TB-500 (Thymosin Beta-4): The Complete Research Guide — Mechanism, Dosing & Applications
Last updated: April 14, 2026 · 17 min read · Reviewed by Grey Peptides Editorial Board
TL;DR
TB-500 is a synthetic fragment of Thymosin Beta-4 (Tβ4), a 43-amino-acid protein naturally produced in virtually every human cell. It is the body's primary intracellular regulator of actin — the structural protein that gives cells their shape and enables them to move. By binding G-actin (monomeric actin), TB-500 promotes cell migration, meaning it mobilizes repair cells (fibroblasts, endothelial cells, immune cells) to travel to damaged tissue. It also reduces inflammation and supports tissue remodeling. TB-500's effects are systemic — it works body-wide regardless of where it's injected, which distinguishes it from locally-acting peptides like BPC-157. The standard protocol uses a loading phase (2.5 mg twice weekly for 4–6 weeks) followed by a maintenance phase (1.5 mg once weekly for 4–6 weeks). TB-500 has zero human clinical trial data for musculoskeletal applications — all evidence comes from animal studies and extensive anecdotal reports.
→ Explore TB-500's profile interactively in the Peptide Encyclopedia.
→ Calculate your TB-500 dosing with the Reconstitution Calculator.
Table of Contents
- What Is TB-500?
- TB-500 vs Thymosin Beta-4
- Molecular Profile
- Mechanism of Action
- Preclinical Research Overview
- Human Clinical Evidence
- Dosing Protocols
- Reconstitution & Administration
- Side Effects & Safety Profile
- Legal & Regulatory Status
- TB-500 vs Other Repair Peptides
- Stacking TB-500
- The Equine Connection
- Frequently Asked Questions
- Sources
What Is TB-500?
TB-500 is a synthetic peptide corresponding to the active region of Thymosin Beta-4 (Tβ4), a naturally occurring protein found in nearly every cell in the human body. Thymosin Beta-4 was first isolated from the thymus gland (hence "thymosin") but is now known to be expressed in virtually all tissue types — blood platelets, wound fluid, inflammatory cells, and tissue fibroblasts contain particularly high concentrations.
The peptide's primary biological function is regulating actin — one of the most abundant proteins in eukaryotic cells. Actin provides the structural scaffolding that gives cells their shape and, critically, enables cells to move. Cell movement (migration) is fundamental to wound healing: repair cells must physically travel to the injury site, immune cells must reach infection sites, and endothelial cells must migrate to form new blood vessels.
TB-500 is the commercial name used in the research peptide market. It is generally understood to be a synthetic version of either the full 43-amino-acid Thymosin Beta-4 sequence or its most active fragment (the 17-amino-acid actin-binding domain, amino acids 17–23 of the parent molecule containing the key sequence LKKTETQ). In practice, most TB-500 products marketed as research peptides contain the full Tβ4 sequence.
TB-500 is not FDA-approved for any indication. It has no published controlled clinical trials for musculoskeletal healing in humans. Its evidence base consists entirely of animal studies, in vitro research, and a substantial body of anecdotal evidence from the peptide therapy and veterinary (equine) communities.
→ New to peptides? Start with the Beginner's Guide for foundational knowledge.
TB-500 vs Thymosin Beta-4: Clarifying the Terminology
The terms "TB-500" and "Thymosin Beta-4" are often used interchangeably in the peptide community, but they are not technically identical.
Thymosin Beta-4 (Tβ4) is the naturally occurring 43-amino-acid protein produced endogenously in human cells. It has been studied in formal pharmaceutical development under the names RGN-259 (for corneal healing) and RGN-352 (for cardiac repair) by the company RegeneRx Biopharmaceuticals.
TB-500 is a commercial/research name used by peptide suppliers. It typically refers to a synthetic version of the full Tβ4 sequence, though some products may contain only the active fragment. The TB-500 name does not appear in published scientific literature — papers reference "Thymosin Beta-4" or "Tβ4."
For practical purposes in the peptide therapy context, TB-500 and Tβ4 are treated as equivalent. The research discussed in this article references Tβ4 studies, which are applicable to TB-500 products containing the full sequence. When purchasing, verify that the product specifies the full Tβ4 sequence or its molecular weight (4,963 Da) to confirm you're receiving the correct compound.
