Krystal Biotech, Inc. (KRYS) Earnings Call Transcript & Summary

Okay. Great. Well, thank you, everyone, for joining us today. We're at the 120 session here on day 2 of the Goldman Sachs Global Healthcare Conference. My name is Graig Suvannavejh. I cover U.S. and European biopharma for the company, and I have the pleasure of hosting Krystal Biotech, a really innovative company out in the Pittsburgh area. And with us today is Krish Krishnan, who's the Chief Executive Officer. And so Krish, thank you so much for joining us today. We've got about 40 minutes and hopefully, we'll make this an entertaining discussion for all. Maybe before we go into kind of formal questions during our fireside chat, let me first obviously welcome you to your first Goldman Sachs healthcare conference. Hope you'll be joining us for many more years in the future. But for those who are perhaps newer to the Krystal Biotech story, maybe let's start with you giving us kind of a little bit about Krystal, when and where the company was founded? And perhaps, if you could, from a high level, get us up to speed on where the company is focused today?

Graig, thanks for having me at the conference. Sure. So we are a gene therapy company, meaning that we are trying to solve problems caused by generic, by issues passed by a single gene. So we go after monogenic skin diseases. And instead of trying to fix the gene, we actually try to supply a replacement copy of the gene to kind of treat the monogenic disease and express the required protein. And the way we deliver that gene is using a modified herpes simplex virus 1 vector, which is -- the majority of the gene therapy programs is focusing -- seem to be focused on AAV. But when we specifically are going after skin diseases and the skin genes seem to be big and not easy to package within the confines of an AAV or an AAD vector easily or a lenti vector for that matter. And so HSV-1, having a huge payload capacity fits really well and nicely, especially when going after large diseases involving where the mutated gene is large, and skin was a great place to start. The company is based in Pittsburgh. And in terms of how we came about this approach and the diseases and indication, we actually did not kind of stop the HSV and try to figure out what indication to fix. We actually were looking at this one indication called EB, epidermolysis bullosa. And we thought that the company's pursuing ways to treat that disease were using somewhat of a cumbersome, autologous approach to treating the disease. And when I say autologous, that implies that the treatment is specific to the individual that something is modified in the treatment that makes it unique. It's kind of custom made. And we thought maybe there is a way to deliver these genes directly to the skin to come up with an off-the-shelf allogeneic approach to treating the disease. And in search of finding the best way to do that, after a couple of failures using MRNA and plasmids, we came across this vector, HSV-1. And what's unique about the story is not as much the HSV-1, not as much that it's the monogenic skin disease. But the idea of thinking about HSV-1 to go after monogenic skin diseases was something that had not been contemplated before. And I think a lot of that came about because of the way we came about founding the company. And once some of the data readout proved out with respect to DEB in the Phase I/II study and even a bit earlier, we then realized to, look, the same approach can work for a variety of monogenic skin diseases. And more recently, we are trying to also imagine and work towards diseases that are not specific to the skin, but have the same mortality in other areas such as pulmonary indications, where the genes are pretty big, the cells are epithelial. And if you could find a way to get the vector to that location, maybe the mechanistic approach would be identical. So that's a quick overview of the company. We're about 65 or so employees. A strong -- we come from a very strong science background. In terms of being very operational focused. We have one GMP facility up and running with -- and having broken ground in a second GMP facility. We're in the early stages of building out a commercial team. So the goal of the company is to be a fully-integrated rare disease company, starting with a huge concentration in skin, but slowly migrating towards pulmonary and other areas.

Man, that sucks. It's a fantastic overview. I appreciate that. I think the first question that I typically get when it comes to Krystal Biotech is really your choice in vector. I know you touched upon HSV. When most investors look at the gene therapy space, they're typically thinking about AAV and perhaps even novel AAV vector design. And then there's also lentiviral-based approaches. Again, you spoke a little bit about kind of the unique properties of HSV. But perhaps if we could drill down a little further, maybe we can compare/contrast why HSV does seem to be the best vector for at least the diseases that you are looking at?

