What Is TB-500?
TB-500 is a synthetic peptide that replicates the active region of thymosin beta-4 (Tβ4), a 43-amino-acid protein that is one of the most abundant and well-studied members of the beta-thymosin family. Your body produces thymosin beta-4 in virtually every cell type, with particularly high concentrations in blood platelets, wound fluid, and developing tissues.
The protein was originally discovered in the thymus gland — a small organ behind your breastbone that plays a critical role in immune system development. Allan Goldstein and colleagues first isolated thymosin beta-4 in the 1960s and 1970s as part of a larger family of thymic peptides. However, researchers later realized that thymosin beta-4 is produced far beyond the thymus. It appears throughout the body wherever tissue repair, cell movement, and growth are needed (Goldstein et al., 2012).
Think of thymosin beta-4 as your body’s internal repair coordinator. When you cut your finger, sprain an ankle, or strain a muscle, thymosin beta-4 levels increase at the injury site. It helps orchestrate the complex process of healing — bringing the right cells to the right place, building new blood vessels to supply nutrients, and calming inflammation so repair can proceed efficiently.
Key characteristics of TB-500:
- Synthetic version of the active region of thymosin beta-4
- 43 amino acids in the full-length natural protein
- Found in virtually all human and animal cell types
- Especially concentrated in blood platelets and wound fluid
- Highly conserved across species (the sequence is nearly identical in mammals)
- Water-soluble, administered via injection in research settings
- Not FDA-approved for any human therapeutic use
One important distinction: TB-500 is not identical to thymosin beta-4, but it contains the same active fragment responsible for the protein’s primary biological effects. The key active sequence is a 17-amino-acid segment known as the actin-binding domain, centered around the sequence LKKTETQ (amino acids 17–23). This is the region that drives most of the cell migration and wound-healing effects attributed to thymosin beta-4.
Why “TB-500”?
The name TB-500 comes from the research and veterinary nomenclature. “TB” stands for thymosin beta, and “500” refers to its cataloging as a research compound. In the equine (horse racing) industry, thymosin beta-4 products have been used for decades under various names to support recovery from leg and tendon injuries. This veterinary history predates much of the current human research interest.
How TB-500 Works: Mechanisms of Action
TB-500 works through several interconnected biological mechanisms. Understanding these helps explain why the same peptide shows up in research on wound healing, cardiac repair, brain injury, and hair growth. It is not targeting one narrow pathway — it is activating a broad repair response.
1. Actin Binding and Cell Migration
The most well-characterized function of thymosin beta-4 is its ability to bind actin — one of the most abundant proteins inside your cells. Actin forms the internal “skeleton” of your cells (called the cytoskeleton), and it is the protein that allows cells to move, change shape, and divide.
Here is an analogy: imagine your cells need to travel to an injury site, like emergency workers heading to a disaster zone. They need roads and vehicles to get there. Actin is both the road-building material and the engine that drives cell movement. Thymosin beta-4 acts as the traffic coordinator — it manages the pool of available actin, ensuring cells can rapidly reorganize their internal structure to move toward the area that needs repair.
Specifically, thymosin beta-4 sequesters (holds onto) monomeric G-actin, the unpolymerized form of actin. By controlling how much free actin is available for polymerization, it regulates how quickly cells can extend projections, crawl toward wound sites, and establish themselves in damaged tissue (Goldstein et al., 2012).
This cell migration effect is central to nearly all of TB-500’s observed benefits. Faster cell migration means faster wound closure, quicker tissue remodeling, and more efficient delivery of repair resources to damaged areas.
2. Angiogenesis Promotion
Angiogenesis is the formation of new blood vessels from existing ones. When tissue is damaged, the injured area needs an increased blood supply to deliver oxygen, nutrients, and immune cells. TB-500 has been shown to promote angiogenesis in multiple research models.
Think of it this way: after an injury, the damaged tissue is like a neighborhood that lost its water and power supply. Angiogenesis is the process of building new pipes and power lines. TB-500 appears to accelerate this process by stimulating endothelial cells (the cells that line blood vessels) to migrate and form new vessel structures (Malinda et al., 1999).
This pro-angiogenic effect is particularly relevant for injuries involving tendons, ligaments, and cardiac tissue — all areas with naturally limited blood supply where healing tends to be slow.
