Vertex Pharmaceuticals Incorporated (VRTX) Earnings Call Transcript & Summary

Great. Good morning, everyone, and once again, welcome to the 40th Annual and, unfortunately, second-time virtual JPMorgan Healthcare Conference. My name is Cory Kasimov. I'm the Senior Large-Cap Biotech Analyst. And it's my pleasure to introduce our next company, Vertex Pharmaceuticals and CEO, Reshma Kewalramani. Please note that following this presentation, we will have a Q&A session. [Operator Instructions] But with that, Reshma, thank you for being here today. Always a pleasure, and let me turn things over to you.

Thanks, Cory. It's good to see you again, and thanks also to JPMorgan for hosting this event virtually today. Good morning, all. I am pleased to be here and to share the significant progress we've made, and I'm really excited to share our vision for where Vertex is headed in 2022 and beyond. To keep us synchronized, I'll call out the slide numbers as I go. Slide 2 is our safe harbor statement. In brief, let me remind that the forward-looking statements made during this presentation are subject to the risks and uncertainties discussed in our SEC filings. Actual outcomes and events could differ materially. All right. With that, let's get started with Slide 3. 2021 was a very important year for Vertex, and one which sets us up for a very bright future. In CF, we have meaningfully increased our leadership position by treating more CF patients than ever before, advancing the next-in-class CFTR regimen into Phase III development and progressing our mRNA program for the last 10% of CF patients. Outside of CF, our pipeline is accelerating and delivering. In heme, we've completed enrollment in both the sickle cell and beta thalassemia trials. We're planning forward for regulatory filings and building commercial readiness for CTX001. And in 2021, we also achieved important risk-lowering milestones in progress in 3 other pipeline programs, VX-147 in APOL1-mediated kidney disease, VX-880 in type 1 diabetes and VX-548 in pain, that highlight our trajectory towards bringing multiple transformative medicines to market. Each of these programs is a first-in-class or best-in-class program, which holds the potential to transform the disease, and each one represents a multibillion-dollar opportunity. Our financial performance, with a 5-year revenue CAGR north of 30% and operating margins now in the 50% range, continue to put us at the very top of our peer group. And we foresee continued, significant top and bottom line growth from CF, well into the middle of the decade, with CF leadership extending into the 2030s, and therapies in the new disease areas adding to that growth, starting with beta-thalassemia and sickle cell disease. I'll review the details under these headlines over the next 20 minutes or so. Beginning with CF, on Slide 4. We've expanded our leadership position in CF in 3 important ways: First, with more than 15 new reimbursement agreements secured in 2021 as well as the launch of TRIKAFTA in patients 6 to 11 in the U.S., thousands of new patients have initiated treatment with TRIKAFTA, or KAFTRIO as it's known, outside the U.S. Second, we continue to accumulate long-term and real-world data with our medicines. We've just now received the first data from the USCF Foundation. These data are truly remarkable, and I'll provide some more detail on these data in just a moment. And third, we've made important progress, advancing new treatments. The advancement of VX-121/tezacaftor/561, with the potential to deliver improved outcomes for patients are now in Phase III. And with our partners at Moderna, we've now demonstrated that we can efficiently deliver full-length CFTR mRNA to the bronchial epithelial cells in nonhuman privates in vivo, solving a long-standing in vivo delivery challenge and in so doing, making a significant step forward in bringing a treatment for the last 10% of CF patients. Based on these data, IND-enabling studies for our CFTR mRNA therapy are now underway, and we plan to file the IND later this year, with clinical trials beginning thereafter. Moving on to Slide 5, our CF growth and market opportunity are shown here. We previously highlighted that there are an estimated 83,000 CF patients in the U.S., Europe, Australia and Canada. We've reached thousands of new patients in the past year. And as a result, our CF business has performed exceptionally well. Yet, there are still more than 25,000 patients, who could benefit from the triple combination but who are not yet on therapy. These patients fall into 3 categories: First, patients who have yet to start treatment in countries where we have recently been reimbursed and, therefore, are early in the commercial launch; second, patients in geographies where we are not yet reimbursed; and third, in younger patients who will be addressed through future label expansions. We're already in clinical trials with the triple combination in 2- to 5-year-olds, having secured approval for the 6- to 11-year-olds in the U.S. and a positive CHMP opinion for 6- to 11-year-olds in the EU. Beyond the 25,000 remaining patients who may benefit from the triple therapy, I also want to highlight another growth opportunity in CF. With our mRNA therapy currently in IND-enabling studies, we're beginning to have line of sight into an additional approximately 5,000-plus patients, represented here by the green wedge. Moving on to Slide 6. In the registrational trials of TRIKAFTA, we showed acute improvements in lung function. Since that time, we've continued to collect long-term and real-world data with the triple combination to evaluate its disease-modifying potential beyond improvements in ppFEV1. In late 2021, we shared the 96-week data from the extension trials, from the pivotals of TRIKAFTA, where we saw no decline in mean lung function, a first for any CFTR modulator. And hot off the presses, we now have the first real-world data for TRIKAFTA from the USCF registry. Across 16,000 patients with TRIKAFTA treatment and captured in the registry in 2020, relative to patients eligible for TRIKAFTA in the year prior to approval, we see an 87% reduction in the risk of lung transplant, a 77% reduction in pulmonary exacerbations and a 74% reduction in the risk of death. For a genetic disease like CF, where patients start medicines at an early age and take them chronically over a lifetime, long term and real-world data like these are incredibly important to patients and physicians. These kind of data take many years and thousands of patients to collect and set a very high bar for any future therapy to meet. Turning to Slide 7. Nevertheless, if it is possible to improve on TRIKAFTA, we're determined to be the ones who do so. The combination of VX-121, tezacaftor and 561, our next-in-class CFTR regimen, has shown superior chloride transport, preclinically, in R HBE cells versus TRIKAFTA. And in Phase II, VX-121/tezacaftor/561 has shown the potential to provide greater clinical efficacy. Skyline 102 and Skyline 103, the 2 global Phase III studies with this regimen, are underway, and we expect to complete enrollment in this pivotal program by the end of this year or early next. The size and duration of follow-up, almost 1,000 patients and 52 weeks in duration, reflect the study design, which is head-to-head against TRIKAFTA. Placebo-controlled trials are, of course, no longer possible, given TRIKAFTA has become the standard of care. We're