And we’re now, as we announced in a pivotal trial where we hope that we will in the – within the next year, perhaps be able to provide the results from that trial, which might confirm this remarkable advance for patients. If it works in this first-line melanoma setting, it really opens up the door to a whole series of other opportunities both in related melanoma settings, such as an even earlier stage melanoma setting such as the adjuvant and perioperative settings, but we could be moving to other cancers as well with that proof of principle. So that’s the nearest term Libtayo checkpoint combination approach. As you know, with our bispecifics, the combination opportunities there are also very exciting, either with Libtayo or with each other.
And we have, in that space shown that our individual agents, the important thing is we have now validated so many of our individual agents as having once again the potential for best-in-class type of activity, whether it’s our agent for myeloma or our CD20 bispecific in, for example, follicular lymphoma and so forth and so on. But we’re also excited about our costim bispecifics. We’ve released the data about the incredible efficacy in, at early stages that we see in combination with Libtayo. But that one – that one is countered by concerns with immune-mediated adverse events that we’re seeing in these patients. It is hard to dramatically increase the extent of immunotherapy benefit without having it associated with increased autoimmune type reactions.
We’re working very hard on that, and we think, based on preclinical data that the trick may be combining our costims with our CD3 bispecifics where we don’t see these dramatic potential increases in the mechanisms that may lead to immune adverse events. So in summary, our checkpoint combinations are very near-term. Our bispecifics are single agents have been validated and hopefully will be being considered by the FDA for approval in the relatively near future. And the combinations are beginning to demonstrate exciting opportunity, and we’re trying to tune that in order to try to present the best efficacy safety profile for patients.
Ryan Crowe: Alright. Thank you, George. Shannon, please the next question.
Operator: Our next question comes from the line of Brian Abrahams with RBC Capital Markets. Your line is now open.
Brian Abrahams: Hey, guys. Congrats on the good launch so far. And thanks for taking my question. You mentioned in the press release some impact of price on EYLEA. I was wondering if you could elaborate a little bit more on this, when you think this might stabilize; any extent that this might affect high-dose EYLEA as well? Thanks.
Marion McCourt: Sure, Brian. So I would comment that in an increasingly competitive category, there of course, there’s been some pressure on EYLEA. I’d also reflect that in 12 years in the market, it’s really modest rebating and discounting if you look at the history of the brand. And of course, that on a brand that has never taken a price increase. But we will continue to be very much watching uptake of EYLEA HD, taking very responsible and appropriate and thoughtful measures on pricing. And certainly, as I reported to early days, we’re making some very strong progress in the marketplace in terms of making sure that physicians gain confidence in reimbursement of EYLEA HD as they initiate patients.
Ryan Crowe: Okay. Thanks Marion. Please the next question, Shannon.
Operator: Our next question comes from the line of Yatin Suneja with Guggenheim. Your line is now open.
Yatin Suneja: Hey, guys. Thank you for taking my question. Question on Dupixent. Could you maybe share your views on the newer mechanism? For example, OX40 or perhaps a longer-acting version of Dupixent on the franchise; maybe if you can talk about your efforts in terms of life cycle management of Dupixent? Thank you.
George Yancopoulos: Yes. Maybe getting back to some of the comments that I made before. The collection of so-called allergic or Type 2 conditions, which Dupixent addresses, are all characterized by a systemic inflammatory problem increase in the so-called Type 2 inflammation, which if you look at the science and literature is really of this digital pathway that largely evolved and was one of the most active parts of the immune system to fight things like fecal parasites, which are really not an issue now in the developed world. This part of the immune system should essentially in the modern world be entirely quiescent. It serves almost no role. The problem is it becomes unleashed abnormally to do things that it shouldn’t be doing, like fighting allergens or attacking the skin or the gut in atopic dermatitis or eosinophilic esophagitis.
What Dupixent does uniquely is that it controls, and the data now demonstrate this, the incredible effect that it puts this useless angry tiger back in the cage where it belongs. And that is why it has this incredible profile of not only efficacy but safety. Because what’s shutting down is it’s shutting down a pathway that should be vestigial in the modern world that becomes unleashed and attacks all different parts of the body. We believe that any of this current competition that’s ongoing doesn’t share these remarkable features that give Dupixent its incredible broad efficacy across the spectrum of diseases with its unique safety profile. Because all of these other approaches, including, for example, the OX40 approach and so forth, are addressing different fundamental immune pathways that are important in the immune system’s function to do a lot of actual useful things in the modern world, like, for example, fighting viral infections in cancer and so forth.
So Dupixent really has a very unique profile, which if we can help explain and if all physicians and patients can understand it, make it the perfect drug for this condition. It uniquely blocks this digital pathway that gets out of control and appropriately and causes disease all over the body. Dupixent shuts down this what should be a vestigial pathway, and it helps disease, whether in the same patients, it could be manifesting in the skin in the lungs, in the nodes, in the gut and so forth, it shuts it down without really untoward effects with regards to the ability of the body to actually fight infections and so forth. In fact, if you look at our clinical studies and some of the data that we published, in many, if not most cases, you actually see unbelievably reduced infections in the setting of the Dupixent treatment.
Because what you’re doing is you’re putting the bad part of the immune system back under control and you’re allowing the rest of immune system to do its function. All of these other approaches are trying to attack critical parts of the immune system that have important other functions, and they don’t address the widespread problem that occurs systemically and causes all of these diseases. So as you’ve seen already with various agents, they may work in one of Dupixent indications, but they don’t work, they failed in other indications. And if they work, they also often come with the concerns about safety because they’re designed to be immunosuppressive, which Dupixent is not.
