Precision BioSciences, Inc. (NASDAQ:DTIL), a clinical stage biotechnology company using its ARCUS® genome editing platform to develop allogeneic CAR T and in vivo gene editing therapies, today announced it will present preclinical data for its chronic hepatitis B virus (HBV) program at the HEP DART 2021 conference taking place in Cabo San Lucas, Mexico, December 5 – 9, 2021.
Presentation Details:
Abstract Number and Title: Abstract #03. Targeting Hepatitis B cccDNA with a Sequence-Specific ARCUS Nuclease to Eliminate Hepatitis B Virus In Vivo
Oral Presentation: Monday, December 6, 2021 at 11:25 AM ET
Poster Reception: Tuesday, December 7, 2021 from 3:00 PM ET to 5:00 PM ET
Abstracts for the HEP DART 2021 Meeting are available on the conference web site, at https://informedhorizonseducation.com/scientific-program-hep-dart-2021.
“Current standard-of-care treatments for chronic hepatitis B work by lowering or suppressing the amount of hepatitis B virus found in infected cells in the body, rarely clearing the virus fully and leaving behind a DNA template for HBV to replicate,” said Derek Jantz, Ph.D., Co-Founder and Chief Scientific Officer of Precision BioSciences. “At HEP DART 2021, we are pleased to share preclinical research illustrating how our ARCUS gene editing technology edited and degraded the covalently closed circular DNA, or cccDNA, responsible for HBV replication and virus persistence. We look forward to building on this research with our PBGENE-HBV gene editing candidate to pursue a potential one-time, permanent treatment for chronic hepatitis B and expect to submit an IND application or CTA in 2024.”
In this preclinical study, ARCUS efficiently targeted and degraded HBV cccDNA and reduced expression of HBV s-antigen (HBsAg) by 77% in HBV-infected primary human hepatocytes. To evaluate ARCUS in vivo, mouse and non-human primate models were developed that utilized an episomal adeno-associated virus (AAV) containing a portion of the HBV genome to serve as a surrogate for cccDNA. In both episomal models, a robust decrease in AAV copy number and high on-target editing in remaining AAV was observed, and a durable 96% reduction of HBsAg was further observed in mice.
