Okay, good afternoon. We'll continue with the next session. I'm Paul Choi, and I cover this mid-cap biotechnology sector here at the firm. It's my pleasure to welcome BridgeBio for this session. From management, joining us is founder and CEO, Neil Kumar. What we'll do is Q&A. If any audience members along the way have any questions for Neil, please feel free to raise your hand, and we'll try and get a mic to you. But maybe before we start with Q&A, Neil, maybe if you wanna provide any high-level comments that you think are of interest. Otherwise, we can just go into Q&A.
Yeah, sure. Happy to. First of all, thanks, everyone, for the time. You know, I think our strategy writ large over the next 18 months or so is informed by two inputs, really. Number one is our continued belief in our late-stage pipeline of phase II or phase III assets in $1 billion+ markets, and we can talk about those, but those are five specific assets inclusive of our TTR cardiomyopathy program, all of which have catalysts in the next 18 months. The second input is that we're at least planning for a very rough tape and a very rough market through the end of next year. What that leads you to is kind of a simple equation of trying to cut burn where you can so that we have a strong cash position.
We've reduced burn through layoffs, fixed cost reductions, et cetera. We've attempted to partner non-essential assets. Those two things together have led to increased runway, about $850 million of cash on the balance sheet, and I think we have opportunities to further that. The final piece of the equation is to deliver solid data. We've started that at the beginning of this year with one of our value driver assets with LGMD2I/R9 proof of concept that'll be moving into a phase III by the end of this year. Last week, we announced positive proof of concept data for our ADH1 program, which also will move into a phase III, likely to read out by the end of next year.
That's kinda how we put it all together, and yeah, happy to answer questions on any of the specific programs or strategy writ large.
Okay, great. Probably, you know, since your top-line data last year and in the ATTR top-line data and, you know, potential competitors' data coming up in the not-too-distant future, the ATTR market obviously is a very high focus point for investors. Maybe, you know, as you've had more time to think about it, you and the Ionis team have looked at the Part A data, is there anything that you would, you know, say now with additional, you know, hindsight of anything that had been determined with respect to the trial conduct, execution, or anything like that or any of the, you know, patient criteria from your perspective that baseline factors that stand out and with subsequent analysis or looking backwards?
Yeah, great question. I mean, I think our primary focus to date has been on Part B and its fidelity. Just as a reminder, we have a nested trial design. Part A was a 12-month readout on six-minute walk, and then Part B is a 30-month readout against mortality and CVH. What we really wanted to do in the first couple months of this year was to look at blinded, blended rates of mortality to ensure what occurred at Part A does not occur at Part B, meaning that we actually have a measurable deterioration against which we can show the drug's activity.
We can walk through it, but I think the conduct and the fidelity of Part B looks good to us so far, meaning a blinded, blended review of mortality at the end of February suggested that death rates were in line with what we would expect from ATTR-ACT and certain of the latest natural history studies that have been published when one corrects for the two-to-one randomization, the moderately more healthy population in class 2 and the hazard ratios that change from class 3 to class 2 to class 1. You know, we had, as I think I've mentioned at JPMorgan, low single-digit levels of TAF drop-in and dropout rates consistent with ATTR-ACT. Everything felt good in terms of the ongoing trial's fidelity.
Furthermore, as we looked at Part A data, it seemed that six-minute walks was discrepant to everything else that we were seeing. As you and I have discussed, we hit on all the rest of what we could measure, inclusive of BNP, which seems to be as good as any a univariate predictor of mortality, serum TTR, quality of life questionnaire, and then we had a 27% reduction in AE-driven death. Against everything else that we could see, it looked fine. Against six-minute walk where it did decline, like in the variant population, we also flatlined it against a -40 declination. Overall, in six-minute walk, we just didn't see a declination against what a healthy volunteer would do.
The question becomes why, and, I'm afraid I don't have a clear answer to that. It's at least one of four hypotheses. You know, the first could be context and training bias, which we could get into. The second is an evolving standard of care, which I think at least plays some role, based on a recent publication, you know, recent-ish publication from the National Amyloidosis Centre, suggesting also an 11 m decrement over 12 months, which was published after our trial started. You know, fewer really control meds, you know, greater and more aggressive use of diuretics. You know, there could be some COVID-oriented changes, less salt in the diet, something that could affect stroke volume. That's very speculative.
