Good morning and welcome to the Inozyme Pharma INZ-701 update call. I would now like to turn the conference over to Stefan Riley, Senior Director of Investor Relations and Corporate Communications, Inozyme Pharma. Please go ahead. Good morning, and thank you for joining us for the review of top-line safety and efficacy data from our ongoing phase 1/2 clinical trials of INZ-701 in adults with ABCC6 deficiency and ENPP1 deficiency. Today's remarks will be followed by a question-and-answer session. Please dial in via telephone to participate. Before we begin our formal remarks, I would like to point you to our forward-looking statements disclaimer. Our speakers from Inozyme today are Dr. Doug Treco, Chief Executive Officer and Chairman of the Board of Directors, Dr. Yves Sabbagh, Chief Scientific Officer, Dr. Kurt Gunter, Chief Medical Officer, and Dr. Matt Winton, Chief Operating Officer. As you listen to this call, we recommend that you access the webcast in the Investors section on our website. I would now like to turn the conference over to Doug. Please go ahead. Thanks, Stefan. I'm delighted to share important top-line results from our trials of INZ-701 in adults with ABCC6 and ENPP1 deficiencies. Additionally, our natural history studies have revealed critical insights into the significant unmet need among children with ABCC6 deficiency. We've invited two experts, Dr. Joyce Liao from Stanford Medicine and Dr. Zulf Mughal of Al Jalila Children's Specialty Hospital in Dubai, who will respectively speak about retinal disease and pediatric stroke in ABCC6 deficiency. We will also provide a brief overview of our ongoing efforts to identify pediatric patients with ABCC6 deficiency and outline our future clinical and regulatory strategies for INZ-701 in this population. We're excited to report that the phase 1/2 trial of INZ-701 in adults with ABCC6 deficiency successfully met all study objectives. In this trial, we investigated the potential for INZ-701 treatment, a recombinant ENPP1 enzyme replacement therapy, to lead to disease modification. We have previously reported positive pharmacodynamic and safety data. For the first time today, we're reporting improvements in vascular pathology, visual function, and patient-reported outcomes, which are suggestive of clinical benefit in these patients. Our natural history studies, which focus on children with early-onset disease, combined with other information, identified stroke and retinal disease as consistent features of ABCC6 deficiency. Using advanced medical record search tools, we were able to identify a substantial pediatric population that is at high risk for stroke and vision loss. Armed with this information, we plan to approach regulators with a plan to gain accelerated or conditional approval based on a measure that is predictive of ischemic stroke. Turning to ENPP1 deficiency, we've completed 48 weeks of INZ-701 treatment in our three twice-weekly dose cohorts. We continue to see a favorable safety and immunogenicity profile, with most patients essentially antibody-free at week 48. The once-weekly dose cohort showed the expected PK profile and supports the use of weekly dosing in our ongoing pediatric pivotal trial and future studies. Moving on to the core of our agenda, I'll remind you that ABCC6 deficiency is mostly understood as an adult disease known by the name of pseudoxanthoma elasticum, or PXE, characterized by progressive calcification of elastic fibers, which cause a unique skin phenotype and which also provides the origin for the name. As shown in the right-hand panel, patients also suffer from progressive arterial calcification that leads to stroke and other neurological disease, cardiovascular complications, and mobility impairment, as well as severe retinal calcification that progresses to geographic atrophy and vision loss. At the other end of the age spectrum, infants born with ABCC6 deficiency suffer from severe arterial calcification, pulmonary hypertension, heart failure, and high mortality. Infants with this condition, termed generalized arterial calcification of infancy type 2, or GACI type 2, present similarly to infants with ENPP1 deficiency, known as GACI type 1, and we plan to treat those babies as part of our ongoing ENERGY-1 study. In the middle is what we believe is an overlooked population of children with biallelic or monoallelic mutations in the ABCC6 gene. We conducted a retrospective natural history study where we collected the medical records from nine children with early-onset disease and diagnosed with GACI type 2. Our findings, combined with literature review and physician experience, uncovered a heavy disease burden highlighted by a high risk of stroke, neurological complications, and severe ophthalmologic disease. We now have evidence for a substantial at-risk pediatric population and are planning an interventional study in these patients. I'll also remind you of the therapeutic hypothesis for the use of INZ-701 in ABCC6 deficiency, which is shown here. ABCC6 moves ATP from the inside to the outside of cells, and defects in this transporter lead to levels of extracellular ATP that are 40%-50% below normal. Calcification and intimal proliferation arise due to low levels of PPi and adenosine, respectively, as we also see in ENPP1 deficiency. The resulting arterial stiffness and blockage leads to vascular disease. In contrast to ENPP1 deficiency, we are not providing the missing enzyme to patients with ABCC6 deficiency. Instead, we aim to increase levels of circulating ENPP1 through administration of INZ-701 to maximize the utilization of lower levels of ATP and generate sufficient pyrophosphate and adenosine. Our data from preclinical models and, as you will see, adults with PXE support this hypothesis. I will now turn the presentation over to Kurt Gunter, our Chief Medical Officer, who will discuss our study of INZ-701 in adults with ABCC6 deficiency. Thank you, Doug. This was a dose escalation study conducted in adults with PXE. Patients were required to have biallelic ABCC6 gene variants, but there were no other patient enrichment selection criteria. The goal of the study was to assess safety and tolerability, immunogenicity, pharmacokinetics, or PK, and pharmacodynamics based on plasma PPi levels. We also evaluated several secondary endpoints for future study planning. Patients were given a single subcutaneous dose of INZ-701, followed for a week to establish the PK profile, and on day 8 began dosing twice per week. Before we turn to the study data, I would like to briefly review the patient demographics. Patient ages ranged from 29-67 years and included six female and four male patients. All the patients were white. Based on past medical history and baseline data, the patients had a heavy disease burden. Although there were no selection criteria for eye disease, all patients had ophthalmic disease and serious cardiovascular disease at baseline. INZ-701 showed a favorable safety profile, one of the study's main goals. Much of this information was presented in our last update in September, and we have not seen any new safety signals since that time. As we previously shared, one patient was withdrawn from the 1.8 milligram per kg cohort due to moderate urticaria. We took this action out of an abundance of caution and believed this patient could have remained on treatment and easily managed in clinical practice. Another patient withdrew due to personal reasons, not due to an adverse event. Because of the early withdrawals, we have 48-week follow-up data on eight patients. Those eight patients remain on INZ-701 home administration, with seven on self-administration for over 631 days. In conclusion, we are very pleased with the favorable safety profile of INZ-701 observed in adult patients with ABCC6 deficiency. Now I will ask Yves Sabbagh, our CSO, to review the immunogenicity profile and PPi pharmacodynamic data. Thank you, Kurt. Overall, we observed a favorable immunogenicity