3. Anti-Inflammatory Effects
Chronic or excessive inflammation is one of the biggest obstacles to efficient tissue repair. While acute inflammation is necessary (it clears debris and fights infection), prolonged inflammation actually damages healthy tissue and delays healing.
TB-500 has demonstrated anti-inflammatory properties in several research contexts. It appears to downregulate pro-inflammatory cytokines (chemical messengers that drive inflammation) and modulate the inflammatory response so it resolves more quickly. This creates a more favorable environment for repair cells to do their work.
In corneal injury models, for example, thymosin beta-4 significantly reduced inflammation markers while simultaneously accelerating the healing process (Sosne et al., 2002).
4. Hair Follicle Stem Cell Migration
One of the more surprising research findings involves TB-500’s effects on hair growth. Researchers discovered that thymosin beta-4 stimulates hair follicle stem cells to migrate and differentiate — essentially reactivating dormant hair follicles.
Philp and colleagues found that thymosin beta-4 promoted hair growth in normal and aged rats by activating hair follicle progenitor cells, increasing the rate at which follicles entered the active growth phase (anagen) (Philp et al., 2004).
This connects back to the actin-binding mechanism: hair follicle stem cells need to physically migrate to the base of the follicle and then differentiate into hair-producing cells. TB-500’s ability to enhance cell migration appears to facilitate this process.
5. Tissue Repair Signaling
Beyond its direct effects on cell migration and blood vessel growth, thymosin beta-4 also acts as a signaling molecule that activates broader repair pathways. It has been shown to:
- Promote extracellular matrix remodeling: Helping the structural scaffolding of tissues reorganize during repair
- Reduce fibrosis (scarring): In cardiac and skin injury models, thymosin beta-4 treatment was associated with less scar tissue formation and more functional tissue regeneration
- Support cell survival: Thymosin beta-4 has anti-apoptotic (anti-cell-death) properties, helping cells survive under stress conditions
- Modulate metalloproteinases (MMPs): These enzymes break down and rebuild the structural proteins of tissue, and thymosin beta-4 helps regulate their activity during healing
The combination of all these mechanisms — faster cell migration, new blood vessel formation, reduced inflammation, less scarring, and improved cell survival — explains why TB-500 appears in research spanning so many different tissue types and injury models.
TB-500 Research Highlights
The research on thymosin beta-4 spans several decades and includes studies on wound healing, cardiac repair, corneal injuries, brain injuries, and musculoskeletal healing. Here are the most significant findings.
Wound Healing
One of the foundational studies on thymosin beta-4’s healing properties came from Malinda and colleagues in 1999. They demonstrated that thymosin beta-4 accelerated wound healing in a rat full-thickness skin wound model. The treated wounds showed faster closure, enhanced angiogenesis (new blood vessel formation), and increased collagen deposition compared to controls (Malinda et al., 1999).
This was a pivotal study because it established the link between thymosin beta-4’s known role in actin regulation and a practical therapeutic application. The researchers showed that the same protein that helps cells move inside your body could be applied topically or via injection to speed up wound repair.
Subsequent studies built on this work, demonstrating that thymosin beta-4 promoted wound healing in aged mice, diabetic mice (which heal very slowly), and other compromised healing models. The consistent finding across these models was that thymosin beta-4 improved both the speed and the quality of wound healing — not just closing the wound faster, but producing better, more functional tissue.
Cardiac Repair
Perhaps the most dramatic research findings come from cardiac studies. In a landmark 2004 paper, Bock-Marquette and colleagues published results in Nature showing that thymosin beta-4 improved cardiac function following myocardial infarction (heart attack) in mice (Bock-Marquette et al., 2004).
The study found that thymosin beta-4 activated a survival kinase called Akt (also known as protein kinase B), which protected heart muscle cells from dying after the blood supply was cut off. When administered after a heart attack in the mouse model, thymosin beta-4:
- Reduced the area of dead heart tissue
- Improved the survival of cardiomyocytes (heart muscle cells)
- Enhanced recovery of cardiac function
This was groundbreaking because the heart has very limited regenerative capacity. Once heart muscle cells die during a heart attack, they are typically replaced by non-functional scar tissue. Thymosin beta-4 appeared to change this equation by keeping more heart cells alive through the crisis period.
