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

Good afternoon, everyone. Welcome to the home stretch Day 3 of Cowen's 2022 Healthcare Conference. I'm senior analyst Ritu Baral, covering analyst on Sarepta. And thanks for joining the Sarepta fireside chat. With us today is CEO, Doug Ingram. Hi, Doug, thanks for joining us. So let's get started.

Literally, every single Sarepta question that I've had since your earnings call has been on your guidance, long-term guidance that you gave unexpectedly, unexpectedly on the call last week, where you promised potential breakeven by 2024, $4 billion in revenue guidance 2025 and potentially $10 billion by the end of the decade. You and I spoke about this briefly, but why now? Did the plan come together internally? Do you get more clarity from FDA on something? Is this the start of corporate strategy, et cetera?

Ritu, really, the reason is because of what I had seen in the external environment over the last 6 to 9 to maybe even 12 months. In this environment, I think few would disagree that folks have become very event-driven, very transactional. People are very focused on trading around milestones. At some point, we have to come back to valuing companies, not simply on the next readout or the next milestone, but on the actual potential of the company itself. And so in a very real sense, to my mind, this is the right time to begin the dialogue about potential. The market -- the biotech market has been suppressed for the last 12 months or so there, in my view, will be a flight to substance back to substance as people come back into biotech. And I think it's important that we think about our potential. And frankly, I didn't tell anybody anything they wouldn't have already known. We're in pivotal trials, registrational trials for both the lead candidates in both gene therapy and of course, our lead candidate SRP-5051 for our next-generation RNA PPMO. So we -- I really was just telling people what they should already know with -- around the edges. The 9001 is successful. If EMBARK is successful, and I have an enormous amount of conviction for that, then the opportunity is enormous. I mean that's the bottom line. Our plans would have us profitable by around the end of 2024, depending on approvals and the like. In 2025, our sales would be in the billions. It could be as high as $4 billion, depending on launch and uptake and the like. And we would certainly be at a $4 billion run rate in 2025. Our plans are successful. And again, I would say we're planning on EMBARK's as our success thesis, and we have a lot of reason to be excited about that. And then if we look to the future and we look to our pipeline, again, this is unrisk adjusted, but if our pipeline performs, we would be approaching $10 billion in yearly revenue by the end of this decade. So this is really the beginning of the conversation to sort of talk about the potential of the organization, not simply myopically what's going to happen next quarter or next month or next 2 quarters?

So these are unrisk-adjusted numbers that we're going to be talking about going forward. But as you think about that $4 billion run rate, can we talk about some of the assumptions behind it? Is this DMD alone? Is it DMD plus some of the limb girdles? And especially as you think of 9001, what do you think the label of the addressable population is going to be? This came up in our orphan neuromuscular panel. So that's going to be -- I think it's going to be a big driver of the TAM, that initial peak, et cetera.

We agree with you. So a couple of assumptions that go into our thinking. First, and it won't surprise you, our basis for approval assumption is EMBARK. It's the end of the [ bark ] will be...

EMBARK perfect.

Yes. [ EMBARK Part 1 ], which is the primary analysis for [ EMBARK ]. So the presumption is that, that's the basis for approval. We will, in the middle of this year, we done dosing and enrolling EMBARK. That means we would have a readout by the middle of next year. We will very quickly thereafter file our BLA. We assume success, and I think we have a lot of reason to believe that we'll be successful with EMBARK. I think it's very well powered and then approval shortly thereafter. The approval would then come in 2024, hopefully earlier rather than later in 2024. It assumes, obviously, a rapid uptake based on our analytics of the marketplace. If the uptake was slower, it would simply mean that those sales would come in the following year or later in that year, it assumes competition. That's an important one. We could -- I could argue about that, but it assumes that we will have significant competition. And it assumes cannibalization, some cannibalization of our RNA therapy sales, although I do believe that there will be a place for the PMO and if it's successful, the PPMO thereafter.

As did our KOLs from the -- as did our KOLs on the orphan neuromuscular panel, yes. So...

Go ahead. Excellent.

But [indiscernible] if this is -- these numbers are driven exclusively by 9001.

9001 and RNA franchise, including some 5051 as well assumes the success of 5051, but no limb-girdle. The label assumption, to answer your question about label and population, the presumption is that we will have a broad label that covers all ages and weights, and I think that should be a very fair assumption given the data that we'll have by the time that EMBARK reads out as well as the way the regulatory structure works in the way 21st-century cures work. So those are...