profile. We measured antidrug antibodies, or ADA, based on dilution titers, with higher titers reflecting greater ADA concentration. Low ADA titers were detected but were not neutralizing, as there was no effect on PK or PPi levels. Eight of the patients had detectable ADA, and the highest titers in individual patients ranged from less than 40 to 2,560. There was no evidence of a relationship between dose and ADA titer. There is evidence of waning of the immune response, as three patients with low ADA titers during the study had no detectable ADA at last follow-up. Interestingly, out of the eight patients that have been followed for 48 weeks or more, five had undetectable or unquantifiable ADA at last follow-up. These ADA titers are generally lower than those observed with some other approved enzyme replacement therapies, as shown here. In conclusion, although ADAs were observed, they had no apparent clinical impact. Now I will be showing you the PPI levels using our validated assay. The black symbols represent samples collected after the first dose. Yellow symbols are pre-dose or trough samples. The majority of the patients had low PPI levels at baseline, as shown by the red symbols. INZ-701 was able to increase plasma PPI within 24 hours after the initial dose, and the plasma PPI levels rose to the normal range, as represented by the green-shaded area in the phase 1 portion at the 1.8 milligram per kilogram dose. This PPI increase was sustained in the phase 2 portion of the trial, as shown on the bottom graph. This clearly shows that the 1.8 milligram per kilogram dose, we had sustained PPi in the healthy volunteer range through 428 days and was significantly different from baseline at week 48. I would like to remind you that most of the PPi values shown are trough levels taken prior to dosing of INZ-701. PPi is therefore expected to be in the normal range transiently in the phase 2 portion at the lower doses, which may still provide a clinical benefit. These results demonstrate that INZ-701 increases plasma PPi into the normal range, and these levels were sustained, which we were very pleased to see. I will now pass it back to Kurt to go over the clinical data. Kurt? Thank you, Yves. We assessed the effect of INZ-701 on the cardiovascular system using carotid intima media thickness, or CIMT, measured by ultrasound. This slide shows a longitudinal section of a carotid artery imaged using ultrasonography. The inner layers of the arterial wall, known as the intima and media, are shown in the magnified box outlined in yellow. Thickening of the carotid intima media leads to narrowing of the artery's lumen and abnormalities in blood flow. CIMT can be easily and precisely measured using ultrasonography. We performed CIMT in all patients using a standardized protocol, and images were analyzed at a central center by qualified radiologists. CIMT is a predictive marker for cardiovascular disease and stroke risk in the general population. In a recent meta-analysis, reduction in the rate of progression of CIMT by as little as 10 microns per year was found to be associated with a reduced risk of both cardiovascular disease and stroke. The figure on the left shows CIMT progression with age. As you can see, CIMT progression is faster in PXE patients, shown in red, compared to the general population, shown in black. At baseline, eight of the 10 patients in our study had abnormally thick CIMT measurements. In a published study, the Treatment of Ectopic Mineralization in PXE, or TEMP study, PXE patients received etidronate and were compared to PXE patients receiving placebo for vascular calcification, CIMT, and other parameters. The placebo patients in the TIMPS study showed a CIMT increase of 20 microns per year, while in our study, patients receiving INZ-701 had an average decrease in CIMT of approximately 4 microns over 48 weeks. Three of the eight evaluable patients had reductions in CIMT, and only one patient showed a CIMT increase in excess of the average increase observed in PXE patients in the TIMPS study. These data suggest that INZ-701 may potentially arrest or reduce CIMT progression in PXE patients. We also assessed the impact of INZ-701 on retinal structures. We used optical coherence tomography, or OCT, to measure choroid thickness. We studied the choroid because it is an important tissue that supplies blood and oxygen to the retina. Choroidal defects, or thinning, may be associated with retinal degenerative changes. Importantly, the choroid is thinner in patients with PXE than in the general population. We used standardized OCT procedures and transferred images to a central center. Our choroid thickness was assessed by two different qualified readers, measuring choroid thickness immediately subjacent to the fovea, as shown here. As shown on the left, choroid thickness is lower in PXE compared to the general population and tends to decrease with age. On the right, looking at baseline data from all patients in our study, we see a similar, relatively strong correlation of choroid thickness with age. This suggests our study population is comparable to the general PXE population and supports the use of choroid thickness measurements in our study. We found that, on average, choroid thickness increased with INZ-701 therapy. The mean increase in choroid thickness across all evaluable patients was approximately 10 microns. Looking at individual eyes, there was an increase in choroid thickness in 12 of 16 eyes. One patient in cohort 3 experienced a decrease in choroid thickness following a grade 2 vitreous hemorrhage following an ocular injection. These data indicate that systemic administration of INZ-701 increased choroid thickness in PXE patients. We assessed patient visual function using the global score from the Visual Function Questionnaire, or VFQ-25. The VFQ-25 is a vision-focused patient-reported outcome measure, which was developed at the US National Eye Institute and was designed for patients with chronic eye disease. The VFQ-25 consists of a 25-question survey assessing various aspects of visual function, including near vision, distance vision, driving, color vision, peripheral vision, and other domains. The subscores from the different domains are averaged to generate a global composite score. Scores above 90 are observed in the general population, and changes by more than 5 units are considered clinically meaningful. As shown on the left, in our study, six patients were below 90 at baseline, and four of those six improved. One patient in cohort three experienced a decline in the VFQ-25, and that may have been associated with a grade two vitreous hemorrhage experienced after an ocular injection. As shown on the right, we also noted that the global VFQ-25 score improvements were greater in older patients. These data indicate that systemic INZ-701 administration stabilized or improved visual function over a 48-week period. We further analyzed the relationship between VFQ-25 score and choroid thickness. Four of seven evaluable patients improved on both choroid thickness and VFQ-25. Together, these data indicate a correlation between VFQ-25 and choroid thickness, which indicates that both parameters are indicative of improvement in eye function following INZ-701. We measure the overall health of patients using the global impression of change, or GIC, patient-reported outcome. As shown on the bottom of the slide, the GIC is a 7-point scale rating the patient's overall health, ranging from -3 to +3, with a score of +3 being very much improved. At each visit, both the patient and the clinician are asked to rate the patient's health compared to baseline using the GIC scale. Here, we plotted the individual GIC scores across the 3-dose cohorts, with the clinician's assessment in the top half of the slide and the patient's GIC assessment in the bottom half. In the clinician's assessment, nine of nine evaluable patients improved from baseline, and in the patient's assessment, seven