Scot Roberts: You know, Roger, in that context, it’s helpful to also understand that the IAH states that 60% to 70% of obese people are dyslipidemic, and the ability of glucagon to drastically change the metabolism of lipids and lower serum lipids and liver fat, as Scott just indicated, certainly creates a special target population in that respect.
Roger Song: Excellent, thank you. I appreciate all the comments, very good. A very quick one in terms of the NASH. I know it’s early stage, you are still finalizing the design, but just in terms of given the multitude, the effect from pemvidutide, what could be the ideal population you will do, like an earlier stage in terms of the NASH stage, or some other consideration you will have for the patient population? Thank you.
Scott Harris: Thanks for the question, Roger. It had been said early on in NASH development that metabolic drugs treat at the early stages of NASH, whereas you need anti-fibrotic drugs to treat the later stages. That paradigm has been turned on its end because we now have two metabolically active drugs, resmiterom and efruxifermin, which have completed Phase III and Phase II respectively, having very meaningful effects on fibrosis. What that shows is that if you affect the liver and have effective liver fat reduction, you’re going to have effective reduction in inflammatory and fibrotic activity which is going to drive activity not only from fat reduction all the way through fibrosis improvement. We actually see the product population for this study being all stages of NASH, up until advanced fibrosis.
That’s been a tough population to treat, and we’d point out that the greater the reduction in the liver fat, the greater the effects that I just mentioned have been in clinical trials. Very happy about the resmiterom results, the reduction of liver fat at 24 weeks was about 49% to 50%, and with efruxifermin it was about 65% to 70%. We’re at 70% to 75%, and based on that, we’re very, very optimistic about biopsy results in the future. But with resmiterom, which we believe will go onto approval, only 25% of people had a response in either NASH resolution or fibrosis improvement. We think that’s great – it lays the regulatory precedent, but we also believe there’s a large amount of room for improvement that we think we can fill.
Roger Song: Excellent, thank you. That’s it from us.
Operator: Thank you. One moment for our next question. Our next question comes from the line of Corinne Jenkins from Goldman Sachs.
Corinne Jenkins: Thanks and good morning. Maybe first from me, just based on what we saw in the NAFLD study, how do you think the dose titration and the 2.4 mg/kg arm could impact safety compliance and then maybe downstream about efficacy in the upcoming MOMENTUM readout?
Scott Harris: Well, thank you for the question, Corrine. We put that short titration in place based on some observation we made in our first-in-human study. With the 2.4 milligram dose, we saw more GI intolerability events, and they were occurring early on, in the first one to two weeks, so we thought that a four-week titration would mitigate adverse events. We saw something to that effect in our NAFLD trial. Whether we continue to use that titration going forward in the future, we’ll have to see based on the data that we accrue. We think that the end of 24 weeks with a four-week titration would probably at that point in time have a minimal effect on the overall weight loss, and certainly by 48 weeks there’d be sufficient time to minimize the impact of the effect of the titration.
