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Peptide Profile

TB-500

Thymosin Beta-4 Fragment 17-23

A synthetic heptapeptide fragment of Thymosin Beta-4. Studied for wound healing and tissue repair, primarily in animal models and equine medicine.

Reviewed March 2026·16 min read·15 citations·Research compoundNot FDA-approved

Regulatory update: February 2026

TB-500 has been announced for reclassification from Category 2 to Category 1, which would allow compounding pharmacies to produce it legally. This change was announced February 27, 2026 but has not yet been formally published in the Federal Register.

Updated March 17, 2026

At a glance

TB-500 is a synthetic fragment of thymosin beta-4, a naturally occurring protein involved in wound healing and tissue repair. It is one of the most popular peptides in the recovery space — but there is a critical distinction most sources fail to make: TB-500 (a 7-amino-acid fragment) and thymosin beta-4 (the full 43-amino-acid protein) are not the same molecule. All human clinical trials have used the parent protein, not the fragment sold online.

Animal studiesModerate50+ studies

Most preclinical research uses full-length thymosin beta-4, not the TB-500 fragment. Strong animal data for wound healing, cardiac repair, and corneal healing — but for the parent molecule. Direct evidence for the TB-500 fragment is primarily from equine medicine.

Human evidenceMinimal0 for TB-500; ~5 for Tbeta4

Zero human clinical trials exist for the TB-500 fragment. Several Phase II trials and one Phase III trial have been completed for full-length thymosin beta-4 in wound healing and dry eye. These used the parent molecule, not the fragment sold online.

Safety dataLimited0 for TB-500

No formal human safety data exists for the TB-500 fragment. Full-length thymosin beta-4 was well-tolerated in clinical trials with hundreds of participants. Whether the fragment shares the same safety profile is unknown.

How are these scores calculated?

TB-500's evidence profile has an unusual structure: the parent molecule (thymosin beta-4) has meaningful clinical data, but the fragment sold online (TB-500) has none. Every claim about TB-500's effects in humans is extrapolated from research on a different — though related — molecule.

New research, delivered clearly

When new studies publish or clinical trials report results, we'll break them down in plain language.

Quick facts

Molecular weight
889.0 Da (acetylated)
Amino acids
7 (heptapeptide fragment)
Parent molecule
Thymosin beta-4 (43 aa, 4,921 Da)
First described
1966 (parent); ~2000s (fragment)
FDA status
Category 2 (pending reclassification)
WADA status
Prohibited (Section S2)

Amino acid sequence

Ac-LKKTETQ


TB-500 vs. thymosin beta-4: the distinction that matters

TB-500 and thymosin beta-4 are routinely treated as interchangeable online. They are not. Understanding this distinction is the single most important thing you can learn about TB-500.

Peptide Garden evidence assessment, March 2026

Thymosin beta-4 is a 43-amino-acid protein found naturally in virtually all human cells, with especially high concentrations in platelets and wound fluid. It was first isolated from calf thymus tissue by Allan Goldstein and colleagues in the 1960s, and its full sequence was determined in 1981.[1] It has been studied in multiple clinical trials for wound healing, dry eye, cardiac repair, and corneal injuries.

TB-500 is a synthetic 7-amino-acid fragment (Ac-LKKTETQ) corresponding to residues 17-23 of thymosin beta-4 — the region identified as the actin-binding domain.[15] It was developed commercially in the early 2000s, primarily for use in equine veterinary medicine.

Here is why this matters:

  • All human clinical trials (wound healing, dry eye, cardiac repair) used full-length thymosin beta-4, not TB-500
  • The TB-500 fragment has zero registered human clinical trials
  • The fragment is missing 36 of the 43 amino acids in the parent protein, including domains that may have additional biological functions
  • No human pharmacokinetic data exists for TB-500 — we don't know how it's absorbed, distributed, metabolized, or eliminated in humans
  • Whether a 7-amino-acid fragment replicates the effects of a 43-amino-acid protein is a genuine scientific question, not an assumption

An analogy: Imagine a 43-page book where researchers identify Chapter 3 as the most important section. TB-500 is like selling only Chapter 3 and claiming it delivers the same experience as the full book. The chapter might contain the key idea — but the full book may work differently than the chapter alone.


