TB-500 (thymosin β4): what it is and what the studies show

TB-500 is a synthetic peptide of seven amino acids. Its sequence, Ac-LKKTETQ, corresponds to positions 17 to 23 of thymosin β4, with an acetyl group at the start. Anti-doping laboratories identified this acetylated fragment in products circulating under the name TB-500 (Esposito et al., Drug Test Anal 2012, PMID 22962027; Ho et al., J Chromatogr A 2012, PMID 23084823).

Thymosin β4 is the full protein: 43 amino acids, present in almost every cell of the body. TB-500 is a small piece of it in synthetic form. It is not the same molecule, something the briefing document of US FDA staff to its advisory committee (July 2026) also states explicitly.

"TB-500" is not an official scientific name. According to the same document, different salts and derivatives, and even different active molecules, circulate under this name.

Thymosin β4 binds actin monomers, the building material of the cytoskeleton, in a 1:1 complex (Huff et al., Int J Biochem Cell Biol 2001, PMID 11311852). A review describes regions of the protein with different roles: the tetrapeptide Ac-SDKP at the start of the chain, studied for inflammation and fibrosis, and the LKKTETQ segment, the central actin-binding region, linked to the formation of new blood vessels and cell migration (Sosne et al., FASEB J 2010, PMID 20179146).

TB-500 comes from this second region. That is why the two names appear together. It does not mean that findings on the full protein also apply to the fragment: • In cell cultures, the non-acetylated LKKTETQ motif showed almost the same activity as full-length thymosin β4 in endothelial cell migration and vessel sprouting assays (Philp et al., FASEB J 2003, PMID 14500546). • For the acetylated form, that is TB-500, researchers at an anti-doping centre wrote in 2024 that its biological effects have not been documented. In their own scratch-closure assay in fibroblast culture, only the metabolite Ac-LKKTE differed significantly from the control group, not TB-500 itself (Rahaman et al., J Chromatogr B 2024, PMID 38382158).

That is why, in this text, every finding states explicitly whether it concerns TB-500 or full-length thymosin β4.

In humans: no clinical studies. A PubMed search on 26/10/2026 (terms: TB-500 or Ac-LKKTETQ, with a clinical-trial filter) found no clinical study of TB-500. Only one report of three cases was found, in which TB-500 is mentioned together with other substances and without a control group; the authors note that causality cannot be established (Froum et al., Front Oral Health 2026, PMID 42876687). The FDA staff briefing document (July 2026) states that no clinical studies and no human exposure data for TB-500 were identified.

In animals: a controlled 2026 study examined an Achilles tendon injury model in 32 rats, 8 per group, over 4 weeks. It compared a control group, BPC-157, TB-500 and their combination (Biçer et al., Jt Dis Relat Surg 2026, PMID 42542926). • Maximum load to failure was higher in the BPC-157 and TB-500 groups than in the control group, reaching statistical significance only in the TB-500 group (p < 0.05). • In the histological assessment, the total Bonar score was significantly lower in the TB-500 group (p = 0.016), which the authors interpreted as better tendon structure. • The combination of BPC-157 and TB-500 showed no additional benefit compared with either substance alone. The authors themselves describe the study as exploratory. It was small, with a single measurement time point.

In cells and metabolism: the 2024 study (PMID 38382158) is one of the few that examined acetylated TB-500 and its metabolites. In rats the main metabolite was Ac-LK. In fibroblast cultures no cytotoxicity was recorded, either for TB-500 or for its metabolites.

The clinical studies found in PubMed concern full-length thymosin β4, not TB-500. They show where research on the protein stands, but they do not carry over to the seven-amino-acid fragment. • Neurotrophic keratopathy, phase 3, 18 patients (Sosne et al., Int J Mol Sci 2022, PMID 36613994): thymosin β4 eye solution vs placebo. Complete closure of the epithelial defect at 4 weeks was recorded in 6 of 10 in the thymosin β4 group and in 1 of 8 in the placebo group (p = 0.0656, not statistically significant). Some authors came from the company developing the formulation. • Dry eye, phase 2, 72 people (Sosne and Ousler, Clin Ophthalmol 2015, PMID 26056426): neither of the two primary endpoints (ocular discomfort and inferior corneal staining) differed significantly from placebo. Differences were recorded in some secondary endpoints. • Venous ulcers, phase 2, 73 patients at 8 European sites (Guarnera et al., Ann N Y Acad Sci 2010, PMID 20536470): a thymosin β4 formulation vs placebo. The adverse event profile was comparable to placebo; for efficacy the authors report only signals. • Healthy volunteers, phase 1, 40 people in 4 groups of 10 (Ruff et al., Ann N Y Acad Sci 2010, PMID 20536472): with thymosin β4, adverse events were infrequent and mild or moderate, with no serious adverse events during the study.