Yes, definitely. So as I mentioned earlier, look, we came from the disease trying to find the perfect delivery vehicle. The skin genes tend to be big. They're at least 9 Kb or more. And so even if you try to squeeze fit into an AAV or a lenti vector, it kind of forces here to take an autologous approach to treating the disease. And so one of the most important attributes, which I just talked about is the payload capacity of HSV-1. It has a payload capacity of about 150 Kb, which means pretty easily you could package 30 to 35 Kb into the backbone without stressing the virus and being able to scale it up pretty nicely. And the other thing with respect to skin cells is skin cells turn over pretty fast. And when you have a fast turnover type environment, unless you find a stem cell, having an integrating virus really doesn't do you that much good. So 1 of the other attributes of this particular vector is that it has huge tropism to the skin cell, which means you get -- and we've seen that in our studies, we get like 98%, 99% transfection efficiency. So HSV, pretty much when it comes into contact with cells and the skin, seems to transfect every cell it comes into contact with. The third attribute being that the vector is inherently episomal, meaning it does not integrate into your DNA, which is, again, great for skin because skin cells turnover relatively fast. And this vector, while it does get into the nucleus, can sustain the nucleus without disrupting your existing DNA, which from a long-term perspective, one could argue, minimizes the risk of oncogenesis. Because any time you disrupt DNA, it has big implications to the company in terms of having to track the patient for life, constantly worrying about what could happen, what may happen in the future. And so an episomal vector kind of minimizes that risk. We -- and HSV-1, even though it's kind of new to this gene therapy kind of space, has been around for a long time. There's a drug called T-VEC Imlygic, an Amgen drug has been in the market, marketed 4, 5 years, it's HSV-1-based. And so there's a lot of literature, not just in the approval of Imlygic but also in past failures where people thought, hey, we could use this vector to go after neuronal indication. So there's actually a lot of literature. So it's easy to understand how to make modifications to the virus that's -- it's kind of well established. And one of the other attributes we have is it's nonreplicating. So in our case, we're talking about a nonreplicating, nonintegrating virus that essentially serves to perform 1 function. Get into the cells efficiently and deliver the gene. And once the gene is delivered into the nucleus, the cell machinery does its job of translating that DNA into RNA and the required protein. So that's another interesting property. So to summarize, huge payload capacity, great tropism to the skin cell, nonreplicating, nonintegrating and now that we are in GMP, the scale-up manufacturing of HSV, especially in the upstream side, tends to be a lot easier than AAV lenti. The downstream is pretty similar. But on the upstream, being able to pack all the deletions into a single cell line and do a single transfection as opposed to AAV scale-up where every deletion is an individual GMP plasmid and co-transfected, causing a lot of variability. That's another important attribute. And last but not the least, the fact that a replicating version of this drug, which is T-VEC, has been given to patients week after week for the last 5 years without any black box implications or immune response or -- and even if there were an immune response, it doesn't seem to affect the efficacy of the drug. That gives us also a lot of confidence that this can be chronically administered.

Great. That was a great overview, and I appreciate that just on the choice of HSV and all the properties. You did touch upon in the last bit of your response there, my next question, which was going to be just around immunogenicity. It's a question that I've gotten from investors who are particularly thinking about in your at least lead indication or lead applications, which are going to be almost topical applications of gene therapy, which is so very unique. But the idea that there is going to have to be repeated applications and thinking about HSV, can you kind of walk us through perhaps some of the reasons why immunogenicity should not be an issue with your programs?