What is TB-500?

TB-500 is a synthetic peptide — a short chain of 7 amino acids — that corresponds to the actin-binding domain of thymosin beta-4. The sequence (LKKTETQ) is typically sold in its N-terminally acetylated form (Ac-LKKTETQ), which may improve stability.

Thymosin beta-4, the parent molecule, is one of the most abundant small proteins inside human cells. It plays a critical role in regulating actin, the structural protein that controls cell shape, movement, and division. When tissue is injured, platelets release thymosin beta-4 at the wound site, where it helps coordinate the repair process — promoting cell migration, new blood vessel formation, and reducing inflammation.

TB-500 gained popularity through equine veterinary medicine, where it has been widely used for soft tissue injury recovery in racehorses. This practical veterinary use is the origin of much of the dosing knowledge in circulation, though controlled equine trials are also limited.

The compound is not extracted from thymus tissue — it is synthesized in a laboratory. The name "TB-500" is a commercial designation, not a scientific one.


How it works

In plain terms, TB-500 contains the specific region of thymosin beta-4 that controls actin — one of the most important structural proteins in your cells. By regulating actin, it influences how cells move, divide, and organize themselves during tissue repair.[4]

Think of actin as cellular scaffolding. When tissue is damaged, cells need to reorganize their scaffolding to migrate to the wound site, build new blood vessels, and lay down new tissue. TB-500's actin-binding domain appears to facilitate this process — based on what we've observed in animal models and in vitro studies.

Detailed mechanism (for advanced readers)

TB-500's mechanism derives from the actin-binding properties of its parent molecule, thymosin beta-4. The established pathways include:

  • Actin sequestration (primary mechanism): Thymosin beta-4 binds monomeric G-actin with high affinity (Kd ~0.5-0.7 microM) in a 1:1 ratio, preventing premature polymerization into F-actin filaments. This controlled release of actin monomers regulates cell motility, migration, and cytoskeletal reorganization critical for wound healing.
  • Angiogenesis: Directly upregulates VEGF expression (2.5-3.8 fold increase in mRNA), promoting new blood vessel formation at injury sites.[3]
  • Anti-inflammatory: Reduces pro-inflammatory cytokine production via NF-kB pathway modulation.
  • Cell survival (Akt pathway): Activates integrin-linked kinase (ILK) and the Akt/PKB survival pathway, reducing cell death in injured tissue.[4]
  • Stem cell mobilization: Promotes recruitment and differentiation of progenitor cells at injury sites.[5]
  • Extracellular matrix remodeling: Modulates matrix metalloproteinase activity during tissue repair.

How it differs from related compounds:

  • vs. BPC-157: BPC-157 works primarily through angiogenesis and growth factor signaling (VEGF, FAK, paxillin). TB-500 works through actin regulation and cell migration. They are mechanistically complementary — which is why they are commonly paired. Neither has clinical evidence supporting the combination.
  • vs. GHK-Cu: GHK-Cu works through copper-dependent gene expression changes, primarily in skin cells. TB-500 has broader systemic tissue repair effects through the actin pathway.
  • vs. Full-length thymosin beta-4: TB-500 contains only the actin-binding domain. The full protein has N-terminal and C-terminal regions that may have additional biological functions beyond actin binding, including immune modulation and anti-apoptotic effects that may not be fully captured by the fragment.

What the research says

Thymosin beta-4 has been published in Nature twice and studied in multiple Phase II and one Phase III clinical trial. TB-500 — the fragment that people actually buy — has zero human trials. This is the central tension of the TB-500 evidence base.

Peptide Garden evidence assessment, March 2026

Research timeline

  1. 1966Preclinical

    Thymosin family discovered

    Allan Goldstein isolates thymosin from calf thymus tissue. Thymosin beta-4 is subsequently identified as a key member of the thymosin family.

  2. 1999Preclinical

    Wound healing demonstrated

    Malinda et al. show thymosin beta-4 accelerates wound healing in rats — 42-61% faster re-epithelialization and increased collagen deposition.

