Rocket Pharmaceuticals, Inc. (RCKT) Earnings Call Transcript & Summary

Well, good morning, everyone, and welcome to day 2 of the UBS Global Healthcare Conference. It is my pleasure to host Rocket Pharmaceuticals here today. From the company, we have Gaurav Shah, the CEO. If anyone has a question, there's a QR code, you can scan it. And all being well, the question should pop up on the iPad here, and I can field it for you. I think -- Gaurav, I'm sure you have a few sort of opening remarks, especially with the positive data recently. So I'll turn it over to you, and then we can dig into some questions.

Thanks, Colin, for having us here, at the UBS. Good to see everybody. Not very often we come back to live conferences, so this feels really good. So Rocket Pharma, we're a gene therapy company. We're a multi-platform or platform agnostic, depending on how you think about it. And we have 2 platforms. One is an in vivo AAV platform. Right now, we apply to a cardiology disease called Danon disease. And we have 3 ex vivo lenti programs with an ex vivo lenti platform that we apply to 3 bone marrow-derived diseases, notably Fanconi anemia, leukocyte adhesion deficiency-I and pyruvate kinase deficiency. All 4 of these programs are in the clinic, 2 of them, notably FA and LAD, are ending or nearing the end of their pivotal Phase II trials that we plan to use for submissions to both FDA and EMA. And Danon disease, AAV program and PKD are both in Phase I, and we're hoping to enter Phase II as we end this year and go into next year. Last week was a big week, I think, for Rocket and also for gene therapy, in general. Both platforms had some further validation, and we found some momentum forward. We read out top line data in LAD-I, which I'm happy to get into a little bit later, which was a big leap for these patients and community because these LAD patients are otherwise children who pass away in early single-digit years, and we think that with restored CD18 function that they may be able to live normal, happy lives and live into -- have a normal lifespan. It's really transformative. This is the power of gene therapy. When it works, it just really works. Fanconi anemia. We also hit the primary end point ahead of planned schedule for a variety of reasons. And both LAD-I and Fanconi anemia, we anticipate filing in 2023. Danon disease is an AAV9 program, and the big jump last week in Danon disease was that we demonstrated acceptable safety on the first 2 pediatric patients. And I feel that was always something that was unclear as to how the safety is going to pan out for Danon patients using AAV9, especially given some of the toxicities that we've seen in the e14 range. We've seen one toxicity of thrombotic microangiopathy in the e14 range, and others have as well. So I think there was some concern about being able to translate safety forward in the mid-e13 range in pediatrics, which will ultimately be our target population. And both of these patients did very well with minimal complement activations, no AEs in the labs or clinical AEs. So that was a great outcome for Danon, Fanconi and LAD-I. And it sets us up to really be a late-stage commercial-focused company that I think we're growing into now.

Great. So maybe let's start with 201. So congrats on the data. You anticipate filing first half of '23. Can you just walk us through the next steps? What has to occur there behind the scenes from your point of view? What do you need to do in terms of the process with the regulators? Flesh that out for us.

Yes. So we have RMAT designation. So because of that, we've been having frequent ongoing dialogues with FDA. So we're pretty confident that we will have a package that supports a robust BLA filing and also an MAA filing. This trial was harmonized across both the U.S. FDA as well as the EMA. So which one goes first? we'll see, but probably a BLA first followed by MAA in Europe. What is the next step? The next step is to formally engage the agency in a pre-BLA meeting. And in preparation for that meeting, we want to make sure that our databases are clean, fully locked, fully validated. We want to make sure that our CMC package is ready to go and robust. And we've learned from our own experiences, there's a lot of late-stage development experts inside the company, but we've also learned from the challenges that other gene therapy companies had faced at this late stage in the game, and we want to avoid those. So we're tightening up the clinical CMC and there's also some preclinical aspects of the package 100% before we even begin that BLA package. So we've guided to one half, first half '23, but we're going to try to do it as soon as possible.

I mean the data themselves are very clean. I think the only question I had was you had one case of grade 4 PAH. Any comments there?

Yes. Some of these patients, these are very, very ill patients without corrected neutrophils. And it's not uncommon to have severe AEs around the time of autologous transplant. You certainly see it in allogeneic transplant cases of PAH and other lung-related toxicities. But you don't see it as common once these patients are starting to get better. You rarely see it in moderate LAD patients as well. So we think that it was related to the transplant itself, and it was clearly marked that's unrelated to the gene therapy.

