I understand SOC has improved with COVID, but is the mechanism of action in these therapies well enough understood at this point? Could someone with more understanding of MOAs comment? Could this be part of the reason why we weren't able to reach primary endpoint in CHF but reduced mortality etc? Is this just something Mesoblast haven't been able to fully get a grip on yet?
Ann: Mesoblast Update on COVID-19 ARDS Trial, page-406
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