  3. 2003Preclinical

    Cancer association identified

    Cha et al. report thymosin beta-4 overexpression increases tumor angiogenesis (4.4-fold) and cell migration in melanoma models. A key safety concern.

  4. 2004Preclinical

    Landmark Nature paper — cardiac repair

    Bock-Marquette et al. publish in Nature: thymosin beta-4 promotes cardiac cell survival and repair after myocardial infarction via ILK/Akt activation.

  5. 2007Preclinical

    Second Nature paper — neovascularization

    Smart et al. demonstrate thymosin beta-4 mobilizes epicardial progenitor cells and induces neovascularization in injured adult hearts.

  6. 2010Human study

    Phase II wound healing trials begin

    RegeneRx Biopharmaceuticals conducts Phase II trials of full-length thymosin beta-4 for venous stasis ulcers and pressure ulcers. Results show accelerated healing.

  7. 2012Milestone

    TB-500 fragment characterized for doping control

    Young et al. synthesize and characterize the Ac-LKKTETQ fragment (TB-500) for anti-doping purposes, confirming its identity as thymosin beta-4 residues 17-23.

  8. 2015Human study

    Phase II dry eye trial (RGN-259)

    Sosne et al. report thymosin beta-4 eye drops significantly improve signs and symptoms of severe dry eye in a randomized Phase II trial.

  9. 2021Human study

    Phase I safety trial (recombinant Tbeta4)

    Wang et al. report a Phase I trial in 84 healthy Chinese volunteers. Recombinant thymosin beta-4 was well-tolerated with no serious adverse events.

  10. 2022Human study

    Phase III neurotrophic keratopathy trial

    Sosne et al. publish Phase III results: RGN-259 (thymosin beta-4 eye drops) significantly promotes corneal healing in neurotrophic keratopathy.

  11. 2023Regulatory

    FDA Category 2 classification

    The FDA places thymosin beta-4 (and TB-500) on the Category 2 restricted list, citing insufficient safety evidence for compounding.

  12. 2026Regulatory

    Kennedy reclassification announced

    HHS Secretary Kennedy announces TB-500 / thymosin beta-4 will be reclassified to Category 1, restoring compounding access. Formal FDA action still pending.

Human clinical trials

There are zero human clinical trials for the TB-500 fragment. All human data comes from studies of full-length thymosin beta-4. Here is what those trials found — with the crucial caveat that they used a different molecule:

2012·Phase II randomized controlled trial·n=72Moderate quality

Phase II: Thymosin beta-4 for venous stasis ulcers

Chronic venous stasis ulcers

Full-length thymosin beta-4 accelerated healing by approximately one month in patients whose wounds healed. Well-tolerated with no serious adverse events. Used the PARENT MOLECULE, not TB-500.

2022·Phase III randomized, double-masked, placebo-controlled·n=18Moderate quality

Phase III: RGN-259 for neurotrophic keratopathy

Neurotrophic keratopathy (Stages 2-3)

6 of 10 treated subjects achieved complete healing at 4 weeks vs. 1 of 8 on placebo. No recurrent defects in treatment group at follow-up. Used the PARENT MOLECULE as eye drops, not TB-500.

2021·Phase I randomized, double-blind, dose-escalation·n=84Moderate quality

Phase I: Recombinant thymosin beta-4 safety

Safety and pharmacokinetics

54 single-dose + 30 multiple-dose subjects received recombinant thymosin beta-4. All adverse events were mild to moderate. No dose-limiting toxicities. Used the PARENT MOLECULE, not TB-500.

Why this matters: These are genuinely encouraging results — thymosin beta-4 appears to promote healing and is well-tolerated. But TB-500 is a 7-amino-acid fragment of a 43-amino-acid protein. Assuming the fragment works identically to the full protein is an extrapolation, not an established fact. In pharmacology, fragments of proteins often have different potency, duration, and side effect profiles compared to the parent molecule.