And can you remind us of the market opportunity for severe LAD? And how well identified are these patients? And you must really be thinking about sort of the commercial infrastructure now and the strategy there. So can you walk us through that?

Yes. So there's 2 segments of LAD patients. They're severe, and there's moderate and there's mild, and how do you break those apart? The real patients who need most acute help are the severe patients. They're patients with less than 2% CD18 expression versus normal. And we think that at peak, that population is 25 to 50. And that's sort of our initial target population for the label. However, if you include moderate patients, who are those patients who have between 2% and up to 30% CD18 expression, these patients, they don't have the shortened lifespan in the early single-digit years, like the severe patients do, but they do have frequent recurrent hospitalizations. And they live longer but not normal life. So that's definitely an addressable population. We think that the market there is up to 100 patients per year. And in terms of how we're going to find these patients, the thing with LAD-I is that there's a very tight community -- immunodeficiency community. There's a consortium. There are many of them immunodeficiency consortiums, but they come together because these diseases are rare and really know most of these families and patients by name. Obviously, we don't, but the consortia do. So we rely on those relationships. We know where a lot of LAD patients are already in the U.S. and Europe. So when we first launch, we'll be able to target those particular families right up front in the first year. Beyond that, the centers of excellence that see these patients, which is probably 5 to 8 per continent, 5 to 8 in the U.S., 5 to 8 in Europe, also have a big catchment area for LAD-I patients. We rely on them. We don't think we need a big commercial endeavor to get to these patients, right? It's relatively modest. Once we get to a much larger disease, we'll have a larger commercial organization, but the first launch is sort of almost self-populating.

Okay. And then from a manufacturing point of view, where will this be manufactured in your Cranbury, New Jersey facility? And I guess just as a broader question as you're moving towards being a more commercial company, can you just talk about your broader manufacturing capabilities?

So we've separated out how we manufacture the ex vivo lenti versus AAV. Right now, for the trials that have read out, everything in both lenti and AAV has been manufactured through a CDMO, different CDMOs obviously. In lenti, you need both the vector supplier and the cell processing site. And with regard to cell processing site, you need one in Europe and one in the U.S., 2 separate ones, right? So you can't really shift these products overseas so easily. You also need another CDMO for AAV. So there's really 4 moving parts here. All the ex vivo lenti will continue to be outsourced to CDMOs in both the vector and cell processing side. That's our long-term plan. We have a way to do that certainly into the early years of commercialization. AAV will now move in-house. We will have Cranbury readiness for clinical AAV manufacturing shortly. We will be tech transferring in from a CDMO to our Cranbury facility, the AAV process, and it's actually a little bit improved. And that will serve as the source for our Phase II clinical trial material as well as our commercial material long term, not just for Danon but other AAV programs that come into the pipeline. What we do with lenti long term remains to be seen. Right now, our goal is -- our method is to continue to outsource the CDMOs, but that may change as we have learned, controlling the product is controlling everything. It control timing, release, quality, and we want to increasingly control that over time. But right now, we're going step by step starting with AAV.

And again, just given your -- the proximity to your interactions or sort of more formal interactions towards approval with the regulators, I guess what have you observed over the last 12 to 24 months? It's been an interesting time in sort of cell and gene therapy. And have you -- does it feel like there's heightened scrutiny or trepidation on the regulator side? What can you say there?

Well, I think gene therapy definitely had an early period of early adoption and excitement. And the field in both lenti and AAV ran into some speed bumps. I wouldn't call them hurdles but some speed bumps that rightfully led health authorities to just take a pause and learn and educate themselves and help us all educate ourselves and one another. And our philosophy has always been that the best consultant in the world is the FDA. So if you're not sure of something, you want to have strong relationships with the FDA and you just call them before you call any consultant, right? I just pick up the phone and call the FDA. And having an interactive, frequent, open dialogue with the FDA is, I think, the path forward because there's clear signals that the FDA wants each of these programs to move forward. They want ex vivo lenti to move forward. They want AAV to move forward. The signals from FDA are questioning but not stopping, right? So educating but not doubting so much, right? So I think engaging the FDA in a disease-by-disease dialogue in a platform-by-platform dialogue is key to each company moving their program forward. And as a result, the whole field forward. So I think we're more at a place where we can turn the tide favorably back toward gene therapy, especially with data that came out, like that came out last week for us and hopefully with other gene therapy companies in the near future. We're in a position to turn the sentiment and sort of move it to a position of inviting more and more innovation and technology and unmet diseases rather than questioning them, and I think we're almost there. I think a couple of the overhangs that were -- that hit the industry last year had to do with AAV toxicities. I think we've put that behind in the sense that it's not so scary. People know how to approach these toxicities. We can talk about our approach for Danon. For the lenti program, the oncogenesis was an issue. And I think we put that behind because it was related to the viral promoter. No one is using that viral promoter and other programs. So I think that we're right at the cusp of coming out of that phase of education and scrutiny and into this phase of more and more therapies coming out there. You heard those remarks from Peter Marks and Dr. Collins last week as well at ASGCT.