Molecular Profile
| Property | Value |
|---|---|
| Full name | Thymosin Beta-4 |
| Commercial name | TB-500 |
| Amino acid sequence | Ac-SDKPDMAEIEKFDKSKLKKTETQEKNPLPSKETIEQEKQAGES |
| Chain length | 43 amino acids |
| Molecular weight | 4,963 Da |
| Key active region | LKKTETQ (amino acids 17–23, actin-binding domain) |
| Half-life | Estimated ~24 hours |
| Natural source | Nearly all nucleated cells; high concentrations in platelets, wound fluid |
| Common vial sizes | 2 mg, 5 mg, 10 mg |
| Storage (lyophilized) | Room temperature stable; refrigeration extends shelf life |
| Storage (reconstituted) | 2–8°C, use within 28 days |
| Solubility | Highly soluble in water |
TB-500 is notably larger than BPC-157 (4,963 Da vs 1,419 Da). This larger molecular weight can mean slightly slower dissolution during reconstitution — gentle swirling may need to be continued for a longer period. If undissolved particles remain after initial reconstitution, refrigerate for 30 minutes and swirl again before use.
→ Look up actin, fibroblast, G-actin, and other key terms at the Peptide Glossary.
Mechanism of Action
TB-500's biological activity centers on its interaction with actin and the downstream effects this has on cell behavior. Unlike BPC-157, which operates through multiple independent pathways, TB-500's mechanisms are primarily connected through the common thread of cytoskeletal regulation.
1. G-Actin Sequestration & Cell Migration
TB-500's core mechanism is binding monomeric (G-actin) to regulate actin polymerization — the process by which individual actin molecules assemble into filaments (F-actin) that form the cell's internal skeleton.
By sequestering G-actin, TB-500 prevents premature or disordered actin polymerization, allowing cells to restructure their cytoskeleton in an organized manner. This restructuring is what enables cell migration — the physical movement of cells through tissue toward an injury site.
The key active sequence LKKTETQ within Tβ4 is the actin-binding domain responsible for this interaction. Studies using synthetic LKKTETQ alone demonstrate cell migration activity, confirming this region as the functional core of the molecule. [1]
In practical terms, this means TB-500 mobilizes the repair workforce. Fibroblasts (which produce collagen and extracellular matrix), endothelial cells (which form new blood vessels), and keratinocytes (which close wounds) all migrate faster in the presence of Tβ4.
2. Anti-Inflammatory Activity
TB-500 demonstrates anti-inflammatory effects through multiple mechanisms. It downregulates pro-inflammatory cytokines (including NF-κB pathway mediators), reduces neutrophil infiltration into damaged tissue, and modulates macrophage polarization — shifting macrophages from the inflammatory M1 phenotype toward the reparative M2 phenotype. [2]
Inflammation is a necessary early phase of healing, but prolonged or excessive inflammation impedes repair. By moderating the inflammatory response without eliminating it entirely, TB-500 helps transition the healing process from the destructive inflammatory phase to the constructive proliferative phase more efficiently.
3. Angiogenesis Support
While BPC-157 is the more potent angiogenic peptide (via VEGF upregulation), TB-500 also supports new blood vessel formation. Endothelial cell migration — enhanced by TB-500's actin regulation — is a prerequisite for sprouting angiogenesis. Studies show that Tβ4 promotes endothelial cell differentiation and tube formation in vitro, contributing to neovascularization in healing tissue. [3]
4. Tissue Remodeling & Fibrosis Reduction
TB-500 appears to influence how damaged tissue is repaired — specifically, whether healing produces functional tissue or nonfunctional scar (fibrosis). Animal studies, particularly in cardiac tissue, suggest that Tβ4 promotes regenerative healing with reduced scar formation. This anti-fibrotic effect may be related to its regulation of matrix metalloproteinases (MMPs), enzymes that break down and remodel extracellular matrix during healing. [4]
5. Cardiac Progenitor Cell Activation
One of the most significant findings in Tβ4 research is its ability to activate epicardial progenitor cells in the heart following injury. These dormant cells, when activated by Tβ4, can differentiate into cardiomyocytes (heart muscle cells) and vascular smooth muscle cells — essentially regenerating functional heart tissue. This discovery, published in Nature, generated significant interest in Tβ4 as a potential cardiac regeneration therapy. [5]
→ See how TB-500's mechanisms compare to BPC-157 and GHK-Cu in the Comparison Tool.
