Good day, and thank you for standing by. Welcome to the Vertex Pharmaceuticals Q2 2021 Conference Call. At this time all participants are in a listen-only mode. After the speaker presentation there will be a question-and-answer session. Please be advised that today's conference call is being recorded. At this time, I'd like to turn the call over to your host Mr. Michael Partridge. Sir, you may begin.

Good evening. This is Michael Partridge. Welcome to the Vertex second quarter 2021 financial results conference call. Making prepared remarks on the call tonight, we have Dr. Reshma Kewalramani Vertex’s CEO and President, Stuart Arbuckle, Chief Commercial and Operations Officer, and Charlie Wagner, Chief Financial Officer. We recommend that you access the webcast slides on our website as you listen to this call. This call is being recorded. A replay will be available on our website. We will make forward-looking statements on this call that are subject to the risks and uncertainties discussed in detail in today's press release and in our filings with the Securities and Exchange Commission. These statements including without limitation, those regarding Vertex’s marketed CF medicines, our pipeline and Vertex’s future financial performance are based on management's current assumptions. Actual outcomes and events could differ materially. I would also note that select financial results and guidance we will review on the call this evening are non-GAAP. I will now turn the call over to Dr. Reshma Kewalramani.

Thank you, Michael. As we reach the halfway point in 2021, our business is performing exceptionally well, and is very well-positioned for the future. Our CF franchise is strong and growing. During the second quarter, we reached a number of new reimbursement agreements with the triple combination, as well as other CFTR modulators in our portfolio, including in major markets like France and Italy, earlier than expected. These reimbursement agreements are occurring in a timeframe that is far quicker than is typical for OUS markets. And importantly, we are achieving reimbursements at levels which are robust and reflect the value of our CF medicines. We also secured regulatory approval for the triple combination in the six to 11 age group for the U.S. Taken together, these additional reimbursement agreements and regulatory approvals provides thousands of new patients with access to our medicines. As such, we're raising our 2021 guidance range by $500 million to a range of $7.2 billion to $7.4 billion, reflecting 18% year-over-year growth at the midpoint of the range. But our work in CF is not done. There are still more than 30,000 people with CF who are yet to be treated. And by reaching these patients, we see continued significant growth for the CF business. With regard to the pipeline, progress is accelerating across the portfolio. We now expect to achieve targeted enrollment in both CTX001 studies in Q3. We have initiated the VX-548 Phase 2 program in acute pain. We are on track to begin the Phase 3 next in class triple combination program in CF shortly.

Thank you, Reshma. I'll begin by reviewing the Q2 revenue performance of our CF medicines. Our Q2 global revenues reached nearly $1.8 billion, driven by increasing revenues outside the U.S. as a result of the launch of KAFTRIO and continued strong performance in the U.S.

Thanks, Stuart. In the second quarter of 2021 Vertex again continued its record of outstanding financial performance. In fact, we're in the midst of our eighth consecutive year of at least double digit revenue growth. Second quarter total product revenues were $1.79 billion, an 18% increase compared to the second quarter of 2020. This growth was primarily driven by strong international uptake of KAFTRIO and continued performance of TRIKAFTA in the U.S. Our second quarter revenues included $1.26 billion in the U.S. and $536 million outside the U.S. Ex-U.S. revenues for the quarter grew 71% over the prior year, reflecting the full quarter effect of prior initiations in Europe, as well as any new patient initiations in countries where patients have access to KAFTRIO. Our second quarter combined R&D and SG&A expenses were $537 million compared to $467 million for the second quarter of 2020, driven largely by investment in our clinical stage programs and our research pipeline. As our pipeline continues to expand and mature, we expect our R&D investments will continue to be substantial, while we drive toward proof of concept data and further clinical and regulatory progress across the pipeline. Our continued growth in revenues combined with carefully managed growth and spending translates to a second quarter operating margin of 57%. With our strong revenue and profitability, we ended the quarter with $6.7 billion in cash following the one-time $900 million payment to CRISPR Therapeutics for the amended collaboration. Our strong financial performance to-date, the future growth profile in CF, and the tremendous potential of our broad and deep pipeline made this the right time for the $1.5 billion stock repurchase authorization that we announced in June. This authorization gives us the opportunity to repurchase stock at very attractive prices as we seek to offset future dilution…

Why don't we go directly to questions and open the phone lines now.