excited to bring forward 121/tezacaftor/561, a once-daily regimen that holds the potential for greater clinical efficacy and enhanced economics with royalties decreasing from low double digits to low single digits. Moving on to Slide 8, turning to the pipeline, which is depicted on this slide. Beyond CF, we have a pipeline that is broad and deep and delivering. This pipeline is considerably more advanced compared to 12 to 18 months ago. The speed at which our clinical programs are progressing is a direct consequence of our R&D strategy, where we target the causal biology, focus on validated targets and on diseases with biomarkers that translate from bench to bedside. Based on this strategy, we're able to generate meaningful, risk-lowering and often transformational data early in development, which significantly accelerates our clinical timelines. A few additional important points as it pertains to the pipeline. First, the number of disease areas, 6 in total, including CF, in mid- and late-stage development, each of which represents a significant market opportunity. Two, the number of modalities at play across the portfolio. The clinical pipeline now spans small molecules, gene editing and cell therapies. And lastly, the balance of internal and external innovation represented in the clinical stage pipeline. On Slide 9, you'll see that the important contribution that business development has made to this picture. Our BD strategy seeks to bring in complementary assets in CF, technologies for our toolbox and programs that fit our R&D strategy. This approach is clearly working. And today, external investments are represented in approximately 40% of our clinical pipeline. Moving on to Slide 10. Highlighted on this slide, are several key pipeline programs where significant advances in 2021 have laid the groundwork for value creation and catalysts in 2022. In 2021, we completed enrollment in the pivotal studies with CTX001, our gene editing program for sickle cell disease and beta thalassemia. We generated the first clinical data for VX-880, our cell therapy program for type 1 diabetes, which, while still early, is very promising. And we established clinical proof-of-concept with unprecedented results in FSGS for VX-147, our small molecule program targeting APOL1-mediated kidney disease. And we initiated 2 Phase II proof-of-concept studies for VX-548, our small molecule NaV1.8 inhibitor in acute pain. The abdominoplasty study in this program has completed enrollment and dosing. Based on this 2021 progress, you can appreciate why we are so optimistic about 2022. We expect to share additional CTX001 clinical data in sickle cell disease and beta-thalassemia this year and to submit filings, globally, towards the tail end of 2022. We anticipate sharing both more patients data and longer follow-up from VX-880 and type 1 diabetes and filing for the IND for the cells plus device program, later this year, with clinical trial initiation thereafter. We see the VX-147 program in APOL1-mediated kidney disease advancing into pivotal development later this quarter, and we project having data from the 2 proof-of-concept studies in acute pain with VX-548, also later this quarter. In the next several slides, I'll walk you through a few of these key programs. Moving on to Slide 11 and to CTX001. This is our most advanced program outside of CF and which we expect will be our next commercial launch. CTX001 is a one-time gene editing treatment with the potential to provide a functional cure for sickle cell disease and beta thalassemia. Physician and patient interest in this program is strong. And our Phase III studies were oversubscribed. We've now completed enrollment in both studies and have dosed more than 70 patients to date across the program. We are wrapping up discussions with regulators to finalize the submission data package, including the number of patients and duration of follow-up. In terms of market opportunity, we see tremendous potential for CTX001. We estimate that there are more than 150,000 patients in the U.S. and Europe, who have beta thalassemia or sickle cell disease, approximately 32,000 of whom have severe disease. 25,000 are severe sickle cell disease patients, and the vast majority of these patients are in the U.S. Published physician surveys in the U.S. consistently indicate that they expect about 1/4 to 1/3 of their sickle cell disease patients would be good candidates for a one-time curative approach using the current busulfan-based conditioning, which is in line with our estimates of the numbers of severe patients. Our pre-commercial efforts are well underway. We have hired many of the key people, who will support the launch, are engaging with the patient and physician communities and are building out manufacturing capability so that we will be ready to bring this potential medicine to patients. Moving on to Slide 12. The data shown here were previously shared at the European Hematology Association Congress in June of 2021. To summarize, at EHA, the data was shown for 22 patients with up to 2 years of follow-up. All 7 patients with sickle cell disease treated with CTX001 were free of vaso-occlusive crises after treatment. And all 15 patients with beta thalassemia, treated with CTX001, were transfusion-free, regardless of the genotype, including the 6 patients who had the most severe genotypes. One of the key considerations for us in choosing the CRISPR-Cas9 gene editing approach over others was safety, and the safety profile of CTX001 has, to date, been very encouraging. Moving on to VX-880 and the type 1 diabetes program on Slide 13. At the turn of the 20th century, patients with type 1 diabetes had a very limited life expectancy, and most patients, unfortunately, died within 5 years of diagnosis. Insulin was discovered in 1921, and the subsequent year, Leonard Thompson became the first patient treated with insulin. For the first time, the medical community could offer a treatment to patients with type 1 diabetes that could manage their glucose levels and, in so doing, save their lives. The headline, seen to the left of this slide, highlighted insulin as a potential cure. But as Banting and Best themselves pointed out, insulin was an extraordinary advance, but it was not a cure for this disease. What does hold the promise of a cure is replacing the islet cells that produce insulin and sense glucose. In 2021, 100 years after the discovery of insulin, we dosed the first patient with a stem cell-derived islet cell therapy, VX-880. The data from the first patient are very encouraging and supportive of this potential for VX-880 to be a functional cure for type 1 diabetes. Turning to Slide 14. In October, we shared the day 90 results from the first patient treated with VX-880, after receiving half the targeted cell dose. Today, for the first time, we're sharing updated day 150 data from this patient. This patient has had long-standing type 1 diabetes and prior to treatment with VX-880 had very-difficult-to-control sugar levels and multiple severe hypoglycemic episodes. No detectable endogenous insulin, that's something we measure by C-peptide levels. He had a hemoglobin A1C of 8.6% and was taking, on average, 34 units of insulin daily. In short, this patient had severe disease. At day 90, C-peptide levels, the hemoglobin A1C values and the exogenous insulin requirements, all showed unprecedented improvements. The day 150 data, shown here, show further improvement