Preclinical Research Overview
TB-500/Tβ4 has a substantial preclinical evidence base across multiple tissue systems. Unlike BPC-157 (dominated by one research group), Tβ4 research comes from multiple independent laboratories worldwide, including major institutions. This broader research base provides greater confidence in the findings.
Cardiac Tissue
The heart is the most extensively studied organ for Tβ4's regenerative effects. Multiple studies demonstrate:
Post-myocardial infarction recovery. Tβ4 administration after induced heart attacks in mice reduces scar size, preserves cardiac function, and promotes survival of cardiomyocytes in the infarcted zone. [6]
Cardiac progenitor cell activation. The landmark Nature study by Smart et al. (2011) showed that Tβ4 "primes" the adult epicardium (the heart's outer layer) before injury, enabling epicardium-derived progenitor cells to contribute to cardiac repair after subsequent damage. This represented a significant advance in cardiac regeneration research. [5]
Anti-fibrotic effects. Tβ4 reduces collagen deposition and fibrosis in cardiac tissue after injury, promoting functional tissue repair rather than scar formation. [4]
Corneal Tissue
Tβ4 has been studied extensively for corneal wound healing, leading to the most advanced clinical development of any Tβ4 application:
Corneal epithelial healing. Multiple studies show accelerated closure of corneal wounds, reduced inflammation, and decreased scarring. This led to the development of RGN-259, a topical Tβ4 eye drop that has completed Phase II/III clinical trials for neurotrophic keratitis (corneal nerve damage). [7]
Musculoskeletal Tissue
Tendon. Tβ4 has shown reduced adhesion formation and improved functional recovery in flexor tendon injury models in rats. The anti-adhesion effect is particularly relevant for hand and wrist tendon injuries where scar adhesion limits range of motion after surgery. [8]
Muscle. Studies demonstrate accelerated skeletal muscle regeneration, reduced fibrosis, and improved functional recovery after crush and laceration injuries. [9]
Nervous System
Peripheral nerve. Tβ4 promotes Schwann cell migration and axonal regeneration in peripheral nerve injury models. [10]
Central nervous system. Multiple sclerosis and traumatic brain injury models show that Tβ4 promotes oligodendrocyte differentiation (the cells that produce myelin) and reduces neuroinflammation. These findings have generated interest in Tβ4 as a potential treatment for demyelinating diseases. [11]
Skin & Wound Healing
Tβ4 accelerates full-thickness wound closure in animal models, with improved angiogenesis, collagen deposition, and wound contraction. These effects have been demonstrated across multiple species and wound types. [12]
Important Caveats
No controlled human musculoskeletal data. Despite the breadth of animal evidence, there are no published controlled clinical trials testing TB-500/Tβ4 for musculoskeletal healing, joint pain, or tendon repair in humans.
Pharmaceutical development challenges. RegeneRx Biopharmaceuticals, the company developing Tβ4 therapeutics, has progressed corneal and cardiac applications but has not pursued musculoskeletal indications. This may reflect the difficulty of demonstrating efficacy in soft tissue healing trials (subjective endpoints, high placebo response) rather than lack of biological plausibility.
Animal-to-human translation. Cardiac regeneration findings in mice may not translate to adult human hearts, which have much more limited regenerative capacity. The corneal data is the most promising for direct translation, given the similarity of corneal biology across species.
Human Clinical Evidence
Published Clinical Data
Corneal healing (RGN-259). RegeneRx's topical Tβ4 eye drop has completed Phase II and Phase III clinical trials for neurotrophic keratitis. Results demonstrated statistically significant improvement in corneal wound healing compared to vehicle control. This is the most advanced clinical application of Tβ4. [7]
Cardiac repair (RGN-352). An injectable Tβ4 formulation was studied in Phase I trials for acute myocardial infarction. Safety data was acceptable, but efficacy data has not been published as of this writing. [13]
Epidermolysis bullosa. Small-scale clinical investigations of Tβ4 for this severe skin blistering disorder have been reported, with preliminary positive findings. [14]
No Published Clinical Data For
- Tendon or ligament healing
- Joint pain or osteoarthritis
- Muscle recovery or sports injuries
- General wound healing (non-corneal)
- Inflammatory conditions
The gap between TB-500's extensive preclinical data and its near-absent clinical data for musculoskeletal applications is the primary limitation in evaluating this compound for the uses most popular in the peptide community.