The fourth could be obviously the standard deviation of the endpoint is almost twice that of the mean, and we could have just drawn an unlucky card. I think we'll learn more about it from, as you mentioned, the competitive landscape, and especially APOLLO-B in the next coming couple months.
Okay. Great. Maybe looking ahead towards the Part B data readout. Under a scenario where the result is positive, you know, how do you think about maybe next steps and your approach to market as, you know, theoretically the second entrant in terms of the stabilizer category? You know, what is your sense of the market outlook with a potential Tafamidis generic coming in the later part of this decade?
Yeah, great question. I think that there, both from our market research as well as from analogs that one might look at in the cardiovascular space, be it the statins or the ACE or ARB, hypertensive categories, you know, a 15% relative risk reduction or more would be considered, I think, superior, as a superior product. In that context, I think we have a pretty solid commercial plan and, you know, I think you'd take a majority of the market share there.
Whether or not one would wanna run in addition to a primary prevention study, some sort of head-to-head potentially in a variant population or something like that to continue to be used post the genericization of Taf, which in the U.S. could occur as early as 2029, although my suspicion is it would be later just given some of the IP that they filed around manufacturing and use. I think we would look at that if we were superior. If we were a me-too product, obviously those things change measurably. This is, you know, obviously the goal of the program here is to provide a relative advantage to Tafamidis, in which case I don't think genericization of the first statin didn't affect Lipitor all that much.
I think you see that in cardiovascular categories as long as you're demonstrably better.
Good. Maybe just in terms of the market dynamic, what are you seeing with regard to the monotherapy utilization versus their combination drug for Vyndaqel versus Vyndamax? You know, how does that factor into your thinking about the market dynamics outside of, you know, the data results?
I mean, they're moving everyone to the 60/1 mg formulation. I think you know, it's only really in Europe where you would think that the 20 mg approach might affect genericization in an earlier timeframe. You know, they're basically moving everyone over there too. It'll be yet to be seen kinda how they deal with that earlier generic window.
Okay, great. Just maybe just lastly on commercialization. How do you think about scaling up and access for Acoramidis when it comes to the market?
Well, it's two very different scenes actually, in Europe versus America. You saw that Tafamidis was actually growing, I think, at 10% clip in Europe and now has more revenue, I think, on an annual basis in Europe, despite not even being available in the U.K. and Spain, I believe. That's because there's a certain price and obviously decreased mortality by 30%. In the U.S., you have the challenge of the Medicare Part D population and, you know, $13,500 or so, if not more, copay, that's not immediately addressable through foundations and, absent any Medicare Part D reform, foundations is really the only way that you can pay for that.
Some 14,000 scripts, I think a minority of them, are being filled right now, just given that gap. I think you can do what you can on the copay commercial coverage side, and then you'd wanna just price responsibly so that you could capture more of the market on the Medicare Part D side, absent any sort of reform.
Okay. There are obviously a lot of moving pieces at Bridge, and you have a very large portfolio. I want to touch on something that you mentioned earlier, which is, you know, pipeline prioritization and just thinking about the cost base here? Can you maybe tell us what's the additional thinking about, you know, potentially partnering up other assets or out-licensing them altogether or perhaps asset sales? And is there anything from your perspective that as investors or analysts we should think about that you'd wanna, like, rationalize or perhaps deprioritize?
Yeah. I think, as I mentioned, we sort of have this barbell approach. When we look at what we can afford, the right-hand side of the barbell are the five large products that we have in phase II or phase III That's ATTR cardiomyopathy, achondroplasia, ADH1, LGMD2I/R9, and then our gene therapy for congenital adrenal hyperplasia. Just two of them have proof of concepts this year. Encaleret proof of concept coming late July, early August. CAH proof of concept coming late this year, early next year, and then a couple of phase IIIs after that in the year to come.
When we couple that with our early-stage research franchise, which is pretty lean, we sort of pride ourselves on being able to do cheap, valuable research, and that's really helmed by our KRAS franchise, which should have its first compound in the clinic next year, and two development candidates this year. That's pretty much all we can afford to do. Everything else that's in between, I think you can expect from us to seek partners. The six announced programs that we put out in our latest earnings report that we're seeking partners on, we immediately cease spend on those. We have, for five of those six programs, term sheets or long-form docs. I expect we'll be able to find solid partners for them.