of nine evaluable patients reported improved overall health relative to baseline. Patients in all cohorts showed improvements in GIC scores, and improvements were sustained throughout the study. Importantly, both the clinician and patient independently assigned similar scores, providing further validation of the clinical outcomes revealed in this trial. Although the data as presented so far are compelling, we would like to present a case study to illustrate the profound impact that INZ-701 treatment had on a study participant. This patient suffered from a substantial disease burden, which included PXE with multiple retinal hemorrhage, gastrointestinal disease, hypertension, nephrocalcinosis, and multiple soft tissue and arterial calcifications. PPi increased with INZ-701 treatment, as it did in all participants, and translated to the clinical improvements noted here. There was a good improvement in both the GIC and PROMIS patient-reported outcomes. CIMT decreased by a mean of 10 microns. Average choroid thickness increased by 0.75 microns. VFQ-25 increased from 71 to 80, a clinically meaningful improvement. Finally, there was no evidence of progression of arterial calcification or nephrocalcinosis by low-dose CT. This is only a single example of the therapeutic benefit of INZ-701 in patients with ABCC6 deficiency. Now I would like to turn back to Doug to provide key takeaways from this study. Thanks, Kurt. In conclusion, we enrolled an unselected adult patient population with biallelic ABCC6 variants and heavy disease burden. Importantly, there was a rapid and sustained increase in PPi observed at the highest dose. CIMT generally decreased or stabilized with INZ-701 treatment, indicating improved vascular function, whereas untreated PXE patients in a different study increased by 20 microns over a comparable time period. Choroid thickness increased, suggesting a beneficial effect on retinal disease. Data from a subset of patients not discussed here showed halting of progression of vascular calcification. The choroidal thickness and CIMT findings, together with preclinical data, suggest a favorable effect of INZ-701 on the vascular system in patients with ABCC6 deficiency. We observed evidence of clinical activity based on the GIC and VFQ-25 patient-reported outcome questionnaires. We believe these findings support additional clinical studies in pediatric and adult patients with ABCC6 deficiency. And now I would like to introduce Dr. Joyce Lau, Professor of Ophthalmology and Neurology at Stanford Medicine, to share an overview of retinal disease in ABCC6 deficiency. It is such a pleasure to talk with you today on pseudoxanthoma elasticum ocular manifestations and vision loss. As you heard earlier, PXE is a syndromic condition that involves multiple organs. In particular, there is eye, blood vessel, and skin involvement, leading to vision loss, vascular compromise such as strokes, and skin abnormalities. Skin is externally most obvious and involved early. However, vision loss is actually what impacts patients the most due to its impact on the activities of daily living. Disease, unfortunately, progresses relentlessly. It starts early, in early childhood, often the first decade, and everyone progresses over time. Unfortunately, eye is involved in essentially 100% of patients, leading to significant visual disability and sometimes blindness. The severity of vision loss and visual impairment can affect multiple aspects of our daily living. This is measured using a very well-established standardized scale called the National Eye Institute Visual Functioning Questionnaire. Now, this is something that has already been investigated in PXE patients, and it measures things like general vision, general health, then activities like driving, and it could affect aspects such as social function and mental health, ultimately affecting the quality of life. In particular, the vision impairment in children with PXE is particularly devastating. This is because they are affected in every aspect of their development, including impacts on education, their psychosocial well-being, and decreases future potential, as well as increases the risk of morbidity and mortality. Let me go over the different eye findings in PXE with you. In stage 1, PXE presents as a discoloration in the back of the eye. We see the eye through our retina, which works like a camera. What you see here is basically the back of the eye turning into an orange peel-like appearance because of the calcium deposition. On the left is a PXE eye versus on the right a healthy eye, and you can see the difference in the texture. Even though at this stage you can see these changes, it is possible that vision is still terrific. That's because of the smoldering effect of the disease progression that then, over time, can suddenly affect vision. In stage 2, you have greater changes in the back of the eye in sometimes what's referred to as angioid streaks. So these are what's pointed in the yellow pointers are as cracks in the Bruch's membrane, a layer in the back of the eye, as a result of further deposition of calcium. They often can form around blood vessels as well. You can see on the left is a color photo of the inside of the eye, and on the right is autofluorescence imaging, which looks grayscale. You can see the cracks in the Bruch's membrane in both types of imaging modalities, making it very easy to visualize. You also see changes on the optic nerve head. These are lumpy-bumpy appearances due to deposition of calcium concretions on the optic nerve head. Optic nerve is the only connection between the eye and the brain, and so any interruption of this information highway from the eye to the brain can lead to visual impairment or sometimes blindness. On the autofluorescence imaging, you can see these optic disc drusen deposits looking like white, bright spots, showing where the calcified deposits are located in the optic nerve head. In the higher stages, in stages three and four, you get vascular abnormalities and neurodegenerative changes. There may be hemorrhages as a result of these abnormal blood vessels leaking and breaking. There may also be atrophy of the back of the eye, so that the camera, which works to capture the visual information in the eye, is no longer able to function. This is when patients can have sudden and severe vision loss, sometimes blindness. The PHENODEX scale is a global scale for disease severity in PXE, which includes eye findings. There are two different slight variants of this scale, but essentially they're similar in that they go over the different stages. In the first decade, there may be changes without any abnormality, such as the peau d'orange appearance or discoloration of the retina that I described earlier. In stage two, you have angioid streaks, where there are calcifications leading to cracks in the Bruch's membrane that we talked about earlier. In stages three and four, are the vascular events and the degenerative changes. So as you can see, the different disease stages of PXE and how it affects vision are actually quite quantifiable and quite visible on a traditional eye exam or eye imaging. As a result, we could quantify these changes over time. And in this study, and also in the Inozyme PXE study, we have found that there is a clear progression of disease over age. Or another way of thinking about it is, as there are longer times that the disease process has had to manifest itself, such as through older age, you get worsening of the scale, as you can see here. The most important thing for our patients is to detect this disease as early as possible, ideally before vision loss or other symptoms occur, so that we could intervene early using novel therapies, which you'll hear about today, and so that we could save vision before they're lost. This is another study looking at the decrease in visual acuity, which is a measurement of central vision with age in patients with PXE. Essentially, the