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Exogenous MG exposure (Figure 4) further revealed two distinct ferroptosis-promoting mechanisms: covalent binding-mediated glutathione depletion, which crippled glutathione peroxidase activity, and suppression of selenoprotein biosynthesis, evidenced by diminished GPX4 and SLC7A11 expression (Figure 5)

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The compound has been shown in cell-based research to upregulate VEGFR2 transcript levels, increase phosphorylation of downstream signalling intermediates after VEGF stimulation, and enhance endothelial tube formation in matrigel assays
