It certainly looks like leronlimab would help.

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Nowadays, it is known that this particular amyloidogenic protein expression is regulated by IL-6, an inflammatory cytokine, which results in increased levels of SAA. Hyperexpression of SAA for long periods of time results in amyloid formation and deposition in tissue, characterizing amyloid A (AA) amyloidosis. This particular type of amyloidosis occurs in chronic inflammation conditions, such as autoimmune diseases or cancer. With the exception of inflammation-induced amyloidosis, such as AA amyloidosis, the role of inflammation in most amyloid diseases is a more recent concept that emerged in the late 1980s with the observation of microglia, a brain immune cell, found near amyloid plaques in postmortem brain tissue from Alzheimer’s disease (AD) patients.

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