That's great. So maybe we should switch gears and talk about 501 and Danon. So what are your expectations here with earlier intervention in the pediatric patients contrasting to what we've seen with adults?

Yes. So our selection criteria for Phase I, and I -- it should be similar for Phase II is that these patients have to have some symptom or sign of cardiomyopathy, right? So it just can't be a genetic diagnosis of data. They have to have some sort of heart disease. So age doesn't really matter, right? The criteria are similar. In fact, if you look at our recent presentation, the baseline BNP for one of the pediatric patients was higher than most of the adult patients. So it's not the age that matters. It's really state of disease. So we think that there should be no difference in how pediatric patients respond versus the adult patients. And if anything, gene therapy has proven itself to be potentially more effective in pediatric patients versus adults, for whatever reasons, a better ability to tolerate, less AAV preexisting immunity, better organ size to BSA ratio. Whatever those factors are, we think that we should see read-through into pediatrics. And we certainly see them in the safety side already as we presented last week. As I alluded to earlier, the first 2 patients with the [ Danon 13 ] therapy did not have really any evidence of lab changes and very minimal, basically negligible evidence of complement activations versus the early patients who had some of those factors.

So it sounds like you are truly age agnostic. Is there -- how early in the disease course would you go? Would you treat a genetic diagnosis at some point? Or...

Yes. So there are something like 250 mutations in Danon disease. We know that 85 to 90 of them are pathogenic. And boys with pathogenic disease almost always, if not always, develop cardiomyopathy. And with the median age of survival of 19, including a heart transplant, and it's probably less than 19 if you -- for patients who don't get a heart transplant. So there's some heterogeneity as to when the severe cardiomyopathy starts in boys, but it always starts, right? The oldest males on record are single cases of a man in his 50s and another man in his 40s. So these patients don't live really past their 30s. And therefore, there's really little downside for boys to treat as soon as one knows that this patient has a pathogenic Danon mutation. Our cutoff right now is age 8, and that will probably be the first label as well because that's what the Phase II will be designed around, but it could go earlier. At some point, if you have a working therapy in a very difficult to treat and fail disease, we could have neonatal screening and sort of a vaccine-like gene therapy early in life, right, just like we have for Fanconi. So I don't think that's impossible. But right now, the age cutoff is 8.

Okay. And then, I guess, one consideration around that is the sort of durability of benefit. And so is this a one and truly done therapy? Or do you think the benefit will weigh in over time?

So -- we think it's a one-and-done therapy, and we've certainly seen ongoing evidence of clinical benefit now out more than 2 years for the first patients who were treated. Obviously, we want to see this for many, many more years to come, and we will follow these patients in a long-term follow-up trial for 10 years, just to make that point. So we'll learn as we go. Cardiomyocytes don't turn over. They don't turn over like liver cells do. We all basically have the same cardiomyocytes that we were born with. There's -- the stem cell thesis in the heart was debunked, right? So -- we think that once you get episomal expression, and it's robust, that expression will continue for a long time, if not for life. Obviously, we don't know if immunogenicity plays in here or weighs in here. We'll only learn that over time. So far, we haven't seen any evidence of transgene destruction beyond the first 2 to 4, we are, say, 3 to 6 weeks after therapy. But between 3 to 6 weeks after therapy, we're treating these patients with both B-cell and T-cell suppression just like you do -- would do with the kidney or heart transplant. And we basically minimized any destruction then. We don't think there's destruction beyond, but time will tell.

A question here. So in the literature, there are studies that show steroids can increase autophagy, you see any effects from immunosuppressants on patients in the ongoing trial?

