Apellis Announces New Data Demonstrating Correlation between Complement Activation and COVID-19 Severity

• Observational study in 41 patients hospitalized with COVID-19 found that nearly all patients had elevated systemic levels of C3a, a marker for C3 activation; median C3a levels were 3.7 times the upper limit of normal

• In a Phase 1/2 interventional study, preliminary open-label safety results in first six patients support advancement of APL-9, an investigational targeted C3 therapy, for severe COVID-19; additional 60-patient randomized, double-blind, controlled study cohort is currently enrolling
  

WALTHAM, Mass., Oct. 15, 2020 (GLOBE NEWSWIRE) -- Apellis Pharmaceuticals, Inc. (Nasdaq: APLS), a global biopharmaceutical company and leader in targeted C3 therapies, today announced observational study results that found a correlation between COVID-19 severity and complement overactivation, which is a key immune response. Additionally, preliminary open-label safety data from six patients in a Phase 1/2 study support advancement of APL-9, an investigational targeted C3 therapy designed for acute interventions, for severe COVID-19. These results also showed that key markers of inflammation were within or near normal range at the end of the APL-9 treatment period.

Observational Study Results
In the 41-patient observational study, data from 40 patients with evaluable blood samples demonstrated that increased complement activation showed a correlation with disease severity. C3a, C4a, Bb and terminal complement complex (TCC) levels each correlated statistically with COVID-19 severity as quantified by the National Early Warning Score (NEWS), a widely used assessment for the need for critical care. A similar correlation was observed with lactate dehydrogenase (LDH), C-reactive protein (CRP) and cytokine interleukin 6 (IL-6).

In addition, 39 (97.5%) patients had substantially elevated systemic levels of C3a, a marker for C3 activation, with median C3a levels 3.7 times the upper limit of normal. Multiple complement pathways were activated as evidenced by systemic elevations of C4a, Bb and TCC. Complement overactivation is known to worsen respiratory diseases by killing healthy cells and causing further complications such as blood clots and multiorgan failure, making it difficult for patients to recover.

“These study results demonstrate that multiple complement pathways are going into overdrive in severe cases of COVID-19, reinforcing the critical need for therapies that can regulate overactive complement and improve patient outcomes in COVID-19,” said Lukas Scheibler, Ph.D., Chief Innovation Officer of Apellis. “Targeting C3 has the potential to control complement activation across all three major pathways due to its central location, so we believe it is a strong target to continue exploring.”