Immune Function

BPC-157 vs TB-500

BPC-157 and TB-500 are both potent healing peptides with vast amounts of research investigating their properties and potential uses. Both are also synthetic derivatives of naturally occurring proteins that have been modified to enhance their already abundant features. Both peptides have been shown to improve immune function, enhance healing throughout the body, and even thwart the ravages of age in some ways. Still, BPC-157 vs TB-500 is a valid comparison as these two peptides are not the same and do not share all of the same functions. Below is a look at why someone might choose BPC-157 over TB-500 or vice versa. 

BPC-157 vs TB-500: General Wound Healing

Both TB-500 and BPC-157 have been shown to accelerate wound healing and tissue repair. BPC-157, a derivative of body protection compound (BPC), has a dose-dependent effect on the growth and migration of fibroblasts, the cells responsible for extracellular matrix repair[1]. TB-500, a derivative of thymosin beta-4 (Tβ-4) has a similar effect that it produces by manipulating actin filaments. Actin is a protein that plays central roles in cell reproduction and migration. Research shows that TB-500 can increase the rate of fibroblast growth and migration as well as boost health and migration of cells of the immune system.

Epithalon Peptide Induces Telomerase Activity and Telomere Elongation in Human Somatic Cells and Overcomes the Hayflick Limit

Each cell contains DNA as an instruction manual for how to divide and grow. The DNA inside of each cell is shielded by proteins called telomeres. During cellular division, a new cell must take some telomeres from its originating cell to shield the DNA of the new cell. The telomeres shorten after every cell division because the new cell can only take a portion of the telomeres from the previous cell, else the previous cell’s DNA will become completely unprotected.Once there are no left over telomeres to take, the cell stops dividing. This happens after a single cell divides and grows about 64 other cells, which is known as the Hayflick limit. This limit exists because cells without shield material are more vulnerable DNA damage. If the DNA of a cell becomes damaged, the cell will follow broken instructions. If the instructions within the DNA of the cell are damaged, then the cell may not be able to eliminate itself through the process of apoptosis like it is supposed to.”The telomere length is increased by approximately 33% in epitalon treated cells [by increasing the telomerase enzyme that strengthens telomeres].” (10)“Telomerase is a reverse transcriptase that has two distinct functions, to replicate pre-existing chromosome ends (telomeres) and to heal broken chromosomes by de novo addition of telomeric sequences directly on to non-telomeric DNA.” (11)

“Addition of Epithalon to aging cells in culture induced elongation of telomeres to the size comparable to their length during early passages. Peptide-treated cells with elongated telomeres made 10 extra divisions (44 passages) in comparison with the control and continued dividing. Hence, Epithalon prolonged the vital cycle of normal human cells due to overcoming the Hayflick limit.” (12)

Thymosin B4 Reduces Inflammation by Upregulating MicroRNA-146a and Promotes Myelin

“Tissue inflammation results from neurological injury, and regulation of the inflammatory response is vital for neurological recovery. The innate immune response system, which includes the Toll-like receptor (TLR) proinflammatory signaling pathway, regulates tissue injury… TB4-mediated oligodendrogenesis results from [up-regulating] miR-146a [causing the] suppression [of] the TLR proinflammatory pathway and modulation of the p38 MAPK pathway.” (8)“By targeting IRAK1 and TRAF6, miR-146 inhibits NF-κB activation. We therefore hypothesized that TB4 regulates the TLR proinflammatory signaling pathway by specifically regulating miR-146a to promote differentiation of OPCs [oligodendrocyte progenitor cells] to mature myelin basic protein (MBP)-expressing OLs [oligodendrocytes]… transfection with anti-miR-146a inhibitor nucleotides significantly inhibited the expression of MBP and phosphorylation of p38 MAPK.” (8)

BPC 157 is a peptide that has demonstrated anti-inflammatory, cytoprotective, and endothelial-protective effects in different organ systems in different species. BPC 157 activated endothelial nitric oxide synthase (eNOS) is associated with nitric oxide (NO) release, tissue repair and angio-modulatory properties which can lead to improved vascular integrity and immune response, reduced proinflammatory profile, and reduced critical levels of the disease. As a result, discussion of its use as a potential prophylactic and complementary treatment is critical.

Figure 2: BPC 157 Molecule

Researchers hypothesize BPC 157 to be a promising future treatment for COVID-19 patients. Plausibly, BPC 157 may offer improved COVID-19 outcomes by mitigating cytokine derailment and subsequent multi-organ failure based on its anti-inflammatory, cytoprotective, and endothelium-protecting effects (e.g., through BPC 157-eNOS interactions). Furthermore, BPC 157 applications may obstruct viral replication, improve clinical and biochemical parameters, attenuate organ damage from the systemic alterations, provoked from SARS-CoV-2. Support for such a hypothesis is explained in further detail below.

What is Thymosin Beta-4?

The beta-thymosins (b-thymosins) comprise a family of structurally related, highly conserved amino acid sequences in species ranging from mammals to echinoderms. Of the 16 known family members, thymosin β4 (Tb4), thymosin β10 (Tb10), and thymosin β15 (Tb15) are found in man.

Thymosin beta-4 (TB4) is a 43 amino acid, 5kDa polypeptide that is an important mediator of cell proliferation, migration, and differentiation. TB4 is the most abundant member of the β- thymosin family in mammalian tissue and is regarded as the main G-actin sequestering peptide. It is found in all tissues and cell types except red blood cells. Thymosin beta-4 is angiogenic and can promote endothelial cell migration and adhesion, and angiogenesis. TB4 also accelerates wound healing and reduces inflammation and scarring when applied in dermal wound-healing assays.

Beta thymosins bind and sequester monomeric actin, thus preventing actin polymerization and formation of filamentous actin. Actin is a vital component of cell structure and movement. Actin is involved in many important non-muscle cellular processes, including cell locomotion, chemotaxis, phagocytosis, and cytokinesis. Of the thousands of proteins present in cells, actin makes up to 10% of the total proteins in a cell, representing a major role in the genetic makeup of the cell.

Animal studies of disease and repair when using thymosin beta-4, the major actin-sequestering molecule in mammalian cells, have provided a base for the ongoing multicenter clinical trials for wound healing, including dermal, corneal, and cardiac. TB4 has multiple biological activities, which include down-regulation of inflammatory chemokines and cytokines, and promotion of cell migration, blood vessel formation, cell survival, and stem cell maturation.

Thymosin beta-4 also inhibits inflammation, microbial growth, scar formation (by reducing the level of myofibroblasts), and apoptosis, and protects cells from cytotoxic damage, including glutamate neuronal toxicity. In addition, it binds to G-actin, blocks actin polymerization, and is released with factor X by platelets. These activities contribute to the multiple wound healing properties that have been reported in animal and human studies.