Okay, I guess we're live. All right. Welcome, everyone. I'm Tiago Fauth. I'm a biotech analyst here at Wells Fargo. I'm joined today by Inozyme. I have Matt from the team here for a fireside chat, and we'll just work through some questions. Generally, I'd like to start with an overview on the company. So again, can you give us, like, the two-minute introduction- Sure. to Inozyme, and then we'll kind of piece it apart? Yeah, no, perfect. So thank you again for having us. Of course. It's been a fantastic conference so far, and we appreciate everybody's interest here in Inozyme. So we are a clinical-stage rare disease company that's focused on disorders of mineralization. They're really driven by the PPi-Adenosine Pathway. So we're working on two genetic diseases and a third disease, which is a complication of end-stage kidney disease, all which involve a similar mechanism of action and pathogenesis, which is calcification of the vascular system as well as intimal proliferation and also effects on bone health. Got it. Perfect. And again, you're kind of addressing all of that with a single asset, INZ-701. So can you just kind of remind us what's the background of that asset, and how the company formed around that? Sure. So maybe we'll take a step back and sort of just kind of explain a little bit on sort of the PPi-Adenosine sort of pathway- Sure ... and how we developed the drug. So, ABCC6 is an ABC-ATP transporter, and that takes ATP from inside the cell to the outside the cell, and there's not a lot of reason to have ATP outside the cell. But one of the reason we think that's critical is to be cleaved by an enzyme called ENPP1 to form pyrophosphate, or PPi, and AMP. Now, PPi has been known for 50-plus years to be a potent inhibitor of calcification. So if you put calcium and phosphate into a test tube, and you add pyrophosphate, it'll precipitate out. If you remove the pyrophosphate, they'll form hydroxyapatite crystals, which is the building blocks of your bones and your teeth. That AMP then travels further down the pathway and gets cleaved to form adenosine. Now, adenosine is critical to maintain healthy blood vessels. It prevents sort of smooth muscle overgrowth in the lumen of the blood vessels and stenosis and intimal proliferation. Now, this drug, INZ-701, is the active domain of ENPP1 attached to an FC domain, so it becomes soluble. So this drug was developed out of Yale University initially to treat ENPP1 deficiency as an enzyme replacement therapy. So these patients are missing ENPP1, and therefore, they have low levels of PPi, which results in abnormal calcification of the vascular system as well as improper mineralization of the bone. And so initially, it was developed to treat ENPP1, to treat one disease as a pure enzyme replacement therapy. We have since kind of expanded that view, by looking at another related disease, with genetic mutations in ABCC6 deficiency. So although this isn't a direct enzyme replacement therapeutic approach, it's still basic enzymatic kinetics. If you have low substrates, right? If you have defects in ABCC6, you have low ATP, and therefore low PPI and low Adenosine. So if you have a low substrate, you know, what you do is you increase the amount of enzyme present to be able to scavenge and mop up all of the ATP to increase PPI, and Adenosine. And we've proven that therapy now in animal models, as well as recently reported data in our first-in-human studies. Calciphylaxis, sort of our third indication, has also had some ties to the PPi-Adenosine pathway. We know, patients with end-stage kidney disease have lower PPi levels than healthy subjects. Patients with calciphylaxis have even lower PPi levels than those with end-stage kidney disease, and those PPi levels track with severity of calcification. They track with lesion size in these patients, and they also, you know, are predictive of six-month mortality. So you get this sort of negative correlation with PPi, and disease severity. We also have some genetic data that suggests some polymorphisms in ENPP1, as well as CD73 can increase your risk for calciphylaxis. So by sort of taking this one sort of unique asset, that is sort of driven by a conserved, you know, biology or sort of pathology in these diseases, you know, we've now shown sort of proof of concept in animals and in humans that this one drug can be used across three indications. So we really look at this as sort of a pipeline and a product. And you know, it's built a robust sort of clinical development program at Inozyme. Perfect. And again, that's super helpful background, and we can get into the more detailed debate in ENPP1. I think let's start there. So to me, like again, the drug is doing exactly what it's supposed to. Like, the mechanism of action here is direct, super direct. So it does feel like from a biology perspective, probability of success should be fairly high for the ongoing trial. So let's perhaps take a step back and just talk about some of these end markets, right? So always challenging for rare disease markets. We know treatment options available, like how well identified those patients are, where they are, and so on and so forth. So can you kind of just give us a brief background on prevalence and patient identification