BPC-157 + TB-500 Blend

Based on Tβ4 research, it has been suggested that TB-500 exerts potential action on cell motility by elevating actin protein levels. More specifically, it has been posited to regulate the cellular actin cytoskeleton and cell migration by sequestering G-actin. TB-500 has a distinct amino acid segment [(17)LKKTETQ(23)] which is hypothesized to be responsible for actin binding and potentially enhancing cell motility. This in turn may exhibit positive action in wound healing processes.(5) TB-500 also appears to amplify the presence of microRNA-146a (miR-146a), which may act as a repressive regulator for certain cell signaling pathways such as those related to the activity of two cytokines linked to inflammation called interleukin-1 receptor-associated kinase 1 (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6). This suggestion was further insisted upon as a potential mechanism of TB-500 by the authors of the research study, who also commented that 'transfection of anti-miR-146a nucleotides reversed the inhibitory effect of Tβ4 on IRAK1 and TRAF6'. Therefore, TB-500 also appears to potentially function for healing by exerting anti-inflammatory action.(6)

It has been suggested that peptide BPC-157 exerts some action through several processes covering nitric oxide production, control of cells pertinent to tissue restoration, growth elements, and inflammatory responses. It is conceivable that BPC-157 may exhibit some engagement with the NO mechanism, possibly providing a safeguard for the endothelium and perhaps fostering angiogenic behaviors by fostering the development of new circulatory routes. Researchers suggest there is a possibility that it may increase the expression of release of early growth response 1 gene, which may play a role in cytokine production and growth stimuli, and possibly aid in the initial assembly of the extracellular framework, including collagen. It is worth noting that BPC-157's relationship with nerve growth factor-induced protein 1-A binding protein 2 may exert inhibitory action on specific elements.(7) As a result, new tissues composed of collagen may be formed, possibly improving wound healing more rapidly.(8)

Given that both peptides TB-500 and BPC-157 appear to exhibit similar pharmacological potential, when mixed, the potential action of both may be maximized – what might otherwise occur with one peptide, could occur at a better and faster rate when combined.

Chemical Composition

• Molecular Formula:
  BPC-157: C62H98N16O22
  TB-500: C212H350N56O78S
• Molecular Weight:
  BPC-157: 1419.5 g/mol
  TB-500: 4963 g/mol
• Other Known Titles:
  BPC-157: Body Protection Compound-157
  TB-500: Thymosin Beta-4

There are no research or clinical studies currently available where both TB-500 and BPC-157 were used in the same experiment or presented in combination, using the same test model. However, listed below are studies observing the potential action of the individual peptides.

In a study with Tβ4 conducted in 1999,(9) experimentally wounded murine models were used as subjects, where half of the murine models were presented with saline solution and the rest were presented with peptide TB-500. The main objective of this study was to determine the peptide's potential tissue repair action. Four days after the experiment, researchers reported that murine models presented with TB-500 showed an apparent 41% increase in the re-epithelialization process (i.e., formation of new epithelial cells to resurface the wound). After seven days, wounds presented with TB-500 had allegedly contracted by at least 11% compared to saline wounds. The authors commented that 'these results suggest that Tβ4 is a potent wound healing factor with multiple activities...'

In another clinical trial from 2006,(10) 72 test subjects with pressure ulcers were presented with TB-500. The main objective of this randomized, double-blind study was to establish the potential of thymosin beta 4 (analogous to TB-500) in the presence of ulcers. The test subjects were divided into two groups, where one group was presented with a placebo for 84 days and the rest were presented daily with various concentrations of the peptide, for up to 84 days. After 84 days, there was an occurrence of the wound healing process where the ulcers exhibited signs of healing.

In a BPC-157 study,(11) three experimental murine models were used as subjects where all were experimentally wounded, with acute or chronic wounds. These murine models were then divided into two groups, where one was presented with a placebo compound and the other was presented with peptide BPC-157. After the experiment, all murine models were examined histologically, and it was determined that the murine models with BPC-157 exhibited a prominently higher number of collagen and blood vessels formed compared to the placebo murine models.

In a study,(12) the medial collateral ligament (MCL) of murine models was transected (cut through) during surgery. All murine models were then presented with a fibrin sealant agent, where some murine models were also presented with thymosin beta 4 (TB-500). Four weeks after surgery, researchers reported that healing tissues in the peptide murine models exhibited apparently formed and uniformly spaced collagen cells. The collagen cells formed in the peptide murine models were allegedly wider compared to control murine models. Additionally, mechanical properties of regenerating tissues, including femur-medial collateral ligament-tibia complexes, appeared to improve in the TB-500 group compared to control.

Another research article indicated that BPC-157 might play a role in aiding connective tissue recovery, potentially promoting tendon explant growth. Interestingly, the study suggested that BPC-157 possibly improves these cells' resistance against oxidative stress. This result could be related to F-actin formation activation, as indicated by FITC-phalloidin staining. BPC-157 also appeared to improve in vitro movement of tendon fibroblasts as indicated by a transwell filter migration test. Furthermore, BPC-157 appeared to accelerate tendon fibroblast dispersal across culture plates. Moreover, the study delved into the possible role of the FAK-paxillin pathway (a pair of proteins linked to focal adhesion that transmit signals after integrins) in transmitting BPC-157 action. Western blot tests hinted that phosphorylation rates of both FAK and paxillin appeared to increase with BPC 157, however, total protein amounts remained constant.(8)

A study(13) was conducted in murine models with experimentally injured gastrocnemius muscle complex. These murine models were initially presented with corticosteroids, which allegedly contributed to severe muscle damage in these murine models. These murine models were then divided into two groups, where one was presented with placebo and the other with BPC-157 daily for up to 14 days. After the experiment, it was reported that BPC-157 murine models appeared to exhibit complete restoration of their gastric muscles along with full ability to function. While the placebo-treated group did not exhibit any apparent change in damaged muscles.

TB-500 may also have a potential effect on muscle cell regeneration, more specifically on heart muscle cells. A study suggests that TB-500 appears to reinforce myocardial resistance under low oxygen conditions, and apparently fosters angiogenesis, possibly paving the way for cardiac cell repair. Researchers have hinted at a potential process where cardiac fibroblasts transition into cells resembling cardiomyocytes.(14) Ultimately, scholars observed that TB-500, when paired with cardiac reprogramming techniques, could collaboratively reduce potential damage to heart cells and foster their regeneration by activating inherent cells within the cardiac region. An examination using coronary artery ligation murine models appeared to exhibit results implying that TB-500 could elevate integrin-linked kinase (ILK) and protein kinase B operations in the heart, possibly increasing early cardiomyocyte resistance and apparently improving cardiac performance.(15) Experts also suggested that TB-500 could support myocardial and endothelial cell movement in the fetal heart and maintains this capability in mature cardiomyocytes.