TB-500 (Thymosin Beta-4): Complete Guide — Benefits, Dosage, Side Effects & Research

What Is TB-500?

TB-500 is a synthetic version of the naturally occurring 43-amino acid peptide Thymosin Beta-4 (Tβ4), one of the most abundant proteins in the human body. Thymosin Beta-4 is produced by virtually all nucleated cells and is found in high concentrations in wound fluid, blood platelets, and other tissues involved in healing and repair.

The distinction matters: TB-500 is the commercially available synthetic analog used in research and by the biohacking community, while Thymosin Beta-4 is the naturally occurring protein. Most published research uses Thymosin Beta-4, but TB-500 replicates the active region responsible for its healing properties.

Thymosin Beta-4 was originally isolated from the thymus gland (hence “thymosin”), where it was initially studied for its role in T-cell differentiation. Later research revealed its primary function: actin sequestration — regulating the polymerization of actin, a critical cytoskeletal protein involved in cell structure, migration, and signaling.

How Does TB-500 Work? (Mechanism of Action)

Actin Regulation

TB-500’s primary molecular function is binding to and sequestering G-actin (globular actin monomers), preventing their premature polymerization into F-actin (filamentous actin). This might sound counterintuitive for a healing peptide, but proper actin dynamics are essential for:

• Cell migration — cells need to remodel their cytoskeleton to move toward wound sites
• Cell proliferation — dividing cells require controlled actin dynamics
• Blood vessel formation — endothelial cell migration depends on actin remodeling
• Cellular signaling — many signaling cascades use actin as a scaffold

By maintaining a pool of available G-actin, TB-500 ensures cells can rapidly reorganize their cytoskeletons as needed during healing (Goldstein et al., 2005).

Anti-Inflammatory Effects

Thymosin Beta-4 has demonstrated significant anti-inflammatory properties. In multiple injury models, it reduces levels of pro-inflammatory cytokines including:

• IL-1β (interleukin-1 beta)
• IL-6 (interleukin-6)
• TNF-α (tumor necrosis factor alpha)

It also promotes the expression of anti-inflammatory mediators. In a rat corneal injury model, Tβ4 treatment significantly reduced inflammatory cell infiltration and suppressed NF-κB activation, a master regulator of inflammatory gene expression (Sosne et al., 2007).

Angiogenesis

Like BPC-157, TB-500 promotes new blood vessel formation. It stimulates endothelial cell migration and tube formation (the functional assay for angiogenesis in vitro). The mechanism appears to involve upregulation of VEGF and its receptor, as well as direct effects on endothelial cell actin dynamics (Malinda et al., 1999).

Cardiac Repair

One of the most exciting research areas for Thymosin Beta-4 is cardiac repair. In murine models of myocardial infarction, Tβ4 treatment:

• Reduced infarct size
• Improved cardiac function (ejection fraction)
• Promoted survival of cardiomyocytes
• Activated cardiac progenitor cells

This led to the development of a synthetic version (RGN-352) that entered Phase I/II clinical trials for acute myocardial infarction, though results were mixed (Smart et al., 2007).

Hair Growth

A somewhat unexpected finding: Thymosin Beta-4 promotes hair growth in mice. Tβ4 appears to accelerate hair follicle stem cell migration and differentiation, leading to faster hair growth in wound-adjacent areas. This has generated interest in dermatological applications (Philp et al., 2004).

Research & Evidence

Wound Healing

In full-thickness dermal wound models in rats, Tβ4 significantly accelerated wound closure. Treatment with Tβ4 (5 μg applied topically) increased wound contraction, re-epithelialization, and collagen deposition compared to vehicle controls. Notably, Tβ4-treated wounds showed better organization of the extracellular matrix with less scarring (Malinda et al., 1999).