initiatives? Sure. Um- ... Yeah. No, yeah, no, it's a great question, and I think it's one we get a lot, and I think it's one everybody asks when you talk about rare diseases. How many patients are really out there? How are you able to find these, you know, patients? And is this sort of a real kind of market? And we think, you know, the answer to, you know, all those questions is yes, and we've done a lot of work to identify these patients and to sort of start preparing for a successful commercial launch if INZ-701 is approved by regulators. So there's a genetic prevalence of ENPP1 is one in 64,000 pregnancies. And this is a number that was published by an independent analysis by some KOLs in the field, looking at the literature and case studies that have been published, looking at genomic population databases, and sort of definition and agreement on different variants in terms of are they pathogenic or are they likely pathogenic? And putting this all together and doing some, you know, basic sort of genetic analysis, this one in 64,000 is sort of the latest number for genetic prevalence. This is sort of a fluid number. I think, like with all epidemiology, as there's more in the literature, more case studies published, as more people are getting genetic tested and whole genome sequenced, and there's more genetic data available to analyze, you know, we think this number will be continued, refined, and improved and actually, you know, continue to increase. In terms of patient identification efforts, so we are doing a lot of activity to identify patients and, you know, continues to produce results. We're very fortunate to have a very experienced team leading our patient identification efforts. Most of them, if not all, have come from other rare disease companies, where they've identified patients, where they've built rare disease markets. And so we're benefiting from the likes of Genzyme and Alexion and, you know, what they've done in the past. This team, in sort of collaboration with some of our partners and folks in other countries around the globe, are out there every day, talking to doctors, going to medical conferences, doing disease education, mining claims data, helping with diagnosis, with trial recruitment. Now we're present in about 15 different countries across the globe, and what we've seen is the more time we spend in a country or a region, you know, the more patients we're able to identify, and I think that's the rare disease story. If you look across the board, be it Pompe, be it Gaucher, Fabry, Hunters, you know, the more awareness, the more improvements in diagnosis and the closer you get to an approved treatment, the more patients sort of come out of the woodwork, and the more patients that you're, you know, able to identify. So to date, we've identified over 1,000 diagnosed or, you know, suspected ENPP1 patients globally. And we're pretty, you know, proud of this number, as when we look at other analogs and other rare disease companies at their, you know, similar time point in their clinical development, you know, we think this number is greater than any analogs, you know, that we can find. We're also starting a patient registry this year, and this is something that's in partnership with the advocacy group, GACI Global, and so this will enroll both ENPP1 and ABCC6, you know, patients across all age groups, and so this will allow us to start, you know, formalizing kind of our patient identification efforts, to continue to identify more patients, you know, kind of build a pool of patients prior to launch, as well as start publishing on the natural history, and, you know, some data on sort of these patients', you know, journey. Another area that we're really focused on is genetic testing and newborn screening, so we have a lot of partnerships with private genetic testing companies to encourage, to support, different regions across the globe with genetic testing. As we know, that's critical for diagnosis of these patients, as well as newborn screening initiatives. You know, one initiative we're particularly proud of is with Genomics U.K., so many of you may know that they've launched a pilot program where they're planning to newborn screen one in every 12 babies that are born in the U.K., and typically with these programs, you know, they want an approved therapy before they add them to the panel, but through sort of lobbying with our KOLs and sort of the patient community, U.K. Genomics added both ABCC6 and ENPP1 to the panel out of their initial 200 genes, so out of the 200 genes, two of them are the diseases you know that we're working on. You know, we continue to spend a lot of, you know, time and resources on patient activities, patient identification activities, because I think a core competency of any- And to your point, like, I think the patients identify they're a significant chunk of the actual theoretical prevalence numbers, correct? Yeah, that's, that's correct. So we estimate there's probably about 10,000 patients in the key markets that we're interested in, and that is the U.S., EU, Japan, and Brazil. We also, you know, know of other patients in other parts of the world, in countries that can pay for a drug commercially, where we have clinical trial sites, where we're enrolling patients. And so we consider