Dosing Protocols
TB-500 dosing follows a distinctive loading/maintenance pattern that differs from most other peptides. This pattern reflects the hypothesis that tissue repair requires an initial period of elevated Tβ4 concentration to mobilize repair cells (loading), followed by a lower sustained level to support ongoing remodeling (maintenance).
Standard Protocol
| Phase | Dose | Frequency | Duration |
|---|---|---|---|
| Loading | 2.5 mg | 2x per week | 4–6 weeks |
| Maintenance | 1.5 mg | 1x per week | 4–6 weeks |
| Total protocol | — | — | 8–12 weeks |
Conservative Protocol (Lower Starting Dose)
| Phase | Dose | Frequency | Duration |
|---|---|---|---|
| Introduction | 1.5 mg | 2x per week | 2 weeks |
| Loading | 2.5 mg | 2x per week | 4 weeks |
| Maintenance | 1.5 mg | 1x per week | 4–6 weeks |
| Total protocol | — | — | 10–12 weeks |
Aggressive Protocol (Significant Injuries)
| Phase | Dose | Frequency | Duration |
|---|---|---|---|
| Intensive loading | 5 mg | 2x per week | 2 weeks |
| Standard loading | 2.5 mg | 2x per week | 4 weeks |
| Maintenance | 2.5 mg | 1x per week | 4 weeks |
| Total protocol | — | — | 10 weeks |
Dosing Principles
Loading phase rationale. The higher-frequency loading phase is designed to rapidly saturate tissue with Tβ4, initiating the cell migration cascade throughout the body. The 2x weekly dosing maintains elevated levels given TB-500's approximately 24-hour half-life.
Systemic action. Unlike BPC-157, TB-500 works systemically regardless of injection location. Injecting in the abdomen, thigh, or arm is equally effective — you do not need to inject near the injury site. This is because TB-500's mechanism (promoting cell migration from throughout the body to injury sites) operates at a systemic level.
Cycling. Most protocols recommend a complete cycle (loading + maintenance) followed by a rest period of 4–8 weeks before beginning another cycle if needed. Some practitioners maintain a low-dose weekly injection (1–1.5 mg) indefinitely for chronic conditions, though long-term safety data is unavailable.
→ Build a complete TB-500 protocol with the Protocol Builder.
Reconstitution & Administration
TB-500 follows standard reconstitution procedures. For a complete tutorial, see the How to Reconstitute Peptides guide.
Quick Reference
| Parameter | Value |
|---|---|
| Common vial size | 5 mg |
| Recommended BAC water | 2 mL |
| Resulting concentration | 2.5 mg/mL |
| 2.5 mg dose = | 100 units (1.0 mL) on U-100 syringe |
| 1.5 mg dose = | 60 units (0.6 mL) on U-100 syringe |
| Doses per 5 mg vial (loading) | 2 doses |
| Storage after reconstitution | 2–8°C, up to 28 days |
TB-500 Reconstitution Notes
TB-500 has a higher molecular weight (4,963 Da) than many other peptides and may dissolve more slowly. When adding BAC water, let it trickle down the vial wall slowly and swirl gently. If particles remain undissolved after 2 minutes of gentle swirling, refrigerate the vial for 30 minutes and try again. The solution should be completely clear before use.
Injection Volume
Note that TB-500 loading doses are relatively large volumes compared to peptides like BPC-157. A 2.5 mg dose at the standard 2.5 mg/mL concentration requires drawing 1.0 mL — the full capacity of a 1.0 mL (100-unit) insulin syringe. If your reconstitution concentration is lower (e.g., 3 mL BAC water = 1.67 mg/mL), the injection volume increases to 1.5 mL, which exceeds insulin syringe capacity and requires a standard syringe.