Yes. Definitely, definitely. Look, the first point I want to make, and there are a few points on this matter. HSV is inherently adept at somehow evading the immune system. And I'm talking about the wild type. And as you know, 90-some-percent of the people are -- have antibodies to HSV. There is a gene within the vector called ICP47. And what ICP47 on the vector does, it tends to avoid the innate immune system. Innate immune system is one that a host uses usually immediately or within a few hours. Innate has got 2 kind of segments, 0 to 4 hours and then 4 to 96 hours. And what ICP47 is able to do, and this is well established, it's not something we had to do is HSV avoids the innate immune response to the -- avoids innate immunity. The second thing you should know is -- and that usually goes somewhere between 0 to about 96 hours, but it could be, give or take a few. If you see the way our vector works, it transfects in a matter of 4 to 5 hours. When I say transfects, it's in the nucleus of the cell in a matter of 4 to 5 hours. And the protein, which is the outcome, is secreted within 24, 48 hours. So within about a 48-hour time window, the vector has done its job, knowing fully well that for the first 96 hours, the vector avoids the innate system anyway. And realize that given the high transfection efficiency and the fact that the vector is inside the nucleus, it's not free floating in systemic circulation, which I'll come to, I'll talk about that in a minute. But the vector has done its job within about 24, 48 hours. So that's with respect to innate immunity. Now if you talk about adaptive immune system, which is like, hey, what happened -- maybe something -- now we're talking B cells, T cells, what happens, delayed? And here, look, from a functionality perspective, we don't particularly care if there was a delayed response, but what tends to happen is to take in the 12 or 13 patients we have treated, we have repeat dosed several times, not just with respect to B-VEC, also with respect to KB105, and we found that we've been able to restore expression without any compromise or issue at all, like -- and on coinciding with showing expression, immune responses tend to be somewhat visible in the sense that you will -- the patient will emit some kind of chills, fever, swelling, maybe. It's not like a silent immune system, but especially in an open skin, and we haven't seen any adverse event on the patient today, drug-related to date on the [ 12, 13 ] on either 103, 105. That's another indicator that, look, we've done it a few times, this issue is behind us. And of course, we have the T-VEC thing to look back at, which is a replicating version of HSV and has been given weekly to patients. I know it's a bit different. It's melanoma. It's not exactly identically EB. But between some of the genes we have removed from the vector, given some of the teams we have retained like ICP47, given we have repeat dosed both in 103, 105 without much issue, without seeing any kind of adverse event, that gives us a lot of confidence that we can continue to administer this drug on a chronic basis. Now there are people who have asked me, Graig, how do you know in 5 years, what would happen? But usually, immune responses, if you're past the first, second, third month, they don't -- and I'm not an expert in this space. But if you don't see anything in the first 0 to 3 months or so, it's unlikely that a few years later, something is going to pop up. But to date, we haven't seen anything. We've treated a bunch of patients, both on 103 and 105, and we're able to repeat the show, repeat expression. And maybe it has to do with 47. Maybe it has to do with the fact that the speed of transfection is high. Maybe it has to do with the fact that there's not much floating in the systemic circulation as we have observed in our bio-shedding studies. There are many ways -- so it's a bunch of dots that -- but there's not one particular reason I can give why. It's a combination of several factors that allows us to evade the immune system and apply the drug chronically.

Okay. This is all great context in terms of thinking about the vector and your platform and maybe as we find ourselves almost halfway through our presentation. Let's turn to your lead candidates, your assets and your most advanced asset is KB103, which is now being described as B-VEC. And certainly, it is going after an orphan dermatology skin condition, EB. And so I'm wondering if you could provide an overview, kind of, of 103 or B-VEC and the data that you've seen thus far, because we are expecting a pivotal trial to -- that's basically where you are right now, you're about to go into a pivotal trial. And so let's talk about that asset and what makes you excited about B-VEC?

Yes. So I have a lot of things to say, and I'll try to speak a bit fast and try to cover a lot of material in short order. Look, it's a disease caused by imitation in a gene called COL7A1 which produces a protein called COL7, collagen VII. Collagen VII holds the 2 layers of your skin together, the epidermis and the dermis. And when you have a mutation in COL7A1, the skin is not held together and hence causes these really debilitating skin condition. And some of these wounds develop squamous carcinoma. So there is a mortality involved in the disease. But more recently, with a lot of these -- there is no treatment, but the universities and the centers of excellence, taking care of the wounds very carefully, they have been able to prolong life by a few years. But mortality is a big [indiscernible] of this disease. And what we essentially do is modify our HSV-1 vector, put it in the gene, a new copy of the COL7A1 gene, formulate it topically and apply it on to the wound. And when we do that, what we have seen today is the vector transfects the cells. It produces the required protein. It holds the skin together and heals the wound. The most important thing to realize is the half-life of collagen VII, not just in patients, but also in healthy individuals. It's about 30 days. So even in normal individuals, every 90 days or 120 days, and it varies by person, like your hair follicle, you have -- you need new collagen and which fits perfectly well with our approach of, you apply the gel, the wound heals. And maybe in 3 months or 4 months, you would start to see blisters and you would reapply the gel on an as-needed basis. That's kind of how we're thinking about this. There are some thoughts about doing something prophylactically for adults at some point. But the essence is to keep applying the gel that synchronizes with the wound healing and starting to blister again. In the Phase I/II, because it's a rare disease, these studies are relatively small, not just -- that's what the agency wants because it's debilitating and there's mortality involved. So you get about 10, 12 patients to figure out the frequency of your application, the dose because there's not that many patients, it's tough to recruit. We have a competitive situation with a couple of other companies in the space. And what we found in the 12 patients is -- and we had a classic design implying we had a placebo, the study was -- we were comparing wounds of similar anatomical nature and seeing how does these wounds get better and we found that when we think about complete wound closure, we separated really nicely from placebo. When I say really nicely, I mean statistically. Peter Marinkovich, my PI, recently at a conference presented the statistical analysis of Phase I/II. And what we found is when you think north of 75% wound closure, 75%, 90%, 100% wound closure, and what I mean by that is if your wound is 100% open, 90% implies that 90% would close because of the drug. So when I talk about 90% closure, I mean a wound that's fully open, it's about 90% closed. So when you look at our Phase I/II, and you think about 75%, 90% or complete wound closure, we separate really nicely from placebo. So we are, as you mentioned, close to starting a pivotal study with the design that's not materially different from the Phase I/II. And we -- if what we see in the 10 or 12 patients reproduces in 22 patients or so, then we have a drug that could potentially, is simple to administer, can be administered by a visiting nurse, health care provider, local doctor, the agency during the last few months has opened the door for us to do home dosing. There are a few -- the timing of home dosing is not tomorrow, but it's maybe in a few months, like 2 to 3 months. But home dosing really makes KB103 B-VEC a very -- because these patients with these wounds, as you can imagine, travel is not easy how these people. They don't like to -- sitting on a plane, delays, airports. There's a lot of burning and itching and pain. So to have someone come to your house or even at your local doctor's office, be able to administer the drug, a gel, which is painless, easy to imagine. And then every 90 days or so, you would see the wound being compromised and you would reapply on an as-needed basis.