Then there are some other programs that we haven't talked about partnering, but if we had NPV positive term sheets on the table that we would take them, and I suspect we'll be able to find partners like that. Yeah, I mean, all collectively, what does that do? It's not gonna be a huge amount of upfront. You know, I think $50 million-$100 million in aggregate additional onto the balance sheet of $850 or so right now. But it alleviates close to 20% of the burn, which I think is gonna be important. You know, just to go back to that first equation, it's really putting the entire picture together. We wanna be able to play those five bets out.
We wanna continue to be able to do early-stage research because we think we can do that and create real value. Then the in-between, it's like, you know, get the burn down to $100 a quarter and really focus on getting that balance sheet. It's at whatever, it was $650 at the quarter. We did the BMS deal and sold our PRV, so it's about $850 and continue to buttress it.
You talked about a barbell shape distribution, but I want to maybe ask about one asset that you didn't mention, which is in the middle there, which is your RDEB program. There are some, you know, relative to the later stage or near commercial stage programs, assets in that particular indication that are just getting up and running here. How do you think about that particular program, just given the data you've shown, which looked, you know, certainly promising on certain metrics?
Yeah. Again, I mean, I think it's a in a different environment we quite like that program and continue to think it has, you know, could have huge usefulness for patients. I mean, obviously the decrease in pain, the systemic nature of it, I think it's a really nice backbone therapy in this space. I just think it's a pretty heavy competitive space, number one. Number two, more importantly, it's pretty high CMC cost. I think people should expect that we're gonna find a partner there to move it forward. You know, there just are programs like that it's not like when we part with a program, we think the science is somehow less strong than it was, you know, a year and a half ago.
It's just we're at a very different environment right now with a very high cost of capital, and the waterline is moving around and there could be better partners out there for us.
Okay. You know, I think probably a question you get frequently is just thinking about your capital structure and your pending debt obligations. You've talked a little bit about pipeline prioritization and managing cash burn here, but you know, what other factors or pushes or pulls could you speak to that would help you address your outstanding converts that down the road, and how do you think about managing for that in the future?
Right. Just as a reminder, as part of the BMS deal and putting the $200 million on our balance sheet, we also kicked our debt out for a couple of years in return for relinquishing $200 of the $300 available that we could pull at a 9% cost of capital. You know, that was a little bit of a yin and yang 'cause 9% cost of capital sounds pretty good right now. But I think, you know, the added debt load is not something that our equity investors are keen for us to access in the near term. What does the debt load look like right now? It looks like $27 million and $29 million debt, with $27 million being the first of that $450 million senior secured.
Between now and 2027 we have seven phase IIIs reading out, including all of those core assets that I talked about, achondroplasia, LGMD2I/R9, CAH, TTR, and ADH1. You know, on a risk-adjusted basis, we should be well able to service that debt handily, unless we're bad at picking assets, in which case, you know, we're not. The company's not creating value commensurate with what it was supposed to do. We feel pretty good about that. And then a number of proof of concepts in the interim as well. Yeah, that's kind of how we're thinking about the capital structure.
Okay, great. If there are any questions along the way, just remind the audience, please feel free to raise your hand and we'll get a mic to you. Maybe continue with the pipeline. Otherwise, can you maybe, you know, help us think through the upcoming ACON data that you mentioned would be possibly in July or August? What in your mind, you know, from a mechanistic perspective, gives you confidence in infigratinib's role here? I guess, you know, what would you consider, I guess, a good result in the context of the approved therapy that's out there from BioMarin?
Yeah, good questions. Just as a reminder that the disease is uniformly driven by gain-of-function mutations in FGFR3, and we're inhibiting FGFR3. Mechanistically, the theory of the case would be that we are targeting the disease at its source, and in doing so, targeting both of the key effector pathways that are responsible for chondrocyte differentiation and proliferation, which are the MAPK signaling pathway and the JAK-STAT signaling pathway. That should lead to an advantage. It did lead to an advantage in preclinical mouse models, a significant advantage, almost some 4 times, on the long bone growth and effects on things like spinal stenosis or things that are tied to that had not been seen with some of the other therapeutic interventions like BioMarin's.
