Jay Luly : Sure. So as you know, our first molecule in the clinic, 938 is a direct-acting antiviral. So it’s a replication inhibitor, in contrast to other approaches that have been tried in the past and in the present, I guess, in terms of entry inhibitors. So we’re focusing on replication inhibitors. We €“ again, we believe that that’s the best way to shut down an active replicating virus in a patient who is presenting. And so to that end, we didn’t want to just have one such class in hand. We’re very committed to RSV over time, and we want to have multiple different approaches over time. Someday, you might think about combining them. Again, there’s no reason, not priority to believe that in the overwhelming majority of patients you would need to have a combination strategy, but we would like to have that possibility for a few different reasons that, I can articulate in just a second.
But 323 is another replication inhibitor. It goes after the polymerase enzyme, and what we do in any of our candidate discovery programs. We’re always focused on finding very potent molecules with good safety, and good pharmacokinetics, and good biodistribution. And so 323 check’s all of those boxes pre-clinically. And so Phase I as is our usual approach, is really just hopefully recapitulating all of those kinds of bits of data in a human Phase I setting. So we’ll be looking for, of course, good safety. We’ll be looking for good PK. All of our, again, preclinical predictions support that, it should have good oral PK once-daily dosing, something we also are always aiming for here. And then we know that, the molecule has extraordinarily good virology.
It’s very, very potent. It’s a picomolar inhibitor of this polymery. So pre-clinically, we believe it’s a good stand-alone molecule on its own right, it’s potentially a good combination partner down the road, again, thinking about different patient populations, ones that might need an extra little support in terms of drug pressure on the virus, maybe in highly immune suppressed patients, for example or — and/or just reading a more normal patient by maybe able to reach a little bit later in the stage of infection by using two agents rather than one and translating that into patient value. It’s potentially widening the treatment window that you might have to come after a person once they present with the infection. So, however, many days of a window — treatment window you might have with one drug, maybe two drugs would just widen up that opportunity, therefore, increasing the addressable patient population.
So these are the kinds of things that we’re looking for, again, it’s always better to have multiple different approaches on any area or any disease indications that you feel very strongly done. And as you know, we’ve been championing RSV for quite a number of years, starting with the earliest discovery efforts a long time ago. And I think now the pandemic, the attention is very high on human respiratory viral treatment. And we’re very pleased to have a second molecule now in the clinic. So next steps, we’ll get the Phase 1 data. We’ll look at it, and then we’ll think about our next steps carefully once we have that data in hand. And you could go a couple of different routes. You could go into a challenge study or you could go directly into a patient population.
And we’re, obviously, thinking about that thing right now, and we’ll have more details at a future time.
Operator: Thank you. And I show our next question comes from the line of Brian Skorney from Baird. Please go ahead.
