Brian Skorney: Hey, good afternoon everyone. Thanks for taking my questions. I had a few quick ones on the 235 SPRINT study. I guess since you’re at seven and 13-fold EC90s for the Omicron variant, are you expecting any dose response on viral load? And it seems like it would be overkill in terms of shutting down the virus. I’m just wondering what, if anything, you expect to see in terms of differences between the dose? And then I noticed on clinical trials, you have a couple of different measures of viral load. Can you just discuss how you’re measuring RNA viral load versus infectious viral load? And then finally, how do you think of the number of days of symptoms you’re enrolling days, I think, five days is where you’re cutting off.
Is that too many to catch separation of the different curve compared to placebo. Just trying to think through the time course of viral load evolution here and if there’s a risk that you’re capturing a lot of patients in the decline phase? Thanks.
Jay Luly: Sure. Maybe I’ll let Tara comment on the viral readouts. So what I would say is on the 200 and 400 milligram doses, we may or may not see — we may see — well, there’s all kinds of but, right, when you look at two doses. But it’s possible that given the strong multiples we have that either of those two doses does what we need it to do. Or there is still a possible that you might see some dose range or dose response and something. These are the two reasonable doses that we chose to evaluate this and it’s exactly why we’re running the study just to see if we can differentiate, if there any differentiating to be done here. The five-day piece Shionogi and Pfizer have shown good viral load dropped in various patient populations with a five-day treatment window.
You can obviously stratify people depending upon what their actual window was, but it won’t be more than five days. So that’s what I would say about that. And then, Tara, do you want to comment on the viral readouts?
Tara Kieffer: Sure, Jay. This is Tara, Brian. So we’ll be looking at the viral load, the RNA and that will be done by PCR. And that’s primarily what a lot of other companies have readout on their programs. We’ll also be looking at infectious virus, and that will be done through culture. So this is actually looking at live infectious virus that is still in the samples. So we’ll be looking at both of those readouts.
Brian Skorney: And those are both just nasal swabs?
Tara Kieffer: Correct.
Brian Skorney: Thank you.
Jay Luly: Thank you.
Operator: Thank you. One moment, while we compile our next question. And our next question comes from the line of Liisa Bayko from Evercore ISI. Please go ahead.
Liisa Bayko: Yes. I think most of the questions have been answered, but maybe just on the COVID study that you announced, can you explain sort of, I guess, the overall goal here? And do you €“ what are you trying to learn from the study? And in terms of enrolling the more kind of lower-risk patients, are you concerned at all that you have a similar outcome than you did in RSV, where you kind of don’t see any necessary kind of separation in terms of resolution of symptoms or any outcomes, just given that you’re not focusing or enriching the study for sort of that higher risk group? So could you comment on — and what your objectives are of the study in light of the focus there on the low-risk patient population? Thanks.