black boxes are vision in the worst eye. In the first few decades, you can see relatively good visual function as measured by central vision. Then over time, you could see the central vision worsening. The vision impact of the central visual acuity is one of the most devastating things in patients with PXE. As we talked about earlier, because there is a progression over time in essentially 100% of patients, the possibility of vision loss is by itself having a huge impact on the quality of life and emotional well-being in PXE patients. Another way that others and Inozyme have investigated these changes in the retina is by segmenting a layer of the blood vessels called the choroid. This is an illustration of how we could use a technology called optical coherence tomography to segment the choroidal layer, which is a vascular layer, just under the retina. You can see that the thickness and the blood flow in the choroid also changes over time, so that the defect in the blood flow worsens in PXE much more dramatically than normal aging. In summary, the eye is an excellent biomarker to monitor the treatment effect of INZ-701, a novel therapy for treatment of PXE patients. In terms of the eye findings, I want to emphasize that the PXE eye changes occur in the first decade of life, very early. However, patients may not manifest as vision loss until later. However, they all progress over time, leading them to a possibility of a future of visual impairment or blindness. As a result, early diagnosis is important. Eye imaging and evaluation are non-invasive and can directly visualize the disease process. Treatment with INZ-701, which increases pyrophosphate levels, has the ability to decrease this progressive ectopic calcification in the eye and in the body. So our goal is to save these patients' vision and to decrease or mitigate the devastating effect of visual impairment. Thank you for your attention. Thank you, Joyce. Now, we would like to present top-line data from our recently completed natural history study of the early-onset form of ABCC6 deficiency in pediatric patients. This was a multicenter retrospective natural history study performed by chart review after obtaining informed consent. Patients were required to have genetic verification of biallelic ABCC6 variants, and the primary objective was to obtain information to support the design of a future study in patients with the early-onset form of the disease. Moving to demographics, there were nine patients with early-onset form of ABCC6 deficiency. The median age was 12.5 years, and the ages ranged from four to 16 years. The patients were split nearly equally between males and females, and the population included four white and two Black or African American patients. Patients with early-onset form of ABCC6 deficiency suffer from a high incidence of major clinical events very early in life. This slide shows the approximate times of important medical events with age on the vertical axis on the left. The age at the time of informed consent is shown by the gray vertical bars. In addition to the nine patients with ABCC6 deficiency from the retrospective natural history study, we have baseline information from three additional patients with ABCC6 deficiency from our prospective natural history study. Two of them are shown here, patients A and B. Stroke events are shown with red dots. 10 of these patients had a history of GACI type two, as would be expected. Note that there were five strokes in these 11 patients. In addition to these five strokes, there are two with cerebral arteriopathy who have not yet had a stroke but are at risk for this severe complication. Therefore, of the 12 ABCC6 deficiency patients we have included in our natural history studies, seven of them have had strokes or are at risk of stroke. Strokes appeared at an early age, prenatally in 1 case, and all before the age of five years. Strokes in these patients were severe, resulting in seizure disorders, paresis, and significant disability. The incidence of severe cardiovascular disease is also noteworthy. This information indicates that pediatric patients with ABCC6 deficiency who survive GACI 2 are still at risk for major morbidity due to their disease. In conclusion, pediatric patients with ABCC6 deficiency suffer from a heavy disease burden. We observed high rates of disabling stroke and cardiovascular disease. Stroke may occur very early in life, even prenatally. Cardiovascular disease is severe, considering the young age of the patients. Renal disease occurs secondary to arterial stenosis and nephrocalcinosis. Retinal disease occurs but was not systematically screened for in this population. We believe that interventional studies in these patients are justified, given the medical need, lack of treatment options, and positive data from INZ-701 in adults with ABCC6 deficiency. Now I will ask my colleague, Matt Winton, our COO, to provide additional color on the pediatric population with ABCC6 deficiency. Thanks, Kurt. In addition to the high rates of stroke observed in our natural history study, we have identified several published case reports of children with ABCC6 mutations presenting with severe cerebrovascular disease, evidence of vascular stenosis, and arterial calcification. We've also been in contact with several physicians who are currently managing the care of these patients. One such physician, Professor Zulf Magal, is overseeing the care of two children with ABCC6 deficiency, and it is now my pleasure to introduce Dr. Magal, who will present the medical history and clinical outcomes of these patients. Good morning, everyone. I'm Zulf Magal. So this morning, I'm going to talk to you about a couple of patients with ABCC6 mutations that I cared for when I was in Manchester, England. This is my disclosure slide. So the proband is a female who is now 14 years old. I met her in 2014 when she was about three and a half years old. She was born to non-consanguineous parents who are of a different ethnic origin. Her pregnancy, perinatal period, and development were all normal up until her presentation to hospital. Before she came into hospital, she developed signs and symptoms of an upper respiratory tract infection like a common cold, and then at presentation, she had weakness of the right side of her face, which was diagnosed as Bell's palsy. Unfortunately, things progressed rapidly thereafter in that she developed recurrent bouts of transient ischemic attacks progressing to full-blown strokes. She underwent extensive investigations. I'll start with genetic analysis. At the time, the next-generation sequencing pediatric stroke panel yielded a negative result. She then had genetic testing for ENPP1 mutations, and no mutation was found. Then our genetic colleagues arranged for targeted exome sequencing for DNA, and she was found to be heterozygous for a mutation in ABCC6 gene. So basically, this girl had generalized arterial calcification of infancy or GACI type 2 caused by secondary to compound heterozygous mutations in ABCC6 genes. Talking more about her clinical picture at the time, her skin was normal, so she did not have the classical plaque-like lesions that one often sees in adults with pseudoxanthoma elasticum caused by biallelic mutations in ABCC6 genes. We undertook a detailed ophthalmic examination, and she did not have angioid streaks. Her blood pressure was slightly raised. Cardiac function showed moderate degree of left ventricular hypertrophy, but her heart itself was structurally normal. Interestingly, her ultrasound scan of the kidney showed bilateral nephrocalcinosis, which is this sort of white sort of shadowing that you see in the substance of the kidney, which is often reported in adults with pseudoxanthoma elasticum. Now, turning to neuroimaging, the proband had a non-contrast CT scan, which showed calcification shown as these white blobs of the right and the left internal carotid arteries. On the MRI scan, again, there was