Sarepta Therapeutics, Inc. (SRPT) Earnings Call Transcript & Summary

Welcome, everyone, to the 40th Annual JPMorgan Healthcare Conference. My name is Anupam Rama. I'm one of the senior biotech analyst here at JPMorgan. I'm joined by Priyanka Grover, Malcolm Kuno and Caleb Smith from the team. Our next presenting company is Sarepta, and presenting on behalf of the company, we have CEO, Doug Ingram. I want to remind all the attendees to use the ask-a-question feature in the portal. If you have a question, I'm happy to ask it on your behalf. With that, Doug, take it away.

Thank you, Anupam, and good morning, everyone, and thank you all for joining us today. I'll wait for the slides to pop up. There we go. Sarepta, hopefully, as you know, is 1 of the world's leading biotechs in the use of precision genetic medicine to treat life-ending rare diseases. And we have the strategy, we have the science, and frankly, we have the execution-focused tenacity to become what I believe to be the next big biotech. Now I can provide a number of proof points to support that prediction. But perhaps there is no better example than SRP-9001 to prove our point that we can use great science and execution to improve the lives of those with rare life-ending diseases. So I'm going to spend the bulk of this discussion, reviewing the top line data from Study 102 Part 2, which is our Phase II trial exploring the use of SRP-9001, our micro-dystrophin gene therapy to treat Duchenne muscular dystrophy. Slide 2, please. I or one of my colleagues may make -- we almost certainly will make statements or predictions about future events today. So please review our public filings for the risks that come with these sorts of forward-looking statements. Slide 3, please. SRP-9001 is intended not merely to treat, but to change the course of this progressively degenerative disease, Duchenne muscular dystrophy or DMD. And so let's briefly review DMD, a rare X-linked to recessive disease. Duchenne results from a mutation on the gene that codes for a protein called dystrophin. Dystrophin is a sort of shock absorber for our muscles. It attaches to our muscle membrane and it distributes force as we move, protecting our muscles from damage. Now boys with Duchenne muscular dystrophy as a result of their mutation, they lack this dystrophin shock absorber to protect their muscles. And the consequences of that are as certain as they are brutal. The course of this disease is predictable. At a young age or Duchenne boy, will begin to struggle sometime typically between perhaps 8 and 11 years old, he will become power wheelchair dependent and he will remain so for the remainder of his life. Then he will begin to lose the use of his arms and his hands and then he will begin to struggle even to breathe, and he may end up on a ventilator. And then usually in his 20s, he will invariably be killed by Duchenne. It is our goal to change the course and inevitability of this disease. Next slide, please. SRP-9001 is a full body or systemic infusion gene therapy, and it's intended to change the course of this disease by restoring the protective shock absorber. It does this by delivering a gene cassette that codes for a truncated but functional form of dystrophin throughout the body, the skeletal diaphragm and cardiac muscle. Now SRP-9001 stands alone as each of the elements of this unique therapy is unique to it alone. SRP-9001 alone uses rh74 as its delivery vector [ rh ], SRP-9001 alone uses a heavy chain MHCK promoter to drive expression and SRP-9001 alone, uses its very specific gene construct, which was designed, empirically tested and optimized by Dr. Louise Rodino-Klapac and Dr. Jerry Mendell over the last nearly 20 years. It is these unique and rationally designed elements of SRP-9001 that explain why this therapy results in superior and properly localized expression of the dystrophin protein across muscle why it has a differentiated unique safety profile and why it results in the functional improvements that we have seen over multiple studies to date. And with that, let's turn to Study 102 Part 2. So let's move to Slide 5, please. Study 102 is a multicenter randomized double-blind Phase II clinical trial. There are 41 participants in the trial, all with Duchenne muscular dystrophy, and age 4 through 7 at the time of study entry. Part 1, which we reported out last year, evaluated the 48-week results of 20 patients on therapy against 21 patients who are randomized to a placebo. At crossover, all of the children remained blinded. So those who previously received the placebo treatment then, receive therapy, while those who previously received therapy, received a saline infusion and that allowed us to maintain the blind. So in addition to expression and safety, the principal analysis for Part 2 of Study 102 is the 48-week North Star Ambulatory Assessment or what I'm going to call NSAA for the crossover patients versus a prespecified prospective external control. Next slide, Slide 6, please. This describes that external control. Our goal of our Part 2 statistical analysis plan was to create a prespecified SAP with such rigor that it can be used for regulatory interaction and potentially a BLA file. The statistical analysis plan for Study 102 Part 2 is a sophisticated propensity score matching analysis that was prospectively defined finalized and submitted to the FDA prior to database lock and unblinding. That's very important to understand. This is all prespecified. None of this is post hoc. In the absence of a placebo arm, the propensity score, external control is a rigorous and commonly employed method to reduce bias and precisely predict treatment effect and numerous therapies have been approved from studies using prospectively designed propensity score external controls. The external sources that we use include the synergy Duchenne history -- natural history study, a prepublication steroid study and the placebo arm of an Eli Lilly study evaluating a treatment for Duchenne muscular dystrophy. The inclusion and exclusion criteria rigorously matched baseline characteristics, and I'll show you that in a moment. And the propensity score weightings included a number of covariants. It was age. It was NSAA. It was rise from the floor and it was 10-meter walk/run. I don't think I'm exaggerating when I say this is almost certainly, the most rigorous prospective external control compared to that's ever been employed for a Duchenne muscular dystrophy trial, and as I said, the primary analysis