocyte migration in a Boyden chamber assay.[2]

Cornea. Thymosin β4 promoted corneal wound healing and decreased inflammation in vivo following alkali injury, the preclinical foundation for the ophthalmic programme that followed.[3]

Heart. In mice, thymosin β4 promoted myocardial and endothelial cell migration in the embryonic heart, enhanced cardiomyocyte survival in culture, and after coronary artery ligation upregulated integrin-linked kinase and Akt activity, enhanced early myocyte survival, and improved cardiac function.[4] A development programme for ischemic heart disease was described on that basis.[6]

Skeletal muscle, where the picture turns. Dystrophin-deficient mdx mice treated twice weekly for six months showed significantly more regenerating skeletal-muscle fibers than untreated mdx mice. They did not show significant improvement in grip strength, in systolic cardiac function, or in skeletal and cardiac fibrosis.[8] Histology moved; function did not.

Human trials exist, but of the protein. Forty healthy volunteers received intravenous synthetic thymosin β4 across four ascending dose cohorts, single dose and then daily for fourteen days; adverse events were infrequent and mild to moderate, with no dose-limiting toxicity or serious adverse events.[11] A phase 2 double-blind, placebo-controlled dose-escalation study across eight European sites randomized 73 patients with venous stasis ulcers to topical thymosin β4 or placebo; safety was deemed acceptable and comparable to placebo, and the authors describe the efficacy findings as suggesting that one concentration may accelerate healing, with complete healing within three months in about a quarter of patients, concentrated among smaller and milder ulcers.[10][7] Two phase 2 randomized, placebo-controlled trials of a thymosin β4 ophthalmic solution reported improvement in signs and symptoms of dry eye.[15][16] Reviews of the field summarize this as a scientific foundation for ongoing and projected trials.[13]

Where the evidence is weak

The substitution at the centre of the page. Every human datum above involves the full 43-amino-acid protein, formulated as an intravenous solution, a topical preparation, or an eye drop. None of it involves N-acetylated LKKTETQ.[11] The inference that a fragment carrying one of the protein's activities will behave like the protein is a hypothesis derived from a review of active sites,[9] and it has not been tested in a person. Treating thymosin β4's trial record as TB-500's trial record is the single most common error made about this compound.

No human study of TB-500 exists. The only peer-reviewed work that studies TB-500 as such is an equine doping-control paper whose purpose was detection.[14]

The recovery claims have no outcome study anywhere. Tendon healing, ligament healing, flexibility, and athletic recovery are the reasons most readers arrive at this page, and no published trial in any species evaluates the compound for them. The nearest relevant animal work, chronic dosing in a muscle-disease model, found tissue-level change without functional improvement.[8]

The human trials that do exist are small, phase 2, and unfinished business. Seventy-three patients in one, a few dozen in the eye studies, forty volunteers in the safety study.[10][15] None led to approval. A cardiac programme was described and did not produce a published positive trial.[6]

The mechanism is not unambiguously benign. Promoting cell migration is what the repair claims rest on, and thymosin β4 overexpression has separately been reported to increase colon cancer cell migration and to associate with clinical metastasis through an ILK/IQGAP1/Rac1 pathway.[12] That is cancer-cell biology, not a demonstrated harm from administration. It is still the same property, and no one has studied what it means in a person with an occult or treated malignancy.

Long-term safety is unknown. Fourteen days of intravenous dosing in healthy volunteers is the longest systemic human exposure in the published record.[11] Nothing speaks to months or years.

Legal and regulatory status

TB-500 is not approved by the FDA for any indication, and neither is full-length thymosin β4. Thymosin β4 entered formal clinical development for ischemic heart disease, dermal wounds, and ocular surface disease and reached phase 2 in several of those programmes,[6][16] which is why it sometimes appears in discussion as though it were an approved drug. It is not one. TB-500 never entered that path at all; it is distributed as a veterinary and laboratory research preparation, which is why every mention of it on this site carries research-only framing.

