Phil Pang: So 24 weeks post treatment, they will — it’s actually somewhat of a mixed bag, but they will — you can continue to expect that they will still be on NUCs. And usually what happens is this, once they have demonstrated that they have lost surface antigen for at least six months off-treatment, their NUC had stopped and then you follow them for another period of time to make sure that they don’t relapse further. I will say though that as you know the NUCs usually only suppress HBV DNA. And therefore, surface antigen loss, which is a protein, would be unexpected to be impacted by the nucleoside reverse transcriptase inhibitor. So although of course, it’s not a perfect match, I think that what we are looking forward to and what we are guiding to is the post treatment data of our drugs but still on the nucleoside reverse transcriptase inhibitor.
Operator: Your next question comes from the line of Patrick Trucchio with H. C. Wainwright.
Patrick Trucchio: First, I am wondering if you can discuss the bar for regulatory approval in HDV or hepatitis delta. And what you would need to see in SOLSTICE to give confidence that this program is on-track? And then secondly, what would be the next steps for the delta program, specifically would you possibly be able to move directly into a Phase 3 program after SOLSTICE readout based on all of the data that’s been generated across HBV and HDV?
Marianne De Backer: So I mean, as you know, the goal of therapy in delta is chronic trial suppression progression as well as reduction of liver inflammation that’s also how the bar is set on the regulatory side. Phil, do you want to add any more color to what we want to see in SOLSTICE?
Phil Pang: So exactly as Marianne said, the regulatory bar is too long decline in HDV RNA and the normalization of ALT, that was one of the bars that was set early on to allow for an incentivized drug development. And I think that that’s one of the bars one to look at. But I think another part to look at is undetectability and HDV RNA, that is another marker that is totally associated with clinical benefit. So we are looking at both of those bars. I do want to remind you that for AASLD we are going to be having a small cohort of patients treated for a relatively short period of time. And I think that we will have to just wait to see what that data looks like to be able to know what the next steps are going to be. But as I have mentioned in my prepared remarks, the regulatory pathway can be accelerated if warranted given the unmet need in this space.
Operator: Your next question comes from the line Roanna Ruiz with Leerink Partners.
Nik Gasic: This is Nik Gasic on for Roanna. Thanks for taking our questions. Maybe first, could you remind us, I guess, what the status is of the next generation 2981 antibody against flu A and B? I guess, could you talk a little bit about how this antibody is differentiated from 2482 aside from the flu B targeting aspect as well? And then secondly, could you discuss some of the learnings which you might apply from your experience developing 2482 in flu A to the development of 2981 in flu A and B? Thanks.
Marianne De Backer: So I’ll start and then ask Phil to provide a bit more depth. So first of all, as you rightly pointed out, one of the major differences between 2482 and 2981 are next generation flu antibody is the fact that it covers both flu A and flu B. It’s also a different mechanism of action. It’s a neuraminidase inhibitor and that is a mechanism of action that has been proven to work before. We have also seen in vitro that the antibody is more potent than 2482. So there’s a lot of differentiating components here for our next generation antibody that we feel are very relevant and interesting. And as it relates to our learnings from 2482, as Phil pointed out in his prepared remarks, there’s some learnings that we already have based on initial data analysis.
