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Moreover, it has been previously shown that GPX4 overexpression in cancer cells inhibits RSL3-mediated ferroptosis, whereas GPX4 deletion increases susceptibility to ferroptosis [22]

Figure 2 1.3 GIP receptor antagonism The physiology of GIP has been explored extensively by exogenous GIP infusions resulting in both physiological and supraphysiological concentrations ( Figure 3 ), and in recent years, the truncated and deactivated form of GIP, GIP(3-30)NH 2 , has proven to be a potent and specific GIP receptor antagonist in humans in high concentrations, and suitable for studies of endogenous GIP physiology and pathophysiology ( Table 1 )

When interpreted with clinical biomarkers and your provider's assessment, this information can support a more personalized treatment strategy