Roy Buchanan: Okay, great. And then just a quick one on [indiscernible] Just any updates you can give us on the progress there? I mean, I know it’s in their hands, probably can’t say much, but any sense of what to expect and maybe timing for the next update for that collaboration? Thanks.
Michael Sofia: Yes, Roy, this is Mike. Good question. Yes, we continue to work with our partners at [indiscernible] to move that program forward as quickly as possible. There’s not much more we can say beyond that. It’s a bit of a slow process in China, as I’m sure you’re aware. But we’re moving as diligently as we can.
Roy Buchanan: Okay, can you just remind me where it’s at at this point, like in development, or is that not public?
Michael Sofia: Where is it in development in China?
Roy Buchanan: Yes.
Bill Collier: We’re still working towards submitting an IMD to Chinese regulatory authority.
Roy Buchanan: Okay, great. That’s it. Thank you.
Bill Collier: Sure. Thank you, Roy.
Operator: Thank you. One moment for our last question. Our last question comes from Brian Skorney of Baird. Please go ahead.
Unidentified Analyst: Hey, good morning. Thanks for taking our questions. This is Charlie on for Brian. Just a couple from us. So I was just kind of curious what your interpretation of the combination data with imdusiran and [indiscernible] is given that in the A1 and B1 cohorts, it looks like, in one or two patients, there’s a sharp drop in surface antigen and then a bit of a rebound. Secondly, we’d be curious if any of the kind of investment calculus has changed for you guys with regards to the coronavirus antivirals, given how the disease landscape has evolved over the past year and a half. And also just kind of, did you set the table with expectations for, when the VTP-300 combination might have an incremental effect from the use of that vaccine and kind of like what you’re thinking about in terms of how that combination might be synergistic. Thank you.
Bill Collier: Okay. Great. Thanks. So let’s chunk this up. Maybe the interferon question first with Karen and then we’ll go across to Mike, Sophia for a comment on coronavirus.
Karen Sims: Yes, sure. Thanks, Bill. So just back to the 201 interferon data that was released. So, as we mentioned earlier, I will remind, you that this is very preliminary data and that the majority of the subjects had not completed the interferon treatment period when we reported this data. So, as we alluded to, I think it’s still too early to draw specific conclusions from the data set that we shared, but, we were encouraged by the performance of imdusiran in the lead-in period doing exactly what it’s supposed to be doing in terms of lowering [indiscernible] antigen and then, the initial data was interferon. To your point, it’s a little variable. Looking at those plots in the poster, perhaps I can refer you back there. The S-antigen data was presented in a log scale.
So while some of those changes look rather dramatic at the low end, these are subjects that are moving from surface antigen values, for example, less than, five to less than low than the quantitation and then back to less than five or less than 10. So the bottom of that scale, there is actually a very small window of surface antigen change that, less than 10 [indiscernible] primal, undetectable where these subjects are moving around. And I don’t think that’s surprising, given the close follow-up, with these subjects, we don’t necessarily expect someone to hit lower limit of quantization necessarily stay there. They may bounce around a little bit before they, settle out into, whichever direction they may go, whether they remain undetectable or have a little bit of surface antigen rebound, to your point.
So, I think the big picture here is we need to keep watching these subjects and let them complete, the full interferon treatment period, let them complete the follow-up period, as with interferon monotherapy data, there are at times, very interesting outcomes and patients after they’ve completed their interferon therapy. So I think we just need to be patient as the data emerges and then, as alluded to, we’ll be providing updates on this study when we have, additional meaningful data to share.
Bill Collier: And then you just want to talk about the second part, the potential impact of VTP-300 in the other study and then we’ll go across to coronavirus.
Karen Sims: So in terms of VTP-300 with the, in the 202 study, so, certainly, as we alluded to, we’ll be sharing some data from that study towards the end of the year. We’ve been following back to text data very closely with their VTP-300 studies, their 002 study, and are, encouraged by their results in terms of surface antigen declines, especially in patients who have low surface antigen at the beginning of the study. So keeping that in mind, we’re very hopeful that imdusiran will continue to, lower surface antigen in the subjects in that study to a point where VTP-300 will hopefully have a similar effect of additional surface antigen decline and then ideally additional immunomodulatory activities that will promote functional cure in those patients.
