COVID-19 is a novel infectious disease that primarily affects the lungs. Many COVID-19 patients with severe disease experience serious, sometimes fatal, respiratory complications caused by an excessive inflammatory response in the lung, primarily driven by T-cells. Recent studies have shown that Neuropilin-2 (NRP2) expression is increased in the lungs of patients who died from COVID-19 related respiratory failure, suggesting this receptor is upregulated in response to SARS-CoV-2 infection in active sites of inflammation. It has also been suggested that the inflammatory lung injury related to COVID-19 may be similar to that of interstitial lung diseases, or ILDs, including the possibility of permanent lung scarring.
ATYR1923 selectively binds to NRP2 and has been shown pre-clinically to downregulate T-cell responses, dampening the inflammatory cytokine and chemokine signaling that has been implicated in severe COVID-19 cases. ATYR1923 has also been shown to improve lung function, as well as to reduce inflammation and fibrosis, in multiple animal models of immune-mediated acute lung injury. By targeting aberrant immune responses via NRP2, we believe that ATYR1923’s mechanism of action has substantial overlap with COVID-19 disease pathology and presents a compelling opportunity to potentially treat the subset of COVID-19 patients with severe respiratory complications for which there are currently no approved therapies.
We are currently enrolling a Phase 2 clinical trial evaluating ATYR1923 in patients with COVID-19 related severe respiratory complications. Click here to learn more.