The results of the controlled clinical studies of thymosin β4 are mixed and the studies small. According to a 2026 publication, no thymosin β4 formulation has been authorised as a medicine (Peng et al., Bioeng Transl Med 2026, PMID 42394899).

Most preclinical data also concern full-length thymosin β4, not TB-500: • Skin (Malinda et al., J Invest Dermatol 1999, PMID 10469335): in a full-thickness wound model in rats, with thymosin β4 re-epithelialisation was 42% greater than in the control group on day 4 and up to 61% on day 7. More collagen and more new blood vessels were also recorded. • Heart (Bock-Marquette et al., Nature 2004, PMID 15565145): thymosin β4 formed a complex with the proteins PINCH and ILK, with activation of the Akt kinase. In mice after coronary artery ligation, better early survival of heart cells and better cardiac function were recorded. Two further studies in mice linked thymosin β4 to the mobilisation of epicardial progenitor cells (Smart et al., Nature 2007, PMID 17108969; Smart et al., Nature 2011, PMID 21654746). • Ligaments (Xu et al., Regul Pept 2013, PMID 23523891): in a medial collateral ligament injury model in rats, with thymosin β4 the mechanical properties of the tissue were significantly higher at 4 weeks. • Muscle (Spurney et al., PLoS One 2010, PMID 20126456): in mice with a Duchenne muscular dystrophy model, over 6 months, with thymosin β4 the number of newly forming muscle fibres increased, with no significant difference in muscle strength, cardiac function or fibrosis. It is one of the findings showing that the picture is not one-sided. • Inflammation (Sosne et al., Exp Eye Res 2007, PMID 17254567): in human corneal cells, in the laboratory, thymosin β4 reduced NF-κB activation after stimulation with TNF-α.

The two peptides are often mentioned together, but they are different molecules: • Origin. BPC-157 is a 15-amino-acid peptide, part of a protein isolated from human gastric juice (Chang et al., J Appl Physiol 2011, PMID 21030672). TB-500 is a seven-amino-acid fragment of thymosin β4. • Mechanisms studied. For BPC-157, activation of the FAK-paxillin pathway in tendon fibroblasts (PMID 21030672) and of the VEGFR2-Akt-eNOS pathway in endothelial cells (Hsieh et al., J Mol Med 2017, PMID 27847966) have been described. For TB-500, the mechanism described is linked to actin binding by the LKKTETQ motif, and data on the acetylated form are scarce. • Direct comparison. The only controlled study found in PubMed that compared them directly is the 2026 Achilles tendon study in rats (PMID 42542926): a statistically significant difference in load to failure only for TB-500, numerical but not significant differences for BPC-157 in the total scores, and no additional benefit from the combination. • In humans. According to two 2026 articles (PMID 41476424; PMID 42578445), data in humans on musculoskeletal tissues are scarce and mostly lack robust controls. • WADA 2026. BPC-157 is named in category S0, thymosin β4 and its derivatives in category S2.3.

In detail on BPC-157 in the article on BPC-157, and on what has been studied when the two are examined together in the article "BPC-157 and TB-500".

The World Anti-Doping Agency (WADA) list for 2026 includes in category S2.3 (growth factors) "thymosin-β4 and its derivatives, e.g. TB-500". The category belongs to the substances on the list that apply at all times, in and out of competition. This concerns athletes who are subject to anti-doping rules. BPC-157 is named in another category of the same list, S0.

Anti-doping laboratories have studied TB-500 since 2012 (PMID 22962027; PMID 23084823).

No. According to the FDA staff briefing document (July 2026), there is no product containing TB-500 authorised by the European Medicines Agency (EMA), and TB-500 is not included in the European or the Japanese Pharmacopoeia. For full-length thymosin β4, a 2026 publication states that no thymosin β4 drug has been authorised (PMID 42394899). The FDA document is a recommendation to an advisory committee, not a decision, and a final decision on TB-500 in the US is pending.

• Data in humans. For TB-500 there are no clinical studies, only one report of three cases involving several substances. For full-length thymosin β4, research in humans is at an early stage, with small studies and mixed results.
• Material identity. Different salts and molecules circulate under the same name (FDA staff document, July 2026), so the finding of one study does not necessarily apply to other material with the same name.
• Safety. According to the FDA staff briefing document, the potential risks of TB-500 in humans are unknown. The staff found no carcinogenicity studies or reproductive toxicity studies, and note that immunogenicity from impurities or peptide aggregates cannot be ruled out.
• New blood vessels and tumours. In mice with melanoma cells overexpressing thymosin β4, metastatic lung nodules averaged 46.7 vs 10.9 in the control group (Cha et al., J Natl Cancer Inst 2003, PMID 14625258). In human tissues, thymosin β4 expression was found to be increased in some tumours, such as osteosarcoma and colorectal cancer (Jo et al., Appl Immunohistochem Mol Morphol 2011, PMID 20975530). These findings concern gene expression, not administration of the peptide, but they show why the question remains open.
• Musculoskeletal research. Two 2026 articles in a sports medicine journal conclude that the data on thymosin β4 and TB-500 come mainly from animal models and that studies in humans are few and mostly lack robust controls (Mayfield et al., Am J Sports Med 2026, PMID 41476424; Tewari et al., Am J Sports Med 2026, PMID 42578445).