I've got a couple of follow-up questions around this product opportunity. It's really intriguing, very exciting in terms of the product presentation, in particular. My first question just has to do with the competitive landscape. There are several other late-stage programs. And for those in the audience who don't know kind of the EB or the DEB competitive landscape, it looks as if there are multiple programs that are in late-stage clinical trials. So could you spend a minute just kind of doing a quick compare and contrast as to why you think B-VEC is well positioned amongst others that are in development?

Yes, I will. Yes. So look, the competition can be divided broadly into 2 categories. There's some of us who actually are working to treat the disease, meaning we try to fix the genetic issue. And there are a couple of companies who provide palliative approaches to mitigating the symptoms of the disease. So -- and this has been tried before too in the past, some kind of cream that relieves -- could be, it relieves your pain, your itch, maybe helps heal the wound temporarily for a couple of days, but basically relieving symptoms. So I'm only going to focus my conversation on those of us who are trying to fix the disease because the palliative side has got many precedences in the past. And it's been a really difficult disease to treat palliatively in the past. But in terms of fixing the disease, look, we're the only company, to the best of my knowledge, that has a direct approach of treating the disease where literally it's the same gel that's applied to any patient in kind of the confines of a home setting, which you can imagine how convenient it is for the patient. The -- there are 2 companies: one is Abeona, which has an autologous way of treating the disease. It's a graft that has to be generated from your skin and then surgically put back on to the wound. Our belief is, in a rapidly turning environment, the skin cells turn around pretty fast. It's tough for us to envision a one and done graft, meaning everything in the skin has to be replaced over and over again because of the -- there is nothing permanent about the skin. And so it makes it a bit more. Look, and it's tough for me to talk about any of my competition in any different kind of meaning because we don't have an approved drug in the market, right? There isn't one. So I'm just talking about what I think about. If the grafting appears to me to be a bit more cumbersome, a bit more demanding on the patient, a bit more having to travel to the university center, having to do it over and over again, a lot of things have to come together when you talk about an autologous approach. The patient has to visit, there should be no infection. There's all -- it's logistically complicated. The other company, and they, I believe, just started a pivotal study maybe early this year. I don't forget. I mean, if I remember right, in 1Q, Abeona announced it started its pivotal trial. The other company is FiberCell, which is also autologous, but instead of a graft, they have a cell-based, where they take some cells and modify them and bring them back. They also started pivotal apparently in 1Q. But both these companies have been in existence a lot longer than we have. I don't think they were materially different in their position when we kind of started as a company. So we've been good at moving fast in this space, a, given we're literally a gel that can be applied onto the wound. But those -- I mean, I'm sure there are some private -- I've heard of BridgeBio, which is making recombinant collagen VII, and that's just IVed into your body. And that's actually been done before by a company called Lotus Biosciences. And recombinant in my prior work experience, I found they are tough to make. And here, you need the protein to go exactly to the basement membrane zone to treat the disease. So when you IV it, you got to make sure that the toxicity doesn't make it go straight to the liver. So to be able to find every wound and be able to go to the basement membrane zone and produce collagen there is difficult. So those are the 3 approaches I know about at the moment.

