Pleased to share our newly published paper entitled: "Clinical C3 Inhibition With AMY-101 Reveals Novel Insights Into IL-8–Driven Inflammation in COVID-19" onlinelibrary.wiley.com/doi/… This work, which was done a few years back, investigated the effects of AMY-101 in treating severe COVID-19, with a focus on understanding how C3 inhibition modulates key elements of IL-8–driven inflammation in these patients. It builds on the promising biological readouts of the ITHACA Phase II trial (see here: science.org/doi/10.1126/scia…) by providing new mechanistic insight that positions C3 activation at the heart of cytokine-driven proinflammatory pathways that can exacerbate lung pathology and neutrophil-driven thromboinflammation across various organs. The study showed that AMY-101 administration not only reduced markers of systemic inflammation, including NETs, CRP, and ferritin but also modulated IL-8, a major chemoattractant for neutrophils. It identified fibroblasts as a major source of increased IL-8 in severe COVID-19 and showed that C3 inhibition can broadly attenuate the proinflammatory consequences of the deregulated fibroblast-IL-8-neutrophil axis in severe COVID-19. These findings underscore the therapeutic potential of C3 targeting in COVID-19 and other neutrophil-driven inflammatory and fibrotic disorders. Moreover, they reveal a crucial mechanistic connection between C3 activation and IL-8–mediated immune responses. onlinelibrary.wiley.com/doi/…

You can read our article here: rdcu.be/egmX8