Thank you. I show our first question comes from the line of Michael Yee from Jefferies. Please go ahead.

Hi, guys. Good evening. Thanks for the question. Reshma, I know that there's an important Phase 2 readout for FSGS later this year, and you've talked about that. And I know you've talked about what you're looking for, in terms of reduction proteinuria. I guess, my question was twofold. One, are there scenarios where reductions are more modest, and you have to think about what that would mean for going forward? And second, if it was really good reductions, reduction of proteinuria is surrogate so when you still need to run a much longer study, appreciate its genetic mutation patient population. So maybe you could talk to those scenarios and how you think about the robustness of data? Thank you.

Yeah. Hi, Mike. The question you asked is about the VX-147 program, for others on the phone this is the APOL1-mediated FSGS program that is currently in Phase 2 and we are on track to readout the Phase 2 results in the second-half of this year. The way I see this program, Mike, and what we're really looking for is safety for sure. It's a Phase 2 program. And on the efficacy side, you're right, it is about percent reduction in proteinuria. And we are looking for double digit reduction in proteinuria because at those levels, it's meaningful. And it is correlated with improvements in GFR, and the hard endpoints of time to ESRD. As with all of our programs, Mike, we have a portfolio approach here. I am excited to see these results. The community, physicians, as well as patient groups, and the regulators, particularly in the U.S. have had multiple workshops and conferences over the last several years. And the regulators have expressed openness for proteinuria to be the regulatory enabling endpoint. Now, whether that's an accelerated approval, whether that's a full approval, all of that, obviously will need to be discussed as we progress the program and have those discussions with the regulators. But I've been really pleased with how the regulators have thought about it and the fact that this is indeed a genetically defined renal disease, and what the regulators have often talked about is a homogeneous proteinuric kidney disease. And that that is what this is. So I feel optimism for proteinuria to be the regulatory enabling endpoint. And obviously, that makes for a more efficient trial.

Thank you. I show our next question comes from the line of Phil Nadeau from Cowen and Company. Please go ahead.

Good afternoon. Thanks for taking our question. A two part regulatory question from us. You recently announced the design of the CF Phase 3 trial. And it's notable because as a non-inferiority primary endpoint, we're curious to know whether simple non-inferiority is sufficient to support FDA approval, or if the FDA asked for superiority or something else from the secondary endpoints? And then second part of the question is, when will we get similar details on what's necessary to file CTX001? I think you've been guiding in FDA update sometime this year, we're kind of curious, is that going to come sooner rather than later? And if you have any preliminary idea of what will be necessary for filing that candidate? Thank you.

Sure. Let me take the CTX001 question first. As I mentioned in my prepared remarks, we are now looking to achieve completion of target enrollment in Q3. So that's really a very near-term completion of the targeting enrollment. So what we're really looking at now, and I've described before, as we've had these conversations with regulators, and we do have the benefit of really virtually every regulatory designation one can imagine, so we've had the opportunity to have productive discussions with the agency. It's about the size of the filing package. It's about the duration of follow up and the CMC manufacturing controls, I'd like to say, achievement enrollment is really short-term. So it's about the duration of follow up and CMC manufacturing. I do expect that we're going to bring those discussions to a conclusion in the next coming months. And I do anticipate filing to be possible in the next or let's call it 18 to 24-months. So that's really what it looks like on CTX001. On the Phase 3 next in class CF program, we've gone through our discussions with the regulators. We've had our end of Phase 2 meetings. And this trial design that you see reflects those considerations and those discussions. I will point out that as I look at the VX-121 data there are three really important elements that stand out to me. The first is that in our HBEF , and you know that our HBE assays translate very well into the clinic, not only qualitatively but quantitatively, singularly or in combination, so one to one alone or in combination with tezacaftor 561. The results are in our HBEs that one to one is more efficacious, more efficacious than even TRIKAFTA. That's really saying something. And in the Phase 2 results, you can look at the sweat chloride, which is the real direct translation of chloride transport in vitro. And you can see that we're looking at numbers that are more like 45 to 45 millimolar with the one to one regimen versus 33 to 39. That's what we saw in Phase 2 with the TRIKAFTA regimen. And then of course, ppFEV1, which is more variable, but even that has indications for being better than TRIKAFTA. So while the primary endpoint is non-inferiority, I see a lot of optimism in these data to even have the potential to be better than TRIKAFTA.