stenosis or narrowing of the internal carotid arteries bilaterally. She went on to have angiography, which again showed this narrowing, which was previously shown on MRI scan. But more importantly, there was this collateral vessel starting to develop. During the phase of the angiography, you could almost see the Moyamoya-type puff of smoke appearance. These are collateral vessels which are developing distal to the stenosis. Some 2 years later, unfortunately, due to recurrent strokes and reduction in blood flow caused by calcification and near-intimal proliferation, which occurs in vessels, she lost a huge amount of brain tissue. So the brain now has these big ventricles and very little brain left here. So this poor girl ended up being severely disabled. You can see that she went on to develop severe scoliosis, the curve in her spine. There's a nasogastric tube in situ to provide feeds because she was unable to feed spontaneously. On the left here, you can see a dislocated hip. So she ended up basically very severely disabled and became a wheelchair user. This is a summary of the problems resulting from recurrent strokes. As I mentioned, she became very disabled. She developed asymmetric spastic quadriparesis. Due to impaired swallowing, she had to have a percutaneous gastrostomy tube sited. She was registered blind, had seizures which were often very difficult to control, severe scoliosis, and subluxed left hip that I mentioned, and this subluxed left hip contributed to chronic pain. Now, the rest of the family was screened for ABCC6 mutations, and her brother, who is currently 12 years old, was found to have inherited the same mutations as the proband. At the time when I saw him, which was about five years ago, his skin was stretchy, but he did not have features of pseudoxanthoma elasticum. The imaging of his brain, just like his sister, showed moderate bilateral narrowing of internal carotid arteries shown on the MRI scan here, and the CT scan showed calcification of both internal carotid arteries and ophthalmic arteries. His heart was normal. As opposed to his sister who had widespread nephrocalcinosis, he had echogenic areas of microcalcification in the cortex of his kidney. ABCC6 mutation is characterized by low serum levels of inorganic pyrophosphate, which is an important biomarker of ENPP1 deficiency, whether it occurs due to ABCC6 mutations or ENPP1 mutations. So with the help of Professor Rutsch in Germany, we measured the brother's inorganic pyrophosphate levels, and it was really unmeasurable, zero as shown here, as compared with 2 control samples. So confirming that his ABCC6 mutations were associated with very low or, in fact, unmeasurable levels of inorganic pyrophosphate. Another metabolite which is important to measure is adenosine, which causes near-intimal proliferation. Unfortunately, that is difficult to measure and was not readily available. So at the moment, this boy remains well, and I last saw him during my visit to Manchester in December last year. He's carefully monitored by the neurovascular multidisciplinary clinic team members. He has annual MRI scans of the brain and the CT scans every couple of years. The current plan is that if he develops transient ischemic attacks or any signs of stroke, then he will be considered for revascularization surgery. However, he's an ideal candidate for enrollment into trial of ENPP1-Fc or INZ-701 replacement therapy because this, as we know from adult studies, helps to restore inorganic pyrophosphate levels in patients who have been treated up to now. The goal of this treatment would be to prevent future cerebrovascular events or ischemic strokes. So from my point of view, the main take-home messages are that mutations in ABCC6 cause significant morbidity in children. We know about ABCC6 mutations causing pseudoxanthoma elasticum, a condition that starts in adulthood affecting the eyes, the skin, and blood vessels. The other important issue which I've sort of touched on with regard to the proband's brother is who, in my opinion, has a ticking time bomb in his head. There is a substantial unmet need in the pediatric ABCC6 deficiency patient population. And finally, ABCC6 and ENPP1 mutations should be included in genetic analysis of children who present with ischemic stroke or severe cardiovascular defects. Thank you very much for listening to me, and. Thank you very much for listening to me, and I'll be happy to answer any questions. Thank you, Dr. Magal. As awareness of our clinical program has increased, so too has the number of requests from physicians seeking potential solutions for their ABCC6-deficient pediatric patients. Notably, in these patients, physicians describe a cerebrovascular pathology that is consistent with the findings from our natural history study and the case study of the two siblings that Dr. Magal just presented. Recognizing the significant unmet medical need, our efforts shifted to understanding the prevalence in this important pediatric population. The genetic prevalence of ABCC6 deficiency is well documented and estimated to be 1 in 25,000 to one in 50,000. Conservatively, this suggests approximately 30,000 patients across our key regions of interest. Assuming, on average, 25% of individuals in these geographies are between 1 and less than 18 years of age, we estimate a genetic prevalence of around 7,000 pediatric patients globally, with approximately 1,900 in North America and 1,700 in the United States. However, in this case, our focus extends beyond the genetic prevalence to the number of pediatric patients presenting with severe neurological, retinal, and/or cardiovascular disease. To address this and gain deeper insights into the phenotypic prevalence of this disease, we engaged with key opinion leaders, talked to physicians who are currently treating these patients, met with patient advocacy groups, attended medical conferences, reviewed electronic health records, and worked with genetic testing organizations and medical claim consultancies. Additionally, in response to a high number of unsolicited requests, we are setting up a limited early access program to gather some initial data on this population. Now, I would like to spend a few minutes talking about one of these key initiatives: a comprehensive longitudinal assessment of US claims data. The results of the study have helped us identify symptomatic pediatric patients, provided insights into the timing and presentation of clinical events, and pinpointed the healthcare providers involved in their care. Through careful inspection of the relevant symptomology, diagnosis codes, and commonly utilized procedures, we created detailed selection criteria that allow us to identify ABCC6-deficient patients between one and less than 18 years of age from US claims data with a high degree of confidence. Following a rigorous test-and-learn approach, we established four mutually exclusive patient groups designed around hallmark symptoms and procedures associated with these pediatric patients. These four groups are ischemic strokes, angioid streaks, retinal imaging by OCT, and cardiovascular anomalies. All identified pediatric patients with suspected ABCC6 deficiency were clinically profiled and evaluated against defined exclusion criteria, as well as a control cohort of over 100,000 patients matched for age, gender, and differential diagnoses. No projection factors were used to identify additional patients that were not already captured in this claims database. Across these four groups, we identified approximately 1,300 pediatric patients, or about 70% of the expected genetic prevalence in the United States. Distribution is roughly evenly split between genders, with slightly more males in the retinal imaging OCT group and slightly more females experiencing stroke and cardiovascular anomalies. Angioid streaks and retinal imaging were more common in older pediatric patients, while stroke and cardiovascular anomalies were observed at a