Animal studies

The preclinical literature for thymosin beta-4 is extensive and high-quality — including two publications in Nature, which is rare for any peptide in this space. Key findings:

Key findings by area
  • Corneal wound healing (mice, rats): Topical thymosin beta-4 produced 50-70% faster corneal re-epithelialization in alkali burn and mechanical abrasion models. Well-replicated across multiple independent labs — one of the strongest areas of evidence.[9]
  • Cardiac repair (mice, rats): After myocardial infarction, systemic thymosin beta-4 reduced infarct size, improved cardiac function, promoted neovascularization, and activated endogenous cardiac progenitor cells. Published in Nature (2004, 2007).[4][5]
  • Dermal wound healing (rats, pigs): Accelerated full-thickness wound closure with 42-61% faster re-epithelialization, increased angiogenesis, and improved collagen deposition.[2]
  • Hair follicle stimulation (mice): Thymosin beta-4 stimulated hair follicle stem cells and promoted hair growth in normal and aged mice.[3]
  • Tendon repair (rats): Improved tendon healing strength and reduced adhesion formation.
  • Neurological injury (rats): Enhanced functional recovery in spinal cord injury and traumatic brain injury models.

What's different about this preclinical data: Unlike BPC-157 (where nearly all research comes from a single lab in Zagreb), thymosin beta-4 research has been conducted by multiple independent groups worldwide, including two Nature publications. The preclinical evidence base is more robust and more widely replicated. However, most of this work uses the full protein, not the TB-500 fragment.


What the evidence shows

People come to TB-500 with specific questions. Here's what the published research actually tells us about the most common areas of interest:

Does TB-500 help with wound healing and tissue repair?

This is the strongest area of evidence — but almost entirely for the parent molecule. Full-length thymosin beta-4 accelerated wound healing in Phase II human trials (venous ulcers, pressure ulcers) and in multiple animal models. The TB-500 fragment contains the actin-binding domain believed to drive these effects, but whether the 7-amino-acid fragment replicates the full protein's wound healing in humans is unproven.

Some supporting evidence

Can TB-500 speed up muscle and tendon recovery?

Animal studies show thymosin beta-4 improves tendon healing and reduces adhesions in rats. Equine veterinary use for soft tissue recovery is widespread, providing practical (though not controlled) evidence. No human clinical trials exist for either TB-500 or thymosin beta-4 in musculoskeletal recovery.

More research needed

Does TB-500 reduce inflammation?

Animal studies demonstrate that thymosin beta-4 reduces pro-inflammatory cytokines via NF-kB pathway modulation. Anti-inflammatory effects have been observed in corneal injury, cardiac ischemia, and wound healing models. No human studies have measured TB-500's anti-inflammatory effects directly.

Some supporting evidence

Can TB-500 promote hair regrowth?

Mouse studies show thymosin beta-4 stimulates hair follicle stem cells and promotes hair growth. The actin-binding domain (which TB-500 contains) appears involved. However, results are from a small number of animal studies with limited replication, and no human data exists.

More research needed

Is the 'Wolverine stack' (BPC-157 + TB-500) effective?

BPC-157 and TB-500 work through complementary mechanisms — BPC-157 via angiogenesis and growth factor signaling, TB-500 via actin regulation and cell migration. The rationale for combining them is mechanistically plausible. However, zero clinical studies have examined this combination in any species. All evidence for the stack is anecdotal, from community self-reports.

More research needed

What do we know about TB-500 safety?

Full-length thymosin beta-4 was well-tolerated in multiple clinical trials with hundreds of participants. No serious adverse events were attributed to the peptide. However, the TB-500 fragment has zero formal safety data in humans. The primary theoretical concern — shared with BPC-157 — is that VEGF upregulation could promote tumor vascularization. Thymosin beta-4 overexpression has been associated with tumor progression in some cancer models.

More research needed

Safety & side effects

What research shows

For full-length thymosin beta-4 (the parent molecule): Clinical trials involving hundreds of participants reported the peptide as safe and well-tolerated. A Phase I study in 84 healthy volunteers found no dose-limiting toxicities or serious adverse events.[11] Phase II wound healing and dry eye trials similarly reported no significant safety concerns.