in all parameters. A further increase in C-peptide, now increased to a little over 400 picomoles, a further reduction in hemoglobin A1C to 6.7%, well within the ADA range for type 1 diabetics of less than 7%, and minimal exogenous insulin use. The safety profile remains unchanged from day 90, and during the extended follow-up period, the patient remains free of symptomatic hypoglycemic episodes. These results offer additional evidence for the efficacy and durability of VX-880 and underscore the potential of this approach to be transformative for the more than 2 million patients living with type 1 diabetes. Advancing now to Slide 15. To recap, type 1 diabetes results from autoimmune destruction of pancreatic islet cells, and we've known this for some time. We've also known that whole pancreas or cadaveric islet transplantation can be curative. The challenge has been quantity and quality of donor tissue. The most important thing to understand about our type 1 diabetes program is that our early results show that we've overcome this challenge. We're the only company that has shown we can make fully-differentiated islet cells at industrial scale. And while still early days, we've now shown that these cells can produce remarkable clinical benefit. Achieving durable results in type 1 diabetes patients requires 2 things: High-quality insulin-producing islet cells, we have that; and two, a method to protect these cells from the immune system. We can address this latter challenge in a few different ways. Today, with VX-880, we're combining the stem cell islets with standard immunosuppression in the Phase I/II study, and we've seen the compelling benefit in the first patient treated. We're also developing approach where these same stem cell islets are encapsulated in an immunoprotective device. In this approach, immunosuppressives would not be needed. The IND-enabling studies for the second approach are already underway, and we expect to file an IND later this year with clinical trials beginning thereafter. And in earlier stages of research, we're also working on genetically altering the stem cell-derived islets to make so-called hypoimmune pancreatic islet cells, cells that are designed to avoid attack from the body's immune system, yet another approach that eliminates the need for immunosuppressives. The bottom line here is that the starting material, the most important component of all of these approaches, is the fully-differentiated stem cell-derived pancreatic islet cells, the same cells that were transplanted into patient Brian, the first patient, and that's why we see the VX-880 results as so foundational. Let me turn to Slide 16 and to VX-147, which could be amongst the first, if not the first precision medicine, to treat the underlying cause of a genetically-driven kidney disease. In renal medicine, one of the most important human genetic discoveries of the last decade was the realization that variance of the APOL1 gene are a key driver of significant kidney disease. VX-147, our small molecule inhibitor, specifically targets this APOL1 protein, and in so doing targets the underlying cause of APOL1-mediated kidney disease. On Slide 17 is the proof-of-concept results for VX-147 in patients with APOL1-mediated FSGS. In the Phase II single-arm study of 16 patients, VX-147 demonstrated rapid and robust reductions in proteinuria, a marker of kidney damage, and was generally well tolerated. Importantly, the almost 50% reduction in proteinuria was on top of standard of care. These Phase II data advance our understanding of APOL1 beyond a causal genetic factor in kidney disease. We've now established that APOL1 inhibition is a powerful, targeted therapeutic mechanism, by which the disease course can be attenuated, and VX-147 thereby holds the potential to be a first-in-class and best-in-class treatment that could transform the lives of patients with kidney disease. Moving on to Slide 18. The potential market opportunity for VX-147 is large. We intend for the pivotal program to address the broad proteinuric kidney-disease population with two APOL1 alleles, including, but not limited to, FSGS. This represents more than 100,000 patients, most of whom are in the U.S. In terms of next steps, we'll have our end of Phase II meeting with the FDA in the near future, and we anticipate initiating the pivotal program later this quarter. Moving to Slide 19. As we close out today's discussion, I want to return to our corporate strategy and business model, which are unique and differentiated by a focus on serial innovation to bring high-value transformative medicines for serious diseases, served by specialty markets. Underpinning this corporate strategy is a very-deliberate R&D strategy to only pursue diseases where we understand causal human biology, have validated targets and biomarkers that translate from bench to bedside. We also expect these programs to have efficient development and regulatory pathways. This strategy has been designed to identify diseases, targets and tools to deliver disproportionate success. CF was the exemplar and the program that put the flywheel in motion. Today, we've demonstrated that this strategy has delivered and is delivering positive proof-of-concept results across multiple programs. We've done it with CTX001 in sickle cell disease and beta thalassemia. We've done it with VX-147 in APOL1-mediated kidney disease. And we're doing it with VX-880 in type 1 diabetes. Moving to Slide 20. Our financial profile and performance continue to be very strong. Our most recent revenue guidance for 2021, which we issued in early November, was $7.4 billion to $7.5 billion, which, at the midpoint represents approximately 20% year-on-year growth and a 36% CAGR since 2017. Looking forward, we anticipate continued, significant top and bottom line growth in CF through the middle of the decade by reaching more patients with our CFTR modulators and as we potentially reach the last 10% with our mRNA therapy. We also expect our business to deliver enhanced top line growth beyond CF, first with the launch of CTX001 and then with multiple programs, VX-147, VX-880 and more. Moving on to the next slide. The operating performance of the company generates significant operating income and cash flow, with an operating margin now in the high 50% range. Our capital deployment priorities have remained clear and consistent as our cash flow has increased. We focus on reinvesting in innovation, both internal and external, which we see as critical to continued value creation. We've invested approximately $3 billion in external innovation and completed more than a dozen transactions since 2019. And as I shared earlier, this has already made a significant impact on our clinical pipeline. We've also conducted targeted share repurchases to offset dilution from stock options of more than $2 billion over that same time period. I'll end with Slide 22. Here's a view of the upcoming milestones and how you can mark our forward progress. In CF, we expect to sustain long-term leadership. With our broad and deep pipeline, we have the ambition to transform many more diseases, and our strategy is designed to allow us to do just that. As we enter 2022, we have the people, the programs and the financial strength to successfully execute on our strategy of serial innovation. And as we do, we will create enormous value for patients and shareholders. Cory, with that, let me turn it back over to you.

