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Towards Cellular Targets for Therapy in SCA3: Lessons from Preclinical Models So far, we have proposed that the primary pathogenic mechanism in SCA3 is indeed the loss of normal quality control of protein folding and interactions, therefore compromising their function

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At worst, it could contain contaminants

This pathway contributes to endothelial function and localized blood flow at sites of tissue injury

Activation of the FAK-Paxillin Pathway: For musculoskeletal applications, BPC-157's effect on the focal adhesion kinase (FAK) signaling cascade is of particular interest