Atea Pharmaceuticals Announces Publication of Data Supporting Bemnifosbuvir’s (AT-527) Novel Mechanism of Action Against SARS-CoV-2 in Nature Communications
Data show bemnifosbuvir’s unique mechanism of action increases barrier for emergence of resistance, making it an ideal candidate for treatment of COVID-19 and for combination therapy
Excerpt from the Press Release:
BOSTON, Feb. 02, 2022 (GLOBE NEWSWIRE) — Atea Pharmaceuticals, Inc. (Nasdaq: AVIR) (“Atea”), a clinical-stage biopharmaceutical company, today announced that new data highlighting bemnifosbuvir (AT-527) were published in the peer-reviewed journal, Nature Communications, in an article titled, “A dual mechanism of action of AT-527 against SARS-CoV-2 polymerase.” The published data demonstrate that bemnifosbuvir’s unique mechanism of action, with dual targets consisting of chain termination (RdRp) and nucleotityltransferase (NiRAN) inhibition, has the potential to create a high barrier to resistance with broad antiviral activity across SARS-CoV-2 variants of concern. Bemnifosbuvir is an orally administered, non-mutagenic, direct-acting antiviral agent derived from Atea’s purine nucleotide prodrug platform. In Phase 2 clinical trials, bemnifosbuvir has demonstrated rapid and sustained antiviral activity in high-risk patients with COVID-19 and has been shown to be generally safe and well tolerated.
Bemnifosbuvir targets SARS-CoV-2 RNA polymerase (nsp12), a highly conserved gene that is unlikely to change as the virus mutates and new variants emerge. This gene is responsible for both replication and transcription of SARS-CoV-2. The inhibition of RNA polymerase has been shown in vitro to effectively block production of coronavirus. In addition, in vitro data confirm that bemnifosbuvir is active against all variants of concern or interest that have been tested.
“These published data provide the first evidence that the NiRAN domain of the RNA polymerase is a key druggable site and highlight the underlying mechanism by which bemnifosbuvir inhibits the NiRAN function to block replication of SARS-CoV-2.
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