Jonathan Wolleben: Thanks for the color, Scot.
Operator: Thank you. And our next question coming from the line of Patrick Trucchio with H. C. Wainwright. Your line is open.
Louis Susser: Good morning, everyone. This is Louis for Patrick. Thank you for taking our questions. I’m going to change gears here and talk a little bit about the HepTcell and the way that the field has been looking at immunomodulation as an accepted necessity and HBV cure for –due to HBV cure. So can you talk about how your treatment is progressing towards the functional cure that could achieve this mechanism — this immunomodulation mechanism where others don’t have that?
Vipin Garg: Sure. I appreciate the question there. What we’ve already demonstrated with HepTcell is that the therapeutic, which is it’s a T cell immunotherapeutic meant to boost the T cell response over the resistance it has to have seen the HPV antigen. We’ve demonstrated in our Phase 1 studies that it’s very safe and that it’s able to significantly increase the T cell response to HBV antigens. And so the next step we felt it was important since this is going to be used as a combination therapy most likely with direct acting antivirals like siRNA or monoclonal antibodies or oligonucleotides and against the surface antigen, for example to show that they come on at activity on its own. And so that’s what this Phase 2 study that’s currently ongoing, and we’ll report out in the first quarter of next year is meant to show.
The advantages of HepTcell have to do with the focus of the T cell response against antigens that are known to be important for functional response. And that is the polymerase antigen and the core antigen. The epitopes that were selected and represented in HepTcell are highly invariant. They’re hydrophobic in nature. And so they’re unlikely to mutate in response to the immune pressure that will be generated. So what we have is an immunotherapeutic that’s expected to be active against all of the circulating genotypes of HBV. And with combination with the adjuvant that we are using IC31, which is preclinically looked very encouraging. And in our Phase I study was shown to be important for these T cell responses. We feel that we’re going to be able to generate a very robust response with surface antigen and other measures of HBV replication.
That will then set us up for purging discussions with companies that have these direct antivirals and allow us to do the Phase 2 studies in combination therapies.
Louis Susser: That sounds great. And do you plan to stratify patients based on surface antigen at baseline. We’ve seen that with the Betty [ph] Phase 3 program. Can you discuss more the baseline characteristics of the Phase 2 trial? And if you’re successful, if you’re going to implement that threshold of surface antigen in the baseline going forward?
Vipin Garg: Sure. That’s a great question. And that’s really one of the unique design elements of the Phase 2 study that’s currently ongoing and report out here shortly, is that we’ve selected patients that are referred to as inactive carriers. And so basically, these folks have low surface antigen levels compared to many chronically infected individuals. And we felt that, that would represent a population that has received direct acting antivirals, has had the surface antigen reduced by the mechanisms that I referred to earlier and then created a better environment for the immunotherapeutic to work and boost the T-cell response. So going forward, we don’t see selecting patients with low surface antigens. We think that the combination therapy, the first part of that with the direct acting — direct acting antivirals will accomplish that goal, and then HepTcell will work as it is in this study.