Okay. Thank you for that review of kind of the landscape. I think one of the questions that we often are asked about gene therapy for skin diseases. And given the fact that this could be a drug for therapy that's going to be used repeatedly and chronically over time versus the traditional paradigm that most of us think about when it comes to gene therapy, which is the promise of potentially one and done. This is clearly a different application. I know it's early days. And -- but for those who are thinking about what the commercial opportunity looks like, maybe the one question I'll ask is, how should one be thinking about potential pricing? Or just how to think about cost of therapy for a year, given that it's going to be repeat dosing in all likelihood?

Yes. Yes, that's a great question. And we are -- with the hiring of Jennifer who used to head rare disease at Sanofi Genzyme, we're embarking on market access, talking to payers now, probably start a pricing study in a few months or so. And we'll have -- I'll have a much better answer to the question maybe end of this year, but here is what we have factually in this space. People are -- patients are spending or parents of patients if it's pediatric, people are spending about 300 -- at least $300,000 a year up in -- with palleted treatments. And the reason for that is, as I mentioned earlier in my conversation, centers of excellence have been able to prolong life by doing some kind of, like, watching the wound, taking care of it, making sure it doesn't get inflamed, antibiotics, anti-inflammatory, pain-soothing creams. And so the floor -- to some extent, we know that people are already spending about $300,000 or so per year. And then the question for Jennifer and the question as we go through our pricing study is how do we price? Because we could price by patient, we could price by dose, we could price by wound, there's a lot of ways to think about this. And no matter how you think about it, people with fewer wounds may either, make it, marginally benefit as people with more wounds? Or do you just have a normalized price per patient? Those are questions we will answer after talking to payers after doing our market research. But the only answer I have, Graig, at the moment is, I know what the burden, the financial burden of the disease is today. And that, to us, provides a certain kind of floor, especially in an area where mortality is involved, but there is no treatment. Everyone really wants a treatment for this disease. And I mean the payers want some treatment, which may sound surprising, but there is -- they know how -- the burdensome nature of the disease. The agency wants some kind of treatment for this disease. Of course, the patients and parents want, given how debilitating this disease really is. So I would say, look, that's where we're working towards of exactly to do it. We have a good existing burden of the disease to work with, and I will probably have a more -- a clearer answer sometime early next year once we have completed the pricing and the payer analysis, which are ongoing.

Makes sense. Well, thank you very much for at least providing that initial high-level view of how you think the value proposition could be. I would be remiss if I didn't bring up 2 recent pipeline developments that I think are very exciting for the company. You reported positive proof-of-concept data for a second candidate, that's KB105. And then separately, you also announced that, as you alluded to at the beginning of this call, expanding beyond dermatology-based diseases and going into lung disease. So perhaps, we've got maybe 6, 7 minutes left. If you could spend just a few minutes on those 2 programs and the reasons why you're excited about 105? And then separately, what you think the opportunity is for a gene therapy for cystic fibrosis using your approach?

