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These differences were recently revealed to have a fundamental impact on the outcome of antagonist engagement of FcRn, as a direct comparison of recombinant versions of efgartigimod (ARGX-113) and two other pipeline antagonistsbatoclimab (HL161BK) and nipocalimab (N027)revealed differential effects on the subcellular trafficking of FcRn [237]

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While challenging the importance of the protein binding hypothesis, it was instead suggested that the key mechanism of cell death involves P450-derived ROS formation during APAP metabolism, which triggers extensive LPO [59, 60]

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