Terrific. Thank you, Reshma. Great presentation. [Operator Instructions] Actually, we have a bunch in here, most on your diabetes program. And we'll get to those. I guess -- starting off, though, I just want to ask you a big picture around CF, and how you're thinking about the growth opportunity for that program here over the next 2, 3 years, given there are still a lot of patients who haven't been treated that might be eligible?

Yes. Yes, Cory. It's a great question. As I mentioned in my prepared remarks, we continue to see significant growth in CF through to the middle of this decade and CF leadership well beyond that into the 2030s. I say that because of 3 real reasons. The first is that there are 25,000 patients out of the universe of 83,000 patients who are eligible for CFTR modulators but who are not yet treated with TRIKAFTA/KAFTRIO. These fall into 3 categories. The first are where we have only recently been reimbursed, think Netherlands, think Spain and we're early in our launch. As you know, once we have reimbursement, uptake is rapid. So I feel very good about getting to those patients. Second, patients who are in countries where we have regulatory approval but we don't yet have reimbursement. Think Australia, think Belgium. As you've seen with the reimbursements we've secured in 2021, we're making good progress there, and I have confidence that we're going to get to all of those patients as well. And the last category is the younger patients. So getting down to the 2- to 5-year-olds and beyond. And those programs are underway. Of course, with the mRNA program now in IND-enabling studies, we're also getting some line of sight into 5,000-plus more patients who don't make any CFTR protein and therefore, would not be eligible for TRIKAFTA/KAFTRIO but would be eligible for the mRNA program.

