# TB-500 (Thymosin Beta-4)

> TB-500 is a research peptide name commonly associated with thymosin beta-4 (Tβ4), a 43-amino-acid, N-terminally acetylated peptide that is the main G-actin-sequestering molecule in most vertebrate cells. Thymosin beta-4 has been studied in cell and animal models of wound healing, cardiac injury, corneal repair and hair growth. Neither TB-500 nor thymosin beta-4 is an FDA-approved drug.

Canonical: https://peptideproperties.com/compounds/tb-500/

## Identity

- **Class:** Tissue-Repair Peptides
- **Also known as:** Thymosin Beta-4, Tβ4, Timbetasin
- **Molecular formula:** C212H350N56O78S
- **Molecular weight:** 4963 g/mol
- **Monoisotopic mass:** 4962.4930 Da
- **PubChem CID:** 45382195
- **InChIKey:** UGPMCIBIHRSCBV-UHFFFAOYSA-N
- **Sequence:** SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES
- **Sequence notes:** N-terminal acetylation (N-acetylserine); free C-terminal carboxylic acid. Sequence shown is full-length thymosin beta-4; products labeled TB-500 may differ.

## Key facts

- Class: beta-thymosin peptide; studied as a tissue-repair research compound
- Length: 43 amino acids with an acetylated N-terminal serine
- Origin: isolated from thymosin fraction 5, a thymic polypeptide mixture; encoded by the TMSB4X gene
- Formula C212H350N56O78S; molecular weight 4963 g/mol (PubChem CID 45382195)
- Primary known function: binds and sequesters monomeric G-actin
- Evidence base: mostly cell and animal studies; eye-drop formulations reached late-stage clinical trials
- Regulatory status: not FDA approved for any indication

## What Is TB-500?

TB-500 is a name used in the research-peptide market for material associated with thymosin beta-4 (Tβ4), a naturally occurring 43-residue peptide. The name is not used consistently: a 2026 narrative review of peptides marketed directly to patients lists Tβ4 and TB-500 as separate entries and describes TB-500 as a thymosin beta-4 fragment.[1] Because of this, the exact identity of a given TB-500 sample depends on its documented sequence. This page describes full-length thymosin beta-4, the molecule behind the PubChem record and most of the published literature.Thymosin beta-4 itself is well characterized. It belongs to the beta-thymosin family and is found in large amounts in many cell types, where it is the main intracellular peptide that sequesters monomeric (G-) actin.[2] It is present in both the cytoplasm and the nucleus.[2]Research interest in Tβ4 centers on tissue repair. Preclinical work has examined it in cardiac ischemic injury, corneal wound healing, colitis, hair growth and neurodegeneration models.[3][4] The same 2026 review notes that many unapproved peptides in this category show favorable tissue repair outcomes in animal models, but that rigorous human safety data are scarce.[1]

## Chemical Structure and Molecular Identity

Thymosin beta-4 is a linear peptide of 43 standard L-amino acids with an acetyl group on the N-terminal serine and a free C-terminal carboxylic acid. PubChem (CID 45382195) lists the molecular formula C212H350N56O78S and a molecular weight of 4963 g/mol. The single sulfur atom comes from the methionine at position 6.The sequence is Ac-SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES. It is rich in lysine and glutamic acid, giving the molecule a high density of charged side chains. Residues 17 to 23 (LKKTETQ) form a short segment that is also sold separately as a fragment.In solution Tβ4 is unstructured, but it folds into a stable conformation when it binds G-actin.[2] A closely related homolog, thymosin beta-10, has similar actin-binding behavior.[5]
### Key identifiers

- PubChem CID: 45382195
- InChIKey: UGPMCIBIHRSCBV-UHFFFAOYSA-N
- Synonyms: thymosin beta-4, Tβ4, timbetasin, thymosin beta-4 acetate
- Gene: TMSB4X

## Research History and Development

Thymosin beta-4 was first isolated as a candidate thymic hormone, was later recognized as an actin-binding peptide, and is now studied mainly for wound healing. It was purified from thymosin fraction 5, a mixture of thymic polypeptides that improved immune response, alongside thymosin alpha-1.[2] Later work showed that none of the isolated peptides were true thymic hormones.[2]Identifying a biological function took years. In 1990, Dan Safer and colleagues recognized that Tβ4 sequesters G-actin, with a dissociation constant in the micromolar range that allows fast binding and release.[2] Research then shifted back toward extracellular effects, describing Tβ4 as a cytokine-like factor that supports wound healing.[2]Ocular repair became the most advanced clinical application. A 2018 review traced work that began at the NIH in 1998 and reported that phase 3 clinical trials of Tβ4 for dry eye and neurotrophic keratopathy were ongoing at the time.[4] In parallel, cardiac researchers documented infarct reduction in preclinical models and called for pharmacokinetic and pharmacodynamic studies and a reliable biomarker to support clinical development.[3]