Thank you. I show our next question comes from the line of Geoff Meacham from Bank of America. Please go ahead.

Great afternoon, guys. Thanks for the question. Just a couple for you guys. So on the pipeline, I know there's been a lot of emphasis on BD. But for what you have today in the pipeline, are there investments that you can accelerate to get into registration trials faster, for example, like in pain? And then, when you look in CF, beyond rolling out across the EU, and maybe adding younger patients across the board, what do you think -- I know you're not going to give long-term guidance, but what is the normalization of the market look like in terms of maybe the incidence rate? What do you guys assuming? I'm just trying to get a sense for when CF is more moderate growth, is that the timeframe where will you think that that you're going to have more of a P&L impact from sickle cell and beta thal from CTX001 or other elements of the pipeline? Just trying to get a sense to put all the pieces together for kind of the long-term growth picture? Thank you.

Yeah, it's a great question, Geoff. And let me set it up for you and then I'm going to ask Stuart to comment on market dynamics. And then I'll come back and address your question about the pipeline and how we see that going. What I see to start with is, I really see continued significant growth for many years to come in our CF franchise. And I'm going to ask Stuart to outline those dynamics for why I say that.

Yeah, Geoff. So as you know, we updated our estimates of the epidemiology for people living with CF in the U.S., Canada, Europe and Australia earlier this year to approximately 83,000 patients. And we're probably treating about half of those patients today. And as you know, we updated our guidance today to a range of $7.2 billion to $7.4 billion. What that means is, and I don't want to gloss over this is that there is more than 30,000 patients remaining, who are eligible for our CFTR modulators. They are likely to benefit from our existing CFTR modulators. And those 30,000 patients really fall into three categories. The first one is people who live in countries where we have regulatory approval, and we've secured reimbursements. And we are beginning the launches in those markets. And as you know, the launches of our CF medicines tend to be very rapid. Second group of patients of those who live in countries where we have regulatory approval, but don't yet have reimbursement. Obviously, we've had a great year securing reimbursement for KAFTRIO, just under a year from the EMA approval, and I have full confidence that we're going to continue that run and secure additional reimbursement agreements in countries where we don't have it today. And then we have to get down into younger patients. And as you know, we've done that with KALYDECO and ORKAMBI, and given the benefit risk profile of TRIKAFTA, we fully expect we'll be able to get down to younger age groups. So over the next several years, we see multibillion dollar revenue growth potential through getting to those more than 30,000 patients. Additionally, we are also working on the 7% to 10% of patients who aren't going to be eligible for our CFTR modulators, using genetic approaches through our collaboration with amongst others Moderna. So, we do see continued growth of our CF franchise for several years to come, based on continuing to execute in the way that we have done over the last few years. And then to tell you how the pipeline is going to layer on top of that, I'll hand it back to Reshma.

