So, we hope and we expect that with lower doses in a much healthier population that this will be a hopefully pretty well tolerated approach.
Leonard Schleifer: And a much shorter.
George Yancopoulos: And a much shorter, yeah. We think that ultimately we make it by with a single short course or very short course of treatment. In terms of whether if somebody takes a holiday, whether one has to then start all over again with the elimination of the IgE cells, we think probably not, because it takes a long time to get to those levels of IgE. So, just delaying for a short period of time, you may not bounce back to those levels. As I said, you may have converted all of those cells to IgG or good cells by that point anyway. But of course, we have to be doing the studies and we have to be looking at these patients in the clinic to really understand. I should mention that the Grade 3 events that I was talking about are reflected by cytokine release syndrome.
A lot of that is also thought to be due to the load of the cancer cells and obviously these normal patients have much less of a load here. So, it’s just another reason to expect hopefully better safety. We’re going to be going with lower doses, more gentle treatment, and they have much less load in there. So, you would expect much less reason to be seeing things like cytokine release syndrome.
Ryan Crowe: Okay. Next question, please.
Operator: Thank you. One moment for questions. Our next question comes from Carter Gould with Barclays. You may proceed.
Carter Gould: Good morning. Thanks for taking the questions. Congrats on all the progress. I wanted to ask another follow-up sort of in bispecifics and autoimmune, but wanted to go down a little bit of a different path acknowledging the BCMA and Dupi effort. But we’ve seen sort of CAR-T efforts and ADC approaches sort of come to the rise in lupus and other autoimmune disorders and naturally people then started talking about T cell engages. This seems like a natural place where Regeneron could leverage its bispecific capabilities and expertise. Are there efforts underway internally on this front? Has Regeneron looked at ways to leverage that expertise? Thank you.
George Yancopoulos: That’s a phenomenal question. And first of all, let me remind you that with our long-term collaboration and recent acquisition of 2seventy, 2seventy had exactly the sort of CAR-T programs that you’re referring to in lupus and other autoimmune settings, which we are now obviously pursuing together with them. But that is one of the reasons why we were excited about turning the collaboration into a situation where we brought all the expertise in the scientists and leadership from 2seventy in-house, because we’re doing exactly what you suggested. We’re hoping to actually literally look in side by side studies, how CAR-T approaches in these settings of autoimmune, severe autoimmune diseases like lupus and so forth compare directly head to head to our bispecifics.
And as you were sort of suggesting, you would think that there would be really little reason to think that the CAR-T solutions would be preferable in this setting, both in terms of off-the-shelfness and the ability to eliminate the normal cells. As I said, it’s usually a lot easier to get rid of normal cells than it is malignant cells. So, whatever advantages you might have in certain settings of CAR-Ts, you would think in the normal disease setting or at least normal cells in autoimmune disease settings that bispecifics might be just as good, much more convenient and much safer. So, together with now our internal Regeneron Cell Medicines group that has involved a lot of the expertise and leadership of 2seventy, we’re exploring that exact question.
I should also say that as clearly been announced by the company and is available in our public disclosures, we have already initiated separately a variety of studies looking at our bispecifics to decrease autoantibodies and autoimmune diseases in other settings as well. So, we were already looking at this, but now we’re looking at these in direct comparison to our CAR-T approaches with our now internal Regeneron Cell Medicines efforts.
Ryan Crowe: Okay. Thank you, George. Next question, please.
Operator: Thank you. One moment for questions. Our next question comes from Brian Abrahams with RBC Capital Markets. You may proceed.
Brian Abrahams: Hi, good morning. Thanks for taking my question, and congrats on all the progress. I know docs are really excited for Dupi in COPD, but it is a new space for biologics. So, I’m curious the amount of education you think is going to be required and how this might affect the initial uptake trajectory? And then, how you’re thinking the introduction of other biologics, which have also been showing promise might impact the overall long-term market here and Dupi’s positioning? Thanks.
Marion McCourt: So, certainly, we look forward to the potential launch of Dupixent in COPD. There’s such unmet need and such opportunity to help those patients with an eosinophilic COPD. Our team, as you know, is very experienced with launches in Dupixent. So, work is very much underway at Regeneron and also with obviously under our collaboration with Sanofi to make sure that we apply the best practices in launch of new indications. I will share that many of these physicians have already experienced use of Dupixent with tremendous results. We’ve made great progress, as you know, in asthma, leading in new scripts and certainly making tremendous overall performance strides. But we will be very thoughtful on how best to reach physicians, how to make sure that we’re aligned with reimbursement and affordability for patients, educating in the way we’ve come to understand is best for Dupixent in the various markets and indications that we’ve entered.
So, we look forward to this opportunity.
Ryan Crowe: Okay. I think we have time for two more questions.
Operator: Thank you. One moment for questions. Our next question comes from Mohit Bansal with Wells Fargo. You may proceed.
Mohit Bansal: Great. Thank you very much for taking my question. I have a question on itepekimab. So, in our conversation and literature search, it suggests that there may be a potential for disease modification with some kind of [AAV modeling] (ph) of this mechanism. Just wanted to see if you think that is possible? And what markers would you be looking forward to in the Phase 3 trial beyond exacerbation when the data come? Thank you.
George Yancopoulos: Well, there’s always the possibility of disease modification. We actually believe, for example, Dupixent in asthma may be doing exactly that sort of benefit. One of the best ways of actually looking at that is looking at overall loss of lung function over time, because as you know in these lung diseases, as Marion said, in both asthma and COPD, these are diseases of the lungs followed largely by pulmonologists, the same sort of doctors. And it is well known that in both of these diseases over time patients start permanently losing lung capacity and lung function. We are and have been and have early data suggesting that Dupixent may prefer that in asthma and we’ll certainly be looking at those sorts of things for not only Dupixent, but itepekimab in the COPD patients in terms of modifying disease and long-term preservation and prevention of this otherwise unstoppable lung function loss.
Ryan Crowe: Okay. Last question, please, Josh.
Operator: Thank you. One moment for our last question. And our last question comes from Chris Schott with JPMorgan. You may proceed.
Unidentified Analyst: Hi. This is [Taylor] (ph) on for Chris Schott. Thanks for taking our question. So, we were wondering, would you be able to elaborate a little bit more about how you’re thinking about the linvoseltamab launch as we approach the August PDUFA? And then, thinking about the field more broadly in myeloma, how are you thinking about MRD negativity as a surrogate? And, thoughts on how you might be able to move into earlier lines in myeloma faster? Thank you.
Leonard Schleifer: Marion can take the question on the launch and everything. I mean, obviously, the MRD negativity as endorsed by that panel gives an opportunity to get these kinds of drugs to patients earlier in a variety of settings. So, we are looking forward to applying that approach in our future studies as we move towards earlier in different lines of therapy. Marion, on the launch?
Marion McCourt: Sure. So, we’re certainly preparing for the potential launch with the August 22 PDUFA date, and we’re really excited because, as I’ve mentioned before, the recent data reinforces linvoseltamab as potentially a best-in-class product for late-stage myeloma patients. So, it’s a wonderful opportunity to extend our oncology franchise in a new disease area.
Ryan Crowe: All right. Thanks, Len and Marion. And thanks to everyone who dialed in for your interest in Regeneron. We apologize to those remaining in the queue that we’ve not have a chance to hear from. As always, the IR team here at Regeneron is available to answer any remaining questions that you may have. Thank you once again and have a great day.
Operator: Thank you. This concludes the conference. Thank you for your participation. You may now disconnect.