is the 21-patient crossover cohort versus propensity score weighted external control. Let's move to Slide 7 now. Just to make that point, you will see on this slide, all of the summary data from our various covariants. I would encourage you to review this slide later to better appreciate the robustness of our external control. But directing your attention to the right side of this slide, you will see there that across all of the various covariants, age, NSAA, rise time and the 10-meter walk/run, the external controls are merely perfectly matched against the crossover patient base lines. Next slide, please. And for those who are tracking, we're at Slide 8 now. Now the functional review today is going to be for NSAA. And that is a composite 17-item, maximum 34-point functional scale. There will be additional yet to be completed analysis, including some timed function test analysis that we will get completed and we'll present in the later medical meeting. However, please know that as has been the case in all of our prior studies, the time test results will be consistent with the NSAA data that you're going to see today. But we're going to focus on NSAA today. NSAA has 3 different scores. Each item is rated as either/or 2 for no obvious modification of function or a 1 for modified activity, but the patient is able to achieve the function or 0 if the patient is unable to achieve the function independently at all. And so we contextualize what 1 point means one really has to understand this by seeing it visually. If we look to the video in this slide on the left screen, and I would ask the -- that video to be played right now. This is a 2-rating. So we'll watch this boy, I mean as you can see, it gets off of the floor. So [indiscernible] . The next video in the center is a 1. It's literally just a 1-point difference and I would ask that, that video to be play. And for those who can't see the video, I will tell you, the boy will struggle to get off of the floor. He will have to use his own body to do it. He will eventually have to use his legs, which is called a Gower's maneuver, but it eventually gets up. That is a single point difference between those 2. And then finally, 1-point difference from that is the boy on the far right. I would ask that this video to be play. Now this is a painful video, and I'm not going to require you to watch the entire video because it goes on for some time. But what you will see here is, unfortunately, with just a 1-point difference, this boy will never get off of the floor. And of course, that loss is permanent. Duchenne moves in only 1 direction toward greater and greater loss of function. So I point all of that out to really make -- emphasize how important single point difference is on this scale. All right. And with that, let us move to the data from 102 Part 2. So let's move to Slide 9. Here are the results for the patients who were dosed at crossover. I want to point a couple of things out. These children are on average, 7.24 years of age at the time of baseline NSAA, which means they're over 8 years old at the last functional visit. That's the oldest group for which we have functional results yet for this therapy. And yet over the course of just 48 weeks, they have achieved a powerfully statistically significant improvement in NSAA over precisely matched external control and they are improving over their baselines. Even with the modest end of 21 patients, the p-value is 0.0009. And the magnitude of effect and the rapidity of its onset is perfectly consistent with the results we have seen across our studies, including Study 101, Study 102 Part 1 and Study 103, and I will review those in a moment. These children are improving, where at this age range, natural history would predict the commencement of what will become a very significant decline. And as we are changing the slope of this disease, this benefit should continue to compound, just as we have seen in past studies. The vast majority of these patients are in the 6- to 8-year-old range, and in fact, many of them are in the 8 year-old range. As you will recall, in Part 1, with a properly matched 4- to 5-year-old cohort, we saw strong statistically significant and clinically meaningful benefit over placebo of about 2.5-points in 48 weeks. So the next question to be answered is whether that benefit has persisted into year 2? And with that, I will move to Slide 10. And here, you will see the answer is a resounding yes. As we previously reported, the 4- to 5-year-old cohort, was properly matched against placebo. And in a small 8-patient cohort versus an 8-patient placebo group, they already saw a clinically meaningful and statistically significant improvement in just 48 weeks. Following these children for the next 48 weeks, you will see here that even as they are getting older, they have maintained the benefits of the therapy. And indeed, they've actually improved an approximate additional point over year 2, and they're now showing a 5-point benefit over their own baselines from the commencement of this study. What is particularly impressive about these results is that we see this result, not only with a small end, but also even though because of titering issues at our manufacturing partner, 60% of these Part 1 patients received less than the target dose for SRP-9001. Additionally, if you look at our Part 1 patient, you should know that the mean NSAA score has remained stable over the entire 2-year period. Now function is extraordinarily important, but we know with respect to gene therapy, safety is equally important. So let's review safety here as well. Let's move to Slide 11 for that. Turning to safety. The safety profile in Part 2 is entirely consistent with the safety profile we saw in Part 1 of the study. We saw no emerging additional safety issues. As has been consistent across our studies, the most common adverse event is nausea and vomiting. There were no treatment-related serious adverse events. No patient discontinued the study for an adverse event. And if we go to Slide 12, for your reference, here are all of the treatment-related adverse events in Part 2 of Study 102, they look entirely consistent with what we saw in Part 1 of Study 102 as well. So now let's move to the conclusions. With the next slide, Slide 13. The conclusions from Part 2 of Study 102 were unequivocal in my view. The patients at crossover have achieved a clinically meaningful, and impressively, statistically significant benefit in just 48 weeks versus a precisely