Okay. Terrific. And then when you think about the clinical bar that TRIKAFTA sets here, I mean how do -- I guess, big picture, considering both your own next-gen triple and of course, there's potential competition that's out there, how do you think about that bar and how hard it is to just meet it, let alone exceed it?

Yes. As we think about the CF landscape in general, we've established a leadership position in CF. And in 2021, not only have we sustained it but we've really expanded it with the kind of long-term data we've generated with TRIKAFTA/KAFTRIO with the advancement of the 121 program into Phase III development and, of course, the mRNA program. And as I think about where we are today, TRIKAFTA has just set an enormously high bar, not just from the data from the registrational programs with the acute improvements in lung function like ppFEV1 but the data that I shared today, with long-term benefit on mortality in lung transplant as well as pulmonary exacerbations. So when I think about drug development in CF, you have to go head-to-head against TRIKAFTA, you have to have better outcomes for patients and that's just table stakes. What you really need is the full package of acute improvements and long-term benefit. And frankly, the only company that has that full package of registrational benefit and long-term benefit is Vertex. And the closest competitor, the most advanced competitor to TRIKAFTA is indeed the VX-121/561/tezacaftor program.

Okay. All right. Makes sense. So moving into the pipeline in the last 10 minutes or so we have here, I want to ask first on your sickle cell program. And do you see CTX001 as meaningfully differentiated from other genetic therapies that are in development for sickle cell disease? And what do you see the -- as those differences and how they may resonate with both patients and physicians?

Yes. No. Cory, the CTX001 approach is different than anything else out there in development, right? This is ex-vivo gene editing, using CRISPR-Cas9 to make a precise edit to increase hemoglobin F levels. This is the only program that has the genetic underpinnings that we can see in diseases like hereditary persistence of fetal hemoglobin. When you have that, when you have high hemoglobins F, what you have is patients with sickle cell disease and beta thalassemia who don't have any real manifestations of their disease. That's what we are recapitulating with our CTX001 program. There is no viral therapy involved in here, no viral delivery, lenti or otherwise. And you can see the benefits of our approach, not only in the preclinical program but in the clinical program now. Efficacy, I showed you the results from last year's EHA, the 22 patients treated were all 3 of the major manifestations of their disease. On the safety side, as I mentioned, the safety is very encouraging. And we're now out to more than a year in a number of patients, more than 2 years in some patients and the durability looks equally good.

