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Beam Therapeutics Presents First In Vivo Data Demonstrating Potential of Multiplex Base Editing Approach to Target Disease Drivers of Chronic Hepatitis B Infection
CAMBRIDGE, Mass., Sept. 19, 2022 (GLOBE NEWSWIRE) -- Beam Therapeutics Inc. (Nasdaq: BEAM), a biotechnology company developing precision genetic medicines

About this update from Beam Therapeutics Inc.
[{"type":"text","content":"CAMBRIDGE, Mass., Sept. 19, 2022 (GLOBE NEWSWIRE) -- Beam Therapeutics Inc. (Nasdaq: BEAM), a biotechnology company developing precision genetic medicines through base editing, today announced new preclinical data demonstrating the potential of the company’s multiplex base editing approach to both reduce viral markers – including hepatitis B surface antigen (HBsAg) expression – and prevent viral rebound of hepatitis B virus (HBV) in in vivo models. The data will be presented today, September 19, 2022, in partnership with Fabien Zoulim’s laboratory at the INSERM Cancer Research Center of Lyon, during a poster presentation titled, “Cytosine base editing inhibits Hepatitis B Virus replication and reduces HBsAg expression in vitro and in vivo,” at the 2022 International HBV Meeting. HBV causes serious liver infection that can become chronic, increasing the risk of developing life-threatening health issues like cirrhosis, liver failure or liver cancer. Chronic HBV infection is characterized by the persistence of covalently closed circular DNA (cccDNA), a unique DNA structure that forms in response to HBV infection in the nuclei of liver cells. Additionally, the HBV DNA integrates into the human genome, becoming a source of HBsAg. While currently available treatments can limit HBV replication, they do not inactivate these HBV genomic elements, which can lead to reinfection and reactivation of the HBV virus. This inability to prevent HBV infection rebound is a key challenge to curing HBV. Base editors are designed to enable direct and irreversible conversion of a specific DNA base into another without inducing double-stranded breaks. In HBV infected cells, cytosine base editors (CBEs) can target both integrated HBV DNA and the cccDNA minichromosome at multiple locations, introducing precise and permanent stop codons in the viral genome. These stop codons are intended to silence the viral genes without the risk of chromosomal rearrangements that can arise with nuclease editing systems that create double-stranded breaks in DNA. “Chronic HBV infection remains a major global health problem, and despite available antiviral medications, there is a significant need for a treatment that can both prevent viral replication and reduce viral protein expression,” said Giuseppe Ciaramella, Ph.D., president and chief scientific officer of Beam. “We a...