Acalabrutinib and ibrutinib are bruton tyrosine kinase inhibitors, used for CLL and lymphoma treatment. Ex vivo analysis revealed significantly elevated BTK activity (BTK regulates macrophage signalling and activation), as evidenced by autophosphorylation, and increased IL-6 production in blood monocytes from patients with severe COVID-19 compared with blood monocytes from healthy volunteers. In a pilot study, 19 patients with severe COVID-19 received the BTK inhibitor acalabrutinib (Roschewski 2020). Within 10-14 days, oxygenation improved “in a majority of patients”, often within 1-3 days, and inflammation markers and lymphopenia normalized quickly in most patients. At the end of acalabrutinib treatment, 8/11 (72.7%) patients in the supplemental oxygen cohort had been discharged on room air. These results suggest that targeting excessive host inflammation with a BTK inhibitor can be a therapeutic strategy. A confirmatory RCT is underway. Some reports have speculated about a protective effect of ibrutinib, another BTK inhibitor (Thibaud 2020).
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Acalabrutinib – Azithromycin – Camostat – Chloroquine – Colchicine – Convalescent plasma – Corticosteroids – Cytokine blockers – Famotidine – Favipiravir – G-CSF – Human recombinant soluble ACE2 – Hydroxychloroquine – Ibrutinib – Iloprost – Interferons – JAK inhibitors – Leflunomide – Lopinavir – Monoclonal antibodies – N-acetylcysteine – Oseltamivir – Protease inhibitors – RdRp inhibitors – REGN-COV2 – Umifenovir