Leonard Schleifer: Yes. I’m not sure we want Marion to get into the details of our strategies, pricing, rebates, things like that. But we can say, Marion, you could add thoughts, that we view it as a very competitive marketplace. There has been some price erosion on some of the products in the marketplace. We’re starting at a new point with EYLEA HD. We think we priced it well. It was received well. It was intended to match on a yearly basis. And so we think the actual price point was fine. I don’t know if Marion wants to add anything at all, but we don’t like to comment specifically on those competitive dynamics.
Marion McCourt: Yes. Chris, really nothing in everyone to add to that.
Ryan Crowe: Okay, all right next question please Shannon.
Operator: Our next question comes from the line of Colin Bristow with UBS. Your line is now open.
Colin Bristow: Hey, good morning and thanks for taking the question. And all the best in the future, Bob. Maybe a couple more on the muscle sparing myostatin program. I’m curious, George, what are your thoughts around the potential concerns of myostatin targeting, increases or preserves muscle volume, but the muscle is less functional. And then any thoughts on the regulatory pathway that you would utilize for these muscle sparing assets? Thank you.
George Yancopoulos: Regulatory. Okay, so o first of all, we’ve done extensive work in preclinical models. And these antibodies have already been in humans. We believe that our studies are actually showing that this muscle is functional and certainly very important from both the metabolic and energy expenditure point of view. So, so far, those studies are very supportive of this whole approach. I should also say there’s a variety of regulatory pathways that we’re pursuing here. Obviously, the easiest, which would come from the possible results that we’re seeing in the animal studies, is if there’s incrementally more weight loss, that might suffice as a regulatory strategy. Alternatively, if it’s just the quality of the white loss, then we would have to show functional outcomes in terms of strength and so forth and so on.
So those are still early in the thinking. We have to see from these initial studies. But as I said, if we simply see increased weight loss, that would be the simplest way forward. And then you have more weight loss but better body composition data, and may also — may be better metabolic benefits, which we also see in muscle, which could also provide additional pass-through approval. So it depends on those results that we’re going to get from the initial studies. I should also mention, in terms of additional programs that we have, obesity. I mean, these are things that are here and now that we’re doing these clinical trials and we hope to be getting results over the course of the next year, 1.5 years that could really inform in terms of all these questions that you have and really validate that there’s real promise here.
But remember, we’re doing a lot of other things as well in obesity that are in earlier stages. So for example, as you probably know, we discovered a brand-new promising target in obesity using our Regeneron Genetics Center, the largest big data set on the planet in terms of human sequence linked to electronic health records, and identified, in some ways, one of the most exciting new targets in obesity that’s been ever discovered. And we have a variety, it’s called GPR75, it was published in a prominent paper in Science about a year or so ago. And we have a variety of promising and not-that-far-away approaches from the clinic in terms of blocking this target for weight loss. And I think that we presented at JPMorgan early preclinical data using siRNA approaches that look very exciting.
I should also mention that, in terms of smaller programs and so forth, we have things like a very exciting leptin receptor-activating antibody that have had very promising human data as well. So there’s a lot of things going on, but I think the muscle preservation program and how it goes forward is going to be very interesting to look at over the next year, 1.5 years.
Ryan Crowe: Thanks, George. Shannon, next question.
Operator: Our next question comes from the line of Evan Seigerman with BMO Capital Markets. Your line is now open.
Evan Seigerman: Hi guys, I have one final question for Bob. So Bob, you’ve done an outstanding job managing the financials of the business and helping drive shareholder returns over the past decade. Looking ahead, how do you believe Regeneron can best use its rapidly growing cash balance to further drive investor returns in the next decade of Regeneron? And thanks for everything, Bob.
Bob Landry: Evan, thanks for the question, and thanks for the video that we were able to show at my retirement party. It was great. On that question, George just laid out earlier today, we have so many opportunities with regards to our kind of research and development. And again, I mean I’m going to hand the mantle over to Chris, but his number one priority within capital allocation is to make sure that that is kind of fully funded. Len and George do a great job with regards to making sure what we’re bringing into the clinic as opportunities, and they’re going to continue to do that, and there’s just a lot coming, particularly when I said kind of 8 to 10 INDs. Proud on buybacks. Maybe I’ve kind of circled the victory too much on that with regards to how much we bought back and at what price.
But we have a good methodology here that Chris is ingrained with, and he’ll continue to do that. And with regards to business development, I mean, just because we can doesn’t mean we’re going to force something. It has to be right, it has to be a franchise, has to be modalities. You’ve heard George mention that has to be kind of incremental to what we currently have in the clinic here with regards to RGC and the targets we develop, and all of that. So we will remain prudent on that. Continue to be proud of the free cash flow that we’re generating. And I trust that Chris, George, Len and the Board will optimize it and put it to great use.
Ryan Crowe: Thank you, Bob. Next question, please, Shannon.
Operator: Our next question comes from the line of Salveen Richter with Goldman Sachs. Your line is now open.
Salveen Richter: Thank you. Good morning. And Bob, you truly will be missed, and enjoy the next stage of life here. With regard to your GA program, can you outline what’s contributing to your confidence in the systemic approach here, and what data you’ve seen to support it given the move from animal models to Phase III?
George Yancopoulos: Okay, geographic atrophy. So basically, the excitement is that, as we show data from our combination approach, we believe that we have the most effective way of blocking the body’s C5 activity. The C5, which is active in the eye, is essentially all coming from the liver. And we’ve shown now in our PNH studies, when we revealed the data from the first portion of our Phase III program, that it looked like we had the best-in-class activity in terms of decreasing the C5 activity. So if you block it at the source, then you don’t have to block it in the eye. And if you block it at the source, then you don’t suffer from all the concerns and side effects and so forth that you have from having to block it in the eye.
So you block it where it’s coming from, then you don’t have to treat local in the eye. You can avoid the local side effects. The concern with systemic blockade is it comes with increased risks of infections and so forth. So we will have to come up with a strategy, which we’re working on, to try to mitigate that in the elderly population that suffers from GA. We believe that we may need for that an approach to identify the patients who might be at risk in those settings. Because we certainly know that, for example, patients with PNH and myasthenia gravis who are immunosuppressed and so forth, not only with our agent, but certainly with this whole class of agents, can suffer from serious systemic infections when you block C5. So we are coming up with a way to mitigate that, in part by probably selecting out the patients who are at the highest risk.