The pipeline is progressing nicely, and I actually would say it's accelerating. And let me tell you why I say that, the pain program is now in Phase 2 for the bunionectomy study and in parallel and very shortly we're going to start up the abdominoplasty study. The CTX001 program, as I said in my prepared remarks, that one is going to achieve target enrollment in Q3 now. And when I think about VX-147 that is absolutely on track to have results in the second-half of this year. And when I put all of that together, it looks like a really important next six to nine months in terms of not only data readouts, but the opportunity to advance to milestones in each of these programs. And that's not even talking about the programs that are in late preclinical development or in Phase 1. So we are investing heavily in our pipeline. It is because the pipeline is accelerating, and there are many opportunities for us to get to the next important milestones in clinical development. I would be remiss if I didn't say a word about VX-880. This is the naked cells only approach. This one is a Phase 1/2 trial, and I would think about this one as similar to CTX001, in that reasonably small number of patients in a reasonably efficient timeframe will really tell us what we have. And so that was another one that I think is going to be important to keep our eyes on and to invest behind.

Thank you. I show our next question comes from the line of Salveen Richter from Goldman Sachs. Please go ahead.

Thanks for taking my questions. For CTX001 on manufacturing, do you have an understanding of the assays required or how differences could play out regulatory wise versus gene therapy given this is a new technology? And then, with your work with Moderna on mRNA and gene editing, maybe you could just help us understand how that's progressing and when those might enter the clinic?

Sure. Salveen with regard to CTX001, we really have had the opportunity to have multiple discussions with the regulators, not just on what the potential filing package could look like, in terms of the clinical data, sample size, et cetera, but also on CMC and manufacturing. And we have a very good understanding of what the agency both here and outside the U.S. would like to see in terms of potency assays and release essays. And that work is going very well. In terms of the mRNA program, you know that we have multiple programs for the last 10% of our CF patients, the most advanced of which is the mRNA program in partnership with Moderna. There's really two components here. It's the mRNA construct itself, and it's also delivery. We have made solid progress on both of those. And I would say the important one is on delivery. A little too early for me to give you timing for when that would enter the clinic, but I will say that the progress has been very good. And I'm feeling very optimistic about our ability to get to that last 10% of patients, maybe even compared to six months ago.

Thank you. I show our next question comes from the line of Robyn Karnauskas from Truist Securities. Please go ahead.

Hi, thanks for the question. Starting first a little bit on -- I have to ask this question. I did not want to be the person who asked this question on the call Reshma, but I have to. Your thoughts on the Galapagos headwind as people are focusing on their data coming up? I know they're behind you. But can you just give any more additional color on the biology perhaps even and how you view their drug? And second on pain, you mentioned like timelines if you can give some clarity on your pipeline over the next six to nine months? When can we actually see data from pivotal trials enroll really quickly? Maybe give us some sense of what your expectations are? Or, your next data set and what the bar might be? Thank you.

Yeah, sure thing, Robyn. Let me start with pain. I'm really excited about our pain program. You know that we have a program in NaV1.8 that's the one that's furthest ahead. In our discovery and preclinical research we also have programs in NaV1.7. The reason I'm particularly excited about NaV1.8 is it's a genetically validated target for sure. But it's also pharmacologically validated by our very own VX-150. The molecule that's in the clinic now VX-548 really is all the attributes we were looking for in terms of potency, as well as in drug like properties, BDIs, manufacturability, et cetera. So this one really looks very exciting to us. It's already in the bunionectomy study that is up and running as a Phase 2 proof of concept study. The abdominoplasty is right behind it and that should start up very shortly. We are also interested in pursuing peripheral neuropathic pain in the NaV1.8 area. And the reason for that is because again, our VX-150 molecule had positive proof of concept data, not only in acute pain, but also in neuropathic pain. So, that one is another study that's coming. With regard to acute pain, the studies are very short in duration because it's a procedure like a bunionectomy, you have treatment that is over a couple of days and so the results can be obtained in a reasonably efficient timeframe. I expect that the bunionectomy results will be ready by let's say the tail end of this year, beginning part of next year, abdominoplasty results thereafter. So that's really how I would have been capsulate the pain program. With regard to the Galapagos data maybe Galapagos AbbVie data, Robyn, I'd rather focus on our portfolio and tell you about how I see our portfolio. And maybe the best way to summarize it is VX-121 561 tezacaftor holds the potential to bring greater patient benefit than even TRIKAFTA, its once daily dosing, which I think adds a level of convenience for our patients. And in all honesty, the greatest threat to TRIKAFTA, the greatest competitor to TRIKAFTA in terms of the most advanced is our very own VX-121 561 tezacaftor.

