TB-500

Description

TB-500 is a synthetic peptide corresponding to the actin-binding domain (amino acids 17–23) of Thymosin Beta-4 (TB4), a naturally occurring 43-amino acid peptide found in virtually all human cells. Thymosin Beta-4 is one of the most abundant intracellular peptides in mammals and is the primary G-actin sequestering peptide in cells. Whether the fragment reproduces the activity of full-length Thymosin Beta-4 has not been established. FDA has identified no human exposure data for the fragment, and evidence generated with full-length Tβ4 does not transfer to it. Unlike BPC-157, which has primarily local healing effects at the injection site, TB-500 provides systemic healing effects throughout the body, making it particularly valuable for widespread injuries, systemic inflammation, or tissues that are difficult to inject directly (such as tendons deep within joints or cardiac tissue). TB-500 has demonstrated remarkable healing effects in animal models of cardiac injury, tendon damage, corneal wounds, and neurological injury. It is commonly combined with BPC-157 for comprehensive tissue repair.

Key Characteristics

Investigated Benefits

• Systemic tissue repair and healing
• Reduced inflammation throughout body
• Improved flexibility and range of motion
• Accelerated muscle recovery
• Cardiovascular tissue repair

* Benefits based on preclinical/animal research unless otherwise noted.

“TB-500” is not a standardised identity. Most material sold under the name is the 7-residue fragment LKKTETQ (~847 Da); some is N-terminally acetylated (~889 Da). Full-length Thymosin Beta-4 is a different molecule at 43 amino acids and ~4,963 Da. Figures for one should not be applied to the other.

Regulatory Status

FDA placed TB-500 in Category 2 (significant safety risks) in September 2023. It is not FDA-approved and is not a lawful dietary ingredient. FDA has identified no human exposure data for the fragment.

Mechanism of Action

“A synthetic analog of Thymosin Beta-4 that promotes systemic healing through actin regulation and angiogenesis.”

TB-500’s primary mechanism involves sequestration of G-actin (monomeric actin) through its LKKTET actin-binding motif. By regulating the balance between G-actin and F-actin (filamentous actin), TB-500 controls cell migration, proliferation, and differentiation — all critical processes in tissue repair. Specifically, it promotes the migration of keratinocytes, endothelial cells, and fibroblasts into wound sites, accelerating wound closure. TB-500 also upregulates VEGF (vascular endothelial growth factor) and its receptor VEGFR2, promoting angiogenesis (new blood vessel formation) that is essential for tissue repair and regeneration. It reduces the expression of pro-inflammatory cytokines (IL-1β, TNF-α) and promotes the transition from the inflammatory to the proliferative phase of wound healing. In cardiac tissue, TB-500 has demonstrated the ability to activate cardiac progenitor cells and promote cardiomyocyte regeneration after ischemic injury — a property unique among peptides studied for cardiac repair.

Reconstitution Guide

Add 2 mL bacteriostatic water to 10 mg vial → 5 mg/mL

For 2.5 mg dose: draw 0.5 mL (50 units on U-100 syringe)

Protocols Featuring TB-500

Unresolved Safety Questions

TB-500 upregulates VEGF and VEGFR2. That pro-angiogenic mechanism carries the same unresolved tumour-promotion questions as other angiogenic agents, and has not been studied for that risk in humans.

Research Highlights

1. 1Demonstrated cardiac repair in myocardial infarction models
2. 2Human trials exist for full-length Thymosin Beta-4 (e.g. RGN-259 in ophthalmology), but none for the TB-500 fragment
3. 3Improved wound healing in Phase II trials

Compatible Peptides

Peptides commonly used alongside TB-500 for synergistic effects.