Dr. Abud Bakri

Yep.

It's modulating a lot of these growth and healing pathways.

Like in the models of damaging the endothelial layer or the epithelial layer of different tissues, you'll get more VEGF signaling.

So that's the vascular endothelial growth factor.

So you get more blood vessels, androgenesis being formed, which creates a lot of the controversy around BPC safety.

You'll get cell migration, especially when coupled with TB500 and TB4.

You'll get more access of the healing factors to the area through androgenic pathways.

On top of that, you'll get an anti-stress effect.

So the other big thing that they did was they'd give corticosteroids with BPC-157 to these mice.

And usually when you have a wound and you give corticosteroids, the corticosteroids will slow or even stop the wound healing from happening.

When BPC was administered, the healing was either the same or even better.

More putting the gas pedal on these processes to bring in the immune system, the healing factors.

For example, in one tendon model, they noticed that it increased the amount of growth hormone receptors on the tendon.

So theoretically, this would allow more growth hormone to dock in and cause the outgrowth of the tendon and the regrowth of it.

So there's that theory there.

Downstream will modulate nitric oxide synthesis.

So that's a big thing when it comes to wound healing because you need to dilate the blood vessels.

You need to call in different cells.

So it's really changing the way cells behave at that level.

But that's only for the tendon side of it.