TB-500 5 mg

Buy TB-500 5mg (Thymosin Beta-4) from our online store. Adapt Peptides is your trusted peptide supplier, with purity levels exceeding 99% independently verified by third-party labs. Get TB-500 for sale, trusted by researchers and institutions for consistent quality and reliable long-term results. Order now for fast, secure shipping, backed by our professional, friendly support team.

What Is TB-500 and What Does It Do?

TB-500 is a synthetic peptide modeled after Thymosin Beta-4 (Tβ4), a naturally occurring protein present in nearly all human and animal cells.

Tβ4 plays an essential role in tissue repair, regeneration, and cellular defense mechanisms. It is typically found in high concentrations at wound and injury sites, where it supports angiogenesis (formation of new blood vessels), modulation of inflammation, and directed cell migration.

While TB-500 is modeled after Thymosin Beta-4, it represents a simplified, synthetic fragment of the natural protein. This design retains the key actin-binding domain responsible for cellular repair and migration, while eliminating the larger and more complex structure of Tβ4.

This design improves stability, ease of synthesis, and more predictable performance in controlled research settings. By focusing on the biologically active region, TB-500 allows researchers to investigate Tβ4-like effects without the variability that can arise when studying the full-length natural protein.

In research settings, TB-500 is widely studied for its potential to promote accelerated recovery in muscle, tendon, ligament, and dermal tissues. Its primary mechanism of interest lies in its ability to regulate actin polymerization, an essential process for cytoskeletal organization and cellular motility.

Because of these properties, TB-500 is frequently utilized in preclinical models of wound repair, post-injury recovery, and fibrosis regulation. It is also being explored in studies related to cardiac tissue repair, corneal injury, and chronic inflammatory conditions.

Disclaimer: Adapt Peptides supplies TB-500 exclusively for laboratory research purposes. This peptide is not approved for human or veterinary use and must not be applied in therapeutic, diagnostic, or clinical contexts.

TB-500 Mechanism of Action (Based on Research)

Thymosin Beta-4 (Tβ4) is a small, highly conserved protein that regulates cell structure, motility, and survival. In biological systems, Tβ4 plays a central role in processes including wound repair, angiogenesis, and inflammation control[1].

Unlike many bioactive peptides that act through extracellular receptors, TB-500 functions primarily inside the cell. Its key mechanism involves binding to globular actin (G-actin) monomers, effectively sequestering them and influencing cytoskeletal behavior[2].

This actin-binding activity enables rapid cytoskeletal reorganization, which is crucial for:

• Directed cell migration toward sites of injury
• Angiogenesis, supporting blood supply to regenerating tissue
• Fibroblast activation and extracellular matrix (ECM) remodeling
• Anti-fibrotic effects, limiting excessive scar formation

Additional research suggests that TB-500 may also influence gene expression related to cellular survival pathways, oxidative stress responses, and inflammatory cytokine modulation. These properties are being explored in preclinical models of organ injury, chronic inflammation, and degenerative conditions[3].

Research Applications (TB-500 Benefits)

TB-500 has been investigated in a wide variety of nonclinical research models for its potential role in tissue repair, cellular migration, and inflammation control.

Research findings suggest that this synthetic peptide fragment of Thymosin Beta-4 supports accelerated wound healing, improved vascularization, and reduced fibrosis, making it a compound of high interest in regenerative biology.

Although promising, all results remain preclinical, and TB-500 is strictly intended for laboratory research only.

Accelerated Wound Closure & Angiogenesis

In injury models, TB-500 has consistently been shown to accelerate wound closure when compared to untreated controls.

According to a study, TB-500 promoted faster re-epithelialization, decreased neutrophil infiltration, and suppressed inflammatory cytokines such as IL-1β and MMP-9[4]. These findings indicate a dual mechanism: enhanced cell migration and modulation of the inflammatory response.

Additional studies in dermal and corneal wound models have demonstrated TB-500’s ability to upregulate VEGF, promoting angiogenesis and increasing nutrient delivery to damaged tissues—both essential steps for robust tissue regeneration[5].

Enhanced Cell Migration & Actin Regulation

A central feature of TB-500’s activity is its influence on actin dynamics. By binding G-actin monomers, TB-500 maintains a reservoir of actin that can be rapidly mobilized for filament assembly. This balance between G-actin and F-actin enables cells to reorganize their cytoskeleton, migrate efficiently to injury sites, and establish focal adhesions necessary for wound closure[6].

