Saturday, August 01, 2020 10:54:51 AM
Lenzilumab targets GM-CSF directly and not GM-CSF receptors, so if GM-CSF is rapidly "consumed" by cells, some (potentially large) proportion of GM-CSF would be able to bind to the cell and do its job before being disabled by lenzilumab. [Or can lenzilumab still bind to GM-CSF after the GM-CSF has been captured by the cell?] I would guess that fine-tuning the dosing and drug delivery are critical, which might help explain why it is delivered IV 3x/day.
A lot of different kinds of cells produce GM-CSF, but maybe Th17 (or Th1) are particularly important in severe covid-19. Temesgen's paper notes elevated levels of CM-CSF-secreting Th17 cells in severe cases (although the paper they cite to support that doesn't mention Th17 but discusses Th1 instead...no idea what the difference is, if any), but it does not report Th17 or Th1, so it's tough to tell.
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