Smart and colleagues followed up in 2007 with research showing that thymosin beta-4 could activate epicardial progenitor cells — a type of stem cell in the heart — to migrate, differentiate, and contribute to cardiac repair. This suggested that thymosin beta-4 was not only protecting existing cells but potentially activating the heart’s own regenerative capacity (Smart et al., 2007).
Corneal Healing
Sosne and colleagues conducted a series of studies examining thymosin beta-4’s effects on corneal wound healing. Their 2002 work demonstrated that thymosin beta-4 promoted corneal wound healing after alkali injury in a rat model, reducing inflammation and accelerating re-epithelialization (the regrowth of the surface cell layer) (Sosne et al., 2002).
The corneal research is particularly notable because:
- The cornea is avascular (has no blood vessels), so the angiogenesis effects are less relevant — yet thymosin beta-4 still promoted healing through its cell migration and anti-inflammatory pathways
- Corneal injuries can be sight-threatening, and current treatments are limited
- This research led to the development of RGN-259, a sterile eye drop formulation containing thymosin beta-4, which has been evaluated in human clinical trials for dry eye disease and neurotrophic keratopathy
RGN-259 represents one of the closest translational applications of thymosin beta-4 research — moving from basic science toward potential clinical use.
Hair Regrowth Research
Philp and colleagues made the connection between thymosin beta-4 and hair growth in 2004, demonstrating that the protein stimulated hair follicle stem cell differentiation and accelerated hair growth in rat models. They found that thymosin beta-4 increased the proportion of hair follicles in the active growth phase and promoted the clumping and migration of follicle stem cells (Philp et al., 2004).
While these findings are from animal models and direct translation to human hair loss treatment is not established, the results have generated significant interest in the hair restoration field. The mechanism — activating dormant stem cells in the hair follicle — addresses a root cause of certain types of hair loss.
Muscle Injury and Inflammation
Research on thymosin beta-4’s role in musculoskeletal healing draws from several lines of evidence:
- Tendon repair: Studies in animal models have shown improved healing of tendons treated with thymosin beta-4, with better collagen organization and stronger mechanical properties
- Muscle regeneration: Thymosin beta-4 has been shown to promote satellite cell activation — the muscle-specific stem cells responsible for muscle repair — and to improve the organization of regenerating muscle fibers
- Anti-inflammatory effects in joints: Research has demonstrated reduced inflammatory markers in joint injury models treated with thymosin beta-4
The equine (horse racing) industry has used thymosin beta-4 products for musculoskeletal recovery for years, which provided some of the early observational evidence for its effects on tendon and ligament injuries. While this veterinary experience is not equivalent to controlled human clinical trials, it represents a substantial body of practical use.
TB-500 vs BPC-157: Key Differences
TB-500 and BPC-157 are the two most discussed healing peptides in research communities. While they share the broad goal of promoting tissue repair, they work through different mechanisms and have different research profiles.
| Feature | TB-500 (Thymosin Beta-4) | BPC-157 (Body Protection Compound) |
|---|---|---|
| Origin | Naturally produced in nearly all human cells; synthetic version used in research | Derived from a protein in human gastric juice; synthetic and not naturally occurring in isolated form |
| Size | 43 amino acids (full-length thymosin beta-4) | 15 amino acids |
| Primary Mechanism | Actin binding, cell migration, angiogenesis | Nitric oxide modulation, growth factor upregulation, gut-brain axis signaling |
| Research Focus | Cardiac repair, wound healing, corneal injuries, hair growth, tendon repair | Gut healing, tendon/ligament repair, muscle injuries, neuroprotection |
| Administration | Subcutaneous or intramuscular injection | Subcutaneous injection, intramuscular injection, oral (orally active in animal models) |
| Systemic vs Local | Acts systemically — effects not limited to injection site | Can act both locally and systemically |
| Angiogenesis | Strong pro-angiogenic effects | Moderate angiogenic effects; also promotes existing vessel repair |
| Anti-Inflammatory | Moderate anti-inflammatory properties | Strong anti-inflammatory, especially in the GI tract |
| Clinical Trials | RGN-259 (eye drop) has entered human clinical trials | No published Phase II or III human clinical trials as of 2026 |
| FDA Status | Not approved for any human therapeutic use | Not approved for any human therapeutic use |
How They Complement Each Other
TB-500 and BPC-157 target overlapping but distinct repair pathways. TB-500’s strength lies in its ability to mobilize cells and build new blood vessel networks — the infrastructure side of healing. BPC-157’s strength lies in its ability to modulate the chemical signaling environment — reducing inflammation, upregulating growth factors, and protecting cells from further damage.