higher rate in younger patients. Given the severity of symptoms, high unmet need, the identified number of highly likely patients in the US, and the expected patient numbers in other regions, we are enthusiastic about advancing the clinical development of INZ-701 for pediatric patients with ABCC6 deficiency. Our comprehensive analysis of the US claims data instills confidence that future clinical trials in this population can be enrolled promptly and that this patient population represents an important and viable rare disease market opportunity. I will now pass it back to Kurt to discuss our clinical development plans for pediatric patients with ABCC6 deficiency. Kurt? Thank you, Matt. Based on data from our adult clinical study, our natural history studies, and information Matt has just shared, we are planning to conduct a future pivotal study in pediatric patients with ABCC6 deficiency. This study is still in the planning stage and is subject in part to discussions with regulatory agencies. We would like to enroll pediatric patients at risk of cerebrovascular disease and follow the progression of cerebrovasculopathy by imaging or another surrogate endpoint. This would be a randomized study, and after an appropriate on-treatment time period, we would transition all patients to INZ-701, and they would be followed long-term for clinical outcomes. We are planning to initiate this study in the first quarter of 2025. We are now working with key opinion leaders and other experts to finalize the study's design and look forward to sharing more details with you in the future. Put it all together, our development plan in ABCC6 deficiency looks like this. We have completed enrollment and 48-week follow-up of the phase 1/2 clinical study in adults, which we have presented today. We are planning to add a GACI type 2 arm to our current INNERGY1 study to allow treatment and generate data from these newborns and infants with no effective treatment options. We plan to conduct a randomized study of pediatric patients at risk of stroke, as we just discussed. This study would be designed to support an accelerated approval and conditional marketing authorization. In addition, we will maintain INZ-701 treatment for all consenting patients who complete all studies and follow them long-term for safety and clinical outcomes. We believe that learnings from the pediatric randomized study, supported by our internal and collaborative research efforts, will inform the future adult treatment strategy. That concludes our discussion of ABCC6 deficiency. Now, I would like to transition to an update from our study of INZ-701 in adult patients with ENPP1 deficiency. Our phase 1/2 study in ENPP1 deficiency is a dose escalation study conducted in adults with confirmed biallelic ENPP1 gene variants. The goal of this study was to assess safety and tolerability, immunogenicity, PK, and pharmacodynamics based on plasma PPi levels. Patients were given a single subcutaneous dose of INZ-701 and then followed for a week. On day 8, patients began dosing twice per week. We have now completed enrollment of Cohort 4, which is testing once-weekly dosing of INZ-701, and we'll be focusing on PK and pharmacodynamic data from this cohort today. We are pleased to report that the safety profile of INZ-701 remains favorable in adult patients with ENPP1 deficiency. 7 of 13 patients experienced mild adverse events related to INZ-701. Mild injection site reactions occurred in 5 of 13 of the patients. There were 2 serious adverse events, but these were not related to INZ-701. No adverse events led to discontinuation of INZ-701, and 11 patients continue to receive INZ-701, and 10 of those have now transitioned to self-administration. Patients from Cohort 1 have now been receiving drugs for almost 800 days and counting. In conclusion, we are very pleased with a favorable safety profile of INZ-701 observed in adult patients with ENPP1 deficiency. Now, I will ask Yves to review the immunogenicity profile, PK, PPi pharmacodynamic data, and some patient-reported outcome data. Thank you, Kurt. We also observed a favorable immunogenicity profile in this clinical trial. The data is represented in the same way as the adult ABCC6 deficiency trial was shown. Low ADA titers were detected but were not neutralizing, as there was no effect on PK or PPi levels. 11 of the 13 patients had detectable ADA, and the highest titers in the individual patients ranged from less than 40-2,560. Again, there was no evidence of a relationship between dose and ADA titer. There is evidence of waning of the immune response since three patients with ADA titers ranging from less than 40-160 had no detectable ADA at last follow-up. Interestingly, out of the eight patients that have been followed for 48 weeks or more, six had undetectable or unquantifiable ADAs at last follow-up. These ADA titers are much lower than those observed with other approved and then replacement therapies, as shown here. In conclusion, although ADAs were observed, they had no apparent clinical impact. Now, I will be showing you the PPi levels of the first three cohorts using our validated assay. As predicted, the patients have really low plasma PPi levels, as shown by the red symbol. Same as before, the black symbols represent samples collected after the first dose, and yellow symbols are pre-dose trough samples. We were pleased to see that INZ-701 increased plasma PPi within six hours after the initial dose, and the plasma PPi levels rose into the normal range and remained sustained through the phase 1 and phase 2 portions of the trial in all three cohorts. I've just shown you the updated PPi data for all three cohorts. We are also happy to report that the significant decrease in serum FGF23 levels in Cohort 3 that we have previously reported is maintained through week 48. Bone biomarker response remained consistent with restoring proper bone mineralization to improve bone pathology. Favorable responses on the PROMIS and global impression of change patient-reported outcome measures were maintained across cohorts, which I will show you on the next slide. We plan on presenting all these data in detail at an upcoming scientific conference. We measured the overall health of patients using the global impression of change, or GIC, patient-reported outcome. The scale shown at the bottom of the slide is similar to what we just described for the ABCC6 deficiency trial. In the clinician's assessment, 6 of 8 evaluable patients improved. 1 patient did not have a clinician's GIC reported. In the patient's assessment, 7 of 9 evaluable patients reported improved overall health relative to baseline. Patients in all cohorts showed improvement in GIC scores, and the majority had improvements that were sustained throughout the study. Importantly, both the clinician and the patient independently assigned similar scores, providing further validation of the clinical outcomes revealed in this trial. Now, I would like to briefly go over data from Cohort 4, where we tested 1.2 milligrams per kilogram once-weekly dosing. INZ-701 was able to increase plasma PPi within 6 hours after the initial dose, and the plasma PPi levels rose into the normal range and remained sustained through day 56 with once-a-week dosing regimen. The PK and ENPP1 activity data from Cohort 4 showed consistent drug exposures and comparable to 0.6 milligrams per kilogram twice-weekly dosing, with a slight increase in drug accumulation with 1.2 milligrams per kilogram once-weekly dosing. These data confirm our previous assumptions based on the previous modeled PK data that once-a-week dosing has the potential to increase PPI. I will now pass it back to Doug for closing remarks. Doug? Thanks, Yve. In conclusion, we've completed 48 weeks of INZ-701 treatment in our three twice-weekly dose cohorts. The once-weekly dose cohorts showed the expected PK profile, which validates our model and supports the use of weekly dosing. We continue to see a favorable