Yes, it's a great question. It's something that we've studied. And we've always known that these patients don't tolerate steroids. These are not like the Duchenne patients in which -- in whom steroids are part of their natural treatment course, and those patients are used to being on steroids. Danon patients are usually steroid-naive. There is a chance that steroids exacerbate autophagy. We've tried to minimize steroid exposure. We learned in the first few patients that were treated, where we had a lot of steroids that they do develop myopathies. And since then, we've learned to reduce the dose. The pediatric patients are getting about half the dose of steroids on a daily basis versus our adult patients. And we're also starting to taper them by day 10 as soon as possible. So the more recent patients in addition to not getting complement activation, we're also not seeing myopathies anymore. So with this new revised regimen, we think that we've solved for both problems pretty effectively.

Okay. You have an ongoing natural history study. I'm curious like what are the key observations that have come out of that study to date?

Yes. So the total study, which includes patients from U.S. and Europe will be over 100 patients, perhaps up to 200. Not all those patients are going to be followed longitudinally for every single time point that we're interested in for our Phase II. However, we are finding that a good number of patients are followed for lab markers, right, just like anyone would follow cardiomyopathy patient for BNP, troponin, et cetera. A lot of patients are being followed for echo. So we can see readouts such as wall thickness and EF and GLS and other echo-based parameters. And some of them are being followed for NYHA class and 6-minute walk, but not all of them. So we're putting the information together. So far, we've been able to identify a couple of markers in natural history that trend very differently from patients in our trial, notably, posterior wall thickness and BNP. Based on the differences, the delta that we see, we think that we can design a relatively modest trial that's well powered, potentially as a single-arm trial for our Phase II, and that's going to be our proposal.

Great. A few more questions. Can you tell us about the choice of reporting posterior wall thickness and septum thickness over other echocardiogram parameters?

Yes. So EF is the obvious one. And another cardiomyopathies, that may be the right end point. And in these patients, in Danon patients, because it's a hypertrophic cardiomyopathy, ejection fraction is usually preserved until very late in the disease. So really not until the last 1 or 2 years do patients have a drop in ejection fraction. So most of our patients have 50%, 60% EF. So there's not much to measure as an outcome. In fact, if you see the graphs that were just presented, the EF stayed in the normal range. They did actually improve overall, which was a surprising positive finding. One of the patients went from 47% to 61%, which is pretty remarkable, but still within normal range. Other parameters like wall thickness are grossly deranged in Danon patients and much easier to follow. And also there's a mechanistic rationale for posterior wall thinning in these patients after gene therapy. So that seemed to be something that we can see a greater magnitude of benefit and potentially design a smaller trial versus something like ejection fraction, which probably needs a lot more patients and it's not as clinically meaningful.

Another question here. Is this protein expression a potential end point? You've shared protein expression quantified by both immunohistochemistry and Western blot and there's quite a lot of variability between the 2 techniques, which do you view as more accurate and why?

Yes. It's my favorite question. I'd love thinking about protein expression, as I'm sure many folks do here. We measure protein expression in 2 ways: One is immunohistochemistry, the other is Western blot. We think that a little protein in each cell goes a long way. Going back to this overused analogy, the autophagy system is like the vacuum cleaner of a cell, and you probably just need to turn the vacuum cleaner on a little bit and give it enough time to clean up the cell. If you turn it on too much, it might damage the cell. So there's a Goldilocks zone. There's sort of a therapeutic index and a needle to thread here. I think that the right Goldilocks zone has a little protein and a lot of cells. So IHC is to better measure. You want broad expression. And over time, and it does take time, we see now that it takes something like 9 to 12 months to see the true clinical effects in these patients, and that's okay. So Western blot is more a measure of Gestalt protein expression. And you could have a little protein in a lot of cells and still have a low Western blot number. We -- so I don't know which one is better for sure, but if I had to pick, I would say IHC. However, I would caution against reading too much into the actual number. And the reason is that there's one shot on goal in these biopsy specimens. It's not like muscle where you can have multiple shots at the muscle and obviously, it's painful for the patient. But these patients are under anesthesia, they're pediatric patients. They're [ cathed ] with anesthesia. We can't keep going in and looking for more specimens from the septum, right? You get one shot on goal. Sometimes it's a 2-millimeter slice, you get what you get, you might hit an area of fibrosis in 1 month. You come back 6 months later and you might hit a great area. So you might get variability from 80 to 20 in the same patient, even though the disease is actually improving, right? So we just want to see that the -- that you are positive on IHC and/or Western. Sometimes you can't even get both. This is a different type of protein readout than what we're used to in other muscle diseases, right? So comparing IHC to Western blot and also time point to time point, I would caution against that. I would rather interpret positive protein expression with clinical outcomes. In terms of an end point, what the FDA wants to understand, and I've heard this directly is analytics that are reproducible and reliable and qualified and ultimately validated. Whether you use IHC or Western blot, the methodology has to be pristine, and that's something that we take very seriously, and we're working ahead of both our BLA -- or end to Phase I meeting, but certainly ahead of our BLA.