matched prospective external control. The total NSAA score for treated patients showed a positive benefit at every single time point post-treatment versus external control. The benefits that were observed in Part 1 of Study 102 persisted and weren't durable, and there have been no new safety signals in Part 2 of Study 102. Study 102 Part 2, adds additional weight to what has become a consistent totality of evidence supporting the thesis that SRP-9001 is a well-tolerated gene therapy that does not merely treat but change is the course of this ferociously-degenerative disease, Duchenne muscular dystrophy. Consider that even before the commencement of the pivotal trial EMBARK, we had already dosed nearly 80 patients with SRP-9001, and the functional benefits we observed in Study 102 Part 2 are consistent with all of our prior studies, and I'll review that right now. Let's go to Slide 14. As you'll recall, in our first study, 101, we saw NSAA benefit at year 1. That was great, but that benefit grew by year 3 to a nearly 9-point benefit over natural history with a p-value of better than 0.0001. Next slide. In Study 102 Part 1, the properly matched 4- to 5-year-old cohort showed a 2.5-point NSAA benefit over placebo with a p-value of 0.017, and as we just saw, that benefit is not only persisted, but has improved another point in year 2 to being 5 points above their baseline now. Slide 16. In Study 102 Part 1, when the 6- to 7-year-olds were actually compared to a properly matched external control, they showed a 2.9-point NSAA benefit and a p-value of 0.0129. And Slide 17. Shows that just as we reported a moment ago, in the crossover patients in Study 102 Part 2, the patients with an average age of 7.24 at time of baseline NSAA at over 8 years at their last functional visit saw a 2-point benefit over external control with a p-value of what is truly an astonishing 0.0009. And finally, Slide 18. With respect to Study 103, which is our commercially representative material, we have seen a 3-point improvement from baseline in the first 11 patients in cohort 1 at just 6 months. So next slide. When we consider the totality of the evidence that we note, over 3 studies, in the widest ranges of ages and child weights, and when we consider the expression levels that we've obtained. And when we consider our safety profile, and when we consider the functional benefits that we consistently observed, you can only imagine the level of confidence and conviction that we have in the success of our pivotal trial EMBARK. So I'm going to talk about EMBARK for a moment. To remind you, EMBARK is our large global double-blind, placebo-controlled trial, which is enrolling and dosing now. And it is designed for success. It is robustly powered. This is an [ N of 120 ] it's the largest study of its kind in Duchenne muscular dystrophy. It is very tightly controlled and have been informed by our prior studies with very tight entrance criteria to reduce standard deviation and to increase our probability of success. Now I know that EMBARK will read out next year. And when it is consistent with the totality of evidence that we have already generated on the benefits of SRP-9001. We will move quickly to file our BLA for the approval of SRP-9001 next year. Of course. We are very well aware and understand that time is not on the side of our patients and that every day's wait is another day of irreversible loss of function or, frankly, worse than that is in the United States alone, 1 child for Duchenne muscular dystrophy dies every day. So we will share these data with the agency this year. And we will discuss with them. The fastest potential pathway to bring this therapy to our community of patients and to their families. Next slide. Now as exciting as SRP-9001 is, it is one of only a number of programs that make up this precision genetic medicine organization that is Sarepta. So let's go to Slide 21. The team has done a simply brilliant job serving the Duchenne patient community with our 3 currently approved therapies. Now announcing to you that quarter 4, we achieved net sales of $178.7 million and that is our 21st straight quarter of consistently strong quarter-over-quarter growth. We achieved full year 2021 net sales of $612 million, that is a nearly 35% year-over-year growth, and it is a 5-year CAGR of greater than 40%. And that growth will continue into 2022. Our guidance for 2022 is to do greater than $800 million in net sales with our currently approved therapies. And I'd like to remind you that we have achieved all of this growth through exceptional commercial execution and through serving the Duchenne community as we have never taken a single price increase since our first therapy was approved. And finally, I should note that in addition to our revenue, we have over $2.1 billion on our balance sheet, to drive our programs. Slide 22, please. Speaking of programs, our multi-platform pipeline, some 40 program rich, is unmatched for a biotech or size or perhaps of a biotech of any size. We are, in fact, in pivotal trials for our lead programs in both of our 2 clinical stage platforms. I've already mentioned earlier, our large gene therapy trial EMBARK. In addition to that, in our RNA platform, we are dosing patients in MOMENTUM, which is our pivotal trial for SRP-5051, our next-generation PPMO for Duchenne muscular dystrophy. To remind you, in Part A of MOMENTUM, we saw 18x greater exon-skipping, 18x greater dystrophin production than the current gold standard of eteplirsen, and we saw that in half the time and at 20% of the drug exposure. So we are very excited by the potential for an accelerated approval to bring SRP-5051 to the community. Moving on to Slide 23. And milestones. So like every year at Sarepta, we have a lot to do, when we have a significant number of milestones to achieve. They will include driving enrollment of EMBARK and MOMENTUM. They will include moving our limb-girdle programs forward. They will include continuing to serve the community of our commercial therapies and, of course, advancing the rest of our pipeline. Final slide. At Sarepta, we have the resources, we have the scientific prowess, and we have the execution-focused team to turn incredible science into life-extending therapies and that is just exactly what we intend to do. Thank you for that. And Anupam, I think it's time for us to turn to Q&A. And I would invite my colleagues, Ian Estepan, Dr. Louise Rodino-Klapac and our Chief Customer Officer, Dallan Murray to join me.

