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We demonstrated that SYNCRIP deficiency sensitizes GBM cells to ferroptosis by inducing ROS accumulation, suggesting that ferroptosis is a key mechanism underlying the antitumor phenotype observed in SYNCRIP-deficient cells

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BPC-157 Research Tissue Repair Cytoprotection Research Use Only Mechanism of Action Research centers on nitric-oxide system modulation and upregulation of growth-factor receptors, with studied roles in tenocyte proliferation, collagen organization, and pro-angiogenic signaling

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As well, single nucleotide polymorphism (SNP) in the promoter region of SIRT1 was linked with the development of PD patients compared to controls (Zhou et al