TB-500 5mg (Thymosin Beta-4)

TB-500 is a 43 amino acid synthetic analogue of thymosin beta-4 (TB-4), which is found naturally in nearly all mammalian cells. TB-500 is known for its effects on actin protein, cell migration, and wound healing. TB-500 has been shown in animal models and in vitro studies to improve blood vessel growth, accelerate wound healing, decrease inflammation, and promote extracellular matrix production. The peptide is under current investigation for its ability to reduce oxidative stress in spinal cord injury, improve recovery following heart attack, and for its many anti-aging effects.

TB-500 is the active domain of TB-4, which has a primary role as an actin binding protein. Actin is a critical component of cell structure and makes up microfilaments. Microfilaments are responsible for giving cells their shape, protecting the integrity of cell membranes, allowing cells to move/migrate, and certain steps in cellular reproduction. Actin is also one of the primary components of muscle protein. Without actin, muscles could not contract. Actin binding proteins, like TB-4, sequester actin monomers, the individual units of actin, so that they are protected from degradation and are available for polymerization into microfilaments when needed.

Research in rats has found that TB-500 encourages central and peripheral nervous system tissues to undergo repair and remodeling following injury. Though the exact mechanism has yet to be elucidated, the research indicates that TB-500 activates the cells that support neurons. These cells, called oligodendrocytes, keep neurons healthy. Boosting their activity actually improves blood vessel and neuron growth in brain regions that have been damaged, a significant laboratory result that is reflected in clinically significant improvements in behavior, motor control, and cognitive measurements.

Recent research shows that TB-500 can reduce oxidative stress following spinal cord injury and help transplanted neural stem/progenitor cells (NSPCs) to survive long enough to enhance spinal regeneration. These findings could make TB-500 and other TB-4 derivatives of great use in treating severe spinal cord injury. TB-500 may offer critical insight into spinal recovery that allows paralyzed individuals to regain use of affected body regions.

TB-500 and TB-4 are potent stimulators of VEGF expression. VEGF is an important signaling molecule in the growth of capillaries (small blood vessels), which are critical to everything from wound healing to hair growth. It is thought that the role of TB-500 is more complicated than this, however. Scientists speculate that the peptide likely underpins a number of steps in the process of blood vessel growth including extracellular matrix remodeling, vasculogenesis, angiogenesis, and the transition of more primitive mesenchymal tissue to the specialized endothelial tissue that lines blood vessels. This speculation is valid because loss of TB-4 has been shown to interfere with blood vessel growth and stability while exogenous administration improves capillary formation and the recruitment of pericytes following injury.

The discovery that TB-500 improves hair growth happened by accident. When mice that were genetically deficient in TB-4 were shaved for laboratory experiments, it was observed that their hair grew back much slower than wild-type mice. When these same scientists investigated hair growth in mice that were genetically modified to produce increased levels of TB-4, they found that their hair grew back much faster than normal. Under the microscope, these mice show increased numbers of hair shafts and grouped hair follicles.

Multi-drug resistance is becoming increasingly common in a number of infections, rendering current therapy ineffective. Unfortunately, there are very few new antibiotics in the pipeline and the process of drug development can take upwards of twenty years on average. A recent study on the effects of TB-4 and its adjuvants, however, provides some hope. Studies of mice suffering from a Pseudomonas aeruginosa infection of the eye have found that TB-4 combined with ciprofloxacin, a standard antibiotic for treating Pseudomonas aeruginosa, increases the effects of the antibiotic, improves healing, reduces inflammation, and promotes faster recovery. The results of just five days of combined therapy showed decreased numbers of colony forming units (CFUs), decreased neutrophil count, and decreased levels of inflammatory reactive oxygen species. This is the first study to demonstrate that TB-500 and similar peptides might be used to promote and enhance the effects of antibiotics.

Two decades of research have shown that TB-4 and its derivatives have a number of beneficial effects in the cardiovascular and renal systems. The exact mechanisms of these positive contributions are not clearly understood, however. Research suggests that the benefits are actually due to several mechanisms. First, TB-500 promotes the growth of collateral blood vessels, which is useful both as a preventative and in restoring function following disease. Second, TB-500 encourages endothelial cell migration and myocyte survival following a heart attack. Finally, it appears that TB-500 works in concert with other natural signaling molecules to reduce inflammation and reduce fibrosis (scar formation).

Recently, research into hydrogels containing a combination of collagen and TB-4 has shown the peptide promotes angiogenesis and epicardial heart cell migration, thus boosting rates of recovering following ischemia and helping to prevent long-term complications by reducing scarring.

Progress in finding a treatment for neurodegenerative diseases like Alzheimer's and prion disease has been slow at best. A recent study into the effects of TB-4 on the ability of the immune system to deal with prion protein has shown that the peptide enhances autophagy. Autophagy is the central nervous system's primary protective mechanism against neurodegenerative diseases. The ability of TB-4 to enhance this natural immunity is the first progression toward real treatment of these debilitating diseases in a long time.