For TB-500 (the fragment): No formal human safety data exists. No preclinical toxicology studies specific to the TB-500 fragment have been published in peer-reviewed literature. Everything we know about TB-500 safety is extrapolated from the parent molecule or from community self-reports.

Community-reported side effects

Among people who have used TB-500 outside of clinical settings, commonly reported effects include:

  • Water retention and bloating (especially during initial weeks)
  • Headache (typically resolves after 1-2 weeks)
  • Fatigue and lethargy
  • Flu-like symptoms initially
  • Injection-site redness, swelling, or tenderness
  • Mild nausea (occasional, more common at higher doses)
  • Lightheadedness (rare)

These are self-reported and not from controlled studies. They should be taken as signal, not as definitive safety data.

Theoretical risks

Angiogenesis and cancer risk: TB-500 upregulates VEGF, promoting new blood vessel growth. Cha et al. (2003) demonstrated that thymosin beta-4 overexpression increased tumor blood vessel formation 4.4-fold in melanoma cells and increased cell migration 2.3-fold.[12] While this does not prove TB-500 causes cancer, it raises a biologically plausible concern — especially for individuals with undiagnosed cancers or a cancer history. The FDA has cited this angiogenesis risk as a primary safety concern.

Contraindications and interactions

Theoretical contraindications (based on mechanism of action, not clinical data):

  • Active cancer or history of cancer (angiogenesis and tumor-promoting potential)
  • Pregnancy and breastfeeding (no safety data)
  • Active infection (theoretical immune modulation as a thymosin-family peptide)
  • Autoimmune conditions (theoretical immune system effects, though not observed in Tbeta4 trials)

Drug interactions: No formal interaction studies in humans. No known drug interactions documented for either TB-500 or thymosin beta-4.


How people use it

TB-500 is most commonly discussed in the context of injury recovery, particularly for muscle, tendon, and ligament injuries. Here's what the landscape of use looks like — with important caveats.

Administration routes

  • Subcutaneous injection (most common): Unlike BPC-157, TB-500 is considered systemically active regardless of injection location. People typically inject in the abdomen, outer thigh, or upper arm — the injection site does not need to be near the injury.
  • Intramuscular: Used by some for deeper tissue injuries.

About dosing information: Specific dosing ranges are not published on Peptide Garden pending legal review. No TB-500 dosing protocol has been validated in a human clinical trial. All dosing knowledge derives from veterinary use and community practice. If you're considering TB-500, the right first step is a conversation with a knowledgeable healthcare provider who can assess your specific situation.

Common stacking context

In community practice, TB-500 is often discussed alongside other peptides:

  • TB-500 + BPC-157 — the "Wolverine stack," targeting healing through complementary mechanisms (actin regulation + angiogenesis). No clinical data supports this combination.
  • TB-500 + GHK-Cu — discussed for comprehensive tissue regeneration. Anecdotal reports only.
  • TB-500 + CJC-1295/Ipamorelin — discussed for GH-mediated recovery alongside direct tissue repair. No controlled studies.

All stacking protocols are community-derived and have not been studied in any controlled setting.

If you plan to reconstitute peptides, see our reconstitution guide for safety-first preparation instructions.


As of March 2026:

FDA status

TB-500 (and thymosin beta-4) is not FDA-approved for any indication. In September 2023, the FDA classified thymosin beta-4 as a Category 2 bulk drug substance — meaning the agency determined there was insufficient evidence that it is safe for human use. Under this classification, compounding pharmacies are prohibited from using it.[13]

On February 27, 2026, HHS Secretary Robert F. Kennedy Jr. announced that approximately 14 of the 19 Category 2 peptides would be reclassified to Category 1, restoring legal compounding access with a physician prescription. TB-500 / thymosin beta-4 is expected to be among those reclassified.

Where it stands now: The Kennedy reclassification has been announced but has not yet been formally published in the Federal Register. Until it is, TB-500's legal status technically remains Category 2. Reclassification to Category 1 would not constitute FDA approval — it would only permit compounding pharmacies to prepare it with a valid prescription.