Okay. And we have a question from our audience. And as you mentioned the depth of safety data for 001, could you please ask Reshma to provide more details there?

Yes. So the safety data really come from 2 sources, right? Preclinically, we have a very deep package, including evaluation of off-target editing, and we see none. Clinically, we've shared data with 22 patients across the program, and you've seen the safety there. We have dosed more than 70 patients across the program. And what I can tell you is that the safety continues to look good and is very encouraging for where we're going with the filings globally towards the tail end of this year.

Okay. We have a lot of interest in your VX-880 type 1 diabetes program. First question I'll put out is, can you discuss the significance of increasing fasting C-peptide, which was undetectable at baseline and now is up to 440? And then also, can you speak to, in the enrollment cascade here, how you enroll patients in this trial?

Yes, yes, yes. Really great questions. So let me tell you a little bit about how to look at these numbers that we're talking about C-peptide, hemoglobin A1C and exogenous insulin levels, right? So the important thing to understand is that this patient had diabetes for well over 30 years and was making no endogenous insulin. So they had no production of insulin from their own pancreatic islet cells. That's measured by C-peptide. Fasting C-peptide levels in normals is somewhere in the mid-250s to about 1,300 picomoles. This patient at day 90 had a level in the high 200s, you'll recall. They're now over about 400 picomoles, well within that normal range. The other really important element to look at, is what happens to C-peptide in response to a mixed-meal tolerance test, because that tells you this is glucose-responsive insulin release. And what you see in day 90 is that's exactly what happens. This is the most substantial improvement in C-peptide levels fasting or in response to stimulus that's been shown in a stem cell-derived program. And what's really impressive is that exogenous insulin goes down by more than 90% while hemoglobin A1Cs have now fallen into the ADA-recommended target range. That package together is really impressive. All right. So where are we going with this program? The program is up and running in the U.S. and Canada, across multiple sites. The way the protocol is structured, the first 2 patients get dosed at half dose. And then after that, we have our patients receiving the full targeted dose. You should expect to hear from us on more patients being dosed and longer duration of follow-up for this program as the year progresses.

Okay. And then on the kidney program, can you talk about the level of education that is going to be needed and the prevalence of APOL1 in the U.S. African population?

Yes, yes. This is a -- this genetic finding of APOL1-mediated kidney disease that 2 APOL1 alleles is a significant driver of a genetically-defined disease is a relatively new finding. It was only really discovered in the last decade or so. So the question around education is an important one, and more education is needed, particularly because while the test to diagnose APOL1, whether you have 2 APOL1 alleles is a fairly simple blood test, it's not a test that's performed very frequently. So we are now involved in making sure that the diagnosis can be ramped up. We ourselves are working on a 510(k)-cleared diagnostic for this disease. And we are working with the community to augment understanding. I think that the most important part of the education is going to be awareness of these Phase II data. As you know, Cory, in rare diseases, but in diseases in general, it's difficult to get patients and physicians to do diagnosis if there's no potential for a therapeutic. And that's the big change now with the availability of these Phase II results.

Okay. Terrific. Perhaps your next upcoming datapoint is with the Pain program. Can you talk about the bar for success for the Phase II studies in pain? And assuming the data look good, what might next steps be? Is it [straight] to pivotal trials from that?

Yes. Yes. So Cory, let's just take one step back on the Pain program. What we're doing here is working on NAV1.8. That's the target. And I'm really excited about this target because it's not only a genetically-validated target, it's pharmacologically validated by our very own VX-150 program. It's the first new target in the Pain area in years. This program is already in Phase II. There's 2 trials, a soft tissue trial in abdominoplasty, a hard tissue trial in bunionectomy. The soft tissue trial in abdominoplasty, that trial has completed enrollment and it's completed dosing, and we are on track for results from both the trials by later this quarter. What we're looking for here is therapeutic pain relief compared to placebo. That's how the trial is designed. And of course, what we're very interested in, is providing therapeutic pain relief without the side effects of opioids, particularly the addictive potential. And there's real reason to believe that that will happen because there are no receptors for NaV1.8 in the central nervous system. So both on the efficacy and the safety side, that's why my enthusiasm for this program is high. Assuming success in Phase II, yes, that is the plan to move forward into Phase III development.

Okay. Terrific. Well, Reshma, we are unfortunately out of time. We have a lot more questions we were unable to get to, but we can follow-up on those off-line. So thank you so much, and good luck for the rest of the week. Appreciate your time.

You bet. Thank you, Cory.