those upside. So we think this 10,000 number is a, a pretty conservative, you know, number. This number also only accounts for biallelic ENPP1 patients. So the more time we're out there identifying patients and talking to doctors, the more symptomatic heterozygote patients we're also identifying. And I think this is sort of consistent to other rare bone disorders like HPP or XLH, where there is some penetrance in the heterozygote, you know, mutations. So we think that's also a potential population, you know, expansion. And there's also some other diseases that have been shown, like OPLL or DISH, that have shown that a subset of these patients have heterozygote mutations for ENPP1, which is believed to be disease-causing. There we go. So again, kind of a typical playbook in rare diseases, but with a fairly advanced patient identification efforts, which is pretty appealing. Let's talk about clinical trials and data- Yep -generated so far. So yeah, I do wanna get into ENERGY-003 and some of the assumptions and what's underlying that, but let's kind of recap what you've seen so far in adult patients. I guess the focus for ENPP1 is gonna be mostly on the biomarkers, 'cause that should be a fairly predictive- Mm-hmm ... biomarker of clinical benefit, and it kind of addresses the root cause of the disease. But what are some of the key highlights from what you've seen so far in humans? Yeah. So, earlier in the year, we released some data in our adult study in ENPP1. It was a small study, but we were very happy with the results. So first and foremost, we showed that INZ-701 was safe and tolerable in these patients. We had a very favorable safety profile. We had minor or a couple patients that had some ADAs, but none of them were able to or were proven to be neutralizing. And overall, the drug was, you know, sort of well-received by patients. It's a subcu injection. We've shown the ability to rapidly increase PPi, which is sort of the critical enzyme that our drug kind of works on, in as early as six hours in many. It was sustained into the normal levels throughout the study. All of these patients have now rolled over to a follow-on safety study, and we're still able to maintain PPI levels into that normal range, which is where we think these patients need to be to see clinical benefit. We also saw improvements in biomarkers, specifically in bone biomarkers in these patients, both bone turnover and bone absorption markers, which we think is a positive sign for our pediatric trial in ENERGY-3, which we can get to. We also saw improvements in six-minute walk test. So, you know, small study, but we think it gives us confidence that, you know, this drug is showing signs of efficacy. And in a larger pivotal study in pediatric population, we should also see positive results. And let's talk about that, 'cause again, you have a slightly different primary endpoint- Mm-hmm Set for U.S. and EU. Can you talk about the ENERGY-3 trial design? Yep. 'Cause the question, the main question here is, like, how translatable are the data generated so far to ENERGY-3? And again, in the us, if I recall correctly, primary is the biomarker effect. Correct. So that feels like a relatively easy bar for pretty nice to achieve. Yeah. Is that fair? Yeah, I think that's fair. So we're very excited that regulators, you know, agree that PPi was a valid, you know, primary endpoint. It's always ideal to get harmonization between EMA and FDA. Sort of in this case, you know, the two agencies suggested different primary endpoints, but for... In our view, it's the same exact study, just the primary endpoint to the data will be analyzed a little bit differently. So kinda let me take a step back, and I'll walk you through the design of the trial, and we can talk about some of the endpoints. So ENERGY-3 is an open-label, randomized, pivotal study in pediatric patients from one to less than 13 years of age. And its goal is to look at the treatment of INZ-701 on both PPi levels and signs of rickets in these patients. So it's being run in the U.S., the E.U., and the Middle East. And so in the U.S., the FDA has agreed that PPi can be the sole primary endpoint, and this is now an endpoint that we've demonstrated the ability to impact positively in animal models and in humans in our adult studies. They did mention that, you know, they would like to see trends in our secondary endpoint, of which RGI-C scale, the Global Rickets Global Impression of Change scale, which is a scale that, you know, rickets from XLH and HPP, you know, derived diseases have used, so it's a well-known, approved endpoint by regulators. But they wanted to see trends, you know, in our secondaries, and we think that's normal for, sort of a- There's a lot. Pioneering, a reasonable ask. It's a new endpoint, you know, trends in the secondary is what we'd expect to be able to show. In the EU, they also wanted to see co-primary endpoint, so PPi or pyrophosphate biomarker as one endpoint, but they wanted to have the RGI-C, the Rickets Global Impression of Change, as a co-primary endpoint. But as our agreed-upon PIP, they are giving us a relaxed p-value of, you know, less than zero point two to the RGI-C scale. So we look at that for all intents and purposes either if it's trends or a relaxed p-value