Its position in sport is stated on the prohibited list itself rather than inferred from anything. The World Anti-Doping Agency names thymosin β4 and its derivatives, giving TB-500 as the example, under section S2.3, growth factors and growth factor modulators. Everything in section S2 is prohibited at all times, in competition and out of it, as a non-specified substance. Detection is not theoretical either: racing laboratories have published and validated methods that confirm N-acetylated LKKTETQ and its metabolites in post-administration equine urine and plasma down to 0.01–0.02 ng/mL, developed specifically to control its misuse in equine sport.[14] The current year's list remains the authority on status, but this is a compound named on it rather than one left to interpretation.

PHL does not sell peptides, does not tell anyone how to obtain them, and takes no position on how unapproved material reaches anyone. What the regulatory status means for a reader is narrower and more useful: there is no label, no approved manufacturer, no assigned indication, and no regulated quality standard behind anything labeled TB-500. The name itself is used inconsistently for both the heptapeptide and the full protein.[13]

Questions to bring to a provider

The useful version of this conversation starts by separating the molecule from its reputation. Questions worth raising:

  • Is the compound under discussion the seven-amino-acid fragment or the full-length protein, and does the evidence being cited actually match it?[14]
  • Given that no published trial has evaluated this compound for tendon, ligament, or muscle injury in humans, what would have to be true for it to be worth considering at all?[8]
  • What is the actual diagnosis behind the injury in question, and what does the standard-of-care evidence base offer for it?
  • Does a personal or family history of malignancy change the calculus, given that the central proposed mechanism is promotion of cell migration and new blood-vessel growth?[12]
  • Are there interactions to think through with anticoagulants, cardiovascular medication, or ongoing cancer surveillance?
  • If competing in a tested sport, what does this year's prohibited list say, and what detection windows have been published?[14]
  • What monitoring (imaging, functional testing, return-to-play criteria) would make it possible to tell whether anything actually changed, rather than relying on how it feels?

A clinician who answers "the evidence for the fragment doesn't exist yet" is giving a precise answer, not a dismissive one.

Evidence by claim

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Identity of TB-500 as a thymosin β4 fragment
Animal studies only animal · review

Well established as chemistry, not as outcome. TB-500 is a synthetic, N-terminally acetylated copy of residues 17–23 of thymosin β4: the sequence LKKTETQ, the central actin-binding domain plus one amino acid. A review mapping the parent protein's active sites attributes angiogenesis, wound healing, and cell migration to that short sequence.

[14] [9]

Endothelial cell migration and angiogenesis
Animal studies only in vitro · review

Thymosin β4 stimulated directional migration of human umbilical vein endothelial cells in culture, and angiogenic activity is the property most consistently attributed to the LKKTETQ region across reviews. Cell-culture and rodent work only.

[1] [9] [5]

Cutaneous wound healing
Animal studies only animal · review

In a rat full-thickness wound model, topical or intraperitoneal thymosin β4 increased reepithelialization by roughly 42% at four days and 61% at seven days over saline controls, with more wound contraction, increased collagen deposition, and increased angiogenesis; keratinocyte migration was stimulated in a Boyden chamber assay. Rodent and cell work.

[2] [13]

Chronic venous ulcer healing in humans
Human RCT evidence human RCT

A phase 2 double-blind, placebo-controlled, dose-escalation study across eight European sites randomized 73 patients to topical full-length thymosin β4 or placebo. Safety was deemed acceptable and comparable to placebo; the efficacy finding is described by the authors as suggesting that one concentration may accelerate healing, with complete healing within three months in about a quarter of patients, mainly those with smaller or milder ulcers. This is the parent protein in a topical formulation, not TB-500.

[10] [7]

Dry eye disease in humans
Human RCT evidence human RCT

Two phase 2 randomized, placebo-controlled trials of a thymosin β4 ophthalmic solution reported improvement in signs and symptoms: one in severe dry eye including graft-versus-host-associated disease, one using a controlled adverse environment model. Again the full-length protein, and again a formulated eye drop rather than a research peptide.

[15] [16]

Corneal injury
Animal studies only animal

Thymosin β4 promoted corneal wound healing and decreased inflammation in vivo after alkali injury, which is the preclinical work the later ophthalmic trial programme was built on.