Great. When do you expect the female trials to begin? And could you just contrast that with the male side?

Yes, there's a lot of interest from the female Danon patients. They do get sick. We don't talk about them that much, but we just host a Danon Disease Day on Rare Disease Day in February this year. We had patients from the Danon community come and join us, both males and females. There's a lot of interest from Danon female patients. They tend to live to a longer age, but still have cardiomyopathy and unfortunately pass away in their 40s. So we want to start that trial. I anticipate it will be sometime next year, but our first goal is to get the male pivotal trial up and running, so as soon as possible.

And then just as we think about the overall opportunity here, sort of 5, 10 years down the line, what is the overall target population in Danon that you expect to be treating?

I think it's going to be all comers. And so I think it will be all comers, males and females. Right now, I would say at least 8 years old, but like I said earlier, potentially earlier than 8 males, should be just about everybody, except males who have preexisting AAV immunity, or patients who are too far gone in fibrosis as we can measure by an ejection fraction of less than 40%, where the benefit is unlikely of gene therapy. How much does that take out? I don't know. We'll find out over time, but I think we still treat most male patients. With females, I would say that Danon disease manifests a little bit differently in females. Cardiomyopathy is later in onset. So females, we might wait until there's more symptomatology from the heart before treating. But it is heterogeneous in females, but homogeneous in the sense that they all still get cardiomyopathy. So it's a pretty big segment of the prevalence that I think we can target.

Great. Maybe we'll switch to 102 now. So again, congrats on hitting the primary end point. Could you just walk us through the path forward here in terms of the regulatory discussions, et cetera? How are they going? When do you anticipate this being on the market?

Yes. First of all, in Fanconi Anemia, this was our first passion when we started at Rocket 5, 6 years ago. And I think these results have certainly helped moved our pipeline forward, help the Fanconi patient and community have an alternative transplant. But also, I think it's moved the field forward because for the first time, we've been able to potentially cure a bone marrow-derived disease without using any conditioning, right? I mean, that's unheard of in history. And I think that because of the courage that Juan Bueren and others at CIEMAT and colleagues have demonstrated, we took a risk, a lot of the community wanted us to try to -- just a ginger dose of Cytoxan to get things going or this and that, but we just stuck with the plan. And every time a patient engrafts with Fanconi, I don't know why I'm still surprised, but I'm very happy. I was surprised that all these patients engrafted, and 51% to 94% MMC resistance. It's almost like a normal person. I mean 94%, even 70%, 80%, you took a healthy person's bone marrow, you might get those same numbers. So these are no longer diagnosable Fanconi patients, right? So the phenotype has been fundamentally converted from Fanconi to normal if you just look at the bone marrow test that is diagnostic for Fanconi Anemia. So the magnitude of that benefit was reassuring, remarkable and, I think, hopefully, uplifting for the lenti field. We hit this end point early for the following reason. During COVID, our medical directors decided to introduce some more flexibility into the protocol. And instead of mandating Q6-month visits, we changed them to Q3-month visits optionally, in case a patient couldn't travel for their 6-month visit, they could come back 3 months later, that had the positive effect of a couple of patients coming in earlier than anticipated. So we had the second MMC confirmation in those couple of patients just a month ago rather than the anticipated Q3. So we were able to read it out early. However, the BLA path and MAA path were still contingent on a Q3 readout. So that's still on track. We didn't really accelerate when we filed, but it derisked whether we file.

Okay. Great. And remind us there, what's the optimum age for intervention? Is there a cutoff?

