Kymera Therapeutics, Inc. (KYMR) Earnings Call Transcript & Summary

Good morning, everyone. Thanks for joining us for another session at the 44th JPMorgan Healthcare Conference. I'm Brian Cheng, one of the senior biotech analysts here at the firm. On stage, we have the CEO from Kymera Therapeutics, Nello Mainolfi. I'll now pass the mic to their CEO for a short presentation, followed by a live audience Q&A. Nello, the stage is yours.

Thanks, Brian. Thanks, everybody, for joining us. Hopefully, the sound is good. Always great to be at JPMorgan in a new room this year. So in the next 20 to 30 minutes, I want to take the opportunity to tell you a little bit about Kymera, where we're going in 2026 and probably more importantly, where we're going in the next 3 to 5 years. So if you look back -- so actually, this year, in May will be the tenth year anniversary since we founded Kymera and we spent the past 10 years building strategy capabilities and team to deliver a whole new generation of medicines. What we're trying to build is something that has actually never been done before: oral drugs with biologics-like activity. And what we've done in the past 10 years, and we'll take a quick look at last year is taking us a step and a step closer to our vision and our goal. So if we just look for a minute on what we've accomplished, 2025 was really a pivotal year for the company. About 2 years ago, around this conference, we presented, for the first time, our STAT6 program. We showed with preclinical studies that if you degrade STAT6, you can deliver activity, the blockade of IL-4 and 13 in cells and in vivo models that can mimic if not being numerically superior to what has been seen with a mega blockbuster drug like dupilumab. So last year, in -- actually in two portions in June and December, we have been able to complete the early clinical translation of KT-621 and demonstrate that actually if you degrade STAT6 in humans either in healthy volunteers and later in patients, you can actually deliver full pathway blockade of IL-4 and 13, and impact both biomarkers and clinical endpoints, at least as effectively as upstream biologics. So we'll talk about that, but there was a really exciting important part of our 2025. We've initiated a Phase 2b study. We'll talk about a new study that we started recently. We also presented a new program, our IRF5 degrade or KT-579, another transcription factor in highly validated pathways where there are effective biologics, but not effective oral convenient drug. And that's where 579 was delivered. And last year, we've not only presented the program, but also completed our IND-enabling work to being able to go into the clinic soon this year. We also had a lot of important corporate updates. We continue to collaborate with Sanofi on our IRAK4 degrader and decided to advance the second-generation degrader in the clinic this year. We entered the collaboration with Gilead on this novel first-in-class CDK2 molecular glue for oncology. And we were able to raise almost $1 billion last year, which gives us about now $1.6 billion that will fund the company through at least into 2029. And importantly, allows us to take several of our programs through proof-of-concept Phase II studies and for KT-621 in several Phase III studies. So this is a snapshot of this 2025 is the foundational pivotal year for what Kymera trying to do. And we can only do this, thanks to both the team, the strategy and the capabilities that we built, as I mentioned, a few days -- a few minutes ago. And maybe it's worth highlighting just a few of the things that I think make Kymera really unique in biotech. One, our target selection strategy. Our target selection strategy was defined about 10 years ago and actually has not changed. We go after untracked targets that have never been drugged before either fully or at all in pathways that have been validated by usually injectable biologics, where we know our oral intracellular degraders can deliver a completely differentiated profile. Again, the concept of oral drugs with biologics-like activity. We have decided about 5 years ago to focus almost solely in immunology, we believe this is the time to advance a whole new generation of oral therapies in immunology. Obviously, we're not the only ones, but we believe we're leading the transformation of how patients with immune inflammatory diseases will be treated in the next decade. We can only do this thanks to the team and the capabilities that we've built. We understand the specificity of our degraders at the molecular level, at the atom level, we know how to make them behave like pharmaceutical agent, selective specific, safe and well tolerated. And importantly, we're rediscovering, redefining these new rules of discovery and development. What does it mean to develop oral drugs that match the activity of biologics? They're whole new concept that we're pioneering at Kymera. And we can only do it thanks to the team in our translational development organization that have been able to build very creative early clinical studies that not only derisks but also validate our mechanisms and allows us to accelerate late development. And you'll see the work that we're doing with STAT6, how it speaks to this particular point. So this is the problem statement. And this is the problem statement that we're very