safety and immunogenicity profile, with most patients essentially antibody-free at week 48. Pyrophosphate remained elevated from baseline and within the normal reference range with long-term treatment. The mechanism of action of INZ-701 is supported by increased PPi levels and improvement in serum phosphate and FGF23 levels. The bone biomarker responses are consistent with restoring proper bone mineralization. The favorable response on clinical outcomes was maintained, although we did not share these data in the interest of time. Based on the encouraging results from this study, we are conducting additional clinical trials in infants and older pediatric patients. Turning back to ABCC6 deficiency, we're excited to report that the phase 1/2 trial of INZ-701 in adults with ABCC6 deficiency successfully met all study objectives, and for the first time today, we're reporting improvements in vascular pathology, visual function, and patient-reported outcomes, which suggests clinical benefit in these patients. Our natural history studies, which focused on children with early-onset disease, combined with other information, identified stroke and retinal disease as consistent features of ABCC6 deficiency. Using advanced medical record search tools, we were able to identify a substantial pediatric population, which is at high risk for stroke and vision loss. Armed with this information, we plan to approach regulators with a plan to gain accelerated or conditional approval based on a measure that is predicted of ischemic stroke. With that, we will now open the line for questions. Operator? We will now begin the question and answer session. To ask a question, you may press star then 1 on your telephone keypad. If you're using a speakerphone, please pick up your handset before pressing the keys. If at any time your question has been addressed and you would like to withdraw your question, please press star then 2. At this time, we will pause momentarily to assemble our roster. The first question comes from Tazeen Ahmad with Bank of America. Please go ahead. Okay, great. Thank you. Good morning, and thanks for taking my questions. I have a couple on ABCC6. Your plan to add an arm to the INNERGY1 study to add data from infants, what information do you think will be helpful to obtain from that study, and do you think you'd need to have additional patients beyond what you plan on studying in order to get a label inclusive of infants? And then secondly, when you talk about the pediatric study at risk of stroke that you would think you could get an accelerated approval, how would that work in terms of seeking approval for the overall ABCC6 population? Should we assume that pediatrics would launch before adults? And then I have another follow-up. Thanks. Okay. Hi, this is Kurt Gunter. Thanks for the question. I'll take the one on the GACI2 patients first. The important data that we want to get from those patients will be changes in PPi, of course, and also, importantly, survival. We'll also want to measure calcium scores on those patients by doing low-dose CT to check their overall vascular calcification levels and other ectopic calcification. We would analyze them separately from GAC1 patients in the same study. Did I answer your question? Yeah. And by how much does that increase the patient population, including infants? In that particular study, we're now planning in that study to have eight patients with GACI1 and about half that many patients with GACI2. Got it. But how does that impact the adjustable patient population at launch? It'll be a GACI 2, will probably be a small portion of our addressable population at launch. Okay. Thanks. And then on the pediatrics study regarding accelerated approval, should we assume that pediatrics would launch before the rest of the adult population for ABCC6? Yeah. I think that our focus is on the pediatric population. We think that's really the push that we want to make with regulators. We're generally optimistic, though, that the data that we've collected in adults would feed into our application and potentially would allow us to get a broad label that would include pediatric and adult patients as well as infants. So I think the need to do another adult study is still being debated. Okay. Thank you. Then maybe one if I may on PPi, how are you thinking about the dosing regimen of weekly versus biweekly as you've collected data so far? We generally think that we'll be using a weekly dose. And ultimately, we plan to develop a flat dosing for adults that would be a single dose in milligrams for all adults in the adult population. So that's our plan moving forward. And that in ENERGY-3, the study that we're doing and the typical study that we're doing in pediatric patients, that is a weekly dose of 2.4 milligrams per kilogram weekly to account for the faster metabolism in children. Okay. Thank you. The next question comes from Doug, excuse me, from Marc Frahm with TD Cowen. Please go ahead. Hi, this is Alex on from Marc. Congrats on the data, and thanks for taking my questions. Just a couple for me. First, could you just comment briefly on the degree of inherent variability associated with the imaging techniques that you use to measure CIMT and choroidal thickness, and maybe how that could have potentially affected the current results and ultimately those of the pivotal ABCC6 study? And then second, could you also just clarify where the efficacy bars are for the imaging and clinical endpoints in ABCC6? More specifically, what are KOLs and regulators kind of wanting to see as clinically meaningful changes, both for CIMT and choroidal thickness as well as vascular event rates and visual function? And then does that potentially differ in pediatric versus adult populations? Thanks. Okay. Hi, this is Kurt Gunter. Thanks for the question. I'll try to answer that. So we actually focused on CIMT measurements and choroidal thickness measurements because of the precision of the measurements. And in fact, I believe our standard deviation for our CIMT measurements was on the order of 2 microns. So it was very precise. I can't speak to the precision. I don't have the numbers on standard deviations for the choroidal thickness, but I do know when we looked at the two different observers on choroidal thickness and plotted them separately, they were almost superimposable. So it's a very, I think, precise and reproducible measurement. Now, you also asked about what the standards of approval would be for these two parameters. And for choroidal thickness, we think it's certainly a good measure of clinical activity of our product. Whether it would be actually an endpoint for approval is yet to be determined, and we would want to discuss that with regulatory authorities. Looking at more recent approvals for agents that are used for geographic atrophy secondary to macular degeneration, rates of improvement or rates of lesion growth have been used to improve those agents. We note that geographic atrophy also occurs in PXE. That could potentially become an ocular endpoint for us. Regarding CIMT, as we mentioned in the presentation, a reduction of 10 microns per year results in reduced rates of stroke and cardiovascular disease. We think that could be a potential benchmark for an approval with that particular endpoint. I hope I answered all the points in your question, but if not, let me know. Nope, that was very helpful. Thank you. The next question comes from Chris Raymond with Piper Sandler. Please go ahead. Thanks. Just a couple of questions. I guess maybe first and foremost on the vision measures you're using, VFQ-25, I know that's a comprehensive measure, but just maybe kind of curious, why not use standard visual acuity tests? I've gotten a few questions from investors. I think folks are just generally used to looking at letters gained, lost, etc. Maybe talk a little bit about that from a clinical standpoint. And then also on the dosing, I don't see any mention of work