Think of rebuilding a house after a storm. TB-500 is the construction crew that moves materials and workers to the job site and builds new roads (blood vessels) to supply the project. BPC-157 is the project manager that coordinates the repair plan, calls off the emergency response (inflammation), and ensures the rebuild follows a functional blueprint (growth factor signaling).
This is why many researchers and clinicians have become interested in combining the two — an approach sometimes called the “Wolverine Stack.”
Research Dosing Protocols
Typical Research Dosing Framework
Research protocols typically follow a two-phase approach:
Loading Phase (Weeks 1–4 to 1–6):
The initial loading phase uses a higher dose to build up tissue concentrations of the peptide. Commonly referenced research doses during the loading phase range from 2 mg to 2.5 mg administered via subcutaneous injection twice per week.
Some research protocols use weight-based calculations, typically in the range of 20–50 mcg per kilogram of body weight per dose. For an 80 kg (176 lb) individual, that would translate to approximately 1.6 mg to 4 mg per dose.
Maintenance Phase (Following the loading phase):
After the initial loading period, research protocols typically reduce to a maintenance dose. Commonly referenced maintenance doses range from 2 mg to 2.5 mg administered once per week or once every two weeks.
Example Research Protocol (Commonly Referenced)
| Phase | Dose | Frequency | Duration |
|---|---|---|---|
| Loading | 2.0–2.5 mg | Twice per week (subcutaneous) | 4–6 weeks |
| Maintenance | 2.0–2.5 mg | Once per week | 2–4 weeks |
| Break | None | — | 2–4 weeks |
Some protocols cycle TB-500 — using it for a defined period, taking a break, and then resuming if needed. This cycling approach is not well-studied in formal research, but it is commonly referenced in practitioner frameworks.
Reconstitution Notes
TB-500 for research purposes typically comes as a lyophilized (freeze-dried) powder that requires reconstitution with bacteriostatic water before injection. General reconstitution guidelines from research contexts:
- Use bacteriostatic water (not sterile water or saline) for multi-use vials, as the benzyl alcohol preservative prevents bacterial growth
- Inject the water slowly along the inside wall of the vial rather than directly onto the powder
- Gently swirl the vial to dissolve the powder; do not shake vigorously as this can damage the peptide
- Store reconstituted peptide in the refrigerator (2–8°C) and use within 25–30 days
- Unreconstituted powder can be stored at room temperature for short periods, but refrigeration or freezing extends shelf life
Injection Protocol Notes
In research contexts, TB-500 is typically administered via subcutaneous (under the skin) injection. Common injection sites include:
- The abdominal area (rotating injection sites)
- The thigh
- The upper arm (deltoid area)
Some practitioners reference injecting closer to the injury site, though thymosin beta-4 is known to act systemically — meaning it circulates throughout the body rather than remaining localized at the injection site.
Side Effects and Safety Profile
What the Research Shows
Thymosin beta-4 has been studied in various research and clinical contexts, and the general safety profile appears favorable compared to many other peptides. The protein is naturally produced in the body, which suggests a lower likelihood of severe adverse reactions compared to entirely foreign compounds.
The clinical trials for RGN-259 (the thymosin beta-4 eye drop formulation) provided some of the most structured safety data. In these trials, thymosin beta-4 administered topically to the eye was generally well-tolerated with a low incidence of adverse events.
In preclinical studies using injectable thymosin beta-4, the compound has shown a wide therapeutic window — meaning the difference between effective doses and toxic doses is relatively large.
Commonly Reported Side Effects
Based on available research data and practitioner reports, the most commonly mentioned side effects of TB-500 include:
- Injection site reactions: Redness, mild pain, or swelling at the injection site — this is the most common side effect and is shared by virtually all injectable peptides
- Temporary lethargy or fatigue: Some research subjects report feeling tired in the hours following injection, particularly during the loading phase
- Head rush or lightheadedness: Occasional reports of brief lightheadedness shortly after administration
- Mild nausea: Infrequently reported, typically resolving quickly
Serious Side Effect Considerations
No serious adverse events have been consistently linked to thymosin beta-4 in published research literature. However, several theoretical concerns deserve mention:
Cancer considerations: Because thymosin beta-4 promotes cell migration and angiogenesis, there has been theoretical concern that it could promote tumor growth or metastasis in individuals with existing cancers. Some studies have found elevated thymosin beta-4 levels in certain tumor types, though whether this is a cause or consequence is not clear. As a precautionary measure, TB-500 is generally not recommended for individuals with active malignancies.