In terms of the approvable endpoint, you're talking about average growth velocity, and the bar there for BioMarin is 1.35, with a single daily injection. You know, in cohort 4, as we read out here, in the summertime, we'd like to be around BioMarin levels in terms of AGV, with a safe once daily oral. We think that's a very competitive profile. In addition, if it's safe, the hope is that the agency would allow us to dose up to the next cohort 5. You know, if it's 5 safe, we can keep going because, you know, the theory of the case is, you only get one chance to find MTD, and that's phase II.
Continue to squeak out more and more efficacy as we move up. Based on preclinical modeling, we should be right around that AUC of 200 animal hours in cohort 4, which should put us around BioMarin efficacy in four already.
Are there any learnings from the Voxzogo launch to date in terms of real-world utilization, patient feedback or parent feedback or physician feedback that's informing your clinical strategy for Infigratinib, even as you continue the dose finding and the dose escalation work?
I mean, it seems to me that it's early. The launch is still early, but I think they announced that they were trending toward $110, which seems like a strong launch to me, even at that elevated price point. You know, that's consistent with the fact that most parents in this space are experiencing de novo mutations with their children and very keen to do what they can to help their children. I guess my learning from that would be that there is a real appetite for medicines that could make a difference here. Secondly is, you know, we have presented some recent data around hypochondroplasia at ENDO, which is a similarly sized market honestly to achondroplasia.
Different mutation in FGFR3, a slightly lower amount of elevated signaling through those two effector pathways. There's a lot of attention within the skeletal dysplasia space to these medicines and an appetite for therapeutics as I think BioMarin is proving out. Yep.
You touched on something interesting, which is, you know, you are focused on lead indications with your early as well as your later stage pipeline, but, you know, you as a management team are clearly thinking about lifecycle management as well as expansion indication here. Maybe, can you touch on that and just, you know, you mentioned one for example for Infigratinib, but what are other areas where you potentially see adjacent opportunities that investors may not be mindful of?
Yeah, I mean, I think they follow in kinda two categories. One is where the mechanism quite obviously is relevant to an adjacent disease. The other is if you're going after a homozygous, you know, recessive disease, for instance, the heterozygous loss of function population might be of interest. You know, maybe in the former, we talked about achondroplasia and hypochondroplasia. We're also exploring uses of our ADH1 calcilytic agent in the context of hypopara, which is, you know, somewhat obvious there as well. In the second category, we have our primary hyperoxaluria type one program, a GO inhibitor, that's, you know, a uniform loss of function in AGXT.
There's a frequent stone former trial that we're also setting up to run in a heterozygous loss of function AGXT patients or just high oxalate patients there as well. Room to expand on all those dimensions that I would say. You know, finally, our hope still on ATTR cardiomyopathy is that we are able to come back to a polyneuropathy trial in a different era and in addition to interrogate that in a primary prevention setting. Lots to do.
Okay, great. Maybe turning to another modality and as well as another disease state, CAH and your gene therapy program efforts there. There are, you know, different approaches to this disease, including, you know, approaches targeting CRF from Neurocrine and Spruce. But in the in that context of those two later stage programs, you know, how do you think about what is considered a good result for a gene therapy approach? As you have data, potentially, as you mentioned, later this year, you know, what would you view for this particular population as a good clinical outcome for your initial data?
Yeah, good question. I think with the Neurocrine and Spruce approaches, they're targeting the upstream part of the pathway which shunts over to you know, aldosterone and testosterone production. What they're not doing is replacing what's missing in this case, which is 21-hydroxylase. By virtue of that, they can't affect you know, I would say half of what is driving this disease, which is the depletion of endogenous cortisol production. What they're showing obviously in their data is reductions in 17-OHP, which are you know, marked and consistent from the adult to the pediatric setting. Hopeful. It's not entirely clear, though, how those port over to reduction in steroid use.
I think that for us, obviously the endpoint and the thing that we're really gonna be focused on is production of endogenous cortisol. I mean, that is the home run hit if we're showing analogous 17-OHP reduction and that alone, that would not be interesting as a gene therapy. I think in that case, there's obviously a one-to-one correlation between elevated endogenous cortisol and not having to use exogenous steroid.
Okay. I guess as you look down the road and think about a potential pivotal trial design here, what does a phase III trial look like for gene therapy in CAH? Assuming positive data there, how does the market there for a gene therapy in this what is a relatively large orphan disease or rare disease population shape out to look like?