passionate about at Kymera. We're just going to talk about order of magnitude and not individual accurate numbers. But if you look at the 10 most common immuno-inflammatory diseases, they are written very small in the slide, but you can imagine, go from AD, asthma , RA, SLE, et cetera. There are about, let's say, more than 100 million patients in the 7 major markets. The patients that access advanced systemic therapy are about 5 million patients. So we have lots of effective therapies, but we have two problems: how the system prescribes advanced systemic therapy, so treatment paradigms. And again, how patients can access advanced systemic therapy. And we believe strongly that if we develop drugs that have the activity, the safety, the efficacy of these advanced biologics but the convenience of oral drugs and the access that we can deliver for patients, we can transform how patients are treated. This is not about the convenience over a biologic. It's about where patients are going to be accessing our drugs. And our vision here is to be our drugs, the first option for all patients with immune inflammatory diseases. So how can we accomplish that? So this is probably the only technical slide of today, so bear with me. But at least on the, let's say, chemistry discovery part. So we know, obviously, how biologics work. You inject the drug that generally a long half-life, and you can cover the target for an extended period of time. And this allows you to have an extended saturating effect on the target and obviously, an extended effect on the clinical manifestation of that disease. Traditional small molecules, let's say, in the past 50, 30, 20 years have tried to get close or replicate that type of pathway blockade. The problem is that for every copy of protein, you can see on the left of the slide, you need one molecule. So you have a stoichiometric inhibition of your target that requires for targets that are expressed usually in the micro -- nanomoral to micromoral levels, you need a large amount of drug for a long period of time, usually for 24 hours. And that's generally extremely difficult to accomplish, if not impossible with a once-a-day oral drug. In fact, I don't remember of a small molecule inhibitor traditional small molecule inhibitor that covers the target more than 95% for 24 hours. So what -- the reason why degraders can accomplish this is because one molecule of our degrader can degrade hundreds, if not thousands of cabrio protein. We can only fit 5 on this slide. But believe me, we can do more than that. And so this allows us to have a catalytic mechanism. So a small amount of drug for a short amount of time, can degrade the protein completely and fully. So when we dose once a day, we can accomplish sustained complete pathway inhibition. I would say, in some cases, if you take a drug every day, you will probably accomplish more pathway inhibition than a saturating dose of an injectable biologic. So just -- we are landing here on our pipeline, just to give you a quick sense of where we are and where we're going. So I think it's fair to say that KT-621 and STAT6 program is probably in the top 3, I would say, the first or the most compelling program in biopharma, but let's say, in the top 3. Given the breadth of opportunity, the validation that is behind it, and also the stage of development. So we've just started Phase 2b study, we started the AD Phase 2b study late last year, actually, we dosed our first patient in, I believe, late October. And then recently, we said we were going to start the asthma Phase 2b study in Q1, we actually ended up starting in week 1 of the year. And both of these studies will have data in 2027. So we'll have about 500 patients worth of data for KT-621 in 2027. We'll talk more about this study soon. Exciting year for KT-579, we are shortly initiating our Phase 1 study, and we'll have Phase 1 data in the second half of the year. We're also planning to start the patient study, hopefully also this year after the healthy volunteer study. We also have, as you know, two programs in collaboration, one with Sanofi, we're on track to initiate our Phase 1 study with the second-generation IRAK4 degrader KT-485. And then we have the exciting partnership with Gilead on this really unique CDK2 molecular glue, which I don't have any time to go into the details of, but hopefully, we'll be able to share more data this year and in the future. So I thought it makes sense to use KT-621, our strategy, our discovery, our data and our development strategy to exemplify how we think about both the drug discovery and development principles at Kymera, our strategy, and more importantly, how we believe we're going to change how patients are treated with our drug. So this -- the introduction slide has been used by myself multiple times. Nonetheless, I think for being comprehensive, it's worth highlighting two key pieces of information here. One, IL-4 and 13 is the most validated biology in Type 2 inflammation. Type 2 inflammation or one could say, allergic inflammation is the most common type of inflammation in the western world with more than 150 million patients suffering from a series of diseases, 8 diseases in which dupilumab has been approved, but there is actually more. There are food allergies and other diseases that have not yet been treated with a Type 