Another study highlighted TB-500’s ability to enhance keratinocyte motility, integrin-linked kinase signaling, and angiogenic capacity[7]. This suggests that TB-500 may serve as a useful model compound for studying cytoskeletal regulation in regenerative and developmental biology.

Anti-Inflammatory & Anti-Scarring Properties

Beyond regeneration, TB-500 exhibits anti-inflammatory effects. Preclinical models demonstrate reduced apoptosis, diminished fibrotic scar formation, and activation of stem cell pathways[1]. Oxidized forms of Thymosin Beta-4 (LTβ4 and UTβ4) have been shown to decrease swelling in carrageenan-induced inflammation models, with LTβ4 reducing edema by nearly 60% at 24 hours[8].

These results suggest that oxidation products of TB-500 may serve as natural modulators of inflammation, blocking neutrophil migration and tempering excessive tissue damage during repair. Researchers have also noted reductions in TGF-β-driven fibrosis, pointing to possible relevance in models of cardiac scarring, pulmonary fibrosis, and chronic inflammatory injury.

Diverse Organ & System Repair

While much of the literature focuses on skin and musculoskeletal tissues, TB-500 has shown broader regenerative activity in systemic models:

Peripheral Nerve Repair

In type II diabetic neuropathy models, TB-500 improved sciatic nerve conduction velocity and restored microvascular density, largely through activation of the PI3K/Akt pathway in endothelial and Schwann cells[9].

Cardiac Repair

Mouse myocardial infarction studies demonstrate TB-500’s role in preserving cardiomyocytes, stimulating epicardial progenitor cells, and thickening the epicardium—mimicking developmental heart processes[10]. This leads to improved vascularization and cardiac function.

Broader Organ Regeneration

TB-500 has also been linked to protective effects in renal and neural tissues. Preclinical data suggest potential neuroprotective mechanisms tied to mitochondrial support and anti-apoptotic signaling, hinting at experimental relevance in brain injury and age-related degeneration[1][11].

Taken together, these findings position TB-500 as a versatile research peptide with relevance across wound healing, fibrosis, neurovascular health, and cardiac biology.

TB-500 Peptide Characteristics

• Chemical Formula: C₂₁₂H₃₅₀N₅₆O₇₈S
• CAS Number: 77591-33-4
• Amino Acid Sequence: SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES
• Synonyms: Thymosin Beta-4 Acetate, Tβ4, TB4
• Molar Mass / Molecular Weight: 4,963.44 g/mol
• Storage Recommendations:
  • Lyophilized Form: Store at –8 °C (46 °F) or below in a sealed, desiccated container for long-term stability.
  • Reconstituted Solution: For short-term use, store at 2–8 °C (35.6–46.4 °F) and use within 14 days.
  • For extended storage, freeze at –20 °C (–4 °F). Avoid repeated freeze–thaw cycles.

Note: Stability data indicate that TB-500 maintains peptide integrity when properly stored under these conditions, ensuring reliable use in controlled laboratory experiments.

TB-500 vs BPC-157 vs Thymosin Alpha-1 Comparison

TB-500 Safety and Side Effects in Studies

Most of the safety data available on TB-500 is derived from preclinical animal research and in vitro cell studies, as no large-scale human clinical trials have been conducted to date. Within these experimental frameworks, TB-500 has generally been well-tolerated at research-level dosages, with no consistent reports of systemic toxicity, organ impairment, or immune dysfunction[1].

Some investigations have observed localized, mild inflammatory responses during tissue regeneration processes — a reaction considered part of the normal healing cascade rather than an adverse outcome. Importantly, no evidence of mutagenicity, carcinogenicity, or acute toxicity has been documented under controlled conditions.

That said, the absence of human data prevents any definitive conclusions about its long-term safety profile. Until further studies are conducted, TB-500 should be regarded strictly as an experimental research compound.

Legal Disclaimer

This product is intended for laboratory research purposes only and is not approved for human or veterinary use. It is not to be employed in diagnostic, therapeutic, or clinical settings, nor resold or repackaged for any such applications.

By purchasing TB-500, the buyer agrees to handle and use it in compliance with all applicable local, state, and federal regulations governing research chemicals.