Thank you. Our next question comes from the line of Cory Kasimov from JPMorgan. Please go ahead.

Great. Thanks. Good afternoon. I appreciate you taking the question. I actually want to follow up Reshma on what you were just talking about kind of on Phil's earlier question on the QDCF study, but from a slightly different point of view. So recognize it's designed to demonstrate statistical non-inferiority from a regulatory standpoint. But what do you think you need to show for this to actually displace a product as good as TRIKAFTA in the market? I'm assuming dosing once versus twice a day isn't enough on its own? And did you say in the prepared remarks I just want to make sure we have this right that the royalty on the QD goes to low single digit from low double digit? Do we get that right?

Yeah. Cory, with regard to the study, you're right. For the regulatory enabling endpoint, it is a non-inferiority study, and that non-inferiority is on ppFEV1. You're also correct that the royalties go from low double digits with TRIKAFTA, KAFTRIO to low single digits. Let me just take a step back, though, and help maybe everyone on the phone line understand our perspective on the one to one program, and why we're really doing this. So, our long standing goals in CF have been threefold. First, bring forward a medicine that can treat up to 90% of patients with cystic fibrosis, give that a check, that's TRIKAFTA, KAFTRIO. Second, get patients who can benefit from CFTR modulators to the highest levels of efficacy. And the way we've discussed that is to bring patients that carrier levels of sweat chloride. And that's really important because as those levels when you look at carriers of cystic fibrosis, they really have no manifestation of disease. And when you look at our own data, other published data, it is absolutely true that the better the sweat chloride results, which is a reflection of CFTR function, the better the outcomes for our patients. And the third big goal has been to get to the last 10% of patients. The VX-121 561 tezacaftor program is all about that big goal number two. Get patients to carrier levels of sweat chloride. And certainly, it is the case that some patients on TRIKAFTA can get there. But we are looking to get many, many more patients to those levels, if not all patients, and that is VX-121 561 teza. And as I reviewed from what we see in the HBE cells, in terms of chloride transport, sweat chloride from the Phase 2 studies, and even ppFEV1, all these measures point us in the direction that this is possible with VX-121 561. And of course, we're busy in the labs working on even more efficacious molecules.

Thank you. I show next question comes from the line of Liisa Bayko from Evercore ISI. Please go ahead.

Hi, thanks for taking the question. I want to ask a little bit more about the FSGS study design. Can you talk about sort of the background therapies that patients will be on? And will they be on study background meds headed into the study? Or, will there be any changes ahead of the study? And when will you allow for the use of steroids? Just curious about some of the other factors. Thank you.

Yeah, sure thing, Lisa, in our Phase 2 study we are looking at patients who have APOL1-mediated FSGS with two APOL1 . And we are looking for patients with heavy amounts of proteinuria. We are allowing patients to be on background therapy. And we are looking for the double digit percent reduction of proteinuria that I was talking about earlier, on top of whatever background therapy our patients may be coming into our trial with.

Okay. Great. Helpful. And then what…

Sorry. Thank you. Our next question comes from the line of Brian Abrahams from RBC Capital Markets. Please go ahead.

Hey, guys, good evening. Thanks for taking my questions. So two questions on VX-121. Can you talk about where you're planning to conduct a Phase 3 triple combo study? And, is that going to be in the U.S. or outside the U.S.? Would you expect any medium-term impact to TRIKAFTA or KAFTRIO revenues? And then, it looks like the sweat core that you've observed, at least in the was dose dependent. I'm wondering, do you feel you've fully explored the dosing curve here any safety or PD reason not to further dose escalate just given the high bar set by TRIKAFTA? Thanks.

