TB-500 vs Thymosin Beta-4: Identity, Evidence, and FDA Status

Reviewed on: August 27, 2026.

This page summarizes published research and official regulatory records. It does not provide medical advice or instructions for using any substance. “TB-500” is used inconsistently in commercial settings, so sequence and terminal chemistry, not the marketplace name, control this evidence review.

Evidence state at a glance

Under the identity convention in FDA’s 2026 review, TB-500 is an N-acetylated seven-residue fragment, Ac-LKKTETQ-OH. It is not the full 43-residue thymosin beta-4 peptide, and it is not the non-acetylated fragment LKKTETQ. FDA found no clinical study or human exposure data for TB-500 and no in-vivo wound-healing pharmacology study of the reviewed TB-500 materials.

TB-500 is not a reliable synonym for full-length thymosin beta-4

Full-length thymosin beta-4 is a naturally occurring peptide with 43 amino acids. FDA’s 2026 TB-500 review uses the name TB-500 for an N-acetylated fragment corresponding to residues 17–23 of thymosin beta-4: Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH, abbreviated Ac-LKKTETQ-OH.[1]

FDA reports the TB-500 free base as C38H68N10O14, with a molecular weight of 889.01 g/mol, UNII QHK6Z47GTG, and CAS 885340-08-9. The acetate contains the same N-acetylated peptide active moiety with acetate and is reported as C38H68N10O14·CH3COOH with a molecular weight of 949.1 g/mol. FDA lists no separate UNII or CAS for the acetate in its identity table and notes that supplier records have reused the free-base CAS.[1]

The non-acetylated fragment LKKTETQ is another related but chemically distinct material. N-terminal acetylation changes the molecular identity. Findings for LKKTETQ, full-length thymosin beta-4, and Ac-LKKTETQ-OH must therefore remain in separate evidence buckets.

Marketplace pages have used TB-500 to mean the seven-residue fragment, full-length thymosin beta-4, or a material with insufficient specification. When names conflict, the complete sequence, terminal groups, counterion, molecular mass, and analytical identity must take priority.

Direct in-vitro evidence: the parent peptide did not improve scratch closure

Rahaman and colleagues examined N-acetylated TB-500 and its metabolites in laboratory systems, including a fibroblast scratch assay. Parent TB-500 did not significantly increase scratch closure compared with vehicle. A shorter metabolite, N-acetylated LKKTE, produced a small statistically significant difference under the tested conditions, but the study did not establish a clear concentration-response relationship or a human outcome.[4]

This is a central null result. A signal for a metabolite does not establish that the parent peptide heals wounds, and a cell-culture scratch assay is not a clinical wound.

Direct animal evidence: detection research is not repair evidence

An equine study identified TB-500 as N-acetylated LKKTETQ and developed analytical methods to detect the parent peptide and metabolites in horses.[5] It provides animal pharmacokinetic and anti-doping detection information. It does not establish wound healing, tissue repair, performance enhancement, or safety.

FDA’s 2026 review reported that it did not identify an in-vivo pharmacological study assessing wound healing for TB-500 free base or TB-500 acetate. FDA also did not identify an adequate toxicology package across major acute, repeat-exposure, genetic-toxicity, reproductive-developmental, and carcinogenicity domains.[1]

Observational- and interventional-human evidence

FDA reported no published human case reports of TB-500 use and no identified clinical study, human pharmacokinetic study, human pharmacodynamic study, or other human exposure data for TB-500 by any route.[1]

FDA’s surveillance search found no FAERS reports through its stated search date. It found two Human Foods Complaint System records mentioning products described as TB-500/BPC-157 blends, but those records did not include safety assessments.[1] Sparse reporting does not establish safety because exposure identity, reporting completeness, and causality are unresolved.

The direct human evidence bucket is therefore empty. Human claims involving wounds, recovery, inflammation, muscle, tendon, ligament, or performance would exceed the evidence.

