William Wood: Appreciate it. And then one last quick one. Your IMPACT trial is enrolling F2/F3 patients. I believe you said 50% have to be F3. Given the difficulties we’ve seen recently in at F4 at the current time, do you foresee pemvi trying to be run in that F4 population?
Vipin Garg: It’s a great question, William. That’s something we’re obviously taking a very, very good look at. We haven’t made any announcements on that to-date. Right now, we’re concentrating on the F2, F3 population, but we’re certainly taking a very good look at cirrhosis and the possibility of engaging that population in a separate clinical trial.
William Wood: Appreciate it. Thanks very much for taking our question and congratulations again.
Scott Harris: Thank you.
Operator: Thank you. And our next question coming from the line of Jonathan Wolleben with JMP Securities. Your line is open.
Jonathan Wolleben: Hey. Thanks for taking the questions. I guess two for me. I want to follow-up from an earlier question. How do you think about an acceptable tolerability profile then in the upcoming little readout given the kind of tweaks Scot, you just discussed you could make going into Phase 3? And then can you also discuss the differentiation from pemvi to the other GLP-1 glucagon dual agonist, Merck and BI compound, either structurally or even from the data we’ve seen, we’ve gotten pretty good datasets from all three at this point. I think that would be helpful to hear? Thanks.
Scot Roberts: Yeah. So we have to point out that any tolerability data that’s been generated to date has been in the absence of dose titration. And the fact that we can achieve comparable safety and tolerability is really — it’s a complement to the drugs, and we believe that arises from the pharmacokinetics of pemvidutide with a slow entry into the bloodstream. Remember that at the 1.2 milligram and 1.8 milligram doses, the adverse event rates leading to discontinuation were low. And again, the 1.8% was given without dose titration and still achieved a 9.4% weight loss at that point in time, which was as good as semaglutide at the same time point when you look at it on a placebo-adjusted basis. Obviously, there is a lot of opportunity to tweak the dosing any way we wish in order to get that profile down even better than it is right now.
And as I mentioned before, Jonathan, we think we can get that to — without adjusting the dose titration by simply allowing for dose reduction in future trials. So we’re obviously optimistic about that. Regarding the other compounds, starting from the structural viewpoint, as one knows that in addition to the ePort domain, which we think is unique and conveys special pharmacokinetics to the drug we also have a 1:1 ratio of GLP-1 to glucagon agonism, which is the highest concentration of glucagon and the glucagon dual agonist that are available today in contrast. The Merck has announced that it’s about 2:1 biostores GLP-1 and the Boehringer compound, pemvidutide is about 8:1. We believe that it’s the higher glucagon content that conveys the properties that we’ve seen.
But it’s also important to note that these compounds have both been associated with heart rate increases and that we’re not seeing these heart rate increases in our program. And we think that’s a very important differentiator. We’ve not seen any liver fat data with the Borger compound. Some discussion has taken place around meetings that they’re not seeing changes in serum lipids. We think that reflects the low glucagon compound content in that compound. And the Merck data, they are seeing relatively comparable reductions in liver fat which we speak to the glucagon activity in both compounds