## Mechanisms Studied in Research

The best-established mechanism of thymosin beta-4 is binding of monomeric actin, which controls the pool of actin available for filament assembly. Working with actin nucleating, severing and uncapping proteins, Tβ4 helps regulate the actin polymerization response in cells.[5]Researchers caution that not every effect fits this model. Adding or overexpressing Tβ4 or thymosin beta-10 alters the cytoskeleton and cell motility, but some effects are inconsistent with simple monomer binding and may involve signaling pathways.[5] Very little is known about how extracellular beta-thymosins act at the molecular level.[2]
### Pathways and products examined

- SRF-MRTF-G-actin signaling: proposed as a route by which Tβ4 indirectly regulates cell motility.[3]
- Angiogenesis and fibrosis: Tβ4 increased blood vessel growth in small and large animal models, and Tβ4 and its degradation products were antifibrotic in vitro and in animal models.[3]
- Derived peptides: effects have been attributed to oxidized Tβ4 and to Ac-SDKP, a tetrapeptide possibly generated from Tβ4.[2]
- VEGF and kinase signaling: in mouse skin, Tβ4 levels tracked with VEGF expression and P38, ERK and AKT phosphorylation.[6]

## Key Findings From Published Studies

Published findings on thymosin beta-4 come mainly from cell culture and animal models, with clinical work concentrated in eye disease. The results below are reported by model.
### Cell and organoid studies
In hCMEC/D3 human brain endothelial cells, Tβ4 increased tight junction protein expression, reduced the F-actin to G-actin ratio and improved vascular permeability dysfunction induced by the prion fragment PrP(106-126).[7] In cerebral organoids derived from stem cells carrying familial Alzheimer disease mutations, expression of TMSB4X was reduced, and Tβ4 treatment rescued neurodevelopmental deficits and beta-amyloid formation; benefits were also reported in 5xFAD model mice.[8]
### Animal studies

- Heart: in preclinical cardiac ischemia models, Tβ4 reduced infarct volume and preserved cardiac function, with effect sizes varying between models.[3]
- Colon: in mice with DSS- or TNBS-induced colitis, an adeno-associated virus delivering Tβ4 to the colon reduced colon injury, epithelial apoptosis, inflammatory infiltration and oxidative stress markers.[9]
- Hair: mice overexpressing Tβ4 in the epidermis regrew hair faster after depilation, while Tβ4 knockout mice regrew more slowly and had fewer hair shafts.[6] A CRISPR/Cas9 Tβ4 knock-in cashmere goat showed a 74.5% increase in cashmere yield without loss of fineness.[10]
- Eye: in a rodent dry eye model, combined mesenchymal stem cell and Tβ4 treatment outperformed either alone, an effect linked to increased corneal glutamine.[11]
### Human evidence
Human data are limited to clinical development of Tβ4 eye drops for corneal disorders.[4] For TB-500 products marketed outside regulatory oversight, reviewers report scarce human safety data and potential for serious harm.[1]Because published names and sequences for TB-500 vary, researchers typically confirm identity with HPLC purity and mass spectrometry data on a batch certificate of analysis.Because published names and sequences for TB-500 vary, researchers typically confirm identity with HPLC purity and mass spectrometry data on a batch certificate of analysis.

## Regulatory and Research Status

Neither thymosin beta-4 nor TB-500 is approved by the FDA for any indication. A 2026 review in Sports Medicine groups Tβ4 and TB-500 with other unapproved peptides sold through a gray market that operates largely outside regulatory oversight.[1]The most advanced clinical program involves Tβ4 eye drops, which reached phase 3 trials for dry eye and neurotrophic keratopathy.[4] Thymosin beta-4 has not received FDA approval for these or any other indications.Thymosin beta-4 and TB-500 are sold as research chemicals for laboratory use. Researchers working with either material should treat the name as a label, not a specification, and rely on the documented sequence and analytical data.Open research questions remain. Reviewers have noted that the molecular mechanisms behind extracellular Tβ4 effects are poorly understood, that effect sizes vary between animal models, and that pharmacokinetic and pharmacodynamic data are needed before clinical use can be evaluated.[2][3] Human safety data for unapproved TB-500 products remain scarce.[1]