Cardiovascular effects: While thymosin beta-4 shows promise for cardiac repair, individuals with existing cardiovascular conditions should exercise caution and consult with their healthcare provider.
Autoimmune considerations: Because thymosin beta-4 modulates immune function and cell migration, individuals with autoimmune conditions should discuss potential interactions with their healthcare provider.
What We Do Not Know
It is important to be transparent about the limitations of the current safety data:
- No large-scale, long-term human safety trials exist for injectable TB-500
- Drug interactions have not been systematically studied
- Effects during pregnancy and breastfeeding have not been established
- Long-term effects of repeated TB-500 cycles are not well-characterized in formal research
- Much of the safety data comes from animal models and small human studies, not large randomized controlled trials
The absence of reported serious side effects is encouraging but should not be confused with proven safety.
TB-500 + BPC-157: The Wolverine Stack
The combination of TB-500 and BPC-157 has become one of the most discussed peptide stacks in research and biohacking communities. The nickname “Wolverine Stack” references the Marvel character’s rapid healing ability — a tongue-in-cheek nod to the combination’s reputation for comprehensive tissue repair support.
Why They Complement Each Other
As discussed in the comparison section above, TB-500 and BPC-157 target different but complementary repair pathways:
- TB-500 excels at: Mobilizing cells to the injury site, building new blood vessels, providing the structural infrastructure for repair
- BPC-157 excels at: Modulating the inflammatory environment, upregulating growth factors (VEGF, FGF, EGF), protecting cells from oxidative stress, and supporting gut-brain axis signaling
When combined, the theory is that you get both the infrastructure (TB-500) and the chemical coordination (BPC-157) working simultaneously.
Commonly Referenced Combined Protocol
| Peptide | Loading Phase | Maintenance Phase |
|---|---|---|
| TB-500 | 2.0–2.5 mg, twice per week, for 4–6 weeks | 2.0–2.5 mg, once per week, for 2–4 weeks |
| BPC-157 | 250–500 mcg per day, for 4–6 weeks | 250 mcg per day or every other day, for 2–4 weeks |
Important Notes
- No published clinical trials have studied this specific combination in humans
- The “Wolverine Stack” is an informal name used in research and practitioner communities, not a standardized medical protocol
- Individual responses may vary significantly
- Always consult a qualified healthcare provider before combining any peptides
For a detailed beginner-friendly protocol, see our BPC-157 + TB-500 12-Week Beginner Guide.
Frequently Asked Questions
What is TB-500 used for in research?
TB-500 is studied for its potential to accelerate tissue repair across multiple tissue types. The primary research areas include wound healing, cardiac tissue repair after myocardial infarction, corneal injury healing, tendon and ligament repair, muscle recovery, and hair regrowth. It is also studied for its anti-inflammatory properties. TB-500 is not approved for human therapeutic use and remains a research compound.
Is TB-500 the same as thymosin beta-4?
Not exactly. TB-500 is a synthetic peptide that replicates the active region of thymosin beta-4. The full-length thymosin beta-4 protein is 43 amino acids long and is naturally produced in virtually every cell type in the human body. TB-500 contains the same key active sequence, particularly the actin-binding domain centered around the LKKTETQ amino acid sequence (positions 17–23), which is responsible for most of the observed biological effects.
How long does it take for TB-500 to work?
Based on research literature and practitioner frameworks, most protocols describe a 4- to 6-week loading phase before evaluating effects. Some research subjects report noticing initial changes within 2–3 weeks, but the full benefits of a TB-500 protocol are typically assessed after completing both the loading and maintenance phases — a total timeline of 6–10 weeks. Individual responses vary based on the type and severity of the condition being studied.
Can TB-500 be taken orally?
TB-500 is a peptide, and like most peptides, it would be broken down by digestive enzymes if taken orally. For this reason, research protocols use injectable administration (subcutaneous or intramuscular injection). Unlike BPC-157, which has shown some oral bioactivity in animal studies, TB-500 does not have established evidence for oral effectiveness. Injectable administration ensures the peptide reaches the bloodstream intact.