Corneal Healing

Multiple studies demonstrate Tβ4’s efficacy in corneal injury models. In rats with corneal alkali burns (one of the most severe eye injury models), topical Tβ4 treatment reduced inflammation, prevented scarring, and improved corneal transparency. This research led to the development of RGN-259 (synthetic Tβ4 eye drops) which completed Phase III clinical trials for dry eye disease with promising results (Dunn et al., 2010).

Brain and CNS

In a rat model of traumatic brain injury, systemic Tβ4 treatment (6 mg/kg IP) improved neurological functional recovery, reduced brain edema, and promoted neurogenesis and oligodendrogenesis in the injured hemisphere. The treated animals showed significantly better outcomes on motor and cognitive tests (Xiong et al., 2011).

Cardiac Studies

The most advanced clinical research on Thymosin Beta-4 has been in the cardiac space. RegeneRx Biopharmaceuticals developed RGN-352 for post-MI cardiac repair. Preclinical studies in both mouse and pig models showed improved cardiac function and reduced scarring. The Phase I safety trial showed the drug was well-tolerated, though the clinical development program has had a complex history (Crockford et al., 2010).

Musculoskeletal

In equine medicine, TB-500 (as synthetic Tβ4) has been more widely studied and used. Research in horses with tendon injuries showed improved healing outcomes, which is partly why TB-500 became a controlled substance in horse racing before gaining attention in human biohacking communities.

Benefits (Based on Research)

• Systemic healing acceleration — promotes healing across multiple tissue types
• Anti-inflammatory effects — reduces inflammatory mediators at injury sites
• Improved tissue remodeling — less scarring, better organization of repair tissue
• Flexibility and mobility support — community reports consistent improvement in joint mobility
• Cardiovascular protection — preclinical evidence for cardiac repair
• Neuroprotection — demonstrated in brain injury models
• Hair growth — accelerated follicle stem cell activity in animal models

Dosage Protocols

⚠️ Disclaimer: No human clinical trials have established dosing for TB-500 as a general healing agent. The following represents community-reported protocols. This is not medical advice.

Common Community Protocols

Loading Phase (first 4-6 weeks):

• Dose: 2–2.5 mg, twice per week
• Total weekly: 4–5 mg
• Purpose: Saturate tissues and establish therapeutic levels

Maintenance Phase:

• Dose: 2–2.5 mg, once per week (or every 2 weeks)
• Duration: 4–8 weeks or as needed

Injection Route: Subcutaneous injection

• Unlike BPC-157, TB-500 is generally injected subcutaneously anywhere — the injection does not need to be near the injury site. Thymosin Beta-4’s effects are considered systemic due to its role in cell signaling throughout the body.

Reconstitution

• TB-500 typically comes as a 5 mg lyophilized powder
• Reconstitute with 1–2 mL bacteriostatic water
• Store reconstituted solution refrigerated (2–8°C)
• Use within 3–4 weeks

Key Difference from BPC-157

TB-500 is generally dosed at milligram levels (2–5 mg per injection), compared to BPC-157’s microgram levels (250–500 mcg). The higher dose reflects the different pharmacodynamics and the peptide’s systemic distribution pattern.

Side Effects & Safety

Reported Side Effects (Community)

TB-500 has a relatively mild side effect profile in community reports:

• Head rush or lightheadedness — reported shortly after injection, typically transient
• Fatigue/lethargy — some users report temporary tiredness, particularly during the loading phase
• Injection site reactions — standard subcutaneous injection reactions
• Headache — occasionally reported, usually mild

Theoretical Concerns

• Cancer proliferation risk: As with BPC-157, the pro-angiogenic and cell-migration-promoting effects of Tβ4 raise theoretical concerns about cancer. Some research has found elevated Tβ4 levels in certain tumor types, though the relationship between exogenous Tβ4 and tumor growth is not established. Studies are conflicting — some show Tβ4 does not promote tumor growth, while others find associations with tumor aggressiveness (Ryu et al., 2012).
• Blood pressure effects: Tβ4 can affect vasodilation, which may transiently affect blood pressure.
• No long-term human safety data — the most critical limitation.