Okay. I guess one of the key questions that I suspect we're going to be getting is it feels like you put maybe accelerated approval potential back on the table with your comments that you will take these data to the FDA as soon as possible and highlighting the unmet need of the disease. Maybe you can expand on that if that's truly on the table now or how you think about it?

Let's first start with a couple of things. First, there is no doubt that the data that we have seen from Part 2 of 102, at least in our strong opinion, adds to the totality of evidence that SRP-9001 is a disease trajectory altering therapy that will benefit kids with Duchenne muscular dystrophy. So we're very excited by the weight of evidence that we have and that the way that the evidence is certainly been enhanced by Part 2 of 102, and by what we've seen in the 4- to 5-year-olds in the second year. So there's no doubt about that. There's also no doubt about the fact that we are executing as fast as we can on EMBARK, our pivotal trial. And that I remain consistent in my view that everyone should see as their base case that, EMBARK, which will complete this year in enrollment, we'll read out next year, and we'll file the BLA if it's successful next year, should be our base case. But certainly, we are going to share the data that we have with the agency, given the wealth of the data and the totality of the data that we have, and considering what the standard is for Accelerated Approval, and considering this is a ferociously degenerative rare disease, and at least talk to the agency about the possibility of a pathway that would be even faster than EMBARK as fast as the EMBARK is. Now one final thing I will say, 1 of the -- for those who are looking at Accelerated Approval for [ EMBARK ], I mean 1 of the interesting issues for us in our discussions is that EMBARK is going to read out so quickly, but they are not that far away from one another. So I think our base case is still very rapid in bringing this therapy to patients.