To keep injection volumes manageable with insulin syringes, reconstitute with 2 mL or less of BAC water.
→ Enter your vial size for exact calculations at the Reconstitution Calculator.
Side Effects & Safety Profile
TB-500/Tβ4 has a generally favorable safety profile in the available data, though the evidence base is more limited than for extensively studied pharmaceuticals.
Observed in Animal Studies & Clinical Trials
No significant toxicity has been observed in animal studies or in the Phase I/II human clinical trials conducted for corneal and cardiac applications. The compound has a wide therapeutic window. [13]
Reported in Community Use
Injection site reaction. Mild redness, swelling, or itching at the injection site. More common with larger injection volumes (the 2.5 mg loading dose is a relatively large SubQ volume).
Fatigue. Transient tiredness reported by some users in the first 1–2 weeks. May be related to the systemic immune modulation effects.
Headache. Occasional, usually mild, more common during the loading phase.
Flu-like symptoms. A small percentage of users report mild flu-like symptoms (low-grade fatigue, mild body aches) during the first week of loading. This may reflect immune system modulation, as Tβ4 has well-documented effects on immune cell function. Typically resolves after the first few doses.
Temporary increase in discomfort at injury site. Some users report a brief increase in discomfort at the healing site during the first few days. This may indicate activation of the inflammatory-to-repair transition at the injury and is generally considered a positive sign that resolves quickly.
Theoretical Concerns
Tumor growth. Like BPC-157's angiogenic concerns, TB-500's cell migration-promoting effects raise a theoretical question about whether it could facilitate tumor cell migration (metastasis). This has not been validated or disproven in controlled studies. Some in vitro data suggests Tβ4 may be overexpressed in certain cancer cell lines, but the clinical significance for exogenous TB-500 administration is unknown. Individuals with active malignancies should avoid TB-500 as a precaution. [15]
Long-term safety. No long-term safety data exists for subcutaneous TB-500 administration in humans at the doses used in the peptide community. The cycling convention is precautionary.
→ Check for interactions with your current supplements or peptides at the Interaction Checker.
Legal & Regulatory Status
TB-500/Thymosin Beta-4 has a regulatory profile similar to BPC-157 — not approved, not specifically banned in most jurisdictions, existing in a gray area.
United States. Not FDA-approved for any indication. Available as a research chemical. FDA has included it on the 503A/503B compounding evaluation list. Compounding pharmacies have produced it under various regulatory interpretations.
European Union. Not approved as a pharmaceutical. Available through research suppliers.
Australia. Classification varies. Some formulations available by prescription through compounding pharmacies.
Sports. WADA lists Thymosin Beta-4 as prohibited under category S2 (Peptide Hormones, Growth Factors, Related Substances). Any athlete subject to WADA testing should not use TB-500.
→ Full legal analysis: Are Peptides Legal? 2026 Guide.
TB-500 vs Other Repair Peptides
| Feature | TB-500 | BPC-157 | GHK-Cu |
|---|---|---|---|
| Primary mechanism | Cell migration (actin) | Angiogenesis (VEGF) | ECM remodeling |
| Action type | Systemic | Local (primarily) | Local/topical |
| Best for | Systemic repair, chronic injuries | Acute injuries, GI healing | Skin, anti-aging, hair |
| Injection location | Anywhere (systemic) | Near injury site | Near target or topical |
| Half-life | ~24 hours | ~4 hours | ~12 hours |
| Dosing frequency | 2x/week (loading), 1x/week (maint.) | 1–2x daily | 1x daily |
| Injection volume | Large (0.6–1.0 mL) | Small (0.1–0.2 mL) | Small |
| Human clinical data | Corneal only | 1 pilot study (GI) | Topical studies |
| Independent research | Multiple labs worldwide | Primarily one lab (Zagreb) | Multiple labs |
| Gastric stability | No | Yes (oral viable) | No |
The key distinction: TB-500 is the systemic mobilizer — it works body-wide to move repair cells to wherever damage exists. BPC-157 is the local builder — it creates blood supply infrastructure at the injection site. GHK-Cu is the remodeler — it restructures the extracellular matrix for better tissue quality. These three mechanisms are complementary, which is why multi-peptide repair stacks are popular.
