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What is a bit strange is that they now posit that the drug works by limiting gut epithelial cell leakage of gut bacteria (leronlimab does this by blocking CCL3). Gut bacteria leakage would lead to an over-reactive inflammatory state. That complete pivot in mechanism of action shows why post hoc analysis is usually not trusted.

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Seems they haven't completely pivoted. They are now making the case for serum creatinine being an ALS biomarker. Muscle loss required to make CRP due to the chronic inflammatory state. Their recent paper indicates overall survival and vital capacity benefits in high CRP and low sCr treated patients.