What are the time lines for meeting with regulators? Has that been outlined? And when you meet with regulators, what will be the disclosure strategy in terms of whether an Accelerated Approval strategy comes forward or if it doesn't, would you disclose that to us?

Yes. So we will meet with the agency sometime this year. We will be cagey about when that will be, to be honest with you. And we will provide updates when we have definitive views with the division. So I think the updates we're going to provide for a while is going to be updates on execution against EMBARK, execution against MOMENTUM and the like. And then we will have conversations with the agency, and we have something that's meaningful and definitive, we'll discuss it with folks later this year.

One of the questions I think that given the FDA's focus on manufacturing that just came to my mind is, do you have enough data with your commercial supply material to have a good argument with the FDA about that portion of the CMC portion, I guess, is tight enough?

We will, we will. I mean we've disclosed now the first 11-patient cohort from Study 103, and I think you've seen that expression look great, the functional signals look great in just 6 months, et cetera. We will by later this year, have more data out of Study 103 as well. We've dosed a significant number of patients on our commercial material just in 103 alone. Louise, perhaps you can provide an update on the number of patients that we've already dosed with 103?

Yes. It's 33.

Yes. So we'll have a good set of data to discuss with the agency to show the consistency from an expression perspective and a safety perspective, and functional signal perspective. And that will be -- and to your very good point on, and that's of course, important.

Maybe just really quickly, one thing to add something about that. Louise just said that 33 patients dosed. That's in a broad spectrum of patients, right? So it's not just 4- to 7-year old, there's [ 24 4- to 7-year ] old and then an additional 13 patients who are older and non-ambulant. So we have not only see efficacy, similar efficacy with the commercial manufacturing material, but also safety in a broad patient population.

Okay. We have an e-mail portal question here, which is, in 2021, you reported 6- and 7-year-old NSAA cohort, which seemed -- which were out of balance at initiation. What happened to these placebo patients and the SRP-9001 cohorts?

I'm sorry, you mean the placebo patients themselves?

Yes.

The placebo patients, the 6- to 7-year-old placebo patients in Part 1 were part of the cohort that was dosed in Part 2. And the interesting thing that someone might ask is, well, are you dividing up what 6- and 7-year-olds look like versus 4- and 5-year-olds at Part 2? And the short answer is that almost all 6- to 7-year-olds are older because remember, there were -- they were 4 to 7 at entry. So essentially, you're seeing those results in the Part 2 data, and they're looking great versus natural history.

What are the -- you reiterated that you expect to complete EMBARK enrollment in the first half of this year. How is enrollment tracking, I guess, for us relative to your expectations? Are there any -- with the new variant and just dynamics around that? Is there any risk to enrollment?

So I've said the 2 things. So first of all, we're on track. So we're on track and we're on track for our time line. So that's all fantastic. I will reiterate what I've said many times, which is, the demand for this therapy is very, very significant, given the need. And so we're not going to have an issue, I think, from a demand perspective or from the interest and investigators. And so there's 2 risks to it is, one, execution, just getting sites up and running and getting them going around the world. We're doing a good job on that. We've got to keep moving on that. And there is always the risk of the country shutting down pandemic-related. But I will put that out there as a theoretical risk. We've done a nice job over the last 2 years managing through that. And frankly, many of our investigators have done a really brilliant job managing through that. So I don't really see that latter risk yet being, something that's impacting us.

What are you hearing competitively about enrollment with Pfizer's gene therapy given the recent safety update? And have they been able to enroll any patients in the U.S.? And is there a chance that you're able to kind of make up some ground here on enrollment in terms of relative to your competition?

I want to be -- again, I'm going to be very careful because Pfizer had a really, really, really unfortunate event recently, and I don't want to look like, I'm talking much about it because they should be the ones talking about it. And I think they have done a nice job of that in the past. My general understanding that has to be confirmed is that they are not dosing anyone on any study right now. They're certainly not dosing in their study in the United States, and I don't think they're dosing outside of the United States right now. And whatever -- I think we'd have to look to them, the time lines about whether they'll be able to dose again and what their goal and plans are for that. But I don't believe unless someone has information that's contrary to this. I don't believe Pfizer's dosing patients right now in light of their event.