→ Full comparison analysis: BPC-157 vs TB-500.
Stacking TB-500
TB-500 is rarely used alone. Its systemic cell-migration mechanism is most effective when combined with compounds that address other aspects of the repair process.
TB-500 + BPC-157 (The Repair Stack)
The most widely used peptide combination for tissue healing. TB-500 provides systemic cell migration and anti-inflammatory effects; BPC-157 provides local angiogenesis and GH receptor upregulation. Strong synergy — complementary, non-overlapping pathways.
→ Full protocol: BPC-157 + TB-500 Stack Guide.
TB-500 + BPC-157 + GHK-Cu (The Wolverine Stack)
Adds extracellular matrix remodeling to the repair stack. Blood supply (BPC-157) + cell migration (TB-500) + tissue structure (GHK-Cu). The most comprehensive repair combination. Commonly used post-surgery or for serious injuries with the goal of optimal tissue quality, not just healing speed.
TB-500 + CJC-1295/Ipamorelin (Recovery + GH)
Combines systemic tissue repair with growth hormone optimization. The elevated GH enhances the repair cell response that TB-500 initiates. Particularly popular among athletes who want comprehensive recovery support.
→ Verify any combination's safety at the Interaction Checker.
The Equine Connection
TB-500's most extensive real-world use history comes not from human medicine but from horse racing. Thymosin Beta-4 was widely used in the equine industry for decades before gaining popularity in human peptide therapy.
Racehorses commonly suffer from tendon, ligament, and joint injuries. Trainers and equine veterinarians adopted TB-500 based on its tissue repair properties, and the compound became one of the most commonly used performance and recovery agents in thoroughbred racing.
This equine history is a double-edged sword for TB-500's reputation. On one hand, decades of widespread use in horses without reports of significant adverse effects provides a degree of practical safety data (though systematic reporting in equine medicine is less rigorous than human clinical trials). On the other hand, the association with horse racing — and the doping scandals that periodically emerge from that industry — has given TB-500 a controversial public profile.
Several high-profile equine doping investigations have involved Thymosin Beta-4 detection. Racing authorities in multiple countries have banned the compound in competition animals. This regulatory history directly influenced WADA's decision to add Tβ4 to its prohibited list for human athletes.
For the purposes of evaluating TB-500's therapeutic potential, the equine connection is relevant primarily as a source of practical (though uncontrolled) efficacy data and long-term safety observation. It is not a substitute for controlled human clinical trials.
Frequently Asked Questions
How quickly does TB-500 work? Most users report initial changes during the loading phase (weeks 1–4), with significant improvement by the end of the full protocol (8–12 weeks). The timeline varies by injury type and severity. Acute injuries may respond faster than chronic conditions.
Do I need to inject near the injury? No. TB-500 works systemically — it promotes cell migration body-wide regardless of injection location. Inject in any convenient SubQ site (abdomen, thigh, upper arm). This is a key difference from BPC-157, which is typically injected near the injury for local effect.
Can I use TB-500 alone, without BPC-157? Yes, though most practitioners recommend the combination for optimal results. TB-500 alone provides cell migration and anti-inflammatory benefits. Adding BPC-157 provides complementary angiogenesis that enhances the overall repair response.
Is TB-500 the same as Thymosin Alpha-1? No. Thymosin Alpha-1 (Tα1, brand name Zadaxin) is a completely different molecule with different functions. Tα1 is a 28-amino-acid peptide that modulates the immune system and is FDA-approved in some countries for hepatitis B and C treatment. Despite sharing the "thymosin" name, Tα1 and Tβ4 have different sequences, receptors, and biological activities.
Will TB-500 help with hair growth? Some users report improved hair density and growth during TB-500 use. There is preclinical evidence that Tβ4 promotes hair follicle stem cell migration and differentiation. However, this is not a well-studied application, and results are inconsistent across user reports.
How should I store TB-500 vials? Lyophilized (powder) TB-500 is stable at room temperature but lasts longer refrigerated. After reconstitution, store at 2–8°C (refrigerator) and use within 28 days. Never freeze reconstituted TB-500 — ice crystal formation can damage the peptide.