Yes. I think that the earlier the better. There's no cutoff. Patients up to -- our patients have been treated up to 6 years old and patients have responded across the spectrum. Ultimately, though, I think that patients who are treated early will have a greater CD34 bone marrow reserve, so they can -- we can create a better product to give back to them. And -- there is going to be a correlation, I think, ultimately, between the quality of the product and outcomes, and our medical directors are working on what we're calling a therapeutic index, how can you predict responsiveness. And that's something that we'll be able to share as we move toward BLA as well.

And maybe just lastly on Fanconi. Could you just again frame the size of this market for us?

So the FANCA complement -- complementation type, we think that the prevalence is 4,000 U.S. plus EU. If you include the other complement types, C and G are the next biggest -- the opportunity is about 6,000.

Okay. And then lastly, in the pipeline, 301, what's the next update there? Just -- and when should we expect it?

So we're -- the pediatric cohort is enrolling. We've so far only demonstrated results from the first 2 patients who are adult patients. They now have a sustained hemoglobin corrections out to 18 months and associated with improvements in hemolysis markers and several improvements in quality of life markers. I think these patients are much, much less sick than they were before the gene therapy. One of the 2 patients had tried the mitapivat drug but did not respond to that and moved to gene therapy, and is now feeling a lot better and has doubled their hemoglobin. I think that the next step here is very straightforward. We enroll pediatric patients. We read them out at the end of the year. We start setting up for Phase II design. The size of that trial should be relatively modest given the magnitude of benefit that I think we're seeing here, maybe something like a Fanconi trial size single arm. And we'll enroll that next year. And both PKD and Danon, I anticipate enroll rapidly as we start up activities at the end of this year and into next year, and we get those ready for filing.

And not that you don't have enough going on already, but as we think beyond your current pipeline, what's at the back of your mind, what areas of interest to you?

Yes. We want to build on the expertise we have. So you don't want to get too diluted because then you lose the power. And I think that bone marrow is something that we've developed expertise about. Cardiac, we're developing, and we'll probably add one more therapeutic area, likely more focused on AAV, but I would say it's going to be a 3x2 matrix. Lenti AAV on horizontal and then therapeutic areas would be bone marrow, cardiac and 1 more, so we'd stop there. I think beyond that, you're no longer a biotech company. So we want to preserve the mindset of biotech.

Very good. And then just can you remind us cash position, cash burn, the runway it gives you?

Yes. So we're about $350 million. And we've now guided that, that cash gets us into the first half of 2024. And I'll say also that as we start thinking about launches for LAD and for Fanconi, at some point, those may result in PRVs. So hopefully, over time, our -- we start seeing internal revenue, and we sort of have that crossing point in the near future.

And then just the IP for the portfolio for 201, 102, 501, just remind us of where that is?

For Danon?

For all of the programs.

Yes. So most of the IP around the lenti programs is expired. There may be some patents that we have to address just for a year or 2 after launch. We don't think those are burdensome at all just because we're launching pretty soon. For AAV, the -- we have a license from REGENX for the AAV9 capsid. So we'll have some obligations there. Beyond that, we own everything.

Okay. Great. And then one question I've been asking all the companies so far is just the -- this is an interesting time in biotech, just given what's happened with the market, et cetera. And there's a lot of discussions of -- around the strategics and their behavior towards the smaller cap companies. Just -- has there -- from your seat, has there been any change in the sort of tone of interactions with the large caps in terms of what they're looking for? Does it feel like they're more looking to be risk-sharing partners versus potentially just kicking the tires for a more definitive transaction?

Yes. It's hard to know for sure. But I think, in general, the bigger strategics are interested in derisked companies, right? Either there's an early platform scientific rationale or there's an asset that's about -- that looks like it can launch, right? So I think most biotech companies probably have had various conversations with strategics. And I think the tone, all I noticed is that the tone changes a little bit as you move more toward commercialization. I haven't seen a big pickup necessarily just because companies are cheaper right now. I think these strategics have enough cash that it's more about the true value add long term. But I think, yes, as companies move more towards late stage, I think the tone shifts a little bit more positive.

Fantastic. I think we're right at the end of time. Any sort of [indiscernible] in your point of view, it's -- you've got a lot going on, you've had a lot great data. So...

Yes. No, it's been a fun journey, and I think it's been important just to learn along the way. And our team is really remarkable, and I believe has the ability to not just get these drugs approved, but launched successfully. So I look forward to the next several years.

Yes, fantastic. We look forward to seeing it Blossom. Thank you.

Thank you, Colin.