Yeah. I think the phase III is gonna have the endpoint of steroid sparing or endogenous cortisol elevation, probably both. I think it will be relatively straightforward. You know, one thing I can say is, you know, I've come to realize that human function doesn't necessarily read the science textbooks. I sort of like these endpoints like we have in ADH1 serum and urine calcium agreed to with the FDA, running a registration trial that reads out next year. You know, percent covariance. It's like you take the drug, if the drug works, we should get a positive result there. Same thing with CAH. Now, we don't know whether. We haven't had a proof of concept, so we don't know whether the drug is working in that context yet.
If it does, I would say the translatability to phase III would be pretty high, and I would expect that would be the endpoint. In terms of the commercial market, I think you could think about it in terms of being more and more important the younger you go. Certainly, you know, children that are exposed to the vagaries of adrenal crisis would be the initial and very interested market. I think we've seen some demand all the way up through older patient population, which is, you know, in aggregate 75,000 people or so. I would say it would skew toward female versus male as you grow older.
You know, we could talk specific numbers, and we've tried to break it out by demand per decade, but I think that's generally a good set of rules.
Right. Maybe more of a theoretical question, but since this question comes up with gene therapy approaches to hemophilia, sickle cell disease, and beta thal, you know, what would be, I guess, in your mind, a good durability outcome on a gene therapy for CAH, conceptually?
A couple of years or more. No. I think. Yeah, less than that, I mean, maybe it would be interesting for people who are immediately, you know, facing adrenal crisis in their youth, but no, it'll be disappointing if it were just a year, per se.
Okay. I think, you know, maybe one of the most overlooked assets in your portfolio is in limb-girdle type 2I. Can you maybe just remind us, you know, what data you've seen so far or shown us so far, and just how does that contextualize for that particular population of limb-girdle, given I think that most people are probably familiar with the Sarepta program in a different area of limb-girdle?
This is the most common of the limb girdles, as far as I know. Sort of out there working on 2B, 2D, and 2E. 2I, which is the one that we're working on, that's uniformly caused by loss of function mutations in FKRP. It is partially active still, not whole loss of function, is about 7,000 patients between the U.S. and EU, and quite a few already identified patients. Like, I think at one of the centers that we were on, VCU, there's about 110 patients already, in a natural history study for a single center, and the trial enrolled very quickly. Reasonably large patient population. You know, the disease happens to be caused by an absence of alpha-dystroglycan glycosylation.
What you can see from the natural history studies as well as the mouse work and preclinical work that's been done is about a 10% increase in glycosylation should drive a therapeutic effect. We ran a phase II clinical trial recently, a six-month trial, and we showed that we were getting about 42% increases in alpha-dystroglycan glycosylation by providing effectively more of the substrate of this enzyme that's you know not working quite as well as it normally does. Simple substrate replacement approach rectified the absence of glycosylation, also decreased creatine kinase levels 70%+. I think the nice thing in that data set was there was a nice correlation between an increase in glycosylation and a decrease in creatine kinase.
You know, you gotta take this with a grain of salt because it was effectively an open-label study. We followed these patients as they came in, and they compared their baseline 10 m walk times and modified North Star to what they had shown before. They were all deteriorating before, and on drug, they were slightly improving. So yeah, that's over six months, but still heartening. I mean, I think all of the data were headed in the right direction, and it set up a very productive discussion with the FDA. The first of many, I think, over the course of the next six months that we'll have, and we continue to anticipate pursuing an accelerated approval in this space based on alpha-dystroglycan glycosylation.
Yeah. You've developed with ribitol and what I would characterize as an elegantly simple solution to what is a, you know, complex disease. Could you maybe speak to some of the other competition in this particular area of limb-girdle, particularly with respect to other modalities? Do you view the, you know, the strategy that you're taking here with ribitol as sort of like setting an efficacy barrier that you view as, you know, challenging to overcome?
An efficacy and safety barrier, I think. Efficacy, I don't know if there would be much, you know, more to be done in terms of glycosylation. The competition in this space, which is just entering the clinic now, is gene therapy. The issue is that you can have too much of FKRP, and that can drive significant toxicity. You know, these types of Goldilocks problems haven't been quite solved elegantly by gene therapy, so you've got that safety issue combined with the fact that, you know, if you have a relatively safe and efficacious substrate replacement therapy, I'm not sure why you go the gene therapy route.