WADA / USADA status

Thymosin beta-4 and its derivatives — including TB-500 — have been prohibited at all times under WADA Section S2 (Peptide Hormones, Growth Factors, Related Substances, and Mimetics). The 2026 Prohibited List explicitly names "Thymosin-beta4 and its derivatives e.g. TB-500" under S2.3 (Growth Factors and Growth Factor Modulators). Athletes testing positive face a standard 4-year ban.[14]

International status

TB-500 is not approved for clinical use in any country. Full-length thymosin beta-4 has been studied in clinical trials by RegeneRx Biopharmaceuticals (US) and Beijing Northland Biotech (China), but has not received regulatory approval anywhere. TB-500 is available as a "research chemical" in most jurisdictions and is widely used in equine veterinary medicine (though banned by some racing commissions).


How TB-500 compares to BPC-157

TB-500 and BPC-157 are the two most commonly discussed healing peptides — and are frequently combined in the "Wolverine stack." Here's how their evidence profiles compare:

TB-500

Fragment of thymosin beta-4 · Not FDA-approved

Animal evidence55%
Human evidence15%
Safety data14%

Primary mechanism

Actin regulation

Human trials (fragment)

0

Parent molecule trials

~5

Best evidence area

Wound healing

BPC-157

Gastric pentadecapeptide · Not FDA-approved

Animal evidence82%
Human evidence12%
Safety data18%

Primary mechanism

Angiogenesis

Human trials

3

Total studies

100+

Best evidence area

GI / tendon

Both peptides share the same fundamental limitation: very limited human clinical data. Where they differ is in structure and mechanism:

  • BPC-157 has more animal studies (100+), but nearly all from a single lab. It works through angiogenesis and growth factor signaling, and shows the strongest evidence for GI protection and tendon repair.
  • TB-500 has fewer studies overall but benefits from higher-quality preclinical research (two Nature papers) conducted by multiple independent labs. Its parent molecule has more advanced human trials. It works through actin regulation and cell migration.

The "Wolverine stack" rationale is that these complementary mechanisms — BPC-157's angiogenesis plus TB-500's actin regulation — might produce synergistic healing effects. This is mechanistically plausible but has zero clinical evidence supporting it. The combination has never been studied in any controlled setting, in any species.



References

  1. [1]
    Goldstein AL, Thurman GB, Low TL, et al.. Thymosin alpha1: isolation and sequence analysis of an immunologically active thymic polypeptide.” Proc Natl Acad Sci USA. 1977. 74(2):725–729 DOI PubMedAnimal study

    Foundational paper establishing the thymosin family of peptides. Thymosin beta-4 was subsequently identified as a distinct member of this family.

  2. [2]
    Malinda KM, Sidhu GS, Mani H, et al.. Thymosin beta4 accelerates wound healing.” J Invest Dermatol. 1999. 113(3):364–368 DOI PubMedAnimal study

    Key early study demonstrating thymosin beta-4 accelerates wound healing in rats via increased re-epithelialization (42-61%) and wound contraction.

  3. [3]
    Philp D, Goldstein AL, Kleinman HK. Thymosin beta4 promotes angiogenesis, wound healing, and hair follicle development.” Mech Ageing Dev. 2004. 125(2):113–115 DOI PubMedAnimal study

    Demonstrated thymosin beta-4 promotes angiogenesis, wound repair, and hair growth in both normal and aged rodents.

  4. [4]
    Bock-Marquette I, Saxena A, White MD, DiMaio JM, Srivastava D. Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair.” Nature. 2004. 432(7016):466–472 DOI PubMedAnimal study

    Landmark Nature paper demonstrating thymosin beta-4 promotes cardiac repair after myocardial infarction via ILK/Akt activation. The highest-impact publication in the thymosin beta-4 field.

  5. [5]
    Smart N, Risebro CA, Melville AAD, et al.. Thymosin beta4 induces adult epicardial progenitor mobilization and neovascularization.” Nature. 2007. 445(7124):177–182 DOI PubMedAnimal study

    Second Nature paper on thymosin beta-4 in cardiac repair. Demonstrated epicardial progenitor cell mobilization and neovascularization.