of point two, it's kind of the same outcome that, you know, we'd like to see. And you know, think that, you know, that's sort of an achievable, you know, ask by the agency. Yeah, and again, to your point, there are precedents for the endpoint. I guess Crysvita in pediatric patients- Yep ... feels very relevant here.... But, I'm curious how you guys thought about potential powering for that. The biomarker feels like it's gonna be fairly achievable, but what's the remaining risk just from a clinical trial design perspective? Yeah. It's a great question. So from a biomarker perspective, you know, we feel pretty confident. We've shown, you know, substantial increases in the biomarker. And in fact, if we actually powered the study on the biomarker, it'd be a very small number- Smaller ... of patients. Yeah. Right? And we didn't think that was appropriate, or regulators would accept that. We took maybe the unusual approach of powering the study on the RGI-C endpoint. Despite that, it was a secondary in the U.S., and a co-primary in the EU with the reduced p-value. We powered the study on the RGI-C at a p-value of 0.05. We used Crysvita as an analog. To go into a lot of our statistical, you know, calculations, we use similar effects and similar deviations that they saw in their trial. Remember, we're powered at a 0.5 p-value, and we only need a 0.2. Point two. Yeah. Point two. Yeah. So I think that's how we kind of adjusted for some of the risk not having used this endpoint in these patients before. We've also, with the RGI-C, although the bones of the scale, no pun intended, but the framework, I should say, of the scale, is the same. It's a seven-point scale. You know, you look at an X-ray at the start of the study, and then at the end of the study, you look at the same X-ray. A blinded team of reviewers looks at them and rates them on a seven-point scale, zero being no change, you know, minus one, minus two, minus three being worsening, plus one, plus two, plus three being improvement. And so we developed our own RGI-C scale for ENPP1. We worked with an academic group that this is sort of what they do, and through our natural history studies, took all of the X-rays that we've had in children, and analyzed them and said, "These are the rickets areas within ENPP1, where the bone sees deficits." That's how we built sort of the scoring manual, the training manuals, and, you know, the blinded reviewers will, you know, determine the score based on those selected areas. There's just two points I do wanna mention. One, we talked about these bone biomarkers that we saw in the adults, the bone resorption, bone turnover biomarkers. Yeah. The bone in children is much more of a dynamic environment. Kids are growing, bone is turning over a lot faster. So, you know, you can hypothesize that if you saw a positive impact in an adult, you would expect to see, you know, a greater impact in children, where you see a bone that has, you know, much more life to it and is growing and turning over a lot faster. So the fact that we saw positive results in our adult study, you know, give us confidence that, you know, we should see an amplified in the peds. You know, the second is, you know, Crysvita and, you know, Strensiq- Strensiq ... which are two drugs that have been approved using the RGI-C score, and so this also gives us confidence that rickets is a treatable, you know, disease, and you can determine effects of efficacy, you know, on rickets using the RGI-C, you know, score, and so, you know, all those sort of points together, you know, give us confidence, you know, to move into the pivotal study, ENERGY-3, you know, using the endpoint. Yeah. But to me, that makes a lot of sense. What's the latest in enrollment and timelines to get to that data point? Yeah. Enrollment is open and going well. It's in full swing. We have active sites now in the us, the EU, and in the Middle East. Enrollment has, you know, picked up greatly over the last couple of months, and so the team continues to work hard, and is excited to get enrollment, you know, fully done, within the next couple of weeks, and we're looking forward to, you know, starting the clock on sort of the treatment period, which will be- Data second half. ... a year-long. Yeah, a year-long kind of period, so hopefully, we'll have data by, the, you know, back half of twenty twenty-five. Got it. And again, between now and then, you also have the ENERGY-1. That one is a little trickier just because it's an infant patient population, less literature, less known, a little harder to establish what the bar is for a- Mm ... successful readout, however you wanna frame that. So how should we frame that? Yeah. So ENERGY-1 is our infant study. And so this is a single-arm, open-label study in infants from zero to less than 12 with biallelic forms of ENPP1 deficiency. And in this study, you know, it's primarily looking at safety and tolerability in this infant population, but it's also really gonna help us determine what dose is appropriate for our pivotal study, ENERGY-2, which we plan to start by the end of the year. And so in addition to safety and tolerability, which are the primary endpoints, we're also looking, you know, at PPi levels. We're looking at growth and development. We're looking at