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These findings confirm that DMH GLP-1R neurons mediate pre-ingestive, cognitive satiation elicited by GLP-1R agonists, a phenomenon that we also observed in a human study [69]

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doi:10.1111/j.1365-313X.2004.02269.x

Conversely, BACH1 knockdown not only inhibited BPC157-induced HUVEC proliferation and tube formation but also blocked the expression of these proangiogenic factors, confirming that BACH1 is the pivotal downstream effector of the BPC157-FBXO22 axis

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A recent injury responds to BPC-157 faster than a 6-month tendinopathy