Because different molecules circulate under the name TB-500, the identity of the material matters in any laboratory research. A certificate of analysis records the purity of the substance measured by HPLC, its identity, the laboratory that ran the analysis and the batch number it refers to. Published certificates are in the COA library.

No. Thymosin β4 is a 43-amino-acid protein. TB-500 is a synthetic fragment of it, seven amino acids long (Ac-LKKTETQ).

No clinical studies. The clinical studies published so far concern full-length thymosin β4. They are small and their results mixed. For TB-500 there is only one report of three cases, which does not allow any conclusion.

Category S2.3 of the 2026 list, as a derivative of thymosin β4. It concerns athletes.

Both are studied in injury models of tendons and other tissues, with different mechanisms. Their combination has been examined in only one controlled study in rats, with no additional benefit (PMID 42542926).

• Esposito S et al. Drug Test Anal. 2012. PMID 22962027 · DOI 10.1002/dta.1402
• Ho EN et al. J Chromatogr A. 2012. PMID 23084823 · DOI 10.1016/j.chroma.2012.09.043
• Huff T et al. Int J Biochem Cell Biol. 2001. PMID 11311852 · DOI 10.1016/s1357-2725(00)00087-x
• Sosne G et al. FASEB J. 2010. PMID 20179146 · DOI 10.1096/fj.09-142307
• Philp D et al. FASEB J. 2003. PMID 14500546 · DOI 10.1096/fj.03-0121fje
• Rahaman KA et al. J Chromatogr B. 2024. PMID 38382158 · DOI 10.1016/j.jchromb.2024.124033
• Biçer O et al. Jt Dis Relat Surg. 2026. PMID 42542926 · DOI 10.52312/jdrs.2026.2951
• Sosne G et al. Int J Mol Sci. 2022. PMID 36613994 · DOI 10.3390/ijms24010554
• Sosne G, Ousler GW. Clin Ophthalmol. 2015. PMID 26056426 · DOI 10.2147/OPTH.S80954
• Guarnera G et al. Ann N Y Acad Sci. 2010. PMID 20536470 · DOI 10.1111/j.1749-6632.2010.05490.x
• Ruff D et al. Ann N Y Acad Sci. 2010. PMID 20536472 · DOI 10.1111/j.1749-6632.2010.05474.x
• Peng H et al. Bioeng Transl Med. 2026. PMID 42394899 · DOI 10.1002/btm2.70144
• Malinda KM et al. J Invest Dermatol. 1999. PMID 10469335 · DOI 10.1046/j.1523-1747.1999.00708.x
• Bock-Marquette I et al. Nature. 2004. PMID 15565145 · DOI 10.1038/nature03000
• Smart N et al. Nature. 2007. PMID 17108969 · DOI 10.1038/nature05383
• Smart N et al. Nature. 2011. PMID 21654746 · DOI 10.1038/nature10188
• Xu B et al. Regul Pept. 2013. PMID 23523891 · DOI 10.1016/j.regpep.2013.03.026
• Spurney CF et al. PLoS One. 2010. PMID 20126456 · DOI 10.1371/journal.pone.0008976
• Sosne G et al. Exp Eye Res. 2007. PMID 17254567 · DOI 10.1016/j.exer.2006.12.004
• Chang CH et al. J Appl Physiol. 2011. PMID 21030672 · DOI 10.1152/japplphysiol.00945.2010
• Hsieh MJ et al. J Mol Med. 2017. PMID 27847966 · DOI 10.1007/s00109-016-1488-y
• Cha HJ et al. J Natl Cancer Inst. 2003. PMID 14625258 · DOI 10.1093/jnci/djg100
• Jo JO et al. Appl Immunohistochem Mol Morphol. 2011. PMID 20975530 · DOI 10.1097/PAI.0b013e3181f12237
• Mayfield CK et al. Am J Sports Med. 2026. PMID 41476424 · DOI 10.1177/03635465251357593
• Tewari K et al. Am J Sports Med. 2026. PMID 42578445 · DOI 10.1177/03635465261464420
• Froum S et al. Front Oral Health. 2026. PMID 42876687 · DOI 10.3389/froh.2026.1907109
• FDA staff. Briefing document on TB-500 for the Pharmacy Compounding Advisory Committee, meeting of 23 and 24/07/2026
• WADA. 2026 List (International Standard), categories S0 and S2.3

An informational text summarising published research. It is not medical advice or usage guidance.