functional performance, cardiac function, hospitalization, healthcare resource utilization, as well as some biomarkers for mineralization and bone. These are very sick babies. The mortality rate is about 50% at six months. And so, you know, we're excited to sort of generate enough data here to give us confidence to move into pivotal trials. But you're right, since it's an open label study, we keep getting asked, you know: So what are you seeing? What's the data? How do you sort of, you know, kind of put into context. So the impact you're seeing, you know, in this population. And so, you know, we agree. We've been enrolling in the study for a little while now, and, you know, we wanna share, you know, all of that data, as well as some data from infants, from our Expanded Access Program. Now, these are infants that were too sick to travel or were not located near a clinical trial site, and were qualified and maintained all the requirements for our EAP program. And so, we'll share some of that data as well. But that speaks just how difficult of a population this is. They're very sick babies. Most of them, unfortunately, are fighting for their lives, right, when they're born. They end up in the NICU, and not everybody can be, you know, born at a Partners Harvard Hospital or Children's Hospital Philadelphia, right? So identifying these babies, getting you know the hospitals to understand sort of what the disease looks like, which can be identified by the second trimester, by a sonogram, you can actually see the calcium deposits light up in these babies, and you know allow us to get treatment early is critical. We've also been working with the agencies to develop some protocols to allow us to start treatment early at you know the home hospital of the baby, and then transfer them to a clinical trial site to you know allow for immediate therapy. And we're also looking to bring mothers to hospitals to give birth where appropriate so we can initiate treatment immediately. Perfect. And, again, we spent a lot of time talking about- Yeah ENPP1, but that lays the groundwork, I guess, for ABCC6. So much larger theoretical addressable market here. Little bit more of an indirect- Mm-hmm mechanism of action, but again, all within the same pathway. So can you just kinda walk us through what the numbers look like from patients identified, the actual addressable market here, and then we'll talk about the regulatory path forward? Yeah. So, you're correct. You know, ABCC6 is a little bit of a larger market. The prevalence estimates are around one in twenty-five thousand to around one in fifty thousand. But it's also a much more developed market. We know of, you know, centers of excellence in Europe and throughout, you know, the us that have three, four hundred, you know, patients, you know, under management. It's very well known in sort of its adult form, you know, called PXE, or Pseudoxanthoma elasticum, which is sort of named based on one of the... a skin phenotype these patients develop. They get calcification of the elastic fibers in the skin in addition to sort of calcification of the whole cardiovascular system. And so that creates kind of a loose sagginess, and that's how it's usually first identified in adolescents and adults. But, you know, these patients end up losing their vision because they get calcification of the Bruch's membrane of the retina, so majority of them end up going blind. They have severe cardiac dysfunction, a lot of peripheral arterial disease, intermittent claudication, a lot of pain, lose the ability, you know, to walk, as adults. Interestingly, the babies in ABCC6 are almost identical to the babies in ENPP1. And you really can only tell the difference by a genetic test. And, you know, usually, you know, you can see the calcification throughout the aorta, throughout the vascular system, and until those genetic tests, it's hard to tell if it's an ENPP1 or ABCC6, you know, baby. For us, you know, our ENERGY-1, we actually have two arms in the study, one arm that treats ENPP1 and one arm that treats ABCC6, because they're a very similar target in terms of, you know, maternal-fetal medicine, in terms of the neonatologists, and so we can treat them. We announced earlier this year that our next study in ABCC6 is gonna be in this in-between population, in this pediatric kind of population, which was sort of misunderstood or not really focused on, you know, by the community until, you know, we started getting involved in doing some natural history studies and doing some, you know, work to better understand this population. These kids are presenting with more of a neuro-cerebral phenotype. These are kids that are having strokes, they're having calcification of the carotid arteries, seizures, as well as sort of a cardiac impact on the disease. So, you know, we think this is a population that's, you know, primed for treatment with INZ-701. You know, if we can use our drug to benefit, you know, a pediatric population that has high unmet need and no approved therapies, I think that's where we'd like to start first. No, that makes sense. Yeah. Again, I guess the question that you guys probably get all the time, like, you do see a lot more variability at baseline for PPi. Yeah. Some patients are actually a little closer