2 drug. So the drug that is most successful at blocking IL-4 and 13 biologists, dupilumab. This is a monoclonal antibody that blocks IL-4 receptor alpha and in doing so, blocks the signaling of IL-4 and 13. We have found that if you degrade STAT6, the selective and obligated transcription factor for IL-4 and 13 signaling, you're able to block the pathway as well as in upstream biologic like dupilumab and this is not only our work, but also if you look at human genetics data, it points to the fact that static is the key transcription factor for allergic diseases. There are many drugs in this pathway, but there is no oral drug that target this pathway intracellularly. And that's really what we're trying to transform. So this slide contains a lot of information. I just want to guide you through like the two important ones. So you can see the diseases on the right, these are indications in which dupilumab has been approved. We're talking about more than 100 million patients the penetration of upstream biologics into this patient population is in the single-digit percentage. So you would ask yourself how is this possible? Well, the challenge is, again, as I said earlier, some diseases are treated, not thinking about the underlying inflammation in the proper way. And actually, they're just treating the symptoms. And then lots of patients and prescribers think twice before prescribing an injectable biologics. So when we talk about the Type 2 drugs, dupilumab and others being $20 billion to, soon, $30 billion drug. While this is obviously an important statement, and it's actually a fact, what we're trying to do is not necessarily competing with these agents in that $20 billion market. We're trying to expand by multiple of that market, the number of patients that we can access. So that's the opportunity that is in front of us. So maybe to spend a couple of minutes of what's stopping the penetration of many of these medicines to even just moderate to severe patients. So obviously, here, we're using asthma and AD. About 60% of patients do not have adequate control of their disease. We have topical drugs that -- or inhaled drug only target mild patients. Current oral therapy is either not active enough or have safety challenges. Biologics, again, they're associated with high treatment burden. So patients go through a needle fear fatigue often and you need to go through several injections before you reach steady state, a complex treatment initiation from some drugs, we need blood testing. So we've done a market analysis. Many companies have done this market analysis. I think the data is absolutely consistent. What patients want is, first, rapid onset of relief of their symptoms, convenience of a neural pill, no treatment initiation requirements, so no blood tests and obviously, a good safety and tolerability profile. So the data that we've generated so far on KT-621 fulfills exactly what patients want. And so this is a drug for all patients. We believe if you have a Type 2 disease, moderate to severe disease initially, KT-621 should be the first option for these patients. And this is why we believe we can expand this $20 billion market to a multiple of that number. So let's go through some exciting data. This is my favorite slide because it was my idea, but we'll see if it works out with the audience. So this was a way to try and summarize everything that we learned on KT-621 in a single slide. So on the left, we have the preclinical data, obviously, highlights extremely potent degrader that blocks IL-4 and 13 in vitro and in vivo completely and at least as well as dupilumab, in many cases, even better. In terms of safety, all the studies that we've run, 4 weeks, 4 months, we're actually about to complete 6 to 9-month talks. We even have completed embryo-fetal development studies in all species, and we have seen no findings, no adverse events. So the most compelling safety profile that I've seen in my career. In humans, we've learned a lot, some of it summarized. Deep -- a complete degradation in blood and skin of STAT6, impact on lesions of AD patients and skin, impact on each of AD patients, impact on FeNO as well as relief of asthma symptoms in comorbid asthma impact on allergic rhinitis. So in -- with 200 humans between healthy volunteers and patients, we have basically derisked the biology of STAT6 and KT-621. And now I'm going to take you through some data. So in this Phase 1b study that we reported last year in December, these were 22 patients with moderate to severe AD we looked at a series of biomarkers in blood, in skin and actually in lungs. And we saw a really robust reduction, all these Type 2 cytokines. TARC, about 74% in patients that had elevated target baseline at least as well as what has been seen with upstream biologics. Eotaxin which is the cytokine [ right ] downstream of IL-4 and 13, we've seen really robust reduction into the 70%, superior to even what has been seen with biologics in this pathway. Ig that requires much longer time to see an effect for biology reasons, we still saw a measurable effect even at 4 weeks. IL-31, which is the most important pruritogenic cytokine, Kymera was the first company to demonstrate you can actually see a reduction -- a robust reduction even after 28 days in the blood of AD patients. And then, again, another creative idea from