## FAQ

**Is TB-500 the same as thymosin beta-4?**
Not necessarily. TB-500 is commonly associated with thymosin beta-4, the 43-residue actin-binding peptide, but the name is used inconsistently. A 2026 review in Sports Medicine lists thymosin beta-4 and TB-500 separately and describes TB-500 as a thymosin beta-4 fragment. The identity of any specific sample should be confirmed from its stated sequence and mass spectrometry data.

**What is the molecular weight of thymosin beta-4?**
PubChem lists thymosin beta-4 (CID 45382195) with a molecular weight of 4963 g/mol and the molecular formula C212H350N56O78S. The molecule is a 43-amino-acid peptide with an acetylated N-terminal serine and a free C-terminal carboxylic acid. A product sold as TB-500 should show a mass consistent with its stated sequence.

**Is TB-500 FDA approved?**
No. Neither TB-500 nor thymosin beta-4 is approved by the FDA for any use. A 2026 review groups both with unapproved peptides sold outside regulatory oversight and notes that rigorous human safety data are scarce. Thymosin beta-4 eye drops reached phase 3 clinical trials for dry eye and neurotrophic keratopathy, but thymosin beta-4 has not been approved.

**How does thymosin beta-4 work?**
Thymosin beta-4 binds monomeric G-actin and limits the actin available for filament assembly, which affects cell shape and movement. It is the main G-actin-sequestering peptide in most vertebrate cells. Researchers also describe indirect effects on signaling, including the SRF-MRTF pathway, angiogenesis and fibrosis, though the molecular mechanisms of extracellular thymosin beta-4 remain poorly understood.

**What does the research on thymosin beta-4 show?**
Most findings come from cell and animal models. Studies report reduced infarct volume in cardiac ischemia models, less colon injury in mouse colitis models, faster hair regrowth in mice overexpressing the peptide, and rescue of deficits in Alzheimer disease brain organoids. Clinical work has focused on eye drops for corneal disorders. Human data on TB-500 products are scarce.

**How is TB-500 different from the TB-500 fragment?**
Full-length thymosin beta-4 has 43 amino acids. The product sold as the TB-500 or thymosin beta-4 fragment corresponds to residues 17 to 23, the seven-residue sequence LKKTETQ, often with an N-terminal acetyl group. The fragment has a much lower molecular weight and is studied separately from the full peptide.

## References

1. Mendias CL, Awan TM. Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance. Sports medicine (Auckland, N.Z.) 2026. PMID: 41966639
2. Hannappel E. beta-Thymosins. Annals of the New York Academy of Sciences 2007. PMID: 17468232
3. Pipes GT, Yang J. Cardioprotection by Thymosin Beta 4. Vitamins and hormones 2016. PMID: 27450736
4. Sosne G. Thymosin beta 4 and the eye: the journey from bench to bedside. Expert opinion on biological therapy 2018. PMID: 30063853
5. Sun HQ, Yin HL. The beta-thymosin enigma. Annals of the New York Academy of Sciences 2007. PMID: 17495248
6. Gao X, Liang H, Hou F, et al. Thymosin Beta-4 Induces Mouse Hair Growth. PloS one 2015. PMID: 26083021
7. Song K, Han HJ, Kim S, et al. Thymosin beta 4 attenuates PrP(106-126)-induced human brain endothelial cells dysfunction. European journal of pharmacology 2020. PMID: 31877278
8. Zeng PM, Sun XY, Li Y, et al. Thymosin beta 4 as an Alzheimer disease intervention target identified using human brain organoids. Stem cell reports 2025. PMID: 40816274
9. Zheng XY, Lv YF, Li S, et al. Recombinant adeno-associated virus carrying thymosin β4 suppresses experimental colitis in mice. World journal of gastroenterology 2017. PMID: 28127198
10. Li X, Hao F, Hu X, et al. Generation of Tβ4 knock-in Cashmere goat using CRISPR/Cas9. International journal of biological sciences 2019. PMID: 31360116
11. Chen X, Zhang C, Peng F, et al. Identification of glutamine as a potential therapeutic target in dry eye disease. Signal transduction and targeted therapy 2025. PMID: 39837870