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Experimental vascular studies using isolated rat aorta preparations reported that BPC-157 modulated vasomotor tone and increased nitric oxide generation through activation of the SrcCaveolin-1endothelial nitric oxide synthase (eNOS) signaling pathway [3]

In renal I/R injury, C3G increases GPX4 expression and GSH level, reverses excessive intracellular free iron accumulation, decreases lipid ROS, ACSL4, 4-HNE, and MDA levels, and significantly inhibits the ferroptosis of renal tubular cells

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There are multiple targets of G i/o activation in alpha cells [38]