Related evidence: non-acetylated LKKTETQ is not TB-500

A 2003 study investigated thymosin beta-4 in diabetic and aged mouse wound models. In diabetic mice, wound contraction and collagen deposition increased, but keratinocyte migration did not differ; the animals were already approaching complete epithelial coverage at the reported observation. A synthetic non-acetylated seven-residue fragment, LKKTETQ, promoted repair in the aged-animal model. Primary mouse study

The fragment finding concerns LKKTETQ as described in that experiment. It is not a direct test of N-acetylated Ac-LKKTETQ, and neither intervention was combined with GHK-Cu and BPC-157. A familiar substring in two peptide names is not sufficient chemical matching.

This distinction is not merely semantic. Changing a terminal group changes the compound’s mass and may change stability, transport, metabolism, receptor interactions, or other properties. Related-fragment evidence can motivate a hypothesis, but it cannot fill the missing direct TB-500 animal or human evidence.

Related molecule, full-length thymosin beta-4 is not TB-500 evidence

Human trials have investigated synthetic full-length 43-residue thymosin beta-4 in particular topical formulations. Those studies concern another molecule and cannot establish clinical effects, safety, or product equivalence for seven-residue TB-500.

A randomized Phase 2 venous-stasis-ulcer study, NCT00832091, reported exploratory wound-closure signals in parts of the enrolled population.[7] It was a small, formulation-specific, condition-specific development study and did not test TB-500.

In a Phase 2 dry-eye study, NCT01387347, selected secondary or later analyses favored a full-length thymosin beta-4 ophthalmic formulation, but neither primary endpoint differed significantly from control.[8] The trial was single-center, limited in duration, and sponsor involved.

A separate severe-dry-eye pilot, NCT01393132, reported differences at selected time points but enrolled only nine participants.[9] A Phase 3 neurotrophic-keratopathy study, NCT02600429, enrolled 18 participants. More complete-healing events occurred in the full-length thymosin beta-4 group, but the primary comparison at the specified time point did not reach statistical significance (p=0.0656).[10]

These studies are useful only when labeled full-length thymosin beta-4 evidence, not TB-500 evidence. Their small samples, formulation specificity, sponsor relationships, and null or borderline primary results prevent broad conclusions even for the full-length molecule.

Negative and null findings

• FDA identified no TB-500 clinical study, human pharmacology study, case report, or human exposure data.[1]
• FDA did not identify an in-vivo wound-healing pharmacology study of TB-500 free base or acetate.[1]
• Parent TB-500 did not significantly improve closure in the direct 2024 fibroblast scratch assay.[4]
• A small in-vitro signal for a shorter metabolite does not establish an effect of the parent peptide.[4]
• A frequently cited mouse fragment study used non-acetylated LKKTETQ, not FDA-defined N-acetylated TB-500.[6]
• Neither primary endpoint was significant in the full-length thymosin beta-4 Phase 2 dry-eye trial.[8]
• The full-length neurotrophic-keratopathy study’s primary result was borderline and not statistically significant at the specified point, and the trial enrolled only 18 participants.[10]
• FDA identified substantial toxicology and human-safety gaps, as well as potential immunogenicity concerns related to aggregation and peptide impurities.[1,3]
• Inconsistent marketplace naming makes product identity an unresolved source of error.

Current U.S. FDA status

Status checked August 27, 2026: FDA states that neither TB-500 free base nor TB-500 acetate is a component of an FDA-approved drug.[1] In its July 2026 briefing, FDA concluded that the statutory criteria weighed against adding either material to the section 503A Bulks List.[1]

The briefing supported a Pharmacy Compounding Advisory Committee discussion, and FDA states that advisory-committee recommendations are nonbinding.[2] It should not be presented as a final rule unless a later final FDA action is identified. FDA’s current compounding safety page lists “Thymosin beta-4, fragment (LKKTETQ), also known as TB-500” among withdrawn nominations. The page states that FDA has not identified human exposure data and flags potential immunogenicity risk associated with aggregation and peptide-related impurities.[3]

What the evidence cannot establish

There is no direct human evidence from which to infer TB-500 clinical effectiveness or safety. The direct animal literature identified here supplies detection and pharmacokinetic information rather than repair outcomes. The direct in-vitro study contains a null result for the parent peptide. These gaps cannot be repaired by borrowing findings from non-acetylated LKKTETQ or full-length thymosin beta-4.