the team, not for me, was actually looking at FeNO in -- so this is Fractional Exhaled Nitric Oxide, is a biomarker of lung inflammation. So we actually learned that even AD patients have a tone of inflammation in their lungs, we're able to reduce the Th2 tone in lungs of AD patients for the first time. So again, just looking at biomarkers effect of KT-621 shows that we have an extremely compelling profile to treat patients with Type 2 inflammation in blood and skin and in lungs. So let's look at some of the efficacy data. So one thing maybe I'll start by saying, obviously, we don't have time today to go through all the data, but the important thing about KT-621 that these two doses that 100 mg and 200 mg that had the same degradation profile gave the same effect on both biomarker or similar effect on biomarkers and clinical endpoints. KT-621 had the same effect whether you had very severe disease or if you had less severe disease. So if you had high easy at baseline or low easy at baseline, a high target baseline, or low target baseline, we had exactly the same type of impact on disease end point. And this is why it goes back to the point I made earlier, a drug for everybody. This is why this drug is so compelling because of the fact that it works just as well regardless of your disease at baseline. And also works just as well, whether you were previously on a pathway biologics like dupilumab or you were naive to a pathway biologics. So that's very important because we want to be able to offer for people that are on injectable biologics and oral auction. So here, we're looking at changes of lesions, whether you measure by EASI or SCORAD, 60% and about 50%. This is, again, in line, if not numerically superior to what has been seen with injectable biologics at day 28. We also had robust effect on categorical endpoints like EASI 50, EASI 75, each, which is the critical effect that the critical symptoms that patients have to deal with every day. We had a really robust effect. Whether you measure it with peak pruritus, NRS or you measure through SCORAD itch, we're able to see between 40% and 45% reduction. You can see in both EASI and itch, very quick impact on symptoms already a date. And importantly, in both cases, I'm actually going back here. And fourth, we see no apparent plateauing of this response. So this leads us to believe that there is much more efficacy to be seen as we continue to dose this drug. Another -- so what we're trying to treat, obviously, we're trying to treat the manifestation of the disease. But importantly, we're trying to make patients' lives better. And so this slide, together with each slide, is actually the most important slide. If you look at the left, this is the measure of sleeplessness, how many times do you wake up at night for scratching. And that is what changes people's lives. If you cannot sleep at night, you can't work, you cannot function. And this -- I believe there isn't a lot of data with other agents with this particular endpoint, but I believe we outperformed many other drugs from this point of view, even at day 8, we have really robust reduction of sleep business and at day 28 to 29, almost 80%. Also other quality of life like DLQI and POEM, really robust responders rates. So this has enabled us to accelerate the development of KT-621 and we initiated this BROADEN2 study. So Phase 2b, this is moderate to severe patients, the criteria on the left, 200 patients, 16 weeks of dosing, 52 weeks of open-label extension, three doses of KT-621, one placebo, 1 to 1 to 1 to 1, primary endpoint and secondary endpoint that are traditionally used for AD. Importantly, we have recently started to also enroll adolescence on this study. Again, it goes back to the drug for everybody. This is a disease of children, so we want to try and bring children into our development and into our label as quickly as possible. So we expect data for this program by middle of next year. So we weren't happy with, obviously, measuring AD in AD patients, we look beyond that. And we're able to validate the effect of KT-621 also in lower and upper respiratory inflammation. So we had 4 patients, small number. We have 4 patients that had comorbid asthma and we looked at FeNO, again, fractional exhaled nitric oxide. If you remember, when we look at all patients, we had about 33% reduction. Now we have uncontrolled mild asthma. So the baseline of FeNO was around 50%. So it was actually quite elevated. And we were able to reduce it between 50% and 60%, very rapidly, at day 8 already we're close to actually above 50%. So this is really telling you that our drug distributes to the lung effectively and has an effect that is as robust, if not superior, to upstream biologics. Not only we measured FeNO, which is a biomarker, we actually measured, at 4 weeks again, also impact on a clinical measure of asthma, which is this ACQ-5 questionnaire. And here, we saw all patients have a reduction of ACQ-5, that was superior than a minimum clinically important difference, which led to 100% responder rate, meaning all patients had a response to our drug. So beyond Asthma so -- lungs, we also looked at allergic rhinitis. This is a very common comorbidity for patients with atopic dermatitis. Here, we had between 6 and 7 patients that were invaluable for this particular comorbidity and also