Operator: Thank you. And I show next question comes from the line of Roanna Ruiz from SVB Securities. Please go ahead.
Roanna Ruiz: Hi. Thanks for taking the question. So maybe tagging on to some of the COVID questions. I was curious about your new PLpro mechanism antiviral. How do you expect that to fit into the treatment landscape in the future, especially when it’s possible there could be multiple 3CL protease inhibitors available assuming they get approved?
Jay Luly: Sure. Thanks, Roanna. So I think, Enanta when we go after a virus, we usually don’t sit tight with one mechanism, especially when it’s a new virus that no one has approved drugs for. So when we started working early on in the pandemic, we went after multiple mechanisms including 3CLpro, and PLpro. 3CLpro gave rise to our first candidate sooner than PLpro. But at the end of the day, no one’s really had the opportunity to study a PLpro in clinical trials. So whereas there may be multiple 3CLpros across the line, ultimately, again, we think the best product profile will win longer term. But we also wonder out loud, could a PLpro have other advantages over a 3CLpro. We know that PLpro, like 3CLpro is a critical enzyme and viral replication.
So either protease inhibitors should be able to knock down the replication part of it. But PLpro also has a role in blunting the innate immune response of the host. And we wonder if there couldn’t be some extra impact that you could have in a treatment by having an PLpro inhibitor that not only shuts down replication, but may also block the suppression of that innate immune response. So in this sort of a situation, more drug choices are better than fewer. We don’t believe at this time that there’s any reason to believe that combination on top of a 3CLpro is necessary, but that might not always be the case. And also there may be special patient populations where you’ll want to have two drugs to try to help the person rather than just one. So for all these reasons and especially where we are and fully understanding this virus.
It’s good to have multiple shots on goal and we think the PLpro is really interesting. We’ve got some great chemical matter and we’re pushing as hard as we can to bring that forward as a candidate.
Operator: Thank you. And I show next question comes from the line of Akash Tewari from Jefferies. Please go ahead.
Unidentified Analyst: Hi, this is Amy on Akash. Thanks so much for taking our question. On the SPRINT trial, I know you indicated that it’s not powered to show viral load reduction, but would love to kind of hear any sort of color on what it is powered to show in terms of symptom benefit or any other endpoints that you think is relevant? And what are you specifically looking for in the data in order to move forward? And additionally, what are the big inflection points in your view where you’re looking to partner out the program ideally? Thanks so much.
Jay Luly: Yes. So I think all this sort of hangs together. The primary endpoint as we’ve disclosed previously is safety and tolerability. It was not powered on these other parameters. It certainly wasn’t powered on a symptomatic readout. But nonetheless, these are things that you look at as secondary endpoints to gather as much information as you can in terms of what factors €“ what symptoms might have been modulated the most in €“ with this current variant that the drug was tested against. So this is all important information to capture as you’re planning Phase 3. We’ll also be looking for trends and viral loads to help us select a dose. Typically with these protease inhibitors, you see €“ maybe about a log, you don’t see profound viral load drops the way these things are measured in these studies.