  6. [6]
    Goldstein AL, Hannappel E, Sosne G, Kleinman HK. The regenerative peptide thymosin beta4 accelerates the rate of dermal healing in preclinical animal models and in patients.” Expert Opin Biol Ther. 2012. 12(S1):S137–S149 DOI PubMedReview

    Comprehensive review of thymosin beta-4 wound healing data from both animal models and early human trials.

  7. [7]
    Treadwell T, Kleinman HK, Crockford D, Hardy MA, Goldstein AL. The regenerative peptide thymosin beta4 accelerates the rate of dermal healing in preclinical animal models and in patients.” Ann N Y Acad Sci. 2012. 1270(1):37–44 DOI PubMedReview

    Reports Phase II wound healing results for thymosin beta-4 in venous stasis ulcers, pressure ulcers, and epidermolysis bullosa.

  8. [8]
    Sosne G, Ousler GW. Thymosin beta4 significantly improves signs and symptoms of severe dry eye in a phase 2 randomized trial.” Cornea. 2015. 34(5):491–496 DOI PubMedPilot study

    Phase 2 RCT of RGN-259 (thymosin beta-4 eye drops) for severe dry eye. Small but well-designed study showing significant improvement in ocular discomfort and corneal staining.

  9. [9]
    Sosne G, Rimmer D, Kleinman HK, Ousler G. Thymosin Beta 4: a potential novel therapy for neurotrophic keratopathy, dry eye, and ocular surface diseases.” Vitam Horm. 2016. 102:277–306 DOI PubMedReview

    Review of thymosin beta-4 in ophthalmology, covering mechanisms and clinical trial data for dry eye and corneal healing.

  10. [10]
    Sosne G, Kleinman HK. 0.1% RGN-259 (Thymosin beta4) 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. 24(1):554 DOI PubMedRCT

    Phase III RCT for thymosin beta-4 in neurotrophic keratopathy. Small (n=18) but well-designed, double-masked trial showing significant healing benefit.

  11. [11]
    Wang X, Liu J, Zhang H, et al.. A first-in-human, randomized, double-blind, single- and multiple-dose, phase I study of recombinant human thymosin beta4 in healthy Chinese volunteers.” Eur J Pharm Sci. 2021. 167:106018 DOI PubMedSafety study

    Well-designed Phase I safety trial of recombinant full-length thymosin beta-4 (NL005) in 84 healthy volunteers. No dose-limiting toxicities or serious adverse events.

  12. [12]
    Cha HJ, Jeong MJ, Kleinman HK. Role of thymosin beta4 in tumor metastasis and angiogenesis.” J Natl Cancer Inst. 2003. 95(22):1674–1680 DOI PubMedAnimal study

    Demonstrated thymosin beta-4 overexpression increased cell migration (2.3-fold) and tumor blood vessel formation (4.4-fold) in B16-F10 melanoma cells. Key reference for the cancer risk discussion.

  13. [13]
    U.S. Food and Drug Administration. Certain bulk drug substances that may present significant safety risks under conditions of use in compounding.” 2023. Link
  14. [14]
    World Anti-Doping Agency. The 2026 Prohibited List — International Standard.” 2026. Link

    Thymosin beta-4 and its derivatives (including TB-500) are explicitly listed under S2.3 (Growth Factors and Growth Factor Modulators).

  15. [15]
    Young JD, Lawrence AJ, MacLean AG, et al.. Synthesis and characterization of the N-terminal acetylated 17-23 fragment of thymosin beta 4 identified in TB-500, a product suspected to possess doping potential.” Drug Test Anal. 2012. 4(Suppl 1):52–61 DOI PubMedIn vitro

    Characterization of the TB-500 fragment for anti-doping purposes. Confirms TB-500 is Ac-LKKTETQ, the acetylated 17-23 fragment of thymosin beta-4.


Medical disclaimer

Peptide Garden is an educational resource, not a medical provider. The information on this page is compiled from published research and is intended for informational purposes only. It does not constitute medical advice, diagnosis, or treatment recommendations. TB-500 is not FDA-approved for any indication. No human clinical trials exist for the TB-500 fragment. Always consult a qualified healthcare provider before making decisions about peptide therapy.