Is TB-500 banned in sports? Yes. WADA prohibits Thymosin Beta-4 under category S2. Athletes subject to drug testing by WADA-affiliated organizations should not use TB-500.
Related Tools & Guides
- Reconstitution Calculator — Calculate exact TB-500 dose units and syringe markings
- Protocol Builder — Build a complete loading/maintenance schedule
- Comparison Tool — Compare TB-500 head-to-head with any peptide
- Interaction Checker — Verify TB-500 stacking safety
- Half-Life Visualizer — See TB-500's 24-hour plasma curve
- Cost Calculator — Estimate loading + maintenance protocol costs
Related Articles
- BPC-157 vs TB-500: Which Repair Peptide Is Better?
- BPC-157 + TB-500 Stack: The Complete Repair Protocol
- BPC-157: The Complete Research Profile
- Best Peptides for Healing Injuries
- Peptide Stacking Rules: What to Combine & What to Avoid
Sources
- Goldstein, A. L. & Kleinman, H. K. (2015). Thymosin β4: actin-sequestering protein moonlights to repair injured tissues. Trends in Molecular Medicine, 11(9), 421–429. PMID: 16099219
- Sosne, G. et al. (2010). Thymosin beta 4: a potential novel therapy for neurotrophic keratopathy, dry eye, and ocular surface diseases. Vitamins and Hormones, 79, 261–286. PMID: 20435055
- Malinda, K. M. et al. (1999). Thymosin β4 accelerates wound healing. Journal of Investigative Dermatology, 113(3), 364–368. PMID: 10469334
- Bock-Marquette, I. et al. (2004). Thymosin β4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature, 432(7016), 466–472. PMID: 15565145
- Smart, N. et al. (2011). De novo cardiomyocytes from within the activated adult heart after injury. Nature, 474(7353), 640–644. PMID: 21654746
- Hinkel, R. et al. (2015). Thymosin β4 is an essential paracrine factor of embryonic endothelium in cardiac development and repair. Circulation Research, 117(1), 52–65. PMID: 25904601
- Dunn, S. P. et al. (2010). Treatment of chronic nonhealing neurotrophic corneal epithelial defects with thymosin β4. Archives of Ophthalmology, 128(5), 636–638. PMID: 20457988
- Ruff, D. et al. (2010). The effect of thymosin beta-4 on tendon healing in an animal model. Plastic and Reconstructive Surgery, 126(Suppl), 91.
- Spurrier, R. G. et al. (2016). Thymosin beta-4 promotes skeletal muscle regeneration. FASEB Journal, 30(Suppl 1), 753.
- Zhang, J. et al. (2012). Thymosin beta 4 promotes oligodendrogenesis in demyelinated brains. Neurobiology of Disease, 48(3), 334–343. PMID: 22820143
- Morris, D. C. et al. (2014). Thymosin β4 treatment of brain-injured rats. Journal of the Neurological Sciences, 338(1–2), 48–55. PMID: 24444756
- Philp, D. et al. (2004). Thymosin β4 increases hair growth by activation of hair follicle stem cells. FASEB Journal, 18(2), 385–387. PMID: 14657001
- RegeneRx Biopharmaceuticals. (2015). RGN-352 Phase I trial results for acute myocardial infarction. Clinical trial data report.
- Treadwell, T. et al. (2018). The regenerative peptide thymosin β4 accelerates the rate of dermal healing in preclinical animal models and in patients. Annals of the New York Academy of Sciences, 1270(1), 37–44. PMID: 23050816
- Huang, H. C. et al. (2013). Thymosin β4 triggers an epithelial-mesenchymal transition in colorectal cancer cells and promotes metastasis. Oncogene, 32(41), 4989–4999. PMID: 23222715
Medical Disclaimer: This article is for educational and informational purposes only. It does not constitute medical advice, diagnosis, or treatment. TB-500 (Thymosin Beta-4) is not FDA-approved for any indication. It is prohibited by WADA for competitive athletes. Peptide therapy should be pursued under the supervision of a licensed healthcare professional. Always consult with a qualified medical provider before beginning any peptide protocol.
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This article is for educational purposes only and does not constitute medical advice. Consult a licensed medical professional before considering any peptide therapy.