Yes. So with respect to 105, that is a natural extension because we're using the same backbone. We're swapping up the gene of interest. It's topical. And so in terms of development time, development cost, the disease is a bit different. The burden of the disease is different. The frequency of application may be different, but it's the same approach. And with CMC behind us, when we go after rare skin diseases, whether it's 105 or 104, we feel that the path should get easier and easier only because the CMC, which is a big part of making it, scaling it, getting the agency to buy into it, is behind us. And so that's understandable [ easily ]. But if you step back and think about our approach, look, if we can get this modified vector with the gene close to a cell of interest, like an epithelial cell, especially for diseases where the gene is big and you cannot fit it in its complete form into any other vector, that provides a great opportunity for us to get into because that -- to at least look into. And so the CFTR gene is really big. If you strip out the introns and exons, we can code for the gene completely into the backbone. The vector seem to survive the nebulizer, especially in in in vitro, in vivo. So it gets to the epithelial cells in the lung. Once it gets there, we know that the vector is high transfection, it will transfect and it will -- what we're seeing in preliminary in vivo studies, not only what we think is good but we've gotten feedback from third parties who likely organize the Hub, which does the organize study for CFTR. And even the CF Foundation, the early feedback has been very positive. We know we're able to chronically administer. And so our thinking was such indications where the gene is big, where we can get the vector without any safety concerns. Of course, it's early days on cystic fibrosis. But even if one assumed Trikafta does a great job for a variety of mutations, there are no treatment for the null mutation. There is nothing today, and it's about 10%, 15% of the population. So we are -- our approach is to go after the null limitation. The studies would be smaller, the path would be faster. It's an unmet medical need. But if you deliver a full copy of the gene, you know you are not mutation-specific. Like it doesn't matter what mutation you have on the gene if you're delivering the whole copy of the gene. But our initial approach is to -- we have a safety study to do in primates, which will encompass most of this year. We have a G&P facility, so we could make the Phase I material in-house. And if all goes according to plan, our hope is to start the Phase I study sometime -- supply an IND sometime in the first half of 2021, and we've had the pre-IND meeting with the agency with respect to what we need to do. So fingers crossed, we still -- 80%, 90% of the company is still rare skin disease. That gravy train will progress slowly, maybe a disease or 2 every year. We are looking at [indiscernible], we're looking at HS, the mild-to-moderate hidradenitis suppurativa, where the mild-to-moderate segment is currently the biggest, treatment is not Humira, but surgery because of the systemic adverse events of Humira. So we're looking at -- so we have a 80%, 90% working on skin. But it will be nice to show the platform can go beyond skin. And if CFTR did were to work, it opens up areas like alpha-1-antitrypsin. It opens up a few indications where the gene is big enough that 1 cannot argue to take easily -- to easily take an AAV lenti approach.

It seems like based on your comments, there's a much broader potential for your platform. So I think that'll be a particular interest for us all over the next coming years. So best of luck there. Maybe with the last few minutes that we have together, I would like to ask you as it relates to cash, I think you just recently completed an equity capital raise, so congrats on the success of financing. With that said, can you just remind us what your current cash position is? And what your cash runway is projected to look like?

Yes. We have about $300 million or so in cash following the secondary, which was done not because we needed cash, but more as to take the COVID risk off the table, if anything were to happen next year or later this year with some kind of resurgence. This $300 million, honestly, puts us well into the second half of 2022 at the moment. And we're hoping by then and it's tough to time and say exactly, but by then, we're actually expecting 103 to launch. So depending on how well the launch goes or not. But just to talk in terms of finance, we're -- I think the cash runway position takes us the second half, June, July, August of 2022, and that includes some of the programs we're contemplating right now and the completion of the second manufacturing facility. But -- so it's good that we kind of -- we really -- there is no reason for us to raise money next year under any circumstance. When you get to the following and you get closer to the $100 million or below $100 million, hopefully, 103 launches by then, and we're all set. But that's kind of how we're thinking about.

And then my very last question, if you could just quickly summarize for investors, what do you think the key milestones upcoming for the company are and potential next catalysts?

Yes, yes. So a bunch. So we have pivotal study initiation shortly, and I hesitate to give you an exact time. We're trying to make sure that everything is right in place, and we don't have to start and stop a study, although things are opening up and looking nice. So initiation of pivotal. We also are filing an IND for an aesthetic indication, which will be in the clinic in the second half, hopefully once the IND gets okay. What we do with the aesthetic asset remains to be seen. We will also initiate a pediatric indication on KB105. Now that the adult indication is complete, that's just the natural progression. So we have 3 clinical studies are coming this year. Going at -- so if you look at -- there is a chance that one or more of these, at least the 105 may readout end of this year, if not at least early next year, depending on timing and COVID and all that. So early next year, we have a bunch of clinical readouts. All 3 of the studies I just mentioned. Then we will have 407 going into the clinic, hopefully, which is for cystic fibrosis. And also the second -- the next rare skin disease. So we have 3 to 5 programs at various stages in the clinic. So it's much of an operation -- clinically operationally exciting year for Krystal.

Okay. Well, that was very comprehensive. Clearly, a lot of news flow you're expecting for the company. With that, we're at the end of our fireside chat. But Krish, thank you so much for joining us today, best on success with your next 6 to 12 months. And thank you to the audience for joining us. So thank you very much.

Thanks. Thanks, Graig. Thanks for having me.