On May 10, 2021, Altimmune announced positive results from a preclinical study of AdCOVID in a SARS-CoV-2 challenge model of infection. In this study, a single intranasal dose of AdCOVID provided sterilizing immunity in the lungs of vaccinated mice, in contrast to the development of dense pulmonary infection and disease in the lungs of non-vaccinated mice following infection with SARS-CoV-2.

In the current study, performed in collaboration with UAB, K18-hACE2 transgenic mice, which are highly permissive for SARS-CoV-2 replication and considered one of the best models for COVID-19, were vaccinated with a single intranasal dose of AdCOVID and challenged one month later with live SARS-CoV-2 virus.

When the lungs of the mice were evaluated for infectious SARS-CoV-2 virus, no detectable levels of infectious virus were observed in the lungs of vaccinated mice, representing a greater than one million-fold reduction of infectious virus compared to the non-vaccinated controls. This demonstration of sterilizing immunity is consistent with the stimulation of local and systemic immunity by AdCOVID shown in previous animal studies, including high serum neutralizing antibody and T cell responses, and most importantly, mucosal IgA responses in the respiratory tract.

In previously reported preclinical studies, AdCOVID was associated with a 29-fold induction of spike-specific IgA and resident memory T cell responses in the lungs of experimental animals, as well as robust systemic serum neutralizing antibody titers and T cell responses in the lung and spleen.

The ongoing AdCOVID Phase 1 clinical trial is evaluating the safety and immunogenicity of AdCOVID following a single dose or two intranasal doses administered one month apart and is expected to report topline data in June 2021. The trial is evaluating three different dose levels of AdCOVID and will measure local mucosal IgA responses in the nasaopharyngeal cavity, systemic serum immune responses, including serum neutralizing antibody relative to COVID-19 convalescent serum, and T cell responses directed against the spike protein receptor binding domain.