here, we had high responder rate, again, in line with what has been seen with upstream biologics. So this has, again, emboldened us and give us the confidence and the excitement to initiate our Phase 2b study today, actually, we're describing for the first time the design of the study. So -- and we've started the study, as I mentioned, about a week ago. So this is a moderate to severe eosinophilic asthma. So we're looking at patients with high eos, 300 and high FeNO, 25. This is because we know, based on the development of other drugs in this pathway like dupilumab. This is the patient population where we expect to see the biggest treatment effect. This is a dose-ranging study, about 264 patients for 12 weeks, again, 3 doses of KT-621, the same 3 doses that we're using for the AD study and one placebo and we're looking at FEV1 as the primary end point. This allows us to actually differentiate doses versus placebo in a short amount of time to allow us to move into a registrational Phase 3 study as quickly as possible. Also for this study, we expect to have data next year. So this concludes , as I said earlier, really the early translation of clinical translation of KT-621 and STAT6 targeting in patients -- in humans, I should say. So we have so much data, starting with human genetics saying that if you target STAT6, you should block type 2 inflammation and potentially deliver this dupilumab in appeal kind of profile that we like to use for simplicity's sake. We've shown in preclinical data, our ability to robustly block the pathway again completely. In healthy volunteers, we were able to show that we can degrade the target exceptionally well and have impact on biomarkers and type 2 biomarkers even in healthy volunteer with an absolutely pristine safety profile. And then now in AD patients, again, we've shown that we can degrade the target in blood, in skin, in lungs, obviously, given the effect of this biomarker. We have impacts on these biomarkers broadly. We have impact on clinical endpoints in both AD asthma and allergic rhinitis. That we have pristine safety, no treatment-related adverse events in this study. And all the numbers that you've seen today really are in line, if not, in some cases, numerically superior to biologics in this pathway is just telling you that we can block IL-4 and 13 exceptionally well. And so we're excited about obviously these Phase 2b studies and what we can do for patients with these diseases. So here's where we are today. And I think the important aspect that I want to kind of highlight is that from these Phase 2b studies, let's start with the one on top, our AD study. The goal is out of these three doses to select one that will go into Phase 3 campaigns. We expect to initiate multiple Phase 3 campaigns in parallel. And hopefully, we can use the same dose without repeating Phase 2b studies for multiple other skin indications using the Phase 3 dose that we select in the AD study. Similarly, for asthma, we hopefully will select the dose to go into Phase 3 with asthma and the same dose we can potentially use for asthma, CRS and other respiratory indications. So in order for us to being able to go into Phase 3 studies directly, in parallel, in multiple indications. And that's really our strategy that we obviously continue to bet and validate as we get closer to initiation of our first Phase 3 study, which is actually quite soon relatively quite soon. So Kymera is obviously not just about KT-621 and STAT6. I like this slide because it gives us an opportunity to look at the programs and the impact. At the end of the day, that's what we're trying to do. And we divide it across, let's say, disease areas. So KT-621, I think, is the best type 2 drug so that treats all these indications you see in the left part of the slide. IRF5, which is a program, again, will generate data this year, is really in the rheumatology space. So IBD, RA, SLE, Sjogren's, et cetera. We have a partnership with Sanofi and IRAK4, this is more Th1, Th17. And here, we're just giving a preview of a couple of programs that are close to disclosure time, hopefully, at least one of them will be able to disclose. So just to give you a sense of the areas that we're going to be looking into developing these drugs, I would say one is more focused on Type 1 inflammation and one is let's say, more focused, if you look on the right side of the slide on autoantibody-driven diseases. Again, these are all oral drugs against targets that have never been drugged with oral molecules. So this is, I believe, my last slide. So 2026, a busy year. The goal is to complete enrollment of the AD study with KT-621, continue to enroll the asthma study to generate data by '27, initiate and complete and release the data for the Phase 1 study of KT-579. As I just mentioned earlier, we hopefully will be in the position to disclose a new program in immunology that will be going into IND-enabling studies later this year. And then, again, continue to advance our partner program to important inflection points. So I wouldn't be able to do anything that I've shown you today without the amazing team that is in Watertown, Massachusetts. So I want to thank them for everything that they've done. The team here for inviting me and all of you for taking the time out of your busy schedule to listen to this presentation.