Is TB-500 legal?
The legal status of TB-500 varies by country and jurisdiction. In the United States, TB-500 is legal to purchase for research purposes. It is not scheduled as a controlled substance. However, it is not FDA-approved for human therapeutic use, which means it cannot be legally marketed or prescribed as a drug for treating any medical condition. It is banned by the World Anti-Doping Agency (WADA) and most professional sports organizations. Always check the specific regulations in your jurisdiction.
Does TB-500 have anti-aging effects?
While TB-500 has not been specifically studied as an anti-aging compound, several of its mechanisms — promoting tissue repair, reducing inflammation, stimulating stem cell activity, and supporting angiogenesis — are relevant to aging-related tissue decline. The hair regrowth research is one example of a visible age-related change that thymosin beta-4 appears to influence. However, it would be premature to classify TB-500 as an anti-aging peptide based on current evidence.
Can TB-500 and BPC-157 be mixed in the same syringe?
In research and practitioner contexts, TB-500 and BPC-157 are commonly described as compatible for mixing in the same syringe and administering in a single injection. Both peptides are water-soluble and reconstituted with bacteriostatic water. There are no published reports of chemical incompatibility between the two. However, some practitioners prefer separate injections to ensure precise dosing and to inject closer to different target areas.
How should TB-500 be stored?
Unreconstituted (lyophilized powder) TB-500 should be stored in the refrigerator for long-term storage, though it is stable at room temperature for short periods. Once reconstituted with bacteriostatic water, the solution should be stored in the refrigerator at 2–8°C and used within approximately 25–30 days. Do not freeze reconstituted peptide solutions, as this can damage the peptide structure. Keep vials away from direct sunlight and excessive heat.
Key Takeaways
- TB-500 is the synthetic form of thymosin beta-4, a 43-amino-acid protein your body naturally produces in virtually every cell type. It plays a central role in wound healing, tissue repair, and inflammation control.
- The primary mechanism is actin binding, which enables cells to migrate to injury sites more efficiently. This single function underlies most of TB-500’s observed effects across different tissue types.
- Research demonstrates benefits in multiple areas, including wound healing acceleration, cardiac tissue repair after heart attacks, corneal injury healing, hair follicle activation, and tendon repair.
- TB-500 and BPC-157 work through different pathways, making them complementary rather than redundant. TB-500 focuses on cell migration and blood vessel formation, while BPC-157 focuses on growth factor modulation and anti-inflammatory signaling.
- The safety profile appears favorable based on available research, with injection site reactions and temporary fatigue being the most commonly reported side effects.
- TB-500 is not FDA-approved for any human therapeutic use. It remains a research compound, and all dosing protocols come from preclinical research, veterinary use, and practitioner frameworks.
- Anyone considering TB-500 should consult a qualified healthcare provider, particularly those with active cancers, cardiovascular disease, autoimmune conditions, or those who are pregnant or breastfeeding.
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References
- Malinda KM, et al. (1999). “Thymosin beta4 accelerates wound healing.” J Invest Dermatol, 113(3), 364-368. PubMed: 10399903
- Bock-Marquette I, et al. (2004). “Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair.” Nature, 432(7016), 466-472. PubMed: 15340005
- Sosne G, et al. (2002). “Thymosin beta 4 promotes corneal wound healing and decreases inflammation in vivo following alkali injury.” Exp Eye Res, 74(2), 293-299. PubMed: 11850419
- Goldstein AL, et al. (2012). “Thymosin beta4: a multi-functional regenerative peptide.” Expert Opin Biol Ther, 12(1), 37-51. PubMed: 23037676
- Philp D, et al. (2004). “Thymosin beta4 increases hair growth by activation of hair follicle stem cells.” FASEB J, 18(2), 385-387. PubMed: 15454081
- Smart N, et al. (2007). “Thymosin beta4 induces adult epicardial progenitor mobilization and neovascularization.” Nature, 445(7124), 177-182. PubMed: 17671655
- Sosne G, et al. (2010). “Biological activities of thymosin beta4 defined by active sites in short peptide sequences.” FASEB J, 24(7), 2144-2151. PubMed: 20179146
- Crockford D. (2007). “Development of thymosin beta4 for treatment of patients with ischemic heart disease.” Ann N Y Acad Sci, 1112, 385-395. PubMed: 17600286