So you're not assuming exon exclusions for safety?

Well, I'm -- [ there'll be some ]. So you will remember that there were -- we have exclusions right now.

For [indiscernible] creations, yes.

Yes, for 1 through 17. That's from our perspective, overly conservative, but rightly conservative right now. We will do some additional work to put ourselves in a position where we can limit those exclusion to the areas that we think would be a risk of an innate immune response to the construct, and they should be much smaller than simply all the 1 through 17.

Is that at the end of the day, do you think that comes down to like less than 10%?

Oh goodness, yes. Yes, just remember, the -- it will be low teens if all of 1 through 17 was excluded or maybe mid-teens of all of 1 through 17 was excluded. But we've dosed about 10 kids in that range. 9 of 10 -- there were no issues. The 10th kid has a very specific kind of mutation. It is not merely being in the 1 through 17 range, but it's also followed by an enormous deletion. It was about 40 exons or so. And as a result of that, this kid would have no possibility of a history of any tolerizing level of dystrophin, and that's what causes the potential for immune response. In the other kids, they were much smaller deletions or point mutations and there were no issues. And so we just need to be thoughtful and careful and cautious about this, but start bringing back into frame those mutations that don't actually associate themselves with a potential issue. So [indiscernible] less than 10%.

And what are your assumptions for [ serotype capacity ]? That was another thing brought up by our KOLs. But if you put the exon exclusions together with the serotype positivity, you may eliminate 50% even around 50% of patients. It was the majority at that point that they were talking about that wouldn't be eligible.

One of the dangers is taking the experience that folks may have had with other constructs and then extrapolating to our construct because they will get these numbers very wrong. So I can speak to our construct and you can speak to others about what they're seeing. But we've done -- first, we've done a lot of work historically on seroprevalence for rh74. Remember, we were screening and even historically, not merely for children with Duchenne muscular dystrophy, but also for adults with various limb girdles. And that had us in sort of the mid- to slightly above mid-teens, but then we did a seroprevalence study, and it's actually below 15%. I think it's in the 14% or so range is the seroprevalence that we're seeing. So that -- so I would assume right now sort of 14% higher, maybe 15% screen up for rh74 positive kids, and that's even using our assay, which is an assay not merely for neutralizing antibodies, but for all binding antibodies, and that's what we see. And then it will probably be another percentage or 2 that would relate to the 1 through 17 once we've actually reduced it to fill a large mutation. So we love to get to a place where we don't have any of those...

Somewhere between 15% and 20%, putting those 2 factors together would be excluded.

Yes, it will be less than 20%.

Yes. Got it. And then pricing, what are some of the pricing assumptions or at least some of the pricing brackets that people should be thinking of as they -- as they model into your guidance.

I'm not prepared yet to discuss pricing. That probably doesn't come as an enormous surprise to you. The fact is that the cost-effectiveness analysis that we would do for this therapy will drive a price higher than we would be willing to charge for it. This -- one of the mistakes that is often made is this belief that gene therapies are very expensive. But when you consider it's a onetime therapy that should benefit child over the course of their life that who's actually extremely cost-effective. I think if you look at Zolgensma, that would be a bit of a tether for us, but considering our cost of goods and the like, I think we could imagine a premium to that. But we're not going to get into a lot of detail on that other than I think it will be a very cost-effective price given the value that will be derived from it in the length of time that it will benefit children.

So as we think about bracket, we should be thinking about Zolgensma as the lower bracket.

[indiscernible]

Okay. Payer coverage needs to be ready pretty much out of the gate. If you're going to hit cash flow, if you're going to hit breakeven by the end of that first year, you should have that lined up. How are those conversations -- I would assume they're starting because you can't really have them until you have the Phase III data in hand, but how are you setting up payer access and then we'll get to logistical access after this.

So we started the process of reaching out to payers and having a dialogue. I mean it's so funny. The pandemic distorts our world view, Ritu, but I mean it has to have been 3.5 years ago. I have personally gone on a number of essentially tours around the United States, starting the process of talking to payers about the value of gene therapy, getting payers onside folks like Steve Miller, who's an enormous representative of the payer community and I have spoken together on stage about the value of gene therapies. We're in constant discussions right now with them to kind of get them prepared for gene therapy to get them to understand the value and the long-term value of it to work out some of the issues that payers worry about, things like portability and the like. So we're kind of working on all of those issues right now.

