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Bottom line is we have no data on any of these things If we limit ourselves to studies conducted outside of the original lab where independent validation is actually necessary and somewhat trustworthy, the best evidence for a primary mechanism of action comes from a study that looked at rat hind limb ischemia In this study, they ligated the femoral artery surgically, and that creates profound ischemia in one leg of the rat Then you treat the rats with BPC 157 or saline ‒ there were 12 rats, 6 in each group This was injected into the abdomen once a day for 7 days 7 days out, the blood flow to the injured limbs recovered much better in the BPC 157 group by about 50% in terms of something called a perfusion ratio, blood in injured limb versus not The treated animals had roughly doubled the number of small blood vessels and a larger share of those vessels expressed VEGF These things taken together suggest that BPC 157 may have influenced VEGF and VEGF receptor-2 signaling There is another study that was done with human endothelial cells This in vitro experiment (done in a dish) used BPC 157 concentrations between 0.1-1.0 μg/mL across these cell cultures They saw more tube formation, which are a marker of new blood vessel growth And they showed an increase in VEGF receptor levels, more VEGF receptor internalization and activation of downstream signaling proteins such as Akt and eNOS These effects were reduced when the cell’s ability to internalize the receptors was blocked Peter cautions, “ But remember, these were not done in actual humans, and that’s not uncommon to see things that work really, really well in cell culture that never work in an organism because you don’t have the pharmacokinetics, you don’t know if these things can even enter a cell under ordinary circumstances of administration
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By screening a phage-displayed random peptide library, the NLN (CNLNTIDTC) and NEW (CNEWQKLSC) peptides that bind to CD44v6-expressing cells were selected