Product identity is an independent limitation. A label saying TB-500 does not reveal whether a vial contains full-length thymosin beta-4, N-acetylated Ac-LKKTETQ-OH, non-acetylated LKKTETQ, or another form. No cited study establishes the identity or biological equivalence of a Serum Research lot.

Frequently asked questions

Is TB-500 the full 43-amino-acid thymosin beta-4 peptide?

Not under FDA’s 2026 identity convention. FDA uses TB-500 for the N-acetylated seven-residue fragment Ac-LKKTETQ-OH. Full-length thymosin beta-4 contains 43 residues.

What is the TB-500 sequence?

FDA’s 2026 review describes TB-500 as Ac-Leu-Lys-Lys-Thr-Glu-Thr-Gln-OH, abbreviated Ac-LKKTETQ-OH.

Is non-acetylated LKKTETQ the same as TB-500?

No. The N-terminal acetyl group changes the chemical identity. Evidence for non-acetylated LKKTETQ must be labeled as related, non-equivalent evidence.

Have human clinical trials tested TB-500?

FDA reported that it did not identify clinical studies or human exposure data for TB-500. Human studies of full-length thymosin beta-4 are not TB-500 studies.

Is TB-500 FDA approved?

No. FDA states that TB-500 free base and TB-500 acetate are not components of an FDA-approved drug.

Why is there no Serum Research TB-500 product link on this page?

The current catalog copy conflicts on whether the material is full-length thymosin beta-4 or the seven-residue TB-500 fragment. The product and every blend containing the disputed component remain blocked until exact identity and lot documentation resolve that conflict.

Does this page explain how to use TB-500?

No. It is an identity and evidence summary and intentionally provides no preparation, administration, or self-use instructions.

Primary and official sources

1. U.S. Food and Drug Administration. TB-500-related bulk drug substances: FDA briefing document, July 2026. FDA media 193349
2. U.S. Food and Drug Administration. July 23–24, 2026 Pharmacy Compounding Advisory Committee meeting. Official meeting page
3. U.S. Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. FDA compounding safety page
4. Rahaman M, et al. Direct TB-500 metabolism and fibroblast scratch-assay study, 2024. PMID 38382158 · DOI 10.1016/j.jchromb.2024.124033
5. Ho ENM, et al. Equine TB-500 detection and metabolism study, 2012. PMID 23084823 · DOI 10.1016/j.chroma.2012.09.043
6. Philp D, et al. Full-length thymosin beta-4 and non-acetylated LKKTETQ in a mouse wound model, 2003. PMID 12581423 · DOI 10.1046/j.1524-475x.2003.11105.x
7. Guarnera G, et al. Full-length thymosin beta-4 venous-ulcer Phase 2 study, 2010. PMID 20536470 · DOI 10.1111/j.1749-6632.2010.05490.x · NCT00832091
8. Sosne G, Ousler GW. Full-length thymosin beta-4 dry-eye Phase 2 study, 2015. PMID 26056426 · PMCID PMC4445951 · DOI 10.2147/OPTH.S80954 · NCT01387347
9. Sosne G, et al. Nine-participant full-length thymosin beta-4 severe-dry-eye pilot, 2015. PMID 25826322 · DOI 10.1097/ICO.0000000000000379 · NCT01393132
10. Sosne G, et al. Full-length thymosin beta-4 neurotrophic-keratopathy study, 2022. PMID 36613994 · PMCID PMC9820614 · DOI 10.3390/ijms24010554 · NCT02600429