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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]

Its primary mechanism is AMPK activation through inhibition of the folate cycle, causing accumulation of AICAR (an AMP analog) [1] [2]

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Reducing exposure while maintaining effectiveness represents a reasonable risk reduction strategy for those concerned about theoretical cancer risk