What should we be thinking about in terms of potential medical conferences for this just now 9001 update? And maybe the spectrum of time -- the functional test that we should be thinking about getting, and how should we think about that?

Yes, Louise, do we have any specific plans for a medical meeting? Are we still sort of taking a deep breath from all the hard work we did to get ready for JPMorgan?

Yes. Yes, we're still figuring that out in terms of the timing -- including the time taking for additional analysis. The team did a brilliant job getting this data, the top line data for this meeting. So we're going to make sure that we continue to do the analysis. So there's certainly meetings that we attend coming up [ NVA ] ASGCT. So we'll provide guidance once we know when we'll be presenting the data in more detail.

Doug, you gave guidance of over $800 million for the commercial products, EXONDYS, VYONDYS, AMONDYS, which is essentially in line with what the street consensus had been modeling. Are there dynamics within the 3 products that we should be considering as part of that $800 million that you think are important because I believe VYONDYS and AMONDYS consensus is roughly equal this year?

Yes, I think that -- and I think there's maybe more opportunity in AMONDYS than we all understood at the beginning of epidemiologically, sorry. But I'm going to turn that to Dallan. Dallan can answer that question for us.

Yes. Thank you, Anupam. As Doug said, the literature has suggested that both the exon 53 amenable population and the exon 45 amenable population are equal size, both being about 8% of the total Duchenne population. But what has become clear to us both in our clinical study execution and now in the commercial setting is that the exon 45 amenable population looks to be a larger population, clearly, a larger population, the 53 population. So we're looking at that very, very closely. And the initial [ epi ] that we based out on, we're just taking a look across. But we are seeing growth in robust growth, still kind of in a launch mode for VYONDYS 53. AMONDYS as Doug said, is a bigger opportunity. And we're looking hard to continue to find opportunities for growth with EXONDYS 51.

We've got a question in the portal here, which is I think a clarification question, Doug. But did the 6- and 7-year-old patients at 2 years show statistically significant benefit versus the natural history cohort?

The Part 2 crossover kits?

No, the 6- and 7-year-old patients that I think originally were dosed that worked out to 2 years?

Well, all the way out, we have additional -- they -- so all of the kids from Part 1 across Part 2 remained stable across it. And then we'll show -- we'll have additional data to share about that, some interesting data in the next upcoming medical meeting.

Got it. Got it. And then when you think about EMBARK and one of the things that we noticed when -- at your mini -- micro-dystrophin R&D Day was there's a real focus on time to rise as the inclusion criteria. And what we've heard from physicians is look, that might be actually more important to control than NSAA at baseline. Like how does that measure specifically help control the heterogeneity that we've observed in trial after trial after trial in this case?

So what we found over time is that, and I'll let Louise talk more about he is probably do a much better job than me. But the bottom line is that time to rise does seem to correlate, very interesting and be very predictive of the time to loss of ambulation. So if you have a child that's over 5 seconds on time to rise, it has a strong correlate with decline in loss of ambulation. And one of the things we saw in Part 1 is having not controlled for that. We have a lot of kids that were over 5 seconds in to reduce that form of heterogeneity, we are excluding over 5 seconds in time to rise. Louise, perhaps you have more color on this, you'd like to provide?

No, I think you captured it well just for 301 in addition to the time to rise, then we also have ceiling and floor on NSAA. And as Doug mentioned, if you would apply that criteria to part 1 of the study, many of those children won't have been enrolled in the study, indicating the severity of the disease. So it is a predictor for loss of ambulation, and this will provide even more, I guess, confidence in our 301 design.

And I will say that's important to understand on Anupam, we've did -- look, we're very excited about 102. We've also learned from 102 and 101 and the like. And so if we look at EMBARK, and on EMBARK is at just a different level and on other DMD studies like this. That's exciting. But also the entrance criteria, exclusion and inclusion criteria as frustrating as it can be for our patients will reduce heterogeneity, will reduce standard deviation, and I think it will greatly enhance probability of success.

All right. Doug and team, I want to thank you guys so much for a super productive session. And I hope you guys have a great rest of the conference.

Anupam, thank you so very much for having us. Really appreciate it. Hopefully, live next year.

Yes.