Banned in Sports

TB-500/Thymosin Beta-4 is explicitly listed on the WADA Prohibited List under peptide hormones, growth factors, and related substances. It is banned both in-competition and out-of-competition. Several athletes, including professional footballers and horse trainers, have been sanctioned for TB-500 use.

Stacking Options

• TB-500 + BPC-157: The classic healing stack. BPC-157 works locally at the injury site while TB-500 provides systemic healing support. Different mechanisms create genuine synergy.
• TB-500 + GHK-Cu: For anti-aging and tissue remodeling. Both promote collagen remodeling through different pathways.
• TB-500 + Ipamorelin/CJC-1295: Adding growth hormone secretagogues amplifies the anabolic and repair environment.

Legal Status

United States

Not FDA-approved for human use. Sold as a research chemical. The FDA’s position on compounded Thymosin Beta-4 products has tightened, with warning letters issued to some pharmacies.

Australia

Classified under Schedule 4 (prescription-only). Used in veterinary medicine (particularly equine) under veterinary supervision.

WADA

Explicitly prohibited under Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Athletes in WADA-tested sports should avoid TB-500.

Horse Racing

Banned in horse racing in most jurisdictions worldwide. TB-500 gained notoriety through several high-profile horse racing scandals.

Frequently Asked Questions

What’s the difference between TB-500 and Thymosin Beta-4? TB-500 is a synthetic peptide that replicates the active region of the naturally occurring protein Thymosin Beta-4. Most published research uses Thymosin Beta-4, while the consumer/research chemical market sells TB-500. They are functionally similar for healing purposes.

Do I need to inject TB-500 near the injury? No. Unlike BPC-157, TB-500 is considered a systemic peptide. Subcutaneous injection anywhere on the body is standard practice, as Tβ4 distributes throughout the body via circulation.

Can I use TB-500 and BPC-157 together? Yes — this is one of the most popular peptide stacks. They work through different mechanisms and are commonly used together for injury recovery. See our BPC-157 + TB-500 stack guide.

How long until I see results? Most community reports describe initial improvement within 2–3 weeks, with more substantial healing progress over 4–8 weeks. The loading phase helps establish tissue saturation.

Is TB-500 detectable in drug tests? Yes. TB-500/Thymosin Beta-4 can be detected by specialized anti-doping tests and is banned by WADA. It is not detected on standard workplace drug panels.

References

1. Goldstein AL, et al. “Thymosin beta4: actin-sequestering protein moonlights to repair injured tissues.” Trends Mol Med. 2005;11(9):421-9. PubMed
2. Sosne G, et al. “Thymosin beta 4 suppression of corneal NFkappaB: A potential anti-inflammatory pathway.” Exp Eye Res. 2007;84(4):663-9. PubMed
3. Malinda KM, et al. “Thymosin beta4 accelerates wound healing.” J Invest Dermatol. 1999;113(3):364-8. PubMed
4. Smart N, et al. “Thymosin beta4 induces adult epicardial progenitor mobilization and neovascularization.” Nature. 2007;445(7124):177-82. PubMed
5. Philp D, et al. “Thymosin beta 4 promotes angiogenesis, wound healing, and hair follicle development.” Mech Ageing Dev. 2004;125(2):113-5. PubMed
6. Dunn SP, et al. “Treatment of chronic nonhealing neurotrophic corneal epithelial defects with thymosin beta4.” Ann N Y Acad Sci. 2010;1194:199-206. PubMed
7. Xiong Y, et al. “Thymosin beta4 treatment of traumatic brain injury in the rat.” J Neurosurg. 2012;116(5):1081-92. PubMed
8. Crockford D, et al. “Thymosin beta4: structure, function, and biological properties supporting current and future clinical applications.” Ann N Y Acad Sci. 2010;1194:179-89. PubMed
9. Ryu YK, et al. “Thymosin beta-4 expression in hepatocellular carcinoma.” Pathology. 2012;44(4):335-8. PubMed

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