Sure thing. Brian, we are going to be conducting the study in the usual countries, U.S., European countries, the standard. Remember, both the studies in the VX-121 program are compared to TRIKAFTA or KAFTRIO, so this is not placebo controlled. So patients are going to be an active therapy in either arm, that obviously makes it a lot easier for patients to enroll into this study. With regard to impact on revenues for TRIKAFTA, no, we don't see any impact on revenues to TRIKAFTA. And with regard to how did we select the dose, how did we think about this program, we shared with you the results from the Phase 2 study. And as is the case with all of our programs, we take all of that data, we do quite a bit of modeling and simulation to settle on the best dose that maximizes efficacy, and has the greatest benefit risk profile. I think that's exactly what we've done with the regimen that we've selected. And as I mentioned, on my response to one of the other questions, what I see in these data with the regimen that we're selecting is in vitro chloride transport that is even better than TRIKAFTA. What chloride levels, which is the most approximate translation of chloride transport, so the sweat chloride levels in our Phase 2 trial that are higher than what we saw with TRIKAFTA. And ppFEV1, which you know, has greater variability that is also showing us potential to be better than TRIKAFTA. I have to say what is obvious, TRIKAFTA is a great medicine. What we saw in the clinical trials has been recapitulated in the real world. You heard Stuart talk about the longer-term data with TRIKAFTA that is just continues to look excellent. But we think we have something that might be even better than that with VX-121 561 tezacaftor, and I'm really looking forward to the Phase 3 results.

Thank you. I show our next question comes from the line of Paul Matteis from Stifel. Please go ahead.

Great. Thanks so much, and congrats on the quarter. I just had a couple other APOL1 questions, if you don't mind. One was just on finding these patients. I know the study or at least preclinical trials, it's been going on for a little over a year, and the implied sample size is estimated to end up at around 10. Has it been difficult to find patients? Is genetic testing a headwind? And then second, Reshma, I know you talked about this is obviously a first study, double digit proteinuria is a goal. Can you just kind of contextualize that in terms of what thresholds have changed in proteinuria have predicted clinical benefit in the past? Is there some sort of minimum change that has been relevant to get FDA comfortable with accelerated approval? Thanks so much.

Yeah. All great questions about the APOL1-mediated FSGS program. Let me start with the clinical trials and the enrollment and such. First and foremost, we are on track to have results in this calendar year in this second-half of the year. It has been a study that has taken some time to enroll, and I'm not surprised about that. The factors that we need to think about are, remember, the study started right in the midst of the pandemic, actually right when the pandemic was hitting a real high point in terms of case numbers here in the U.S. The second is that this is a disease for which we don't routinely employ genetic testing in renal medicine. So it takes a little bit of time to find the patients, genetically test them and have them enroll in our studies. And the third thing is APOL1-mediated FSGS is the smaller of the spectrum of APOL1-mediated kidney disease and the APOL1-mediated FSGS patients, because it's a smaller component, they are spread across the U.S. and they don't necessarily live close to a testing center. And so that was particularly difficult in the pandemics. With regard to what we are looking for, we are looking for percent decreases in proteinuria. And I think double digit decreases in proteinuria in this Phase 2 study, which is a first-in-class molecule for this genetically validated target would be just excellent. And the question around what is the agency looking for and such, it really depends on the kidney disease of interest. We are looking at a homogeneous kidney disease, it is all genetically defined. And I think that that falls into a category in and of itself. And as I said that there is no precedent for this, we are the first to bring a targeted of therapy for APOL1-mediated kidney disease. But I do think a percent reduction in the double digits would be very, very meaningful.

Thanks a lot.

Thank you. I show our next question comes from the line of Brian Skorney from Baird. Please go ahead.

