But nonetheless with the trial that’s roughly around 200 patients we did over enroll the study. But I think hopefully it’s set up to give us what we need to know about safety and tolerability between doses, look for trends in the virology between the doses and anything else we can get out of this study is gravy, so to speak, as we’re planning Phase 3 studies. So this data is obviously what we’re trying to achieve in the SPRINT data and you indicated questions about what’s appropriate for a partner. Partners always have what they want to see, but suffice it to say, the data package that we’re putting together continues to build into something that’s very interesting and perhaps best in class.
Operator: Thank you. And I show our next question comes from the line of Matthew Hershenhorn from Oppenheimer. Please go ahead.
Matthew Hershenhorn: Hey, this is Matt on for Jay Olson as well. Thank you so much for taking our questions. So we were wondering for the hMPV/RSV dual-inhibitors, could you just talk about the potential utilization in the real world? How common, for example, is it for patients to have a co-infection and also how will the dual inhibitor impact EDP-938 and EDP-323 development? Really appreciate it. Thank you.
Jay Luly: Sure. Thanks for the question. So the dual inhibitor, to be clear, we’re not looking for co-infected patients, although they could exist. I think that would be a relatively rare thing. It might be more common to be infected with COVID in RSV or COVID in human metapneumo. But even that co-infection in these specific instances is probably rather rare. And so instead, the way we’re thinking about it is more of a broad spectrum antiviral one that we could use to treat either infections so that regardless of whether it was RSV or human metapneumo in the diagnosis, you could just use one drug to take care of both of them. RSV also a virus that most pediatricians can tell an RSV infection just based on bronchiolitis and other sorts of symptoms.
And so, someday it might even be used to treat patients presumptively for those infections. And having the comfort that you could treat either RSV or human metapneumo would be a great advantage. I’ll kind of go back to my earlier point. When we get into an area, we don’t usually just pick on one mechanism for a drug or one drug class. We like coming forward really understanding especially in an area like RSV and human metapneumo, where there are no approved drugs. We want to have as many different mechanisms in classes that we can bring forward. Ultimately, there will be comparative data that we’ll have. We may elect to select them into different patient populations. And in some instances, there may be reasons to do combinations. You didn’t ask about our health protein inhibitor for RSV 323, but that’s another mechanism that we have in addition to 938.
So we have a lot of optionality going forward.
Operator: Thank you. And I show our next question comes from the line of Ed Arce from H.C. Wainwright & Co. Please go ahead.
Ed Arce: Hi, Jay. Thanks for taking our questions. Really just one on EDP-323 in RSV with data in second quarter, as you mentioned. Just wondering this study is obviously in human volunteers. So there’s really no opportunity yet for virological data. But I’m just wondering what kind of €“ what criteria are you looking at? How should we judge this early safety and PK study results? How would you judge it to move forward? And as you think about next steps, when do you think we could get initial efficacy data? Thanks.