But you do anticipate having them pretty much buttoned down upon launch.

Yes. If we're good at -- I mean, we'll see and with -- gene therapy is new, but I think [ if SRP is ] good at anything, it's good at R&D and it's good at serving the community and working with payers. I think we've seen that over the last 5 years. So we will be ready to launch this therapy as soon as we get an approval, patients are waiting for it.

So what about logistics? Are there enough centers qualified, I guess, now or a couple of years from now to administer the -- administer the therapy and to monitor the patients. This was -- I mean, this is something I've seen you guys actually working on for a couple of years at World Muscle. This has been the lunchtime presentation. And I think that was literally a recruiting effort for some of the centers. But what is the capacity to actually deliver if price wasn't even an issue?

I think we -- there are a number of sites now. We have benefited from the launch of Zolgensma in that regard. Certainly, a lot of centers have worked through the process dealing with a therapy that at least a very costly infusion. So how do you deal with that issue? How do you handle it? How do you get it through the pharmacy? How do you get it into the infusion center. There are more -- we need more sites up between now and full launch with all of the -- with the full label, but we're working on that.

You know how many you lead?

Okay. I mean I know we're looking to have at least, I think, something like 50 sites by the time we launch that are ready to go.

And then just going back to price do you anticipate that the range that you're looking at will impact the rapidity of uptake? Or do you think that the pharmacoeconomic arguments are going to be so beyond even the range that you're talking about, that there's some sensitivity around that?

Well, there's always a sensitivity between price and discussions and uptake. If we're wrong on any of those, it will simply -- it will be a bad answer for patients, of course, it would just attenuate the launch curve itself as we work through the prevalent population. And that's why we have to do a lot of work now. If we just sat sort of subterranean and didn't talk to payers now and get the dialogue going with payers now and then launch the therapy, then I think you could end up having to have a lot of those conversations post-approval that you could have had in advance of approval. So there is definitely discussions when you're dealing with things like a significant onetime therapy and the newness of a significant onetime therapy. But I am convinced of a couple of things. One, the cost effectiveness of SRP-9001 will be compelling, certainly for payers when we consider the value of this therapy. And second of all, we're not dealing with [ regular the Alzheimer's disease ]. We're dealing with a really compelling therapy for an underserved degenerative disease that ends in death 100% of the time, and that is very rare. And so I think payers will be will listen loudly when we talk about getting these kids access as soon as possible.

Is that $4 billion in sales, is that sort of peak annual treatment rate of the prevalent population. We talked about how the sales curve is going to look because if you are addressing the prevalent population, you're drawing down that pool. So ostensibly after a certain point, your revenues should decline to the incident population. Is that the peak? Or will the peak come a couple of years after that.

It comes later.

It comes later. So it's not $4 billion is not peak, $4 billion is a couple of years after that, but you do model a decline.

Yes. We'll work through the prevalent population. And then the -- and when that -- when we work through the prevalent population will relate to the speed with which we can get kids on therapy and get payers to reimburse that length of time will relate to that. So it's an interesting issue, which is in aggregate, it will be about the same. So from an investor perspective, it isn't that significant. The aggregate value will be the same. The value in getting kids on therapy as fast as possible as for the families who are waiting and losing muscle while they wait. But to your question, we don't assume peak year sales to occur in 2025, nor do we assume the peak year sales are $4 billion, they're higher than that.

And the year of peak sales, however they're modeled internally, sort of what percent of the prevalent population do you think that you're treating? Like do you think there's a year where you could be treating 10% of the prevalent population? Or will it always be sort of in the single digits?

It will be greater than the single digits. Our assumption is a pretty lofty and how fast we can get this therapeutic kids because we're very committed to it. But it will be a few years to get to peak year sales.

But that would be 15%, 20%? Do you think you could pick off 20% of the...

I don't have the numbers in front of me, but I think it will be -- we're assuming pretty significant uptick.

Okay. Got it. Great. And how much cannibalization are you assuming, say, in the 2024 to end of decade -- I'm sorry, 2024 to 2027 time frame, how much of the PPMO is it going to [ weigh at ]?

