Seamus Fernandez : Great. And maybe just a follow-up on the MASH program. Can you just remind me the doses? My recollection was that the plan was to explore only up to the 1.8 milligram dose. But where we saw more meaningful weight loss in the obesity program was at the 2.4 milligram dose. So just wanted to see where the sort of dose range is going? And then you mentioned weight loss in MASH patients, but my recollection is that there was very limited weight loss in the NASH sort of Phase Ib/II program that you ran previously out to 12 weeks. Just trying to get a better understanding because I my recollection is you explore the 1.8-milligram dose there, but we didn’t see much weight loss and that, I guess, was partially attributed to the patient population recruited but just trying to get a better understanding of how this Phase II will differ from your initial Phase Ib/II program?
Scott Harris: Right, Seamus. So we’re seeing a different dose response curve for liver fat than we are for weight loss. With weight loss, we’re seeing increasing weight loss with increasing doses of drug. And in fact, we believe that if we were to go to even higher doses of pemvidutide in the future, even greater weight loss would be achieved, very happy with the weight logistics we’ve achieved in the obesity program. We think it’s very telling along with the other effects that Vipin described, but we have the opportunity to go higher because the dose response curve in obesity continues as you go up. When you get 70.5% plus liver fat reduction at 1.8 milligram dose, there’s really very little place to go further with the 2.4 milligram dose in the dose response.
So that’s the way the trial was designed, looking at the 1.2 milligram and 1.8 milligram doses. We always have the opportunity to add that on Phase III. That’s always a possibility that exists for us, but right now in the Phase II design, we’re going to be looking only at the 1.2 milligram and 1.8 milligram doses.
Operator: Our next question comes from Roger Song with Jefferies.
Roger Song : Great. Thanks for sharing the new data and the update and taking our questions. So another question related to the partnership, maybe a little bit more specific. Can you let us know how much discussion is contingent upon this more detailed Phase II obesity MOMENTUM data, at the words, your Phase II MASH data kind of upcoming? And just remind us the discussion is a combination of both programs moving forward or you will different partners have different interest in certain programs?
Vipin Garg: Yes, Roger. I would say the good news is that most of our partnership discussions are actually focused on both obesity and MASH program. Most of the players that are looking at pemvidutide are interested in both because they’re very related indications that you can imagine. So it’s going to be hard to separate them anyway. But in terms of developing and commercializing a product, it’s a very similar pathway. So the good news is that most of our partnership discussions are focused on both of those programs. So we think ultimately, our ideal partner would be a multinational player that has the ability to develop both obesity and MASH and commercialize in both of these and really take this program forward in parallel. So we’re in good shape from that perspective. The partners are clearly getting the message in terms of the value proposition, the differentiation that pemvidutide brings. And therefore, we’re very excited about those discussions.
Roger Song : Got it. And then another mechanistic question. So it seems very compelling this muscle preservation, which is very interesting. So how do you think about pemvidutide can be differentiated in the maintenance or the rebound kind of mechanism, given you are more liver lipid — or additional liver lipid targeting versus the GLQ-1 mostly is the hypocaloric mechanism?
Vipin Garg: Yes, that’s a great question, Roger. Scott, do you want to take that?
Scott Harris: Yes, Roger. We feel that every time we generate data, we’re showing the really incredible differentiating effect with glucagon compared to other mechanisms. So we’re very familiar with GLP-1 and GIP, and those drugs have very nice effects on weight loss and they also have other benefits that have been seen in clinical trials that are ongoing or soon to be completed. Glucagon brings a whole different dimension here. That’s extremely valuable for not only achieving weight loss but maintaining weight loss, healthy weight loss and having long-term effects in cardiovascular outcomes. So we really think in that sense, glucagon is a game changer. We’ve seen, as you’ve mentioned, the effects on serum lipids and liver fat.
And now on top of that, we’re seeing a very potent effects on preserving lean body mass as people lose weight. This has been a very important point of differentiation and discussion in the obesity circle for the last 2 years because now, people are turning away from the absolute amount of weight loss to the quality of the weight loss. And that’s important, especially for long-term maintenance. So the ability to hit a certain number acutely doesn’t really matter if someone stops the drug and regains the weight or regains the weight that’s mainly fat or not lean. So we think this could be an incredibly important mechanism for maintenance. As you know, there was a suggestion in the obesity data at the 2.4 milligram dose that the weight loss was continuing in an aggressive manner at 48 weeks.
We think this would also represent a fundamental effect of glucagon on intermediary metabolism and energy expenditure that could continue in the future basically changing the metabolic balance and having in that score, real differentiation from the GLP-1s and the GIPs. We don’t have that data at this point. It certainly would be of great interest to study this going forward, and it’s something that we’re strongly considering in our Phase III program.
