Janssen&Janssen schreef op 20 mei 2021 22:04:
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Belangrijkste stuk in het geheel
The optimal complement pathway component inhibition target is also not yet clear,
even in the more studied complementopathies. Ongoing trials in SARS-CoV-2 target
complement inhibition at the level of C1 esterase, C3, C5, C5a, C5aR, or MASP. To address
hyperinflammation, it is theorized that upstream targets (e.g., C3 inhibition) would yield
the greatest anti-inflammatory effects [59]. However, this may come at the cost of an
increased risk of infection, thus some proponents favor C5a or C5aR over C5 inhibition
due to the retained ability to generate C5b-9 or MAC [29,98]. Alternatively, C1 esterase
inhibition with its kallikrein effects has also been proposed as a promising target to address
the elevated bradykinin levels caused by dysregulated ACE2 activity in SARS-CoV-2 [81]