Well, so the working assumption inside the model, I think, is more aggressive than what we'll bear out in real life. And without giving you the exact numbers, we are assuming a pretty aggressive amount of cannibalization of RNA franchise with the gene therapy. I think it may vary -- and I think that's a smart conservative approach to take in building a strategic plan. I think it would just assume that the RNA franchise can coexist with the gene therapy at sort of essentially the same rate, we might find ourselves in trouble in our modeling. I like to believe that we will only know this as we develop additional data, and we launched this therapy because a lot of what we're doing is new. No one's ever launched a gene therapy of this size before. This is multiple larger than, for instance, Zolgensma and SMA would be, nobody has ever launched the therapy and had the ability to serve the community both with a really compelling RNA therapy as well as a onetime therapy. So a lot of what we're doing is new and first. But I think our assumption -- all of which is to say our assumptions are significant cannibalizations, whether that actually occurs or whether there is a real value to having both the RNA franchise and the gene therapy franchise for these families together is something that...

You mean adjunct treatment, combination treatment?

Yes. There's definitely going to be the case. There are going to bex when kids just simply don't have access to gene therapy from an access to reimbursement perspective, but we'll get access to an RNA therapy and vice versa. There will be places regionally around the world where that will be the case as well. But I think in addition to that, the potential for adjunct therapy is something that we're looking at and working on right now. But that's going to require more data. Go ahead.

What would the driver of adjunct therapy be yesterday during our KOL panel roll-off durability of treatment was debated. And I think consensus between the 2 doctors was this is going to last definitely longer than hemophilia treatment, but nobody really knows is it 10 years, is it 15, is it 20? And at some point, you're going to need you might need adjunct. Is there the potential that you might need adjunct for other tissues or other manifestations that gene therapy just can't seem to get to or transduce tissues that you can't transduce? How in your model are you assuming that adjunct?

Yes. So a couple of thoughts on it. One, from a sort of the durability perspective, our working assumption is that actually we will -- by the time we have to think about durability really significantly, we'll have solved the issue of redose. That is one of our assumptions from a doing in proposition. We believe...

We do see 9001.

Yes. We believe that that will come. Like it's an engineering problem. It's not a basic innovation problem. Just how do you clear out neutralizing antibodies long enough to be able to safely redose and get expression again. We can't do it today, but we have a number of mechanisms we're working on. So the real issue for adjunctive therapy is just the confidence at value of having an ongoing chronic therapy and a microdystrophin. And there's a number of potential thesis. I mean, one just basic thesis is that having an additive, early full length additional dystrophin in the -- if all goes well, 10% range, could just add value to these kids in addition be an additional way to create a shock absorber for their muscles. But also beyond that, know that these -- what we do with respect to SRP-9001 is it's brilliant it goes just about everywhere, skeletal muscles, diaphram, cardiac muscles, all those places that it's extraordinarily well needed. But remember, there's dystrophin also in smooth muscle. And the SRP-9001 doesn't code for protein and smooth muscle. Now historically, you don't hear a ton about the problems associated with the lack of dystrophin in smooth muscle and Duchenne muscular dystrophy children. But that's may very well be because they don't live into significant adult. But you could envision a world where you could use an RNA therapy that does benefit smooth muscle to be additive to SRP-9001, so that if we are [ target product ] profile bears out, and we are able to do what our aspiration is, which is to give these kids a very long life and stop talking about Duchenne boys and young man and talk about Duchenne adults. I think there would be a really compelling potential need and opportunity for a chronic therapy that can benefit them broadly as well as in smooth muscle.

What's the dose -- the redosing interval that your model assumes?

It doesn't assume. Right now, it doesn't assume redosing. So I'm assuming redosing, but our numbers do not.

Your numbers don't. Okay, got it.

There's nothing -- let me say, there's no -- that's one thing that we should know, I mean, with respect to our strategic plan. There's no magical thinking in our strategic plan. And I've seen this before, and I've been around a long time, and you'll often look at some company, and you'll see the strategic plan. And they'll just be like a bar for stuff that we're going to either get. We don't do that at Sarepta. We try to be very fact-based. Now it is success driven. So it's not risk adjusting. With respect to the near-term opportunity, I don't think that's a significant issue because, of course, we have an enormous amount of conviction around EMBARK as well as momentum. But for instance, I can tell you that I think we're going to solve the redosing paradigm. But we haven't solved it yet. We haven't dosed children read those children. So our strategic plan wouldn't presume that. That's an additional opportunity that's not found in our -- even our long-term strategic plan right now.