[3]

Cardiac repair after ischemic injury
Animal studies only animal · review

In mice, thymosin β4 promoted myocardial and endothelial cell migration, formed a complex with PINCH and integrin-linked kinase, activated Akt, and after coronary artery ligation enhanced early myocyte survival and improved cardiac function. A development programme for ischemic heart disease was described on this basis; no completed positive human cardiac trial is available in the peer-reviewed literature.

[4] [6]

Skeletal muscle repair
Animal studies only animal

The one chronic study located reported increased skeletal-muscle regenerating fibers in exercised dystrophin-deficient mice after six months of treatment, but no significant improvement in grip strength, systolic cardiac function, or fibrosis. The honest reading is a histological signal without a functional one.

[8]

Tendon, ligament, and athletic recovery in humans
Anecdotal reports only animal · review

No published trial, randomized or otherwise, has evaluated TB-500 or thymosin β4 for tendon injury, ligament injury, or athletic recovery in humans. The recovery claims attached to this compound are the claims made for a veterinary preparation, catalogued as such in the doping-control literature, and they are not supported by an outcome study in any species for those indications.

[14] [13]

Cell migration as a two-sided mechanism
Animal studies only in vitro

Thymosin β4 overexpression was reported to increase colon cancer cell migration and to associate with clinical metastasis via an ILK/IQGAP1/Rac1 pathway. This is mechanism, in cancer cell lines and tumor material, not a demonstrated risk from administering a peptide. It is also the same migratory property the repair claims rest on, which is why it belongs on this page rather than in a footnote.

[12]

FOR RESEARCH PURPOSES ONLY

Typical protocol range in the research

  • The only published administration of TB-500 as such: a single dose given to horses in a racing-laboratory doping-control study, reported so the investigators could characterize the compound and its metabolites in urine and plasma

    A single dose of a veterinary preparation containing 10 mg of N-acetylated LKKTETQ per horse. This is a detection study, not an efficacy study, and a horse is not a person. [14]

  • Full-length synthetic thymosin β4 given intravenously to healthy human volunteers in a phase 1 dose-escalation study (four cohorts of ten, single dose then daily for 14 days). This is the parent protein, not this fragment.

    42, 140, 420, and 1260 mg intravenously [11]

  • Full-length thymosin β4 applied topically in a phase 2, double-blind, placebo-controlled, dose-escalation venous-ulcer study across eight European sites (73 patients randomized). Again the parent protein, and a topical formulation.

    Escalating topical concentrations; the report identifies 0.03% as the concentration whose efficacy signal it describes as suggestive [10]

  • Full-length thymosin β4 in dystrophin-deficient (mdx) mice, given twice weekly for six months

    150 µg per animal per administration [8]

No published trial establishes a human dose of TB-500 for any indication, and none of the ranges above is a TB-500 human range. The equine figure is a single administration in a detection study; the human figures belong to the 43-amino-acid parent protein in formulations that have nothing to do with reconstituted research material.

Ranges are what published research reports, not a recommendation. PHL does not prescribe, and nothing here is personalized to you.

Side effects & safety signals

  • No established human safety profile for the fragment

    Not established · Unknown. This is an absence of data, not a finding of safety. Every human safety observation in the thymosin β4 literature belongs to the full-length protein in a pharmaceutical formulation. Nothing published characterizes what N-acetylated LKKTETQ does in a person.

    [11] [14]

  • Tolerability of the parent protein in short, small trials

    Adverse events infrequent and mild-to-moderate in the phase 1 intravenous study; the topical venous-ulcer study reported a safety profile deemed acceptable and comparable to placebo · Reassuring within its limits and easy to over-read. Forty subjects dosed for fourteen days and seventy-three patients treated topically for eighty-four days is not a safety database, and neither study used this fragment or a subcutaneous research preparation.

    [11] [10]

  • Promotion of cell migration and angiogenesis as the central mechanism

    Consistently reported across the preclinical literature · Not an adverse effect in itself, but the same property that is framed as repair is the property tumor biology cares about. Thymosin β4 overexpression has been reported to increase colon cancer cell migration and to associate with metastasis through an ILK/IQGAP1/Rac1 pathway. A personal or family history of malignancy is a reason to raise this with a clinician before considering anything.