to normal range. So having just a biomarker as a primary endpoint might be kind of a tall ask. Mm-hmm Just because that might actually be a difficult endpoint, so what is the regulatory plan as of now, and how have been regulatory interactions with FDA? Yeah. So, yeah, we completely agree, right? Right. I think you're spot on. We don't think PPi or biomarker is the right endpoint for ABCC6. Just to put into context, PPi levels in these patients are about 50% to healthy individuals, compared to ENPP1, which is more like 10%, you know, to healthy individuals. These patients also have a wild type ENPP1, right? So it's not as direct, right? And so we think it's- it is not, you know, an endpoint that regulators, you know, will approve as a primary. Definitely, one we'll have in our trials, you know, as, as a secondary, you know, endpoint.... So, you know, and we want our next study, you know, which is still subject to sort of review by regulators, which we're, you know, planning to meet with by the end of the year, and we'll share publicly once, you know, we get confirmation from the regulators. But we want that study to be in pediatric ABCC6 patients who have a history of or a risk of cerebrovascular disease or cardiovascular, you know, disease. Initially, we thought the best way to do this was through imaging endpoints or a surrogate endpoint, which are the endpoints we used in our adult study. Looking at vascular pathology by CIMT or sort of cardiovascular through, and optic disease through choroid thickness and cardiovascular disease, looking at calcium imaging, you know, in the body, and so the more we spoke to experts about this, the more we sort of looked deeper into the literature. Although there's lots of data in adult patients, and there's lots of data on these surrogate markers in like diseases like Moyamoya, there wasn't a lot of data in the pediatric population, and that's the population we want to run the trial on. So we thought that was a little risky, maybe too risky to sort of go in, which not having a great sense of what the variation in some of these endpoints could be or, you know, what a clinical meaningful result in a pediatric patient could be. And, you know, the more we looked at, can we extrapolate from adults or what about from like diseases? We just couldn't get comfortable, you know, with that. Thought that was too much risk to the program. So in collaboration with a lot of our experts and KOLs in the space, you know, we've aligned to sort of look at more harder clinical endpoints. Look at endpoints, you know, and and clinical events like stroke, like MI, like hospitalization, like death in these patients, and to have a sort of a composite type of endpoint on those harder clinical endpoints. We think that gives us a better chance of success to take to regulators and to prove efficacy of the drug. And I'll just mention, in our natural history study in ABCC6 pediatric patients, the number of patients that had strokes were sort of upwards of 40%, and ones at risk had, you know, severe cerebral angiopathy. So they already were starting to see stenosis in some of their cerebrovascular system. So those were at risk of stroke, and others had MI. We think, you know, this population and using a harder endpoint approach is probably a better way to go. That's a very helpful slide- Yeah. You guys have on the deck about that specifically? Yeah. Um- Again, we're running out of time, but I do want to touch on calciphylaxis. Yeah. Just because, again, that one is just a little harder to, again, understand exactly what a successful readout would be on that one. So I'm assuming that phase 1 data, it's going to be fairly exploratory. Mm-hmm. But again, directionally, what are we looking for in that readout? Yeah. So Calciphylaxis is a third indication. We have a phase 1 trial ongoing, and it's not in calciphylaxis, it's in patients with end-stage kidney disease. Yeah. We started in that population for a couple of reasons, and exploratory is the best, you know, word you could use. This is our first population that does not have a genetic deficit that we are treating. This is a population that has high comorbidities and is undergoing dialysis, hemodialysis, three times a week. We want to see what the activity of our drug is, what are the properties of our drug is in this environment? Are we able to raise PPi the same levels that we saw in sort of the genetic diseases? Is it safe and tolerable in these patients? This data is gonna drive the next, you know, study, which will be in calciphylaxis patients, and we're planning to release data at Kidney Week at ASN on the phase 1 study in... I guess it's the end of October. Got it. No, looking forward to it. Yeah. Awesome. Last question. Yeah ... is cash and runway. I have to ask. Yeah. Check the box. Yeah. So, my CFO is in the room, so hopefully I get this right, and if I don't he'll correct me. But we have, you know, cash through the end of next year with $144 million in the bank. Got it. Perfect. And a few data points from here until then, so- Yeah. Awesome. That's perfect timing, I guess. Perfect. So again, I appreciate you guys making the trip and- Yeah ... joining us at conference. It was great. Appreciate it. Awesome. Thanks, everyone. All right. Thank you.