Certificate of Analysis (COA)

At Evolve Peptides, every batch of TB-500 is subject to independent third-party laboratory testing to confirm identity, purity, and structural integrity. Analytical methods such as high-performance liquid chromatography (HPLC) and mass spectrometry (MS) are employed to verify that each lot meets rigorous specifications.

Our Certificates of Analysis consistently demonstrate purity levels exceeding 99%, reflecting the high standards we maintain in sourcing, manufacturing, and quality control.

For transparency and reproducibility, COAs are made available upon request and may be provided directly with your order, ensuring researchers have the documentation needed for reliable experimental use.

Scientific References

1. Xing Y, Ye Y, Zuo H, Li Y. Progress on the Function and Application of Thymosin β4. Front Endocrinol (Lausanne). 2021 Dec 21;12:767785.

https://pmc.ncbi.nlm.nih.gov/articles/PMC8724243/ 

2. Khandoker Asiqur Rahaman, Anca Raluca Muresan, Hophil Min, Junghyun Son, Hyung-Seop Han, Min-Jung Kang, Oh-Seung Kwon,

Simultaneous quantification of TB-500 and its metabolites in in-vitro experiments and rats by UHPLC-Q-Exactive orbitrap MS/MS and their screening by wound healing activities in-vitro, Journal of Chromatography B, Volume 1235, 2024, 124033, ISSN 1570-0232.

https://www.sciencedirect.com/science/article/pii/S1570023224000412 

3. Kumar S, Gupta S. Thymosin beta 4 prevents oxidative stress by targeting antioxidant and anti-apoptotic genes in cardiac fibroblasts. PLoS One. 2011;6(10):e26912.

https://pubmed.ncbi.nlm.nih.gov/22046407/ 

4. Sosne, G., & Kleinman, H. K. (2015). Primary mechanisms of Thymosin β4 repair activity in dry eye disorders and other tissue injuries. Investigative Ophthalmology & Visual Science, 56(9), 5110–5117.

https://iovs.arvojournals.org/article.aspx?articleid=2423767 

5. Sosne G, Qiu P, Kurpakus-Wheater M. Thymosin beta 4: A novel corneal wound healing and anti-inflammatory agent. Clin Ophthalmol. 2007 Sep;1(3):201-7.

https://pmc.ncbi.nlm.nih.gov/articles/PMC2701135/ 

6. Carlier MF, Jean C, Rieger KJ, Lenfant M, Pantaloni D. Modulation of the interaction between G-actin and thymosin beta 4 by the ATP/ADP ratio: possible implication in the regulation of actin dynamics. Proc Natl Acad Sci U S A. 1993 Jun 1;90(11):5034-8.

https://pmc.ncbi.nlm.nih.gov/articles/PMC46648/ 

7. 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 Nov 25;432(7016):466-72. 

https://pubmed.ncbi.nlm.nih.gov/15565145/ 

8. Girardi M, Sherling MA, Filler RB, Shires J, Theodoridis E, Hayday AC, Tigelaar RE. Anti-inflammatory effects in the skin of thymosin-beta4 splice-variants. Immunology. 2003 May;109(1):1-7.

https://pmc.ncbi.nlm.nih.gov/articles/PMC1782938/ 

9. Wang L, Chopp M, Szalad A, Liu Z, Lu M, Zhang L, Zhang J, Zhang RL, Morris D, Zhang ZG. Thymosin β4 promotes the recovery of peripheral neuropathy in type II diabetic mice. Neurobiol Dis. 2012 Dec;48(3):546-55.

https://pmc.ncbi.nlm.nih.gov/articles/PMC3533234/ 

10. Zhou B, Honor LB, Ma Q, Oh JH, Lin RZ, Melero-Martin JM, von Gise A, Zhou P, Hu T, He L, Wu KH, Zhang H, Zhang Y, Pu WT. Thymosin beta 4 treatment after myocardial infarction does not reprogram epicardial cells into cardiomyocytes. J Mol Cell Cardiol. 2012 Jan;52(1):43-7.

https://pmc.ncbi.nlm.nih.gov/articles/PMC3664360/ 

11. Xiong Y, Zhang Y, Mahmood A, Meng Y, Zhang ZG, Morris DC, Chopp M. Neuroprotective and neurorestorative effects of thymosin β4 treatment initiated 6 hours after traumatic brain injury in rats. J Neurosurg. 2012 May;116(5):1081-92.

https://pmc.ncbi.nlm.nih.gov/articles/PMC3392183/