Mike Ulz: Yep, that’ll make sense. And then your thoughts on the need for PEG, I guess. Shorter with PEG might work, but longer maybe doesn’t make sense.
Phil Pang : So I would say that the — let me answer that in two ways. Let me answer that from a biological perspective, and then from a patient perspective. From a patient perspective, I think that it is really going to depend on what the efficacy is. So imagine you’re a patient right now, and someone says, I’m going to give you a year-long course of therapy, it’s going to have some side effects, but you only have a one in 20 chance of it actually benefiting you at all. Most people say, I’m not willing to roll the die in that circumstance. However, if you were to come back to that same patient and say, I’m going to give you a year of therapy, but if I do it in combination with these other drugs, I could increase your chance of cure to, one in three or one in two, I think that’s a very different story.
So I don’t think it’s just about absolute duration. I think it’s about efficacy in the context of that duration. As far as the biological need for interferon, I think there are things in favor of suggesting why it might be necessary. I think the fact that, it is the only known way to cure hepatitis B right now that has been approved is one interesting point. But I think it points more broadly to the need for an immune modulator to really achieve a functional cure, which is really an immunologically-induced remission. So, one of the aspects about VIR-3434 that we’re really excited about is the fact that it’s not just a neutralizing antibody. It has a modified Fc domain, which allows it to act as a potential therapeutic vaccine. And if that aspect of the VIR-3434, which we believe may allow it to act as a substitute or an alternative to interferon alpha.
So of course the jury’s still out on that. We’re going to see what 24 weeks looks like on treatment this coming Q4. And then we’ll of course have what 48 weeks of that treatment look like next year.
Mike Ulz: That’s helpful. Thank you.
Operator: All right. Our next question comes from Joseph Stringer from Needham & Company.
Joseph Stringer : Hi. Thanks for taking our questions. Two from us. First on the HIV program, you were previously evaluating your 1111 and Phase 1 trials. What’s different about 1388 and what gives you confidence that this T cell vaccine is the right approach and what are timelines around initial data? And then secondly, given current cash balance, what are your thoughts on external BD? What’s your appetite for bringing in external assets, whether they be early or late stage? Thanks.
Marianne De Backer : Thank you, Joe. So maybe I’ll start with the last question first. And obviously, we are in a very unique position where we have a strong balance sheet that will allow us to really fund our critical Phase 2 and phase one assets for the next stages of inflection. It also offers us the opportunity to remain opportunistic. And if we see assets or opportunities out there that can really strengthen our pipeline and our capabilities within field biotechnology, then of course we will take advantage of that. For your first question related to the differentiation of VIR-1111 versus VIR-1388. Maybe Phil you can take that one.
Phil Pang : Thanks, Marianne. So, Joseph, we are on track to dose our first patient this quarter in Q3 with VIR-1388, which as you noted is a prophylactic HIV vaccine. In terms of what’s different about it compared to VIR-1111, I think that, obviously, we need to wait for the results in humans, but at least we can say in tissue culture, the biggest difference is that VIR-1111 was deliberately attenuated, which means we made it less able to replicate in tissue culture, because we wanted to really get some basic understanding of how this vector, which is based on human CMV, behaves in people. We now have the opportunity with 1388, based on that safety information from VIR-1111, to take what we call the less attenuated virus into the clinic.