Hey, good afternoon, everyone. Thanks for taking my question. Mine is really on the diabetes program. Just strictly thinking about the opportunity in patients who are going to require lifetime immunosuppression, how do you think about differentiation from your cell line from sort of a cell trans donor cells, which, I think should probably get approved in the next month? Is there a supply constraint there due to sourcing that you think you overcome with the sort of the stem cell line? Are there other characteristics of differentiation that you think can make your technology work better? And then in terms of -- I know, you're working on sort of encapsulation for protecting the differentiated islet cells to reduce immunoreactivity. But are you exploring other ways, such as the induction of immunetolerance or cell editing to get around the need for immunosuppression as well? And any thoughts on sort of those pathways?

Yeah, really, really great questions, Brian, and thank you for those. I'm really happy to talk about the type 1 diabetes programs. I'm sure you can hear from the enthusiasm in my voice, it's one of the ones that is really holds enormous potential for patients. So let's just start at the very top of the funnel, there are more than 2 million patients, 2 million patients with type 1 diabetes in the U.S. and Europe. So the potential to help patients is enormous when you look at it from that perspective. I'll take your second question first about encapsulation, I do think that it will be important to have the cells being encapsulated in a device, or in some way be immune evasive, so that you don't require immunosuppressives to be able to get to all of those patients. I think that the device approach is elegant, because it has the benefit of simplicity. That's not to say that it's a simple device, but it is to say that the cells encapsulated with this device, then don't require any further manipulation which is elegant. That all being said, we are very interested in all other approaches, and we are pursuing other approaches to immune evasion. The lead approach is with the cells encapsulated in the device. With regard to the cadaveric cells and the cells that are available currently, the big differentiator and this is really important to understand because it's fundamental. Those cells are cadaveric cells. And those cadaveric cells have all of the limitations that have made the procedure difficult for patients to undergo. That is to say quality and quantity of cells are limited. Our approach is a stem cell derived, fully differentiated, insulin producing islet cells. And that makes quantity not an issue and quality not an issue. And so, that's really the foundational difference between our approach and the other.

Great. Thank you, Reshma. That's very helpful.

Yeah, sure thing.

Operator, we have time for one more question.

Thank you, sir. Our last question comes from the line of Alethia Young from Cantor Fitzgerald. Please go ahead.

Hey, guys, thanks for squeezing me in. Just a quick question on how you’re kind of thinking about maybe kind of external deals, maybe are there an interest in kind of proof of concept? Are you still kind of focused on kind of earlier stage deal? Thanks.

I'm sorry, Alethia. We couldn't hear your question in the room? Could you repeat your question?

Yeah. With your external deals kind of in the early stage or in the late stage? But then, I guess, just some thinking about maybe significant timelines with the program being a little bit more delayed than we thought? Thanks.

I think the question is about deals, external deals, we’re looking at what phase might we be looking at?

Alethia, we are interpreting your question.

Can you hear me now?

We can hear you.

Yeah, basically, I'm just asking about kind of external timelines or external development, kind of aspirations like whether you're looking at more proof of concept deal? Or, are you looking at kind of earlier stage development programs, but you kind of have gone with in light of what's been going on without ?

Sure thing. I think you're asking about business development and how we’re doing and external innovation. Alethia, we have been and we remain today very focused on innovation, both internal and external. And we've talked in the past about our areas of interest and how we view this, namely in CF in tools to augment our toolbox and assets that fit our sandbox diseases. All of those stay exactly the same. Our R&D strategy encompasses both internal and external innovation. You have never seen us invest more in our internal innovation. Our pipeline has both sources of assets, from our own pipeline and what we brought in from acquisitions like Semma and Exonics, and partnerships like CRISPR, and Moderna. And you should expect us to continue in the same way.

Great. Thank you.

Thank you. This concludes our Q&A session. At this time, I'd like to turn the call back over to Mr. Partridge for closing remarks.

Thanks, operator. Thanks, everybody, for tuning into tonight's call. The Investor Relations team is in the office, and we look forward to any additional questions that you have. Have a good night.

This concludes today's conference call. Thank you for participating. You may now disconnect. Good day.