on a q-weekly dose in ABCC6 patients. Are there any plans there maybe to harmonize that dose schedule between the two, or is it even necessary? And I have a follow-up. Okay. I'll take the question about visual acuity. So we actually did collect, if that's correctly, visual acuity data in the study. And I'll abbreviate that as BCVA if you don't mind going on. So as Dr. Liao presented, BCVA doesn't generally deteriorate until the fifth or sixth decade in patients with PXE. And we had a relatively wide age range in our study. So today, we focused on the VFQ-25 because we felt it would capture aspects of PXE retinal disease that appeared earlier in life. But here, I'll just summarize, if you don't mind, the BCVA data verbally. So at baseline, 8 or 10 patients had abnormal BCVA. And the worst was a patient who could not read the top row of a Snellen chart and whose vision was limited to counting fingers at one foot. We got VCVA follow-up data on 7 patients, and 2 of those 7 improved on VCVA. Looking at those 2 that improved, one went from a VCVA of 20/200 to 20/40, and this was associated with an 11-point increase in the VFQ-25. And then the other patient improved from 20/32 to 20/20, and this was associated with an essentially stable VFQ-25. It was a -1 change, technically, at the end of the study. And nobody had a decrease in VCVA during the study. So that's our VCVA information. Do you want to take the dose question, or would you like me to handle that? No, you can do it. Okay. So the dose is we want to look at flat dosing. That's something that we're planning to do. In fact, we're planning a study in the future that will incorporate a fixed dose for all adults. And we'll be giving you more information about that in the future. I don't know if there's much more I can say. Our models indicate that flat dosing or fixed dosing will provide exposures in adults equivalent to what we get with 1.8 twice a week. And so that's what we plan to do. Okay. Thanks. And then maybe just on the ABCC6 patient identification efforts, you guys have gone through great lengths to look at patients. You've done some patient estimates, etc. But any plans for a registry sort of in parallel to ENPP1 efforts? Yeah. Hi, Chris. It's Matt. Good question. So our current patient registry that we launched this year will accept ABCC6 patients with infantile onset. So as the registry continues to get up and running and sites gets on board, we'll be collecting pediatric ABCC6 patients through that registry as well. Good. Thank you. The next question comes from David Nierengarten with Wedbush Securities. Please go ahead. Hi. I had another question on the potential pediatric ABCC6 study. Because the pediatric patients seem to already have significant or frequently have significant carotid narrowing on presentation and diagnosis and things like that, I guess how are you thinking about getting the baseline for the patients and the placebo group here given the variability in presentation and that it's a rare disease? Like Dr. before presenting the siblings, I mean, obviously, you had very different outcomes to date. Obviously, the brother is still at risk of stroke and such. But I'm just curious, how do you control for that, and how are you planning to size the study properly to have a placebo group and such, and how that feeds into the recruitment and time to conduct it? Thanks. Yeah. Hi, David. This is Doug. So our hypothesis is that we want to do this under controlled circumstances, but we can't do it for 3 years or 4 years. And we know that the strokes and eye progression that children have are going to take longer than a year study. So our plan was to follow them for a year using an imaging metric predictive of stroke, and there are many out there that could be used that we're contemplating right now. And then after a year, switch everybody back switch everybody to drug and then monitor them against a natural history population assembled from various sources, including patients in our registry. We think it's going to be a reasonably sized trial, and we think that the heterogeneity within the patients should be generally addressed by the size of the population. So we believe that although, as you point out, there's heterogeneity in symptoms, if you actually look, the fact that these children are all having strokes before 5 years old, they all have calcification in the eye at a very early age, I mean, there is a fair amount of homogeneity within the population too that we think. So we think the study will be large enough to account for any heterogeneity. And I would also point out that we've looked at a lot of these images, and they all look very similar with this constriction in cerebral arteries. And so we think that is homogeneous enough that we're going to be able to get a good data set out of it. Okay. Thanks. The next question comes from Joseph Stringer with Needham & Company. Please go ahead. Hi. Good morning. Thanks for taking our questions. Just a quick one on PPi. It looks like in the biweekly dosing, I think it was in the 1.8 mg per kid group in ABCC6, it looks like had one time point that was a little bit above the healthy level. Just curious, is that something that you think would be mitigated with once-weekly dosing, and what's the risk of sort of seeing a spike in PPi levels? And then follow-up for Dr. Lau, just curious if you can comment on some of the improvements that we've seen with 701 and ABCC6 patients, specifically on the VFQ-25 and the choroidal thickness. What's your take on this and clinical meaningfulness, and what could this mean for patients? Hi. This is Doug. Joyce, if you heard the question, I'll let you answer that first. Sure. Thank you for your question. In terms of the VFQ-25, as was pointed out earlier, improvement or change in five points is considered clinically significant. And the amount of change, I think, it will not depend on the VFQ-25 by itself. As you heard earlier, the best-corrected visual acuity, those two improvements are really astonishing, actually, going from 20/200 to 20/40 and then going down to 20/20 in one patient. So the combination really is the most important. The choroidal thickness improvement and, at the minimum, stabilization is meaningful, but that, as an endpoint, will have to be discussed with the FDA. So overall, for vision trials, we typically measure quite a few different modalities, usually a combination of disease-relevant visual endpoints, lifestyle modifications, and imaging modalities, which are relatively objective compared to the other two. So I feel confident that the kind of changes that we already have so far in a small study will likely be quite promising for the future clinical endpoints for PXE. Thank you. Thank you, Joyce. And thanks for the question on the PPi. This is Yves Sabbagh talking. So yeah, we did see a spike, and it's actually a spike in one patient only. But again, just to remind people, there's alk phos or TNAP. That's in these patients that's working normally, so it would try to prevent the continuous. This is a single time point. We're not concerned about this at all. But to your point, yes, once-weekly dosing will still lead to the proper drug exposures but should not have an impact on spikes like this. But this is just one sample out of many that we saw the spike. So we're not concerned about that at this point. Great. Thank you so much for the color and thanks for taking our questions. Again, if you have a question, please press star, then one on a touch-tone phone. This concludes our question-and-answer session. I would like to turn the conference back over to Doug Treco for any closing remarks. Thank you. Before we sign off, I want to extend our deep appreciation to the patients who participated in our studies. These were challenging studies, and their perseverance helped make the study successful. Thank you all for listening in today. I hope you all get a chance to enjoy the solar eclipse this afternoon.