Thanks, Nello.

I took too long.

No, no, not all. Let's start the Q&A. [Operator Instructions] I'll just start off with more of a broader picture question. Can you put 621's data last -- from last month into a bit of context. I think as we think about your portfolio overall, is there -- do you see a read-through to your next work and so on? And overall, how does that derisk the underlying technology to roll out the next degrader?

Yes, a great question, Brian. I think this, I believe -- I should know this, I believe this is our sixth program that goes into the clinic. And in all the programs that we've advanced in the clinic, we've shown an absolute amazing fidelity of translation between the data we have generated preclinically and how we've seen safety, target engagement early clinical impact. And so I think, obviously, we've also learned a ton in the past 10 years. I always say that KT-621, KT-579, 485 and others that you'll see. These are -- I like to call them second generation degraders, meaning it's -- they're benefiting from years of learnings that we've had with the first programs that we discovered and then advance into a clinic. And I think the data, the 621 data, which I think for many ways that you look at it is as good as you could ever hope for just speaks to the fact that we have really absolute control on how we design these degraders and how they behave clinically. So yes, the short enter is, I think it validates the work that we're doing for 579 with second-generation IRAK4 degrader and all the future programs that we're bringing forth because all programs are following this type of strategy of high specificity, high potency and good physical chemical properties and the right targets.

And we'll take a question from the audience.

I actually have two questions. The first one is you explained the logic of like choosing PROTAC compared to the inhibitor very well. But I want to ask like what is the clinical consequence of PROTAC? Is it leading to like stronger efficacy or is leading to a less frequent dosing? That's the first question. And then second question is like we all know that DUPIXENT is doing very well with AD and asthma. So did we try to compare the maybe the efficacy on the animal test or whatever like compared to DUPIXENT?

So the first question is what can degraders offer? So many things. First, as I said, there are no small molecules that can block a target completely 24/7 because the PK and the PD relationship is one to one. And extremely difficult to have enough drug on board 24/7 to block the target. So it allows you to actually have maximal target inhibition, which should lead to blockade, which should lead to superior clinical benefits. I would also say that in many cases, not in all cases, proteins have more than one function. So when you remove the protein, you can actually benefit from removing all functions of the protein and not the catalytic function that the small molecule is able to block. And then your second question is about -- so we've done plenty of preclinical studies comparing KT-621 to dupilumab. I'm always very careful to claim superiority because dupilumab is such an exceptionally effective and successful drug. And I cannot use a few preclinical studies to claim that we're a better drug. All I can say is that in these preclinical studies, when we degrade the target 90% or more, we see an effect that is at least as good as what you see with the saturating dose of dupilumab in these models. But we're still close to generating robust placebo-controlled clinical data. And so I would love to use that data to delve more into these comparisons. I like it. We have audience. I never get audience questions in this day and age. So thank you.

Thank you for your presentation. So I have two questions. The first one is we noticed that you have a QD but I also noticed that you're empathizing the lasting effect, especially for asthma [indiscernible] efficacy. So do you have a plan to do QW dosing?

So a great question. Actually, you also asked a similar question. I forgot to answer. So the question is, yes, the -- sorry, I'm not used to repeat questions. I apologize. You guys have all heard the question. So QD is what we believe to be the most commercially viable dosing paradigm that we believe, based on analysis, will allow for maximum compliance. We know if you look at our data in Phase 1, we know that actually one dose of KT-621 is able to retain maximal degradation for multiple days. So it is possible that you could dose less frequently. It's not something we're exploring clinically today, but it's something that could be explored at some point.

So second point is just my curiosity because degrader and the PROTAC and the molecular glue noticed that's the first one that's [indiscernible] as PROTAC and CDK2 is molecular glue. So what's your basic criteria some technology to which one you would choose for which target [indiscernible]?

Yes. Excellent question. very simple answer. It's really, really driven by the problem we're trying to solve. If we want to degrade a target that we can find a small molecule binder for selectively. There is no better technology that heterobifunctional integrators, you have complete control of specificity and of the mechanism. If we cannot find a specific binder to the protein X or, for example, for CDK2, we cannot find the specific binder that is specific for CDK2. As you know, there is high homology between CDK2 and CDK1 so we choose this protein-protein interaction enabling technology, which many call molecular groups. So that's how we separate the two.

Well, thank you so much for your time, and that's all the time we have. Thanks for coming.

Thank you, everybody.

Thank you.