    [12] [1]

  • No functional benefit in the one chronic skeletal-muscle animal study

    Reported in dystrophin-deficient mice over six months · A caution about expectations rather than a harm. Treated mice showed more regenerating skeletal-muscle fibers, but grip strength, systolic cardiac function, and fibrosis were not significantly improved versus untreated animals. Histological change without functional change is a recurring pattern worth knowing about.

    [8]

  • Anti-doping exposure

    Detectable at sub-nanogram-per-millilitre concentrations · Racing laboratories have published methods that confirm N-acetylated LKKTETQ and its metabolites in post-administration urine and plasma at 0.01–0.02 ng/mL. Anyone subject to drug testing is dealing with a compound that analytical chemists have specifically built assays to catch.

    [14]

  • Unverified identity and purity of unapproved material

    Not quantified · With no approved manufacturer, nothing about the composition, concentration, or contaminant profile of material labeled "TB-500" is regulated or independently guaranteed. The label itself is ambiguous too, since the name is used for both the heptapeptide fragment and, loosely, for full-length thymosin β4. This is a category-level risk sitting on top of whatever the molecule does.

    [14] [13]

Published lists are never exhaustive, so report anything unexpected to a licensed provider.

Storage, handling & reconstitution

Lyophilized storage
Lyophilized short peptides are conventionally kept refrigerated at 2–8 °C and protected from light, with freezing used for long-term holding. No published stability study addresses the shelf life of N-acetylated LKKTETQ in a vial, and because there is no approved manufacturer of this material there is no label, no assigned beyond-use date, and no lot-level stability testing behind any storage claim. The conventions here come from general lyophilized-peptide practice, not from a TB-500 study.
Reconstituted storage
Once in solution, peptides are conventionally refrigerated at 2–8 °C, protected from light, and treated as short-dated rather than indefinitely stable. No published source establishes a solution shelf life for this fragment. The two forms with published human data are a topical gel and an ophthalmic solution of the full-length protein. Both were formulated pharmaceutically and say nothing about how research material behaves.
Reconstitution diluent
Bacteriostatic water is the conventional diluent for lyophilized research peptides, including this one. It is sterile water preserved with 0.9% benzyl alcohol. Sterile water without a preservative is used where a preservative is contraindicated and is treated as single-use.
Reconstitution & handling
Conventional handling: sanitize the stopper before piercing it, add the diluent slowly down the inside wall of the vial rather than directly onto the powder, and let it dissolve on its own. Swirl gently if needed, never shake. A properly reconstituted solution is clear; anything cloudy, discolored, or carrying visible particulate is discarded. PHL does not publish volume or unit calculations, because those are dosing decisions and dosing decisions belong with a licensed clinician.
Handling notes
Because a short peptide is more chemically tractable than a 43-amino-acid protein, TB-500 is sometimes described as intrinsically more stable than thymosin β4. That is a plausibility argument, not a measurement; no comparative stability data for the two is published.

The how-to guides cover the conventions behind these fields, and what the published stability data does and does not establish: Storage, Reconstitution, Handling.

Goal pages that include TB-500

Each one starts from the goal rather than the molecule, and grades what the evidence supports for that goal specifically.

  • Recovery

    A research reference for the peptides mapped to injury recovery and tissue repair, covering what the animal literature established, what the handful of human trials actually measured, and how to tell the two apart.

Questions for your provider

Bring this page to a licensed provider. A provider can order labs, review your medications and history, and tell you whether anything here is relevant to your situation. This page can't. Peptide Health Lab does not prescribe and does not sell peptides.

Want a structured starting point for that conversation? The Stack Builder turns your goals into a research-cited outline you can review together.

Citations

16 sources · every identifier checked against PubMed

Before you act on any of this

This page is educational only and is not medical advice. It does not diagnose, treat, or prescribe. Review it with a licensed provider before making any health decision. Peptide Health Lab does not sell peptides.

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