There's also, you know, other mutations that occur upstream, that could also be, you know, treated with gene therapy and then downstream mutations that could be very interestingly solved with our substrate replacement therapy. There's a couple diseases there that we would either include some patients, like Fukuyama and some others in the registration trial or look to follow up with, you know, phase IV trials post our first LGMD 2I/R9 trial.
Maybe at a high level, those adjacent populations, how does that theoretically expand the TAM in your mind for ribitol?
Probably by about 1,200 patients, 1,200 to another 2,000. You know, it's the chunk of it is still in LGMD2I/R9.
Okay.
Yeah.
Great. We're coming up on time, but I wanted to spend a few minutes on Encaleret here. You just provided an update. Maybe you could provide a recap for the data that you recently presented here at ENDO, and then just how that has figured into your regulatory discussions for your planned phase III?
Yeah. Really exciting data. This is one of the more exciting programs I think that we're working on. ADH1 is a disease that's uniformly caused by hyperactivating mutations in the CASR, calcium sensing receptor. We're just basically have a negative allosteric modulator of that receptor. What we had shown in an inpatient setting that we then expanded to the outpatient six-month setting in this most recent bevy of data is that we can normalize both urine and serum calcium levels for these patients. What the standard of care doesn't normalize anyone. It's 0%, as we saw, from our run-in, and that makes some sense because you're taking vitamin D and calcium supplements. Even if you're addressing serum calcium, you're actually exacerbating the urine calcium elevation in many ways.
You know, the mean of both urine and serum calcium were fully normalized, some 80%+ responder rate. We took that data to the agency and had a good discussion with them about what a registration trial should look like. You know, we're pleased to come out with effectively endpoints that are serum and urine calcium randomized against a standard of care arm. That's a fairly straightforward trial that we expect to start enrolling sometime this year and to read out late next year.
Yeah. I agree. Seems like a pretty good line of sight through what is largely a similar phase III relative to your phase II.
Yeah.
A line of sight to the regulatory stage. Can you maybe talk about how these patients are identified? You know, what is the, you know, current market landscape or treatment landscape like in terms of patient identification and, you know, how you think about the build-out and, you know, promotion of Encaleret here in the market?
Yeah. Right now there's about 3,500 patients that are identified, which is just a small minority or a fraction of the some 12,000 patients that are thought to be prevalent within the United States alone. We get to that through four different of the statistical genetic databases. That's a fairly consistent number. Right now, they tend to be diagnosed based on acute symptomatology, typically due to the low serum calcium. Fainting, seizures, things of that nature. You know, in a future state, the hope is that we can pick up many more of these patients because they're likely to be hiding within the hypoparathyroidism population. There is a test that we're conducting alongside Invitae, who is our partner here, where one can run a panel.
We had published some recent results—not we, sorry, another group had published some recent results suggesting 13% of a hypoparathyroidism population within the healthcare system actually had ADH1 or hyperactivating mutations in the CASR. I think that would be the next round. I mean, interestingly, you know, while most of the patients that we pick up today and most of the patients writ large of those 12,000 are moderate to severe, even mild patients go on to have a lot of the symptomatology associated with the high urine calcium levels, so nephrolithiasis and CKD toward the middle and end stages of their life. I think there's a role for this medicine in a lot of different patients, if we can find them.
Okay. We're almost out of time here, but Neil, maybe just to touch briefly on the earlier stage pipeline. If you had to call out a single asset that you would suggest investors follow closely over the next 12-24 months, you know, who would you pick as sort of your favorite child from the early stage program?
I think that we're really focused right now on trying to simplify the story and it's those big five value drivers that I mentioned, plus KRAS. I suppose that would qualify. I think we have a very interesting GTP-bound G12C inhibitor that'll head into the clinic sometime mid-next year. Then we have a SHP2 breaker program as well that should head into the clinic a little bit after that. So those I think are interesting, and we're gonna publish more data on those in the next coming months. But outside of that's really where we want people to focus and that's really where we wanna focus as an organization to deliver some good, clean wins for investors so that we can, you know, kinda start to build our way back.
Okay. Great. We're out of time, so my thanks to Neil and BridgeBio, and we'll end the session on that note. Thanks, Neil.
Thanks.
Thank you.