Gilead Sciences is ditching a new avenue of treating hepatitis B as it cuts ties with Precision Biosciences less than two years into their research pact.
Back in September 2018, Gilead laid up to $445 million on the table in biobucks that saw the pair collaborate on gene therapies aimed at eliminating viral infections in vivo by using Precision’s genome editing platform.
Under the deal, Gilead was on tap to fully fund the effort and run clinical trials while Precision was on the hook for early development, formulation and preclinical work.
Current HBV treatments may suppress viral replication, but they do not completely clear out the virus; the infection’s covalently closed circular DNA, or cccDNA, enables HBV replication to restart if treatment is stopped.
Precision’s ARCUS editing platform is derived from a natural enzyme called a homing endonuclease that can target long sequences and is used to insert or delete DNA. The Durham, North Carolina-based company’s fully synthetic version can be designed to locate and disrupt particular sequences and minimize off-target effects.
Gilead’s preliminary, in vitro studies using ARCUS nucleases had shown significant activity against cccDNA and integrated HBV DNA in human liver cells. But, two years down the line, Gilead no longer wants in.
Precision, which is predominately working on next-gen cancer therapies, will regain the license to its hep B program. It’s not clear what prompted the decision, but the biotech could be on the lookout for a new partner.
“This was a highly productive and well-aligned collaboration, and we deeply value the opportunity to advance our ARCUS genome editing technology and a potential cure for HBV alongside a global leader in infectious disease,” said Derek Jantz, Ph.D., co-founder and chief scientific officer of Precision.
“Key learnings from this program and how to develop liver-directed gene editing therapeutic candidates are directly applicable to our in vivo pipeline. While we consider new partnership opportunities for HBV, we are focused on progressing our internal lead proprietary gene correction program for primary hyperoxaluria type 1 for which we expect to nominate a clinical candidate later this year.”