Got it. How much would these numbers change if you did get Super Duper accelerated approval before EMBARK Part 1. And do you think that the supportive data behind that ask is growing rapidly? Are there things that haven't been disclosed that make a much better pace than some of us skeptics think that the data currently does, the data set currently does?

Well, I not being a sceptic and obviously being biased. I think the data that you've all seen is compelling. The 101 data, the 102 Part 1 data, the 102 Part 1, 6 to 7 against natural listric cohort though 102 Part 2 data, the early read on the 103 data, but there is more data than that available. We have not disclosed it publicly because we want to share it first with the FDA, which has been a strong recommendation from our regulatory colleagues to let's share this with the FDA and have those discussions first. There's a number of things that we haven't disclosed. There's an integrated analysis. There's 103 data. There's more data out of 102, and then we'll share it with the world they're after. I would say 2 things on accelerated approval. The first is that I think the data is very compelling from an accelerated approval perspective. But I would also immediately thereafter say that I don't think people should presume, accelerated approval is the pathway for the approval of this therapy. It hasn't to the best of my knowledge, been used by OTAT in connection with maybe any therapy certainly not in selling gene therapy to the best of my knowledge, other than perhaps in oncology, but that's an oncology issue where accelerated approval is quite common. And so there's far too much uncertainty. I think one of the ironies is that if you were going to worry about getting accelerated approval, to my mind, it's not the data. It may just be that EMBARK is so close to being ready to read out. So I just want to be very clear. I don't want to sell accelerated approval. We would be irresponsible not to have the conversation with the FDA. And I certainly feel strongly about the data, but I think people should assume EMBARK as the path. If we got accelerated approval, it would certainly impact the uptake, it would make up for a faster uptake, it might even pull forward our profitability a little bit. In the long run, the aggregate sales would be about the same likely, although we would probably benefit significantly from having more time to spend with payers and families getting families on therapy even before EMBARK reads out. So there would be -- there would definitely be a benefit to it for sure.

Okay. So as you talked to FDA this year, you're going to put forward the 102 Part B natural history comparison. Can you talk about -- talk a little bit about why you chose that particular stats analysis, can you talk to how the covariants were balanced as you did that?

Yes. The beauty of Part 2, I mean that was the primary analysis. What is it -- what are the kids, all of which were dosed at the target dose. You will recall in Part 1, unfortunately, as a result of an assay that was used by our manufacturer before, not today. We had an issue in the 60% or so of the kids had less than a target dose. At crossover, we had 2 things that we were able to do that could address to drawbacks in Part 1. One was everyone could be on target dose as they were. And second of all, we could match them against the natural history cohort that acted like a synthetic [ placebo ], and that is this propensity-matched score that we use that balance very well these kids against a number of different data sets, including a placebo data set across the long coverage, NSAA, age, I think 100-meter walk and then time to rise. So these kids were very well matched. And of course, the beauty of it had an extremely impressive p-value and show that it was disease-modifying. And that's the most important thing to understand. This is one of the -- I believe one of the errors that people get when they look at the therapy. They think that we're dealing with some palliative therapy or symptomatic help. And then they say, how many points did you get here? That's not the way to look at it. The way to look at it is simple question. Does SRP-9001 act like a shock absorber and therefore, is it disease-modifying? Does it change the trajectory of this disease? The answer across all the studies is yes, so far. And the second question is, how confident are you that the result that you're seeing is actual, is real? And the answer to that is in the p-value for those who understand statistics, look to the p-value and [indiscernible].

Rather than the delta. And that was something that was brought up at the panel yesterday. One of our SMA KOL didn't believe that the 2-point change for the age looked at in Part B was outside the variability of the measure. He thinks that -- he thinks it should have been more in order to be a conclusive evidence of benefit. Let's put it that way. How do you see the variability of the measure?

