AstraZeneca has submitted a request to the U.S. FDA for an Emergency Use Authorization for AZD7442, its long-acting antibody (LAAB) combination, for prophylaxis of symptomatic COVID-19.
 
If granted, AZD7442 would be the first LAAB to receive an EUA for COVID-19 prevention. It is the first LAAB with Phase III data demonstrating a statistically significant reduction in the risk of developing symptomatic COVID-19 compared to placebo.
 
Results from the PROVENT pre-exposure prophylaxis trial showed AZD7442 reduced the risk of developing symptomatic COVID-19 by 77% compared to placebo. Importantly, the trial population included people with co-morbidities and who may be in need of additional protection from SARS-CoV-2 infection. Greater than 75% of participants in PROVENT presented with co-morbidities associated with an increased risk of severe disease or a reduced immune response to vaccination. The trial accrued 25 cases of symptomatic COVID-19 at the primary analysis. AZD7442 was well-tolerated.
 
The EUA request filing includes safety and efficacy data from the PROVENT and STORM CHASER Phase III trials and the Phase I trial.
 
AZD7442 was optimized using AstraZeneca’s YTE half-life extension technology, which more than triples the durability of its action compared to conventional antibodies.
 
Preliminary ‘in vitro’ findings demonstrate that AZD7442 demonstrates broad anti-COVID activity, and in particular neutralizes recent emergent SARS-CoV-2 viral variants, including the Delta and Mu variants.
 
Discussions regarding supply agreements for AZD7442 are ongoing with the U.S. Government as well as other governments around the world.
 
AZD7442 is a combination of two LAABs – tixagevimab (AZD8895) and cilgavimab (AZD1061) – derived from B-cells donated by convalescent patients after SARS-CoV-2 virus. Discovered by Vanderbilt University Medical Center and licensed to AstraZeneca in June 2020, the human monoclonal antibodies bind to distinct sites on the SARS-CoV-2 spike protein and were optimized by AstraZeneca with half-life extension and reduced Fc receptor and complement C1q binding.