I think there's a lot of variability in Duchenne muscular dystrophy. And that's why when you look at the data, you look to the p-value. So the answer is in the p-value, we've done the math. It's not a -- this is not a subjective issue. This is not an opinion issue. This is the p-value tells you whether the therapy's disease-modifying and it's 0.0009, I believe. I mean the chance that this was -- the chance that this wasn't a disease-modifying is exceptionally low, far lower than the standard for statistical significance, as we all know. This therapy is disease modifying and it's very consistent. We're seeing the same consistent results in 101 and then they grow over time. You saw these kids at 5 years or about 8.7 points better than natural history. You saw that in 102, you saw it in 102 Part 1 in the 6- to 7-year-olds when you did an actual matched set of kids. You see it in the 102 Part 2 kids, very well matched. This propensity matching is probably the most sophisticated approach that anyone's ever taking the natural history in Duchenne, and it's been the basis for approval of other therapies. And then you see the 103 kids, that's just 6 months, they had a 3-point benefit on NSAA. So this is -- I am quite confident that SRP-9001 is bringing not just the benefits of these kids, but a change in the course of this disease.

So -- you mentioned other products have been approved on propensity-matched natural history. Do you remember which ones they are?

I'll follow up. As soon as I said...

I'll follow up. No problem. And...

We have a couple of recent approvals on that basis.

Okay. So FDA knows propensity matching. And did you talk to them in advance before unblinding?

No, we did not. We have not. We have not had these discussions with them. But what we did do is to ensure that there was no debate or a question about the fact that all of the analysis we did in Part 2 of 102 would be prespecified, not post hoc. We provided to the FDA in advance of unblinding the statistical analysis plan that we're going to use for not only Part 2 102, but also for our integrated analysis 101, 102 and 103, so it's all prespecified. Now that doesn't mean the FDA has come back and said, "This is great. This will be the basis for...

Did they provide any feedback on it, whatsoever?

No.

They don't have to say they like it, but usually, when they hate it, they tell you that.

Yes. They haven't commented it on.

Got it. So just as we think about the 2 data sets, the 4- to 5-year-olds move 6- to 7-year-olds, and you think about how you're going to price this drug versus the clinical benefit confer, right? It's going to be an important -- it's going to be an important driver where you set the price. If we think about like the 5-point gain in the 4- to 5-year-olds versus like stability in the 6- to 7-year olds, [ is that ] worth something different? Do you know what I mean? Which benefit are you going to price it towards the best benefit or the okay benefit?

The interesting thing is they're all great benefits, and they're very similar, great benefits. And the reason that one might see them differently is because we don't consider the trajectory of the disease. So it is easier to get a pump and a benefit in a really young kid because they have -- they still in the growth phase. When you arrest the decline in a child that would otherwise be greatly declining the actual delta versus the natural history cohort is -- it can be the same or bigger and you may not notice it because you didn't consider it. So just think about the data. Study 101, we saw a great benefit initially, but then you look out 3 years, and these kids are 8.6 points improved. Why? Because the natural history cohort is going to start going down and eventually more aggressively going down. If you look at 102 Part 1 in the 4- to 5-year-olds against placebo, we saw a 2.5-point benefit in the Part 1 6- to 7-year-olds, we saw just about a 3-point benefit actually, actually better in the 6- to 7-year-olds when you considered a properly matched NSAA matched natural history cohort. If you look at Part 2 of 102, you see a 2-point improvement against a propensity match natural history. And all of these are -- P-values are off the charts in every one of these I just mentioned. And then, of course, you have 103, you see a 3-point benefit in just 6 months when they would have actually been modestly declining. So the fact is it's [ somewhat of a loser ] to imagine that in this group, 4 to 5 is working well, this 6 to 7 is working less well. It's working well in all of them. And like, let's go out, if you go out to a 10-, 11-, 12-year-old, they are in an aggressive, if they're not already in [ wheels ], they get an aggressive decline mode. If you could arrest that decline. I mean it...

It should be worth, okay. Well, we are giving our operator a complete heart attack because we're 6 minutes over, which I did not realize, I'm so sorry. I was -- [ sorry, K ], I was having such a good time growing you, Doug. Thank you for all the time. Thanks for your patience. Thanks for letting me do this to you. And thanks for all you. I really appreciate it. I'll follow up with you on those propensity examples. And for our audience, anybody's got outstanding questions, derivative questions, shoot them to me. I'll make sure it gets answered. Thanks so much.

Thank you so much.

Thanks, Doug. Bye.